PVD ● Lesser blood pressure, weaker compared to

ARTERIES the arteries and has a more tendency to

● carry rich and oxygenated blood away from collapse with stress.
the heart.
● Branches off into sections with smaller ● Blood pressure from the veins is low
diameters called: Arterioles. because it does NOT come from the heart
● Thicker - as they bear strong blood flow but from the body.
pressures generated by the heart. ● Because of the low blood pressure from the
*If blood pressure changes, arteries also change in veins of LE to the heart, it cannot withstand
diameter. * gravity. This is why veins have VALVES.
● Strength - has to withstand high pressures ● Venous reflux
from the heart. ○ Blood will backflow because the
● Elastic - it can change in diameter. If low valves are destroyed which is
blood pressure, diameter lessen, If high responsible for preventing the
blood pressure, diameter increases. backflow.
● Strong and durable - to keep their ● Veins are susceptible to the movement of
cylindrical shape when stretched the body.
● Movement will actually help the blood move
Have (3) layered walls that give them strength and back to the heart. (faster blood flow) .
elasticity :
1. Tunica Adventitia - outermost and Three types/layers of veins
strongest layer; composed of collagenous ● Superficial veins - outermost, runs above
and elastic fibres; limiting barrier, protecting the fascia of the muscle. You can actually
the vessel from overexpansion 2. see the veins as it runs across the fascia of
2. Tunica Media - middle and thickest layer; the muscle.
primarily smooth muscle; not only provides ● Deep veins - run below the fascia. You
support for the vessel but also changes cannot see this.
vessel diameter to regulate blood flow and ● Perforating veins - only connect both deep
blood pressure and superficial veins
3. Tunica Intima - innermost layer; consists of
flat epithelial cells; allow fluid to flow Peripheral Vascular Disease
smoothly and are interspeed with valves ● general term used to describe any disorder
that ensure the flow continues in one that interferes with arterial or venous blood
direction. flow of the extremities

