IM Shelf - Amboss
IM Shelf - Amboss
Post Myocardial Infarction; there will be venous pressures, crackles S3, AV block and ST
changes;
- There will show that the heart is not pumping blood forward;
- Management; vasopressors; and inotropes
Pericarditis; This is a common cycle for cardiac tamponade. It may occurcur in cases in which
the pericardium becomes less elastic, this can release increased amounts of inflammatory fluids
into the pericardial space. Other causes include uremia and aortic dissection.
Uremia Induced pericarditis; Patient presents with positional chest pain, and a pericardial
friction rub
Pathogenesis; uremia; this is the most likely cause of the patients findings; this doesn’t present
with classic diffuse ST elevations; indications for hemodialysis
DVT In Pregnancy
Overview; there is a tender, palpable cord in the lower extremities; this is regarded as
superficial thrombophlebitis;
Management; this will be with duplex US; this will be a risk especially with obesity and venous
isufficiency
Immediate Cardioversion;
There will be atrial fibriation; the patient is hemodynamically unstable, immediate
cardioversion
there will be attempt to restore rate
If cardioversion fails; then use B-blocker and calcium channel blocker
Drug Induced HTN: OCPS can cause a rise in BP in many women; includes HTN, obesity, woman
older than 35 years old;; it will resolve post discontinuing OCPs
ECG:
THe patient presents with anticholinergic toxicity; AMS< hyperthermia, tachycardia and
pupillary dilation; this wll cause QT prolongation. This corresponds to the likelihood of
ventricular arrhythmias and seizures; sodium bicarbonate will counter the cardiotoxic effects of
TCAs.
SIRS; Overview; this will present with fever and AMS post abdominal surgery; there will also be
tachycardia and abnormal WBC count; caused by SIRS:
- Note this is caused by the patients bowel
- Presentation, fever, tachycardia, warm skin, neutropenia and thrombocytopaenia
Post MI management;
Asymptomatic left ventricular systolic dysfuction is common
- Management ACE inhibitors; this will revent concentric hypertrophy
Nonvalvular Afib;
Afib; this leads to blood and clot formation in the atrium; so once we convert back to sinus
rhythm, we will administer a DOAC
Atrial Fibrilation
Presentation; it will manifest as palpations, lightheadedness and irregular heart rate; this is a
diagnosis of Afib; this will have risk factors including HTN and CAD
Management; rate control and anticoagulation
Mechanism of warfarin; long half ife and interference wih gamma carboxylation of VKOR; 2, 7, 9
and 10 along with protein C and S
- There will be shorter half lives; ad this is a therapytic bridge
- PTT; this will monitor heparin therapy
Atrial FIbrilation; this will be the most common type of arrhythmia; it is associated with
cardiomyopathy; note it wil be flared with alcohol intake, cocaine, amphetamines, theophuline
- Management rate control
-
Edocarditis caused by prosthetic valves; staphylococcus epidermidis; this is the most common
cause for prosthetic valve endocarditis;
Pathogenesis; it will create a biofilm over the prosthetic valve and will have a subacute course;
B-blockers
IV glucagon is the initial treatment for IV fluids, atropine----b adrenergic agonist in severe case
- IV glucagon is part of the initial treatmen for symptomatic patients (along with IV fluids
and atropine alone_, there will be profound myocardial depression and activation of AC
which enhances cardiac contractility
- Additional treatment includes depending on the severity of the symptoms,
Hypertensive Emergency;
Clinical presentation; this will have headache, blurry vision and AMS,
Management; this will be treated with nitroprusside to prevent end organ damage.
Includes labetolol, nitroprusside and nicardipine.
Complication; nitroprusside, this will cause CN toxicity, this will also reduce renal perfusin,
Bradycardia Management;
Atropine is an aticholingeric agent, that will raise HR
Cardiomyopathy;
Clinical picture; there will be palpatations, exertional dyspnea, hypoxia and JVD, there bilateral
crackles and s3 gallop.
- Management; because of the chronic alcohol use, there will lead to ventricular dilation
and reduced contractility.
- Treatment, alcohol cessation
Atrial Fibrillation; measure TSH this will diagnose hypothyroidism, there will be associated with
increased MR, tremor, warm skin and palpations.
Clinical manifestation; anxiety, weight loss, and enlarged thyroid gland
Managmet; antithyroid drugs and b-blockers such as propranolol.
HTN reduction;
Weight loss is the most effective method to reduce BP in obese patients, there will b a
reduction in BP by 1 mmhg for every 1 kg of weight loss. Maintaining a normal BP will reduce
BP.
Theory; peripheral insulin resistence, leading to hyperinsulinemia, this will trigger sodium and
fliod resorption.
Aneurysm;
Femoral artery, aneurysm, painless at the midinguinal point. There is a palpable thrill
characteristics features of a femoral artery aneurysms----age, hypertension,
hypercholesterolemia, chronic smoking all risk factors.
Hyponatremia;
Patient is euvolemic; neurologic and respiratory distress and psychiatric; thiazides will ihibit
sodium resorption
Fibromuscular Dysplasia;
Overview; this will lead to RAS: there is early onset HTN that is refractory to pharmacotherapy;
there is also an abdominal bruit; this will be diagnosed by duplex imaging. This is suggestive of
RAS; young women with early onset of pharmacotherapy are the most common cause for DMF
Management percutaneous transluminal US
AV Block;
Patients ECG will show ventricular rate of 40/min, and an atrial rate of 100/min, the placement
of transcutaneous pacemaker is indicated
- Dyspnea, dizziness and syncope episodes with bradycardia. This will be consistent with
third degree heart block.
- P waves and ventricles will beat independently of one an other.
Syncope;
Situational syncope; is one type of neutrally mediated reflex syncope, triggers include cough,
swallowing, or micturition, parasympathetic hyperactivity it turns to peripheral dilation.
- A LOC can be caused by cerebral ischemia, the absence of postictal period (tounge
biting), bladder incontinence, neurologic findings make it less likely.
Myocarditis;
Presentation; Subacute onset of dyspnea, chest pain, JVD with inspiratory crackles on lung
auscultation consistent with CHF, most likely secondary to myocarditis
Hypovolemic Shock; there will be evidence of bleeding, rapid pulse, and free fluid. BP- CO x
SVR,
The combination of decreased CO, PCWP, and increased SVR and decreased CVP, this will have
hemorrhagic shock.
- Low right heart failure result in decreased blood delivery with decreased PCWP. Low CO,
causes hypotension so the peripheral vasculatre constricts (increased SVR) to maintain
adequate BP for organ perfusion
Management; correction of the underlying cause
Infective Endocarditis;
Clinical picture, there will be fevers, chills, murmur, and splinter hemorrhages and Janeway
lesions, vegetation of the mitral valve and cultures growing coag negative staph.
Associated with infected peripheral venous catheter; with IE; will most likely be staph
epideridmis. This will be linked to IV catheter, pacemakers and will form a biofilm related to
prosthetic material
Infective Endocarditis;
IV drug users, there is an increased of IE that can manifest as bacteremia, there will be raised
risk of PE due to bacterial embolisms, the right heart is ratrely involved in IE,notably with mitral
or tricuspid involvement
Left sided IE; will cause emboli to the retina, janeway lesions, osler nodes (kidney, brain and
spleen)
Pathogenic agent in right sided endocarditis; there will be rapid progression, a sudden onset of
symptoms and high fever.
- This is most likely linked to staphylococcus aureus, this will be associated with IVDU,
however subacute endocarditis, will be insidious onset.
Pleural Effusion; Patients history of subacute viral pleuritis, chest pain, fever, and a friction rub
suggest infection.the condition is self resolving and will attenuate within a few weeks.
Manage with NSAIDS, ibuprofen, indomethacin.
Pleural effusion
Overview; patient has a productive cough and fever that will progress to SOB and this is
suggestive of pneumonia and it is complicated by paranpneumonic effusion
Acute Limb Ischemia , this is most commonly caused by thrombosis, dissecton, trauma and
stent/graf occlusion, there will originate from thrombus formation (Afib, valvular heart disease
or ventricular aneurysms.
Drug induced vasoconstriction; this is characterized by bilateral necrois of the toes and
coldness of all extremities
Drug induced vasoconstriction is associated with septic shock and the MAP > 65, NE will be
associated with increased SVR and prolonged a receptors will cause constriction and
downstream necrosis
Ventricular Tachycardia;
Polymoprhic ventricar tachycardia, there will be syncope or life threatening arrhythmias, such
as torsade de pointes. It can be promoted via amiodarone, hypokalemia, hypomagensiumia and
hypocalcemia
Other drugs that promote QTC prolongation are ondansetron and methadone
Hypertrophy;
There will be a QRS complex > 30, there will be a diastolic dysfunction in this case, leading to
impaire filling and elevated left ventricular and left atrial and pulmonary venous pressure
Aortic Dissection;
There will be a strong association with fibrillin 1 gene mutation. This will lead to subluxation of
lens and cardiovascular anomalies include dilation of the aorta.
Aortic Dissection
Clinical presentation, there is sudden and severe chest pain accompanied by an assymetric
blood pressure on the x-ray, this is consistent with aortic dissection
There will be Mufflied heart sounds, this is a common complication of aortic dissection type A, if
the dissection results in the tunica intima, it can leak into the pericardium and muffle
transmission of the heart sounds.
Acute Myocardial infarction; this will last a duration > 20 minm there are two types UAm
NSTEMI; this is part of the continuum of ACS
Aortic Dissection
Overview; this is a condition that presents with chest pain that radiates to the back will cause a
diastolic decrendeo murmur that is best heard at the right upper sternal border;
Management; depends on the origin, will be managed surgically (Stanford A) or BP control
(Stanford B), because patient is hemodynamically unstable (will do TEE)
DVT:
Superficial thrombophlebitis; thrombosis that manifssts in the lower extremities.
- Risk factors; obesity and smoking. This is consisting of NSAIDS affects lower limb and
compression therapy.
Aneurysm;
US guided thrombin injection, this will initiate formation of the of clot stopping hematoma. This
is the gold standard for uncomplicated post catheterization.
Myocardial Infarction
ECG gindings; show anterior chest leads, in the left anterior ventricular wall, this is a late
complication of MI, the murmur might be heard as a result of MR, third heart sound is also
common in patients
- Mural thrombus, this can develop several weeks to months, this will include thinning
and weakening of the vessel wall. There will be heart failure, ventricular arrhythmia and
myocardial rupture
Statins;
The patient presents with generalized weakness, elevated concentration of CK, this will have
discontinued simvastatin, post discontinuation for a period of 2-4 weeks, there will be
myopathy
Cardiogenic Shock
Key parameters, PCWP, will show increased CVP increased PCWP and increased SVR
Pathogenesis; MI secondary to CAD, this will be the most common cause for cardiogenic shock.
