CLERKSHIP RECORD

Jawaharlal Nehru Technological University, Kakinada in

Partial fulfilment of requirement for the award of degree in

DOCTOR OF PHARMACY

Submitted by
D. HANUMA NAYAK (19CR1T0003)

PharmD V Year

NALANDA INSTITUTE OF PHARMACEUTICAL SCIENCES

SIDDHARTHA NAGAR, KANTEPUDI (V), SATTENAPALLI (M), GUNTUR
(Dt), ANDHRA PRADESH-522438
2023 – 2024
 NALANDA INSTITUTE OF PHARMACEUTICAL SCIENCES
SIDDHARTHA NAGAR, KANTEPUDI (V), SATTENAPALLI (M),
GUNTUR (Dt), ANDHRA PRADESH-522438

CERTIFICATE
This is to certify that Mr. / Mrs.___________________________________
bearing Regd no.__________________ is a student of ________ year in
_____________ department and he/she has collected______ patients data sheets
in the GBR hospital during clerkship for the academic year_____________.

The lab exam conducted on_____________

Signature of lab-in-charge Signature of H.O.D

Internal Examiner External examiner

 INDEX

S.NO: DATE NAME OF THE CASE STUDY PAGE.NO;

S.NO: DATE NAME OF THE CASE STUDY PAGE.NO;
 INTRODUCTION TO CLERKSHIP

MISSION:

To provide an experiential learning environment which will assist the students to

become confident caring ethical pharmacy practitioner with the ability to think critically and
apply their knowledge and skills in the best interest of their parents regarding individualized
pharmacotherapy planning, intervention and outcome evaluation. The clinical experiences we
provide will help students to enter their choice of clinical speciality, to continue successfully
in their lifelong learning and practice, to meet their responsibilities to patients and the society.

GOALS:

i. To develop a sufficient relevant, and experimental knowledge base to utilize

appropriate resources necessary to provide direct patient care regarding individualized
therapeutic planning, intervention and evaluation.
ii. To master the clinical skills necessary to assume accountability and responsibility for
therapeutic outcomes in the process of providing pharmaceutical care.
iii. To develop professionalism and interpersonal skills as a member of team of health
care providers, necessary for the provision of optimal patient care and pharmacy
services.

OBJECTIVES:

This clerkship/internship will help and prepared the students for their future
professional pharmacy practices. The details are mentioned below.

A. Management of disease state:

After successful completion of the clerkship, the student will be able to:
1. Take and record the patient history and record the findings of clinical
examination.
2. Interpret the information from the patient’s laboratory examination in
assessing the disease state(s) and reaching/ confirming the final diagnosis of
the patient.
3. Discuss the currently acceptable options of investigation and treatment for the
patient’s disease state based on the best evidence available.
4. Utilize information from 1,2 and 3 in formulating an individualized
therapeutic plan for the patient, which will include:
 a) Therapeutic objectives, with end point of therapy.
b) b. Pharmacologic and non-pharmacologic treatment
c) c. Follow up evaluation plan.
d) d. Evaluation of therapeutic outcomes
5. Discuss various therapeutic options with the patient as well as with the other
health care providers, if asked for.
6. 6. Discuss potential drug-disease, drug-drug, drug-laboratory test, and drug
dietary problems prior to making recommendations on drug therapy. These
recommendations will include:
a. Selection of drug or non-drug therapy
b. Dosage
c. Route of administration
d. Frequency of administration
e. Duration of therapy
f. Drug dosage adjustment consultation
B. Patient monitoring:
After successful completion of the clerkship the student will able to:
1. Monitor daily progress of the patient’s disease state and drug therapy based
upon relevant laboratory data, physical findings and consultation with
medical.
2. Identify existing or potential adverse reaction and/or treatment of failure,
provide assessment and recommend and abuses to assess their clinical
significance and to discuss potential solution
3. Utilize the medication history and patients medical record to identify drug
incompatibilities, and abuses to assess their clinical significance and to
discuss potential solution.
4. Apply pharmacokinetic dosing principal to dosing of selected drug and
monitor specific drug therapy
C. Patient chart/Data review:
After successful completion of the clerkship the student will be able to:
1. Demonstrate the ability to retrieve required information from the medical
record (paper or electronic) and assess patient specific information necessary
for drug Therapy monitoring. In that regard student will familiarize
him/herself with Regard to:
 a. Chart arrangement.
b. Specific type of information contained therein. For example,
admission Note history and findings from physical examination,
physician order, Laboratory results, progress note.
c. Medication administration record, diabetic management sheet and
progress etc
d. Medical abbreviation
2. Plan intervention based on the information retrieved, if asked for
3. Present the information in a concise and complete manner.
D. Laboratory findings:
After successful completion of clerkship, the student will be able to:
1. Recognize the significance of both normal and abnormal laboratory tests and
reports.
2. Interpret the lab findings regarding to the patient disease state in diagnosis
and follow up evaluation.
3. Utilize the lab finding in formulating the individualized drug therapy plan,
follow up evaluation and identifying the drug therapy problem.
E. Medication history:
After successful completion of the clerkship the student will be able to, obtain
through direct interview, a patient medication history to identify, prescription and
nonprescription usage, medication administration habits, procurement sources for
drugs, Compliance with prescribed therapy, and previous adverse drug reaction or
allergies.
F. Drug information:
After successful completion of the clerkship the clinical pharmacy student will Be
able to:
1. Apply skills related to utilizing the drug information resources to Answer
question related to drug use and toxicity.
2. Demonstrate the ability to retrieve, evidence-based drug information,
Critically evaluate and utilize when providing answer to a question.
3. Respond to drug information requests appropriately and in a timely Manner.
4. Communicate information verbally and in written.
G. Discharge medication counselling:
 Prior to counselling a patient, the student should have a comprehensive
understanding of the medication to be discussed, including the drugs indication,
mechanism of action, pharmacology, appropriate use and administration, storage,
common adverse effects and precautions. The students should review this
information with the preceptor prior to interacting with the patient
After successful completion of the clerkship the clinical pharmacy
student will be able to
1. Provide organized and individualized instruction to patient about their
disease and drugs prescribed to improve the patients understanding and
willingness to accept proper treatment.
2. Advice patients on proper utilization of prescription and nonprescription drug
including expected drug effects and potential drug drug, and drug-dietary
interaction warning, storage etc

ACTIVITIES OF THE STUDENT:

Each student will be assigned a preceptor and thus to a specific medical team and he is
expected to become an actively participate in patient care as outlined below:

1. Maintain rotating activist’s log, duly signed by the preceptor daily.

2. Attend daily rounds and morning meetings with the assigned medical team.
3. Attend the outpatient clinics related to his/her clerkships.
4. Monitor patients assigned by his/her preceptor
5. Meet your preceptor daily for any potential discussion which may include:
a. Giving informal oral presentation of assigned patients to your preceptor and
fellow students.
b. Providing daily updates on patient you have been following.
c. Reading material provided by your preceptor.
6. Conduct at least two patient interviews to obtain drug histories.
7. Maintain follow up of two patients at least at any giving time.
8. Conduct drug consultation in support with your preceptor.
9. Deliver any information about the drug, if the preceptor asks for it but don’t
volunteer or comment on any issues not asked for.
10. Attend clerkship meeting as per schedule given by the preceptor
 11. Attend all other activities scheduled by the preceptors, other than the above
mentioned.

MANDATORY AREAS OF ROTATION:

1. Hospital pharmacy
2. Internal medicine
3. Cardiology/ CCU/critical
4. Surgical, ICU and nutritional support
5. Emergency medicine
6. Ambulatory care
7. Haematology and oncology
8. Nephrology
9. Infectious diseases
10. Paediatrics

TEXT BOOKS/ REFERENCES:

1. Materials as assigned by preceptor or participating health care professionals

2. Robert j. cipolle, peter c. morley: pharmaceutical care practice the clinical guide
3. Behlid; pharmacy practice clinical manual, zed lippincot, 2002
4. Pharmacy clerkship manual by Ruth and Karen. Mc Graw-Hill, New York. NY, 2002
5. Dipiro JT, talbert RL, Yeege, matzkc GR, wells BG, posey LM, eds.
6. Pharmacotherapy, a pathophysiological approach, latest Ed.MC Graw-Hill New York.
 ROLES AND RESPONSIBILITIES OF PHARM D STUDENTS IN

CLERKSHIP

DEFINITION- CLERKSHIP:

Clerkship is an organized, directed, post graduate training program in a defined area of

Pharmacy practice, which is to be carried out under the supervision of a well-trained
preceptors Who have expertise knowledge in drug therapy and clinical skills for better patient
care. Clerkship aims to provide students with a practical and stimulating learning experience
where They are given an opportunity the participate in ward rounds along with the health care
team And provide a wide variety of clinical services

ROLES AND RESPONSIBILITIES OF PHARM D STUDENTS IN CLERKSHIP

1. Assist the providers in the selection, utilization and monitoring of the most
appropriate drug therapy, based upon patient specific information. This will be
accomplished by
a. Interviewing the patients for medication histories, and to determine efficacy,
toxicity, adherence, drug interactions and (if) cost issues for each medication.
b. Regular chart review with recommendations for optimal therapy.
c. Responding to patient problems concerning their medications.
d. Being available to assist in answering drug therapy questions by doctors.
2. Optimized patient care
a. See patients as needed for counselling, medication adjustment, monitoring and
follow up for chronic diseases.
3. Survey as a drug information resource for healthcare providers
a. After discussing with preceptors, provider complete answers and
recommendations for medication related questions from providers.
b. May require a literature search, reviewing several references and providing
documentation
 GATHERING RELEVANT INFORMATION OF THE PATIENT

Medication History
Patient/
• Caregiver
• General
Medical History and records of Practitioner
initial clinical Investigations
• Healthcare
provider
Construction of an abstracted chart with clinical and pharmaceutical data

SYSTEMIC ANALYSIS OF DRUG THERAPY DURING PATIENT’S STAY IN

• No indication for a current drug

• Indication for a drug- but none prescribed
• Wrong drug regimen prescribed/ more efficacious choice possible
• To much of the correct drug
Source of Information:
• Too little of the correct drug
• Adverse drug reaction/ drug allergy Reference books, Hospital
• Drug-drug, drug-disease, drug -food interactions formulary, Data Relating to
• Patient not receiving a prescribed drug the Evidence Based Medicine
• Routine monitoring (labs, screening, exams) missing
• Otherproblems, such as potential for overlap for adverse effects

Addressing the query

Are Drug-Related Problems identified??

INTERVENTIONS OF OPTIMIZE PRESCRIBING

Requestor’s demographics
• Discuss the DRP Background questions
• Propose a solution
Categorization of a question
• Seek acceptance
• Ensure the follow up Search strategy
Data evaluation, analysis and synthesis
D. HANUMA NAYAK(Doctor of Pharmacy )
(
Formulation and provision of response
Nalanda Institute of Pharmaceutical Sciences
Follow up, follow through and documentation
GBR Hospital, Narasaraopet.
 4. Assignments/ projects ( inclusive list, all may not be required to be determined by the
preceptor )
a. Oral assignment
• Formal case presentation
This is a 30–45-minute oral presentation of an interesting patient (plus 10 minutes For
questions). A handout must accompany the presentation.
• Noon or morning conference in-service
This is a 45-minute presentation, 10 minutes of questions, reviewing the
Pathophysiology, treatment, and monitoring of a specific disease/ condition Presented
to medical faculty members and medical residents.

b. Written assignment (drug information paper)

• Formal 3–5-page paper evaluating a specific drug information question that arouse
During clinic; should include the question asked, a brief review of the literature, and
Your conclusion and recommendation with reference.

c. Journal club presentation

This is a 30–40-minute presentation of a significant clinical trial plus a 1 page

double Sided or 2-page summary handouts.

d. Topic discussion

This is a 1-1.5-hour presentation of a major clinical guideline with discussion of

Pathophysiology, diagnosis, treatment, risk factors, monitoring, prevention and
Complications. Should include all pertinent drug information.
Date Clerkship

CASE STUDY ON MIGRAINE HEADACHE

DEFINITION:
Migraine is a familial disorder characterized by recurrent attacks of headache widely variable
in intensity, frequency and duration.
Attacks are commonly unilateral and are usually associated with anorexia, vomiting and/or
photophobia, photophobia. Migraine is one of the common causes of recurrent headaches.
➢ According to IHS , migraine constitutes 16% of primary headaches.
➢ Migraine afflicts 10-20% of the general population.
➢ In India, 10-20% of people suffer from migraine.
➢ Migraine is under diagnosed and under treatment
➢ According to headache classification committee of the international headache society,
Migraine has been classified as:
➢ Migraine without aura[common migraine]
➢ Migraine with aura[classic migraine]
➢ Complicated migraine
PHASES:
1. Prodrome
2. Aura
3. Headache
4. Postdrome
According to headache classification committee of the international headache society,
Migraine has been classified as:
➢ Migraine without aura[common migraine]
➢ Migraine with aura[classic migraine]
➢ Complicated migraine
AURA:
• Flashing lights, silvery zig zag lines moving across visual field over a period of 20 mins
• Sometimes leaving a trail of temporary visual field
• Sometimes auditory, olfactory, gustatory hallucinations
• Sensory aura-spreading front of tingling and numbness, from one body part to another

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PRPRODROME:
Vague premonitory symptoms that begin from 12to36hours before the aura and headache
Symptoms
Yawning
Excitation
Depression
Lethargy
Craving or distaste for various food
DURATION: 15 -20mims
HEADACHE: headache is generally unilateral and is associated with symptoms like anorexia,
nausea, vomiting, photophobia, phonophobia, tinnitus.
POSTDROME: following headache patient complaints of fatigue, depression, fever exhaustion,
some patients feel usually fresh.
DURATION: few hours to 2 days
ETIOLOGY:
Family history of migraine headache 70% to 80%
Medication (birth control pills, vasodilators)
Fatigue or emotional stress
Specific food or alcohol or caffeine
Exertion
Lack of sleep
Noise, light, diet
EPIDEMOLOGY:
Migraine affects 18% of women and 6% of men in the united States and has an estimated
worldwide prevalence of about 10%
For both men and women, the prevalence of migraine rise throughout early life and fall
after midlife
In girl’s women, the rate almost triple between age and 10 and 30years
SIGN AND SYMPTOMS:
Defects in visuals, dysphasia, headache, severe pain, vomiting, photophobia, pallor,
anorexia, phonophobia, hemiparesis, confusion, apathy, numbness

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RISK FACTORS:
• Genetic factors
• High frequency of attacks anxiety and depression
• Stressful life events
• Obesity
• Heavy caffeine consumption
• Tobacco use
• Overuse of abortive headache medication
• Snoring
• Sleep related problems
• Tempomansibular disorder
• Other pai pain syndrome
• Psychiatry problem
PATHOPHSYIOLOGY: Migraine was once thought to be initiated by problems with blood
vessels. This theory is now largely discredited.Current thinking is that a phenomenon known as
cortical spreading depression is responsible for the disorder.In cortical spreading depression,
neurological activity is depressed over an area of the cortex of the brain. This situation results in
the release of inflammatory mediators leading to irritation of cranial nerve roots, most particularly
the trigeminal nerve, which conveys the sensory information for the face and much of the head.

This view is supported by neuroimaging techniques, which appear to show that migraine is
primarily a disorder of the brain (neurological), not of the blood vessels (vascular). A spreading
depolarization (electrical change) may begin 24 hours before the attack, with onset of the headache
occurring around the time when the largest area of the brain is depolarized. The effects of migraine
may persist for some days after the main headache has ended. Many sufferers report a sore feeling
in the area where the migraine was, and some report impaired thinking for a few days after the
headache has passed.

In 2005, research was published indicating that in some people with a patent foramen ovale (PFO),
a hole between the upper chambers of the heart, suffer from migraines which may have been
caused by the PFO. The migraines end instantly if the hole is patched. Several clinical trials are

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currently under way in an effort to determine if a causal link between PFO and migraine can be
found. Early speculation as to this relationship has centered on the idea that the lungs detoxify
blood as it passes through. The PFO allows uncleaned blood to go directly from the right side of
the heart to the left without passing through the lungs.
Migraine headaches can be a symptom of Hypothyroidism.
Diagnosis:
Pulsatile
Hours
Unilateral
Nauseating
Disabling
TREATMENT
Conventional treatment: focuses on three areas: trigger avoidance, symptomatic control,
and preventive drugs. Patients who experience migraines often find that the recommended
treatments are not 100% effective at preventing migraines, and sometimes may not be
effective at all.
Trigger avoidance:
Patients can attempt to identify and avoid factors that promote or precipitate migraine
episodes. Moderation in alcohol and caffeine intake, consistency in sleep habits, and
regular meals may be helpful. Beyond an often-pronounced placebo effect, general dietary
restriction has not been demonstrated to be an effective approach to treating migraine.
Abortive treatment:
Migraine sufferers usually develop their own coping mechanisms for the pain of a migraine
attack. A cold or hot shower directed at the head, a hot or cold wet washcloth, a warm bath,
or resting in a dark and silent room may be as helpful as medication for many patients, but
both should be used when needed.

Some headache sufferers are surprised to learn that a simple cup of coffee is used daily
around the world to control minor vascular headaches that are not quite migraines. Minor
vascular headaches are frequently associated with the hormonal fluctuations of menstrual

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periods, irregular eating, and unusually hard work. For migraineurs, a well-timed cup of
coffee can prevent outright migraine under the same conditions.

GOALS OF TREATMENT:
Ergot alkaloids
Until the introduction of sumatriptan ergot derivatives (see ergoline) were the
primary oral drugs available to abort a migraine once it is established.
Patient specific goals:
Rapid headache relief with minimal adverse effects , and symptom recurrence, and minimal
disability and emotional distress
Patient specific goals:
Rapid headache relief with minimal adverse effects , and symptom recurrence, and minimal
disability and emotional distress
Limit use of acute migraine therapies to fewer than 10 days/month to avoid medication
misuse headache.
Reduce reliance on poorly tolerated, ineffective, or unwanted or acute pharmacotherapies.
Disease specific goals:
Reduce attack frequency and severity.
Reduce disability .
Improve quality of life and prevent headaches.
Avoid headache medication escalation[a rise].
Reduce headache related distress and psychological symptoms.

TREATMENT PLAN:
a trail of metoclopramide vs sumatriptan for the emergency department treatment of
migraine was done in patient:
This study compared metoclopramide 20mg/IV over 6 hr with sumatriptan 6mg/SC for
initial treatment of emergency migraine headaches.
By measuring the pain intensity, it concluded that metoclopramide preferable therapy for
migraine presenting to the patient .

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Because, at 2 hrs, pain free rates were 59% with the metoclopramide to 35% with the
sumatriptan.
NON PHARAMCOLOGICAL TREATMENT:
❖ apply ice to the head.
❖ recommended periods of rest or sleep, usually in dark or quite environment.
❖ Identify and avoid triggers of migraine attacks.
❖ Behavioural interventions[relaxation therapy, biofeedback, cognitive therapy] may help
patients who prefer nondrug therapy or when drug therapy is ineffective or not tolerated.
❖ Decrease the use of OTC medication.
❖ Massage, passive mobilization of the cervical facets.
❖ Stress and pain management.
❖ Physiotherapy[daily exercise programme and posture correction].
❖ References:
https://www.slideshare.net
https://my.clevelandclinic.org
https://www.mayoclinic.org

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CASE STUDY ON DENGUE FEVER WITH THROMBOCYTOPENIA

DEFINITION: A debilitating viral disease of tropics, transmitted by mosquitoes and causing

sudden fever and acute pain in joints .
Thrombocytopenia is a common feature in both mild and severe dengue disease. (1)
ETIOLOGY:
• Caused by dengue virus.
• Spread by aedes mosquito
• Increased platelet destruction and clearance from peripheral blood
• Decrease production of platelets in bone marrow.
EPIDEMIOLOGY:
• Since 2010, the incidence of dengue has increased to 15 per million people annually in
different states.
• Every year more than 100,000 infections and 200- 400 deaths occur.
CLINICAL FEATURES:
• Head ache
• Muscle, bone or joint pain
• Nausea
• Vomiting
• Pain behind eyes
• Swollen glands
• Reddish rash
• Unusual weakness
• Bleeding.
SEVERE DENGUE FEVER SYMPTOMS:
• Severe stomach pain
• Persistent vomiting
• Bleeding from your gums or nose
• Blood in your urine, stools or vomit
• Bleeding under the skin, which might look like bruising

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• Difficult or rapid breathing

• Fatigue
• Irritability or restlessness
DIAGNOSIS:
• Complete blood picture
• Polymerase chain reaction
• Antibody titter for dengue virus type.
COMPLICATIONS:
• Liver damage
• Low platelets
• Dehydration
• Neurological damage
• Bleeding
• Meningoencephalitis (2)

PATHOPHYSIOLOGY:
Bites of Aedes mosquito

The virus penetrate into the skin

The virus infects and replicates inside the Langerhans cell

Langerhans cells release interferons (to limit the spread of infection)

Infected Langerhans cells go to the lymphatic system to make immune system alert

Then travels to circulation

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Results in viraemia – high levels of virus in the blood stream

Activation of immune response - increases lymphocytes

Decreases neutrophils in White Blood Cells

Release of pyrogen causes fever and increased blood pressure in blood vessels causing rashes

Dengue

COMPLICATIONS:
• Severe dengue fever can cause internal bleeding and organ damage. Blood pressure can
drop to dangerous levels, causing shock. In some cases, severe dengue fever can lead to
death.
• Women who get dengue fever during pregnancy may be able to spread the virus to the baby
during childbirth. Additionally, babies of women who get dengue fever during pregnancy
have a higher risk of pre-term birth, low birth weight or fatal distress.

TREATMENT:
Goals of treatment:
• To improve quality of life
• To prevent and treat complications

NON-PHARMACOLOGICAL TREATMENT:
• Advised to take more fluids
• Avoid non steroid anti- inflammatory drugs.
PHARMACOLOGICAL TREATMENT:

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• Paracetamol
• Multivitamins
• Ranitidine
• Domperidone
• Ondansetron
• Dexamethasone
• Cefixime
• Vitamin C (ascorbic acid)
• Cetirizine
• Electrolytes for maintaining fluid balance.

Table 1-guidelines for transmission of platelets

Blood component Indication
Packed red cells Loss of blood – 10% or more of total blood volume
Refractory shock despite adequate fluid administration and declining
hematocrit
Replacement volume should be 10ml/kg body weight at a time and
coagulogram should be done
If fluid overload is present packed red cells are to be given
Platelets In general, there is no need to give prophylactic platelets even at less than
10000/cumm in absence of bleeding manifestations
Prolonged shock; with coagulopathy and abnormal coagulogram
In case of systematic massive bleeding, platelet transfusion may be
needed in addition to red cell transfusion
Fresh frozen Coagulopathy with bleeding,
plasma/Cryoprecipitate Patients clinical condition may be considered or as per the advice of the
physician
PREVENTION:
• Advised to use mosquito repellents.
• Keep surroundings hygiene.

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• Avoid maintaining stagnant water.(3)

REFERENCES:
1. World Health Organization (WHO) Global Strategy for Dengue Prevention and Control
2012-2020. Geneva: WHO Press; 2012.
2. WHO. Dengue Guidelines for Diagnosis, Treatment, Prevention and Control. Geneva:
World Health Organization; 2009.
3. Thomas SJ, et al. Dengue virus infection: Prevention and treatment.
https://www.uptodate.com/contents/search. Accessed Oct. 30, 2020.

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CASE STUDY ON PNEUMONIA

DEFINITION:

An inflammation of the lung parenchyma (the respiratory bronchioles and the alveoli) is known
as pneumonia. It is an inflammatory condition of the lung that is caused by a microbial agent.

"Pneumonitis" is a general term that describes an inflammatory process in the lung tissue that
may predispose a patient to or place a patient at risk for microbial invasion. It is the leading
cause of death from the infectious disease.

EPIDEMIOLOGY:

Common illness affecting approximately 450 million people a year occurring in all part of the
world and 4 million deaths yearly. Rates are greater in children less than five years and adult
older than 75 years.

It occurs five times more in the developing world than in developed world.

It is the eighth leading cause of death in US resulting in almost 70,000 deaths per year. In
persons 65years of age and older, it is the fifth leading cause of death.

In India it is the single largest cause of death in children resulting in nearly 120 million cases a
year.

CLASSIFICATION:

1. ACCORDING TO THE CAUSATIVE ORGANISMS:

a) BACTERIAL PNEUMONIA: Caused by bacteria.

* Pneumococcal pneumonia caused by Streptococcus pneumoniae.

* Staphylococcal pneumonia caused by Staphylococcus aureus.

* Influenza Pneumonia caused by Haemophilus influenza.

* Gram negative bacterial pneumonia caused by Klebsiella pneumonia.

b) VIRAL PNEUMONIA:

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* Rhino virus, corona virus, influenza virus, respiratory syncytial virus (RSV), Adeno virus
and para influenza.

* Herpes simplex virus rarely cause pneumonia in newborns persons with cancer, transplant
recipients and people with significant burns.