2 Contractile abilities - Happens when the Epidemiology

sympathetic division of the autonomic nervous ● Affects 30 percent of the adult population,
system (ANS) is triggered. and two-thirds of all cases are
● Vasoconstriction asymptomatic
○ Tighten to make the space inside ● Is uncommon until middle age and then
smaller. increases dramatically.
● Vasodilation ● Prevalence of PVD is slightly higher in men
○ opens your blood vessels to make than women, yet this tends to diminish with
the space inside bigger. age
○ ● M>F
VEINS
● Return oxygen-depleted blood from tissues ARTERIAL INSUFFICIENCY
and organs to the heart. ● lack of adequate blood flow to a region or
● Thinner than arteries but have the same 3 regions of the body. It loses its ability to
layers. contract and dilate.
● Cause: smoking, heart disease, diabetes
mellitus, neuro hypertension, renal disease,
 increased cholesterol and triglycerides,
obesity and sedentary lifestyle. Raynaud’s Disease
● A phenomenon characterised by recurrent
vasospasms of fingers and/or toes
● Typically occurs in response to emotional
stress or exposure
Disorders That Occur With Abnormal Arterial ● a vasomotor disease of small arteries and
Blood Flow arterioles.
● VASO means vessel and MOTOR means
Arteriosclerosis contraction.
● general term for artery loss of elasticity, This means Raynaud’s disease is the loss of ability
thickening and hardening of the blood of the artery to contract.
vessels. ● Symptoms
Atherosclerosis ○ Fingers & feet are pallor (unhealthy
● most common form of arteriosclerosis pale appearance)
● associated with damage to the endothelial ○ Rubor (reddish discoloration)
lining of the vessels and the formation of ○ Cyanosis (bluish discoloration)
lipid deposits can eventually form into a ○ Oxygen did not reach the fingers
clot/blood clot and feet because the vasomotor
ability of the arteries are destroyed.
Arteriosclerosis Obliterans (ASO)
● Peripheral atherosclerosis - plaque The common clinical manifestations of AI
formation is seen in the distal part of the ● Wounds will most frequently be located on
body/ peripheral parts of the body. the LEs When wounds are present on an
● Seen in lower extremities (ankles, feet) ischemic limb, atherosclerotic occlusion of
● Causes intermittent claudication, rest pain, the peripheral vasculature is almost always
and trophic changes. present.
● This is the arterial disease most likely to ● Diabetic
lead to ulceration. ● Trophic changes
● Known risk factors for development of the ● Skin is cool on palpation.
disease are smoking, diabetes mellitus, ● Intermittent claudication
hypertension, hyperlipidemia, and ● Wounds are painful and patients may also
hyperhomocysteinemia. describe the pain in the legs and/or feet.
● Wound base is usually necrotic and pale,
Thromboangitis Obliterans (TAO) lacking granulation tissue.
● Buerger’s disease ● Skin around the wound may be black,
● NOT caused by plaque formation; caused mummified (dry gangrene)
by inflammation
● Inflammation leads to arterial occlusion (a VENOUS INSUFFICIENCY
sudden blockage or closing of one of your ● Lack of blood going to the heart
peripheral arteries that interrupts blood flow) ● Inadequate drainage of venous blood from
and tissue ischemia (interruption in the a body part, usually resulting in edema
arterial blood supply to a tissue) and/or skin abnormalities and ulcerations.
● Nicotine sticks to the walls then inflames the ● Venous insufficiency is related to ageing.
walls. Inflammation swells, gets bigger &
turns red, if it gets too great, there will be Chronic Venous Insufficiency
arterial occlusion. (BF cannot flow; there is ● most common condition
ischemia = lack of oxygen in the tissues. ● most common cause of leg ulcer
● - MC : young men who smoke. ● Also known as Venous hypertension
(because of too much
*Note : ASO & TAO have the same symptoms but ● blood in the veins, leads to high blood
different causes. pressure)
Pathology: ● paresis, Immobility causes DVT
○ blood will not go back to the heart -> too ● Risk Factors
much blood in the ● Most common prevention: ankle pump
○ veins -> high blood pressure in the lower
extremities -> stays in Precaution
○ one area -> ulceration ● If the clot has already formed or there is a
Risk Factors pre-existing DVT-> it can lead to embolism
● Aging (thrombus can dislodge from the venous
● Lack of exercise walls and move to other parts of the body)
● Sedentary lifestyle -> This can lead to pulmonary congestion or
● Pregnancy stroke.
● Obesity
● Hereditary THROMBUS VS. EMBOLUS
● Thrombus is blood clot formation within the
Clinical Manifestations arteries. If there is too much pressure, it will
● Edema push the thrombus away and it becomes an
● Relieved by elevation (because of gravity, embolus.
fluids would go down once elevated. ) ● Embolus is a blood clot which moves away
● Itching from the vessel of origin. Usually the
● Fatigue embolus would either go to the veins going
● Aching to the lungs or brain (which causes a
● Heaviness stroke) or the extremities.
● Skin changes- hemosiderin staining.
● Fibrosis of Dermis
● Increased temperature in LE
● Hot to the touch
Arterial insufficiency Venous insufficiency
● Most commonly seen proximal to medial
malleolus ● Decrease or ● Normal pulse
● Usually not painful. absent of pulse ● Normal
● More on dull aching and heaviness ● Cold LE temperature on LE
● Pale and pain in ● Relief of pain upon
Acute Venous Insufficiency elevation elevation
● varicose veins ● Dusky red on ● Pain of dependent
● Swollen distended superficial veins dependent position position
(swollen/stretched) ● +gangrene and
● Dark, enlarged, twisted veins. rest pain
● Happen anywhere in the body, but are more
common in the legs.
● Blood already pools/stays in the veins as it
Diagnostic Procedures:
does not go back to the heart.
Ankle-Brachial Index (ABI) Test
● Affected: Valves due to increased pressure
This simple, non-invasive test is usually the
in the LE, prolonged standing, obesity,
physician’s first choice in screening for peripheral
pregnancy or prolonged cross leg position
vascular disease. The systolic blood pressure in
the ankle is compared to the systolic blood
Deep Vein Thrombosis
pressure in the arm. Calculates ABI by dividing the
● Usually seen in deep veins Seen through
blood pressure in an artery of the ankle by the
ultrasound
blood pressure in an artery of the arm.
● There is clot in the deep veins
● Prolonged immobility, Oestrogen use,
Ankle-Brachial Index (ABI) Test
Increasing age,
● History of thrombosis, Increase age,
Extremity Greater than Calcification/ Refer to
 Bypass surgery
1.4 Vessel vascular
● performed to reroute blood flow so that it
hardening specialist
travels around a narrowed or blocked area
1.0 - 1.4 Normal None of a blood vessel.
● They will remove the plaque formation part
0.9 - 1.0 Acceptable and replace it with a plastic tube.
● Remove the affected part and remove an
0.8 - 0.9 Some Arterial Treat risk artery elsewhere (own or donor) and
Disease factors replace the affected part (coronary bypass
grafting/surgery)
0.5 - 0.8 Moderate Refer to
● Difference between plastic tube and own
Arterial vascular
vessel. Using plastic tubes, it would have to
Disease specialist
be replaced once or twice a year. Using
Less than 0.5 Severe Arterial Refer to your own blood vessel means having to
Disease vascular operate only once.
specialist Course
● Acute cases of PVD are reversible and
Doppler manageable however for chronic cases of
Ultrasound An ultrasound can be used to monitor PVD it leads to gangrene of the affected
blood flow through the blood vessels. This is used extremity resulting in an amputation to
to notice if there is a blockage in the arms or legs if prevent damaging proximal healthy cells.
you have PVD. Prognosis
● In most cases, the prognosis (expected
MEDICATIONS outcome) for patients who have PVD is
● Anticoagulants - which prevent blood clots good. The condition often can be controlled
● Beta blockers - which slow heart rate and with treatment, including lifestyle
lower pressure modifications, regular exercise,
● Cilostazol - which relaxes arteries and medications, and in severe cases, surgery.
allows them to enlarge Patients who have uncontrolled risk factors,
such as diabetes, high blood pressure, and
Surgical Procedures: high cholesterol, are at increased risk for
Percutaneous Transluminal Angioplasty, or heart attack, stroke, and gangrene (tissue
"angioplasty” death and decay that often requires
● technique for enlarging an artery that is amputation).
blocked or narrowed without surgery.
● A diagnostic angiogram is done first to
locate the blockage or narrowing and
determine the severity.
○ minor blockages - treated with
medicine.
○ If the obstruction is significant,
especially in a larger artery,
angioplasty may be reasonable.
● The angioplasty is performed through a thin
tube called a catheter inserted with a needle
into the affected artery. It has a tiny balloon
attached to the end. The balloon is inflated,
pushing aside the plaque and widening the
artery so that it no longer restricts blood
flow.
● The balloon is then deflated and removed
from the artery.
 b. Allow drainage of excess and waste
fluids, to minimise the possibilities of
infection.
c. Clients will need to stay in the
hospital for a longer period of time.
1. Decrease the possibility of infection
2. Close Method
a. Reduce the number of days in
hospital but decrease drainage.
b. Increased possibility of infection and
the possibility of draining again.
3. Bone Bending
a. Smoothening the edges of the bone
for it to become functional.
b. Has to be done since the body will
actually try to regrow the bone
(normal body response).
AMPUTATION c. In these cases there could be a
● The loss of limb whether a result from possibility for bone spur which can
disease, injury or congenital causes. be painful.
EPIDEMIOLOGY 4. Myodesis
● Calculation of the number of individuals with a. Suturing or sewing muscle to bone. -
limb amputations worldwide → difficult to This is done to smoothen.
complete because many countries do not 5. Severing of the blood vessels and the
keep records of these data nerve
● Major cause of lower limb amputation: a. Need to be sewed to avoid bleeding
○ PVD, often associated with smoking of the limb.
and diabetes b. Some cases, the blood vessels
● The second leading cause of lower limb would be closed and some would
amputation attach and sew the anterior and
○ trauma posterior blood vessels in order to
● Lower limb loss (80%) → more prevalent have a continuous flow. -
than c. Another method is to cut the nerves
○ upper limb loss (10%) or to allow the nerve to retract, this is to
○ multiple limb loss (10%) remove residual limb pain.
● Upper limb loss due to trauma is increased
during times of active warfare. Complication of Amputation
● Cause of approximately 75% of upper limb ● the higher the level of amputation → would
amputations in adults implicate the amount of motor function loss
○ Trauma on the respective joints in the extremity that
ETIOLOGY: was lost.
(3) major causes : disease, injury and congenital Neuroma
● MC type of disease causing amputation is ● a small ball of nerve sa distal stamp due to
PVD - the nerve that keeps trying to grow.
● Elective Amputation : amputation by choice ● massages and stretches to try to flatten out
○ Severe or complete brachial plexus the nerve bal
injury, you can’t move the UE Phantom Limb
SURGICAL TECHNIQUES ● The sensation that an amputated or missing
1. Open Method limb is still attached to the body and is
a. The site of the surgery was not moving with other body parts, causing pain,
closed. tingling, or creating sensation.
Phantom Sensation
 ● Sometimes after a body part has been a. For example: if the cause is related
amputated, it feels as if that part is still to PVD or diabetes- so the lab test
there. It is a normal part of healing after needed for PVD or diabetes would
surgery. be needed.
● Phantom sensation is not pain, but is a During and after surgery, the primary goal → form a
tingly, cramping, or itching feeling where the residual limb that maintains maximal function of the
missing part used to be. It is not a very remaining tissue and allows maximal use of the
unpleasant sensation. prosthesis.
Sensation
● Loss of sensory feedback from the Medications
amputated limb NSAIDS - relieve pain
● Residual limb hyperesthesia or an overly 1. Beta-blockers - relieve constant , dull,
sensitive limb → limits functional use and burning phantom limb pain
causes discomfort. 2. Opioid Analgesics - may be effective in
Edema relieving postoperative pain.
● Development of residual limb edema during 3. Anticonvulsants- control stabbing and
the post prosthetic phase → usually cramping pain.
indicates an ill-fitting socket. 4. Tricyclic antidepressants - may not only
● Proximal tightness of the socket may result alleviate phantom limb pain but may also be
in distal edema. prescribed to improve mood and coping
ability.