Gastroenterology
Hepatocellular Carcinoma;
THis is associated with a hepatitis C infection, will present with liver cirrhosis, palmar erythema,
telangectasia, nodular live surface and a solitary hepatic lesion on US, this makes HCC the most
likely diagnosis.
Risk factors; Hepatic infections, liver cirrhosis,----this will manifest wiehg tweight loss, cachexia,
ascites and jaundice.
Wilson Disease;
There is a combination of wing beating tremor, excessive drooling, hyperreflexia, signs of
depression, gait abnormalities and dysmetria. This will be seen with those with Wilson Disease
Management; penicillamine is the treatment of choice for Wilson disease, once acute
treatmentis done--- trrientrene and zn can be done
IBS (diarrhea Predominant); this will have abdominal pain, changes in bowel habits; this will
have normal BC normal erythrocyte; and psychological support;
Management; loperamide
Emphysematous cholecystitis;
The crepitus in the abdominal wall and thickened gall bladder wall; most likely the cause for the
patients abdominal pain; the pain is in classically elderly men; manage with cholecystectomy as
delays are linked to gall bladder perforation
Portal HTN;
Overview; reported episode of bright red hematemesis, upper GI bled will focus on
resuscitation and stabilization, hemodynamically stable with AMS
managmenet; endotracheal intuation; will secure airway
Inherited Hyperbilirubinemia;
Dubin Johnson benign condition ----direct hyperbilirubinemia this is identified as an incidental
darkly pigmented black liver (mild and moderate jaundice)
Inherited Hyperbilirubiemia;
Inherited hepatic storage and reuptake of conjugated is underlying cause of RS; OAT1B/3
responsible for the inability of the liver to store conjungated BS (LFTs are characterized
normal)-----urinary bilirubin and urine corproporpyn
Hepatic Adenomas;
Overview; the patient is a young woman on OCPs, she has benign findings of periphera
enhancement, the first strep is stopping anabolic steroids and removing any hormones. Then
we will FU with the mass within a few months
Pancreatic pseudocyst; this is a technique used to drain if the cyst is > 6 cm or is symptomatic;
it is the first line treatment as CT pericutaneous drainage is the next appropriate step
Hypercalcemia;
Familal hypercalcuric hypercalcemia; FHH results from inactivating mutation---serum calcium
levels are normal with low excretion-
Acute Pancreatitis;
Summary; it will epigastric pain radiating to the back, vomiting, guarding, and reduced bowel
sounds, leukocytosis, and elevated lipase
- Management; IV fluids, will aggressive hydration with crystalloids, LR is the most
important measure with acute pancreatitis signs of hypovolemia, tachycardia and
elevated hematocrit and BUN/creatinine
Acute Pancreatitis Management;
- Management; PCA pump; there will have effective analgesic this will minomize risk of
underdosing, this will be monitored to prevent RDS
Pancreatic Cancer;
Even if ultrasonography does not show a pancreatic lesions (increased ALP, conjugated
hyperbilirubinemia), worsening epigastric pain, significant weight loss---increased 65 year old
patient.
Abdominal CT; contrast enhanced abdominal CT---there will elucidate its resectibility, it can
appear as an ill defined hypodense mass, this will be diagnosed with contrast enhanced
abdominal CT
Pancreatic Cancer;
THe patient most likely suffers from malignant biliary obstruction with elevated bile acids, pale
stools direct/conjungated bilirubinemia---there will also be elevated serum glucose levels.
Acute Pancreatitis;
A presentation of severe epigastric pain radiating to the back and elevated pancreatic enzymes,
amylase and lipase----abdominal distension, decreased bowel movement
Risk factors; alcohol and gallstones
Acute Pancreatitis;
Overview; damage to this retroperitoneal structure should be considered in patients preseting
delayed symptoms
Pancreatic ductal injury; this with blunt trauma, pancreas is compressed against the vertebral
bodies, common from the seatbelt, or handlebar injuries, motor vehicles or bicycle acccidents
Diarrhea;
Medication Abuse; hypermagesiumia caused by surreptitious use of magnesium containing
laxatives and melaosis coli, there will be sennna, rhubarb ad bisocodyl.
- This is more associated with bulimia
- Biopsy; showed pigment laden macrophages will have chronic colitis ,
NASH;
Summary; history of type II DM, ALT/AST < 1. Hepatocyte ballooning degeneration and
macrovascular steatosis.
- NASH is a common finding, intype II DM, will have raised risk for cirrhosis AST?ALT
(100.130) , progression to cirrhosis can be prevented with optimizing diabetes
treatment
Bacterial Gastroenteritis;
Clinical manifestation; inflammatory bloody diarrhea, with association with domesticated
animals
- There will be fever, generalized aches, pseduappendicits, and acute periumbilical pain in
the RLQ,
- Mode of transmission; fecal and oral/associated with undercookied meat and
unpasteurized milk
Giardia;
Hepatorenal Syndrome
This will present with ascites, jaundice, and labs that inhibit the fenal function,
Labs show LFTs, anemia prolonged PT and low platelet count thiat is suggestive of
decompensated liver cirrhosis
- Decompensated renal perfusion, will be hepatorenal syndrome, this will lead to renal
hypoperfusion, this will reduce GFR, it is prerenal FenA <1 and Br/cr > 20
Nephrotic syndrome; FSGS; this will present with typical features of nephrotic syndrome due to
FSGS; this will appear as segmental sclerosis underlight microscopy; associated with heroin use
obesity, SCD and HIV infection
AIN: New onset rash, fever and elevated Ck; this is consistent with AIN; there will be
cephalosporins, TMP-SMX, and cipro
Penicillin; this is most commonly used for gram positive cocci
Penicillin allergy will cause rash; anaphylaxis, hemolytic anemia and elevated CK; with WBC
casts and eosinophilia
IGA Nephropathy;
Renal glomerular damage will show dysmorphic RBC and RBC casts; notably IgA nephropathy;
this will deposit in the meangium; will cause hematuria; and mild proteinuria with recent 1
week pharyngitis;
Vasculitis;
The patient presents with nonspecific symptoms (fever, arthralgia, and weight loss/cutaneous
symptoms and cardiac abnormalities; chest pain, dyspnea and palpations; (proteinuria,
hematuria); there will be elevated ESR and leukocytosis.
Celiac Disease; This woman presents with diarrhea, abdominal bloating, signs angular
stomatitis, and positive iGA with TTG, she also has Turner syndrome associated with celiac
disease
Management; this will be managed with gluten free diet, this will
Esophageal perforation
Iatrogenic trauma, most common etiology of upper endoscopy as seen in this patient,
THe findings suggest pneumomediastinum. Gastrogaffin is preffered it is water soluble and less
irritating.
Hepatitis B;
Because HbAg is positive, this is going to limit to active chronic----
Envelope antigen indicates the patient has an active infection, there will be IgM antibodies
showing chronic Hep B infection
Achalaia;
Management; this will first be managed with endoscopy at the GE junction, this will be
pseudoacalasia.
Because the patient had smoking and weight loss, we need to suspect esophageal cancer
GI Bleeding;
Presenation; tarry stool, naproxen and hypotension are representative of GI bleed
EGC is preferred diagnostic method for upper GI bleeding, there is shock and active GI bleeding.
NASH; note for the obese individuals, there will be adipokines that are released, this leads to
post prandial hyperglycemia, the hyperinsulinemia will trigger lipid uptake and lipogenesis
within the hepatocytes, NASH will induce oxidative stress that leads to cirrhosis and HCC
Clostridium Difficle Infection;
Clinical presentation; there will be accordian trapping, of contrast material, thickened haustral
folds, this will be with pseudomembrane colitis.
This can adversely damage the endogenous flora, there will be release of exotoxins A and B, this
will damage the colonic epithelium leading to exotoxin mediated inflammation of the colon
Zenker Diverticulum;
This is an outpiuching of the hypopharynx, this is most common in middle aged and elderly
patients. This will be complicated with swallowed saliva, liquid and food entering the airway.
GERD; there will be risk of esophageal strictures, this is a common sequelae of GERD in which
gastric acid leads to inflammation and it can form strictures
Esophageal Perforation;
There will be chest pain, tachycardia, tachypnea, and crepitis that occurs due to endoscopy
Esophageal perforation, there will be associated with EGC with iatrogenic procedure, fever can
occur as a result of secondary infection
Esophageal Cancer;
Overview; increasing retrosternal pain, weight loss and anemia with 40 pack year smoking
history
Management; esophageogastrduodectomy will confirm suspected cancer. There will be
anemia, melana dysphagia
Next steps; biopsy, must assess lymph node involvement, this can determine adenocarcinoma
or SCC
Acute cholelithiasis;
Overview, there will be recurrent intermittment and post prandial RUQ pain with biliary colic,
this is due to cholelithiasis. This will be a risk as the patient just had an MI
- In uncomplicated disease, can do ursodeoxycholic acid and a low fat diet
- If no contraindications, laparoscopic cholycystectomy.
Gastroporesis;
Dietary manifestations; early dumping syndrome, this is the initial treatment of choice, there
will be large amounts of carbohydrate leading to fluid shifts and SNS activation, early treatment
leads to small and low carbohydrate meals.
- 1st line, lifestyle modification and second line, treat with octreotide
Crohn Disease;
There will be abdominal pain, nonbloody diarrhea, and perianal fistula with colonic ulceration;
this will show enteropathic arthritis and erythema nodosum; treatment depends on the activity
and severity of disease
Management; infliximab; and azathioprine for severe CD;
- This wil include fever, abdominal pain and weight loss;
Constipation;
Note the elderly woman presents with abdominal bloating secondary to partial intestinal
obstruction.
- Management, regular physical activity, there will be risk with advanced age, female sex,
dehydration, low fiber diet and absence of physical activity.
Management; PEG should be used.
Hemochromatosis;
Management; regular phlebotomy
Pathogenesis of hemochromatosis, iron overload and this will cause multiorgan involvement,
such as cardiomyopathy, arthritis, (symmetric, oligoarticular, and there is hepatomegaly,
hyperpigmentation and bronze diabetes). Manage with phlebotomy.
