Pathophysiology Module 7

Front 1

atherosclerosis

Back 1

loss of elasticity or irregular narrowing of artery secondary to atheroma (macrophages, lipids, and connective tissue that accumulates to make a plaque)

sclerosis means hardening and loss of resilience

Front 2

coronary arteries

Back 2

made up of intima (inner most (pliable, elastic fibers)(prone to injury), media (smooht muscles), externa (collagen)

Front 3

theory of endothelial injury

Back 3

tissue damage from high volume of circulating lipids that cause local and focal activation of endothelium (LDL), taken up into endothelium, initiates inflammatory response. activates signaling cascade (platelets adhere to endothelium through glycoprotein 1a receptors, ramp up activation-induce expression of VCam1- vascular cell adhesion molecule 1- monocytes bind and become macrophages. ALL of these accumulate in endothelial level. macrophages engulf LDL which oxidizes it by endocytosis, forms FOAM CELL (macrophages that engulf and phagocytized low density lipid)- activate inflammation, recruit more macrophages or induce smooth muscle cell migration to the area which secrete matrix proteins (collagen) to stabilize plaque. form FIBROUS CAP which makes STABLE ATHEROMA

Front 4

nuclear stress imaging

Back 4

shows you where the plaque is forming, eat something fatty before hand.

nucleotide missing after stress is indicative of coronary artery disease of heart

Front 5

coronary artery disease

Back 5

atherosclerosis, myocardial ischemia (angina), myocardial infarction

Front 6

ischemia

Back 6

strangling, decrease of blood flow to myocardium, aerobic metabolism to anaerobic, irritating to cells so initiate pain response from cardiac plexus which inervates from t1-t4 which causes the anterior chest pain

s/s chest pain, pressure, tightness, heaviness, radiates into shoulder, activates sympathetic ns, nausea/v omiting, shortness of breath.

stable myocardial ischemia- over exert themselves, exceeded supply, goes away with rest

unstable- symptoms start to increase or occur at rest

prince metal's angina- form of ischemia- spasm of vascular bed (calcium channel dysfunction) (local increase of nitric oxide)

EKG anywhere from normal to nonspecific ST changes, Twave inversions

cardiac enzymes- only reside in cardiac cells. Troponin. should not be outside cell, if it is, then there has been injury to myocardial cells. should not be elevated in ischemia.

lifestyle changes, weight loss, decrease Na and fat, less smoking, beta antagonist medication.

nitroglycerin can be given to relieve pain.

Front 7

myocardial infarction

Back 7

non ST infarction- myocardial cell death, complete cut off of coronary artery, myocardial cells die, unstable plaque, factors make plaque rupture (change in blood flow, macrophages make enzyme to attack collagen, apoptosis of plaque constituents which lead to necrotic pore) (when it ruptures there is exposure of thrombotic substances which call other thrombotic substances to area leading to clot and vasoconstriction)

ST infarction- symptoms of chest pain, no elevations in EKG, troponin is elevated

(?)

balloon or stent placement

Front 8

risk factors for coronary artery disease

Back 8

advanced age, genetics, males, smoking, hyperlipidemia, hypertension, poor dentition (cavities), vasculitis, cowasaki's disease, diet

Front 9

what is cholesterol

Back 9

breakdown of bile and sterol (from liver),

synthesized mostly in liver

acetyl coa becomes cholesterol

can also come from diet

carried in blood as VLDL and LDL and HDL

LDL should be less than 100 and HDL should be greater than 60

Front 10

myocardial infarction interventions

Back 10

supplemental oxygen, aspirin, nitroglycerine, morphine (decrease sympathetic ns), plavix (signaling mechanism for platelet congregation), glycoprotein lib/llla, fibrinolytics (break down fibrin clot), percutaneous coronary intervention (form balloon or stent or vaccuum out clot)

Front 11

12 lead EKG

Back 11

diagnostic tool for evaluation of chest pain, records electrical activity from many different planes, T wave may be depressed in ischemia or may be normal, when cells are dead ST segment elevations occur (STEMI),

Front 12

cardiomyopathy

Back 12

deterioration of myocardium resulting in change of structure and function of heart. result of ischemia or hypertension that lead to remodeling of heart.

