PATHO FINALS CUMULATIVE STUDY GUIDE

week 1-15

what is pathophysiology and what factors does it contain?

study of abnormal changes in body that are the cause of disease process

contains: etiology, pathogenesis, manifestations, treatment

what is etiology and what are the classifications and its meaning?

study of cause

1. idiopathic: cause unknown

2. iatrogenic: cause relating to unwanted treatment (i.e. chemo)

3. congenital

4. infectious

5. multifactorial

what is pathogenesis?

development/evolution of disease

sign and symptom, which is subjective and which is objective?

sign: objective (something that is observed)

symptom: subjective (feeling of abnormality)

what are the stages of diseases?

1. exposure

2. latent period

3. prodromal period

4. illness

5. decline

6. convalescence

what is reliability when it comes to diagnostic assessments?

what is validity? what is predictive value?

reliability: test’s ability to give same result repeatedly

validity: test’s ability to reflect on true value intended

predictive value: test’s ability to differentiate between presence/absence of person’s condition (i.e. pregnancy test)

• sensitivity: true + rate

• specificity: true - rate

what is epidemiology and what are the types?

study of patterns of disease involving populations

type:

• endemic (particular region - low spread)

• epidemic (spread rapid thru large population)

• pandemic (worldwide)

what are the levels of prevention?

1. primary (health & risk promotion) (i.e. vaccinations)

2. secondary (screening of risk of individual - early prevention)

3. tertiary (rehab, prevention of complication, improve quality of life)

describe the terms below:

1. homeostasis

2. allostasis

3. stress

4. stressors

5. distress

6. allostatic overload

1. state in which body system is in balance at ideal

2. ability to adapt to challenges (body undergoes adjustments to establish homeostasis)

3. tension of body/mind

4. agents that produce stress and endanger homeostasis

5. inability to cope w/ stressors

6. inadequate adaptation that lead to disease/death

what is general adaptation syndrome (GAS) and what are the stages?

stage that describes physiological changes body goes through when under stress

stages:

1. alarm reaction: fight or flight response due to stressful stimulus

2. resistance (adaptation): increase activity of nervous system and return to homeostasis

3. exhaustion: body can no longer return to homeostasis

what hormones do the body releases in respond to stress? what are there physiological effects of each hormone?

catecholamines:

• norepinephrine: constrict blood vessel & raise BP

• epinephrine: enhance muscle contractility

adrenocortical steroids:

• cortisol: stress hormone (anti-inflammatory, energy burst)

• aldosterone: promote absorption of sodium and water in kidney

endorphins:

• oxytocin: produces during childbirth/sex/lactation (calming effect)

• cytokines: secreted during stress response

what organs are affected during stress?

Stress generally affects all systems of the body including cardiovascular, respiratory, endocrine, gastrointestinal, nervous, muscular, and reproductive systems

what do these terms mean?

1. perfusion

2. ischemia

3. hypoxia

1. delivery of oxygen and nutrients

2. reduce blood flow (leads to hypoxia) (injures cells faster due to metabolic waste)

3. low levels of O2 in tissue (results from ischemia) (cause power failure in cell)

what is the cause(s) of cellular injury?

most common is ischemia

other causes:

• hypoxia

• nutrition

• infections

• chemical injuries

• physical injuries

• radiation injuries

what are some reversible cell injuries?

hydrophic swelling, intracellular cell injury, cellular adaptation

what are some irreversible cell injuries?

necrosis, apoptosis, cellular aging

what is hydropic swelling?

intracellular edema

what is intracellular cell injury and what are some example?

excess accumulation of substance in cell (fat, glucose, protein)

examples: fatty liver, gaucher disease, pigment

what is cellular adaptation and what are the different types?

definition: cells adapting to ongoing stressors

types:

1. atrophy: cells shrink and functionality reduces

2. hypertrophy: cell mass increase and augments functionality (takes up space)

3. hyperplasia: increase in functional capacity r/t increase cell number (i.e. callus)

4. metaplasia: conversion of one cell type to another

5. dysplasia: disorganized appearance of cell

what are the 4 types of necrosis?

what is gangrene? (describe what dry, wet, gas gangrene are)

what does gangrene result from?

4 types:

1. coagulative

2. liquefactive

3. fat necrosis

4. caseous necrosis

gangrene: necrosis in large area of tissue which results from ischemia

• dry: formation of coagulative necrosis (dry, black, wrinkled)

• wet: liquefactive necrosis (internal organs and can be fatal?

