Topics B2-7. Cardio 2: MI, SCD, Angina, Ischemic Heart Disease, Endocarditis, Valvular Heart Disease, Cardiomyopathies, Myocarditis Flashcards Preview

Y Pathology I (Dustin) > Topics B2-7. Cardio 2: MI, SCD, Angina, Ischemic Heart Disease, Endocarditis, Valvular Heart Disease, Cardiomyopathies, Myocarditis > Flashcards

Flashcards in Topics B2-7. Cardio 2: MI, SCD, Angina, Ischemic Heart Disease, Endocarditis, Valvular Heart Disease, Cardiomyopathies, Myocarditis Deck (62)
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Note: Topic A5 includes myocardial infarction as well as B2, so will repeat some questions but not everything. I will ask more detailed questions and use the book more for these cards, since the other one I kept it too simple and this is really important

OK, mark this card 5 and hopefully it won't come back


How does ischemic heart disease rank as far as cause of death in developed countries?

How many people who have heart attacks normally die from them?

#1 cause of death in developed countries

1/3 of people with MI die from it, and half of those before they get to the hospital


What is the major underlying cause of MI in the vast majority of cases?

Coronary atherosclerosis ("fixed coronary") that are then involved in thrombogenesis.

Fixed coronary + dynamic changes like rupture of plaque -> AMI.


How do plaques rupture and cause thrombosis?
(answer has some general review of formation of thrombus too)

A plaque is disrupted (usually at its "shoulder") by mechanical forces or intraplaque hemorrhage
-> subendothelial collagen and necrotic plaque contents get into the blood
-> platelets adhere and aggregate, releasing Thromboxane A2, ADP, and serotonin, causing further platelet aggregation and vasospasm
-> Coagulation cascade is actvated by tissue factor/VIIa and thrombus develops with fibrin network
Thrombus grows to completely occlude the lumen


What is a "transmural" versus "subendocardial" myocardial infarction?

What is the "wavefront theory?"

Transmural: traverses the entire ventricular wall from endocardium to the epicardium

Subendocardial infarction: limited to the interior 1/3 of the wall (of the left ventricle because RV infarcts are very very rare)

Wavefront: Myocardial infarctions always start in the subendocardial area, then progress to the transmural area step-by-step as a "wave-front." Fast treatment limits extent of necrosis.


What are the 3 reasons behind the Wave-Front Theory?

1. Coronaries run in the subepicardium, and the endocardium only gets the distal branches
2. Myocardial fibers twist like a spiral, and subendocardium works harder (more sensitive to O2 deprivation)
3. Ventricle has higher pressure, which compresses the subendocardium more than subepicardium


Which gender is more prone to myocardial infarctions, but how does this change over time?

Men are more susceptible with MIs, but women lose the protective effects of estrogen after menopause, and so their risk of MI is also high when they are elderly.

Ischemic heart disease is still the leading cause of death in elderly women. Plus, if they smoke or have other factors that increase their risk, the estrogen benefit is less important.


7 notable time periods that mark MI progression via how the tissue changes (patient symptoms and EKG are not relevant here)
it's a lot but going to write these as simply as possible to pack in key details, it's better to be able to link them together

1. 0-30 min: no real morph changes, reversible
2. 30min-4hrs: only change is dilated cells. Diaphorase rxn may be used to detect infarct in lab
3. 4-12 hours: begin coagulation necrosis, usually not grossly apparent yet
4. 12-24 hrs: full-blown MI w/ firm, pale (or dark mottled) area. Preciptated proteins in histo
5. 1-2 days: degeneration, hyperemic red ring around pale necrotic area. Macrophages infiltrate, soften tissue
6. 3-12 days: capillarization of tissue, early scar formation with fibroblast infiltration. Risk of myocardial rupture
7. 12-20 days: scar tissue replaces necrotic area. white, "egg-shell" color.


What is the functional consequence of acute ischemia? Why does it occur?

How long does it take for reversible changes to occur?