Skin
● Skin complications -> account for most post
surgical problems. COURSE :
● Complications in the pre-prosthetic phase ● stable if the cause → traumatic; may also
○ Delayed healing and extensive skin be worsening over time and may need more
grafting amputation from other extremities if ever the
● Complication in the prosthetic phase nature of
○ Skin breakdown, ulcers, infected ● cause → severe and chronic conditions
sebaceous cysts and allergic such as cancer, diabetes, and peripheral
reactions. vascular diseases.
Bone Spurs
● Little bone growth
● Formation of bone spurs
Factors to Consider for Prognosis
● Occurs during the pre prosthetic phase
Wound Healing GOOD POOR
● For clients with LE amputations -> delayed
wound healing and excessive skin grafting ● Cause of ● Cause of
are potential complications during the pre amputation is amputation is due
prosthetic phase. traumatic to non-traumatic
● Postoperative infection from external or ● Lower level of causes such as
internal sources is a major. amputation which PVD, diabetes,
preserves the cancer etc.
DIAGNOSTIC PROCEDURES function of the ● Higher level of
1. X-ray - To check for the status of the bones residual limb. amputation which
of the residual limb and presence of bone ● Absence of corresponds to
spurs growth. post-surgery significant
2. Other lab tests may be required depending complications. functional loss of
on the comorbid conditions associated with ● Good fit of residual the limb.
amputation or the cause of amputation limb (stump) to ● Presence of
especially for non- traumatic causes. prosthetics. post-surgery
 Merkel Cells (Tactile epithelial Cells)
● Only unilateral complications such
● Contacts sensory neurons called merkel
amputation. as bone spurs
disc
● Patient is with formation and poor
● Which is responsible for tactile sensation
intact cognition wound healing.
● Poor fit or misfit of
STRATUM CORNEUM
residual limb
● (25-35 layers of flattened dead
(stump) to
keratinocytes)
prosthetics.
● Cells are continuously shed and replaced
● Bilateral
by cells from deeper strata
amputation or
● Multiple layers of dead cells help protect
multiple limb
deeper layer from injury
amputation.
● Constant exposure of skin friction ->
● Patient with
Stimulates cell & keratin production ->
impaired cognition.
Formation of callus