• gas: from infection of necrosis by bacteria (bubble)

what is apoptosis and what can trigger it?

definition: type of cell death (normal for cell growth and no inflammation)

triggers:

• withdrawal of survival that suppresses apoptotic pathway

• extracellular signal that bind to cell and trigger death cascade

• intrinsic pathway: sever cell damage leads to increase in protein which can cause own cell death

what is the cause of cellular aging?

what are theories about cellular aging?

cause: decline in proliferation and exposure to damaging environmental and metabolic factors

theories:

• DNA damage accumulates overtime

• stem cell decline

• free radical theory (accumulated cell damage)

• programmed senescence theory (finite # of cellular replication)

what is somatic death? general features of it? what enzyme is released during somatic death?

definition: death of entire organism

features: cessation of respiration and heartbeat, stiffened muscle due to calcium in body (riggor 0-6hrs, flaccid 24-48hr)

enzyme: lytic enzyme in body tissues

Which type of irreversible cell injury initiates an

inflammatory response?

A. Apoptosis

B. Necrosis

C. Hydropic swelling

D. Intracellular accumulations

B. Necrosis

what are the layers of the skin and the function of the skin?

layer: epidermis, dermis, hypodermis

function:

• protective barrier for internal organs

• regulate temperature

• sense change in temp., pressure, pain

• excrete fluid and electrolytes

• store fat

• synthesizes vitamin D

• provide site of drug absorption

what are the age related changes when it comes to the integumentary (skin)?

• epidermis thins

• cell reproduce more slowly

• dermis less elastic (decrease elastin)

• decrease SQ fat

• hair loss (thinning in males)

• loss of melanocytes (hair is grey/white)

• dull, brittle, hard, thick nails

• increase longitudinal striations that cause splitting in nails

• decrease sebum secretion and sebaceous glands

• protective function, sensory nerves, blood vessels decline

• skin easily injured and heals slowly

what are the types of skin lesions?

• macule: flat discolored

• patch: elevated pimple like bump

• papule: elevated solid (1cm)

• plaque: plateu-like, elevated, <1cm

• vesicle: small fluid filled blister

• bulla: big fluid filled blister

• pustule: small pus filled

what do these terms mean?

1. excoriation

2. lichenification

3. scar

1. repetitive itching of skin leading to lesion

2. skin becomes thick and leathery

3. left over mark thats not completely healed

what are the distributions of skin lesions?

• diffuse

• localized

• discrete (separate; not joined)

• confluent (multiple small macules/papules that forms patches in net-like pattern)

• linear

what are some infectious and bacterial skin conditions? (explain each one and treatments for it)

1. impetigo (staphylococci): starts as red itchy sore and heals as crusty honey colored scab

   • Tx: antibiotic (mupirocin)

2. syphilis: primary stage on tongue then moves to palms and rash on back

   • Tx: IM antibiotic (penicillin)

3. cutaneous abscess: break in skin

   • Tx: drainage & oral antibiotic

what are some infectious and viral skin conditions? (explain each one and treatments for it)

1. verrucae: warts caused by human papillomavirus

2. herpes simplex: virus causing contagious sores

   • Tx: antiviral for severity & recurrence

3. chicken pox: contagious itchy blister like rash on skin

   • Tx: childhood vaccine

4. herpes zoster: also known as shingles and those w chicken pox can develop this

   • Tx: vaccine and antiviral

what are some infectious and fungal skin conditions? (explain each one and treatments for it)

1. tinea corporis (neck, arms, legs)

2. tinea cruris (groin)

3. tinea pedis (foot)

4. tinea unguis (toenail, fingernail)

Tx: topical anti-fungal (clotrimazole)

what are some examples of skin preparation drugs?

isopropyl alcohol, iodine (betanide), chlorhexidine

what are some topical antipruritic drugs?

antihistamines

corticosteroids

what is pressure injury?

what are the risk, cause, and stages?

what are the treatments, prevention, and what tool used to assess risk?

definition: localized areas of necrosis resulting from ischemia r/t prolonged pressure

risk: poor nutrition, aging, immobility, sensory loss, incontinence

cause: pressure overtime, shear/friction, moisture, poor nutrition, poor circulation

stages:

1. stage 1: non-blanchable eythema

2. stage 2: partial thickness loss

3. stage 3: full thickness loss

4. stage 4: full thickness loss (able to see muscle, tendon, bone, cartilage)

5. unstageable: eschar (black) w/ slough (yellow) (undermining and tunneling present)

