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MED233 Cardiovascular > Cardiac Pathology 1 - HF, IHD, HTN HD, > Flashcards

Cardiac Pathology 1 - HF, IHD, HTN HD, Flashcards

1
Q

What 3 changes occur in an aging heart?

A

1) myocardium and chambers - LV increased size, increased epicardial fat, myocardial changes*
2) Valves*
3) Vascular changes*

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2
Q

What myocardial changes occur with aging?

A
  • Lipofuscin and basophilic degneration

- Fewer myocytes, increased collagen fibers

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3
Q

What valvular changes occur with age?

A

AV and MV annular calcification
Fibrous thickening of leaflets
-Lambl excresences

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4
Q

What happens to LA with age?

A

Increases in size due to MV leaflets bucking toward left artrium

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5
Q

What vascular changes occur with age?

A

Coronary atherosclerosis

Stiffening of the aorta

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6
Q

What is congestive heart failure?

A

Heart unable to pump blood at a rate to meet peripheral demand (or can only do so with increased filling pressure).

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7
Q

What does CHF result from (2)?

A

1) Loss of myocardial contractile function (systolic dysfunction)
2) Loss of ability to fill vents during diastole (diastolic dysfunction)

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8
Q

What 2 settings do cardiac myocytes become hypertrophic?

A

1) Sustained pressure or volume overload

2) Sustained trophic signals (b-adrenergic stim)

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9
Q

What do cardiac myocytes look like in setting of Pressure Overload Hypertrophy? Is this a diastolic or systolic dysfunction?

A

They become thicker and LV WALL THICKNESS INCREASES CONCENTRICALLY.
Diastolic dysfunction - difficulty filling bc LV too small

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10
Q

What do cardiac myocytes look like in setting of Volume Overload Hypertrophy? Is this a diastolic or systolic dysfunction?

A

Myocytes elongate and VENTRICULAR DILATION is seen.

Systolic dysfunction - insufficient expelling capacity.

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11
Q

What is a hypertrophic heart vulnerable to?

A

Ischemia. Because the increase in size is not matched by increased blood supply.

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12
Q

What is the best measure of hypertrophy?

A

Heart weight!

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13
Q

Is left sided heart failure (L-HF) systolic or diastolic failure?

A

Either!

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14
Q

What are 4 things that commonly result in L-HF

A

1) Myocardial ischemia (atherosclerosis)
2) HTN (LV struggles to pump against increased BP)
3) Left-sided valve disease
4) Primary myocardial disease

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15
Q

What are clinical effects of left sided heart failure due to?

A

1) Congestion in pulmonary circulation (then edematous).

2) Decreased tissue perfusion.

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16
Q

What is the clinical presentation of L-HF?

A

Cough, dyspnea, orthopnea, paroxysmal nocturnal dyspnea.

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17
Q

What areas of hypertrophy/dilation do you see if L-HF?

A

Left ventricular hypertrophy.

LV dysfunction leads to LA DILATION (can lead to afib, stasis, thrombus)

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18
Q

What can be affected systemically as the result of L-HF?

A
  1. Kidney - Decreased Ejection Fraction = decreased GLOM PERFUSION.
  2. Brain - decreased cerebral perfusion = HYPOXIC ENCEPHALOPATHY
  3. Lungs - PULM EDEMA
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19
Q

What is the most common cause of right sided HF (2)?

A

1) L-HF!
2) Isolated R-HF results from any cause of pulmonary HTN (COR PULMONALE; **parenchymal lung dz, primary pulmonary HTN, pulmonary vasoconstriction.

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20
Q

What are signs of PRIMARY R-HF?

A

Minimal pulm congestion, but marked venous congestion

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21
Q

In Primary R-HF, what does venous congestion result in (5)?

A

Liver congestion (nutmeg). Splenic congestion=SM. Effusions in peritoneal, pelural, and pericardial spaces. Edema in ANKLES. Renal congestion.

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22
Q

What causes ischemic heart disease (IHD)?

A

Insufficient coronary artery flow (resulting in insufficient perfusion to meet metabolic demands of the myocardium).

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23
Q

What are consequences of IHD?

A

MI, angina, chronic IHD with HF, sudden cardiac death

24
Q

What is the leading cause of death in the US?

A

IHD! 90%+ are secondary to atherosclerosis (Chronic vascular occlusion and Acute plaque changes like thrombi)

25
Q

Definition of angina pectoris.

A

Transient, often recurrent CHEST PAIN induced by myocardial ischemia insufficient to cause MI.

26
Q

What are the three clinical variants of angina?

A

1) Stable angina
2) Prinzmetal variant angina
3) Unstable (“crescendo”) angina

27
Q

What does this person have? Stenotic occulsion of the coronary artery, feels like a “squeezing” or burning sensation with exertion. Relieved by vasodilators.

A

Stable angina - what is it and what does it feel like? How is it relieved?

28
Q

What does this person have? Episodic coronary artery vasoSPASM. Relieved with vasodilators.

A

Prinzmetal variant angina - what is it and what does it feel like? How is it relieved?

29
Q

What does this person have? Caused by rupture of plaque and partial thrombosis. Pain that increases in frequency/duration/severity (eventually at rest). 1/2 have myocardial necrosis.

A

Unstable (“crescendo”) angina - what is it and what does it feel like?