Functional consequence is rapid loss of contractility, within ~1 min of ischemia onset

Loss of myocardial blood supply -> impaired aerobic glycolysis and anaerobic glycolysis causes lactic acid buildup

Reversible ultrastructural changes include myofibrillar relaxation, glycogen depletion, cell and mitochondrial swelling occur but may not be visible before 30 minutes. After 30-40 minutes, starts to get irreversible.


When is the ideal time for reperfusion therapy in myocardial infarction? Why?
(4 specific effects are listed)

3-6 hours after infarction. Effects:
1. Free radicals are produced after reperfusion, damaging myocytes
2. Myocyte hypercontracture: ischemia caused high intracellular calcium levels, impaired calcium cycling and sarcolemma damage. Reperfusion causes uncontrolled contraction because they lack ATP to undergo relaxation. Can also kill myocytes
3. Leukocytes aggregate + platelets and complement are activated, injuring tissue and the microvasculature
4. Vascular injury/leakiness can cause bleeding into necrotic area (major risk)


Ways to perform reperfusion therapy?

1. Thrombolysis, for example by tPA
2. Angioplasty: balloon catheter opens the coronary artery, usually followed by a stent placement to ensure it stays open
3. Coronary arterial bypass graft (CABG)


Which artery is most commonly occluded in an MI? What about the other two?

Most common: LAD (40-50%). Infarcts the anterior wall, septum, and much of apex.

RCA: 30-40% of infarcts. Affects right ventricle, but usually RV can compensate without infarction. LV can instead be affected on posterior septum etc, depends on left vs right dominance of the heart

LCX: 15-20% of infarcts. Affects lateral left ventricle


What 3 clinical signs and symptoms are heart attacks based on?

1. Chest Pain: crushing pain. Patient typically quiet and sweating. Pain may radiate to the left shoulder, arm, or neck. Posterior infarcts may cause abdominal pain. Pain is not relieved by nitroglycerin (like with angina pectoris). However, may still have painless AMI (especially with diabetes).

2. ECG: transmural necrosis marked by ST elevation. Other signs: T-en-dome, T wave inversion

3. Enzyme alteration: most used are Troponin T and I, creatine kinase, maybe also lactate dehydrogenase. Leak from myocardium when the cells undergo necrosis.


What are 5 consequences of myocardial infarction? (from lecture.. there are more in book)

1. Pump failure / heart failure: can cause hypotension, pulmonary edema, cardiogenic shock
2. Arrythmias: conducting system impaired
3. Myocardial rupture: usually 5-6 days after due to inflammatory cells digesting tissue. May cause hemiparcardium, cardiac tamponade
4. Aneurysm: soft infarct tissue bulges from pressure
5. Chronic ischemic heart disease: heart failure in long run, hypertrophy


What happens to non-infarcted zones in a survived myocardial infarction?

Non-infarcted zones undergo compensatory hypertrophy and dilation.

This + scarring/thinning from infarcted zone = "ventricular remodeling"


People who undergo Sudden Cardiac Death are categorized into 2 groups, what are they?

1. All those sudden cardiac deaths relating to AMI. Severe atherosclerosis is present. Accounts for 80-90% of cases.

2. Any other cause besides AMI, also don't have significant atherosclerosis. Maybe 10-20% of cases.


What are the 4 non-myocardial infarction causes of sudden cardiac death?

1. Congenital heart malformations. May have been undetected, then they could die while exercising

2. Any developmental problem of the conductive system: causes arrhythmias again often after exercising. This is the most common one, and it's a reasoning for AEDs in many gyms.

3. Myocarditis: may be related to viral/bacterial infections, flu, etc (later topic, B5)

4. Cardiomyopathies: hereditary disorders of myocardium (later topic, B7)


How occluded is a coronary artery to be considered "fixed?"

What percentage is called the "critical stenosis?"