Clostridiodes Difficile;
Summary; this will have watery, foul smelling stools streaked with blood includes blood
leukocytosis as well as tenderness throughout the lower abdominal quadrents. EIA this will
have GDH this is the est for clostriodes, with c. diff toxin A and B
Choledocolithiasis
ERCP; post cholecystectomy syndrome, elevated cholestatic patterns that are due to residual
gallstones, an ECRP is the most common cause for biliary dysfunction and sphincterectomy is
indicated
Hepatic Adenoma;
There will be a 4 cm liver mass with central hypoattenuation, the ocal nodular hyperplasia is a
common benign tumor at age 20-50; follow up at between 5-6 months will be recommended.
Ambulatory;
Influenza, this is a live attenuated-inactivated vaccine that is recommended during the flu
season and during May-October in the Southern Hemisphere, this may not always be
antigenically identical.
PUD;
Nonbillous emesis following food intake, early satiety, weight loss, epigastric tenderness,
succession splash, GOO, stent placement, age, weight loss and alcohol use
- This is concerning for gastric cancer. Therefore upper endoscopy is a diagnostic choice
Overview; dyspepsia, severe epigastric pain relieved by by food but worsened can be caused by
an ulcer, this wll have succession splash, hypokalemia and hypochloremia. GOO is caused by
PUD
ENT
Elderly Diabetic patients, are at greatest risk for developing malignant otitis media and
malignant otitis externa, the association may not be fully understood but may related to the
strong association between the two conditions.
Menierre Disease
This will be vertigo with unilateral tinnitus, sensorineural hearing loss.
Management; will be with reduction of caffeine intake---this is is the initial nonparhmacological
treatment.
Uncomplicated AOE;
Uncomplicated AOE is managed with topical steroids such as hydrocortisone, betamethasone
and acetic acid, this is an antibiotic that is managed against AOE. The treatment includes aural
toilette to remove debris and NSAIDs for relief.
Intestinal Ischemia;
CT angiography; abdominal CT angiogram, this is a comfirmatory test for chronic mesenteric
ischemia, this will be stenosed with atherosclerosis. (there will be postprandial pain)/intestinal
angina.
CMI; there will be HTN, hypercholesterolemia and CAD
Hematology Oncology
AIHA; Direct Coombs Test; RBC membrane, negative---direct Coombs test,, hemoglobinopathy.
Sezary Syndrome; this will manifest with weight loss, fatigue, pancytopaeia; this will show end
stage mycosis fungoides; this is a variant of T cell lymphoma
- It will have > 10% of TBSA
- Management; ; total skin electron beam therapy
Transplantation Management; there will be fever, decreased urinary output with elevated
BUN/ this wil indicate acute allograft reaction
Biopsy confirmed acute cell reaction; with IV methylprednisone;
Oncologic Emergency;
Based on the characteristic history, there will risk of increased cell turnover; includes
potassium, phosphate, and urate nephropathy leading to AKI and death
Myeloproliferative Neoplasm;
there will be constitutional symptoms; fatigue, weight loss, night sweats; and a punctio sicca on
bone marrow aspiration; making myelofibrosis the most likely diagnosis
- Ruxolitinib; this is a Jak2 inhibitor with primary myelofibrosis;
Multiple Myeloma;
There will be renal failure, oligiuria, elevated BUN/CK; there will be fatigue bone pai,
constipation
There will be anemia, hypercalcemia;
IG Light chains; most common cause for myeloma cast nephropathy
Positive urine sulfosalicylic acid and SPEP
Acute Leukemia;
The bone marrow here shows multiple auer rods;
Myeloperoxidase; this is found in the peroxidase positive granules and it delineates it from ALL:
which myeloperoxidase negative; there will be fatigue, weakness and thrombocytopaenia
Mutation in JAK 2 kinnase; this will cause monoarticular elbow pain, tender erythema, and
hyperuricemia; this is connsistennt with acute gout; this will have normal BMI, exercise
regularly and moderate amounts of alcohol;
- Jak2; will have P vera, essential thrombocytosis and PMF. This will lead to increased uric
acid levels; with marked erythrocytosis (elevated Hb)
DIC In the setting of meningitis;
It will have neck pain, headache dizziness, nausea and vomiting; this will indicate meningitis;
this will be whe n the hip is flexed to 90 degrees
- It is a consumptive coagulopathy; associated with excessi fibrin formation, platelet
microthrombosis;
Factor 5 Leiden;
Association; this will be linked to PE, warfarin use, and clinical features of calf tenderness and
noncompressable popliteal vein.
- Mutation of coagulation cascade, doesn’t allow for activated protein c,
TTP: Thrombocytopaenic Purpura; this will have a congenital deficiency against ADAMTs13; this
will cleave WVF multifmers; FAT FN; will have decreased hb, elevated LDH, indirect
hyperbilirubinemia; pregnancy is a known risk factor
Leukemoid Reaction; this will have profound leukocytosis and increased neutrophils, immature
and mature precursoros and elevated LAP; there will be secondary to lung cancer
TTP; The patient has the classic constellation of symptoms, including neurological
abnormalities, stroke, confusion, fever and impaired renal function
- This will cause a deficiency of ADAMSTS12; this will accumulate on the endothelial cells,
platelet adhesion and thrombosis
- Management; plasma exchange
Fundamentals of Pharmacology;
Warfarin is a substrate of cytochrome p450 prevention of clots, with Afib, this bruising is
suggestive of elevated warfarin levels
- Omeprazole is a cytochrome p450, inhibitor this will increase warfarin amounts,
other relavent, sulfamethazole, and grapefruit juice,
AML:
The patient has cytoplasmic inclusions regarded as auer rods; these are pathonomonic for
disease
- They wil present with fatigue, petechiae and splenomegaly, especially M3; this will show
aueur rods
Multiple Myeloma;
Clinical presentation; there will be lethargy, confusion, and nausea due to hypercalcemia, there
will be recent episodes of pneumonia and UTIs
Pathogenesis; this will have lab abnormalities indicating MM, this is a plasma cell dyscrasia with
unctrolled proliferation of plasma cells. Clinical presentation, leukopenia, thrombocytopenia
and anemia
Multiple Myeloma;
MM is characterized by uncontrolled proliferation and diffuse infiltration of the bone marrow;
this will manifest as lytic and painful boe lesions as seen in this patiet; there will be elevated
Bence Jones Protein
- > 10% clonal plasma cells,
Mycosis Fungoides;
Diffuse erythema with intense prurits, generalized lymphadenopathy and blood smear will
show cerebroform nuclei, there will arise from another CTCL arise de novo---
Managements; topical corticosteroids, topical nitrogen mustards, eg. Phototherapy,
chemotherapy and monoclonal antibodies
Oral Anticoagulents;
Overview; the patient notes that taking warfarin for Afib and high dose acetaminophen
comntributed to the retroperitoneal hematoma
- Why? Acetaminophen, inhibits vitamin K dependant carboxylase. This will involve 2, 7. 9
10
Polycythemia Vera;
Clinical presentation; CT scan will show range of stroke. This will be associated with erythema,
blurry vision, and labs show elevated WBC counts
- Repeated phlebotomies will show P. Vera, this will have increased cell count
- Management; phlebotomy should be done until Hb is < 45
Polycythemia Vera;
Patient presents with fatigue, sweating pruritis and cyanotic lips with increased in
erthryocytosis, leukocytosis thrombocytosis, there will be low serum iron, ferratin andnormal
TIBC
Management; phlebotomy, this will show reduced cell counts and hyperviscosity. Manage
prophylaxis with aspirin with cytoreduction and IFN-A
Paranenteral Anticoagulation;
HIT Type II: this will be 5 days post surgery after obtaining unfractionated heparin, HIT II will
have necrotic skin lesions around the injection sites.
- Others will cause swelling and tenderness with + homen sign
Mnagemnt; switch unfractionated heparin with a direct thrombin inhibitor such a sbilvarudin
and agatroban .
CHemotheraputic Agents;
Vincristine adverse effects; this will be used in NHL it is limited by potential neurotoxicirty,
there will be decreased intestinal motility, and mixed symmetric and motor neuropathy
- Course; there will be improved with cessation of the drug,
Hemacrhromatosis;
The patient has an increased risk of cardiomyopathy, liver cirrhosis and HCC
Diagnosis; there will be fatigue, symmetric arthralgia this will affect MCP 2 and 3 along with
skin hyperpigmentation and DM, this will suggest hemochromatosis
- Note this will be delayed in premenopausal women due to menstruation. However, it
will show iron deposition in many organs
- Diagnosis; iron studies and genetic testing for C282Y and H63D
- Other damage sites, include puitary damage and can deposit in the gonads.
Management R-CHOP
Hodgkin Lymphoma
B symptoms; there is classic signs and symptoms (night sweats, fever, weigh loss),
Management; Adriamycin, bleomycin, vinblastine and dacarbazine; this will treat Hodgkin
lymphoma
Dermatology:
Biopsy of the lesions, this is the next best step in the management of leukoplakia. It can
predispose to SCC. This is important as we need to biopsy for dysplasia
Pyogenic Granuloma;
This is a benign vascular tumour that will have bleeding profusely post minor trauma; this will
develop at the sites of skin trauma of the face and hands;
Psoriasis;
Limited plaque psoriasis, this is treated with topical medications and moisturizers; calcipotriene
and corticosteroids, and retinoids---there will be intertrignous facial areas. There will be
functional impairment and psychosocial distress
Lichen Planus; this will be purple, polygonal, pruritic rash with wickham striae; this will be
associated with hepatitis c infection, penacilamine, ACE inhibitors and sulfonylureas
Cutaneous Squamous Cell Carcinoma;
Diagnosis; punch biopsy, lesion suspicious of skin cancer—biopsy with malignancy
- sCC will be managed with punch biopsy.
Bullous Impetigo
Overview; there will be direct immunoflouorescence that is the gold standard for diagnosis of
BP, there will be linear depositis of IgG and C3 along the basement membrane, IgG is directed
against the basement membrane, it will present in adults > 60 with tense bullae
Lichen Planus;
White atrophic papules on the glans and prepuce and the male associated with pruritis,
urethral meatus are indicative of lichen sclerosis
- biopsy of lichen sclerosis; increased risk of squamous cell. Potent topical steroids such as
clobestol
Dermatofibroma
Overview; this is a benign and asymptomatic skin lesion with a positive dimple sign, this has
squeezing and retraction post insect bites and trauma.
- This is asymptomatic and slow growing this will also show Fitzpatrick sign
- Management; observation
SCC;
The patients condition, most commonly manifests in the face and neck
SCC; this will be the most frequent malignancy with everted edges but it is friable and bleeds
easily.