* People following organ transplantation or immune compromised present high rates of

cytomegalovirus pneumonia.

c) FUNGAL PNEUMONIA: Fungal pneumonia caused by histoplasmosis, blastomycosis,

coccidioidomycosis, aspergillosis, candidiasis.

d) PARASITIC PNEUMONΙΑ:

Parasitic pneumonia (caused by protozoa, nematodes, Platyhelminthes); common organism is

Pneumocystis firoveci.

2. ACCORDING TO ENVIRONMENT:

a) COMMUNITY ACQUIRED PNEUMONIA: Pneumonia which develops in an otherwise

healthy person outside of hospital or have been in hospital for less than 48 hours.

b) HOSPITAL ACQUIRED PNEUMONIA: Pneumonia that was not incubating upon admission
developing in a patient hospitalized for greater than 48 hours.

c) VENTILATOR ASSOCIATED PNEUMONIA (VAP): VAP refers to

Pneumonia that arises more than 48-72hours after endotracheal intubation

d) PNEUMONIA IN THE IMMUNO COMPROMISED HOST: It is a complex infection and

inflammation of lower respiratory tract, complicated by wide spread multi drug

3. ACCORDING TO THE AREAS OF THE LUNG INVOLVED/ AFFECTED:

a) Lobular pneumonia

b)Multi lobular pneumonia

c)Bronchial pneumonia

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d)Interstitial pneumonia Alveolar pneumonia

e) Necrotizing pneumonia

f)Segmental pneumonia

4. ACCORDING TO THE CAUSE:

a)Bronchiolitis obliterans organizing pneumonia (BOOP)/cryptogenic organizing

b)Pneumonitis (COP).

c)Eosinophilic pneumonia occur in response to infection.

d)Chemical pneumonia.

e)Aspiration pneumonia. Antibiotic resistance.

f)Dust pneumonia.

g)Bilateral pneumonia.

ETIOLOGY:

There are many causes of pneumonia including bacteria, viruses, mycoplasmas, fungal agents
AMD protozoa. It may also result from inhalation of toxic or caustic chemicals, smoke, dusts, or
gases or aspiration of food, fluids or vomitus Pneumonia may complicate to chronic illness.

RISK FACTORS:

a)Age

b)Smoking

c)Air pollution

d)Altered consciousness

e)Tracheal intubation

f)Upper respiratory tract infection

g)Immune suppression

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h)Prolonged hospital stay.

PATHOPHYSIOLOGY:

Gastric content aspiration/entry virus into the lung

Inflammatory response.

: Cavity extend to the bronchus

Promotion of abscess into encapsulated.

Tissue necrosis.

Increased production of sputum.

Pneumonia.

CLINICAL MANIFESTATION:

1.Fever

2.Chills and sweating

3.Productive cough

4.Shortness of breath

5.Pleuritic chest pain

6.Hypoxemia

7.Fatigue Tachypnoea

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8.Hemoptysis

9.Dyspnea

10.Headache

11.Crackling sounds over affected area

12.Decreasing in breath sounds

13.Unequal chest expansion

DIAGNOSIS:

a) Gram stain and culture and sensitivity tests of sputum

b) Chest X-ray
c) Blood culture
d) Immunologic test to detect microbial agents
e) CT scan thorax

Physical examination

a) Fibreoptic bronchoscopy or transcutaneous needle aspiration/ biopsy.

b) Tracheal aspirate
c) Transcutaneous Oxygen level analysis or ABG.
d) Fibreoptic bronchoscopy or transcutaneous needle aspiration/ biopsy.

COMPLICATION:

1.Emphysema

2. Lung abscess

3.Sepsis

4.Bacterimia

5.Pericarditis

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6.Bronchiolitis obliterans

7.Acute respiratory distress syndrome (ARDS)

8.Atelectasis

9.Pleural effusion

MANAGEMENT:

1.Oxygen therapy

2.Nutritional support

3.Fluid and electrolyte management

4.Broncho dilators medications: Albuterol sulphate, metaproterenol

5.Deep breathing exercises and spirometry.

6.Chest physiotherapy

7.Percussion and vibration

8.Postural drainage

9. Nasotracheal suctioning

PHARMACEUTICAL TREATMENT FOR VIRAL PNEUMONIA

For influenza virus

Name of the Dose ROA Frequency Duration

drug
Oseltamivir 75mg PO BD 5-10 days
zanamivir 5mg 2 inhalations BD 5-10 days

For respiratory syncitial virus

Name of the Dose Frequency ROA Duration

drug

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Ribavirin 6gm BD IV 5 days

For Adeno virus

Name of the drug Dose ROA Frequency

cidofovir 5mg/kg IV BD

For Herpes simplex virus and varicella

Name of the drug Dose ROA Frequency

Acyclovir 10mg/kg IV q 8 hours

REFERENCES:

1. Torres. A., Cilloniz, C., Niederman, M.S et al. Pneumonia. Nat Rev Dis Primers 7,25(2021).
https://do 1.org/10.1038/s41572-021-002590.

2. Olli Ruuskanen, Prof, MD, Elina Lahti, MD, Lance C Jennings, PhD and David R Murdoch,
Viral Pneumonia (2011).

3. Olalekan Bakare, Fadaka Ade wale, Oluwaseun, Ashwil Klein, Ashley Pretorius, diagnostic
approaches of pneumonia for commercial scale biomedical applications: an overview (2020). All
life 13(1): 532-547 do 1: 10-1080/26895293.2020.1826363

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CASE STUDY ON CAD WITH NSTEMI

INTRODUCTION

Acute coronary syndrome (ACS) can be divided into subgroups of ST-segment elevation
myocardial infarction (STEMI), non-ST-segment elevation myocardial infarction (NSTEMI), and
unstable angina. ACS carries significant morbidity and mortality and the prompt diagnosis, and
appropriate treatment is essential. STEMI diagnosis and management are discussed elsewhere.
NSTEMI and Unstable angina are very similar, with NSTEMI having positive cardiac biomarkers.
The presentation, diagnosis, and management of NSTEMI are discussed below.
ETIOLOGY
The etiology of NSTEMI varies as there are several potential causes. These include tobacco abuse,
lack of physical activity, high blood pressure, high cholesterol, diabetes, obesity, and family
history.
EPIDEMIOLOGY

The median age at the time of presentation for ACS in the United States is 68 years. Males
outnumber females by a 3:2 ratio. The incidence of ACS in the United States is over 780,000,
and of those, approximately 70% will have NSTEMI.

PATHOPHYSIOLOGY

ACS is simply a mismatch in the myocardial oxygen demand and myocardial oxygen
consumption. While the cause of this mismatch in STEMI is nearly always coronary plaque rupture
resulting in thrombosis formation occluding a coronary artery, there are several potential causes
of this mismatch in NSTEMI. There may be a flow-limiting condition such as a stable plaque,
vasospasm as in Prinzmetal angina, coronary embolism, or coronary arteritis. Non-coronary injury
to the heart such as cardiac contusion, myocarditis, or presence of cardiotoxic substances can also
produce NSTEMI. Finally, conditions relatively unrelated to the coronary arteries or myocardium
itself such as hypotension, hypertension, tachycardia, aortic stenosis, and pulmonary embolism
lead to NSTEMI because the increased oxygen demand cannot be met.
HISTORY AND PHYSICAL

The “typical” presentation of NSTEMI is a pressure-like substernal pain, occurring at rest or

with minimal exertion. The pain generally lasts more than 10 minutes and may radiate to either

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arm, the neck, or the jaw. The pain may be associated with dyspnea, nausea or vomiting,
syncope, fatigue, or diaphoresis. Sudden onset of unexplained dyspnea with or without
associated symptoms is also a common presentation. Risk factors for ACS include male sex,
older age, family history of coronary artery disease, diabetes, personal history of coronary artery
disease, and renal insufficiency. Atypical symptoms may include a stabbing or pleuritic pain,
epigastric or abdominal pain, indigestion, and isolated dyspnea. While all patients presenting
with ACS are more likely to present with typical symptoms than atypical symptoms, the
likelihood of atypical presentations increases with age over 75, women and those with diabetes,
renal insufficiency, and dementia.

Physical Exam for ACS and NSTEMI is often nonspecific. Clues such as back pain with aortic
dissection or pericardial friction rub with pericarditis may point to an alternative diagnosis for a
patient’s chest pain, but no such exam finding exists that indicates ACS as the most likely
diagnosis. Signs of heart failure should increase concern for ACS but are, again, nonspecific
findings.

EVALUATION

History, ECG, and cardiac biomarkers are the mainstays in the evaluation. An ECG should be
performed as soon as possible in patients presenting with chest pain or those with a concern for
ACS. A normal ECG does not exclude ACS and NSTEMI. ST-elevation or anterior ST
depression should be considered a STEMI until proven otherwise and treated as such. Findings
suggestive of NSTEMI include transient ST elevation, ST depression, or new T wave inversions.
ECG should be repeated at predetermined intervals or if symptoms return.

Cardiac troponin is the cardiac biomarker of choice. Troponin is more specific and more
sensitive than other biomarkers and becomes elevated relatively early in the disease process.
While contemporary cardiac troponin may not be elevated within the first 2 to 4 hours after
symptom onset, newer high sensitivity troponin assays have detectable elevations much earlier. It
is also true that the amount of troponin released, and therefore the time to elevation, is
proportional with infarct size, so it is unlikely to have a negative initial troponin with larger
infarcts. Regardless of infarct size, most patients with true ischemia will have elevations in
troponin within 6 hours, and negative troponins at this point effectively rule out infarct in most
patients. Most assays use a cutoff value of greater than a 99th percentile as a positive test. In

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older, contemporary troponin assays, no detectable troponin is reported in most healthy

individuals without the disease. Newer high sensitivity troponin assays often will report a
normal detectable range in healthy individuals without the disease.

Several tools and scores have been developed to assist in the workup of ACS. These tools must
be used with caution and in the appropriate context as none have been definitively shown to be
superior to clinician judgment. Some common tools available are the TIMI (Thrombolysis In
Myocardial Infarction) risk score, the GRACE (Global Registry of Acute Coronary Events) risk
score, the Sanchis score, the Vancouver rule, HEART (History, ECG, Age, Risk Factors, and
Troponin) score, HEARTS3 score, and Hess prediction rule. The HEART score was specifically
developed for emergency department patients and has gained popularity in this setting.

DIAGNOSIS

NSTEMI is diagnosed in patients determined to have symptoms consistent with ACS and
troponin elevation but without ECG changes consistent with STEMI. Unstable angina and
NSTEMI differ primarily in the presence or absence of detectable troponin leak.

TREATMENT/ MANAGEMENT

Initial management strategies aim to reduce cardiac ischemia and prevent death. Oxygen, aspirin,
and nitrates are administered based on initial concern for ACS and prior to a definitive diagnosis.
Subsequent treatment depends on confirmation of diagnosis or a high index of suspicion with or
without a definitive diagnosis.

Oxygen was previously recommended for all patients presenting with concern for ACS, but
newer data suggests this strategy may be harmful in patients who otherwise do not warrant
supplemental oxygen. Supplemental oxygen is now recommended in patients with oxygen
saturation less than 90%, those with respiratory distress, or when high-risk features of
hypoxemia are present.

Chewable, non-coated, aspirin 324 mg should be given to all patients who present with concern
for ACS unless otherwise contraindicated. Patients who cannot take aspirin may be given
prasugrel 60 mg PO.

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Patients with ongoing symptoms should receive 0.4 mg sublingual nitroglycerin every 5 minutes
for up to three doses or until the pain is relieved, unless otherwise contraindicated.
Contraindications include the recent use of phosphodiesterase inhibitors and
hypotension. Nitrates should be used with extreme caution in patients with concerns for right-
sided infarction. Continuous intravenous nitroglycerin should be considered in patients with
persistent signs of heart failure or hypertension.

Many patients will present with concern for ACS but will not have positive findings of ischemic
ECG changes or positive troponin on initial workup. These patients may be observed with serial
ECG and troponin measurements every 3 to 6 hours. Patients also may undergo provocative
testing such as the treadmill stress test or myocardial perfusion imaging prior to discharge or
within 72 hours. Low-risk patients often may be discharged with a referral for further outpatient
testing after initial ACS is ruled out.

In patients where NSTEMI has been definitively diagnosed or is highly likely, anticoagulation
should be initiated. Protocols will vary by institution, so cardiology consultation should be
obtained if readily available. This is especially true when there is the possibility of percutaneous
intervention, as this may change anticoagulation strategies. Unfractionated heparin with bolus
dosing and a continuous infusion is commonly used, with most institutions having protocols
available. Other strategies may include the use of enoxaparin, bivalirudin, fondaparinux, and
dual antiplatelet therapies. Fibrinolytic therapies should not be used in NSTEMI.

When NSTEMI has been diagnosed, patients should be admitted to cardiac care units for further
management. Beta-blocker therapy should be started within 24 hours after the presentation in
patients who do not have a contraindication. Contraindications include signs of heart failure,
hypotension, heart conduction block, or reactive airway disease. Unless otherwise
contraindicated, ACE Inhibitors should be initiated in patients with an ejection fraction less than
40%, hypertension, diabetes, or chronic kidney disease. High-dose statins should be initiated for
cholesterol management. Invasive and non-invasive testing strategies are employed. Both early

intervention strategies with diagnostic angiography and intervention are applied as indicated, and
conservative medical management strategies are employed. The rationale for choosing one
strategy over the other is often patient and institution-specific and beyond the scope of this
review.

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DIFFERENTIAL DIAGNOSIS

Clinical conditions that can present with chest pain and have nonspecific ECG changes with an
elevated troponin marker include:

1. Myocarditis

2. Pericarditis

3. Pulmonary embolism

4. Left ventricular aneurysm

5. Prinzmetal angina

6. Anxiety Disorder

7. Aortic Stenosis

8. Hypertensive emergency

PROGNOSIS

Patients who present with NSTEMI have a lower 6-month mortality rate than those who present
with unstable angina. Morbidity and mortality further depend on the degree of troponin elevation
as well as comorbid conditions such as the severity of diabetes, presence of peripheral vascular
disease, presence of renal dysfunction, and dementia.

COMPLICATIONS

Complications of NSTEMI are secondary to the systemic effects of the disease rather than
structural complications of STEMI. Cardiomyopathy with diffuse hypokinesis may be seen but
left ventricular aneurysms or papillary muscle dysfunction is rare. Pulmonary edema due to poor
cardiac output may be seen in severe cases. Other complications of poor cardiac output such as
renal dysfunction may be seen as well

Deterrence and patient education

Patients with NSTEMI need extensive counselling regarding medication compliance as well as
lifestyle modifications to prevent repeat events and improve morbidity as well as mortality.
Smoking cessation is essential. Smoking cessation counselling by the provider is recommended

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Enhancing healthcare team outcomes

The diagnosis and management of NSTEMI are best managed with an interprofessional team
that consists of a cardiologist, internist, nurse practitioner, and a pharmacist.

In patients where NSTEMI has been definitively diagnosed or is highly likely, anticoagulation
should be initiated. Protocols will vary by institution, so cardiology consultation should be
obtained if readily available. This is especially true when there is the possibility of percutaneous
intervention, as this may change anticoagulation strategies.

When NSTEMI has been diagnosed, patients should be admitted to cardiac care units for further
management. Beta-blocker therapy should be started within 24 hours after the presentation in
patients who do not have a contraindication. Unless otherwise contraindicated, ACE Inhibitors
should be initiated in patients with an ejection fraction of less than 40%, hypertension, diabetes,
or chronic kidney disease. High-dose statins should be initiated for cholesterol management.
Invasive and non-invasive testing strategies are employed. Both early intervention strategies with
diagnostic angiography and intervention are applied as indicated, and conservative medical
management strategies are employed.

The outcomes of patients with NSTEMI depend on the severity of the myocardial injury,
compliance with treatment and other comorbidities. Patients who do not change their risk factors
for the coronary disease have a poor outcome. (Level V)

REFERENCES

1. Gilutz H, Shindel S, Shoham-Vardi I. Adherence to NSTEMI Guidelines in the Emergency

Department: Regression to Reality. Crit Pathw Cardiol. 2019 Mar;18(1):40-46.

2. Piątek Ł, Wilczek K, Janion-Sadowska A, Gierlotka M, Gąsior M, Sadowski M. Outcomes

of a routine invasive strategy in elderly patients with non-ST-segment elevation myocardial
infarction from 2005 to 2014: results from the PL-ACS registry. Coron Artery Dis. 2019
Aug;30(5):326-331.

3. Manfredonia L, Lanza GA, Crudo F, Lamendola P, Graziani F, Villano A, Locorotondo G,

Melita V, Mencarelli E, Pennestrì F, Lombardo A, De Vita A, Ravenna SE, Bisignani A, Crea
F. Diagnostic role of echocardiography in patients admitted to the emergency room with

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suspect no-ST-segment elevation acute myocardial infarction. Eur Rev Med Pharmacol
Sci. 2019 Jan;23(2):826-832.

4. Rupprecht HJ, Geeren M, Geeren M, Weilemann S, Schuster HP. [Acute coronary

syndrome without ST-elevation (NSTE-ACS)]. Herz. 2019 Feb;44(1):10-15.

5. Kamińska J, Koper OM, Siedlecka-Czykier E, Matowicka-Karna J, Bychowski J, Kemona

H. The utility of inflammation and platelet biomarkers in patients with acute coronary
syndromes. Saudi J Biol Sci. 2018 Nov;25(7):1263-1271’.

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CASE STUDY ON BREAST CANCER

DEFINITION

Breast cancer is a malignant tumour stars in the cells of the breast tumour is a group of Cancer
cells that can grow into surrounding tissues has spread to distant area of the disease occurs
almost entirely in women but men can get it to

TYPES OF BREAST CANCER

there are many types of breast cancer ductal carcinoma invasive ductal carcinoma in breast
cancer metastatic breast cancer some other specific type

TYPES OF CANCERS:

Pathologically, tumours are generally classified by four ways

BASED ON ORIGIN: It is based on the tumour is developed from which part or organ or
region of the body.

EX: Breast cancer, Liver cancer, Prostate cancer etc.….

BASED ON TISSUE TYPE: It involves which type of tissue having Neoplasm or Tumour.

Carcinoma: Carcinoma refers to a malignant neoplasm of epithelial origin or cancer of the

internal or external lining of the body.

Sarcoma: Sarcoma refers to cancer that originates in supportive and connective tissues.

Myeloma: Myeloma is cancer that originates in the plasma cells of bone marrow.

Leukaemia: The disease is often associated with the over production of immature WBC.

Lymphoma: Lymphomas develop in the glands or nodes of the lymphatic system.

Mixed types: The type components may be within one category or from different categories (1).

• Benign Tumour: A tumour that remains confined to its original location, neither
invading surrounding normal tissue nor spreading to distant body sites is known as
benign tumour.
Ex: Skin wart

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• Malignant Tumour: A tumour which is capable of both invading surrounding normal

tissue and spreading (metastasis) throughout the body via the circulatory or lymphatic
systems is known as malignant tumour. Only malignant tumours are properly referred to
as cancer.
• Pathologically, cancers are classified into three categories: carcinomas, sarcoma, and
leukaemia. (2)

Cancers cells are formed from normal cells due to a mutation or modification or changes of
DNA and/or RNA. Cancer develops if the immune system is not working properly and/or the
number of cells produced is too great for the immune system to eliminate. The rate of DNA
and RNA mutations can be too high under some conditions such as: unhealthy environment,
chemical carcinogens, radiation energy, food products, infectious agents and genetic
predispositions to mutations.

Worldwide, Breast cancer 10.4%of all cancers incidences among women, making it the
second most common type of non-skin cancer and the fifth most common cause of cancer
death. Breast cancer is about times more common in women than in men, although males
tend to have poorer outcomes due to delays in diagnosis. (3)

EPIDEMIOLOGY

most common cancer in women worldwide leading floor of the lifetime risk of dying breast
cancer is approximately 34%

ETIOLOGY

Age or gender family history reproductive study environmental factors endocrine factors

Pathophysiology

• Normal
• Hyperplasia increase in number of cells
• Atypical Hyperplasia or abnormal increase in number of cells maker of breast cancer
• Carcinoma in in slides are cancer but no effort to the locals whose it originally developed

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RISK FACTORS

• Gender
• Age
• Genetics Related
• Family history
• Personal history of breast cancer
• Menstrual periods
• Birth control
• Breast feeding

SIGNS AND SYMPTOMS

1. Skin dimpling
2. Lump
3. Change in now the nipple looks like pulling in of the nipple
4. clear or blicirys fluid that leaks out of the nipple
5. change in the colour or texture

INVESTIGATIONS

Mammography
Breast ultrasound
magnetic resonance imaging
breast biopsy

TREATMENT

• Surgery
• Lumpectomy- removal of cancerous tumour without removing the entire Brest
• Mastectomy- removal of the entire Brest
• Chemotherapy
• Radiotherapy
• Hormonal therapy

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PREVENTION

• Breast Prevention begins with various factors

• Control the weight
• Get plenty of physical activity
• Brest feed
• Healthy diet
• Discontinue hormonal therapy
• Avoid exposure to environmental pollution
• Screening
• Mammogram- clinical Brest exam Brest self-exam
Treatment
Now pharmacological therapy
• Taking Aspirin avoid exposure pesticides non-alcohol
• Maintain healthy diet
• Avoid it hormone therapy
• Stay physically active
• Eat high fibre food emphases olive oil
Pharmacological treatment
• Antimetabolites
• 5flurouracil
• Capecitabine
• Gemcitabine
• Antibiotics
• Doxorubicin
• Epirubicin
• Alkylating agents
• Cyclophosphamide
• Cytotoxin
• Microtubule inhibitors
• Docetaxel

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• Paclitaxel
• Vinblastine
• Vincristine
• Advent chemotherapy
• Neoadjuvant chemotherapy

Regimens

• TRASTUZUMAB+DOCETAXEL+DOXORUBICIN+CYCLOPHOSPHAMITRASTUZ
UMAB+DOCETAXEL+DOXORUBICIN+CYCLOPHOSPHAMIDE
• DOCETEXEL
• DOCETAXEL,EPIRUBICIN,CYCLOPHOAPHAMIDE
• ADRIAMYCIN,CYCLOPHOSPHAMIDE+PACLITAXEL
• ADRIAMYCIN+CISPLATIN
• PACLITAXEL+ADRIAMYCIN+CYCLOPHOSPHAMIDE
• TRASTUZUMAB+DOCETAXEL+DOXORUBICIN+CYCLOPHOSPHAMIDE
• EPIRUBICIN+CYCLOPHOSPHAMIDE
• DOCETAXEL+CYCLOPHOSPHAMIDE+TRASTUZUMAB
• EPIRUBICIN+CYCLOPHOSPHAMIDE
• PACLITAXEL+ADRIAMYCIN+CYCLOPHOSPHAMIDE
• ADRIAMYCIN+CYCLOPHOSPHAMIDE+ZOLENDRONIC ACID
• ADRIAMYCIN+CYCLOPHOSPHAMIDE+DOCETAXEL+TRASTUZUMAB

REFERENCES

1. MR.Ataollani et al ., Breast Cancer and associated factors journal of medicine and life
2015:8(spec Iss4):6-11
2. Anthony Howell et al., Risk determination and prevention of Brest cancer Brest cancer
research 2014.16:446

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CASE STUDY ON ECLAMPSIA

DEFENITION:

Eclampsia is the onset of fits in a woman whose pregnancy is usually complicated by pre-
eclampsia. The fits may occur in pregnancy after 20 weeks gestation, in labour, or during the
first 48 hours of the postpartum period.

TYPES OF ECLAMPSIA:

Based upon the timing of eclamptic seizure onset in regards to gestational age three types
of eclampsia exist.

1. Antepartum eclampsia (occurring prior to labor) most often occurs preterm (before 37 weeks
of gestation)

2. Intrapartum (during labor) and

3. Postpartum (after delivery of the fetus and placenta) occur more often at term .

STAGES OF ECLAMPSIA:

Premonitory stage:

This lasts 10-20seconds, during which: The eyes roller stare

• The face and hand muscles may twitch.

Tonic stage:

This lasts up to 30seconds, during which: The muscles go into violent spasm

• The fists are clenched and arms and legs are rigid The diaphragm is in spasm, so that breathing
stops and the colour of the skin becomes blue or dusky (cyanosis)

• The teeth are clenched The eyes bulge.

Clonic stage:

• This lasts 1-2minutes and is marked by:

• Violent contraction and relaxation of the muscles
• Increased saliva causes "foaming" at the mouth and there is a risk of inhalation
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• deep Noisy breathing

• The face looks congested (filled with blood) and swollen

Coma stage:

This may last for minutes or hours. The woman is deeply unconscious and often breathes
Noisily. The cyanosis fades buther face may still be swollen and congested. Further fit

ETIOLOGY:

The mechanism(s) responsible for the development eclampsia remain(s) unclear. Genetic
predisposition, immunology, endocrinology, nutrition, abnormal trophoblastic invasion,
coagulation abnormalities, vascular endothelial damage, cardiovascular maladaptation,
dietary deficiencies or excess, and infection have been proposed as etiologic factors for
eclampsia. Imbalanced prostanoid production and increased plasma anti phospholipids have
also been implicated in eclampsia.

