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3 Patho > CVS 1 > Flashcards

CVS 1 Flashcards

1
Q

Cardiac hypertrophy: the compensatory response due to pressure overload?

A

Concentric. Increased wall thickness; reduced cavity diameter.

The heart has to pump harder to overcome the systemic pressure.

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2
Q

Cardiac hypertrophy: compensatory response due to volume overload?

A

Hypertrophy with dilation; increased ventricular diameter.

Too much blood in the heart would mean the heart harder to eject blood from the chamber.

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3
Q

Some causes of pressure overload in the heart?

A

systemic hypertension –> LV hypertrophy

pulmonary hypertension –> RV failure

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4
Q

Characterized by Diminished CO and/or damming back of blood in the venous system.

A

Heart failure, congestive heart failure

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5
Q

Most common cause of CHF

A

systolic dysfunction

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6
Q

Major s/sx of systolic dysfunction:

A

pulmonary congestion

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7
Q

Causes of diastolic dysfunction:

A

LV hypertrophy, amyloid deposition, contrictive pericardits

restrictive conditions –> reduced compliance

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8
Q

Left-sided HF in lungs presents with:

A

acute: congestion and edema
chronic: with heart failure cells

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9
Q

Left-sided HF in kidneys:

A

decreased renal blood flow –> activation of RAAS –> hydrostatic pressure increases –> peripheral and pulmonary edema

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10
Q

Left-sided HF in brain:

A

hypoxic encephalitis

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11
Q

Right-sided HF in liver:

A

nutmeg liver, chronic passive congestion

centrilobular necrosis, sclerosis

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12
Q

Right-sided HF in spleen:

A

congestive splenomegaly

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13
Q

Right-sided HF in heart:

A

RV hypertrophy/dilatation

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14
Q

Right-sided HF in kidneys:

A

congestion

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15
Q

Right-sided HF in brain:

A

hypoxic encephalopathy

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16
Q

Patient presents with pulmonary edema, dyspnea, and orthopnea?

Describe the heart failure

A

Left-sided

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17
Q

Heart failure results in nutmeg liver, hepatojugular reflex, edema

A

right-sided

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18
Q

Manifestations/syndromes of ischemic heart disease:

A
  1. Acute MI
  2. Angina
  3. Chronic IHD
  4. Sudden cardiac death
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19
Q

70% of a coronary artery lumen occluded with atherosclerotic plaque:

A

critical stenosis

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20
Q

Causes of non-atheromatous coronary arterial occlusion

A 
embolism
dissecting aneurysm
vasospasm
congenital anomaly
trauma
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21
Q

Most common form of angina pectoris

A

Stable AP

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22
Q

Chest pain with progressive, recurrent pain at rest

A

Unstable AP

23
Q

Chest pain secondary to vasospasm at rest

A

Prinzmetal AP

24
Q

Chest pain secondary to atherosclerosis

A

Stable

25
Q

Chest pain with ST depression

A

Stable AP

Unstable AP

26
Q

Chest pain associated with acute plaque change with superimposed partial thrombosis or vasospasm

A

Unstable AP

27
Q

Chest pain with thrombosis but no necrosis

A

Unstable AP

28
Q

Chest pain with exertion

A

Stable AP

29
Q

Chest pain with ST elevation

A

Prinzmetal’s AP

30
Q

Sequence of coronary artery thrombosis

A 
Tear/fissure
collagen exposed
extrinsic pathway (coagulation)
activated platelets release factors causing vasospasm
occlusive thrombosis
31
Q

Indicator of irreversible damage in MI

A

sarcolemmal membrane damage

32
Q

Time it takes for irreversible damage in MI

A

20-40 minutes

33
Q

Gross changes 0-18 hours after MI

A

None

34
Q

Yellow pallor in heart is seen how long after MI?

A

1-7 days

35
Q

Vague pallor in heart is seen how long after MI?

A

18-24 hours

36
Q

White scar is seen in heart how long after MI?

A

months

37
Q

Central pallor with hyperemic border seen how long after MI?

A

7-28 days

38
Q

Dark mottling or tigering effect is seen how long after MI?

A

12-24 hours

39
Q

How long post-infarct is this microscopic change seen: wavy myocyte fiber

A

1-4 hours

40
Q

How long post-infarct is this microscopic change seen: neutrophilic infiltrate

A

1-4 days (within 1 week macrophages and neutrophils)

41
Q

How long post-infarct is this microscopic change seen: granulation tissue

A

7-28 days

42
Q

How long post-infarct is this microscopic change seen: macrophages

A

4-7 days (within 1 week macrophages and neutrophils)

43
Q

How long post-infarct is this microscopic change seen: coagulative necrosis

A

4-24 hours

44
Q

What pathologic form of MI is associated with diffuse stenosing coronary artery atherosclerosis without thrombosis and acute plaque change?

A

subendocardial

45
Q

What pathologic form of MI is associated with chronic atherosclerotic obstruction, acute plaque change, and superimposed complete thrombosis?

A

transmural

46
Q

Type of infarct with greater necrosis

A

transmural

47
Q

Type of infarct with ST depression?

A

subendocardial

48
Q

Type of infarct with ST elevation and pathologic Q waves?

A

transmural

49
Q

Characteristic MI microscopic change seen 12 hours post-infarct:

A

hyper-eosinophilia with surrounding congestion

50
Q

First change seen (electron microscope):

A

myofibril relaxation
glycogen loss
mitochondrial swelling

51
Q

ECG feature in MI

A

new Q waves

52
Q

Cardiac proteins seen an hour after MI, peaking at 16 hours

A

troponin I

troponin T

53
Q

Most specific protein marker in MI?

A

Troponin I

54
Q

CK-MB is also found in

A

skeletal muscle

3 Patho (8 decks)

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