6. deep tissue injury: maroon/purple discoloration with either skin intact or not

Tx: skin dry & clean, fluid & protein, vitamin supplement, avoid infection

prevention: reposition, area clean, bed linen clean & no wrinkle, pillow

tool: braden scale (sensory perception, activity, mobility, moisture, nutrition, friction/shear)

what are some wound care medications and explain each one? what are the adverse effects of each?

vitamin C, zinc, topical such as:

• dakin’s solution: bleach + baking soda that treat & prevent tissue infection

  • adverse effects: redness, irritation, pain, swelling of treated skin

• cadexomer iodine: clean wound and promote healing; remove slough & debris

  • adverse effect: allergic reaction

• collagenase: debriding agent; remove necrotic tissue (may increase risk of serious infection)

  • adverse effect: pain, burning, redness, irritation

• medihoney: clean & promote healing; reduce inflammation; promote moist environment and protective barrier

  • adverse effect: none

• silvadine: treat/prevent burn

  • adverse effect: pain, burning, itch

everything about the bone:

1. how many are there?

2. whats it’s function?

3. shapes and classification?

4. components?

5. what hormones influences bone growth?

6. what does absence of bone stress lead to?

7. how does modeling/remodeling happen? (sequence)

1. 206

2. storage, protection, stability, stem cells

3. long, short, flat, irregular, sesamoid

4. mineral (Ca & phosphorus), water, fibrocytes, osteocytes

5. calcitonin, PTH, estrogen

6. demineralization

7. hematoma form → fibrocartilage form → callous form → ossification → remodel

what is wolff’s law?

bone in healthy person will adapt to the loads of work under which it’s placed (load bearing activity activates osteoblasts which increases bone density and lack of activity decrease is)

what are the three connective tissues and explain?

how does the joint respond to injury/stress?

cartilage (ends of bones - cushion)

tendons (muscle to one - flex)

ligaments (bone to bone - stabilize)

joints (point of contact between bones; responds to stress by cartilage becoming thin and surface irregular/rough and lead to swelling of joint cavity and lead to pain/stiffness)

what are the changes in older adults regarding the muscular system?

• size and number of muscle mass decrease

• muscle less responsive to neurotransmitters and hormones

• decrease muscle strength and endurance

what are the changes in older adults regarding the skeletal system?

• bone breakdown

• synovial fluid thickens

• bone mass decrease

• kyphosis

• narrowing of disk space (decrease height)

what are s/s and tx of muscle and connective tissue injuries?

explain for each (cartilage, ligament, muscle)

cartilage

• s/s: pain, swelling, crepitus, stiff, locking

• tx: NSAIDs, surgery, glucosamine

ligament

• s/s: “snap,” pain, limited ROM, wt. bearing intolerance

• tx: brace, RICE, NSAIDs, PT, surgery

muscle

• s/s: pain, erythema, limited ROM, spasm, swell, weakness

• tx: RICE, NSAIDs

what are the types of fractures?

1. nondisplaced (remain at alignment)

2. displaced (fracture separate and unaligned)

3. simple (skin not broken)

4. compound (skin broken)

5. transverse (straight line)

6. spiral (twisting motion)

7. longitudinal (along axis)

8. oblique (angle)

9. depressed (below level of bone surface)

10. comminuted (fracture line + fragment)

11. impacted (drives fragments to each other)

12. complete (clean break)

13. incomplete (break crack - “greenstick”)

14. pelvic fx (heal w/o complications; shortening ht., weak difficulty, pain sitting down)

what are some interventions, procedures, and assessment done w bone injuries?

interventions: ice & elevate, immobilize, meds., surgery

procedure: internal fixation, external fixation, bone graft (auto-: self, allo-: deceased, xeno-: non-human, synthetic)

circulation assessment: pain, pulse, pallor, paresthesia, paralysis

carpel tunnel

(definition, s/s, and tx)

narrow passageway of ligaments and bone surrounding median nerve at base of hand

s/s: weakness, pain, burn, numb, tingle (worst at AM & PM)

tx: rest, NSAIDS, steroids, surgery

compartment syndrome

(definition, s/s, and tx)

soft tissue injury and swelling due to compartment size decrease

tx: reduce pressure and swelling, surgery

DVT

(definition, s/s, and tx)

blood clot forming within large vessel r/t decrease circulation

s/s: erythema, edema

tx: anticoagulants (heparin & warfarin), thrombectomy, greenfield filter

pulmonary embolism

(definition, s/s, and tx)