EPIDEMIOLOGY:

World Health Organization estimated, at least 16% of maternal deaths in low- and middle-
income countries (LMICs) result from hypertensive disorders of pregnancy, of which
eclampsia is the primary contributor. Largely on the basis of clinical data, the incidence of
eclampsia ranges between 2% and 10%, depending on the population studied and the
definition of eclampsia used. The proportion of deliveries impacted by eclampsia in Indian
women ranges from as low as 0.9% to as high as 7.7%.

RISK FACTORS:

MODERATE RISK FACTORS:

• Maternal age ≥ 40 years.

• Maternal BMI ≥ 35 at initial presentation
• . Family history of pre-eclampsia.
• Pregnancy interval > 10 years Multiple pregnancy.

HIGH RISK FACTORS:

• Chronic hypertension

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• HTN,
• pre-eclampsia or eclampsia in previous pregnancy.
• Pre-existing chronic kidney disease
• Diabetes Mellitus
• Kemane diseases (e.g. SLE, anti-phospholipid syndrome)

COMPLICATIONS:

Maternal Complication :

• Death
• Adult respiratory distress syndrome
• Stroke(encephalopathy or cerebral haemorrhage)
• Pulmonary oedema
• HELLP syndrome with or without liver haemorrhage
• Acute renal failure

Fetal complications:

• Fetal growth restriction

• Oligobyramnios
• Hypoxia-acidosis
• Preterm delivery
• Death
• Long term morbidity

PATHOPHYSIOLOGY:

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SIGNS AND SYMPTOMS:

• Elevated blood pressure

• Swelling in face or hands
• Headaches
• Excessive weight gain
• Nausea and vomiting
• Vision problems, including episodes with loss of vision or blurry vision
• Difficulty urinating
• Abdominal pain, especially in the right upper abdomen
• Seizures
• Loss of consciousness
• Agitation

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DIAGNOSIS:

CT Scanning and MRI of the Head:

Computed tomography (CT) scanning of the head, with or without contrast, can
exclude cerebral venous thrombosis, intracranial haemorrhage, and central nervous system
lesions, all of which can occur in pregnancy and present with seizures. CT scan findings may
include the following: Cerebral oedema, Diffuse white matter low-density areas, Patchy area
of low density, Occipital white matter oedema, Loss of normal cortical sulci, Reduced
ventricular size, Cerebral haemorrhage, Intraventricular haemorrhage, Parenchymal
haemorrhage (high density), Cerebral infarction, Low attenuation areas, Basal ganglia
infarctions.

Abnormal magnetic resonance imaging (MRI) findings of the head have been
reported in up to 90% of women imaged. These include an increased signal at the gray-white
matter junction on T2-weighted images, as well as cortical edema and hemorrhage. The
syndrome of posterior reversible encephalopathy (PRES), indicative of central vasogenic
edema, has been increasingly recognized as a component of eclampsia.

Electroencephalography and CSF Studies:

Electroencephalograms and cerebrospinal fluid studies are rarely useful in

management; however, they may be indicated if epilepsy or meningitis is considered in the
diagnosis.

Liver Function Tests:

Liver function test results may reveal the following (20-25% of patients with
eclampsia).

*Aspartate aminotransferase (SGOT) level higher than 72 IU/L "Total bilirubin levels higher
than 1.2 mg/dL.

*LDH level higher than 600 IU/L

*Elevated levels due to hepatocellular injury and HELLP syndrome

Serum Creatinine level:

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The serum creatinine level is elevated in eclampsia because of a decreased intravascular

volume and a reduced glomerular filtration rate (GFR). Creatinine clearance (CrCl) may be
less than 90ml/mi/1.73m².

Urinalysis and Uric Acid levels:

Proteinuria is typically one of the presenting symptoms in patients with eclampsia. A

timed collection has been the criterion standard for urinalysis to detect proteinuria (>300 mg
24 h or 1 g/L). Protein per unit time measured over 24 hours has been used traditionally:
however, 12-hour collections have proved to be as accurate. In addition, it is now common to
rely upon a spot protein to creatinine ratio to assess proteinuria, instead of a timed collection.
The degree of proteinuria or change in proteinuria is helpful in diagnosing preeclampsia, but
does not have any significant effect on clinical management.

MANAGEMENT:

The management of eclampsia involves the following stages:

• Making sure the airways are clear and the woman can breathe.

• Controlling the fits Controlling the blood pressure. General care and monitoring, including
controlling fluid balance.

• Monitoring carefully to prevent further fits and identify complications.

CONTROLLING FITS:

Fits are controlled by giving the woman anticonvulsant drugs. The drug of
choice for both the prevention and treatment of eclampsia is magnesium sulphate. If
magnesium sulphate is not available, diazepam may be given.

Magnesium sulphate:

Loading dose:

Give 4 g of 20% magnesium sulphate IV slowly over 5 minutes. Magnesium sulphate should
not be given as a bolus. Follow immediately with 10g of 50% magnesium sulphate solution,
5g in each buttock as deep IM injection, with Iml of 2% lignocaine in the same syringe.

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Good aseptic technique is essential when giving IM magnesium sulphate. The woman may
have a feeling of warmth during the injection, but this is normal. If convulsions Recur after
15minutes, give 2g magnesium sulphate (50%solution) IV over 5minutes.

Maintenance dose:

Give 5g magnesium sulphate (50%solution) together with Iml lignocaine 2% in the same
syringe every 4hours into alternate buttocks. Continue the treatment with magnesium
sulphate for 24 hours after delivery or the last convulsion, which are occurs last.

Diazepam:

Use only if magnesium sulphate is not available.

Loading dose: Give diazepam 10mg IV slowly over 2minutes. If convulsions recur, repeat
the loading dose.

Maintenance dose: Give diazepam 40mg in 500ml IV fluid (Ringer's lactate or normal
saline) titrated to keep the woman dated but able to be roused.

CONTROLLING BLOOD PRESSURE:

Antihypertensive drugs:

Antihypertensive drugs should be given if the diastolic blood pressure is 110mmHg

or more. The aim is to keep the diastolic blood pressure between 90-100 mmHg to prevent
cerebral hemorrhage. Hydralazine is the drug of choice.

Hydralazine:

Give hydralazine 5mg IV slowly every 5minutes until blood pressure is lowered.
Repeat hourly as needed or give hydralazine 12.5mg IM every 2hours as needed. If
hydralazine not available, give another antihypertensive drug, e.g. labetalol 10mg IV. The
dose can be doubled to 20mg, 40mg and 80mg. with a 10-minute interval between each
increased dose, until a satisfactory response is achieved, i.e. the blood pressure falls.

FLUID MANAGEMENT:

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One of the main causes of maternal death is cardiorespiratory failure. Eclamptic

women, although possibly hypo voluaemic, are grossly fluid overloaded if total body fluid is
skin into account. This is due to edema which is common in these patients and any fluid
management policy should take this into consideration. In order to reduce the chances of
iatrogenic complications, especially pulmonary edema, left ventricular failure and adult
respiratory distress syndrome, both fluid input and output should be closely monitored. In an
effort to increase the plasma osmotic pressure, colloid solutions are often used. Intravenous
fluid should be given at a rate of 80 ml/hour (1 ml/kg/hour) or the previous hour's urine put
plus 30 ml. Urine output is best monitored by siting an indwelling urethral catheter
maintaining an hourly fluid balance chart.

REFERENCES:

1. Pathologic basis of disease, 7th edition by Robbins and cotran.

2. http://teachmeobgyn.com/labour/emergencies/eclampsia
3. http://emedicine.medscape.com/article/253960-overview#a15
4. http://www.nhp.gov.in/disease/gynaecology-and-obstetrics/preeclampsia

5. Text book of pathophysiology 5th edition by Harsha Mohan.

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CASE STUDY ON GOUT

DEFINITION:
Gout is a form of inflammatory arthritis that develops when there is a high level of uric acid
in the blood (hyperuricemia). The acid can form needle-like crystals in a joint and cause sudden,
severe episodes of pain, tenderness, redness, warmth, and swelling.
EPIDEMOLOGY:
The prevalence of gout as the 125. hac men over the last twenty y 1.3 million (44) Americans.
Contis mors The having gout rises with age, with a page of 75, menopause. Among the US
population, abs 21% verd d condition known as bygerunamis. However, hyperuricemia will
actually develop post. It pumps have gist. the of developing it

ETIOLOGY
Mainly associated with the slower in the purse metabolism
• Hypouricemia -Over production & under excretion of uric and in the hog
• Excess nucleoprotein trover
• Psoriasis (1 cell proliferation or death
• Genetic disorder (Lesh-Nyhan Syndrome)
• Drugs & thiarides, loop diuretics, PZA, Cyclosporine’s
• Alcohol abuse
• Dehydration

RISK FACTORS:
• Diet rich in meat, seafood, alcohol (beer)
• Obesity produces more uric acid
• Medical conditions-diabetes, metabolic syndrome, and heart and kidney disease
• Certain medications thiazide diuretics, aspirin
• Family history of gout
• Age & Sex more often in men & between age of 30-50 years
• Recent surgery or trauma

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SIGNS & SYMPTOMS

• Intense joint pain
• Lingering discomfort
• Inflammation & redness
• Limited range of motion
• Tophi accumulation of uric acid crystals
• Red or purple skin around the joins
• Swelling & warm

COMPLICATIONS
People with gout may develop complications if untreated
Advanced gout:
• if untreated, uric acid crystals can get deposited under the skin in called as sophii
• This can be present is fingers, hands, feet, elbows or Achilles etc
• Usually painless, during gout attacks these may become swollen and tender
Recurrent gout:
• For some people gout may reoccur again multiple times a year these could damage joints
Kidney Stone:
• Uric acid crystals deposited on the kidney tubes can be kidney stone

PATHOPHYSIOLOGY:

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DIAGNOSIS

• Joint fluid test - Urate crystals may be visible when the flood in examined under
microscope
• Blood test- To measure the levels of arc acid and creatinine in the blood.
• X-ray imaging Joint X-rays can be helpful to take her ses inflammation
• Ultrasound-Musculoskeletal ultrasound can detect wate cystic inapot or in a tophus.
• Dual energy CT scan - This type of anaging can detect the presence of weste tryna ina joint,
even when it is not autely inflamed

TREATMENT

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• Non-steroidal anti-inflammatory drugs (NSAIDS) art frequently and to lieve the pain
and swelling of an acute gout episode. They can shorten the artask, especially if kan in the
first 24 hours
• Corticosteroids These drugs can be taken by mouth or opested into an end to quickly
relieve the pain and swelling of an aur atack. Content working within 24 hours after they
are takes.
• Colchicine This anti-inflammatory medicine works best if taken within the fire 24
beurs of a gout atack. Colchicine is also given to reduce inflammation during an acute
gout attack
• Allopurinol reduces the amount of uric acid your body produces.
• Colchicine prevents white blood cells from sttacking gout crystal, A standard dose is
0.6 mg once or twice a day. In addition to helping prevent future attacks, colchicine
may effectively reduce inflammation during an acute gout attack

• Probencid helps your kidneys filter out more uric acid from your body
• Febuxostat lowers uric acid levels. Although more expensive than allopurinol,
febuxostat is an option for patients who cannot take probenecid or allopurinol
REFERENCES:
1. https://orthoinfo.aaos.org/en/diseases-conditions/gout/
2. https://www.msk.org.au/gout/
3. complications of gout-Bing
4.https://www.rheumatology.org/I-Am-A/Patient-Caregiver/Diseases-Condition/Cout
5. Hyon K Chol David Mount, Anthony M Reginato. Pathogenisis of Gout. Research
Gate.2005;143(7):499-516
6. https://www.versusarthritis.org/about-arthritis/conditions/gout/

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CASE STUDY ON BELL’S PALSY

DEFINITION:

• Bell's Palsy is an idiopathic condition caused by a dysfunction in Cranial Nerve VII (CN
VII), also known as the Facial Nerve.
• CN VII has motor, sensory and parasympathetic components. CN VII innervates the
muscles of facial expression, sensory for taste to the anterior 2/3 of the tongue and
parasympathetic innervation to the lacrimal gland (tear duct) and most of the salivary
glands.
• Factors that may increase the risk of Bell’s Palsy are diabetes, high blood pressure,
toxins, infections
(herpessimplexvirus1(HSV1),humanimmunodeficiencyvirus(HIV),shingles/chickenpox,
Lyme Disease, Epstein-Barr Virus and ischemia .
• Bell's Palsy can occur at any age, but it is most common between 15-60 years of age, and
is believed to be a possible reaction to a viral infection that causes inflammation and
swelling to CN VII.

HISTORY:

• Patients present with rapid and progressive symptoms over the course of a day to a week
often reaching a peak in severity at 72 hours. Weakness will be partial or complete to
one-half of the face, resulting in weakness of the eyebrows, forehead, and angle of the
mouth. Patients may present with an inability to close the affected eyelid or lip on the
affected side.
• The key physical exam finding is a partial or complete weakness of the forehead. If
forehead strength is preserved, a central cause should be investigated. Patients may also
complain of a difference in taste, sensitivity to sound, nostalgia, and changes to tearing
and salivation. Ocular features include the following:

• Corneal exposure

• Brow droop

Paralytic ectropionise of the lower lid

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Upper eyelid retraction

Decreased tear output

SYMPTOMS:

• Loss of nasolabial fold

• Drooling, Headache, Facial swelling.
• Muscle weakness or paralysis.
• Overall droopy facial appearance.
• Impossible or difficult to blink.
• Lusty eating and drinking.
• Difficulty speaking, Forehead wrinkles disappear.

EPIDEMIOLOGY:

The annual incidence is 15 to 20 per 100,000, with 40,000 new cases yearly. The lifetime risk is
1 in 60. The recurrence rate is 8% to 12%. Even without treatment, 70% of patients will have
complete resolution.

There is no gender or racial preference, and palsy can occur at any age, but more cases are seen
in mid and late life, with the median age of onset at 40 years. Risk factors include diabetes,
pregnancy, preeclampsia, obesity, and hypertension.

CAUSES:

Although the exact reason Bell's palsy occurs isn't clear, it's often related to having a viral
infection. Viruses that have been linked to Bell's palsy include viruses that cause:

• Cold sores and genital herpes, also known as herpes simplex.

• Chickenpox and shingles, also known as herpes zoster.

• Infectious mononucleosis, caused by the Epstein-Barr virus.

• Cytomegalovirus infections.

• Respiratory illnesses, caused by adenoviruses.

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• German measles, also known as rubella.

• Mumps, caused by the mumps virus.

• Flu, also known as influenza B.

• Hand-foot-and-mouth disease, caused by a coxsackievirus.

RISK FACTORS:

Bell's palsy occurs more often in people who:

• Are pregnant, especially during the third trimester, or who are in the first week after giving
birth.

• Have an upper respiratory infection, such as the flu or a cold.

• Have diabetes.

• Have high blood pressure.

• Have obesity.

It's rare for Bell's palsy to come back. But when it does, there's often a family history of repeated
attacks. This suggests that Bell's palsy might have something to do with genes.

PATHOPHYSIOLOGY:

Bell palsy is thought to result from compression of the seventh cranial nerve at the geniculate
ganglion. The first portion of the facial canal, the labyrinthine segment, is the narrowest; most
cases of compression occur in the labyrinthine segment. Due to the narrow opening of the facial
canal, inflammation causes compression and ischemia of the nerve. The most common finding is
a unilateral facial weakness that includes the muscles of the forehead.

DIAGNOSIS:

This case presented a patient, Mrs. S age 34, with a diagnosis of Bell's Palsy, who presented with
acute right- sided facial muscle weakness and facial droop, dry eye and functional difficulty with
speaking and drinking. Her facial weakness is classified as moderately severe on the House-

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Brackman facial nerve scale. The patient's primary concerns were jaw pain, functional
difficulties with speaking and drinking and trouble working at the computer due to dry eye.

• Electromyography (EMG). This test can confirm the presence of nerve damage and determine
how serious it is. An EMG measures the electrical activity of a muscle in response to stimulation.
It also measures the nature and speed of the conduction of electrical impulses along a nerve.

• Imaging scans. Magnetic resonance imaging (MRI) or computerized tomography (CT) may be
needed on occasion to rule out other possible sources of pressure on the facial nerve, such as a
tumour or skull fracture.

• Blood tests. There is no blood test for Bell's palsy. But blood tests can be used to rule out
Lyme disease and other infections.

MANAGEMENT:

Non pharmacological therapy:

Physical therapies including tailored fa- coal exercises, acupuncture to affected muscles,
massage, thermotherapy and electrical stimulation have been used to hasten recovery.

However, there is no evidence for any significant benefit. A Cochrane review concluded from
poor- quality evidence that tailored facial exercises can help improve facial function, mainly for
moderate paralysis and chronic cases.

Early facial exercise may reduce recovery time, long-term paralysis and number of chronic
cases.

Pharmacological therapy:

• The treatments considered for Bell's palsy include oral corticosteroids (prednisolone) and
antiviral drugs. Although the aetiology of Bell's palsy is uncertain, it is known that
inflammation and oedema of the facial nerve are response blew for the symptoms.
Corticosteroids have therefore been used for their anti-in- amatory effect.
• Corticosteroids The maximum benefit is seen when steroids are commenced within 72
hours of the onset of sump- toms. There is no optimum regimen, but in adults 50-60 mg
prednisolone daily for 10 days has been commonly used.6.7 Prednisolone has been used

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at a dose of 1 mg/kg/day up to a maximum of 80 mg in some studies. Doses of more than

120 mg/day have been used safely in partier↑ with diabetes.
• In a randomised controlled trial, the re- cover rate at nine months with pred nisolone was
94%. It was 81.6% in patients who did not receive prednisolone.
• A systematic review of trials that used prednisolone showed that at six months 17% of
patients had incomplete recovery compared with 28% of patients who received no
treatment. There was also a significant reduction in motor silkiness in those who received
prednisolone. There was no significant reduction in cosmetically disabling squeal.
• Antiviral drugs. The role of antivirals is not certain. Antivirals alone have shown no
benefit compared with placebo. Antivirals added to steroids may benefit some people
with Bell's palsy, but this is still not proved.
• Despite this, an antiviral medicine, such as Val acyclovir (Valtrex) or acyclovir, is
sometimes given in combination with prednisone in people with severe facial palsy.
Physical therapy:
Paralyzed muscles can shrink and shorten, which may be permanent. A physical therapist
can teach you how to massage and exercise your facial muscles to help prevent this from
occurring.
Surgery:
In the past, decompression surgery was used to relieve the pressure on the facial nerve by
opening the bony passage that the nerve passes through. Today, decompression surgery
isn't recommended. Facial nerve injury and permanent hearing loss are possible risks
associated with this surgery.
• Rarely, plastic surgery may be needed to correct lasting facial nerve problems. Facial
reanimation surgery helps make the face look more even and may restore facial
movement. Examples of this type of surgery include an eyebrow lift, an eyelid lift, facial
implants and nerve grafts.

COMPILATION:

Mild symptoms of Bell's palsy typically disappear within a month. Recovery from more-
complete facial paralysis can vary. Complications may include:

• Irreversible damage to your facial nerve.

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• Irregular regrowth of nerve fibbers. This may result in involuntary contraction of certain
muscles when you're trying to move other muscles, known as silkiness. For example, when you
smile, the eye on the affected side may close.

• Partial or complete blindness of the eye that won't close. This is caused by excessive dryness
and scratching of the clear protective covering of the eye, known as the cornea.

CONCLUSIONS:

• The symptoms of Bell's palsy vary from mild to severe. The aetiology is still un- clear,
but it is known that the symptoms are caused by swelling and inflammation of the facial
nerve. Eye protection re- mains crucial in preventing long-term eye complications.
• Drug treatment is controversial, given that over 70% of patients will eventually recover
normal facial function without treatment. Early treatment with prod- nisolone can hasten
recovery and reduce long-term squeal. Although the quality of evidence is low to
moderate, there may be some benefit in adding antiviral drugs to prednisolone.

REFERENCE:

1. Rhizopodial. Bell's Palsy. Available from: https://www.physio- pedia.com/Bell%27s_Palsy

(accessed 8 May 2020)

2. John Hopkins Medicine. Bell's Palsy. Available from:

palsy: a review. J

Neurol. 2019. https://doi.org/10.1007/s00415-019- 09282-4

4.1 Mayo Clinic. Bell's Palsy. Available from

https://www.mayoclinic.org/diseases- conditions/bells-palsy/symptoms- causes/syc-20370028

(accessed 15 May 2020)

5. National Institute of Neurological Disorders and Stroke. Bell's Palsy Fact Sheet. Available
from:

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https://www.ninds.nih.gov/Disorders/P patient-Caregiver-Education/Fact- Sheets/Bells-Palsy-

Fact-Sheet (accessed 14 May 2020)

6.1 6.0 6.1 Murthy JMK, Sabena AB. Bell's palsy: treatment guidelines. Ann Indian Aced
Neurol. 2011;14:S70-S72.

7. John Hopkins Medicine. Bell's Palsy. Available from: https://www.hopkinsmedicine.org/healt

h/conditions-and-diseases/bells-palsy (accessed 8 Mav 2020)

8.1 Mayo Clinic. Bell's Palsy. Available from

https://www.mayoclinic.org/diseases- conditions/bells-palsy/symptoms- causes/syc-20370028

(accessed 15 May 2020)

9. National Institute of Neurological Disorders and Stroke. Bell's Palsy Fact Sheet. Available
from: https://www.ninds.nih.gov/Disorders/P patient-Caregiver-Education/Fact- Sheets/Bells-
Palsy-Fact-Sheet (accessed 14 May 2020)

10. Macho VB, Gayer I, Daly F, Saundra D, Sullivan M, Gammier F et al. Corticosteroids for
Bell's Palsy (idiopathic facial paralysis) (Cochrane review). Cochrane Database Sits Rev 2016;
(2):CD001942

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CASE STUDY ON CHRONIC KIDNEY DISEASE (CKD)

DEFINITION:
Chronic kidney disease (CKD) is a progressive, irreversible deterioration of renal function in
which the body ability to maintain metabolic, fluid and electrolyte balance fails, resulting in
uraemia or azotaemia (retention of urea and other nitrogenous waste in blood)

STAGES OF CKD:

Stages Description Percentage

Stage 1 Kidney damage with normal kidney function 90 – 100%
Stage 2 Kidney damage with mild loss of kidney function 89 – 60%
Stage 3a Mild to moderate loss of kidney function 59 – 45%
Stage 3b Moderate to severe loss of kidney function 44 – 30%
Stage 4 Severe loss of kidney function 29 – 15%
Stage 5 Kidney Failure Less than 15%

EPIDEMIOLOGY:
• CKD is estimated to be more common in women than in men (16% vs 13%)
• According to Nephrology Dialysis Transportation there are 7.85 million CRF patients in
India. Etiologically diabetes (41%), hypertension (22%), chronic glomerular nephritis (16%),
chronic interstitial disease (5.4%), ischaemic nephropathy (5.4%), obstructive uropathy
(2.7%) and unknown cause (5.4%) constituted the spectrum.