- There will be risk of prolonged sun exposure with smoking and light skin
- Diagnosis; wedge biopsy should be performed to confirm the diagnosis
HSR Reaction;
This will have rash exasperated by occupational hazard
- Irritiant contact dermatitis, most common form of contact dermatitis. It can be
chemical, water detergents, or physicial (wood), this will cause xerosis, erythema,
scaling and fissuring.
- Management; avoidance of irritants, moisturizers to restore skin barrier and
symptomatic treatment with glucocorticoids.
SJS/TEN
Overview; there will be fever, mucositis skin tenderness, this will be immune mediated
cutaneous reaction
Other associated symptoms, fever mucositis and skin tenderness, TEN > 30%
Other features; mucositis, dysphagia, and photophobia all from the skin peeling that we see.
Hidradentis Suppurativa;
In an obese woman, painful lumps, intertriginous folds below the breast and armpit, there will
be malodorous and this will be suggestive of hidrandentis supperitiva
- Groin, this will be hormonal active apocrine glands and inframammary glands with
perianal, perineal skin and genital skin
Melasma;
Chloasma, is a benign disorder with irregular patchy hyperpigmentation seen in reproductive
age with exposure to sunlight
Management; avoid triggers or sunscreen. Hydroxychloroquine can be used in severe cases
Icthylosis Vulgaris;
Characterized by dry skin and a fish scale appearance, will be in the air, also groin, axilla---there
is also xerosisi risk
Management; skin products and retinoids
Neuroscience;
Postoperative anteromedial thigh/lower leg paresthesia.-----the patient has evidence of femoral
nerve injury. Anteromedial thigh with decreased strength in hip flexion/hip extension.
Polyneuropathy;
This is seen in alcohol use disorder or poorly controlled diabetes
Polyneuropathy; this is associated with tingling and distal sensory loss. THis is associated
Pathogenesis; diabetes, alcohol use disorder and GBS
Creutzfeldt Jacob Disease; CJD this is a neurodenegerative disease called prions, the normal
PrPc are found on the surface of cortical neurons, misfolded proteins PrPsc, this will have more
b-sheets,
Most patients die within 12 months of diagnosis
Labs will show increased 14-3-3 concentration, S100 protein, tau protein on CSF
ALS: there will be destruction of the UMN and LMN and this will affect the cranial, cervical and
thoracic and lyumosacral nerves, UMN will cause increased tone and spasticity, LMN causes
atrophy.
- There will be choking on secretions/dysphagia.
- Other standards of evaluation, include MRI and EMG
Subarachnoid Hemorrhage
Ruptured aneurysm; this is the most common cause for ontrumatic SAH; this will be corrected
with surgical clipping and endovascular coiling. CT angio will ID the aneurysm location, clipping
is done to attenuate rebleeding,
- Disclaimer; endovascular coiling has gained popularity, it is preferred over the age of 70
Subarachnoid Hemorrhage;
The patient presents with the signs of cerebral ischemia with new onset focal weakness post 5
days after SAH< pathology is going to be coronary vasopasm
ICH;
The patiet presents with acute onset of headache, weakness, hyperreflexia (poorly controlled
HTN is major risk factor)
Rupture; small penetrating artery; most likely ICH, penetrating artery in the subcortical region,
- Single ICH will cause lipohylaosis that can rupture these weakened vessels severe
headache, nausea, confusion and focal eurological deficits.
Cerebellar Syndrome;
Romburg test; the patient would most likely not be able sto stand with feet and eyes open.
Left sided cerebellar defect will cause gait ataxia, dysarthia, nystagmus, dysmetria and
didiadodyskinesia. It will manifest on the lesion side of the cerebellum
Multiple Sclerosis;
Clinical presentation, we have a patient who presents with acquired colour blindness, a
decrease in visual acuity this is corresponding with MS.
Optic neuritis, this will be caused MS in 35% of cases and is the harbringer , there is also acute
to subacute colour blindness, a reduction in visual acuity.
Right thalamic Stroke; will cause contralateral hemiparesis, there will also be miotic and
nonreactive pupils. This is called wrong way eyes.
Stroke;
Sudden onset of right arm numbness and weakness coupled with right facial droop will show
stroke in the left MCA,
Risk factor; HTN, this will be suggestive of stroke, it will be caused with large artery
arthrosclerosis.
Syringomyelia;
THis will occur months to years post whiplash injuy of the necl, there will be classical fndings of
of central cord syndrome. (vibration and position senses ae slectviely spared). As it progressies,
it will develop in the upper arm and the lower arm
Myasthenia Crisis
LEMS; overviewl weakness, in the lower extremitiy,
There will be autoantibodies against the presynaptic neurons.
The result, is that there will be increased ach release with added stimulation.
Assocation; underlying malingnany, therefore must do x-ray or CT scan
Patients with LEMS can develop autonomic dysfunction (diplopia, ptosis and dysphagia, CXR
and CT scan should also be undertaken
LEMS;
Weakness of the lower legs, improves with
Intracerebral Hemorrhage;
Arterial HTN is the most important feature for ICH, there will be leading to microaneurysm, this
leads to acute rupture.
Path; HTN
Management; for ICH, must lower BP, but we have to do so gently
If too high, must do craniotomy.
Parkinsons Disease
Overview; there is progressive degeneration of DA neurons, this is particularly of the substantia
nigra pars compacta.
- DA deficiency of the straum will modulate activity.
- There is bradykinesia, resting tremor and postural instability
- PD with non-ergot includes MAOB, pramiprexole ropinrole. =
Rheumatology;
Granulomatosis with polyangiitis;
Overview; nephritic syndrome with elevated creatinne and blood urea nitrogen, there will be
kidney and lung involvement, will show chronic sinusitis saddle nose deformity and necrotic
skin lesions
- This will target small and medium vessels, there will be necrotizing granulomas
- Management; includes immunosuppression, such as cyclophosphamide and rituxmab
Neck Soreness; this will be managed with a supervised trial without the color; this is
approprirate
Rheumatoid Arthritis; There will be a mass at the popliteal fossa; this will be characteristic of a
Bakers Cyst;
RA; this inflammation of the synovium; leading to Bakers cyst; with low grade fever/fatigue
Paget Disase of the Bone ? 55; years of age; deformed tibia (saber shin and osteolytic lesions
and elevated ALP); this will have bowing of lone bones with impaired hearing loss; (conductive)
Vasculitides;
The patient presents with cough, bloody sputum and a UA and a palpable purpura on
examination and skin biopsy, in the absence of granuloma formation---
MPO; 90%, fatigue, myalgia, weight loss, (skin or kidney)
Temporal Arteritis; this will manifest as a unilateral pain while chewing; it is key to implement
glucocorticoid therapy as soon as possible; temporal arteritis
- This is associated with PMR: this will show tenderness in the neck and torso
Dwarfism; there will be short stature and family history of inherited disorder; includes
macrocephaly; frontal bossing and midface retrusion; this is an AD disease
Pathogenesis; there will be chondrocytes in cartilage; there will be FGFR3 dysfunction and the
bones can no longer lengthen
Osteoarthritis;
THis is joint pain associated with movemet and stiffness > 30 minutes and crepitus suggesting
OA
Joint space narroiwing; chronic trauma; will decrease proteoglycans cause loss of elasticity and
inflammation of cartilage
Mixed Cryoglobulinemia;
This is associated with Hep C infection; there will be triggered compliment this will have
compliment activation and inflammation of blood vessels due to cryoglobulinemic vasculitis
- Another important cause for mixed cryoglobulemia; this will be AI disease and SLE;
Inflammatory Myopathies
Anti-Jo1, this is specific to polymyositis and dermatomysotis; there will be also anti-mi2 in DM
and PM
Septic Arthritis;
Clinical presentation, permanent joint destruction is a dreaded complication
Hematogenous spread of infection will cause septic arthritis, this will manifest as fever, jont
pain and restricted range of motion. This will cause hematogenous spread of bacteria most
commonly via staphylococcus.
Features; there will be synovial WBC over 50000 and dominance of PMNS
Septic Arthritis;
Patient presents with fever, joint pain, and restricted range of motion
Risk factors; poorly controlled DM and history of right total knee replacement
Labs; will show WBC > 50000, low glucose levels, and s. aureus
Parvovirus B19n Arthrovirus
Clinical picture; recent history of flue, acute bilateral upper extremity and exposure to children
- Parvirus will affect adult with mild febrile illness
---this can effect adults wit mild febrile nillness and severe polyarthritis in the fingers, hands
knees and ankles
Management NSAIDs and analgesics;
Rheumatoid Arthritis
There will also be joint space narrowing, with chronic RA and additional septic arthritis,
disseminated gonococcal infection, and gram negative diplococci.
- There will be joint space narrowing, erosions of the cartilage and bone and
demineralization.
Rheumatoid Arthritis; the patient has all of the classical RA signs, including positive ESR and
positive rheumatoid factor
- Xray of cervical spine is recommended for diagnosis and will cause atlantoaxial and
subaxial subluxation
Ankylosing Spondylitis;
C2 vertebral fracture, will have history of back pain of inflammation, this will range with
morning stiffness and worsen with rest. There is risk for osteoporosis and pathological fracture
Associated with extraarticular findings such as anterior uveitis there will be eye redness and
pain.
IBD and aortic insufficnecy, AV block are other findings
Reactive Arthritis;
Arthritis, urethritis and conjunctivitis
Reactive arthritis, this is caused by infection of chalmydia, shigella and campylobacter jejuni
- This will be linked to an HLA B27 genitype,
- Must also screen for HIV too
Paget Disease of Bone; this will show elevated ALP and normal calcium, phosphate and PTH;
this is a marker of bone formation (osteoblatic activity); there is raised bone turnover; bone
resorption, PTH levels are normal
- Note that increased bone turnover will cause normal lamellar bone formation; it is
deformed and highly susceptible to fractures
Hypercalcemia
Bisphosphanates; this includes zolendronic acid, it will reduce osteoclast mediated bone
respoption, this is linked to malignancy linked hypercalcemia and breast cancer
- The patient will show moderate hypercalcemia 12-14,
- Long term therapy is recommended for avoidance of hypercalcemia sequelae
Osteomalacia;
- the patient’s x-ray has pseudofracture has pseudofractures (low calcium, low phosphate
and elevated PTH, the patients medications predisposed her to osteomalacia
Vitamin d; this is a underlying cause of phenytoin, a cytochrome p450 and metabolites, there
will be hypocalcemia with stimulate PTH
1. PTH activates osteoclasts
2. PTH will simulate calcium resorption, in distal tubule and decrease phosphate resorption
in the proximal tubule
Sarcoidosis
CXR; there will be raticular opacities and hllar adenopathy, this will be a common finding
- Most common symptoms are going to be pulmonary symptoms, this includes SOB and a
non-productive/dry cough. There is also iridocyclitis, and arthralgia in the ankles
Sarcoidosis;
Clinical presentation, we have a patient with 6 months of cough, tere will be local immune
hyperactivity, with granulomas. There will be local hyperactivity, the lungs and the lymphatic
system are the most involved, there is increased in macrophages that hydroxylates 25
hydroxyvitamin D to increase calcium resorption
Lung Cancer;
Follow up after being involved in an automobile accident
As the solitary lung nodule is < 3 cm or equal in size; there is a 40% chance of malingnancy;
The lesion is located in the upper lobe; surgical management is the next best option for
management
Treatment; surgical excision is the gold standard
Reactive arthritis
Clinical presentation, there is back pain, stiffness in the hips/knees and pain on urination., there
will be spondyloarthropahy with ankylosing spondylitis and inflammatory back pain, there can
keratoderma blenorrhagicum
ALS;
Overview; medications used ALS are rilouzole and edavarine
ALS; this is a disease presents age 50-70, there is worsening features of UMN and LMN signs.