foreign substance obstructing circulation in lung tissue

s/s: chest pain, hypoxemia, tachycardia

tx: ventilatory support, anticoag. (heparin), greenfield filter

fat emboli

(definition, s/s, and tx)

fat particles release into blood stream and lodge in lungs

s/s: shortness of breath, tachypnea, rash, altered mental status

tx: ventilatory support

osetomyelitis

(definition, s/s, and tx)

infection of bone

s/s: acute pain in bone, tender, heat, swell, erythema, fever, chills, drainage

tx: long term antibiotic, surgery

osetoporosis

(definition, s/s, and tx)

metabolic disease of skeleton where rate of resorption is greater than bone formation

s/s: short ht., muscle waste, back muscle spasm, difficulty bending over, humpback

tx: exercise, heat, calcium and vit. D supplement, bisphosphonate, PTH

paget’s disease

(definition, s/s, and tx)

idiopathic dysfunctional bone formation

s/s: pain, fracture, headaches, kyphosis, deafness, misshapen bone, increase ALP level

tx: bisphosphonate, calcitonin, monitor ALP

osteomalacia

(definition, s/s, and tx)

bone growth due to vitamin deficiency due to lack of building materials

s/s: bone pain, fracture, muscle weakness, low Ca

tx: vit. D, phosphate, calcium supplements

what is rheumatism?

disease marked by inflammation

osteoarthritis

(definition, s/s, tx)

joint disorder associated w aging wear and tear from repetitive stress

s/s: crepitus w/ movement, bony enlargement, spurs, coolness, DIP & PIP nodes

tx: PT, wt. reduction, NSAID, corticosteroids, assistive device

rheumatoid arthritis

(definition, labs, s/s, tx)

autoimmune inflammatory disease that lead to immune cells and production of antibody RF and infiltration of synovium

labs: RF present, ESR & WBC elevated

s/s: pain improves w/ activity, warm erythema, malaise, fatigue, sjogren syndrome

tx: NSAID, corticosteroids, DMARD, TNF, surgery

lupus (SLE)

(definition, labs, s/s, tx)

inflammatory autoimmune disorder of connective tissue (immune injury to basement membrane)

labs: elevated ANA & ESR, decrease C3, C4, WBC, PLT and anemia

s/s: butterfly rash, photophobia, renal insufficiency

tx: NSAIDs, immunosuppresents, antimalarials, methotrexate, glucorticoids

scleroderma

(definition, labs, s/s, tx)

inflammatory connective tissue disease which affects skin, blood vessel, synovium, organ

labs: ANA elevation

s/s: polyarthritis in small joints, edema of finger/hand/feet, limited ROM, CREST, atrophy

tx: vasodilator, anatcids, PPI, ACE inhibitor, prostaglandins

ankylosing spondylitis

(definition, s/s, tx)

fusion of inflamed vertebrae

s/s: low back pain relieved w/ activity, severe s/s upon waking, limited ROM in lower back

tx: stretching, ROM exercise, NSAIDS, corticosteroids, methotrexate, joint replacement

psoriatic arthritis

(definition, s/s, tx, five types)

inflammatory autoimmune disease

s/s: patches of thick red skin covered by white/silver scales, stiffness

tx: corticosteroids, NSAID, immunosuppressants, TNF

five types:

1. symmetric (all joints)

2. asymmetric (not all joints)

3. distal (ends of fingers/toes)

4. spondylitis (spine and neck)

5. mutilans (severe deformities of small joints in fingers and toes)

gout

(definition, cause, phases, s/s, tx)

limited excretion of uric acid by kidneys (urate acids buildup in blood stream and deposit in joints)

cause: genetic, renal insufficiency, diet high in purine

phases:

1. asymptomatic

2. gouty arthritis

3. complicated arthritis

4. tophaceous arthritis

s/s: warm, erythema, tender

tx: may resolve within 10-14 days, elevate, immobilize, cold pack, colchicine

fibromyalgia

(definition, s/s, tx)

chronic widespread muscle stiffness, fatigue, and tender point pain that lasts 3months (idiopathic & no diagnostic)

s/s: pain, tenderness, muscle fatigue, stiffness

tx: exercise, duloxetine, milnacipren, pregabalin, gabapentin

lyme disease

(definition, s/s, tx)

caused by borrelia burgorferri bacteria carried by deer tick

s/s: flulike symptom, erythema migrans (rash at site), stiff neck, arthritis, nerve pain, facial palsy

tx: oral or IV antibiotic

rheumatic fever

(definition, s/s, tx)

group A streptococcal infection

s/s: fever, polyarthritis, muscle spasm, eythema, carditis

tx: antibiotic, NSAID, corticosteroids

what are the mechanism of action of NSAIDs

inhibit leukotriene and prostaglandin and blocks chemical activity of enzyme COX that cause inflammatory response

hemostasis:

1. what is it?

