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Y2 - Path - Exam 4 > 4: Ischemic heart disease > Flashcards

4: Ischemic heart disease Flashcards

(56 cards)

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1
Q

2 key causes of Ischemic heart diease?

Which of the two accounts for the majority of the cases?

A
  • Reduced Perfusion (*>90% of cases due to obstructive atherosclerotic lesions in coronary arteries)
  • Increased myocardial demand
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2
Q

Which pathological cause of ischemic heart disease is associated w/ the following causes?

  • Coronary emboli, myocardial vessel inflammation, spasm
  • Hypoxemia, systemic hypotension
A

These cause REDUCED PERFUSION –> resulting in ischemic heart disease

(recall: >90% of cases due to obstructive atherosclerotic lesions in coronary arteries)

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3
Q

Which pathological cause of ischemic heart disease is associated w/ the following causes?

  • Due to increased contractility, HR, ventricular wall tension/thickness (myocardial hypertrophy)
A

Due to increased myocardial demand

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4
Q

Percentage occlusion of coronary artery assoc with the 3 stages of ischemic disease?

  1. asymptomatic
  2. stable angina
  3. unstable angina
A
  1. asymptomatic - <70% occlusion
  2. stable angina - >70% occlusion
  3. unstable angina - >90% occlusion
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5
Q

four key clinical presentations of Ischemic heart disease?

A
  • angina pectoris (chest pain)
  • congestive hear failure
  • myocardial infarction
  • sudden cardiac death
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6
Q

definition: intermittent chest pain caused by transient, reversible myocardial ischemia

(15 sec-15 min)

A

angina pectoris

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7
Q

what is the pathological cause of Angina (chest pain)?

A

pain is a consequence of the ischemia-induced release of adenosine & bradykinin

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8
Q

type of ischemic heart disease assoc with the following description?

  • Predictable chest pain associated with exertion
  • Crushing/squeezing, substernal chest pain radiating down left arm/jaw
  • Pain relieved by rest, drugs (nitoglycerin)
A

Typical/stable ischemic heart disease– most common

  • reversible w/ medications (nitroglycerin)
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9
Q

type of ischemic heart disease assoc with the following description?

  • Coronary artery spasm, can affect normal vessels
  • Responds to vasodilators (relieved/reversible w/ medications)
A

Prinzmetal/variant – uncommon

(Responds to vasodilators (relieved/reversible w/ medications))

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10
Q

type of ischemic heart disease assoc with the following description?

  • increasingly frequent pain, occurs at rest
A

Unstable ischemic heart disease

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11
Q

type of ischemic heart disease assoc with the following description?

  • necrosis of heart muscle due to ischemia
  • Epi: 10% occur <40 y/o; M>F
  • Causes: atherosclerosis, vasculitis, amyloid, sickle cell disease
A

Myocardial infarction;

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12
Q

what is thought to cause “women being protected against MI during reproductive years?”

A

HORMONES are thought to have PROTECTIVE EFFECT

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13
Q

Describe the pathogenesis of myocardial infarction?

A
  1. Preexisting atherosclerotic occlusion
  2. New, superimposed thrombosis
  3. +/- vasospasm/ vasoconstriction
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14
Q

Preexisting atherosclerotic occlusion:

where does it occur?

A
  • LAD, LCX – first cm from aorta takeoff
    • (left anterior descending)
    • (left circumflex artery)
  • RCA – along entire length
    • (right coronary artery)
  • “critical stenosis” - if fibrous cap is eroded and ruptures –> completely occludes the lumen
  • Collateral perfusion
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15
Q

define: critical stenosis

A

critical narrowing of an artery (stenosis) that results in a significant reduction in maximal flow capacity in a distal vascular bed

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16
Q

New, superimposed thrombus:

process of superimposed thrombsis

A
  • Eroded/ruptured plaque
  • Platelets adhere, aggregate, and are activated
  • Coagulation is activated
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17
Q

+/- vasospasm / vasoconstriction:

describe this third stage of pathogenesis of ischemic heart disease

A
  • Compromised lumen diameter
  • Increases local shear forces –> further damaging the fibrous cap –> plaque disruption
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18
Q

review the acute plaque changes

A
  1. atherosclerosis –>
  2. plaque disruption –> healing –> severe fixed coronary obstruction (chronic ischemic heart disase)
  3. Plaque disruption –?
    • mural thrombus w/ variable obstruction/ emboli
    • occlusive thrombus
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19
Q

factors contributing to acute plaque change –> MI?

A
  • vulnerable plaques
  • adrenergic stimulation

*In the majority of cases, culprit lesions in myocardial infarction patients were NOT critically stenotic OR symptomatic before plaque rupture

(slide 11)

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20
Q

what are: large atheromatous cores or thin fibrous caps

A

VULNERABLE / UNSTABLE PLAQUES:

these are more prone to rupturing

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21
Q

how does adrenergic stimulation affect/contribute to acute plaque change?