ETIOLOGY:
• Diabetes
• Hypertension
• Obstructed urine flow
• Kidney diseases

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• Kidney artery stenosis

• Certain toxins - including fuels, solvents (such as carbon tetrachloride), and lead etc.
• Fetal developmental problem
• Systemic lupus erythematosus
• Malaria and yellow fever
• Some medications - for example, NSAIDs
• Illegal substance abuse - such as heroin or cocaine.
• Injury - a sharp blow or physical injury to the kidney

PATHOPHYSIOLOGY

Due to Etiological Factors

Decreased GFR

Hypertropy of remaining Nephrons

Inability to Concentrate Urine

Further loss of Nephron Funtion

Loss of Non - Excretory and Excretory Function

Chronic Kidney Disease (CKD)

CLINICAL MANIFESTATIONS:

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According to
• URINARY SYSTEM
▪ . Polyuria
▪ Oliguria
▪ Anuria
• CARDIAC
▪ HTN
▪ Heart Failure
▪ Pericarditis
▪ CAD
• GASTRO INTESTINAL SYSTEM
▪ Anorexia
▪ Nausea
▪ Vomiting
• SKIN :
▪ Pruritus
▪ Pallor
• NEUROLOGICAL
▪ Altered Mental Ability
▪ Seizures and coma
▪ Dialysis encephalopathy
▪ Restless leg syndrome
▪ Muscle twitching
▪ Irritability
▪ Decreased ability to concentrate
• Hematologic :
▪ Anaemia
▪ Altered immune response and function
▪ Diminished inflammatory response
• Pulmonary :

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▪ Crackles
▪ Tachypnoea
▪ Kussmaul - type respirations
▪ Uremic pneumonitis
• Reproductive :
▪ Amenorrhea
▪ Infertility
▪ Decreased libido
• Electrolyte imbalance :
▪ Hyperkalaemia
▪ Metabolic acidosis
▪ Hyponatremia
• Musculoskeletal :
▪ Muscle cramps
▪ Loss of muscle strength renal osteodystrophy bone pain
▪ Bone fractures
▪ Foot drop

RISK FACTORS
• Diabetes Mellitus
• Hypertension
• Cardiovascular Disease
• Obesity
• Age and Race
• Acute Kidney Injury
• Malignancy
• Family history of CKD
• Kidney Stones
• Infections like Hepatitis C and HIV
• Autoimmune diseases
• Nephrotoxic like NSAIDS
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COMPLICATIONS
• Fluid retention
• Hyperkalaemia
• Cardiovascular disease
• Weak bones and an increased risk of bone fractures
• Anaemia
• Decreased sex drive, erectile dysfunction or reduced fertility.
• Damage to your central nervous system.
• Decreased immune response.
• Pregnancy complications that carry risks for the mother and the developing fetus
• Irreversible damage to your kidneys (end-stage kidney disease)

DIAGNOSIS:
1 History Collection
2 Physical Examination
3 Urine output measurements : Measuring how much urinate in 24 hours
4 URINE TESTS
a) Urinalysis: Dipstick test, urine albumin and creatinine.
b) Twenty - four - hour urine tests: The urine may be analysed for protein and waste products
(urea, nitrogen, and creatinine).
c) Glomerular filtration rate: As kidney disease progresses, GFR fall.
5 BLOOD TESTS:
a) Creatinine and urea (BUN) in the blood
b) Electrolyte levels and acid-base balance
c) Blood cell counts
d) Erythropoietin
6 OTHER TESTS:
a) Abdominal ultrasound: Kidneys with CKD are usually smaller (<9 cm) than normal
kidneys.
b) Renal Biopsy

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c) Abdominal CT scan
d) Abdominal MRI
e) Renal scan

Treatment:
Pharmacological treatment:
1 Treatment of underlying conditions such as diabetes, hypertension, autoimmune diseases
etc.
2 Treatment of fluid overload
Diuretics: Furosemide, oral/IV 4-120mg daily
3 Treatment of hypertension (goal of BP<130/80 mm of Hg)
• ACE inhibitors: Lisinopril, oral 5-40 mg daily
Ramipril, oral 2.5-10mg daily
• ARB's: Losartan, oral, 25-100mg daily
Valsartan, oral, 80-160mg daily
4 Treatment of Anaemia
• Injection of erythropoietin 50-100 units IV/SC 3 times weekly Treatment is initiated at
HB<10gm/dl
• Tab ferrous sulphate 200mg 3 times daily
5 Treatment of hyperkalaemia/metabolic acidosis
• 10% calcium gluconate, IV 10-20ml over 2-5 mins plus
• Sodium bicarbonate IV 8.4% 50mEq over 5 mins plus
• Regular insulin, IV 10 units in 50-100 ml glucose 50%
6 Treatment of hyperphosphatemia
• Phosphate binders (calcium acetate / calcium carbonate 2 capsules (1334mg) orally
with food)
7 Treatment of hypocalcaemia
• Calcium citrate 1 gm./day
• Vitamin B supplements; 2 tablets (800 IU) once daily
8 Treatment of pruritus
• Capsaicin cream/cholestyramine

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9 Treatment of bleeding
• Desmopressin 0.3mcg/kg IV over 15-30 mins.
10 Renal replacement therapy (RRT)
• Kidney transplant with immunosuppressive agents
11 Dialysis
12 Kidney transplantation and then immunosuppressive therapy

GOALS OF TREATMENT:
▪ To preserve renal function
▪ To delay the need for dialysis or transplantation as long as feasible.
▪ To alleviate extra renal manifestations as much as possible.
▪ To improve body chemistry values.
▪ To provide an optimal quality of life for the client & significant others.

NON-PHARMACOLOGICAL TREATMENT:
▪ Diet maintenance
▪ General health advice like smoking cessation
▪ Water and electrolyte balance
▪ Daily weighing
▪ Avoid Nephrotoxic like NSAID's, Herbal medication
▪ Admit patient especially in stage of exacerbation.

REFERENCES:
1 https://www.mayoclinic.org/diseases-conditions/chronic-kidney
disease/symptomscauses/syc-20354521
2 https://www.kidney.org/tez/content/about-chronic-kidney-disease
3 Chen TK, Knicely DH, Grams ME. Chronic Kidney Disease Diagnosis and Management:
A Review. JAMA. 2019; 322(13):1294-1304. Doi: 10.1001/jama.2019.14745

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CASE STUDY ON SCRUB TYPHUS

Definition:

Scrub Typhus is a disease caused by bacteria called "orientia tsutsugamushi". It is also known as
Bush Typhus.

Epidemiology:

It is a common Re-emerging rickettsial infection in India, South East Asian countries.

It is distributed in "tsutsugamushi triangle" bound by Japan, through China, the Philippines,

tropical south Australia, Pakistan, possibly to Tibet to Afghanistan, southern parts of USSR in
north.

Etiology:

It is caused by Orientia tsutsugamushi. It is transmitted to humans by a bite of an arthropod

vector of "Thrombiculidae family" (Leptotrombidium deliensse, L. akamushi).

Vector Infected chiggers (Larval mites)

Host - Small rodents, particular wild rats of sub species Rattus and acraine hosts

Pathogenesis:

Severity depends on strain involved in causing the fever.

* Orientia tsutsugamushi invades endothelial cells

I To Produce

Disseminated Vasculitis & Perivascular inflammatory lesions

I Results in

Significant vascular leakages & End organ injury [Lung, Heart, Kidney]

Orientia tsutsugamushi

I Induces Formation of

Several Cytokines

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[Granulocyte Colony Stimulating factor (CSF), Macrophages-CSF, Interferon y, TNF-y]

Cytotoxic T lymphocytes, NK cells, playplay important role in destroying infected host cells.

The Organism down regulates host defense mechanism by downregulating GP 96 on

macrophages and endothelial cells which plays a primary role in Antigen presentation, function
of dendritic cells, antibody production, cross primary immune system Response Immune

I Against

Orientia tsutsugamushi

1.Humoral immunity 2. Cell Mediated immunity

1.Production of strain specific antibodies against organism.Reduces organisms’ capacity to enter

cells by altering non specific attractions between infections agents & infected cells.

2.T Lymphocytes are involved producing interferon Y by mononuclear cells in peripheral blood.

Clinical Features: Incubation period of O. tsutsugamushi in humans is 10-20 days.

This is characterized by

Fever.

O Pyrexia of unknown origin (POU).

O Head ache.

O Myalgia.

O Cough.

Gl symptoms.

Mental changes ranging from confusion to coma.

*Severity of symptoms depends up on susceptibility of host, virulence of bacteria strain or both.

*The first sign of scrub typhus is vesicular lesion at site of mite where feeding, which in turn
converts into an “ESCHAR”.

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Risk Factors:

1.Presence of scrub vegetation around the house.

2.Presence of wood piles around the house.

3.Presence of cattle and pets around the house 121.

Diagnosis:

Fever and Eschar presence supports the diagnosis.

1. Serology

In case of primary infection,

*IgM antibodies appear at end of the first week.

*IgG antibodies appears at end of second week.

In case of reoccurrence with O. tsutsugamushi IgG antibodies are detectable at day 6 and IgM
antibodies are variable .

2. Gold Standard test: Indirect immunofluorescence antibody (IFA).

This test detects specific antibodies bound to SMEARS of S.T antigen.

o It is very expensive.

* Requires specialized lab & equipment's.

3. Rapid Diagnostic test: Immuno Chromatographic test (ICT).

4. Weil-Fleix test (WF test):

Cheapest test and widely available serological test.

It's a very tedious process. Cell culture time consuming 4 weeks.

5. Loop Isothermal Amplification:

Amplifying DNA that makes use of 3 Specially designed Primer pairs and best DNS polymerase.
It’s very simple but expensive process.

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6. PCR-Conducted by collecting ESCHAR sample.

Treatment:

* Doxycycline or tetracycline are most commonly prescribed antibiotics. Chloramphenicol.

* Strains resistant to azithromycin and rifampicin are reported in northern Thailand.

Rifampicin, Azithromycin is alternative.

When doxycycline resistance is suspected in children less than 8 years and pregnant women,
azithromycin is alternative.

Ciprofloxacin cannot used in pregnancy as it may associated with still births. Miscarriage

Combination therapy of doxycycline and rifampicin is not recommended due to possible

antagonism 14).

* Doxycycline 100mg/200mg IV BD or PO BD/OD.

* Doxycycline 100mg BD for 7 days 151

In severe conditions 500mg 6th hourly for 7 days

50-75 mg/kg/day in children.

Rifampicin 600mg PO BD for 5 days.

* Azithromycin 500mg PO OD for 5 days.

0 Other supportive and symptomatic treatment are suggested to minimize the risk.

Prevention:

* NO vaccines are available for Scrub typhus.

Reduce the risk by avoiding contact with infected chiggers.

References:

1. Sayantani chakra borty, Nilendu sarma. Scrub Typhus: An Emerging Threat. Indian
journal f ermatology. 2017 sepoct, 62 (5): 478485: doi: 10.4103/ijd_388_17 PMCID:
PMC J618834.

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2. 2. Tina George et al., Risk Factors For Acquiring Scrub Typhus among the Adults.
Journal of Global Infectious Diseases.2018 Jul-Sep; 10(3): 147-151. Doi:
10.4103/jgid.jgid_63_17.
3. 3. Dasch GA. Halle S, Bourgeosis AL. Sensitive microplate enzyme-linked
immunosorbent assay for detection of antibiotics of antibiotics against scrub typhus
ricettesia, Ricettessia tsutsugamushi.j. clin.1979;9:38-48.

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CASE STUDY ON HAEMORRHAGIC STROKE

INTRODUCTION:

There are two types of strokes, haemorrhagic and ischemic. A haemorrhagic stroke is either a
brain aneurysm burst or a weakened blood vessel leak. Blood spills into or around the brain and
creates swelling and pressure, damaging cells and tissues in the brain. Haemorrhagic strokes are
less common, in fact only 15 percent of all strokes are haemorrhage, but they are responsible for
about 40percent of all stroke deaths.

• There are two types of haemorrhagic strokes called intracerebral and subarachnoid.
• Intracerebral haemorrhage: The bleeding occurs inside of the brain. This is the most
common type of haemorrhagic stroke.
• Subarachnoid haemorrhage: The bleeding occurs between the brain and the membranes
that cover it.

EPIDEMIOLOGY:

• There are approximately 800 to 1000 new or recurrent strokes per year in the United
States, of which-10% to 15% are haemorrhagic.

ETIOLOGY:

• Uncontrolled high blood pressure

• Overtreatment with blood thinners (anticoagulants)
• Bulges at weak spots in your blood vessel walls (aneurysms)
• Trauma (such as a car accident)
• Protein deposits in blood vessel walls that lead to weakness in the vessel wall (cerebral
amyloid angiopathy)
• Ischemic stroke leading to hemorrhage.

SIGNS AND SYMPTOMS

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RISK FACTORS:

• Factors associated with a higher risk of stroke include:

• Age People age 55 or older have a higher risk of stroke than do younger people.
• Race African Americans have a higher risk of stroke than do people of other races.
• Sex-Men have a higher risk of stroke than women. Women are usually older when they
have strokes, and they're more likely to die of strokes than are men.
• Hormones-Use of birth control pills or hormone therapies that include estrogen increases
risk

PATHOPHYSIOLOGY

DIAGNOSIS:

The ICH score is a widely used grading seale for risk stratification. Parameters used to calculate
the ICH score include Glasgow Coma Scale (GCS) (0 to 2 points) at presentation, patient age
280 (1 point), ICH volume ≥30 ml. (1 point), presence of intraventricular blood (1 point), and

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infratentorial origin of blood (1 point). Scores range from 0 to 6 with a score of 0 conferring 0%
mortality and a score of 6 with estimated 100% mortality.

Blood tests Complete blood count, electrolytes and creatinine, glucose and coagulation studies
should be obtained.

Neuroimaging :

• NON-CONTRAST COMPUTERIZED TOMOGRAPHY: Non contrast

• computerized tomography (NCCT) is a fast technique with excellent sensitivity for
identifying acute ICH. Beyond the diagnosis of ICH, NCCT can provide useful elements
such as, presence and degree of edema, and midline shift or brainstem compression
secondary to the mass effect from the hematoma.
• CT ANGIOGRAPHY: CT Angiography (CTA) is the most widely available, non-
invasive technique for the detection of vascular abnormalities as secondary causes of
ICH. Presence of extravasation within the hematoma on CTA images, also termed spot
sign, is an independent predictor of hematoma expansion and poor outcome in patients
with supratentorial ICH.
• MAGNETIC RESONANCE IMAGING: Magnetic resonance imaging (MRI) can be a
useful technique to detect underlying secondary causes of ICH such as neoplastic lesions
or haemorrhagic transformation of ischemic stroke.

TREATMENT:

NON-PHARMACOLOGICAL TREATMENT:

• Controlling high blood pressure (hypertension). Having a stroke, lowering your blood
pressure can help prevent a subsequent stroke. Healthy lifestyle changes and medications
are often used to treat high blood pressure
• Lowering the amount of cholesterol and saturated fat in diet. Eating less cholesterol and
fat, may reduce the buildup in arteries.
• Quitting tobacco use. Quitting tobacco use reduces risk of stroke.

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• Managing diabetes. Diet, exercise and losing weight can help keep blood sugar in a
healthy range.
• Maintaining a healthy weight. Being overweight contributes to other stroke risk
• factors, such as high blood pressure, cardiovascular disease and diabetes.
• Eating a diet rich in fruits and vegetables. The Mediterranean diet, which emphasizes
olive oil. fruit, nuts, vegetables and whole grains, may be helpful.
• Exercising regularly. Aerobic exercise reduces risk of stroke in many ways. Gradually
work up to at least 30 minutes of moderate physical activity such as walking. jogging,
swimming or bicycling.
• Drinking alcohol in moderation. Heavy alcohol consumption increases risk of high blood
pressure, ischemic strokes and haemorrhagic strokes. However, drinking small to Date
• Genk dap record
• moderate Amounts of alcohol, such as one drink a day, may help prevent ischemic stroke
and decrease blood's clotting tendency,
• Avoiding illegal drugs. Certain street drugs, such as cocaine and methamphetamine, are
established risk factors for a stroke.

PHARMACOLOGICAL TREATMENT:

• Haemorrhagic strokes are caused by bleeding into the brain and so treatment focuses on
controlling the bleeding and reducing the pressure on the brain that it is causing
• Treatment can begin with drugs being given to reduce the pressure in the brain, overall
blood pressure, prevent seizures and prevent sudden constrictions of blood vessels. If the
patient is taking anti-coagulant or anti-platelet medication like Warfarin or Clopidogrel,
they can begin drugs or blood transfusions to counter the medication's effects,
• Surgery can be used to repair any problems with blood vessels that have led or could
lead to haemorrhagic strokes. Surgeons can place small clamps at the base of aneurysms
or fill them with detachable coils to stop blood flow to them and prevent rupture.

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REFERENCES:

• www.AHA.com
• https://medscap.com
• https://svn.bmj.com
• https://www.health.harvard.edu/a_to_z/hemorrhagic-stroke-a-to-z
• https://www.mayoclinic.org/diseases-conditions/stroke/symptoms-causes/syc20350113
• HAEMORRHAGIC STROKE pathophysiology - Bing images
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC25089075/pdf/nihms801072.

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CASE STUDY ON VIRAL ENCEPHALITIS

Definition:-Encephalitis is defined as an inflammation of the brain caused either by infection or

by virus or from a primary autoimmune process.

Encephalitis:-Inflammation of brain.

Meningo encephalitis: Meningo encephalitis is a serious condition of inflammation of meninges

and the brain itself caused by virus, bacteria and more.

Epidemiology:-

• 20,000 cases annually occur among worldwide.

• Incidence of cases are altered by routine vaccinations.
• Vinises are most common cause,

Etiology:-

Infectious

1. Viral-Herpes virus, varicella zoster virus, Epstein bar virus.

2. Alphavirus
3. Flavivirus
4. Mumps
5. Dengue virus
6. Measles virus
7. Bacteria
8. Rickettsia
9. Fungal
10. Parasites

Non-infectious

1. Allergy of post vaccine

2. Heat hyperpyгеxіа
3. Antibody-associated encephalitis.

TYPES:-

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There are two main types of encephalitis:

• Primary encephalitis: This condition occurs when a virus or other agent directly infects
the brain. The infection may be concentrated in one area or widespread. A primary
infection may be a reactivation of a virus that had been inactive after a previous illness.
• Secondary encephalitis: This condition results from a faulty immune system reaction to
an infection elsewhere in the body. Instead of attacking only the cells causing the
infection, the immune system also mistakenly attacks healthy cells in the brain. Also
known as post-infection encephalitis, secondary encephalitis often occurs two to three
weeks after the initial infection.

Clinical features:

• Headache
• Fever
• Altered consciousness
• Confusion
• Cognitive impairment
• Personality changes
• Seizures
• Weakness and movement disorders
• Presence of focal neurologic findings in addition to fever and headache

Risk factors:-

Age: Some types of encephalitis are more common more severe in certain age groups. In
general, young children and older adults are at greater risk of most types of viral encephalitis.

Weakened immune system: People who have HIV/AIDS, take immune-suppressing drugs or
have another condition causing a weakened immune system are at increased risk of encephalitis.

Geographical region: Mosquito or tick-borne viruses are common in particular geographical

regions.

Season of the year: Mosquito- and tick-borne diseases tend to be more common in summer in
many areas of the United States,

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Diagnosis:-

• History
• Physical examinations
• Cerebrospinal fluid profile mild Mod lymph pleocytosis normal or slightly elevated
protein and normal glucose.
• Viral cultures-detection of viral nucleic acid, serology of cerebrospinal fluid and serum
MRI-Magnetic resonance imaging.
• Electroencephalogram-non specific with more characteristic changes.
• Computed tomography scan.

Pathophysiology:-

Complications:-

• Loss of memory

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• Behavioral changes
• Epilepsy
• Fatigue
• Physical weakness
• Vision problems
• Coma
• Difficulty in breathing
• Death

Transmission of virus:-Viruses spread by different means, and some are more infectious than
others. Some of the modes of viral transmission include:

• Coughs or sneezes from an infected person that release airborne viruses, which are then
inhaled by others.
• Infected insects (such as mosquitoes or ticks) and animals, which can transfer some.
• Viruses directly into the bloodstream via their bite.
• Eating contaminated food or drink.
• The transfer of some viruses can occur through touching an infected person.
• There is evidence to suggest that some cases of viral encephalitis are caused by a dormant
viral infection (such as herpes simplex virus) becoming active again.

Treatment goals of treatment:-

• To reduce fever and pain

• To maintain fluid balance
• To enhance cerebral tissue perfusion.

Non- pharmacological treatment:

• Oxygenation bi nasal cannula.

• Mechanical ventilation is necessary in cardiorespiratory insufficiency.

Pharmacological treatment:

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•Active Viral encephalitis

1. Herpes simplex virus land 2-Acyclovir

2. Varicella zoster virus (including Cerebellitis) – Acyclovir corticosteroid
3. Human herpes virus-6-Ganciclovir, foscamet
4. Rabies-ketamine, amantadine, ribavarin

•Sub acute or chronic encephalitis

1. In the immunocompromised

Varicella-zoster virus – Acyclovir

Cytomegalovirus-Ganciclovir, foscamet, cidofovir

Measles inclusion body encephalitis – Ribavarin

Enterovirus – pleconaril, specific immunoglobulin

Progressive multifocal leukoencephalopathy in HIV patients highly active antiretroviral

therapy (HART), cidofovir

2. In the immunocompetent

Sub-acute sclerosing panencephalitis-interferon alpha, ribavirin

Progressive multifocal leukoencephalopathy arabinoside

Progressive rubella panencephalitis – Plasma exchange

Rasmussen’s encephalitis – IVIg Immune mediated encephalitis.

Acute disseminated encephalomyelitis corticosteroids’ IV1g/ Plasma exchange

Paraneoplastic-Treatment of underlying tumour, consider immunosuppression Voltage gated
K channel limbic encephalitis – IVIg/plasma exchange corticosteroids.

Other types of therapy:-

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Physical therapy to improve strength, flexibility, balance, motor coordination and mobility
Occupational therapy to develop everyday skills and to use adaptive products that help with
everyday activities.

Speech therapy to relearn muscle control and coordination to produce speech.

Psychotherapy to learn coping strategies and new behavioural skills to improve mood
disorders or address personality changes.

Supportive care:

• Breathing assistance, as well as careful monitoring of breathing and heart function

• Intravenous fluids to ensure proper hydration and levels of essential minerals
• Anti-inflammatory drugs, such as corticosteroids, to reduce swelling and pressure
within the skull.
• Anticonvulsant medications, such as phenytoin (Dilantin), to stop or prevent seizures.

Prevention:-

• Practice good hygiene. Wash hands frequently and thoroughly with soap and water,
particularly after using the toilet and before and after meals.
• Don’t share utensils. Don’t share tableware and beverages.

References:-

1. Tom Solomon, lan hart, Nick beeching. Viral encephalitis: A clinician’s guide, review
article, November 2007.
2. Bennett JE, et al. Encephalitis. In: Mandell, Douglas, and Bennett’s Principles and
Practice of Infectious Diseases. 8th ed. Philadelphia, Pa: Saunders Elsevier,
2015.http://www.clinicalkey.com. Accessed Jan. 24, 2017.
3. Hardarson HS. Acute viral encephalitis in children: Clinical manifestations and diagnosis.
http://www.uptodate.com/home. Accessed Jan. 31, 2017.
4. Ferri FF. Encephalitis, acute viral, In: Ferri’s Clinical Advisor 2017. Philadelphia,
Pa:Elsevier, 2017. http://www.clinicalkey.com. Accessed Jan. 24, 2017.

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CASE STUDY ON URINARY TRACT INFECTION

Definition: -

UTI TI refers to infections caused by microorganisms in urinary system, UTI is characterised by

inflammation of urinary tract which causes discomfort. The most predominant components of the
urinary tract to be infected are the kidneys, urinary bladder UTI occur in all age groups both the
genders. Women are more prone to UTI compared to men.

Aetiology: -

Causative organisms: E. coli is the most important causative agent for UTI Staphylococcus
saprophytes, a gram +ve microorganism causes cystitis and pyelonephritis in women. Other
organisms, which causes UTI are species of gram -ve bacteria (enteric) like klebsiella, proteus
mirabilis, pseudomonas aeruginosa, Enterobacter enterococci etc.

Other factors: Other causative factors that are responsible for UTI are structural abnormalities
like kidney stones, tumours, or urethral structures (constriction), instruments such as catheters.
stunts, etc. metabolic abnormalities like DM, renal failure and kidney transplantation.

Types/classification of UTI: It is of 2 types.

1. Acute infection

2. Chronic infection

Acute infection. It involves of urinary bladder termed as cystitis and urethra known as urethritis.
This infection is termed as cysts-urethritis.

Symptoms:

• Frequent micturition

• Dysuria (painful micturition)

• Pain in perineum (region between anus and urethral opening).

• Pyuria (presence of pus cells in urine) Septicaemia (destruction of tissue) occurs

in pregnant women.

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• Chills, fever or leucocytosis (increase WBC count)

• If acute infections are not treated properly, then they may lead to recurrent and
chronic infections.

Chronic infection: It involves infection of kidneys. It includes acute pyelonephritis involves

acute infection of one or both kidneys along with lower urinary tract. The cause of chronic
pyelonephritis is unclear.

Symptoms:

• Polyuria (production of large volume of urine)

• Weight loss

• Anaemia and HIV

• Pyuria

• Fever, vomiting's, abdominal pain is seen in infants and children.

Pathophysiology: Bowel is the most predominant site from where the microorganism enters the
urinary tract. In women the distance between the bowel and urethra is comparatively less the
organism tend to colonise in the vaginal and periurethral space. From here, the bacteria ascents
into the urethra and bladder the subsequent colonisation or destruction of microorganism in the
vaginal is determined by the pH. If the pH is suitable, then the microorganisms continue to
multiply, however males are not as susceptible as females to UTI. This is mainly due to
anatomical distance is in males the distance between the bowel and perineum is large. Upon
gaining assess into the urinary bladder, the organism to depended upon the host defence
mechanisms. If the defences are strong then, the bacteria will eventually be exerted in urine
within 2-3 days. However, if the defence is weak and it suffer from structural abnormalities
(stones, catheters) then bacteria may invade the bladder epithelium.

Defense mechanism in the host (human): There are many defence mechanisms by which the
host can inhibit the growth of bacteria, they are: a. High urban concentration in urine.
b. Increased osmolarity and pH of urine.
c. WBC helps in ingesting and destroying the bacteria, when the bladder is infected. In
response to intracellular replication of bacteria the infected bladder cells undergo

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apoptosis to remove bacteria by means of urine. In addition, apoptosis, the mucosal

cells of tract generate chemokine which are alternates for neutrophils. The neutrophils
phagocytise the bacteria such inflammation response is accountable for the local
symptoms like pain, burning etc. experienced by the patient.