dilated cardiomyopathy- heart is responding to ischemia or vascular disease or alcohol/ drugs (cocaine), infection. remodeling of left ventricle making it much bigger and an inneffective pump

s/s shortness of breath, dyspnea, fatigue, jugular venous dystention, pedal edema,

ace inhibitors, diuretics, angiotensin converting enzyme

hypertrophic cardiomyopathy- hypertrophied, sarcomeres become enlarged, increase in size of myocyte, causes myocardial dysarray, disruption of normal allignment of myocyte, signal to contract is disrupted. arrhythmias occur. typically genetic. dysruption in coronary artreies, decrease in blood flow and cardiac ischemia. can be asymptomatic, shortness of breath, syncope. leading cause of sudden death in young athletes

restrictive cardiomyopathy- least common, rigid and noncompliant muscles, amyloidosis, hemochromatosis, s/s: heart failure, dyspnea, jugular venous dystention, congestive hf,

diuretics, cardiac transplant,

Front 13

heart failure

Back 13

inability of heart to effectively pump,

from: myocardial infarction, hypertension, valvular disease, alcohol abuse

pathophys: alterations in myocardium cycling of calcium,

left ventricular: inadequate stroke volume pumped out, blood left over leading to increase in pressure inside left ventricle and in pulmonary vasculature leading to pulmonary edema, injection fraction of left ventricle (amount squeezed out) falls below 35%

s/s: shortness of breath, dyspnea on exertion, fatigue, orthopnea, pedal edema, pulmonary edema, nocturnal dyspnea,

BNP blood- amino acid secreteed by ventricles in response to stretch.

right ventricular failure: normally a result of left ventricular failure, decrease in pulmonary circling, COPD, overload of right ventricle due to left ventricular function, chronic hypoxia, peripheral edema in legs and arms, treatment: treat underlying cause,

Front 14

aortic stenosis

Back 14

allows for blood to enter systemic circulation. comprises of three leaflets.

narrowing of aortic valve, related to age and calcification, pneumatic fever (from streptococcus pyogenes)

exertional syncope, high indicator of death, angina, systolic murmur, ecchocardiogram shows valve dysfunction

aortic valve replacement

Front 15

mitral valve prolapse

Back 15

prevents back flow from left ventricle to left atrium,

excess in connective tissue for mitral valve

tendon like structures help support the valve leading to elongated chordae tendonae and a floppy mitral valve

risk: rheumatic fever, s. pyogenes, graves disease, connective tissue disorders,

hear murmur during systole

on exam they have s/s of heart failure

prone to endocarditis (infection of heart valve) due to change of turbulance

can have congestive heart failure

sudden death (unsure as to why)

diagnosis: echocardiogram

treatment: beta antagonist, aspirin, coumadin, mitral valve replacement

Front 16

deep vein thrombosis

Back 16

venous disease, blood clot in one main vein in any part of body

three factors related to it: virchow's triage, venous stasis, hypercoagulability, changes in blood vessel wall

Front 17

thrombus

Back 17

formation of blood clot that remains attached to vessel wall- final product of coagulation cascade

formed by aggregation of platelts, fibrin, and erythrocytes

Front 18

thromboembolism

Back 18

when thrombus breaks off

leading to possible stroke, pulmonary embolism,

Front 19

embolus

Back 19

detached traveling intervascular mass (blood clot, cholesterol emboli, air emboli, amniotic fluid, tissue, foreign body)

Front 20

venous stasis

Back 20

inefficient venous flow, stagnation in venous flow, immobility (cast or splint even), bed ridden, advanced age (comorbidities), surgery, heart problems

Front 21

endothelial damage

Back 21

can lead to DVT, trauma, ecchymosis, surgery, catheters (exposes tissue factor which initiates thrombin)

exposes tissue factor in subendothelial tissue which initiates thrombin which is involved in the coagulation cascade to convert fibrinogen to fibrin