While dysphagia is a late feature, it indicates a poor prognosis
Enterovirus Mediated Meningitis;
Presentation, headache, fever and photophobia along with positive Brudzisnki sign, and this will
have a lymphocyte predominance, slightly raised protein, this can indicate aseptic meningitis
- This will have peak incidence in summer and early fall, this can also cause carditis,
herpangina, HFMD,
Crytococcal Meningitis;
Clinical presentation; fever, headache, AMS with oral candidiasis with positive HIV
This will be associated with crytococcus neoformans;
Management; this will be done with IV amphotericin B and oral flucytosine; this will be then
followed with oral fluconazole
Meningioma; Besides bilateral schwannomas, NF2 will manifest with cerebral and spinal
tumors, the patient may be asymptomatic, however they will have generalize symptoms such
as tumors, there will be cerebral and spinal tumors along with meningiomas.
- Clinical features; of schwannoma, there will be compression of vestibulocochlear nerve
(VIII) there will be sensorineural eharing loss, tinnitus, dizziness, unsteady gait and
disequilibrium
Type I HSR; the localized urticaria is consistent with a mild/moderate type I HSR allergy to latex;
this is caused by preferomed antibodies from prior sensitization ; leads to rapidly releasing
histamine
Managemet first generation histamies (diphenhydramine, chlorphenramine and hydroxyzine)
-
Meningitis;
Patient presents with acute headache, fever, photophobia, neck stiffness
CT scan before LP is indicated because of signs of increased ICP, neuroimaging before LP should
be before to reduce risk for herniation (FAILS< focal neurologic eficit , AMS,
immunocompromised/increased ICP, new onset seizures
Dengue Fever;
Mosquito repellent is an effective for preventing bites aedes aegypto. This will have exanthem
and lymphadenopathy.
Pulmonology;
Lung Cancer; glandular tumor cells; mucin producing tumor cells, this is a characteristic of
adenocarcinoma other causes (bronchiectasis, pneumonia and chronc inflammatory response).
This will lead to persistant DNA damage.
Chronic PE
There will be pedel edema, JVD, and catheterization (Increased MAP) without left heart failure
CTEPH; single/recurrent episodes of PH; there will be malignancy,r ecent surgery (VQ scan can
elucidate CTEPH from PAH
Lung Cancer
Evaluation of an incidetial solitary lesion will be
1. Large nodule size
2. Location in upper lung fields
3. Irregular, spiculated and scalloped borders
Risk factors; malignancy, history of smoking, asbests, and positive family/personal history of
malignancy
Samters Triad
1. Rhinosinusitis
2. Nasal polyposis
3. NSAID HSR and asthma
Pseudoallergic reaction; resembles type I HSR with decreased breath sounds, cutaneous
flushing post administration of asthma medication. AERD is caused by COX inhibition. This will
inhibit conversion to leukotrienes
Asthma; the patient has a severe asthma exasperation, with AMS, and accessoru muscles. This
with rising pCO2 > 42 mmHg, those are linked to worsening airway obstruction and increasing
respiratory fatigue.
The wheezing is not heard as there is not enough air moving out.
Theophyline Toxicity; Overview; the patient presents to the ED with dyspnea headache and
vomiting; this will indicate obvious distress; and drug drug toxicity;
Mechanism of theophylline; it is used to treat asthma; it will act through CAMP and cause
nausea, vomiting, headache, anxiety and diarrhea
Sarcoidosis;
Management; X-ray of the chest, erythema nodusum is thought to be a delayed HSR, there will
be circulating immune complexes, there will be cutaneous manifestation of underlying disease.
– CBC and ASO
Sarcoidosis; this will manifest as SOB, weight loss and symptoms of hypercalcemia; this will be
lined to stones, groans, bonnes and psychiatric overtones
- Sarcoidosis; this is a granulomatosis disease affecting numerous organ systems and the
skin; it will be linked to over production of 1,25 hydroxvitamin D by granulomas.
Diagnosis is confirmed by histology
COPD;
x-ray will show hyperinfilated lungs; there will be decreased FEV1 In obstructive diseases such
as asthma and COPD; this will have decreased FEV1, severity increases
COPD; this will present with dyspnea, productive cough and weight loss; risk factors include
smoking multiple cigarettes a day; this will have decreased FEV1/FVC; spirometry is a gold
standard for COPD diagnosis
COPD: this will present with progressive dyspnea and cough post significant signs of smoking
history
Supplimenntal 02; indicated in COPD; with hypoxemia; Sp02 <88%;
Best treatment s to reduce mortality; Supplimental 02 and smoking cessation
Diabetes Insipidus;
There will be hypercalcemia and elevated PTH;’
The history of polydipsia and polyuria in combinated with increased urine osm and water
deprivation suggestive of response to desmopression
Management; lithium and demeclocycline
Diabetic Ketoacidosis
ABG; reveals increased anion gap acidosis; this will show decreased HCO and decreased PCO2;
the ABG and ketonuria will reveal DKA
Extracellular potassium shift; will trigger shift to the extracellular compartment; K+, requires
insulin; cannot easil shift back into the intracellular compartment
Tubulointerstital disease;
This will have crystal precipitatin; this is secondary to IV bolus injections; ; will reveal hematuria
pyuria, and crystal; and administration of acyclovir in preventing crystal induced AKI
Hypocalcemia;
An elevated urinary protein; this will be a sign of lupus nephritis, this is a commo n
complication, it can manifest with neohrotic syndrome, lupus nephritis can manifest with
nephrotic syndrome will cause HTN, hypoalbuminemia, and peripheral edema, free ioized
calcium typically stays normal. It will have no signs of hypocalcemia, this is called
pseudohypocalcemia
Primary Polydipsia;
The patient presents with history of excessive thirst---polyyrua, hyponatremia, all of which
findings with polygenic polydipsia, the water deprivation allows for it to be differentiated from
diabetes insipidus. Normal values of serum, urine osm, water deprivation test
- In patients with primary polydipsia, an excess in free intake, causes a compensatory
reduction in the secretion of ADH, excretes excess fluid
Acute Interstitial Nephritis; the patient shows rash, fever, skin rash and peripheral eosinophilia;
Pathogenesis; Penicillins, cephalosporins, sulfonamides, and quinolones
- This will show WBC casts, pyuria, varying degrees of proteinuria and eosinophils
-
Methanol Intoxication
Overview; this will show decreased arousal, abdominal pain, and visual chages with metabolic
acidosis and elevated anion gap (NA- Cl-HCO3); fompiezole is the most appropriate for acute
treatment for methanol intoxication; this will be competitively inhibiting
Diuretics;
Patient presents with +Rinne test and lack of lateralization on the Weber test, this will be
caused by the diuretic she receives, the patient was treated with IV furosemide for
decompensated HF by inhibiting the ascending limb
- There will be sensorineural hearing loss via the cochlear stria vasicularis
Tubulointerstitial Nephritis;
Labs show kidney dysfunction, fatigue, anemia, uremia, elevated Cr with pyuria negative
cultures and CKD. Long term use of naproxen
- This will enhance RBF by dilating the capillaries, but by inhibiting NSAIDS we will cause
renal papillary necrosis. THis can lead to analgesic nephropathy
NSAIDs and CKD, will cause CKD with aspirin and caffeine
Renal Replacement Therapy; CVD, this will cause the leading cause of death in patients
undergoing dialysis. This will cause mortality rate in 20 fold.
- MI will have higher mortality rate
- CVD, would be the most common cause of death for patients undergoing a kidney
transplant
Nephrotic Syndrome;
Recall, hepatitis B, there is an increased risk of membranous nephropathy, this leads to the
HBV associated nephritic syndrome, recall loss of ATIII, there will be arterial thrombosis, renal
venin thrombosis can manifest in pulmonary embolis, there is also acute complete vein
thrombosis
Hyponatremia;
This will offer massive hemorrhage that is dilutional, physiological ADH will be secreted by the
pituitary and lead to hyponatremia, there will rapidly correct with serum sodium levels.
However, if we correct rapidly, this can cause central pontine myelinolysis
Nephrolithiasis
THe morbidly obese patient with colicky flan pain, vomiting will cause urethroliasis.
- Ureteroscopic with stone removal is first line for patients. It is ffecaious in even obese
patients.
- After removal we have to assess the composition of the stone so specific guidance can
be provided.
Renal Failure; this will be prerenal as there is reduced oral intake of food and liquids; this will
also show fatigue, malaise and orthostatisis, Fe<1% is this will refect prerenal failure;
hypovolemia;
Patients with anemia; mid systolic murmur, there will be increased blood flow across aortic
valve
EPO therapy; The patient presents with ESRD, it can be managed with EPO stimulating agent,
this is used to treat anemia. There is increased RAAS and decreased NO production
- She may require antihypertensive therapy
Pyelonephritis;
Overview; there will be CVA tenderness, patients UA, and diabetic
Management; there will be inpatient treatment with IV ciprofloxacin, note that those with
pyelonephritis have raised risk for sepsis, therefore we have to manage with floroquinolones
Patient can be switched to orla medications once culture negative
Nephrolithiasis;
Diagnosis; NCCT of the abdomen and pelvis is the gold standard for most adult patients, the
sensitivity is 95%. This can ID calculus location, size and density,
Nephrolithiasis;
Envelope shaped crystals are seen, there will be malabsorption of the fatty acids due to bile
acids this includes short bowel syndrome
- Risk factors; intestinal lumen, undigested fatty acids chelate calcium,
Diabetic Nephropathy
Clinical picture; undiagnosed diabetes type 2 will show diminished two finger point
discrimination, this will show an elevated HbA1c, there will be also elevated creatinine that is
consistent with diabetic nephropathy
- Morphology on kidney; will show nodular glomerularsclerosis; this will be managed with
ACE inhibitors
- Management; lifestyle changes, medical nutrition therapy and insulin
Diabetes Arthropathy;
Overview; there will be history of insulin dependant diabetes and peripheral neuropathy, there
is risk of charcot foot.