STRATUM LUCIDUM
● Can be found in palms and sole of the foot
● “Clear layer of the skin”
● 4-6 layers of flattened dead keratinocytes
● has large amounts of keratin and thickened
plasma membrane which adds the level of
toughness
● helps keep other foreign substances from
penetrating the deeper layers of the skin
and causing infections.
INTEGUMENTARY SYSTEM
● Largest Organ in the body
● 15% of total body weight STRATUM GRANULOSUM
● Has three layers of tissue: Epidermis, ● 3-5 layers of flattened keratinocytes
Dermis & Hypodermis undergoing apoptosis (cell suicide)
● Dermis: Papillary & Reticular Dermis ● responsible for the early stages of
● 4th layer: Subcutaneous layer keratinization, lipid secretion, and the
differentiation of keratinocytes into
EPIDERMIS corneocytes.
● Outermost layer of the skin
● Composed of epithelial tissues STRATUM SPINOSUM
● Avascular (No vessels) ● Also knowns as “Spiny layer”
● Contains several layers of keratinocytes
Contains 5 layers: and projections of melanocytes
1. Stratum Corneum ● provides strength and flexibility to the skin
2. Stratum Lucidum
3. Stratum Granulosum STRATUM BASALE
4. Stratum Spinosum ● Also known as “stratum germinativum” cell
5. Stratum Basale formation
● Deepest layer of the epidermis responsible
Langerhans Cells (Intraepidermal for mitosis in the epidermis which actively
Macrophages) divides and produces new keratinocytes.
● Responsible for Immune Responses
against KERATINIZATION & GROWTH OF EPIDERMIS
● Microbes 1. Cell division in the stratum Basale - Mitosis
● Easily damage by UV light in the 1st layer
 2. Keratinocyte Migration - Moves upward to ● Structure: composed of dense irregular
higher layers connective tissue, which contains a
3. Keratinocyte maturation - As they move up meshwork of thick collagen and elastin
they -> process of maturation fibers
4. Formation of the stratum Granulosum ● Collagen and Elastin: The collagen fibers in
5. Formation of the stratum corneum the reticular layer provide tensile strength,
6. Desquamation (Shedding) Continual which helps the skin resist tearing and
7. Renewal shearing forces. Elastin fibers give the skin
elasticity, allowing it to return to its original
RETE PEG REGION shape after being stretched.
The "rete pegs" are structures found in the junction ● Thermoregulation: by dilating (expanding) to
between the epidermis and the underlying dermis release excess heat from the body's core or
in the skin. They are also sometimes referred to as constricting to conserve heat during colder
"dermal papillae. " This region plays a crucial role conditions.
in maintaining the structural integrity and
attachment between the epidermis and dermis
Sensory Location Sensation
● Function: Increase surface area, Reservoir receptor
of skin, overcome friction
● DysFx:Blisters from abrasion and poor Free Nerve Epidermis Pain and itch
adherence of new epidermal tissue endings