2. what does it involve? (organs)

3. what essentials elements are involved?

4. whats the process?

5. what are the stages?

1. arrest of bleeding/prevention of blood loss after blood vessel injury (body allows blood flow while repairing the wall)

2. vessel wall, circulating PLTs, plasma protein, liver, bone marrow, kidney

3. calcium and vitamin K

4. injury → vascular spasm → PLT formation → coagulation

5. primary, secondary, and final stage

explain the stages of hemostasis (primary, secondary, final stage)

1. primary: exposure to collagen → vasoconstrictions to minimize blood loss → release of TF → PLT activate → forms PLT plug

2. secondary: clotting factor activates → forms insoluble fibrin strands

3. final: clot retraction → tissue buildups → plasmin activates to dissolve clot (increase of thrombin levels → ingests fibrin → dissolve)

what are the two components of blood?

PLT and insoluble fibrin strands

whats the role of TF and vWF?

TF: activates due to exposed blood/disruption in vessel wall

vWF: released due to injury to blood vessel and joins PLTs together and promote production of clotting factors

Platelets:

1. where is it produced?

2. function/role?

3. how much in % in circulation?

4. whats the normal levels?

5. resting vs activated (explain the difference of state of PLT during rest and activation)

1. bone marrow

2. self adhere in presence of vWF and form mechanical plug

3. 75% in circulation and 25% stored in spleen and liver

4. 150,000 - 400,000

5. resting: spends more time free floating in resting state

   activated: process: adhesion (PLT - vessel wall) → aggregation (PLT - PLT) → degranulation

what organ produces coagulation factors?

liver and majority are in inactive form

what drives the coagulation cascade? what are the two pathways?

clotting factors secreted by liver, PLT, endothelium

pathways:

1. intrinsic: initiated by exposed collagen

2. extrinsic: initiated by release of TF

bleeding:

1. what are the sources of active bleeding

2. what are some nursing considerations?

1. arteries: spurting & bright red

   veins: steady flow & dark red

   capillaries: slow even flow

2. education (any activities that causes bleeding), fall prevention, avoid IM injections, avoid prolonged constrictive item, and manual BP

what are the lab findings and their normal range?

CBC: identify anemia (RBC, WBC, HCT, HGB)

PLT: # of PLTs (15-40)

PT/INR: extrinsic pathway (10-14)

PTT: intrinsic pathway (33-45)

Fibrinogen: common pathway (200-400)

FDP: (<3)

D-Dimer: fibrinolysis (<200)

thromboctopenia

(define, lab values, tx)

lack of PLT caused by inadequate PLT production, hyperactive PLT destruction, dilution (low PLT to circulating volume), excessive splenic pooling

lab values: low PLT, normal PTT, PT/INR

Tx: antimicrobials, splenectomy, PLT transfusion

hemophilia

(define, lab values, tx)

blood does not clot properly due to decrease ability to form fibrin strands

lab values: elevated PTT, normal PLT, PT/INR

Tx: factor VIII/IX replacement, frozen plasma (FFP), cryo 1

vonwillebrand disease

(define, lab values, tx)

lack of vWF (PLT won’t be sticky w/o vWF) and impacts primary hemostasis

lab values: elevated PTT, normal PT/INR, PLT

Tx: DDAVP & cryo

vitamin K deficiency

(define, lab values, tx)

needed for liver to synthesize coagulation factors

lab values: elevated PT/INR, normal PLT, PTT

Tx: vit. K replacement, FFP

Disseminated intravascular coagulation (DIC)

(define, lab values, tx)

abnormal clotting and bleeding

lab values: elevated PT/INR, PTT, FDP/FSP & low PLT

Tx: transfuse FFP, cryo, PLT and anticoagulants

liver disease

(define, lab values, tx)

large number of clotting factor produced in liver

lab values: elevated PTT, PT/INR and low PLT

Tx: Vit k supplement and transfuse FFP, PLT, cryo

thrombosis

1. definition

2. what can it lead to?

3. what is the cause?

