CVS 1 Flashcards

(54 cards)

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

23
Q

Chest pain secondary to vasospasm at rest

A

Prinzmetal AP

24
Q

Chest pain secondary to atherosclerosis

25
Chest pain with ST depression
Stable AP | Unstable AP
26
Chest pain associated with acute plaque change with superimposed partial thrombosis or vasospasm
Unstable AP
27
Chest pain with thrombosis but no necrosis
Unstable AP
28
Chest pain with exertion
Stable AP
29
Chest pain with ST elevation
Prinzmetal's AP
30
Sequence of coronary artery thrombosis
``` Tear/fissure collagen exposed extrinsic pathway (coagulation) activated platelets release factors causing vasospasm occlusive thrombosis ```
31
Indicator of irreversible damage in MI
sarcolemmal membrane damage
32
Time it takes for irreversible damage in MI
20-40 minutes
33
Gross changes 0-18 hours after MI
None
34
Yellow pallor in heart is seen how long after MI?
1-7 days
35
Vague pallor in heart is seen how long after MI?
18-24 hours
36
White scar is seen in heart how long after MI?
months
37
Central pallor with hyperemic border seen how long after MI?
7-28 days
38
Dark mottling or tigering effect is seen how long after MI?
12-24 hours
39
How long post-infarct is this microscopic change seen: wavy myocyte fiber
1-4 hours
40
How long post-infarct is this microscopic change seen: neutrophilic infiltrate
1-4 days (within 1 week macrophages and neutrophils)
41
How long post-infarct is this microscopic change seen: granulation tissue
7-28 days
42
How long post-infarct is this microscopic change seen: macrophages
4-7 days (within 1 week macrophages and neutrophils)
43
How long post-infarct is this microscopic change seen: coagulative necrosis
4-24 hours
44
What pathologic form of MI is associated with diffuse stenosing coronary artery atherosclerosis without thrombosis and acute plaque change?
subendocardial
45
What pathologic form of MI is associated with chronic atherosclerotic obstruction, acute plaque change, and superimposed complete thrombosis?
transmural
46
Type of infarct with greater necrosis
transmural
47
Type of infarct with ST depression?
subendocardial
48
Type of infarct with ST elevation and pathologic Q waves?
transmural
49
Characteristic MI microscopic change seen 12 hours post-infarct:
hyper-eosinophilia with surrounding congestion
50
First change seen (electron microscope):
myofibril relaxation glycogen loss mitochondrial swelling
51
ECG feature in MI
new Q waves
52
Cardiac proteins seen an hour after MI, peaking at 16 hours
troponin I | troponin T
53
Most specific protein marker in MI?
Troponin I
54
CK-MB is also found in
skeletal muscle