- Rocker bottom.
Diabetic Nephropathy;
Clinical presentation, there will be painless ulcers located along the pressure point, decreased
sensation.
In the untreated patient, there will be elevatd blood glucose that can lead to progressive
sensorimotor neuropathies and peripheral nerves. This will explain why diabetic foot ulcers are
painless.
- There will be regular screening for neuropathy
- There will testing with tuning fork and we can assess for pain with pinprick test.
SIADH;
There will be dilutional hyponatremia decreased serum osm and inapproropiatly concentrated
urine. This is due to unrestricted ADH secretion
Medication adverse effect; SIADH, for PAN, if left untreated will cause hyponatremia, vomiting,
weakness and severe cases, AMS< and disorientation
Opthamology
Orbital Cellulitis: this is a disorder caused by rhinosinusitis
Clinical presentation, nasal congestion, headache, tenderness, and right nasal discharge
Most alarming feature; pain with eye movement, fever, edema, erythema and tenderness.
Management; with oral antibiotics (antibiotics, vancomycin, ceftriaxone, cefotaxime,
augmentin, pip-tazo
Carotid Artery Stenosis; Stenosis of the ICA, will cause retinal ischemia whih will cause
microemboli, diagnosis with carotid duplex US
Risk factors; HTN, hyperlipidemia, DM and smoking
Management CEA;
Infectious Diseases
Multivesicular Herpes zoster; this will show immuncompromised patient, this will treat herpes
simplex or varicella zoster. There are more likely to involve multiple dermatomes.
PCP pneumoniae;
The patient is immunocompromised;
Management of PCP; TMP/SMX
Glucocorticoids; if administered will promote mortality
Schistosomiasis;
Patients urinary microscopy revealed parasitic eggs with terminal haematobium; this is endemic
to Africa and the middle east; this will be treatmed with praziquanntal.
- If left untreatrd genitourinary schistomasis can cause hydronephrosis
Helminth infection;
THe patient went on hunting trip recently; there is now fever, myalgia and periorbital edema,
splinter hemorrhages and elevated CK; this all suggests infection with trichonella spirilli
- This will cause trichenllosis; acquired via ingestion of spres, such as bears that contain
encysted larvae; they will eventually develop to adult worms
- Management; mebendazole and albendozole; associated with arrhythmias, encephalitis
and respiratory failure
Conjunctivitis; the most common organism is streptococcal pneumonia, and Hib; this will be
most commonly caused by staphycoccus aureus; making it the empiric antibiotic of choice
Chagas Disease;
Overview; the patient presents with left ventricular dilated cardiomyopathy, global hypokinesis
with dilated cardiomyopathy with CHF, progressive exertional dyspnea, JVD S3 gallop
- This will also cause fever, fatigue, lymphadenopathy and chagoma
Aspirgillosis; Itraconziole; for several weeks to months, this is the first line for allergic
bronchoscopic asthma. ABPA, there will be with CF this is seen
- ESR, eosinophilia and very hgh concentrations of serum IgE
- Confirm with skin antigen testing and measurement of the aspergillus specific IgE
Epididymitis;
Overview; this sexually active young man has dysuria, there is increased blood flow
Chlamydia trachomatis in sexually active post pubertal man < 35, this will be cased by
chlamydia and n.gonorrhea
Manage with ceftriaxone and doxycycline
Mycoplasma Pneumonia;
This is the cause for mycoplasma pneumonia, an atypical pathogen causing CAP; there will be
extrapulmonary symptoms such as pharyngitis
Diagnosis; PCR is the best test for M. pneumoniae
Chlamydia; this will have L1, L2 and L3 serotypes; this is STI lymphogranuloma venereum; this
will be seen with MSH; this includes fever, malaise, chills and myalgia; this will lead to chronic
genital lymphedema
Meningitis;
CSF; subacute low grade fevers, headaches in combination, T lymphocytes---count AIDS illness,
Cryptococcus pneumonia; AIDS caused by Cryptococcus---mass lesions, confirm this as well.
This is specific and sensitive (3-7) days to result.
TB meningitis;
This will present with a two week history of low grade fever, headache; this wil cause subacute
meningitis with increased CT scan and ADA
- Latent TB; will cause moderately elevated opening pressure cell count and reduced
glucose concentration
Nosocomial infections;
overview; fever, hemodynamically instability, and purulent discharge is associated with CRSBI,
Management; combination related therapy, vancomycin, cefipime and capseofungin, this will
be associated with CRBIS---femoral is also at risk of pseudmonas
Malaria;
Clinical preentatio, high-grade fever, decreased Hb, jaundice, hemolytic anemia, ring shaped
inclusion body with erythrocytes,;
- P. Falciparum; causative organism; this is the most dangerous type of malaria, there will
be irregular spikes with high fever, there can be hemoglobinuria, heart failure and coma.
- Managemet; atovaquone/progranul
Chikungunya Virus;
Acute feer, malaise, myalgia, symmetric maculopapular rash in comination with leukopenia and
thrombocytopaenia---most commonly caused by aedes aegypti and albopictus.
Diagnosis; RT-PCR
Managementl supportive—
IVDU and low CD4 count, indicative HIV---the ring enhancing lesion are most like Toxoplasma
Management; cerebral oxoplasmosi, pyrathine and sulfadiazine inhibit folic acid---this is a
common AIDS defining condition, CD4+ < 100,
Bladder Outlet Obstruction and Sepsis; this is the most likely explanation given the patients
BPH, this can occur spontaneously or post operatively, there will be lower abdominal pain and
palpable lower abdominal mass
- This will raise risk for UTIs via urosepsis
- Mamagement; foley catheter or suprapubic catheter.
Management of chalmydia
Treatment will be with a one week course of doxycycline,
Note that the common adverse effects of doxycycline will be exposure to UV light and will lead
to damage in the bones ad the teeth through complex formation impairing growth and causing
tooth discolouration
CAP:
Fever, dyspnea, cough and CXR will be at risk of pneomnia---
Gram positive diplococci—gram staining pneumonia,
CAP:
Productive > 48 admission, gram negative bacilli (pseudomonas), and staphylococcus
- Should be started post blood cultures.
- Control potential infection focus remove lines and drains, debridement
Bacilliary Angiomatosis;
HIV positive patients present with constitutional symptoms and bacteria is detected via
warthrin starry stain, this is the most likely diagnosis, bacillary angiomatosis is caused by
bartonella and can manifest with GI lesions
Management; erythromycin, this is the firs line treatment, patients should take it for 3 months
titier < 1:64
Sinusitis;
Acute viral rhinosinusitis; this will present with watery nasal discharge, fveer, headache, and
facial pain-this will lead to superinfection, mucopurulent discharge and will present with
bacterial rhinosinusitis caused by streptococcus pneumonia or hib
Managememtn amoxicillin clauvulnic acid; this will be combined with b-lactamase
CMV influenza
IV Gancyclovir; renally dosed for severe and life threatening CMV with fever, cough, dyspnea
and diffuse pulmonary intestinal infilitrates, this will include +Pp65
- If ganciclovir resistant, use foscarnet
Amphotericin B;
Risk factors; include pneumonia, splenomegaly with histoplasma (Mississipi River valley), this
will be pathogenesis by binding ergosterol and it will dusrpt the fungal cell membrane.
Advese effects hypomagnesemia; this will bind to the fungal cell membrane, this will effect the
renal tubular cells.
This will lead to increased masnesium excretion
Complication; will cause type I RTA
Asplenia;
Review; asplenic patients have a lifelong risk of fulminant life threatening conditions such as
with encapsulated bacteria. Note tha vaccination immediately does not promote ideal response
- 13 valent, meningococcal, and Hib, will be 8 weeks post administration of PCV13 after
surgery.
- Elective splenectomy, 14 days prior to surgery
Molluscum Contagiosum;
There will be pearly and painless growths with a dimpled center;
Large DNA virus, includes molluscum, this wil affect children and they will be managed with
chemotherapy or extensive glucocorticoid therapy
Botulism;
Botulism is caused by botulinum toxin, this will irreversibly inhibit Ach release from the motor
endplate, this will include CN nerve abnormalities such as paralysis and mydriasis. There will
also be difficulty swallowing and breathing.
Mollucum Contagiosum;
Disseminated molluscum contagiosum, this will raise concerns for underlying
immunocompromised states;
Management; disseminated cryotherapy/surgery, curettage, and IFN-a
Shingles Reactivation;
There will be multiple vesicles with crusting lesions and severe burning pain that will
correspond to the dermatome, this is typical of the shingles infection
- Viral reactivation in the DRG leads to HSV infection---there will be 1-3 dermatomes with
intense pain.
Shingles;
The photograph inpatient, will show acyclovir with antiviral medication---this is at higher risk for
eveloping zoster,note that this can evolve and become disseminated.
Demeclocycline;
This can cause an acute exaggerated skin reaction; note this will have an adverse effect profile
similar to other tetracyclines. UV light will interact with the metabolites and will cause damage
to the surrounding sun exposed skin.
Helminth Infection
Cystircerosis; this is endemic to south Africa and Central America, this will be transmitted from
taneia solium from human fecees. The stool will conglomerate in the muscles leading to
myalgia, there is also ocular cysts leading to ophthalmologic examination abnormalities.
Helminth Infection
Overview cutaneous larvae migrans this is a common travel associated infection contracted
with walking barefoot; this will follow migratory path humans are an accidental host
- This will cause initial small red papule with burrowing through the epidermis and the
bug will secrete hyaluronidase and protease but no collagenase is going to prevent
mgration
Transplantation
Prophylaxis for transplant, will include for AIDS
TMP/SMX for PCP
Valgancyclovir for CMV
TB management;
Administration of isoniazid for 2 months with rifampin, pyrazinamide and ethambutol followed
by rifampin for and isonadiz for two months, this will optimize response and minimize
resistence
- Caution; should monitor against hepatotoxicity, optic neuritis
Must administer pyridoxine, this will be an essential neurotransmitter, along with heme
While B6 deficiency is rare, it is associated with INH treatment. To prevent this, utilize B6
Isonaizid, this will also cause hepatotoxicity, must assess for elevated liver enzymes, nausea,
vomiting and abdominal pain----there will be continued.