A
  • Adrenergic stimulation adds to plaque stress
  • Causes of adrenergic stimulation:
    • Surge in adrenergic stimulation associated with waking and rising
    • Intense emotional stress
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22
Q

what are the 3 REVERSIBLE changes in the myocardial response to ischemia?

A
  1. Aerobic metabolism ceases ↓ATP ↑lactic acid
  2. Loss of contractility
  3. Ultra-structural changes on cellular level
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23
Q

what are the 2 irreversible changes in the Myocardial Response to Ischemia?

Study These Flashcards
A

Irreversible changes occur in 20-40 minutes of prolonged ischemia

  • Coagulative necrosis of myocytes
  • Microvascular thrombosis
24
Q

which aspect of the artery is MOST SUSCEPTIBLE to infarction?

Study These Flashcards
A

SUBENDOCARDIAL ZONE is most susceptible;

susceptible to developing ischemia due to being FURTHEST AWAY from coronary artery

(endocardial zone is typically spared during periods of ischemia)

25
which type of infarcts **involve full thickness of ventricle?** What is seen on ECG?
* **TRANSMURAL INFARCTS** involve full thickness of ventricle * Yields **ST segment elevations on ECG** (aka STEMI) Slide 14
26
which type of infarcts involve **limited to inner third or myocardium?** What is seen on ECG?
* **SUBENDOCARDIAL INFARCTS;** limited to inner 1/3 or myocardium * Typically show ST segment depressions (aka non-STEMI or NSTEMI Slide 14
27
**Left anterior descending (LAD) artery occlusion:** * what is it? * where does it occur? * what % of MIs? * nickname for this occlusion?
* type of heart attack that's caused by a **100% blockage of the left anterior descending (LAD) artery** * Location: Anterior LV wall, anterior 2/3rds of septum, apex * 40-50% of MI; accounts for most of the causes of MIs * "**widow maker"**
28
**Right coronary artery (RCA) occlusion** * where does it occur? * what % of MIs?
* Location: RV and posterior 1/3rd of septum and posterior LV (if PDA arises from RCA) * 30-40% of MIs (2nd most common)
29
Left circumflex artery (LCX) occlusion: * location * % of MIs
* Lateral LV wall * 15-20% of Myocardial Infarction
30
which artery perfuses 1/3rd of septum and posterior LV artery? what's its course?
**Posterior descending artery;** * Arises from RCA (90%) or LCX --\> dominant vessel * PDA is often a branch off of Right Coronary Artery; but CAN be a branch off of Left Coronary (Left Circumflex Artery) -- termed "Left Dominant Circulation"
31
how does the gross appearance of a myocardial infarct differ from hours: * \<4 hours * 4-12 hours
* **\<4 hours – no changes appreciated** * If preceded death by 2-3 hours, area can be highlighted by immersing tissue in *triphenyltetrazolium chloride* * **• 4-12 hours – _occasional dark mottling_** (dark discoloration, on myocardium)
32
when do **microscopic changes** of myocardial infarct appear? what are these changes?
* microscopic changes usually require \>4 hrs * changes: * EM changes in first 4 hrs (**sarcolemmal disruption, mitochondrial amorphous densities**) * Early **coagulation necrosis** * **Edema** * **Hemorrhage** Slide 22
33
the image is of a **triphenyltetrazolium chloride stain;** where is the ischemia?
**Lateral Left Ventricle experienced ischemia:** due to Left Circumflex branch being occluded --\> ischemia (can't pick up the stain)
34
what are the gross findings of **myocardial infarct at 12-24 HOURS?**
**Dark mottling** (red-blue discoloration)
35
what are the **microscopic findings** of myocardial infarct at **12-24 HOURS?**
* Coagulation necrosis * **Pyknotic nuclei (shrunken and dark)** * Myocyte hypereosinophilia * **Contraction band necrosis** * Early neutrophilic infiltrate
36
gross anatomical changes in a **24-72 hour myocardial infarct?**
Mottling with **yellow-tan infarct center**
37
MICROSCOPIC anatomical changes in a **24-72 hour myocardial infarct?**
* Coagulative necrosis * Loss of myocyte nuclei * Loss of muscle cross-striations * Brisk neutrophilic infiltrate
38
gross anatomical changes of a **3-7 day old myocardial infarct?**
* Gross changes are most prominent at 3-7 days * Hyperemic border, central yellow-tan softening * Central softening (feels gelatinous/ soft to touch), depression due to removal of dead tissue
39
microscopic anatomical changes of a **3-7 day old myocardial infarct?**
* Dead myofibers removed * Neutrophils disappearing * Macrophage infiltration
40
gross anatomical appearance of **7-14 day old myocardial infarct**
* Maximally yellow-tan and soft (7-10 days) * Red-gray (10-14 days)