Free Nerve Dermis Pain

DERMIS endings
● Also known as “Corium” or “True Skin”
● Second layer of the skin located beneath Merkel Disks Stratum light touch and
the epidermis Spinosum superficial pain
● Contains: Blood vessels, lymphatics,
Meissner's Papillary Dermis 2-point
nerves, collagen and elastic fibers Corpuscles discrimination
● Encloses epidermal appendages: sweat
ducts and sebaceous glands, and hair Ruffinis Papillary Dermis Warmth
follicles -> source of epidermal cells for
Krause's end Papillary Dermis Cold
wound healing
bulb
● 20-30x thicker than the epidermis
● Collagen and elastic fibers: Structural Pacinian Reticular Pressure and
support, strength and elasticity of the skin Corpuscles Dermis vibration
has 2 layers: papillary & Reticular
OTHER FUNCTIONS OF THE SKIN
PAPILLARY LAYER ● Temperature Regulation
● Location: Superficial of the 2 layers of the ● Secretion of Oils and sweats
dermis ● Substances
● Structure: composed of loose connective ● Vitamin D sythesis
tissues & contains smaller, finer collagen ● Contribute to cosmetic appearance and
fibers identity
● Contains thin collagen and fine elastic fibers ● Sensation
● Dermal papillae - contains capillary loops ● Protects body from external Environment
(blood vessels) Meissner Corpuscles (tactile ● Wound Healing
receptors), nerve endings (sensitive to
touch); free nerve endings (sensitive to WOUND HEALING
pain, temperature, tickling and itching) Two types of wound healing
RETICULAR LAYER ● Epidermal Wound Healing
● Location: situated beneath the papillary ● Deep Wound Healing
layer
EPIDERMAL WOUND HEALING
 ● refers to the repair and regeneration of the ● Angiogenesis: involves the formation of new
epidermis, which is the outermost layer of blood vessels.
the skin. This process typically occurs in ● Extensive growth of epithelial cells beneath
response to superficial wounds that affect the scab.
only the epidermis or the uppermost part of ● Fibroplasia: migrate to the wound site,
the dermis. Common examples of wounds proliferate (multiply), and synthesize
that undergo epidermal healing include collagen and other extracellular matrix
minor cuts, abrasions, and superficial burns. proteins.
● Collagen is essential for wound strength
DEEP WOUND HEALING and stability.
refers to the repair of more extensive wounds that ● Fibroblasts also help to remodel the tissue
extend deeper into the dermis and sometimes as it heals.
involve underlying tissues like muscle, fascia, or ● Skin Integrity is restored =
bone. Examples of wounds that require deep re-epithelialization Duration: day 3 - day 20
wound healing include surgical incisions, traumatic
injuries, and severe burns. MATURATION PHASE
● More complex healing process ● Also known as “Remodelling”
● Four phases: Inflammatory, Migratory, ● scab soughs off once epidermis has
Proliferative & Maturation Phase restored to normal thickness
● Scar formation: hallmark of maturation
INFLAMMATORY PHASE phase
● Normal Immune system Reaction ● Collagen fibers become more organized ->
● Central Activity in wound healing maturation of the tissue
● A vascular and cellular response helps ● New skin: 15% of normal tensile strength ->
eliminate microbes, foreign substances in 80% original tensile strength
PREPARATION for repair ● blood vessels restored to normal Duration:
● wound: Periwound edema/ swelling, ● Day 9 - 2 years
erythema and drainage (accumulation of
fluid = pus) FACTORS AFFECTING WOUND HEALING
● Vasodilation & vasoconstriction: blood ● Oxygen - Increase blood flow -> improve
vessels at the wound site constrict rate of wound healing
(vasoconstriction) to minimize blood loss. ● Moisture - optimal wound healing; dry
This is followed by vasodilation, where. wound causes scar and eschar
● blood vessels expand to increase blood flow ● Nutrition - Iron, Vit B12 and folic acid
to the area. Duration: day of injury - day 10. (oxygen); Vit C and Zinc (tissue repair), Vit
A (collagen production) and Arginine
MIGRATORY PHASE (healing and immune function)
● Cell Migration: movement of several types
of cells into the wound site TYPES OF WOUND CLOSURE
● Fibroblasts: are connective tissue cells that ● Primary Intention: surgeon closes a wound:
are essential for wound healing. staples, sutures, glue, skin grafts, skin flaps
● Endothelial cells: play a crucial role in ● Secondary Intention: wound is left to heal
angiogenesis, the formation of new blood on its own
vessels ● Tertiary Intention: delayed primary;
● Keratinocytes: helps close the wound and secondary then primary as final treatment;
restore epidermal barrier. usually owing to presence of infection
● Granulation Tissue Formation: Fibroblasts,
as well as other cells, play a role in the SCAR FORMATION
formation of granulation tissue. (temporary, FIBROSIS – process of scar tissue formation
pinkish tissue that fills the wound gap) ● Too much scar tissue à raised scar elevated
above normal surface = HYPERTROPHIC
PROLIFERATIVE PHASE SCAR
 ● Too much scar tissue à extend beyond the ● Non blanching erythema with intact
boundaries of normal tissue = KELOID epidermis
SCAR Stage II
● Partial thickness involving epidermis and
SKIN RELATED CONDITIONS dermis
● Pressure Ulcers Stage III
● Burn ● Full thickness ulcer extending dermis into
subcutaneous tissue
PRESSURE ULCERS Stage IV
● Also known as “Pressure Sores” or ● Deep tissue destruction extends through
Decubitus Ulcers or “Bed sores” fascia and may involve muscle, bone and
● localized injuries to the skin and/or tendons.
underlying tissue, usually over bony
prominences, as a result of prolonged Course and prognosis
pressure and reduced blood flow to the Stage I and II: Pressure ulcers in these early
area. stages are generally less severe and have a better
● Blistering = superficial damage prognosis. Can heal within weeks.
● Reddish-blue discoloration = deep tissue Stage III and IV: Pressure ulcers in these advanced
damage stages involve deeper tissue damage, and their
● prolonged pressure = tissue ulceration prognosis is typically less favorable.
● Small breaks/ ulcers in epidermis ->
infected = damages deeper tissues MEDICATIONS
● Treatment: relieve every 15 minutes or ● Topical Antiseptics
every 2 hours ○ solutions or creams may be used to
help prevent or treat infection in
EPIDEMIOLOGY pressure ulcers.
● M=F ● Topical Growth Factors
● Common in older individuals age 60 above ○ Topical agents containing growth
Patients with Spinal Cord Injury, CVA, TBI, factors, such as recombinant human
Parkinson’s Disease, Multiple sclerosis, epidermal growth factor (EGF), have
Diabetes & Vascular diseases are more been used to promote wound
susceptible to pressure ulcers. healing in pressure ulcers.