Management; metronidazole, this will cause infection with anerobic bacteria, this is the first
line for amebiasis and extraintetstinal complication,
Tosilitis;
Summary; the patient has acute onset sore throat, dry cough, headache and erythema and
tonsils and pharynx (without tonsillar exudates); complication---
HSV Keratitis;
THis will present with a dendritic corneal ulcer; this will cause unilateral eye pain, watery
discharge, and will manifest with primary ocular infection.
Management; trifluridine and ganciclovir
HSV Encephalitis
Overview the patient presents with 5 days of fever and headache followed by AMS< and focal
neurologic defects---thhis is suggested of HSV encephalitis
Management; this will be managed with acyclovir
Clinical course; prodromal phase followed by subacute encephalopathy will show seizures, AMS
and behavioural change
Lyme Carditis;
Mobitz type 1 wenkeback, this will have progressively longer PR intervals,
Epidemiology; NE
Management; lyme carditis is managed with third generation cephalopsporine
Diagnosis; must do serology before testing
HIV Encephalopathy;
CD4+ less than 200, this indicates that the patient has AIDS, there wll be a neurologic causing
AIDS defining illness, this can be disseminated throughout the white matter
PML; this will cause a progressive decline in cognitive function, there will also be behavioural
changes, AMS, and there will also be PML
Tuberculosis
Clinical presentation, young man who immigrated to the US and has a + skin test
Management; following PPD< there will be high risk especially in Nepal where Tb is endemic,
there will be other symptoms such as sweats and hemoptysis.
Latent TB;
Definition, no TB symptoms or TB findings on CXR
We will manage with isoniazid for 9 months
Suppliment with B6 to prevent peripheral neuropathy
TB;
Can diagnose with a diagnostic throacocentesis, pleural LDH to serum LDH > 0.6 and protein to
serum >0.5 and this will be 2/3 of upper limit for LDH, there will be an exudate, this is due to
increased vascular permabiltiy as opposed to decreased oncotic pressure
TB: there will be generalized pitting edema, JVD< paradoxical increase in JVD with inspiration:
Kussmaul sign and pericardial calcifications; TB)
Overview; this is caused by mycobacterium TB; this will be immigrated from Indonesia; with
SOB, low grade fever, patchy infiltrations in the right lung; TB may affect any organ including
the heart, it is also a common cause for pericarditis in developing nations
Pericarditis; NSAIDs; ibuprofen and colchie this will be associated with acute pericarditis;
The NSAIDS will improve respiratory symptoms and will correlate with a history of Uri
Patients should restrict activity until infection has resolved and CRP has normalized
Brain Abscess;
Overview; Risk factors recurrent
Overview; there will be aspiration and brain abcscess ? 2.5 cm, there will be management with
stereotactic aspiration. Drain and manage with 4th generation cephalosporine and
metronidozle
HIV encephalopathy;
Asociated with candidial esophagitis; this is an AIDS defining condition, with neurologic
detoriation, in recent months, this can occur with CD4+ count less than < 200
HIV encephalopathy, this is an AIDS defining illness, CD4+ <100, there will be associated with
ataxia, didiadodyskinesia, and esophagitis, begin with antiretroviral therapy.
HSV; Viral culture can confirm HSV infection, vesicular lesionsa re present, other tests that
confirm include serum antibody test. Tzank smear is nonspecific
Pneumonia;
Fever, productive cough, pleuritic chest pain and crackles, this will present 3-5 days post
surgery. This will be associated with upper abdominal surgery
Incentive Spirometry;
This is an effective method for maintaining and improving function post surgery. Patients are at
increased risk for pneumonia, tere will be increased risk due to pain, intubation related change,
impaired surfactant production
Osteomyelitis;
Vertebral osteomyelitis; this will include worsening back pain at night this is associated with
osteomyelitis, risk factors; include DM, SCD, recent corticosteroid use.
Pathogenesis; this disease will seed, most likely from the thrombophlebitis. Infectious agent
staphylococcus aureus.
Hepatitis A;
Overview; the combination of symptoms in the stomach, scleral icterus, dark urine and dark
stool is associated with fever, hyperbilirubinemia and rapid transaminases, this makes acute
hepatitis the most likely diagnosis
Hepatitis A Vaccination
Note that Hep A is distributed around SA, Africa, Asia
Treponemal Test;
This will include the fluorescent treponemal antibody (FTA-Abs), the treponema, this will show
positive romburg test (there will be tabes, Argyll Robertson pupil, there is association with
consequent heart failure.
Nephogenic DI; HCTZ, in a low salt diet, low protein diet, it will be with nephrogenic DI, leading
increased sodium and water resorption in the tubules.
Subacute Thyroiditis;
Pathogenesis; there will granulomatous inflammation of the thyroid gland and granulomatous
substype of thyroitidtis (women 30-50 with vital UTI, tachycardia, widened pulse pressure and
resting tremor
Hyperparathyroidism;
Overview; there will be fatigue, weakness hyporeflexia and hypercalcemia; this is due to
hyperPTHism;
- Note this can cause a bone disease called osteitis fibrosa cystica; with excessive
osteoclastic bone resorption
Endocrinology;
THis will be associated with HTN, severe acne, obesity, and purple striae; this is consistent with
cushing syndrome; due to exogenous corticosteroid administration;
We will elevated cortisol and this is even though adrenal cortisol secretion is absent low
Kallmann Syndrome;
This will be a congenital GNRH deficiency; this wll be due to failed migration of the GnRH
neurons; this will also show decreased FSH and LH levels, anosmia, colour blindness, nerve
deafness and rena disorders
Pheochromocytoma;
This is a period of sustained elevated BP; causing hyperadrenergic spells with diaphoresis,
headache, tremor and pallor;
Management; fractioned catecholamine and metanephrine leves
Thyroid Cancer;
Total thyroidectomy is an effective treatment for most patients, note that thyroid cancer more
common in women than in men, and orior radiation is a common established risk factor---will
have partial resection hemithyroidectomy.
Hypoglycemia;
Clinical presentation; patient has a history of type II DM, with recent dietary changes and
nausea, diaphoresis, palpatations, seizures, will suggest hypoglycemia; the fingerstick glucose <
30
Management; IV dextrose, will show suspected hypoglycemia, management is to administer IV
glucose.
Thyroid Nodules;
Patient presents with hyperthoudism decondary to a toxic adenoma, this is a GOD secondary to
TSH stimulation, without negative feedback will transform into a toxic adenoma.
Glucagonoma;
There will be necrolytic micratory erythe,a. normocytic normochromic anemia with elevated
glucose levels which are characteristic features of a glucagonoma, the diagnosis wil be with
elevated glucagon levels. US will show a mass in the onacras
- Prevention, octeotride, this will reduce the secretion of glucagon to stop hyperglycemia,
diarrhea, necrolytic migratory erythema
Carcinoid Syndrome
There is secretory diarrhea, episodic flushing, wheezing and this means the patient is most
likely undergoing carcinoid syndrome. This will metastisize the liver and lead to carcinoid
symptoms such as flushing.
Risk factors; eating, drinking, defecation and palpations of the liver or anesthesia
Hashimoto Thyroiditis;
Hashimotos; TPO, and thyroglobulin, this will be sequestered from the systemic immune
system.
There will be positive Tg and TPO
Acromegaly;
Overview; the patient presents with acromegaly, this is going to have effect IGF-1, a common
organic manifestation is cardiomyopathy, which may progressive to CHF and will manifest with
reduced CO.
Insulinoma;
Clinical picture, palpations, nausea, fatigue and diaphoresis
Management; there will be with 72 hour fasting test, spontaneous hypoglycemia, there will be
involving measurement of insulin, c-peptide, and proinsulin.
Hyperparathyroidism;
Overview; there will be elevated serum calcium with low phosphorpus and elevated urinary
calcium.
Pathogenesis; abnormal PTH growth, hyperplasia, adenoma or carcinoma
Indications for surgery; age under 50, skeletal compromise, renal compromise with GFR < 60
Diabetes Mellitus;
Patient presents with diabetic ulcer, there will be ulcer base and calloused margin, this is a good
medium for bacterial proliferation, predisposes to bacterial infection
Management; sharp surgical debridement with scalpel blade
HHS;
In those with type II DM, those with a UTI, raise suspicion for HHS, woth redued insulin
secretion, there will be hyperglycemia in times of stress, infection and surgery----willl show
polyuria, polydipsia and dcecreased skin turgor and hypotension
Adrenal Insufficiency;
Overview; the patient has a history of autoimmune defieicny, this will be a constellation of
symptoms (shock, abdominal pain and thyroiditis, this is suggestive of adrenal crisis, there will
be no symptoms until the stressful trigger occurs
Cushing Syndrome;
Clinical picture; hirsutism, thin bruisable skin, and moon facies along with flushing of the face,
acne, weight gain and irregular menstrual cycle.
- There will make Cushing syndrome the most likely cause
- In individuals with Cushing, there will be inhibition of calcitriol synthesis. There will also
be avascular necrosis in the femoral head.
Causes; prolonged glucocorticoid therapy is the most common cause. This will be an exogenous
cause.
There will endogenous causes such as adrenal adenomas, pituitary adenomas and
paraneoplastic syndrome.
Screening; peripheral neuropathy, this will have positive monofilament test or vibration test.
Also recommend daily self examinations
Multiple endocrine Neoplasia;
There are two types MEN1 and MEN2; this will have evidence of kidney stones, joint pain,
nausea, vomiting and psychiatric overtones.
- Prolactinoma, pancreatic tumors and PTH tumours indicate MEN1, which is defective in
the gene Menin
- Management; surgical excision of tumors
Hyperthyroidism;
RAIU, this will only be taken up functioning thyroid tissue, the entire thyroid gland is
hypersecreting,and this is caused by thyroid stimulating antibodies. RAIU will lead to
permanent hypothyroidism
- We need to remanage with life long l-thyroxine
Secondary Hypothyroidism;
Overview; we will see fatigue, weight gain, obesty, ED and decreased thyrid function
- There will be caused by pituitary adenoma.
- Order of loss, there will be between loss of GH/ LH/FSH, TSH and ACTH
-
HHS:
There will be symptoms and labs that suggest DM: there will be orthostatic hypotension
(Whitened togue and skin turgor)
Osmotic diuresis; there will be hyperosmotic, hyperglycemic syndrome; HbA1c, polyuria, and
dehydration; there will be water pulling out of the cells. For example, water loss exceeds
sodium loss
- GI: There is diarrhea, vomiting
- Dermal fluid loss; burns, excessive sweating
Gastrinoma;
Fasting gasrtrin levels; b this is the best way to image, increase in gastrin is conclusive for
gastrin secreting tumors
Pheochromocytoma;
Presentation; there will be recurrent episodes of high blood pressure, this is suggestive of
catacholamines due to pheochromocytoma, there will be an elevated metanephrine level.