41
microscopic anatomical appearance of **7-14 day old myocardial infarct**?
* **Granulation tissue at margins (7-10 days)** * 10-14 days: * Well-established granulation tissue * New blood vessel formation *(angiogenesis)* * Collagen deposition *(pink on histo slide is the new collagen being deposited)*
42
gross and micoscopic anatomical features of **2-8 week old myocardial infarct?**
* Gross: Gray-white scar * Microscopic: * Increased collagen deposition * Decreased cellularity * *Macrophages are leaving the area*
43
gross and micoscopic anatomical features of **a \>2 month old myocardial infarct?**
* Gross - **Scarring complete** * Microscopic - **Dense collagenous scar** **area is all scar tissue; nonfunctional tissue (can't determine how old it is, but we know it's older than 2 months)**
44
what is **REPERFUSION**, and what can be done to stimulate this?
* Restoration of blood flow, which improves long and short-term survival * \*\*Goal is to reperfuse early\*\* * **Thrombolysis (tissue plasminogen activator), angioplasty, or coronary arterial bypass graft**
45
what is **reperfusion injury?** what are the pathological changes that result locally upon reperfusion?
* **Late restoration of blood flow to ischemic tissue can incite local damage** * Changes * Mitochondrial dysfunction – mitochondrial contents are released and promotes apoptosis * Myocyte hypercontracture * Free radicals form and cause myocyte damage * Leukocytes aggregate and may occlude microvasculature * Platelets and complement are activated
46
how do **hemorrhagic lesions** occur after reperfusion injury?
* vasculature is injured during ischemia --\> bleeding after flow is reestablished * brown bc it's experienced hemorrhage
47
JUST ONE CRUEL AND UNUSUAL HISTO QUESTION BC PROFS SUCKKK: what does this histo image show?
* Contraction band necrosis – intensely eosinophilic stripes (closely-packed sarcomeres) * dark pink vertical lines; buildup of calcium --\> contraction bands form due to excess excitation (can't relax, stuck in contracted state
48
how do we diagnose a myocardial infarction?
* clinical symptoms (\*\*but 10-15% of pts may be asymptomatic) * Severe, crushing substernal chest pain * Radiation to neck, jaw, epigastrium, left arm * Diaphoresis, nausea, vomiting * labs * EKG changes/ abnormalities * STEMI and ST segment depression
49
what do irreversibly damaged myocytes release?
intracellular macromolecules (such as Creatinine Kinase enzyme, Troponin free int he cytoplasm)
50
what are the 3 key biomarkers for myocardial ifnarctions? * Which are most sensitive and specific? * Which is best to identify subsequent MIs?
* Troponin I and T are MOST sensitive and specific * CK-MB is more helpful to identify subsequent MIs
51
key consequences of myocardial infarction?
* **Arrhythmias:** *risk for V. fib is greatest in first hour* * **Mural thrombus:** *impaired contractility leads to stasis, endocardial damage creates thrombogenic surface* * **Myocardial rupture** * **Papillary muscle dysfunction --\>** *post-infarct mitral regurgitation* * **Pericarditis:** *2nd or 3rd day after transmural infarct (full thickness of wall)* * **Ventricular aneurysm:** *dilation/ballooning outward; can occur in the ventricle*
52
myocardial rupture: ## Footnote *epidemiology, adn causes*
* Epi: 1-5% of MIs and fatal * Left ventricular free wall most common --\> leads to hemopericardium, cardiac tamponade * Occurs 3-7 days after infarction * Ventricular septum --\> leads to VSD * Papillary muscle rupture --\> leads to MR
53
the gross image is of what?
**post-MI ventricular aneurysm;** *Wall is dilated; there's a dilation of the wall (myocytes have been degraded by macrophages; --\> so the area is more prone to formation of aneurysm)*
54
**Chronic Ischemic Heart Disease:** * define? * classic type of patient?
* Progressive heart failure secondary to ischemic myocardial damage -- **ischemic cardiomyopathy** * Patient: * **Prior infarction(s) & compensatory mechanisms fail** (hypertrophy of residual viable myocytes) * **Severe coronary artery disease** (microinfarcts and replacement fibrosis without clinical evidence of a frank infarct)
55
**Chronic ischemic heart disease**: morphology
* LV dilation and hypertrophy, areas of gray-white scars * myocyte hypertrophy, diffuse subendocardial myocyte vacuolization, fibrosis
56
histological features in subendocardial zone after a myocardial infarct?
diffuse subendocardial myocyte vacuolization

Y2 - Path - Exam 4 (13 decks)

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