30
Q

What are 90% of MIs caused by? What are 3 other causes?

A

1) ATHEROMATOUS PLAQUE + associated risk factors
2) Embolus
3) Vasospasm
4) Ischemia secondary to vasculitis, shock, hematologic abnormalities (i.e. sickle cell that causes ischemia in cap beds)

31
Q

Presentation of what?
*Crushing chest pain radiating to left arm or jaw for more than 30 min.
*Diaphoresis
Dyspnea, NV

A

Classic presentation of an MI

32
Q

Do all MIs present with the typical symptoms?

A

No - 25% are “silent MIs” due to: i.e. people with neuropathy or people with denervated transplanted hearts

33
Q

What is the area of the subendocardium is first at risk after an arterial occlusion? What happens? Time of evolution?

A

The area farthest away - ischemia and necrosis of subENDOCARDIUM first, then MYOCARDIUM, then EPICARDIUM (1/2 of zone by 2hrs, full zone by 24hrs).

34
Q

How long is the injury-reversible phase after a MI?

A

Approx 20-30min for complete recovery.

35
Q

What 3 coronary vessels are at highest risk of infarct?

A

1) LAD (40-50%)
2) RCA (30-40%)
3) LCX (15-20%)

36
Q

Where areas do the LAD , RCA, and LCX supply?

A

LAD - Apex, LV ant wall, ant 2/3 of septum
RCA - RV free wall, LV post wall, post 1/3 of septum
LCX - LV lateral wall

37
Q

What does triphenltetrazolium chloride stain and what does it show?

A

It stains tissue containing lactate dehydrogenase RED. This signifies infarcted tissue.

38
Q

Evolution of MI (gross and micro)

A

Generally (1day to months):
Gross - dark to yellow to red to white.
Micro - coagulation necrosis to PMNs to granulation tissue to scar (collagen deposition=blue)

39
Q

What is the goal of reperfusion?

A

Limit the infarct size by rescuing the at risk myocardium.

40
Q

What are four methods of reperfusion?

A

(1) Thrombolysis. (2,3) Angioplasty and Stent placement. (4) CABG (Coronary Artery Bypass Graft - i.e. vein)

41
Q

What happens and what do you see (grossly) after reperfusion of an infarcted area?

A

NECROSIS occurs and CONTRACTION BANDS form.

42
Q

After temporary occlusion, does tissue immediately have increased viability after reperfusion?

A

No. It still decreases slightly in viability after and remains its reperfusion injury. The ventricles never fully regain pre-ischemic levels of function.

43
Q

What are the three useful biomarkers for MI?
Which is the most cardiac myocyte-specific lab findings?
Which peaks earliest?
Which is best for detecting re-infarction days after an MI?

A

1) Troponins I and T are most specific/sensitive. Peaks about 24 hours after MI.
2) Myoglobin peaks earliest - before symptoms.
3) CK-MB is best for detecting re-infarction because it is normal after 72 hours. rises before troponin, but is not heart specific.

44
Q

What are 1/2 of all MIs secondary to (and occur within what time frame of onset of this)?

A

MI within 1 hour of ARRHYTHMIA onset. Arrhythmia reoccur as a result of permanent damage to conducting system from MI.

45
Q

What are 5 complications of MI?

A

1) Contractile dysfunction
2) Fibrinous pericarditis
3) Myocardial rupture*
4) Infarct expansion *
5) Ventricular aneurysm *
6) Arrhythmia

46
Q

When does a myocardial rupture (as a complication of an MI) occur after an MI and what are 4 risk factors?

A

Occurs 2-4 days post-MI.
When inflammation and necrosis weaken the wall - (1) increased age, (2) large transmural anterior MI (LAD), (3) first MI (no scar tissue), and (4) absence of LV hypertrophy.

47
Q

What is an infarct expansion (as a complication of an MI)?

A

Muscle necrosis results in weakening, stretching, and thinning of the wall. Mural thrombus often seen.

48
Q

What are characteristics of a ventricular aneurysm (as a complication of an MI)?

A

Late complication of large transmural infarct with early EXPANSION.
Composed of thinned wall of scarred myocardium, normally no rupture occurs, associated with mural thrombus.

49
Q

What precipitates Sudden Cardiac Death and what is SCD?

A

Coronary artery disease precipitates SCD in 80-90% of cases.
Occurs without symptoms or within 1-24 hours of symptom onset. FATAL ARRHYTHMIA from ischemia-induced myocardial irritability.

50
Q

What are characteristics of L-sided Hypertensive disease?

A

Pressure overload results in LV hypertrophy (concentric thickening).
Diastolic dysfunction = LA enlargement = afib

51
Q

What can L-sided Hypertensive disease lead to?

A

CHF and risk factor for SCD

52
Q

What are characteristics of R-sided Hypertensive disease?

Most common cause?

A

Isolated causes of R-sided HTN disease is the result of pulmonary HTN.
Most common cause is L-sided Heart Disease

53
Q

What can cause an acute cor pulmonale?

A

A large pulmonary embolus.

54
Q

Cor pulmonale definition

A

RV failure due to increased vascular resistance or pulmonary HTN.

55
Q

Cocaine use, MV-prolapse, cardiomyopathy associated with what?

A

Sudden Cardiac Death

MED233 Cardiovascular (18 decks)

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