Clinical manifestation:

According to different ages of patient, features of UTI are:

• Infant and newborn: growth impairment, emesis fever, diarrhoea,
• Children: whose age group exceed more than two years' experience frequent
maturation, dysuria, haematuria (blood in urea) abdominal pain, vomiting.

• Adult: suffering from lower UTI, frequent micturition, dysuria, urgency in

micturition.

• Geriatrics: In these UTI is usually a symptomatic, but they experience frequent

urination, dysuria and urinary incontinence, (inability to control urination) due to
age related factors.

Diagnosis:

• Dip stick test

• Urine analysis

• Urine culture

Treatment:

Goals of treatment include: Eradicating the causative organism by the use of antibiotics.
UTI in pregnant women and children requires prompt attention as they are prone to further
complications.

Drugs used for UTI:

2) Urinary antiseptics: Nitrofurantoin, Methenamine and Phenazopyridine.

a) Nitrofurantoin: It is a urinary antiseptic whose antibacterial effect depends upon

the level it attains in plasma.

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MOA: Nitrofurantoin exert deleterious effect on the bacterial DNA, the drug also exhibits,
it's antibacterial activity by interfering with the data synthesis of acetyl coA. This
eventually invades the essential bacterial processes such as carbohydrate metabolism, cell
wall synthesis etc.

ADRS: Nausea, vomiting, peripheral neuritis and other neurological effects,

haemolytic anaemia, hepatic damage etc. Dose: 50-100mg TID for 5-10 days.

b) Methenamine mandelate: It is a urinary antiseptic; it is obtained by utilisation

reaction between an acid like mantellic acid and a base like methenamine. ADRS gastritis,
haematuria, cystitis.

c) Phenazopyridine. It is an ago dye which provide symptomatic relief in pain,

burning sen-sation and urgency in micturition associated with lower UTI. ADRs,
epigastric pain and nausea may occur.

2)Fluoroquinolones: First generation Fluoroquinolones such as ciprofloxacin and

norfloxacin are used in UTL

3) Cephalosporins: They are effective against E. coli and proteus species, resist due to
other drugs: The newer cephalosporins are also active against Enterobacter and
pseudomonas species.

4) Cotrimoxazole: It is active against most of the common urinary pathogens particularly

protease and E. coli. It is usually in the dose of 960mg, BD for 7 days. It should be
avoided in pregnancy.

5) Aminoglycosides: They are highly active against Proteus, pseudomonas, and E. coli.
Gentamicin and amikacin are commonly used in UTI but due to their neurotoxicity
their use is restricted.

6) Piperacillin: It is affective against gram negative like pseudomonas arogenosa. It is

used along with gentamicin in severe UTI septicaemia.

7) Ampicillin or Amoxicilin; Ampicillin was initially employed as drug of choice in UTI

Mostly amoxicillin and clavulanic acid is preferred.

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8) Sulphonamides: They attain effective anti-bacterial cone in urine and tissues. They are
used along with other drugs for suppressive and prophylactic therapy of UTI.

9) Tetracyclines: They are less commonly employed due to the development of resistance.

Treatment for lower UTI

1. Acute and uncomplicated cystitis and urethritis in women. This can be treated by one of
the following three regions.
a) Single dose regimen: this therapy includes administration of single dose of
Sulfisoxazole (2g) orally, cotrimoxazole 6 tabs, orally or ampicillin/amoxicillin (3g)
orally, Fosfomycin trimethamin 3g in pregnant women.

b) There day regimen: this regimen involves administration of cotrimoxazole 2 tabs

ampi-cillin 250-500mg (QID), cephalexin 500mg (QID)

c) 7-14 days regimen: In patients above 65yrs of age or if the infection persist for more
than 7 days. Drugs like cipro floxacillin 250-500mg BD, norfloxacin 400mg BD.

3) Recurrent infection: it is usually within 1 month and successful treatment

contraceptives
like diaphragm and spermicide can lead to the recurrent infection
Drug regiment:
A. Cotrimoxazole or fluoroquinolones should be given to patient for at least 4 to 6
weeks B. Amoxicillin + clavulanic acid or 3rd generation cephalosporins like cefixime
can also

3. Chronic persistent infection: This type of infection occurs in patients with implanted
catheters into the larder. Induction is associated with pyuria and bacteriuria.

4. Asymptomatic bacteriuria: Usually this type of infection doesn't require any treatment

5. Acute urethral syndromes: This is syndrome, we are crossing woman. The infection is
Drug regimen: doxycycline-100mg bd or erythromycin-500mg for seven days can be
given.

Prevention:

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• There are several measures that can be taken to reduce the risk of developing a
UTI Drink lots of water and urinate frequently.
• Avoid fluids such as alcohol and caffeine that can irritate the bladder. Wipe from
front to back after urinating and bowel movement.

• Keep the genital area clean.

• Showers are preferred to baths and avoid using oils.

• Sanitary pads or menstrual cups are preferred to tampons.

• Avoid using a diaphragm or spermicide (contraceptive substance) for birth control.

• Avoid using any perfumed products in the genital area.

• Wear cotton underwear and loose-fitting clothing to keep the area around the
urethra dry.

Reference:

1) Clinical Pharmacy and Therapeutics by Roger Walker and Cate Whittlesea, 5th edition.

2) Chronic Urinary Tract Infections, Healthcare: Women's Health & Maternity, Baylor
Medicine.
3) James Mcintosh, what to know about urinary tract infection, Medial news today, 2018

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CASE STUDY ON ACUTE GASTROENTRITIS

Definition:
Gastroenteritis is an inflammation of the lining of the intestines caused by a virus, bacteria, or
parasites. The cause is often a virus infection. It spreads through contaminated food or water or
by contact with an infected person.

EPIDEMIOLOGY
The second most common cause of death in children<5years. Viral gastroenteritis is these second
most common illness in the U.S. Account for 1.5million death of children/year globally.
Mortality due to diarrhoea has declined cause of Rota virus vaccine, improved nutritional status,
better management of disease.

ETIOLOGY:
• Feco-oral route transmission.
• Ingestion of contaminated food or water.
• Person to person transmission occur in pathogens infectious in small inoculum, like
Shigella. campylobacter, EHEC, Norovirus, Rotavirus, E. histolyticum and Giardia.
• Most common cause is viral like Rota, norovirus (Norwalk) then adenovirus and enteric
viruses.
• Bacterial causes like salmonella, Shigella and E. Coli
• Water borne outbreaks of diarrhea caused by cryptosporidium commonly and others like:
Shigella, E. coli, Norovirus and Giardia.

SYMPTOMS

• Common symptoms include malaise, anorexia, abdominal pain and cramping, watery
diarrhea, nausea and vomiting, and low-grade fever. If caused by Campylobacter jejuni or
Shigella, symptoms may progress to colitis, bloody diarrhea, and tenesmus,

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PATHOPHYSIOLOGY:

DIAGNOSIS
• Doctors perform sigmoidoscopy or radiological examination to exclude the
possibilities of inflammatory bowel disease (e.g. Chron's disease) and pelvic abscesses
(pocket of pus). Viral gastroenteritis is contagious and spread through close contact
with infected persons especially by sharing food, water or eating utensils or by touching
surfaces contaminated by an infected person and then touching one's mouth. Viral

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gastroenteritis is familiar to most of us as 'stomach flu' and only the common cold
occurs more frequently.
Laboratory Diagnosis
Diagnosis of bacterial gastroenteritis is by the routine stool culture. Exceptions to this are
the use of antigen and/or nucleic acid amplification tests for the detection of
a) C. difficile and to a lesser extent
b) Shiga toxin-producing Escherichia coli (STEC) and
c) Campylobacter
TREATMENT
• Generally, bacterial gastroenteritis can be treated at home by getting plenty of rest, drinking
enough fluid to stay hydrated, eating small amount of mineral rich food at regular intervals.
avoiding dairy products food high in fiber and fruit.
• Bacterial gastroenteritis often clears up on its own without any treatment. However,
vomiting and diarrhea can cause denydration, so it is necessary to stay hydrated at home
by drinking plenty of fluids especially water.
• Treatment is important for symptomatic cases, although some parasitic and bacterial
infections require specific anti-infective therapy. Common antibiotics used to ireal
gastroenteritis include penicillin, cephalosporin, antifolate sulfa combinations,
nitroimidazole, glycopeptide and mono lactam antibiotics.
• Vomiting and diarrhea cause the individual to lose essential minerals such as sodium,
potassium and calcium.

• Eating soups or broth can replace body fluids and minerals. Fluid and mineral replacement
solutions are sold in pharmaceutical stores.
• Where a person cannot keep fluids down or become too dehydrated, the hospital should be
visited so as to be given intravenous fluids and electrolytes.
• One's doctor should be contacted before taking any over the counter (OTC) medications to
treat bacterial gastroenteritis, as some medications may prolong symptoms.
• Anti-vomiting drugs or antidiarrheal drugs must avoid unless prescribed or recommended
by one's doctor because they are likely to keep infection the body.

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PREVENTION

Infectious gastroenteritis can be prevented by several means, some of these methods are
highlighted as follows:.
a) Personal hygiene practices generally prevent gastroenteritis.
b) Thorough hand washing with soap before handling food and after using the toilet.
c) Clean the toilet and bathroom regularly, especially the toilet seat, door handles and taps
d) Washing hands thoroughly with soap after touching animals, particularly farm animals
e) Avoiding close contact with people infected with gastroenteritis.
f) Using a separate cutting board for raw meat.
g) Avoiding eating of raw meat and fish.
h) Keep all kitchen surfaces and equipment clean
i) Store food appropriately and discard expired or spoilt product.
j) Drinking only bottled water when travelling especially in developing countries,

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REFERENCES

1. Guerrant RL, Oria RB, Moore SR, Oria MO, Lima AA (2008) Malnutrition as an enteric
infectious disease with long-term effects on child development. Nutrition reviews 66, 487-505.

2. Guerrant DI, Moore SR, Lima AA, Patrick PD, Schorling JB, et al. (1999) Association of early
childhood diarrhea and cryptosporidiosis with impaired physical fitness and cognitive function
four-seven years later in a poor urban community in northeast Brazil. The American journal of
tropical medicine and hygiene 61: 707-713.

3. Niehaus MD, Moore SR. Patrick PD, Derr LL. Lorntz B. et al. (2002) Early childhood diarrhea
is associated with diminished cognitive function 4 to 7 years later in children in a northeast
Brazilian shantytown. The American journal of tropical medicine and hygiene 66: 590-593

4. Checkley W. Buckley G. Gilman RH. Assis AM. Guerrant RL, et al. (2008) Multi- country
analysis of the effects of diarrhoea on childhood stunting. International journal of epidemiology
37: 816-830.

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CASE STUDY ON TUBERCULOSIS

Definition: Tuberculosis (TB) is a dangerous and highly contagious bacterial disease caused by
Mycobacterium tuberculosis. It primarily affects the lungs, but if left untreated, it might spread to
different parts of the body.
TYPES OF TUBERCULOSIS:
There are two different types of tuberculosis:
● Pulmonary Tuberculosis.
● Extrapulmonary Tuberculosis,

PULMONARY TUBERCULOSIS:
it is an endemic infection affecting the lungs. It is further classified into:
Primary Tuberculosis Pneumonia: Associated symptoms include coughing and high fever. It can
also arise in patients with HIV/AIDS.

Miliary Tuberculosis: This form of TB is named so because of a distinctive pattern seen on a

chest radiograph, where many small spots are distributed throughout the lung fields, bearing an
appearance similar to millet seeds. The infection can eventually spread to the extrapulmonary
organs, such as the spleen, liver, and kidneys,

Latent Tuberculosis Infection: This infection is mainly seen in those patients having the bacteria
within their body, but does not display any of the symptoms of the disease. This infection is
primarily detected through the tuberculin skin test.

EXTRAPULMONARY TUBERCULOSIS:
It is usually seen in immunocompromised patients. There are several types:
● Tuberculosis Meningitis
● Osteal Tuberculosis
● Lymph Node Disease
● Renal Tuberculosis
● Adrenal Tuberculosis.

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SYMPTOMS:
TB bacteria or Mycobacterium tuberculosis multiply once it gets into the lungs. It can cause severe
symptoms such as:
● Coughing up blood and mucus from deep inside the lungs
● A bad cough that lasts three weeks or longer.
● Weakness or fatigue.
● Sweating at night.
● Pain in the chest.
● Weight loss.
● No appetite.
● Chills and Fever.
CAUSES:
● TB is caused by type of bacteria called mycobacterium tuberculosis.
● It spreads from person to person through microscopic droplets released into air.
RISK FACTORS:
● HIV Infection
● Substance Abuse
● Diabetes Mellitus
● Severe Kidney Disease
● Low body weight
● Age

COMPLICATIONS:
● Spinal Pain
● Back Pain and Stiffness
● Joint Damage
● Liver and Kidney Damage
● Heart Disorders

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DIAGNOSIS:
● BLOOD TEST:
Blood tests can confirm or rule out latent or active tuberculosis. These tests measure your immune
system reaction to TB bacteria. Blood test might be useful at high risk of TB infection but have a
negative response to the skin test, or if you've recently received the BCG vaccine.

IMAGING TESTS:
● A chest X RAY or CT scan to look for changes in your lungs.
● Acid fast bacillus tests for TB bacteria in sputum, the mucus that comes up when you cough.

SKIN TEST:
● This is also known as the Mantoux Tubercule skin test. Injects a small amount of fluid into
the of lower arm. After 2 or 3 days, they'll check for swelling on arm, if results are positive,
probably have TB bacteria.

PATHOPHYSIOLOGY OF TB:
● The whole cycle begins when an individual inhales a Mycobacterium which travels down the
airways into the alveoli. Here the Mycobacterium will start to multiply, and in some cases,
bacilli may also travel across the body through the lymphatic system.
● The infection may occur anywhere between 2 to 20 weeks after being exposed to the
Mycobacterium. Naturally, the body goes in Defence Mode and starts an inflammatory
reaction.
● This allows the bacteria to be engulfed by Phagocytes, and the bacilli to be destroyed by TB
Specific Lymphocytes. However, while the TB Specific Lymphocytes are busy attacking the
bacilli, they are also attacking healthy tissue.
● The breakdown of normal tissue will lead to a build-up of Exudate in the alveoli, which in
turn causes Bronchopneumonia. The live and dead bacilli start to accumulate and form
Granulomas, which over time transform into a Fibrous Mass.

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● The centre part of this fibrous mass is called Ghon Tubercle. Eventually, some of the bacteria
and macrophages from the Fibrous Mass become necrotic and form a slimy mass. Which in
turn will calcify and create collagenous scars.
● At this point, the bacteria will sleep, and there is no more advancement of active disease. After
the first infection is over, the active disease might come back if the person does not have a
strong immune system, or if he gets re-infected. In the case of re-infection. the Ghon Tubercle
ulcerates and pushes the bacteria out into the bronchi.
● Here the bacteria will become airborne and increase the chances of infecting other people. The
ulcers on the Ghon Tubercle will eventually close up and form even more scar tissue.
Naturally, the build- up of scar tissue will irritate the lung, so the lung becomes more inflamed,
which creates more Tubercle and develops Bronchopneumonia.
MANAGEMENT:
● Pulmonary TB is treated primarily with antituberculosis agents for 6 to 12 months.

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NON-PHARMACOLOGICAL TREATMENT:
● Medical staff must wear high efficiency disposable masks. Isolate patients with possible
tuberculosis infection in a private room. Encouraged patients to follow good cough hygiene.
● Provide vitamins and minerals supplements when required.
● Integrated nutritional assessment counselling and support for the duration of illness.
REFERENCES:
1. Pharmacotherapy A pathological approach by Joseph. T. Dipiro 8th edition.
2. Clinical pharmacy and Therapeutic by Roger Walker, 5th edition.
3. K. D. Tripathi Essential of Medical Pharmacology, 7th edition.

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CASE STUDY ON POLY CYSTIC OVARY SYNDROME

DEFINITION:

Polycystic ovary syndrome (PCOS) is a hormonal disorder common among women of

reproductive age. Women with PCOS may have infrequent or prolonged menstrual periods or
excess male hormone (androgen) levels. The ovaries may develop numerous small collections of
fluid (follicles) and fail to regularly release eggs.

ETIOLOGY:

✓ The exact cause of PCOS isn't known. Factors that might play a role include:
✓ Excess insulin. Insulin is the hormone produced in the pancreas that allows cells to use
sugar, your body's primary energy supply. If your cells become resistant to the action of
insulin, then your blood sugar levels can rise and your body might produce more insulin.
Excess insulin might increase androgen production, causing difficulty with ovulation.
✓ Low-grade inflammation. This term is used to describe white blood cells' production of
substances to fight infection. Research has shown that women with PCOS have a type of
low-grade inflammation that stimulates polycystic ovaries to produce androgens, which
can lead to heart and blood vessel problems.

Heredity. Research suggests that certain genes might be linked to PCOS.

Excess androgen. The ovaries produce abnormally high levels of androgen, resulting in hirsutism
and acne.

SIGNS AND SYMPTOMS:

✓ Signs and symptoms of PCOS often develop around the time of the first menstrual period
during puberty. Sometimes PCOS develops later, for example, in response to substantial
weight gain.
✓ Signs and symptoms of PCOS vary. A diagnosis of PCOS is made when you experience
at least two of these signs:

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✓ Irregular periods: Infrequent, irregular or prolonged menstrual cycles are the most common
sign of PCOS. For example, you might have fewer than nine periods a year, more than 35 days
between periods and abnormally heavy periods.

✓ Excess androgen: Elevated levels of male hormone may result in physical signs, such as
excess facial and body hair (hirsutism), and occasionally severe acne and male-pattern baldness.

✓ Polycystic ovaries: Your ovaries might be enlarged and contain follicles that surround the
eggs. As a result, the ovaries might fail to function regularly. PCOS signs and symptoms are
typically more severe if you're obese.

PATHOPHYSIOLOGY:

✓ The pathophysiology of PCOS involves primary defects in the hypothalamic pituitary

axis, insulin secretion and action, and ovarian function. Although the cause of PCOS is
unknown, PCOS has been linked to insulin resistance and obesity. The association with
insulin function is expected; insulin helps to regulate ovarian function, and the ovaries
respond to excess insulin by producing androgens, which can lead to an ovulation.
Follicular maturation arrest is a hallmark sign that an ovarian abnormality exists.
✓ Clinical signs of PCOS include elevated luteinizing hormone (LH) and gonadotropin
releasing hormone (GnRH) levels, whereas follicular-stimulating hormone (FSH) levels
are muted or unchanged. As a result of the increase in GnRH, stimulation of the ovarian
thecal cells, in turn, produces more androgens. Follicular arrest can be corrected by
elevating endogenous FSH levels or by providing exogenous FSH. Some studies suggest
that PCOS is a primary defect in young girls who are entering puberty and who have a
family history of the disorder. Approximately 25% of patients with PCOS have elevated
prolactin levels.
✓ Therapeutic interventions are designed to reduce insulin levels and ovarian androgen
production, ultimately correcting sex hormone binding globulin (SHBG) levels. This
increase in SHBG levels can be used to effectively manage the symptoms of PCOS.
Studies have reported that thecal cells in patients with PCOS produce higher amounts of
testosterone, progesterone, and 17- hydroprogesterone than in normal patients. These
cells have been altered in PCOS patients whose cytochrome P450 (CYP) 11A, 3-HSD2,

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and CYP17 genes exhibit elevated levels. Obesity is a common comorbidity of PCOS but
is not required for diagnosis.

RISK FACTORS:

Risk factors for PCOS including:

➤ Irregular menstruation.

Family history of infertility and diabetes

➤ Mother's irregular menstruation

Unpleasant mood and

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➤ Lack of physical exercise.

COMPLICATIONS:

Complications of PCOS can include:

➤ Infertility

➤ Gestational diabetes or pregnancy-induced high blood pressure

➤ Miscarriage or premature birth

➤ Nonalcoholic steatohepatitis a severe liver inflammation caused by fat accumulation

in the liver

➤ Metabolic syndrome a cluster of conditions including high blood pressure, high blood sugar,
and abnormal cholesterol or triglyceride levels that significantly increase your risk of
cardiovascular disease.

Type 2 diabetes or prediabetes

➤ Sleep apnea

➤ Depression, anxiety and eating disorders

➤ Abnormal uterine bleeding

➤ Cancer of the uterine lining (endometrial cancer)

➤ Obesity is associated with PCOS and can worsen complications of the disorder.

DIAGNOSIS:

✓ Three tools can be used to diagnose PCOS. In 1990, the National Institute of Child
Health and Human Development (NICHD) of the National Institutes of Health (NIH)
hosted a panel of experts who developed the first known criteria for PCOS. Over the next
Decade, it was discovered that ovarian morphology was a key component in the
diagnosis. The European Society of Human Reproduction and Embryology (ESHRE) and

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the American Society for Reproductive Medicine (ASRM) sponsored a workshop in

Rotterdam. During the workshop, polycystic ovarian morphology on pelvic ultrasound
was added to the NICHD/NIH criteria. It was then decided that only two of the three
criteria had to be met for a diagnosis of PCOS.

Diagnostic Tools for Polycystic Ovary Syndrome.

TREATMENT:

TREATMENT GOALS:

✓ Correcting an ovulation,

Inhibiting the action of androgens on target tissues

✔Reducing insulin resistance.

NON-PHARMACOLOGICAL APPROACHES

Because the primary cause of PCOS is unknown, treatment is directed at the symptoms. Few
treatment approaches improve all aspects of the syndrome, and the patient's desire for fertility
may prevent her from seeking treatment despite the presence of symptoms.

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✔ Laparoscopic ovarian drilling is an outpatient surgical intervention in which multiple

perforations are created in the ovarian surface and stroma. It is thought that this intervention
destroys androgen-producing tissue, which should lead to decreased androgen levels.

LIFE STYLE CHANGES:

➤ Regular exercise is advised.

➤ Diet modification:

➤ Limit carbohydrate intake, avoid junk foods.

➤ Advise protein rich food,

PHARMACOLOGICAL APPROACHES ANOVULATION

Clomiphene: (Prescribed to who were anxious to conceive):

The drug of choice for inducing ovulation in PCOS is clomiphene citrate (Clomid, Sanofi),
although the precise mechanism of action is unknown. Initially, a dose of 50 mg/day for 5 days is
given. If ovulation occurs but no pregnancy results, 50 mg/day for 5 days is continued for the
subsequent cycles. However, if ovulation does not occur after the first cycle, the dose may be
increased to 100 mg daily for 5 days at least 30 days after the previous course of therapy.

ANTI DIABETIC AGENTS:

Other medications may be added to clomiphene to yield a more favourable outcome for
ovulation. Antidiabetic drugs can be used to improve fertility, decrease insulin resistance, and
reduce circulating androgen levels. More data are available for metformin (Glucophage, Bristol-
Myers Squibb) than for the thiazolidinedione's in treating. In a meta-analysis comparing
pioglitazone (Actos, Eli Lilly) with metformin among patients with PCOS, pioglitazone was
more effective in reducing fasting insulin levels and metformin was more effective in reducing
body weight.

GONADOTROPINS:

Human menopausal gonadotropin (IMG) and FSEI can also be used to induce ovulation if
clomiphene and/or metformin therapy fails. Although gonadotropins might be more effective

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than clomiphene for inducing ovulation, the comparative expense and ease of administration of
clomiphene favoured clomiphene as a first-line therapy for fertility in PCOS.

AROMATASE INHIBITORS:

Letrozole (Femara. Novartis) is an aromatase inhibitor approved for patients with hormone-
responsive breast cancer, but it has also been studied for the induction of ovulation in PCOS. The
difference between the efficacy of anastrozole (Arimidex, AstraZeneca) and letrozole was
studied for ovulation induction.

ANDROGENIC SYMPTOMS:

Cosmetic treatment of hirsutism, acne, and alopecia is an option for women dealing with the
hyperandrogenic manifestations of PCOS. The use of depilatories, waxing, and shaving for
managing hirsutism is limited by adverse effects such as skin redness and irritation. Other more
expensive options may include medical spas that offer laser hair removal and electrolysis. Over-
the-counter products can be used for acne, but they have limited effectiveness and are associated
with treatment-site irritations. Alopecia can be treated topically or with oral antiandrogens.

ANTIANDROGENS:

Spironolactone (Aldactone, Pfizer), flutamide (Eulexin, Schering/Merck), and finasteride

(Propecia, Merck) are antiandrogens that work in PCOS by decreasing androgen levels, thereby
reducing the signs of hirsutism and acne. These antiandrogens may also improve lipid levels,
which can be elevated in patients with PCOS. The effects of spironolactone 100 mg, flutamide
250 mg, and finasteride 5 mg daily were compared in 40 women with hirsutism for 6 months. All
three drugs were found to be efficacious, although there was no significant difference between
the groups. Spironolactone, at a dose of 25 to 100 mg twice daily, is the most commonly used
antiandrogen because of its safety, availability, and low cost. Because of the increased. Risk of
teratogenicity to the male fetus (opposing genital formation), contraception is recommended
when patients are using antiandrogens for the treatment of PCOS.