1. blood clot reduces blood flow through affected vessel

2. ischemia, necrosis, MI, PE, ATN

3. Virchow’s triad:

   1. abnormal blood flow

   2. hyper coagulability

   3. injury to vessel wall (needle that exposes collagen which activates PLT and clot formation happens)

catheter thrombosis

(definition, s/s, tx)

thrombosis due to catheter

s/s: sluggish flow of catheter, edema, erythema, tender, increase WBC

tx: remove line, tPA

atherosclerosis

(definition, tx, risk)

artery stiffens and narrows due to buildup of plaque

tx: diet, exercise, control HTN & cholesterol, ASA, Plavix

risk: stroke and heart attack

acute coronary syndrome

(definition, s/s, tx)

blockage and narrowing coronary vessel that reduce blood flow

s/s: angina, jaw pain, diaphoresis, anxiety, ECG changes, sudden cardiac death

tx: vasodilator, ASA, plavix, anticoag., tPA, bypass graft, cardiac cath

ischemic stroke

(definition, tx, sign)

impairment of cerebral circulation in one or more blood vessel supporting the brain

tx: tPA, TNK, embolectomy

signs: B.E.F.A.S.T. (balance, eyes, face, arms, speech, time)

what is the difference between ischemic and hemorrhagic?

ischemic: blood clot blocks blood flow

hemorrhagic: artery rupture and causes bleeding around brain

atrial fibrillation

(definition, what can it lead to, tx)

absence of coordinated and rhythmic atrial contractions

leads to: stasis of blood and clot formation

tx: ablation, MAZE, peacemaker, anticoags., antirrhythmics

what is hematopoiesis?

what are the two stages?

formation of blood cellular components

stages: proliferation and maturation (RBC, PLT, WBC)

RBC

1. function

2. lifespan

3. manufactured where?

4. made up of what?

1. deliver O2 to tissues via hemoglobin chain

2. 120 days

3. bone marrow by stem cells

4. hemoglobin

erythropoiesis

1. define

2. how is it stimulated?

3. what does it require?

4. stages

1. process of production of RBC

2. decrease in O2 which is detected by kidneys which release erythropoietin

3. Vit. B12, iron, folic acid

4. stage:

   1. kidney secrete erythropoietin

   2. pro erythroblast into erythroblast (huge nucleus)

   3. turns into normoblast (nucleus shrinks)

   4. reticulocyte (nucleus ejected & matures)

RBC demise, what is it?

spleen removes old/ages/dead RBC and broken down into iron and bilirubin which then recycled to make new RBC (stored in liver) or secreted as waste

anemia

1. define

2. insufficient production of what?

3. what does it lead to?

4. s/s?

1. lack of mature healthy RBC (insufficient delivery of O2)

2. iron, folic acid, B12

3. increase O2 demand

4. fatigue, tachycardia, hypotension, pallor, lightheadedness, enlarged spleen

iron deficiency anemia

(define, s/s, tx)

lack of iron and leads to small RBCs that are unable to carry O2

s/s: s/s of anemia, PICA, koilonchychias, blue sclera

tx: diet (citrus but no tea since it can impair iron absorption)

folic acid anemia

(define, s/s, tx)

lack of folic acid crucial to proper brain function and fetal development

s/s: depression, forgetfulness, ulceration of cheek and tongue, fissure on mouth

tx: folate supplement

vitamin B12 anemia

(define, s/s, tx)

lack of B12 where RBC can’t synthesize and lead to large RBC with poor O2 carrying capacity

s/s: brain fog, mood swing, muscle weakness, depression, dementia

tx: B12 supplement

aplastic anemia

(define, s/s, tx)

lack of healthy material in bone marrow caused by toxic/radiant injury

s/s: low PLT and WBC

tx: blood transfusion, bone marrow transplant

chronic renal failure

(define, s/s, tx)

impaired renal endocrine function resulting in decreased erythropoietin production

s/s: low EPO, general s/s of anemia

tx: epogen or aranesp

hemorrhagic anemia

(define, acute vs chronic, s/s, tx)

lack of total circulating blood volume

acute: large volume in short amount of time

chronic: short volume in long amount of time

s/s: low RBC, HGB/HCT

tx: transfusion

hemolyctic anemia

(define, s/s, tx)

RBC are being destroyed faster than they are replaced

s/s: low RBX, HGB/HCT, jaundice, splenomegaly, dark/red blood urine

tx: transfusion

sickle cell anemia

(define, s/s, tx)

misshaped RBC leading to RBC destruction

s/s: jaundice, splenomegaly, stunted growth

tx: voxelotor, hyrocyurea, folic acid supplement, bone marrow transplant, gene therapy