Front 22

hypercoagulability

Back 22

can lead to DVT, malignancy, cancer, pregnancy, inherited disorders, overstimulation of inflammatory cascade (cancer), protein C or S deficiency, antiphospholipid syndrome, factor 5 latent disease

protein C deficiency: rare disorder that predisposes to DVT, protein C feedback/ block factor 5 and 8 which activates thrombin,

protein S deficiency: similar but with factor 5a and 8a

antiphospholipid syndrome: hyperimmune, lupus anticoagulant, antibeta 2 antibody, inactivate protein c/s or bind to prothrombin increasing it- hypercoagulable state

factor 5 laten: factor 5 can't be inactivated by protein c

Front 23

DVT s/s

Back 23

pain, swelling, erythema, dilated collateral veins, palpable cord (rare), phlegmasia cerulea dolens (whole leg is clotted, cyanotic looking extremity), homan's sign

dilation of colateral veins due to backflow (rare),

Front 24

d dimer test

Back 24

breakup of clot will also be there when there's a clot

dimer is fibrin degradation product

very sensitive test

not very specific other things can lead to positive result

Front 25

DVT treatment

Back 25

anticoagulant (heparin, coumadin), have to bridge heparin into coumadin (takes a while for coumadin to take effect) (inhibits vitamin K),

compression stockings,

IVC filter (wire or mesh net in inferior vena cava to collect clots)

treat underlying cause

prevention- early ambulation, etc.

Front 26

hypertension

Back 26

pressure in arterial system is elevated (bp)

requires heart to work harder

Risks: CVA, kidney disease, aneurysmal disease, etc.

Front 27

primary hypertension

Back 27

polygenic disease (multiple genes associated)

advanced age predisposes, family history, gender (male), african american, smoking, overweight, diet (high in salt, low in potassium)

Front 28

pathophysiology primary hypertension

Back 28

sympathetic ns involved leading to increase in peripheral vascular resistance, sodium retention, increase in production of renin and angiotensin

Sympatheticc ns is stimulated by smoking, diet, genetics, obesity

Front 29

renin angiotensin system

Back 29

angiotensinogen is broken down by renin into angiotensin I where ACE converts it to Angiotensin II in the lungs, which interacts with kidney to promote aldosterone secretion which promotes sodium retention and vascular/ cardiac remodeling,

Front 30

obesity

Back 30

overstimulation of sympathetic NS and reninangiotensinaldosterone system.

release of adipokine (type of cytokine called leptin- proinflammatory, overstimulates SNS/ RAAS- released by fat cells, acts on hypothalamus to inhibit appetite) that is produced and released by fat cells which overstimulates RAAS system,

secondary effects are proinflammatory

Front 31

secondary hypertension

Back 31

renal disease, hyperthyroidism, pregnancy, epinephrine, norepinephrine, tumors in gastroingtestinal tract,

s/s no symptoms until end organ dysfunction, headaches, vertigo, tinnitus, retinopathy, chest pain, congestive heart failure, renal disease, hemorhagic stroke,

diagnose: two readings, two minutes apart on two seperate occassions that are above 140/90

elevated creatinin levels

EKG: nonspecific ST to T changes

enlargement of cavities in heart

Front 32

aortic aneurysm

Back 32

constant stress on arterial wall (hypertension), risk factors: atherosclerosis, infections (syphillis),

Front 33

collagen diseases

Back 33

risk factor for aneurysmal disease, collagen deposition and synthesis,

marfan's disease: fibrolin 1 which is involved in elastic fibers and connective tissues, characterized by tall, thin, long extremities, long flexible fingers, arteries are at risk for an aneurysm and aortic dissection which is when blood dissects layers of arteries,

Front 34

signs and symptoms of aortic dissection

Back 34

assymptomatic until it ruptures

screening can be done if there is a family history

dysphagia (trouble swallowing), short of breath, abdominal pain,

beta blockers given

Front 35

paracarditis

Back 35

paracardium is fibrous sac around heart that has fluid inbetween layers which allows the layers to slide over each other

inflammation of paracardium

seen in lupus, seen after MI (dressler's syndrome), uremia (crystals) (end stage renal disease), cancer (radiation irritates paracardium), viral infection, bacterial infection

pleuritic chest pain (worse when they take a deep breath), sharp chest pain that gets better when leaning forward, fever, dry nonproductive cough, fatigue, myalgia, arthralgia, pleuritic chest pain, friction rub

ST elevation, PR interval depression.