ORAL CONTRACEPTIVES:

Women with PCOS who do not wish to become pregnant may consider oral contraceptives
(OCs). The mechanism of action for OCs in the treatment of PCOS is primarily through the

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regulation of menstrual periods. These drugs also reduce hirsutism, acne, and androgen levels.
Estrogen and progestin combinations are the primary OCs used in the treatment of hirsutism and
acne associated with PCOS.

Although data are sparse, some newer OCs contain anti- androgenic progestins, such Bayers
risperidone (e.g., Yaz) and dienogest (e.g.. Natazia). Theoretically, these drugs are more
effective for treating androgenic symptoms compared with older formulations. Women with
hirsutism usually notice clinical improvement after approximately 6 months of treatment with
OCs. The data also suggest that OCs can be combined with anti-androgens for synergy.

OTHER THERAPIES

Medroxyprogesterone acetate:

In a dosage regimen of 5 to 10 mg/day for 10 to 14 days each month, medroxyprogesterone

acetate (MPA) can be used to treat amenorrhea or dysfunctional uterine bleeding in women with
PCOS who do not wish to conceive and who are not at risk for pregnancy.

STATINS:

Statins are considered to have a place in the treatment of PCOS because of their ability to reduce
testosterone levels, as well as low-density lipoprotein-cholesterol (LDL-C), triglycerides, and
total cholesterol.

REFERENCES:

✔ https://www.healthline.com/health/rheumatoid-arthritis#medications

✓ https://www.medicinenet.com/rheumatoid_arthritis/article.htm

✓ https://www.webmd.com/rheumatoid-arthritis/guide/rheumatoid-athritis-symptoms-types

✓ https://www.rheumatology.org/I-Am-A/Patient-Caregiver/Diseases-
Conditions/Rheumatoid-Arthritis

✓ https://www.medscape.com/answers/331715-5335/what-is-the-global-prevalence-of-
rheumatoid-arthritis-ra-among-different-age-groups-and- ethnicitie

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CASE STUDY ON BENIGN INTRACRANIAL HYPERTENSION

Benign intra cranial hypertension (BIH), sometimes called by the names idiopathic intracranial
hypertension (IIH), or pseudo tumour cerebri (PTC).

• Characterized by an increased intracranial pressure in the absence of a tumour or other

diseases.
• The fluid surrounds the spinal cord and brain is called cerebrospinal fluid or CSF if too
much fluid is made or not enough is reabsorbed, the CSF can build up. This can cause
symptoms like those of a brain tumour.

BIH CLASSIFIED INTO THESE CATEGORIES:

❖ ACUTE: Symptoms happen suddenly often because of a head injury or stroke.

❖ CHRONIC: Symptoms develop over time. They may be caused by an underlying health
problem.
❖ IDIOPATHIC: The cause is unknown.

ETIOLOGY:

Causes are not known for IIH. But some medicines have been linked to a higher risk of it.

• Birth control pills

• Certain antibiotics
• Chemotherapy drugs
• Steroids
• Some acne medicines

EPIDEMIOLOGY:

• 0.9 case per 100,000 population.

• 1.6 cases per 100,000 women.
• 3.3 cases per 100,000 females aged 15-44years.
• 7.9cases per 100,000 obese women aged 15-44years..

PATHOPHYSIOLOGY:

• The cause of IIH is not known.

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• The Monro Kellie rule states that the intracranial pressure is determined by the amount of
brain tissue, cerebrospinal fluid (CSF) and blood inside the bony vault. Three theories
therefore exist as to why the pressure might be raised in IIH: an excess of CSF
production, increased volume of blood or brain tissue, or obstruction of the veins that
drain blood from the brain.
• The first theory, that of increased production of cerebrospinal fluid, was proposed in
early descriptions of the disease.
• A second theory posits that either increased blood flow to the brain or increased blood
flow to the brain or increase in the brain tissue itself may result in the raised pressure
Little evidence has accumulated, but both biopsy samples and various types of brain
scans have shown an increased water content of the brain tissue.
• A third theory suggests that blood flow from the brain may be impaired or congested.
Only in a small proportion of patients has underlying narrowing of the cerebral sinuses or
only in a small proportion of patients has underlying narrowing of the cerebral sinuses or
veins been demonstrated. Congestion of venous blood may result from a generally
increased venous pressure, which has been linked to obesity.

RISK FACTORS:

• Women of child bearing age 20-45 years

• Obesity
• People who have a thyroid condition or chronic kidney failure.

SYMPTOMS:

• IIH mimic those of a true brain tumor

• Changes in eye sight such as blurry vision or double vision
• Vision loss, especially in the peripheral vision.
• Felling dizzy or nauseated.
• Vomiting
• Neck stiffness
• Trouble walking
• Frequent headaches, often along with nausea or vomiting

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• Tinnitus
• Forgetfulness
• Depression

DIAGNOSIS:

• Brain imaging such as MRI or CT scans

• Lumbar puncture to withdraw a sample of fluid from around the spine for testing
pressure.
• Exam to test vision and check the back of your eye.

MANAGEMENT:

Weight loss

• Including via bariatric surgery

Pharmacological Treatment

▪ Acetazolamide (250-500 mg orally three times daily,increasing slowly two to four times
daily) reduces formation of cerebrospinal fluid; furosemide, Digoxin and analgesia
▪ Steroids are controversial, but a short course is sometimes used.
▪ eg: Prednisolone 60-80 mg daily.

Surgical

▪ LV/VP shunt
▪ Optic nerve fenestration
▪ Transverse dural sinus stenting
▪ IV mannitol or LP are usually reserved for acute severe exaberations.

REFERENCES

1. Gary. Y.Shaw, Stephanie k. Million, "Benign intracranial hypertension: A diagnostic

Dilemma", case reports in ptolaryngology, col.2012, article ID 814696, 8 pages, 2012. https://do
Lorg/10.1155/2012/814696.

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2. Hamdan A.R., Tay el, A.M., El Khatteb, E.E.et al. Benign intracranial hypertension is a
misleading name for a more serious disease: analysis of visual outcome in cases with idiopathic
intracranial hypertension. Egypt J Neurosurg 34, 38 (2019).

https://DLL.org/10.1186/s41984-019-0064-5.

3. Maxine A. Papadakis, Stephen J.Mcphee, Associate Editor Michael W. Rabow, current

medical diagnosis & treatment 60th anniversary edition 2021, Pg. No: 1009-1011

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STUDY ON NEURO ENDOCRINE TUMOR WITH MESENTERIC

NODULAR LESION

Definition
Small bowel neuro endocrine tumor
Neuro endocrine tumours as defined as epithelial tumours with predominant neuro endocrine
differentiation
Mesenteric nodular lesion
It is a mesenteric thickening or mass that can be nodular in consistency and focal or diffuse within
the small bowel mesentery the root of the mesentery and the tissues surrounding the superior
mesenteric vessels are commonly involved
Mesenteric tumours are rare and consists of a heterogeneous group of lesions masses may arise
from any one of the mesenteric components
Peritoneum lymphatic tissue fat and connective tissue cellular proliferation can also vary from
infectious or inflammatory process

Epidemiology
● Duodenal nets comprise 1%-3% of all primary duodenal tumours and 28% of all carcinoid
tumours.
● According to SEER program the adjusted annual incidence of NETS arising from jejunum
and ileum is 0.67 per 10,000 and for appendix NCT it is 0.16 or 10000 Mesenteric masses are
mostly of lymphatic origin the induced cystic mesenteric
● masses is estimated at 1 by 10000 in the United States
● Lymphoma is the most common solid mesenteric tumor
● Endocrine tumor of the small intestine is rare metastatic lymph node
● The annual incidence of desmoid tumours 2.4 to 4.3/100000
Etiology
● Genetic syndromes associated with increased risk for carcinoid include
● Multiple endocrine neoplasia type
● Neuro fibromatosis type 1

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● Tumeroul sclerosis complex

Pathophysiology
● Enterochromaffin sails stain yellow brown after chromate fixation and are the diffusely
distributed in the tissues derived from the primitive gut
● Intestinal Enterochromaffin cells are the kulchistiky cells in the crypts of lieberkuhn of the
small intestine
● Carcinoid tumors arise from the enterochromaffin cells
● Tumor cells and kulchitsky cells both reduce silver salts thus the term argentaffin Oma is used
to describe carcinoid tumors.
● Endocrine cells in the Pituitary gland thyroid gland lungs pancreas and gastrointestinal tract
Secrete polypeptides are shared common cytochemical and ultrastructural characteristics.
● Tumors that histologically appeared to be carcinoids may also produce
Calcitonin
Vasoactive intestinal peptide
Neurotensin catecholamines
Corticotrophin
Diagnosis
➤ Asymptomatic-many/incidentally/autopsy

➤ Symptomatic depends on location size and metastasis

➤ Complications

➤ Partial intestinal obstruction

➤ LGI bleeding

➤ Intestinal ischemia infraction -decimo plastic reaction agiopathy

➤ Malignant carcinoid syndrome

Symptoms
● Small intestine
● Appendix
● Colon
● Rectum

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Risk Factors
● Consumption of red meat
● Ingestion of smoked or cured foods
● Crohn disease
● Peutz jeghers syndrom
● Familial adenomatous polyposis
Diagnostics tests
● Barium
● CT sca
● CT Angio
● In-Labelled syntigrapghy
● MRI-hepaticmetic
● Endoscopy
● Radio nuclear scanner
● Positron emission tomography
Treatment
Medical therapy
● Symptomatic relie
● Octreotide
● Symptom relief
● Tumor regression
● Newer drugs-sandostatin
Pasireotide
● Broad somatostatin reseptor inhibitor
● 40 fold increase in binding affinity
Methysergide
● Serotonin receptor antagonist
● No longer use
Cytotoxic chemotherapy

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● Used for metastatic disease who are symptomatic

● High tumor proliferation rates
Antiangiogenesis therapy
● Bevacizumab with cytotoxic drug still being investigated
● Sunitinib -under study
● Iv octreotide 50-100mcg infusion at 50 mcg/hr
● Iv antihistamine hydrocortisone
Surgical debulkin
Hepatic artery embolisation
Medical therapy
Chemotherapy
● Cyclophosphamide
● 5-fluorouracil
● Streptozocin
Antiangiogenesis therapy
● Bevacizumab
● Sunitinib-under study
Prognosis
● Best prognosis of all small bowel tumours whether localized or metastatic
● Resection of primary tumour locized to its primary site-100% survival
● 5 year survival
● Regional disease -65%
● Distant metastasis 25-35%
● Serum chromaganin a level is independer predictor of adverse prognosis

References
1.www slideshare net byDR Sumit KR Kansal
2. review article of management os small bowel neuro endocrine tumour by Aaron T Scott, James
R. Howe

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CASE STUDY ON OSTEOARTHRITIS

DEFINITION:

Osteoarthritis is a noninflammatory degenerative condition of joints characterized by

degeneration of articular cartilage and formation of new bone ie, osteophytes Osteoarthritis is
also known as degenerative arthritis/ hypertropic arthritis. Common in weight bearing joints such
as hip and knee Both male and females are affected. But more common in older women ie, above
50 years of age particularly in menopausal women.

Classification of osteoarthritis:

1. Primary osteoarthritis

2. Secondary osteoarthritis

Primary osteoarthritis:

Primary osterarthritis is caused by the breakdown of cartilage, a rubbery material that euses the
friction in your joints. It can happen in any joint but usually affects your fingers, thumbs, spine,
hips, knees, or hig toes.

Causes

Breakdown of cartilage, wear and tear of bones.

It is more common in older people where there is no previous pathology is mainly due to wear
and tear changes occurring in old ages mainly in weight bearing joints

It is sub divided into 2 types

Localized osteoarthritis-Involving only 1 tor) 2 sites.

Generalized osteoarthritis-Affecting 3 (or) sites.

Secondary osteoarthritis:

Secondary osteoarthritis occurs when your cartilage is damaged by any other disease or medical
condition. Things that can cause it or make it more likely include: Obesity, which puts more
stress on your joints, especially your knees.

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Causes

Injury to joint

Previous infection

Rheumatoid arthritis

Deformity

Obesity

Hyperthyroidism

EPIDEMIOLOGY:

Internationally osteoarthritis is the most common articular disease

On the basis of radiographic criteria for osteoarthritis, more 50% of adults older than

65 years are affected by the disease In individuals older than 55 years, the prevalence of
osteoarthritis is higher among

Women than men.

PATHOPHYSIOLOGY:

Cartilage helps joint to move easily and comfortably.

As joins are used, it gets thin in some people with its short of osteoarthritis

Cartilage away and bones against each other

Rubbing causes pain, swelling, decreased motion of joint.

Bones start to grow too thick and ends where they meet to make a joint.

Hits of cartilage loosen and get in a way of movement, pain swelling, stiffness.

CLINICAL FEATURES:

Early stage:

Swelling, diffness, increased warmth, tenderness of proximal finger joints and the wrists.

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Disease progression:

Joint movement becomes restricted, Isolated tendon ruptures at wrist.

DIAGNOSIS:

Medical history

Physical examination

X-rays

Laboratory investigations

Joint aspiration

TREATMENT:

PHARMACOLOGICAL TREATMENT:

Analgesics:

Acetaminophen 325-600mg, every 4-6hrs/day.

Tramadol 50-100mg, every 4-6hes.

NSAID

Ibuprofen 1200-3200 mg/day in 3-4 divided doses

Naproxen 250-500 mg BID

Topical analgesics:

Capsaicin 0.025% 0.075%

Apply to affected joint 3-4 times/day

Nutritional supplements:

Glucosamine sulphate/chondroitin sulphate 500rog TID

Hyaluronate Injections:

To promote lubrication with motion and shock absorbency during rapid movements.

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Sodium hyaluronate – Hyalgan 20mg/2ml

Hyalumman orthorise 30mg/2ml

Aids and applications:

Braces splints

Shoes/imoles

Mobility aids

Joint replacement therapy:

Complications: Sepas, loosening of muscle/joints

TEENS (Electrical Nerve Stimulation)

NON PHARMACOLOGICALTREATMENT:

Advice to reduce to overweight.

Physical therapy with heat or cold treatments. It helps maintain & restore joint range of motion.

REFERENCES

1. Osteoarthritis. National Institute of Arthritis and Musculoskeletal and Skin Diseases.

https://www.niams.nih.gov/health-topic/osteoarthritis. Accessed March 7, 2021.
2. Curtis L., et al. (2021). Facet joint disease
Statpearls.com/ArticleLibrary/viewarticle/21534

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CASE STUDY ON ULCERATIVE COLITIS

INTRODUCTION:

Is a long-term condition that results in inflammation and ulcers of the colon and rectum.

The primary symptoms of active disease are abdominal pain and diarrhea mixed with blood.
Weight loss, fever, and anaemia may also occur. Often, symptoms come on slowly and can range
from mild to severe. Symptoms typically occur intermittently with periods of no symptoms
between flares.

Complications may include megacolon, inflammation of the eye, joints, or liver, and colon cancer.

EPIDEMIOLOGY:

• Together with Crohn's disease, about 11.2 million people were affected as of 2015.
• Each year it newly occurs in 1 to 20 per 100,000 people, and 5 to 500 per 100,000
individuals are affected.
• The disease is more common in North America and Europe than other regions.
• Often it begins in people aged 15 to 30 years, or among those over 60. Males and females
appear to be affected in equal proportions.
• It has also become more common since the 1950s. Together, ulcerative colitis and
Crohn's disease affect about a million people in the United States.
• With appropriate treatment the risk of death appears the same as that of the general
population.
• The first description of ulcerative colitis occurred around the 1850s.

ETIOLOGY:

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• The cause of UC is unknown. Theories involve immune system dysfunction, genetics,

changes in the normal gut bacteria, and environmental factors.
• Rates tend to be higher in the developed world with some proposing this to be the result
of less exposure to intestinal infections, or to a Western diet and lifestyle.
• The removal of the appendix at an early age may be protective. Diagnosis is typically by
colonoscopy with tissue biopsies.
• It is a kind of inflammatory bowel disease (IBD) along with Crohn's disease and
microscopic colitis.
• No direct causes for UC are known, but many possible factors such as genetics and stress
play a role.

• Genetic factors: A genetic component to the etiology of UC can be hypothesized based

on:
➢ Aggregation of ulcerative colitis in families.
➢ Identical twin concordance rate of 10% and dizygotic twin concordance rate of
3%.
➢ Ethnic differences in incidence.
➢ Genetic markers and linkages.
• Twelve regions of the genome may be linked to UC, including, in the order of their
discovery, chromosomes 16, 12, 6, 14, 5, 19, 1, and 3, but none of these loci has been
consistently shown to be at fault, suggesting that the disorder is influenced by multiple
genes.
• For example, chromosome band 1p36 is one such region thought to be linked to
inflammatory bowel disease.
• Some of the putative regions encode transporter proteins such as OCTNI and OCTN2.
• Other potential regions involve cell scaffolding proteins such as the MAGUK family.
• Human leukocyte antigen associations may even be at work. In fact, this linkage on
chromosome 6 may be the most convincing and consistent of the genetic candidates.
• Multiple autoimmune disorders have been recorded with the neurovascular and
cutaneous genetic porphyrias including UC.

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• Crohn's disease, celiac disease, dermatitis herpetiformis, diabetes, systemic and discoid
lupus, rheumatoid arthritis, ankylosing spondylitis, scleroderma, Sjogren's disease and
scleritis. Physicians should be on high alert for porphyrias in families with autoimmune
disorders and care must be taken with the use of potential porphyrinogenic drugs,
including sulfasalazine.

• Environmental factors: Many hypotheses have been raised for environmental factors
contributing to the pathogenesis of ulcerative colitis. They include:
➢ Diet:
▪ As the colon is exposed to many dietary substances which may encourage
inflammation, dietary factors have been hypothesized to play a role in the
pathogenesis of both ulcerative colitis and Crohn's disease.
▪ Few studies have investigated such an association; one study showed no
association of refined sugar on the prevalence of ulcerative colitis.
▪ High intake of unsaturated fat and vitamin B6 may enhance the risk of
developing ulcerative colitis. Other identified dietary factors that may
influence the development and or relapse of the disease include meat
protein and alcoholic beverages.
▪ Specifically, sulphur has been investigated as being involved in the
etiology of ulcerative colitis, but this is controversial.
▪ Sulphur have been investigated in patients with UC and animal models of
the disease.
▪ The theory of sulphur as an etiological factor is related to the gut
microbiota and mucosal sulphide detoxification in addition to the diet.

• Breast feeding:

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➢ Some reports of the protection of breastfeeding in the development of IBD

contradict each other. One Italian study showed a potential protective effect.
➢ One study of isotretinoin found a small increase in the rate of UC.

SIGNS AND SYMPTOMS:

Increased risk of blood clots in veins and arteries the main symptom of ulcerative colitis is bloody
diarrhea. There might be some pus in your stools, too.

Other problems include:

• Cramping belly pain

• Sudden urges to empty your colon right away
• Not feeling hungry
• Weight loss
• Feeling tired
• Fever
• Dehydration
• Joint pain or soreness
• Canker sores
• Eye pain when you look at a bright light
• Too few red blood cells, called anaemia
• Skin sores
• Feeling like you haven't completely emptied your colon after you use the bathroom
• Waking up at night to go
• Not being able to hold your stool.

Your symptoms can flare up, go away, and come back. Sometimes they might not bother you for
weeks or years at a time.

Other gut diseases can have some of the same symptoms. Crohn's disease causes inflammation,
too, but it affects other places in your digestive tract. Ulcerative colitis involves only your large
Intestine and its lining.

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Irritable bowel syndrome has some of the same symptoms as UC, but it doesn't cause inflammation
or ulcers. Instead, it's a problem with the muscles in your intestines.

EXTRA INTESTINAL FEATURES:

As UC is believed to have a systemic (i.e., autoimmune)origin, patients may present with co

morbidities leading to symptoms and complications outside the colon. The frequency of such extra
intestinal manifestations has been reported as between 6 and 47%, and includes:

• Aphthous ulcer of the mouth

• Ophthalmic
➢ Iritis or uveitis, which is inflammation of the eye's iris
➢ Episcleritis
• Musculoskeletal:
➢ Seronegative arthritis, which can be a large-joint oligoarthritis (affecting one or
two joints), or may affect many small joints of the hands and feet
➢ Ankylosing spondylitis, arthritis of the spine
➢ Sacroiliitis, arthritis of the lower spine
• Cutaneous (related to the skin)
➢ Erythema nodosum, which is a panniculitis, or inflammation of subcutaneosas
tissue involving the lower extremities
➢ Pyoderma gangrenosum, which is a painful ulcerating lesion involving the skin
• Deep venous thrombosis and pulmonary embolism
• Autoimmune hemolytic anemia
• Clubbing, a deformity of the ends of the fingers
• Primary sclerosing cholangitis, a distinct disease that causes inflammation of the bile ducts

COMPLICATIONS:

Possible complications of ulcerative colitis include:

• Severe bleeding
• A hole in the colon (perforated colon)

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• table
• Severe dehydration
• Liver disease (rare)
• Bone loss (osteoporosis)
• Inflammation of your skin, joints and eyes
• An increased risk of colon cancer
• A rapidly swelling colon (toxic megacolon)

DIAGNOSIS:

Different tests can help your doctor diagnose UC. This disorder mimics other bowel diseases such
as Crohn's disease. Your doctor will run multiple tests to rule out other conditions. Tests to
diagnose ulcerative colitis often include:

• Stool test: A doctor examines your stool for blood, bacteria, and parasites.
• Endoscopy: A doctor uses a flexible tube to examine your stomach, oesophagus, and small
intestine.
• Colonoscopy: This diagnostic test involves insertion of a long, flexible tube into your
rectum to examine the inside of your colon.
• Biopsy: A surgeon removes a tissue sample from your colon for analysis.
• CT scan: This is a specialized X-ray of your abdomen and pelvis.

Blood tests are often useful in the diagnosis of UC. A complete blood count looks for signs of
anemia (low blood count). Other tests indicate inflammation such as a high level of C-reactive
protein and a high sedimentation rate. Your doctor may also order specialized antibody tests.

PATHOPHYSIOLOGY:

An increased amount of colonic sulphate-reducing bacteria has been observed in some patients
with ulcerative colitis, resulting in higher concentrations of the toxic gas hydrogen sulphide.

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Human colonic mucosa is maintained by the colonic epithelial barrier and immune cells in the
lamina propria (see intestinal mucosal barrier) N-butyrate, a short-chain fatty acid, gets oxidized
through the beta oxidation pathway into carbon dioxide and ketone bodies. It has been shown that
N-butyrate helps supply nutrients to this epithelial barrier.

Studies have proposed that hydrogen sulphide plays a role in impairing this beta oxidation pathway
by interrupting the short chain acetyl-CoA dehydrogenase, in enzyme within the pathway.

Furthermore, it has been suggested that the protective benefit of smoking in ulcerative colitis is
due to the hydrogen cyanide from cigarette smoke reacting with hydrogen sulphide to produce the
non-toxic isothiocyanate, thereby inhibiting sulphides from interrupting the pathway.

An unrelated study suggested that the sulphur contained in rod meats and alcohol may lead to an
increased risk of relapse for patients in remission.

MANAGEMENT:

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PHARMACOLOGICAL:

Ulcerative colitis treatment usually involves either drug therapy or surgery. Several categories of
drugs may be effective in treating ulcerative colitis. The type you take will depend on the severity
of your condition. The drugs that work well for some people may not work for others, so it may
take time to find a medication that helps you. In addition, because some drugs have serious side
effects, you'll need to weigh the benefits and risks of any treatment.

Anti-inflammatory drugs

Anti-inflammatory drugs are often the first step in the treatment of ulcerative colitis. They include:

• 5-aminosalicylates. Examples of this type of medication include sulfasalazine

(Azulfidine), mesalamine (Asacol HD, Delzicol, others), balsalazide (Colazal) and
olsalazine (Dipentum). Which one you take, and whether it is taken by mouth or as an
enema or suppository, depends on the area of your colon that's affected.
• Corticosteroids. These drugs, which include prednisone and hydrocortisone, are generally
reserved for moderate to severe ulcerative colitis that doesn't respond to other treatments.
Due to the side effects, they are not usually given long term.

Immune system suppressors

These drugs also reduce inflammation, but they do so by suppressing the immune system response
that starts the process of inflammation. For some people, a combination of these drugs works better
than one drug alone.

Immunosuppressant drugs include:

• Azathioprine (Azasan, Imuran) and mercaptopurine (Purinethol, Purixan). These are

the most widely used immunosuppressant's for treatment of inflammatory bowel disease.
Taking them requires that you follow up closely with your doctor and have your blood
checked regularly to look for side effects, including effects on the liver and pancreas.
• Cyclosporine (Gengraf, Neoral, Sandimmune). This drug is normally reserved for
people who haven't responded well to other medications. Cyclosporine has the potential
for serious side effects and is not for long-term use.