>70% of the artery is covered by plaque. If it's less than 70%, then they usually will be asymptomatic

>90% occlusion is "critical stenosis" - have chest pain even at rest (unstable angina)


What is ischemic heart disease (NOT chronic)

What are 4 diseases covered by this blanket term?

Discrepancy between blood supply and myocardium that makes ischemia

Covers: AMI, Angina Pectoralis, Chronic Ischemic Heart Disease, and Sudden Cardiac Death


What is Angina Pectoris?
What are the 3 types? (just the name, will elaborate in other cards)

Intermittent chest pain caused by transient, reversible ischemia. Pain may be due to bradykinin/ adenosine released by ischemia.

1. Stable/ "Typical"
2. Prinzmetal / "Variant"
3. Unstable / "Crescendo"


What is stable / typical angina pectoris?

How does it appear on EKG?

What medication is regularly used to treat it?

Patient has no symptoms at rest, but on physical exertion or emotional stress they have crushing and radiating chest pain similar to MI. Strong sign that patient has fixed coronary >70%.

Appears as ST depression on EKG

Medication: normally nitroglycerin is given to cause coronary vasodilation. They should also rest, and then get some sort of angioplastic surgery like stent placement before they have a MI.


What is Prinzmetal / variant angina pectoris?

What medication is used to treat it?

Chest pain occurs at rest, but it's because of a functional malformation that causes vasospasm. May or may not have atherosclerosis.

Usually it's well-treated with nitroglycerine


What is Unstable / crescendo angina pectoris?

Chest pain that is increasing in frequency, lasting longer, generally getting worse. They have a fixed plaque, maybe have self-resolving thrombus or microinfarcts.

It's a very bad sign, developing >90% occlusion. Needs intervention soon.


What is chronic ischemic heart disease?
What are 3 causes?

Progressive heart failure secondary to ischemic myocardial damage.

1. History of MI and compensatory mechanisms begin to fail

2. Atherosclerosis: many coronaries with plaques that don't make ischemia in one area, but more a "global shortage" of blood supply - distributed ischemia with small infarcts

3. Hypertension: causes hypertrophy, limit is 500-600g weight and then start to get small necroses throughout, coronaries can't handle the size


Ischemic heart disease that occurs after MI: why does it occur?
How does it look macroscopically?

Infarcted area loses its contractile force, and so other muscle hypertrophies to compensate. However, atherosclerosis means it can't get enough O2.

Results in "spotty fibrosis"


What are 3 clinical risks with ischemic heart disease?

1. Severe progressive heart failure
2. New episodes of angina or infarction
3. Arrhythmias


What bacterial infection is related to Rheumatic Fever? More specifically, what causes it?

What type of acquired stenosis is it essentially the only cause for?

Bacteria: Streptococcus pyogenes (group A β-hemolytic strep). But rheumatic fever itself is not caused by the bacteria, but rather a cross-reactivity of antigens (namely M protein) that is present on both the bacteria and myocardium/ cardiac valves. Only ~ 3% of people with S. pyogenes infection develop RF.

Essentially the only acquired cause of mitral stenosis (causes deforming, fibrotic mitral stenosis)


With Rheumatic Valvular Disease, what special substance becomes deposited in the leaflets?

Verruca: "verrucous endocarditis" with immune complexes, coagulated fibrin, and necrotic cell debris

Rarely, may cause microemboli


What 2 special things that are named after some dudes appear histologically in the myocardium during Rheumatic Fever?
(the naming is particularly annoying here)

Anitschkow cells: plump activated macrophages. Have abundant cytoplasm and central nuclei with chromatin condensed to form a wavy ribbon (so they're also called "caterpillar cells"). Can fuse together to form multinucleated "Aschoff cells"

Aschoff bodies: granulomatosus myocardial inflammatory lesions / nodules. Contain lymphocytes, plasma cells, and the Anitschkow cells


What is the type III hypersensitive reaction part of rheumatic fever?

Immune complexes deposit in kidney glomeruli, causing activation of complement, attracting neutrophils and macrophages, triggering inflammation. This leads to glomerulonephritis

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