Diagnosis; CT scan will confirm suspicion
Niacin; ; there will have alcohol use disorder, glossitis, diarrhea, dementia and progressive
memory loss.
B3; this will result in constellation of clinical findings known as pellagra, diarrhea, dementia,
dermatitis----; there will be a precursor to to serotonin and niacin
Acetominophen Toxicity;
This is attempted suicide post intentional OD; and scleral icterus; prolonged INR suggesting
acute hepatic injury; this will be managed with NAC this is a precursor to glutathione; and it will
prevent further liver injury
Antidepressent;
Combination of antimuscarinic (sedation, dry mouth and a1 blockade, this is associated with
MDD depression and migraine prophylaxis
- Fast sodium blockade, TCA will inhibit fast sodium channels, will coorelate positively
with QRS complex.
Frostbite;
There will be mild hypothermia; management for 95 C
Will use circulating water which is warm; rewarming measures should be done and this will
enhance peripheral circulation
KOH poisoning;
KOH is a storng alkali in the drain and toilet bowel cleaners, it can manifest with heavy
salivation, odynophagia and dysphagia. KOH ingestion can lead to esophageal perforation and
liquefactive nercrosis with perforation.
Management; decontamination, airway management and fluid resuscitation.
Antihistamine poisinong; this will cause confusion, drowsiness mediated by H1; this wil show
dry skin, dry mucous membranes, mydriasis, tachycardia and constipation.
Heatstroke
Elderly has classic heatstroke, anhidrosis and AMS to keep up with the hot summer
temperatures, classic nonexertional heatstroke will have _ hypothalamic thermoregulatory
response, there will be peripheral vasodilation that will dissipate the heat into the
environment.
Treatment; rapid reduction, by cold water spraying fanning and cold IV crystalloids
CO poisoning;
Note that in the winter, basements ae cold, this places patient risk for chronic carbon monoxide
poisoning, increased somnolence and fatigue that can rise to unsafe levels especially during the
winter months, note CO has an affinity 240xx, there will be a chronic hypoxic state and there
will also have a normal sp02
Ambulatory:
Immunization schedule > 6 months, need to obtain influenza vaccine
HPV; recommended 11-26
Meningococcial recommended at 16 or above or high risk individuals, such as those in resident
dormitory
Vaccination;
Vaccination in HIV infected individuals follows a schedule including for live attenuated vaccine
( MMRV should be given if CD4 count is sufficient. Specifically > 200
PE; the patient has a sudden onset of stabbing chest pain that worsens with inspiration, there is
tachycardia, friction rub and lower limb swelling.
PE: will arise from the deep vein system, and is asosicated with a hstory of immobility, will
diagnose with CT angiogram with contrast and we should initiate therapeutic anticoagulation
PE: The patient presents with acute dyspnea pleuritic chest pain, dry cough and hypoxemia; this
should raise suspiscio for PE; with value of 3; test for D-Dimer; will do a CTPA
Blunt Trauma;
Endotracheal itubatio with PEEP is indicated for those with RDS; (Hypoxia, tachypnic despite O2
supplimetation. PEEP will have a splinting effect and this will enhance respiration
ARDS;
The patient has ARDS: pathogenesis is acute pancreatitis; this will show diffuse bilateral
infiltrates on a CXR; this is suggestive of ARDS;
- This will be associated with SIRS leading to progressive hypoxemia
There will be decreased tidal volume
Recall PH;
1. Idiopathic or hereditary
2. Left sided heart disease
3. Chronic hypoxic disease
4. Chronic thromboembolism;
5. Unknown disease
Anaphylaxis;
Presentation, there will be cutaneous hives, lip swelling RDS, (dyspnea, cough, wheezing,
tachycardia
Managemennt; epinephrine; this will be given to prevent progression to RDS and cardiovascular
failure; this will be liked to mortality, IV fluid and suplimental 02
OSA:
In laboratory polysonography, there is a gold standard test for OSA< diagnostic polysonography,
preferred---olysonography will demonstrate apnea, and desaturation, there will also show EEG,
and fragmentation, polysonography will elucidate CPAP treatment
Bronchiectasis;
Overview; there will be a chronic cough with copius sputum indicating bronchiectasis; this will
show a + Signet sign
Damage; this will be caused by erosion, and rupture of the dilated bronchial wall vessels leading
to mild self limiting hemoptysis
Pneumothorax;
Partially occlusive dressing (clear plastic treatment for open pneumothorax) with confirmed
and definitive treatment, there is occlusion.
- Once patient has been stabilized, pneumothorax, chest tubes are sufficient.
Pulmonary Embolism;
Risk factors for PE; HRT, recent long distance flight, and clinical presentation (chest pain, cough
right HF) suggests PE
- Iliac vein; DVT, vast majority, 90% occurs iliac vein, proximal deep veins, also go onto PE,
signs for DVT
Pulmonary Examination;
Initial steps to management of massive hemoptysis (with bleeding lung with cardiovascular
support), after the patient beem stabilizing. Transfusion of blood products, the next appropriate
step Is bronchoscopy
X-ray should find pulmonary nodule combination, SOB and cough productive of blood sputum,
30 pack year smokig history, potential occupational exposure to asbestos and brochogeic
Pneumonia;
CAP;
Clinical presentation will show cough, fever, pleuritic chest pain and CAP
- CURB -65=0
Outpatient; Amoxicilli CA; with CURB 65----will hav resp < 30, and SBP >90, and < LDH
Oxygen Therapy;
With COPD, continued O2 therapy, there will be reduction of pulmonary HTN
- This includes tobaccocessation and O2.
Anaphylaxis;
Type 1 HSR, this will cause sudden onset SOB, hypotension, and tachycardia/tachypnea with B-
lactam. This is consistent with type I HSR,
- Drug induced iGE there will be basophils and release of vasoactive substances
Airway management;
Tracheostomy; this is indicated for patients who require mechanical ventilation and will be in
patients with upper airway obstruction. A tracheostomy will provide airway that bypasses the
tumor and is used for long term mechanical ventilation
Goodpasture Syndrome;
Clinical picture; there will be microscopic hematuria and pyuria with HTN < 3+ on dipstick
making a nephritic syndrome more likely, there will be hemoptysis, dyspnea and pulmonary
infiltrates. This indicates pulmonary renal syndrome.
Labs will reveal anti-GBM antibody, this will target the noncollagenous domain of the a3
subunit in type IV collagen. This is a component of the basement membranes. There will be
lung and kidney involvement leading to nephritic syndrome
Nephritic Syndrome;
the patient has oligura, HTN and Bun/Cr < 15, and peripheral edema, dyspnea and crackles, this
will indicate AKI, this is secondary to streptococcal pharyngitis,
- Mild but significant leukocyturia, will result in nephritic syndrome, RBC casts indicate
sterile pyrua, leukocytira, the inflammation is 1+ or 2_
PFT;
Dry cough, worsened with lying down, there will be S3 gallop, in this case we will see
decreased DLCO but normal PFTS, showing that the fluid depresses gas exchange
Salt Retention;
Patient presents with nephritic syndrome, I.e. glomerular hyperfiltration secondary to SLE,
there is going to be associated with HTN and edema
Pulmonary examination;
Pneumonia evaluation will show consolidation, fluid accumulation, air filled tissue increasing
transmission of low frequency sounds, wil show low frequency sounds with dullness
Cough;
Bronchial asthma, caused by airway hyperresponsiveness and bronchial obstruction
Path; type I HSR, this will be common in older patients, nonallergic pathologies,
Presentation, exercise induced exasperation and diffuse end expiratory wheezing
Diagnosis; methalcholine challenge
Obstructive Sleep Apnea;
Complications; RVH with bilateral ankle swelling, increased JVD and ECG leads to right ventricle
dysfunction.
Chronic hypoxia, leads to smoking, snoring and occaisionally choking, this will be associated
with OSA leading to hypoxia during apneic episodes. There can be RV dysfunction
Electrolyte Abnormalities
Hyperkalemia; this will have life threatening hyperkalemia this will cause rhabdomyolysis (CK,
myoglobinuria that causes dark urine post trauma, and immobilization, CKD will contribute to
accumulation of K+
Management insulin is a rapidly acting treatment for hyperkalemia, glucose is simultaneous
administered to prevent hypoglycemia.
COPD
Overview; the patient has a decreased FEV1, and FEV1/FVC< 70% - there will be increased lung
compliance. This will also cause worsening dyspnea and end expiratory wheeze. There is also an
occasional dry cough
GOLD class 2; with FEV1
Managementl with salmeterol or formeterol
Heme Onc
Polycycthemia; the patient has an elevated RBC count (elevated Hb, and hct, with constitutional
symptoms such as fatigue like hyperviscosity syndrome (triad of mucosal bleeding, neurologicl
symptoms and water when getting ready for work)
- Pathogenesisis mutated, Jak2 mutation there will be present in almot all cases of
polycycthemia. With ET and PMF
Hemolytic Anemia;
Normocytic Anemia; elevated LDH, haptoimmunoglobulin. These findings are related to the
exercise regiment. Exertional hemoglobulinemia form to intravascular hemolysis. The most
likely etiology in the lab abnormalities seen is in the marathon. It is thought to be due to
mechanical trauma
Management; eculizumab
Opthalmology;
Chloqoruine Toxicty; this will cause visual deficits with irreversible retinopathy, the key finding
is going to be retinopathy. Discontinue chloroquine to prevent further toxicity
Clinical features; night blindness, floaters, and bulls eye maculopathy suggest retinopathy
Germ Cell tumour; this wil produce the majority of all testicular cancers; this will represent half
of all testicular cancers; this will have painless lump or swelling in the scrotum; notably this will
be consistent with testicular seminoma
- There will be dull ache in the abdomen and the groin and pain in the testes or scrotum
Social Sciences
Patient safety reporting systems; omnipresent and can ID patient safety events and quality
problems; frontline personel include nursing physicians pharamcisits and maintainace staff
Health Maintaintaince;
- This will not require preauthitorization before services are provided
Multiple Sclerosis;
Overivew; this is diagnosed based on prior vision changes; dissemination in time and space; this
will be managed by steroids given 3-5 days and it will be tapered wth symptom improvement