Pathb2: Heart Ii Ihd

Front 1

Dark red-blue mottling, gross appearance 12-24 hrs post MI, stagnant blood

Back 1

-

Front 2

yellow pallor due to coagulative necrosis, occurs in the first week post MI acute inflammation (neuts=>macs), note the risk of fibrinous pericarditis

Back 2

-

Front 3

Wavy fibers and coagulative necrosis within 1 day of infarct

Back 3

-

Front 4

Papillary rupture within 1 week post MI, complication of macrphoage degradation of structural components during the inflammation stage

Back 4

-

Front 5

define IHD

Back 5

imbalance between supply and demand for oyxgen and nutrients and removal of metabolites, ischemia worse than hypoxia

Front 6

main cause of IHD (90%)

Back 6

reduced coronary blood flow due to atherosclerotic narrowing (fixed plaque, acute plaque change, thrmobosis, vasospasm)

Front 7

Describe the degree of stenosis required to cause ischemia with exercerise (stable angina) and at rest (unstable angina)?

Back 7

with exercise-70%, at rest 90%;

Front 8

describe acute plaque change

Back 8

unpredictable abruput converstion of stable plaque to an unstable atherothrombic lesion that results in ischemia. Rupture/fissure/ ulceration exposes underling thrombogenic substnaces, hemorrhage into atheroma expands the plaque and narrows the vesseel lumen further. results in acute coronary syndromes: MI, unstable angina, sudden cardiac death

Front 9

Causes of acute plaque change (intrinsic and extrinsic)

Back 9

intrinsic-composition of the plaque(large area of foam cells/lipid with thin cap), most dangerous lesions are the moderately stenoti lipid rich atheromas, abundant inflammation, few SMCs. Extrinsic-adrenergic stimulation -upon awakening, emotional

Front 10

outcome of coronary thrombosis total vs. incomplete occulsion

Back 10

total-acute transmural MI or sudden death, incomplete=unstable angina, acute subendocardial infarct, sudden death, emboli

Front 11

Causes of vasoconstriciton leading to severe but transient reduction in coronary blood flow

Back 11

adrenergic agonist, locally released platelet contents, endothelial dysfxn, mast cell mediators

Front 12

four syndromes of IHD

Back 12

angina, MI, CIHD, sudden cardiac death

Front 13

define angina

Back 13

paroxysmal and recurrent attacks of chest pain caused by transient myocardial ischemia 15 seconds to 15 minutes

Front 14

three patterns of angina

Back 14

stable, prinzmetal, unstable

Front 15

cause of stable angina

Back 15

produces by physical activity or emotinoal excitement, stenosis of coronary artery 70-90%, subendocardial ischemia, reversible injury

Front 16

cause of prinzmetal angina

Back 16

coronary vasospasm at rest, reverislbe injury, transmural ischemia

Front 17

cause of unstable angina

Back 17

>90% stenosis, or acute plaque change=> thrombosis w/ incomplete occlusion, often prodrome of MI, reverisble injury, subendocardial ischemia

Front 18

risk factors for MI

Back 18

M>F, age, atherosclerosis (HTN, smoking, DM, increased cholesterol/ lipids)

Front 19

Pathogenesis of MI

Back 19

90%=acute plaque change resulting in thrombisis and emoblism of coronary a., 10% vasospasm, emboli, or unexplained

Front 20

Transmural vs. subendocardial vessel distribution, degree of obstruciton, ECG

Back 20

transmural-confined to 1 vessel districution, complete obstruction, ST elevation; subendocardial-non-occlusive thrombus or hypotension, extends laterally beoynd 1 vessel, ST depression

Front 21

timeline of myocardial response to ischemia

Back 21

60sec- loss of contractility, 20-40 min-irreversible damage

Front 22

frequency of arteries occluded in MI

Back 22

LAD-40-50%> RCA-30-40%> LCA-15-20%

Front 23

pattern of ischemia with global hypotension

Back 23

circumfrential subendocardial

Front 24

describe the progression of gross myocardial findings post MI

Back 24

<4 hrs=none. 1 day=dark red-blue mottling, post 1 day- 1 week=yellow pallor , post 1 week- 1 month=red boarder at edge of infarct=>white scar (hint: 1 day 1 week 1 month, necrosis, inflammation, healing0

Front 25

describe the progression of microscopic myocardial findings post MI

Back 25

<4hrs=none, 1 day=coagulative necrosis,contraction bands, 1day-1 week=marcophages, 1 week-1 month=granulation tissue=>fibrosis (hint: 1 day, 1 week, 1 month, necrosis, inflammation, healing)

Front 26

describe the progression of clinical complication you would expect post MI

Back 26

<4 hrs=cardiogenic shock, CHF, arrythmia, 1 day=arrhythmia, 1day-1 week=fibrinous pericarditis-rupture, months=aneurysm, mural thrombis, Dressler's syndrome

Front 27

when in the course of an MI is arrhthmia a risk

Back 27

early, less than 1 day

Front 28

When in the course of an MI is fibrinous pericarditis a possible complication

Back 28

earnly in the inflammation phase (1 day-1 week), only transmural infacrt, note chest pain w/ friction rub

Front 29

when in the course of an MI is rupture a risk. What can rupture

Back 29

Late in the inflammation phase (1day-1 week), macropahges degrade structural components-ventricular free wall-tamponade, IV septum-shunt, Papillary m.-MV insufficiency (if RCA infarct)

Front 30

when in the couse of an infacrt is aneurysm ,mural thrombus, and Dressler's syndrome a risk

Back 30

post healing phase, months,

Front 31

what is dressler's syndrome

Back 31

occurs months after MI, rate autoimmune reaction due to Ab's angainst pericardial antigens

Front 32

Coagulative necrosis would be found when after an MI

Back 32

4hrs-1 day, note loss of myocyte nuclei, wavy fibers, contraction bands

Front 33

Neutrophils would be present in a sample of myocardium when after an MI

Back 33

early in the inflammation phase (1 week-1 day), note the risk for fibrinous pericarditis

Front 34

macrophages would be present in a sample of myocardium when after an MI

Back 34

late in the inflammation phase (1day-1 week), note the risk of rupture of ventricular free wal, TV septum, or papillary m.

Front 35

Granulation tissue would be present in a sample of myocardium when after an MI

Back 35

during the healing phase (1 week-1 month), note plump fibroblasts, collagen and vessels

Front 36

A white scar and fibrosis would be present in the myocardium when after an MI

Back 36

post healing phase (1week-1 month) note the risk of aneurysm, mural thrombus, Dresseler's syndrome

Front 37

wavy fibers would be present when after an MI

Back 37

acute inflamation phate less than 1 day post

Front 38

describe reperfusion injury

Back 38

reperfusion prevents necrosis if occurs in less than 20 min but can lead t ohemorrhage into infarcted tissue, contraction bands, free radiacal release and microvascular injry, platelet and complement activation

Front 39

Clincial signs/ sxs of MI

Back 39

severe crushing substernal chest pain that radiates into the l. arm, neck, jaw, epigastrium, last several minutes to hours, no relief by NG, rapid weak pusle, diaphoresis, dyspnea

Front 40

Acute and long term MI prognosis factors

Back 40

acute-depends on infarct size, site, extent of wall penetration, Long term-depneds on quality of LV fxn and extent of vascular obstruction