ETIOLOGY BURN
● Pressure: Prolonged pressure on a specific Tissue damage that results from heat,
area of the body. overexposure to Thermal, other radiation, chemical
● Immobility: limited mobility is at higher risk or electrical contact that causes pain and other
because they are unable to relieve pressure integumentary, musculoskeletal or neurological
on vulnerable areas by changing position. symptoms.
● Reduced Sensation: Conditions that reduce
the ability to feel pain or discomfort, such as EPIDEMIOLOGY
neuropathy ● Gender: M(69%) > F(31%)
SIGNS & SYMPTOMS ● Highest incidence of injury: Men (16-40 y.o)
● Pain or Discomfort ● Usually happens on summers
● Infection Most common causes of injury:
● Changes in Skin color or texture ● Children (1-5) = Scalding
● Foul odor Fever ● Adolescents & Adults = Hot liquids
● Systemic symptoms Admission causes
● Fire/flame = 44%
Stages of pressure sores ● Scalding = 33%
Stage I ● Electrical = 4%
● Chemical = 3%
 ● Other = 7% c. <124F (51C) = exposure time
Place of occurrence: needed to damage tissue is
● Home: 69% extremely brief
● Occupational:9% 2. Duration of exposure
● Street/highway: 7% 3. Type of Insult: (flame, liquid, chemical or
● Recreational sport: 5% electrical).
● Other: 10%
COURSE & PROGNOSIS
ETIOLOGY Three Zones of a Burn:
● Thermal: 95% of burn admissions 1. Zone of Coagulation: Point of maximum
● Chemical: Contact with chemical irritants damage, irreversible tissue loss due to
● Electrical: High voltage 100,000 – 200,000 coagulation.
volts |Low voltage 500 – 1000 volts | 2. Zone of Stasis: Decreased tissue perfusion,
Iceberg Phenomenon – wound of entry might be potentially salvageable tissue, Increase
small but there may be gross necrosis of deeper tissue perfusion and prevents damage.
tissue; skin may not reflect deeper necrosis 3. Zone of hyperemia: Site of minimal cell
immediately. damage; recover within several days.
● Radiation: Over exposure to sunlight,
exposure to radioactive substances (rare) COURSE & PROGNOSIS
Factors affecting a burn Px’s prognosis
BASIC MEDICAL SCIENCE ● Depth
Skin: ● Extent
● Largest organ of the body, composed of ● Type of Burn: Worst = Electrical burns due
15% of total body weight to its “Iceberg Effect”
● Functions: Protection, sensation, ● Age:>2 y.o. are prone to infection; >65 are
thermoregulation, Vitamin D productions decreased assistance: the higher the age,
Layers of the skin: Come Let's Get SunBurn the worse the prognosis
1. Stratum Corneum: Topmost layer ● Delay treatment
2. Stratum Lucidum: Clear transparent layer
3. Stratum Granulosum: Water Retention COMPLICATIONS OF BURNS
4. Stratum Spinosum: “Spiny layer” The two major systems affected in burn injuries are
progressive keratinization the cardiac and pulmonary systems
5. Stratum Basale: Inner most layer, Pulmonary Complications
regenerates upper layers, production of new ● Inhalation injury: inhalation of hot gasses
cells. and potentially toxic fumes change/
dyspnea, loss of consciousness, soot in
airways, mucosal changes
● Inhalation injury signs: Facial burns, harsh
cough, hoarseness, hypoxemia, pneumonia
leading cause of death.
Cardiovascular Complications
PATHOPHYSIOLOGY ● Significant edema / edema formation d/t
Three primary factors that influence the amount of inflam. respo.
tissue destruction: ● Decrease of cardiac output to 15% of
1. Temperature normal
a. >111F (44C) = local tissue damage ● Loss of circulatory fluid and blood plasma
will not occur unless the exposure is
prolonged. EDEMA
b. 111F & 124F (44C & 51C) = rate of The accumulation of excess fluid in the body's
cellular death doubles with each tissues is a natural immunological response to burn
degree rise in temp. and short injuries.
exposure to cell destruction. Occurs in several reasons:
 ● Increased capillary permeability ● Excision and Escharotomy: In cases of deep
● Plasma loss partial-thickness and full-thickness burns, the
● Inflammatory response burned tissue, known as eschar, must be
● Vasodilation surgically removed.
● Lymphatic System Impairment Skin Grafting:
Edema contains: ● Autograft: involves taking a piece of healthy skin
● Water from one part of the patient's body and
● Electrolytes transplanting it to the burn site.
● Allograft or Homograft:involve using skin from
● Proteins (Albumins, globulins)
another human donor (cadaveric skin) to
● WBC & RBC
temporarily cover burn wounds.
● Inflammatory Mediators (histamine,
● Xenograft or Heterograft: Xenografts involve
cytokines, prostaglandins)
using skin from animals, typically pigs, as a
temporary covering for burn wounds.
SIGNS & SYMPTOMS ● Isograft:Involve using skin from identical twin