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• Infliximab (Remicade), adalimumab (Humira) and golimumab (Simponi). These

drugs, called tumor necrosis factor (TNF) inhibitors, or biologics, work by neutralizing a
protein produced by your immune system. They are for people with severe ulcerative colitis
who don't respond to or can't tolerate other treatments.

NON-PHARMACOLOGICAL:

Sometimes you may feel helpless when facing ulcerative colitis. But changes in your diet and
lifestyle may help control your symptoms and lengthen the time between flare-ups.

There's no firm evidence that what you eat actually causes inflammatory bowel disease. But certain
foods and beverages can aggravate your signs and symptoms, especially during a flare-up.

It can be helpful to keep a food diary to keep track of what you're eating, as well as how you feel.
If you discover that some foods are causing your symptoms to flare, you can try climinating them.

Here are some suggestions that may help:

Foods to limit or avoid

• Limit dairy products.

➢ Many people with inflammatory bowel disease find that problems such as diarrhea,
abdominal pain and gas improve by limiting or eliminating dairy products.
➢ You may be lactose intolerant that is, your body can't digest the milk sugar (lactose)
in dairy foods. Using an enzyme product such as Lactaid may help as well.
• Limit fiber, if it's: problem food.
➢ If you have inflammatory bowel disease, high-fiber foods, such as fresh fruits and
vegetables and whole grains, may make your symptoms worse.
➢ If raw fruits and vegetables bother you, try steaming, baking or stewing them.
➢ In general, you may have more problems with foods in the cabbage family, such as
broccoli and cauliflower, and nuts, seeds, corn and popcorn.
• Avoid other problem foods.
➢ Spicy foods, alcohol and caffeine may make your signs and symptoms worse.

Other dietary measures:

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• Eat small meals.

➢ You may find you feel better eating five or six small meals a day rather than two or
three larger ones.
• Drink plenty of liquids.
➢ Try to drink plenty of fluids daily. Water is best. Alcohol and beverages that contain
caffeine stimulate your intestines and can make diarrhea worse, while carbonated
drinks frequently produce gas.
• Talk to a dietitian.
➢ If you begin to lose weight or your diet has become very limited, talk to a registered
dietitian.

Stress:

Although stress doesn't cause inflammatory bowel disease, it can make your signs and symptoms
worse and may trigger flare-ups.

To help control stress, try:

• Exercise.
➢ Even mild exercise can help reduce stress, relieve depression and normalize bowel
function.
➢ Talk to your doctor about an exercise plan that's right for you.

• Biofeedback.
➢ This stress-reduction technique helps you reduce muscle tension and slow your
heart rate with the help of a feedback machine. The goal is to help you enter a
relaxed state so that you can cope more easily with stress.
• Regular relaxation and breathing exercises.
➢ An effective way to cope with stress is to perform relaxation and breathing
exercises.

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➢ You can take classes in yoga and meditation or practice at home using books, CDs
or DVDs.
• Turmeric.
➢ Curcumin, a compound found in the spice turmeric, has been combined with
standard ulcerative colitis therapies in clinical trials.
➢ There is some evidence of benefit, but more research is needed.

Surgery:

Surgery can often eliminate ulcerative colitis. But that usually means removing your entire colon
and rectum (proctocolectomy).

In most cases, this involves a procedure called ileal pouch anal anastomosis. This procedure
eliminates the need to wear a bag to collect stool. Your surgeon constructs a pouch from the end
of your small intestine. The pouch is then attached directly to your anos, allowing you to expel
waste relatively normally.

In some cases, a pouch is not possible. Instead, surgeons create a permanent opening in your
abdomen (ileal stoma) through which stool is passed for collection in an attached bag.

REFERENCES:

• Pharmacotherapy A Pathological approach by Joseph T.Dipiro.7th edition.

• KD Tripathi Essential of Medical Pharmacology, 7th edition.
• Clinical pharmacy and Therapeutics by Roger Walker, 5th edition.

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ALCOHOLIC LIVER DISEASE

DEFINITION:

Any pathological conditions of liver as a result of chronic and excessive alcohol consumption
leading to a spectrum of conditions from ranging from asymptomatic fatty liver to alcoholic
hepatitis to end stage liver failure with jaundice, coagulopathy and encephalopathy.

EPIDEMIOLOGY:

Alcohol abuse is the most common cause of serious liver disease in Western societies. The true
prevalence of alcoholic liver disease, especially of its milder forms, is unknown, because patients
may be asymptomatic and never seek medical attention.

ETIOLOGY:

Alcoholic liver disease occurs when the liver is damaged by the excessive consumption of
alcohol. How alcohol damages the liver and why it does so only in a minority of heavy drinkers
is not clear. It is known that the process of breaking down ethanol, the alcohol in beer, wine and
liquor produces highly toxic chemicals, such as acetaldehyde. These chemicals trigger
inflammation that destroys liver cells. Over time, web-like scars and small knots of tissue replace
healthy liver tissue, interfering with the liver's ability to function. This irreversible scarring,
called cirrhosis, is the final stage of alcoholic liver disease.

Heavy alcohol use can lead to liver disease, and the risk increases with the length of time and
amount of alcohol drink. But because many people who drink heavily or binge drink never
develop alcoholic liver disease or cirrhosis, it is likely that factors other than alcohol play a role.
These include:

Other types of hepatitis: Long-term alcohol abuse worsens the liver damage caused by other
types of hepatitis, especially hepatitis C.

Malnutrition: Many people who drink heavily are malnourished, either because they cat poorly
or because alcohol and its toxic by-products prevent the body from properly absorbing and
breaking down nutrients, especially protein, certain vitamins and fats. In both cases, the lack of
nutrients contributes to liver cell damage.

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Sex: Women have a higher risk of developing alcoholic liver disease than men do This disparity
may result from differences in the way alcohol is processed by women.

Genetic factors: A number of genetic mutations have been identified that affect the way alcohol
is broken down in the body. Having one or more of these mutations may increase the risk of
alcoholic liver disease.

SIGNS AND SYMPTOMS:

CLINICAL PRESENTATION

Signs and Symptoms

More specific findings include:

• Hepatomegaly.
• Splenomegaly jaundice.
• Ascites
• ankle edema, and
• Spider angiomas.

With advancing disease, encephalopathy and hepatic coma may ensue, resulting in death.

Other less specific signs of alcoholic liver disease include

• Anemia
• Purpura
• Ecchymosis
• Gingival bleeding
• Palmar erythema
• Nail changes, and parotid gland enlargement (known as sialadenosis).

Pathophysiology:

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DIAGNOSIS:

Common considerations in alcoholic patients with jaundice include chronic pancreatitis with
biliary strictures and pancreatic biliary neoplasms.

Changes in the mental status of patients with alcoholic liver disease do not always imply the
presence of hepatic encephalopathy. Entities (e.g. subdural hematomas) should be excluded by
obtaining a computed tomography (CT) scan of the brain.

CBC COUNT:

• A complete blood cell (CBC) count commonly reveals some degree of neutrophilic
leucocytosis with bandemia. Usually, this is moderate; however, rarely, it is severe
enough to provide a leukemoid picture.

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• Alcohol is a direct marrow suppressant, and moderate anemia may be observed. In

addition, alcohol use characteristically produces a moderate increase in mean corpuscular
volume.
• Thrombocytosis may be observed as part of the inflammatory response, conversely,
myelosuppression or portal hypertension with splenic sequestration may produce
thrombocytopenia.

SCREENING BLOOD TESTS:

Screening blood tests to exclude other conditions (appropriate in any patient with alcoholic liver
disease) may include the following:

• Hepatitis B surface antigen (HBsAg) detects hepatitis B.

• Anti-hepatitis C virus by enzyme-linked immunosorbent assay (ELISA) detects hepatitis
C
• Ferritin and transferrin saturation detect hemochromatosis
• Jaundice with fever can be caused by gallstones producing cholangitis and is suggested
by a disproportionate elevation of the alkaline phosphatase (ALP) level.

LIVER FUNCTION TESTS:

Liver enzyme levels exhibit a characteristic pattern. In most patients, the aspartate
aminotransferase (AST) level is moderately elevated, whereas the alanine aminotransferase
(ALT) level is in the reference range or only mildly elevated. This is the opposite of observed in
most other liver diseases.

ULTRASONOGRAPHY: Ultrasonography is the preferred imaging study in evaluating

patients with suspected alcoholic liver disease. This modality provides a good evaluation of the
liver and other viscera, and it permits guided liver biopsy.

TREATMENT

NON PHARMACOLOGICAL THERAPY:

• Avoid alcohol consumption, do not reduce the intake at a time reduce it slowly.
• Eat easily digestible foods like bread, less protein because heavy meal can further

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damage the liver.

• Avoid meat intake.

• Drink amount of water.

ADVISED

➢ Coconut Water.
➢ Fresh vegetable soups, salads, juices.
➢ Sugarcane juice.

AVOID

➢ Alcohol
➢ Smoking
➢ Non-Veg, Packaged food
➢ Frozen food, Artificial food
➢ Junk Food, High protein diet
➢ Soft Drinks
➢ Pain Killers
➢ Citrus fruits and Yogurt and heavy, greasy, cheesy diet.

PHARMACOLOGICAL THERAPY:

Corticosteroids:-

➢ PREDNISOLINE-5mg/day.
➢ HYDROCORTISONE-80-100 mg/day.

Supportive therapy:-

➢ Vit. K
➢ Lactulose.

Alcohol Withdrawal syndrome:

➢ DISULFIRAM-200mg/day.
➢ THIAMINE- Vitamin supplement.

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PATIENT COUNSELING :

✓ Alcohol use must be stopped.

✓ Care should be taken to ensure good nutrition providing supplemental vitamins, minerals
including folate and thiamine.
✓ Salt restrictions may be required.

REFERENCE:

➢ Joseph. T. Dipiro, pharmacotherapy a pathophysiological approach – 7th edition, pg.no:

923-935.
➢ World journal gastroenterology 2014 March 7th, 20(9) 2159 – 2167, published online.
➢ K. D. Tripati, essentials of medical pharmacology 7th edition pg.no: 275 – 290.

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 International Journal of Pharmaceutical Research and Applications
Volume 9, Issue 1 Jan-Feb 2024, pp: 985-989 www.ijprajournal.com ISSN: 2249-7781

A Comprehensive Review of Prescription Patteren in Breast

Cancer Patients
D. Hanuma Nayak1*, Dr. D. Rama Brahma Reddy2, Dr. T. J. Mohan Rao3.
1
Doctor of Pharmacy (PharmD) V year, Department of Pharmacy Practice,
2
Professor and Principal, Department of Pharmacognosy and Phytochemistry,
3
Associate Professor, Department of Pharmacology,
Nalanda Institute of Pharmaceutical Sciences. Kantepudi (Village), Sattenapalli (Mandal), Dist. Guntur-522438
Andra Pradesh, India.
----------------------------------------------------------------------------------------------------------------------------- ----------
Submitted: 20-01-2024 Accepted: 30-01-2024
---------------------------------------------------------------------------------------------------------------------------------------
ABSTRACT: A tumour or mass of cells made up of these
We go into the topic of breast cancer and examine aberrant cells may stay contained in the original
the intriguing world of prescription patterns in this tissue, or it may start to spread to neighbouring
review paper. We give a general review of breast tissues. Worldwide, breast cancer is the most
cancer, covering its incidence and effects on common malignancy in women to receive a
women globally. Furthermore, we examine the diagnosis. In 2020, there were 22,61,419 new
many aspects of breast cancer therapy prescription instances of breast cancer reported and 6,84,996
patterns. We seek to shed light on current deaths from the disease. The incidence of breast
prescribing practices and pinpoint areas for cancer is fewer than 200 cases per million in
improvement by thoroughly examining the underdeveloped nations, while it exceeds 1000
literature. We can improve patient care and cases per million in industrialized nations. Because
treatment outcomes by comprehending the of late-stage detection, a lack of knowledge about
subtleties of prescription patterns. The purpose of breast cancer signs and symptoms, and poor health
this evaluation is to support further efforts to care facilities, the death rate from breast cancer is
enhance treatment approaches for breast cancer. higher in low- and middle-income nations.
Studies on medication prescriptions help in Normally, a mass known as a tumour form
observing the typical anticancer medication when healthy breast cells undergo uncontrollable
prescribing trend. For this reason, the purpose of growth and alteration, leading to breast cancer.
this review is to track medication prescription With the exception of skin cancer, breast cancer is
patterns for breast cancer. Any of the several cell the most prevalent cancer diagnosed in women in
types in the body might proliferate abnormally and the US. Breast cancer is the most common type of
result in cancer. A tumour or mass of cells made up cancer worldwide. Genetic and inherited
of these aberrant cells may stay contained in the predispositions are among the several risk factors
original tissue, or it may start to spread to linked to the development of breast cancer.One
neighbouring tissues. An invasive tumour is percent of cases of breast cancer are in males. Male
considered malignant, and tumour cells released breast cancer may be related to genetic
into the bloodstream or lymphatic system have the predisposition and family history, hormonal
potential to spread to other parts of the body and imbalances brought on by clinical illnesses (such as
form new tumours. When a tumour’s growth cirrhosis and gynecomastia), and radiation
interferes with the function of other tissues and exposure.
organs, it can be fatal.Studies on medication The most frequent type of cancer in
prescriptions aid in observing the typical anticancer women and the second leading cause of cancer-
medication prescribing trend. Therefore, the related deaths in women is breast cancer. In
purpose of this review is to track medication actuality, 15% of female cancer fatalities and 22%
prescription trends for breast cancer. of all female malignancies are caused by breast
Keywords:Prescription medications, breast cancer, cancer.
anti-cancer drugs, breast cancer therapy. The primary factors contributing to
increased BC-related morbidity among Indians are
I. INTRODUCTION inadequate access to competent medical treatment
Any of the several cell types in the body and a lack of information regarding BC screening.
might proliferate abnormally and result in cancer.
DOI: 10.35629/7781-0901985989 | Impact Factor value 7.429 | ISO 9001: 2008 Certified Journal Page 985
 International Journal of Pharmaceutical Research and Applications
Volume 9, Issue 1 Jan-Feb 2024, pp: 985-989 www.ijprajournal.com ISSN: 2249-7781

Thus, it’s critical to comprehend how anti- Pharmacists communicate with their patients
neoplastic and supportive treatments are now used. regarding their prescriptions by performing
Over the past 20 years, there has been an increase prescription analysis.
in breast cancer incidence with an overall slight Understanding the ever-changing
decline in mortality in the United States, which landscape of treatment options is made possible in
today accounts for around 20% of the one million large part by the prescription pattern analysis of
cases happening worldwide. Thus, much more breast cancer. Breast cancer is the most common
work has to be done in the areas of primary breast cancer in women worldwide; hence, prescribing
cancer prevention and prevention of breast cancer treatment approaches needs to be thoroughly
recurrence in breast cancer survivors, even though examined. Higher death rates are a result of late-
treatment and early diagnosis have made some little stage discovery, a lack of knowledge, and
progress in these areas. Breast cancer is largely inadequate healthcare facilities, especially in low-
caused by gene-nutrient interactions, and little is and middle-income countries.
known about the genetic and environmental factors The context for examining the prescription
that affect a person's susceptibility to breast cancer. patterns used in breast cancer treatment is
established by this introduction. In order to assess
PRESCRIPTION PATTEREN the efficacy and safety of ongoing treatment, it is
Analysing how prescribed drugs are used crucial to examine the use of anticancer drugs and
is part of the process of creating a prescription comprehend the pharmacological classes that are
pattern. Periodically assessing prescribing patterns recommended. As the study progresses, it seeks to
is necessary to give prescribers feedback and raise offer insightful information about present
their understanding of appropriate drug use. As a procedures, prospective advancements, and how
result, it’s essential to assess and track the prescription patterns affect patient care
prescription patterns for supporting and anticancer optimization in the context of breast cancer.
medications. The pattern of drug prescriptions in This study of drug use evaluation can be
healthcare facilities is assessed using standardized helpful because improper prescriptions are a major
prescribing indicators. As of yet, there isn’t a issue in developing nations like India. The majority
single, widely recognized protocol for improving of drug use evaluation research has employed
the therapeutic care of breast cancer. efficient techniques to ascertain its results.
One way to analyse prescription drug use There aren’t many studies on prescription
is to look at prescription patterns. It is employed to drugs for cancer in India. Additionally, no research
examine the anticancer medications and has been done on the off-label use of anticancer
pharmacological classes being administered for medications and other medications used to treat
treatment. It is employed to gauge the continuous cancer patients in India, despite the fact that this
treatment’s effectiveness and safety. Compared to practice is well-known to exist and is particularly
all other drug classes, antineoplastic medications common among those with breast cancer.
appear to be responsible for the majority of adverse Using the terms “breast cancer,”
drug reactions. By substituting the target drug with “prescription medication,” and “treatment” in the
an appropriate substitute or altering the drug dose title field, we searched the Google Scholar and
schedule, the identification of ADRs may aid in PubMed databases for relevant literature for this
limiting the harm. study. The search was conducted between 2015 and
One possible method for determining the 2023. For this review, we carefully chose the
place of drugs in society is to look at prescription pertinent publications after reading the abstracts.
patterns. It is quite beneficial for creating This review looks at several prescription treatments
healthcare budgets. Analysing prescription drug use for breast cancer and looks into current practices as
is the technique of prescribing pattern analysis. well as potential developments in the field of breast
Inappropriate drug use is the main cause of cancer medications.
potential patient hazards. One method of
preventing such risks for patients and ensuring the II. DISCUSSION
security and efficacy of treatment is to conduct Study 1: Basini J et al., (2023):The study assessed
periodic reviews of drug usage. When it comes to the prescription pattern of chemotherapeutic agents
healthcare-related decision-making, including how in 75 breast cancer patients in a tertiary care
best to use resources, doctors are essential. But hospital. The most prescribed combinational
when it comes to medications, pharmacists serve as regimen was Adriamycin, Cyclophosphamide, and
a link between patients and how they take them.
DOI: 10.35629/7781-0901985989 | Impact Factor value 7.429 | ISO 9001: 2008 Certified Journal Page 986
 International Journal of Pharmaceutical Research and Applications
Volume 9, Issue 1 Jan-Feb 2024, pp: 985-989 www.ijprajournal.com ISSN: 2249-7781

Taxanes (ACT) in 29.33% of patients, while III. CONCLUSION

Trastuzumab was the most prescribed The worldwide effect of breast cancer and
monotherapeutic agent in 10.6%. Promethazine and the critical role that prescribing practices play in
PEG filgrastim were used in 53.3% and 44% of enhancing treatment results are both highlighted by
patients, respectively. Neoadjuvant chemotherapy this study. The study that has been emphasized
was used in 13 patients, adjuvant chemotherapy in highlights persistent problems and indicates that
30 patients, and chemotherapy alone in 32 patients. more research is necessary to improve the
Study 2: Gurung S et al., (2022):Breast cancer is treatment of breast cancer. The paper highlights the
a significant issue in Nepal, with socioeconomic importance of prescription pattern analysis,
disparities, insufficient financial resources, and lack covering both monotherapeutic and combination
of awareness hindering prevention and treatment. A regimens, and offers informative data on drug
study assessing drug prescription patterns among utilization trends. The conversations are deepened
breast cancer patients at Bhaktapur Cancer Hospital by the inclusion of demographic information and
found that the majority were aged 40-59, with 51% drug-related side effects. The review emphasizes
in stage II and 29% in stage III. Anticancer drugs the ongoing need for research and development in
like Cyclophosphamide, Doxorubicin, Taxane, and primary prevention and recurrence prevention,
5-fluorouracil were prescribed from the national despite improvements in breast cancer detection
essential medicine list 2016 and WHO essential and treatment over the past 20 years. The prudent
drug list 2019 with brand names. use of anticancer drugs is ultimately critical to the
Study 3: Adhikari et al., (2018):The study aimed safe and successful treatment of breast cancer, as
to evaluate the drug prescription pattern of breast evidenced by prescription trends.
cancer patients in a tertiary care hospital in West
Bengal. The study involved 28 female patients Acknowledgments
diagnosed with breast cancer, with the majority We, the authors, express our sincere
found in the middle age group. The most prevalent gratitude to our guide for patiently editing our
type was invasive ductal carcinoma, accounting for drafts, skillfully guiding us, and encouraging us
75% of the population. The most common throughout this review process. We also extend our
chemotherapeutic agents used were 5-fluorouracil, heartfelt gratitude to the management of Nalanda
epirubicin, doxorubicin, cyclophosphamide, Institute of Pharmaceutical Sciences for providing
docetaxel/paclitaxel, and carboplatin. the necessary support.
Study 4: Manichavasagam M, et al., (2017):The
study examines the prescribing pattern of Conflicts of interest:
anticancer drugs in a tertiary care hospital’s The authors confirms that this article’s conflict has
medical oncology department. It reveals that the no conflict of interest.
majority of cancer cases are in the age group of 55-
65 years, with breast cancer being the most REFERENCES
prevalent. The majority of drugs prescribed are [1]. Kadam, R. L. (2018, January 15). Study of
alkylating agents, antimetabolites, plant prescription pattern and adverse drug
derivatives, cytotoxic antibiotics, and reactions of antineoplastic drugs in
glucocorticoids. The study concludes that the patients with breast cancer in a tertiary
utilization of anticancer drugs is rational, with over care teaching hospital. Indian J Pharm
70% prescribed from the National Essential Drug Pharmacol.
List. https://www.ijpp.org.in/article-
Study 5: Renuka L. Kadam et al., (2017): The details/5524
study analysed the prescription patterns of drugs [2]. M, M. (n.d.). Prescribing Pattern of
and adverse drug reactions (ADRs) in breast cancer Anticancer Drugs in a Medical Oncology
patients. It found that Cyclophosphamide was the Department of a Tertiary Care Teaching
most commonly prescribed drug, followed by Hospital. Retrieved from
Doxorubicin and 5-FU. Nausea was the most https://www.amhsr.org/articles/prescribing
common ADR, followed by alopecia, vomiting, -pattern-of-anticancer-drugs-in-a-
and nail blackening. The most common medicaloncology-department-of-a-
combination was Cyclophosphamide + tertiary-care-teachinghospital-4090.html
Doxorubicin + 5 FU. Out of the total ADRs, [3]. Adhikari, A., Chakraborty, D., Indu, R.,
60.11% were considered "definitely preventable," Bhattacharya, S., Ray, M., & Mukherjee,
while 74.15% were mild level 1 severity.
DOI: 10.35629/7781-0901985989 | Impact Factor value 7.429 | ISO 9001: 2008 Certified Journal Page 987
 International Journal of Pharmaceutical Research and Applications
Volume 9, Issue 1 Jan-Feb 2024, pp: 985-989 www.ijprajournal.com ISSN: 2249-7781

R. (2018, March 1). DRUG CARCINOMA BREAST RECEIVING

PRESCRIPTION PATTERN OF SYSTEMIC CHEMOTHERAPY IN
BREAST CANCER PATIENTS IN A TERTIARY CARE HOSPITALS.
TERTIARY CARE HOSPITAL IN https://doi.org/10.22159/ajpcr.2021.v14i4.
WEST BENGAL: A CROSS- 40826
SECTIONAL AND QUESTIONNAIRE- [13]. Assessment of Prescribing Pattern of Anti-
BASED STUDY. Cancer Agents in Breast Cancer Patients
https://doi.org/10.22159/ajpcr.2018.v11i3. at West Indian Oncology Hospital.
23180 Retrieved from
[4]. wjpps | ABSTRACT. (n.d.). Retrieved https://actascientific.com/ASCB/ASCB-
from 04-0247.php
https://www.wjpps.com/Wjpps_controller/ [14]. Claessens, A. K. M., Ibragimova, K. I. E.,
abstract_id/15975 Geurts, S., Bos, M. E., Erdkamp, F., &
[5]. Basini, J. (2023). A Prospective Study on Tjan‐ Heijnen, V. C. G. (2020, September
Drug Prescription Pattern of 1). The role of chemotherapy in treatment
Chemotherapeutic Agents in Breast of advanced breast cancer: an overview
Cancer Patients in a Tertiary Care for clinical practice. Critical Reviews in
Hospital. Retrieved from Oncology/Hematology.
https://ijopp.org/article/1020 https://doi.org/10.1016/j.critrevonc.2020.1
[6]. Guduru, H. (2019). A prospective study on 02988
the prescription pattern of anti-cancer [15]. Pentareddy, M. R., Suresh, A., Shailendra,
drugs and adverse drug reaction in a D., Subbaratnam, Y., Prasuna, G., Naresh,
tertiary care hospital. Retrieved from D. T. V., & Rajshekar, K. (2015, May 16).
https://pesquisa.bvsalud.org/portal/resourc PRESCRIPTION PATTERN OF
e/pt/sea-200033 ANTICANCER DRUGS IN A
[7]. Manjesh, P., Shetty, Y. C., Chinnaswamy, TERTIARY CARE HOSPITAL. Journal
G., & Patankar, P. (2021, January 1). of Evidence Based Medicine and
Prescription pattern of drugs in pediatric Healthcare.
cancer patients in a tertiary care hospital: https://doi.org/10.18410/jebmh/2015/435
An observational study. [16]. Taghizadeh-Ghehi, M., Amouei, A.,
https://doi.org/10.4103/oji.oji_20_21 Mansouri, A., Kohneloo, A. J., &
[8]. Bhushan, A., Gonsalves, A., & Menon, J. Hadjibabaie, M. (2018, May 15).
U. (2021, May 14). Current State of Breast Prescribing Pattern and Prescription-
Cancer Diagnosis, Treatment, and writing Quality of Antineoplastic Agents
Theranostics. in the Capital City of a Middle-income
https://doi.org/10.3390/pharmaceutics130 Developing Country. PubMed.
50723 https://doi.org/10.4103/jrpp.jrpp_17_74
[9]. Mary, S. B. V. (2022, October 27). [17]. Conyers, R., Devaraja, S., & Elliott, D.
Alarming rise in breast cancer cases in (2017, December 29). Systematic review
India. Retrieved from of pharmacogenomics and adverse drug
https://www.thehindu.com/life-and- reactions in paediatric oncology patients.
style/october-marks-breast-cancer- Pediatric Blood & Cancer, 65(4).
awareness-month-heres-what-we-need-to- https://doi.org/10.1002/pbc.26937
know-and-do-to-keep-the-disease- [18]. Singh, A., Mishra, R., & Mazumder, A.
away/article66030432.ece/amp/ (2023, November 2). Breast cancer and its
[10]. Breast cancer. (2023, July 12). Retrieved therapeutic targets: A comprehensive
from https://www.who.int/news- review. Chemical Biology & Drug Design,
room/fact-sheets/detail/breast-cancer 103(1).
[11]. CARE Fund. (n.d.). Retrieved from https://doi.org/10.1111/cbdd.14384
https://give.breastcancer.org/give/294499/ [19]. Prescription drug use patterns around
#!/donation/checkout?c_src=clipboard&c_ fragility fractures. (2016, September).
src2=text-link Reactions Weekly, 1617(1), 12–12.
[12]. Shah, S., Singh, A. P., & Mundhava, S. https://doi.org/10.1007/s40278-016-
(2021, April 7). A STUDY OF DRUG 20791-y
UTILIZATION IN PATIENTS OF
DOI: 10.35629/7781-0901985989 | Impact Factor value 7.429 | ISO 9001: 2008 Certified Journal Page 988
 International Journal of Pharmaceutical Research and Applications
Volume 9, Issue 1 Jan-Feb 2024, pp: 985-989 www.ijprajournal.com ISSN: 2249-7781

[20]. Shyamala, K., Girish, H. C., & Murgod, S.

(2014, January 1). Risk of tumor cell
seeding through biopsy and aspiration
cytology. Journal of International Society
of Preventive and Community Dentistry.
https://doi.org/10.4103/2231-0762.129446

DOI: 10.35629/7781-0901985989 | Impact Factor value 7.429 | ISO 9001: 2008 Certified Journal Page 989
 03-05-2024

CASE STUDY ON MIGRAINE HEADCHE

DEFINITION:
NALANDA INSTITUTE OF Migraine is a familial disorder characterized by recurrent attacks of headache widely variable in intensity, frequency and duration.

PHARMACEUTICAL SCIENCES Attacks are commonly unilateral and are usually associated with anorexia, vomiting and/or photophobia. Migraine is one of the common cause of recurrent headaches.

 According to IHS , migraine constitutes 16% of primary headaches.

 Migraine afflicts 10-20% of the general population.
 In india, 10-20% of people suffer from migraine.
CASE PRESENTATION ON  Migraine is under diagnosed and under treatment
 According to headache classification committee of the international headache society, Migraine has been classified as:

MIGRAINE HEADCHE 

Migraine without aura[common migraine]
Migraine with aura[classic migraine]

BY  Complicated migraine

PHASES:
D. HANUMA NAYAK
1. Aura
REGD.NO. 19CR1T0003 2. Headache

PHARM.D V YEAR 3. Prodrome

4. Postdrome
• According to headache classification committee of the international headache society, Migraine has been classified as:
 Migraine without aura[common migraine]
 Migraine with aura[classic migraine]
 Complicated migraine

RISK FACTORS:
ETIOLOGY:
 Genetic factors
• Family history of migraine headache 70% to 80%  High frequency of attacks anxiety and depression
• Medication (birth control pills, vasodilators)  Stressful life events

• Fatigue or emotional stress

 Obesity
 Heavy caffeine consumption
• Specific food or alcohol or caffeine
 Tobacco use
• Exertion
 Overuse of abortive headache medication
• Lack of sleep  Snoring
• Noise, light, diet  Sleep related problems
 Tempomansibular disorder
EPIDEMOLOGY:
 Other pai pain syndrome
• Migraine affects 18% of women and 6% of men in the united States and has an estimated world wide prevalence of about 10%
 Psychiatry problem
• For both men and women, the prevalence of migraine rise throughout early life and fall after midlife
PATHOPHSYIOLOGY:
• In girl’s women, the rate almost triple between age and 10 and 30years
Migraine was once thought to be initiated by problems with blood vessels. This theory is now largely discredited. Current thinking
SIGN AND SYMPTOMS:
is that a phenomenon known as cortical spreading depression is responsible for the disorder. In cortical spreading depression,
• Defects in visuals, dysphasia, headache, severe pain, vomiting, photophobia, pallor, anorexia, phonophobia, hemiparesis, confusion, apathy, neurological activity is depressed over an area of the cortex of the brain. This situation results in the release of inflammatory
numbness mediators leading to irritation of cranial nerve roots, most particularly the trigeminal nerve, which conveys the sensory information
for the face and much of the head.

This view is supported by neuroimaging techniques, which appear to show that migraine is primarily a disorder of the TREATMENT
brain (neurological), not of the blood vessels (vascular). A spreading depolarization (electrical change) may begin 24 hours
before the attack, with onset of the headache occurring around the time when the largest area of the brain is depolarized. TREATMENT PLAN:
The effects of migraine may persist for some days after the main headache has ended. Many sufferers report a sore feeling
• a trail of metoclopramide vs sumatriptan for the emergency department treatment of migraine was done in patient:
in the area where the migraine was, and some report impaired thinking for a few days after the headache has passed.
• This study compared metoclopramide 20mg/IV over 6 hr with sumatriptan 6mg/SC for initial treatment of emergency migraine headaches.
In 2005, research was published indicating that in some people with a patent foramen ovale (PFO), a hole between the
upper chambers of the heart, suffer from migraines which may have been caused by the PFO. The migraines end instantly • By measuring the pain intensity it concluded that metoclopramide preferable therapy for migraine presenting to the patient .
if the hole is patched. Several clinical trials are currently under way in an effort to determine if a causal link between PFO
and migraine can be found. Early speculation as to this relationship has centered on the idea that the lungs detoxify blood • Because, at 2 hrs, pain free rates were 59% with the metoclopramide to 35% with the sumatriptan.
as it passes through. The PFO allows uncleaned blood to go directly from the right side of the heart to the left without
NON PHARAMCOLOGICAL TREATMENT:
passing through the lungs.
 apply ice to the head.
Migraine headaches can be a symptom of Hypothyroidism.
 recommended periods of rest or sleep, usually in dark or quite environment.
Diagnosis:  Identify and avoid triggers of migraine attacks.
• Pulsatile  Behavioural interventions[relaxation therapy, biofeedback, cognitive therapy] may help patients who prefer nondrug therapy or when drug
therapy is ineffective or not tolerated.
• Hours  Decrease the use of OTC medication.
• Unilateral  Massage, passive mobilization of the cervical facets.
• Nauseating  Stress and pain management.

• Disabling  Physiotherapy[daily exercise programme and posture correction].

1
 03-05-2024

Case study PAST MEDICATION HISTORY:-

Patient details :-  Nil
Name :- Mrs. XY IP. NO:- 230120 PHYSICAL EXAMINATION:-
AGE:- 30 SEX:- Female Conscious, oriented
D. O. A:- D. N. D:- Temp:- 98.6of B.P:- 140/70 mm of Hg
PR :- 98 bpm RR:- 24 bpm
Chief complaints:-
SYSTEMIC EXAMINATION:-
Tingling sensation (6AM), blurred vision, giddiness.
CVS:- S1S2+ CNS:- NFND
HISTORY OF PRESENT ILLNESS:-
LAB INVESTIGATIONS:-
Headache, blurred vision PCV:- 30.4% Hb:- 10.4 g/dl
PAST MEDICAL HISTORY:- FBS:- 130 mg/dl RBS:- 145 mg/dl
Headache since 1 month, chills Direct bilirubin:- 0.8 mg/dl
Indirect bilirubin:- 0.3 mg/dl

• DIAGNOSIS :- Viral headache/ Migraine PATIENT COUNSELLING:-

• TREATMENT Manage stress
• DRUG CHART:- Take medication regularly
• DRUGS DOSE R.O.A FREQUENCY Daily exercises
• Tab. Pantop 40mg PO BD
• Tab. Encorate 300mg PO BD
• Tab. Zevert 16mg PO OD
• Tab. Dome 40mg PO BD
• Tab. Nexto 20mg PO BD THANK YOU

2
 PACKAGE LEAFLET: INFORMATION FOR THE USER
Cisplatin 1mg/ml Concentrate for Solution for Infusion
Cisplatin

The name of your medicine is ‘Cisplatin 1 mg/ml Concentrate for Solution for Infusion’ but in the rest of the
leaflet it will be called “Cisplatin Injection”.

What is in this leaflet:

1. What Cisplatin Injection is and what it is used for
2. What you need to know before you use Cisplatin Injection
3. How to use Cisplatin Injection
4. Possible side effects
5. How to store Cisplatin Injection
6. Contents of the pack and other information

1. What Cisplatin Injection is and what it is used for

Cisplatin forms part of a group of medicines called cytostatics, which are used in the treatment of cancer.
Cisplatin can be used alone but more commonly Cisplatin is used in combination with other cytostatics.

What it is used for?

Cisplatin can destroy cells in your body that may cause certain types of cancer (tumour of testis, tumour of
ovary, tumour of the bladder, head and neck epithelial tumour, lung cancer and for cervical cancer in
combination with radiotherapy).

2. What you need to know before you use Cisplatin Injection

Do not use Cisplatin if:

• you are allergic to cisplatin or to any of the other ingredients of this medicine (listed in section 6
• if you have had hypersensitivity to similar anti-cancer medicines in the past
• you have severe kidney disease you have hearing difficulties
• if you have very low numbers of blood cells (called ‘myelosuppression’), (your doctor will check this with
a blood test)
• you are dehydrated
• if you need to have a vaccine for ‘yellow fever’
• you are breast-feeding

Warnings and precautions

Talk to your doctor, pharmacist or nurse before using Cisplatin Sterile Concentrate:
• if you have any symptoms of nerve damage (peripheral neuropathy) such as pins and needles,
numbness or poor sense of touch
• if you have had radiation therapy to your head

Other medicines and Cisplatin Sterile Concentrate

Tell your doctor or pharmacist if you are taking/ using, have recently taken/ used or
might take/ use any other medicines, for example:
some antibiotics, such as cephalosporins, aminoglycosides and amphotericin B and
some substances used in medical imaging may make the side effects of cisplatin worse;
particularly kidney problems
 • some antibiotics, such as cephalosporins, aminoglycosides and amphotericin B and some substances
used in medical imaging may make the side effects of cisplatin worse; particularly kidney problems
• some water tablets called loop diuretics, antibiotics called aminoglycosides and an anti-cancer
medicine called ifosfamide may make the hearing loss side effect of cisplatin worse
• bleomycin (anti-cancer medicine), methotrexate (used to treat cancer or arthritis) and paclitaxel (anti-
cancer medicine) may produce more side effects if cisplatin is also being used
• the effectiveness of oral anticoagulants may be affected. Your doctor will monitor with blood tests
• use of certain antihistamines may hide the symptoms of balance changes (such as dizziness or
tinnitus)
• the effectiveness of medicines used for the treatment of convulsions (e.g. phenytoin) may be reduced,
so blood levels may need to be checked
• cisplatin may make the side effects of the anti-cancer medicine ifosfamide worse

Pregnancy, breast-feeding and fertility

If you are pregnant or breast-feeding, think you may be pregnant or are planning to have
a baby, ask your doctor or pharmacist for advice before using this medicine.
Due to the possible risk of birth defects, male and female patients should take
contraceptive measures both during treatment with cisplatin and for at least six months
after treatment has ended.
Treatment with cisplatin can potentially cause permanent sterility in men. It is
recommended that those who wish to become fathers in the future discuss the possibility
of cryoconservation
(freezing) of their sperm prior to treatment. Tell your doctor if you have any
concerns.

Driving and using machines

Do not drive or use machines if you experience any side effect which may lessen your
ability to do so.
Cisplatin injection contains sodium
This medicine contains 3.5 mg sodium (main component of cooking/table salt) in each ml. This is equivalent
to 38.3% of the recommended maximum daily dietary intake of sodium for an adult.
3. How to use Cisplatin Injection

Dosage and method of administration

Cisplatin should only be given by a specialist in cancer treatment.
The concentrate is diluted with a sodium chloride solution.
Cisplatin is only given by injection into a vein (an intravenous infusion).
Supportive equipment should be available to control anaphylactic reactions.
Cisplatin should not come into contact with any materials that contain aluminium.
The recommended dosage of Cisplatin depends on your well-being, the anticipated effects of the treatment,
and whether or not cisplatin is given on its own (monotherapy) or in combination with other agents
(combination chemotherapy).

Cisplatin (monotherapy):
The following dosages are recommended:
• A single dosage of 50 to 120 mg/m² body surface, every 3 to 4 weeks.
• 15 to 20 mg/m² per day over a 5-day period, every 3 to 4 weeks

Cisplatin in combination with other chemotherapeutical agents (combination chemotherapy):

• 20 mg/m² or more, once every 3 to 4 weeks.

For treatment of cervical cancer cisplatin is used in combination with radiotherapy.

A typical dose is 40 mg/m² weekly for 6 weeks.
In order to avoid, or reduce, kidney problems, you are advised to drink copious amounts of water for a period
of 24 hours following treatment with Cisplatin.

If you take more Cisplatin than you should

Your doctor will ensure that the correct dose for your condition is given. In case of overdose, you may
experience increased side effects. Your doctor may give you symptomatic treatment for these side effects. If
you think you received too much Cisplatin, immediately contact your doctor.

Always use this medicine exactly as your doctor or pharmacist has told you. Check with your
doctor or pharmacist if you are not sure.

4. Possible side effects

Like all medicines, this medicine can cause side effects, although not everybody gets
them If any of the following happen, tell your doctor immediately:
• severe allergic reaction - you may experience a sudden itchy rash (hives), swelling of the hands,
feet, ankles, face, lips, mouth or throat (which may cause difficulty in swallowing or breathing), and you
may feel you are going to faint
• severe chest pains possibly radiating to the jaw or arm with sweating, breathlessness and nausea
(heart attack)
• pain or swelling at the injection site during the injection (may be due to the injection not going
into the vein properly, which can lead to serious damage to the tissues around the injection site)
• stroke
• brain dysfunction (confusion, slurred speech, sometimes blindness, memory loss and paralysis)

These are serious side effects. You may need urgent medical attention.

Very common: may affect more than 1 in 10 people:

• decrease in bone marrow function (which can affect the production of blood cells)
• decrease in white blood cells, which makes infections more likely (leukopenia)
• decrease in blood platelets, which increases the risk of bruising and bleeding
(thrombocytopenia)
• reduction of red blood cells which can cause weakness and your skin to look pale
(anaemia)
• reduced level of sodium in the blood
• high temperature

Common: may affect up to 1 in 10 people:

• severe pain or swelling in either of your legs, chest pain, or difficulty breathing (possibly
indicating harmful blood clots in a vein)
• fast, irregular or slow heart beats
• sepsis (blood poisoning)

Uncommon: may affect up to 1 in 100 people:

• severe allergic reaction (see above)
• damage to the ear (ototoxicity)
 • reduced level of magnesium in the blood
• abnormal sperm production

Rare: may affect up to 1 in 1,000 people:

• increased risk of acute leukaemia
• seizures (fits)
• fainting, headache, confusion and loss of vision
• loss of certain types of brain function, including brain dysfunction characterised by
• spasms and reduced level of consciousness
• heart attack
• inflammation of mucous membranes of the mouth (stomatitis).
• peripheral neuropathy of the sensory nerves, characterised by tickling, itching or tingling
without cause and sometimes with loss of taste, touch, sight, sudden shooting pains from the neck through
the back and into the legs when bending forward

Very rare: may affect up to 1 in 10,000 people:

• heart arrest

Not known: frequency cannot be estimated from the available data:

• signs of infection such as fever or sore throat
• haemolytic anaemia
• inappropriate release of vasopressin hormone (ADH) which may lead to low sodium
• in the blood and water retention
• blood amylase (enzyme) increased
• dehydration
• reduced level of calcium, phosphate, potassium in the blood
• high level of uric acid in the blood
• muscle cramping
• spinal disease which may cause a sensation of electric shocks passing into your limbs • loss
of taste
• problems with your eyesight (blurred vision, odd colours, loss of vision or eye pain)
• ringing in the ears or deafness
• heart problems
• unusually cold or white hands and feet
• tingling, numbness or tremor in your hands, feet, arms or legs
• persistent headache
• feeling or being sick
• loss of appetite, anorexia
• hiccups
• diarrhoea
• liver enzymes increased; bilirubin increased
• difficulty breathing
• problems with your kidneys or urine
• hair loss
• rash
• extreme tiredness/weakness
• swelling or soreness where the injection was given
• cramps or spasms
• burning or prickling sensation
• unexpected bruising or bleeding
 • haemolytic uremic syndrome which may cause changes to the kidneys and blood

Cisplatin may lead to problems with your blood, liver and kidneys. Your doctor will take
blood samples to check for these problems.

Reporting of side effects

If you get any side effects, talk to your doctor, pharmacist or nurse. This includes any possible side effects
not listed in this leaflet. You can also report side effects directly via the Yellow Card Scheme at:
www.mhra.gov.uk/yellowcard. By reporting side affects you can help provide more information on the safety
of this medicine.

5. How to store Cisplatin injection

Keep this medicine out of the sight and reach of children.

Keep the vial in the outer carton (to avoid exposure of Cisplatin to light).

Concentrate for solution for infusion 1 mg/ml

Keep container in the outer carton in order to protect from light. Do not refrigerate or freeze.

If a crystal or precipitate has formed as a result of exposure to low temperatures, redissolve by keeping the
vials at room temperature till clear solution is obtained.
The product should be discarded if the solution doesn’t become clear after vigorous shaking.

Do not use this medicine after the expiry date which is stated on the vial and the outer carton after ‘exp’. The
expiry date refers to the last day of that month. Do not use this medicine if you notice visible signs of
deterioration.

All materials that have been used for the preparation and administration, or which have been in contact with
cisplatin in any way, must be disposed of according to local cytotoxic guidelines

If you find the solution cloudy or a deposit that does not dissolve is noticed, the bottle should be discarded.

6. Contents of the pack and other information

What Cisplatin Injection contains:

Cisplatin Injection contains the active ingredient cisplatin.
Each millilitre (ml) of solution contains 1 milligram (mg) of cisplatin. This medicine is presented in amber
glass containers called vials.

Presentations 10 ml 25 ml 50 ml 100 ml
Amount of cisplatin 10 mg 25 mg 50 mg 100 mg

It is available in packs containing a single vial (not all the presentations mentioned may be marketed).

The other ingredients include water for injections, sodium chloride, hydrochloric acid (for pH adjustment)
and/or sodium hydroxide (for pH adjustment).

What Cisplatin Injection looks like and content of the pack:

Cisplatin Injection is clear, colourless to pale yellow solution in an amber glass vial practically free from
particles with flip off transparent seal.
Packaging with 1 injection vial of 10 ml, each injection vial containing 10 mg cisplatin.
Packaging with 1 injection vial of 25 ml, each injection vial containing 25 mg cisplatin.
Packaging with 1 injection vial of 50 ml, each injection vial containing 50 mg cisplatin.
Packaging with 1 injection vial of 100 ml, each injection vial containing 100 mg cisplatin.

Not all pack sizes may be marketed.

Marketing Authorisation Holder and manufacturer:
Accord Healthcare Limited,
Sage House, 319 Pinner Road,
North Harrow, Middlesex,
HA1 4HF,
United Kingdom.

Manufacturer:
Accord Healthcare Limited
Sage House, 319, Pinner Road,
North Harrow, Middlesex,
HA1 4HF,
United Kingdom

Accord Healthcare Polska Sp.z o.o.,

ul. Lutomierska 50,95-200 Pabianice, Poland

Accord Healthcare B.V.,

Winthontlaan 200,
3526 KV Utrecht,
The Netherlands

This leaflet was last revised in 04/2021.

(Please note this is a Prescriber Information Leaflet NOT the SPC. For full details regarding this
product please refer to the SPC.)

The following information is intended for medical or healthcare professionals only:

Preparation and handling of the product

Like with all anti-neoplastic products caution is needed with the processing of cisplatin. Dilution should take
place under aseptic conditions by trained personnel in an area specifically intended for this. Protective gloves
should be worn for this. Precautions should be taken to avoid contact with the skin and mucous membranes.
If skin contact did occur anyway, the skin should be washed with soap and water immediately. With skin
contact tingling, burns and redness have been observed. In case of contact with the mucous membranes they
should be copiously rinsed with water. After inhalation dyspnoea, pain in the chest, throat irritation and nausea
have been reported.

Pregnant women must avoid contact with cytostatic drugs. Cisplatin should not be used during pregnancy
unless the clinician considers the risk in an individual patient to be clinically justified.
Bodily waste matter and vomit should be disposed with care.

If the solution is cloudy or a deposit that does not dissolve is noticed, the bottle should be discarded.

A damaged bottle must be regarded and treated with the same precautions as contaminated waste.
Contaminated waste
must be stored in waste containers specifically marked for this. See section “Disposal”.

Preparation of the intravenous administration

Take the quantity of the solution that is needed from the bottle and dilute with at least 1 litre of the following
solutions:

- sodium chloride 0.9%

- mixture of sodium chloride 0.9% / glucose 5% (1:1), (resulting final concentrations: sodium chloride
0.45%, glucose 2.5%)
- sodium chloride 0.9% and 1.875% mannitol, for injection
- sodium chloride 0.45%, glucose 2.5% and 1.875% mannitol for injection

Always look at the injection before use. Only a clear solution, free from particles should be administered.

If precipitate or crystal observed inside the vial, keep vial at room temperature (20 - 25°C) until till clear
solution obtained. Protect unopened container from light. The product should be discarded if the solution
doesn’t become clear after vigorous shaking.

DO NOT bring in contact with injection material that contains aluminium.

DO NOT administer undiluted.
With respect to microbiological, chemical and physical stability with use of the undiluted solutions, see below
“Special precautions for storage”.

Disposal
All materials that have been used for the preparation and administration, or which have been in contact with
cisplatin in any way, must be disposed of according to local cytotoxic guidelines. Medicines should not be
disposed of via wastewater or household waste. Ask your pharmacist how to dispose of medicines no longer
required. These measures will help to protect the environment.

Incompatibilities
Do not bring in contact with aluminium. Cisplatin may interact with metal aluminium to form a black
precipitate of platinum. All aluminium-containing IV sets, needles, catheters and syringes should be avoided.

Cisplatin decomposes with solution in media with low chloride content; the chloride concentration should at
least be equivalent to 0.45% of sodium chloride.
In the absence of compatibility studies, this medicinal product must not be mixed with other medicinal
products.

Antioxidants (such as sodium metabisulphite), bicarbonates (sodium bicarbonate), sulphates, fluorouracil and
paclitaxel may inactivate cisplatin in infusion systems.

Special precautions for storage

Medicinal product as packaged for sale:

Concentrate for solution for infusion 1 mg/ml

Undiluted solution: Keep container in the outer carton in order to protect from light. Do not refrigerate or
freeze. If the solution is not clear or a dissolvable precipitate is formed the solution must not be used.

Diluted solution:
For the storage condition of the diluted medicinal product: see
below “Concentrate for solution for infusion after dilution”. Do
not refrigerate or freeze.

Concentrate for solution for infusion after dilution:

After dilution
Chemical and physical in-use stability after dilution with infusion fluids described in section “Preparation and
handling of the product”, indicate that after dilution with recommended intravenous fluids, Cisplatin Injection
remains stable for 24 hours at 20 - 25 °C room temperature.
From a microbiological point of view, the diluted solution should be used immediately. If not used
immediately, infuse storage times and conditions prior to use are the responsibility of the user and dilution
should take place in controlled and validated aseptic conditions.