DIFFERENTIAL DIAGNOSIS
Cellulitis
● primarily caused by a bacterial infection, often
due to Staphylococcus or Streptococcus
bacteria.
● Similarities: Both affect the skin and underlying
tissues, leading to redness, swelling, and
potential tissue damage.
Vasculitis
● damage blood vessels by causing inflammation,
or swelling.
● Similarities: Both involve inflammation, which is
the body's response to injury or damage.
Inflammation in both conditions can cause
redness, swelling, and pain.
Toxic Epidermal Necrolysis (TEN)
● A life threatening skin condition. Causes peeling
and blistering skin over much of the body,
including the mouth, eyes, and genitals.
● Similarities: Both TEN and burns cause severe
damage to the skin, leading to the loss of the
skin's protective barrier function.

LAB TEST
● Complete Blood Count (CBC):Measures the
number of red blood cells, white blood cells, and
platelets in the blood. It can help identify signs
of infection, anemia, or other blood-related
issues that may arise due to a burn injury.

SURGICAL MANAGEMENT
 ● Metastases
● Tumor
● Staged
Types:
● Carcinoma - within an organ
● Sarcoma - connective tissue
● Chondorma - cartilage
● Lymphoma - lymphatic tissue
● Leukaemia - blood forming tissue
Malignancy (metastasize fast if high grade)
● Low-grade
● High grade

Paraneoplastic Syndrome
● Hormonelike substances secreted by tumor→
dysfunction of organs
● Lab tests: Blood Tests
● Quadriparesis

Most Common Cancers

WOMEN
1. Breast
2. Lung
3. Stomach
MEN
1. Lung
2. Prostate
3. Colon
CHILDREN
1. Acute lymphocytic Leukemia
ADOLESCENTS
1. Hodgkin’s lymphoma
2. Thyroid carcinoma
3. Brain and CNS
a. Also common in children
(neuroblastoma)

Classification of Cancers
According to Tumor:
MALIGNANT BENIGN

● Carcinoma ● Papilloma
● Leukemia ● Adenoma
● Lymphoma ● Chondoma
● Sarcoma ● Osteoma
● Myeloma ● Rhabdomyoma
● Leiomyoma
● Angioma
● Neurofibroma

Oncology
Cancer
According to Appearance:
● Mutation of cells
1. Alveolar - deformed microscopic sacs
● Broad grouping of diseases linked by
2. Annular - circular
● presence of malignant tumor cells in
3. Cystic - fluid filled sacs
● body
 4. Diffuse - spreading evenly through tissue Discontinued cell IF:
5. Fungating - mushroom pattern 1. (+) retinoblastoma gene→ apoptosis
2. (+) proteolytic degradation → apoptosis
According to TNM: 3. No hormones
4. No nutrition
Stage Primary Tumor

I Tumor 5 cm or less No No BMS

in size; no invasion regional distant SYNTHESIS PHASE (S-Phase)
of adjacent tissues positive metastasi ● DNA replication phase
nodes s ● Genetic footprint
● Replicate lacking chromosomes from mitosis
II 5 cm in size; no (-) (-)
invasion of
adjacent tissues G2 (GAP 2 PHASE)
● Preparation for mitosis
III Tumor outside (-) (-) ● Ribosome formation
organ in fat and
surrounding tissues
MITOSIS
5 cm or less; no (+) (+) ● Cell will enter mitosis if its ready
invasion of ● 4 stages
adjacent tissues or ○ Prophase
>5 cm no invasion ○ Metaphase
of adjacent tissues ○ Anaphase
○ Telophase
IV Tumor outside (-) or (+) (+)
organ in fat and
surrounding soft BMS– Cell Death
tissues, or tumor
APOPTOSIS NECROSIS AUTOPHAGY
invading adjacent
organs ● Programmed ● Unprogramm ● Consumpti
cell death ed Due to on of cells
5 cm or less; no
● Autonomous outside ● Due to lack
invasion of
● Happens to factors of nutrition
adjacent tissues or
excess or ● Due to
tumor outside
damaged autolysis
organ or invading
cells
adjacent organs
● Presence of
death
BMS receptors
Cell Cycle Phases:
G1 → SYNTHESIS → G2 → Mitosis BMS–Cell Life Span
● 4 typical phase
SHORT MODERATE LONG
● 1 atypical phase
2 wks 2 wks to 1 yr lifespan
BMS
G0 (GAP ZERO) Cells Osteoclast Cardiac Muscle
● Quiescent Phase Neutrophil (2 weeks) (5 to 10 years)
(1-5 days)
● A cell goes into G0 FROM G1
Skin Fat Cells
Eosinophils (2-5 (2 weeks) (8 yrs)
G1 (GAP 1) days)
● Growth Phase Paneth cells Bones
● Considered the FIRST phase Small intestine (20 days) (25-30 yrs)
● Chromosome replication; organelles form (2-4 days)
● Cells prepare for DNA synthesis B cells CNS Neurons
Stomach (4-7 weeks) (lifetime)
● Longest period (mins → hrs)
(2-9 days)
Transient Checkpoint
Phase between G1 and S Large intestine Trachea Oocytes
 (3-4 days) (1 to 2 months) Lens Cells
(lifetime) Radiation
Cervix Osteoblast ● Radioactive materials directly on tumor ro kill
(6 days) (3 months) Skeletal Muscles ● cancer cells
RBS (lifetime) ● Pellet to the body (radioactive seed
Lung alveoli (4 mos to 60 implantation)
(8 days) days)
● or beam of radioactivity to generalized body
● Side effect:
Platelets Liver
(10 days) (6 mos to a ○ Burns→ mobility dysfunction
year)
Medical Procedure
● Laboratory Exams
Pathophysiology ○ CBC, Blood Protein Testing, Tumor
● Quality check system of the body but NOT ALL Marker Test, Tissue Biopsy,
mutations are stopped. Mammogram, Ultrasound, MRI, and CT
scan
Etiology ● Chemotherapy or Radiation
Carcinogenic factors ● Surgery
● Nonmodifiable ○ Removal of the mass or resection of
○ Genetic tissue
○ Age ● Medication
○ Gender ○ opioids - pain
● Modifiable
○ Environment Treatment
○ Chemicals Preventive Stage
○ Radiation ● Change of habits and behaviors
○ Repetitive injury ● Self examination and cancer detection tests
● Vaccines
Warning Signs
1. Changes in bowel and bladder Early Post Diagnosis Phase
2. A sore that does not heal ● Education and training
3. Unusual bleeding or discharge in women
4. Thickening lump Postoperative Phase
5. Indigestion or difficulty swallowing ● Encourage and enable clients to participate in
6. Obvious change of warts or wounds daily occupations
7. Unintended or unusual weight loss ● Special movement precautions
8. Nagging cough ● Training for equipments or techniques
9. Severe anemia
Chemotherapy and Radiation
Signs and Symptoms Acute hospitalizations
Depends on type of cancer ● For prolonged bed rest
● PAIN ● Peripheral neuropathy
● FATIGUE ● Anxiety and fear
● Burns
Chemotherapy
● Use of variety of toxic chemicals to kill cancer Rehabilitative Phase
cells within body ● Intensive (3 hrs)
● Side effects: ● Goal: restoration and support of function
○ Alopecia ● Impaired mobility
○ Peripheral neuropathy ○ Impaired sensation
○ Thrombocytopenia ○ Edema
○ Fatigue ○ Impaired vision
○ Changes in rbc ○ Impaired cognition
○ Function limiting anxiety or fear ○ Chronic fatigue
Assessment Tools
● MOntreal Cognitive Assessment
● Mini Mental State Examination
● Fatigue Severity Scale
● WHOQOL-BREF

Palliative Care
● Achieving comfort and ease of participation in
activity
● Hospice
○ Home hospice care or inpatient facilities
○ OTs with the client, caregivers,
volunteers, families for QUALITY OF
LIFE
■ Adapt the environment
■ Train caregivers to assist in daily
tasks
■ Counsel for issues related to
disease process
■ Provide assistance with issues
concerning
■ death and dying