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Cardiovascular 2 > Cardiac Pathology 1 > Flashcards

Cardiac Pathology 1 Flashcards

1
Q

Myocardial and chamber changes with aging

A
  • Decreased LV size
  • Increased epicardial fat
  • Lipofuscin buildup in myocytes, basophilic degeneration
  • Fewer myocytes, increased collagen (STIFF)
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2
Q

What is lipofuscin? Pathologic?

A

Normal breakdown product stored in cells

- No known damage to cell

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3
Q

Valvular changes with aging

A
  • Annular calcification (L side valves)
  • Fibrous thickening
  • Mitral valve buckling toward L atrium –> increased atrial size
  • Lambl excrescences
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4
Q

What are lambl excrescences? Pathologic?

A

Frond-like papillary projections off of cusps

- Pathologic IF abnormally large and embolize

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5
Q

Heart vascular changes with aging

A
  • Coronary atherosclerosis

- Stiffening of aorta

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6
Q

CHF

A

Heart can’t pump to meet peripheral demand with normal filling pressure

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7
Q

2 causes (general) of CHF

A

Systolic dysfunction - loss of contractility of myocytes

Diastolic dysfunction - loss of filling ventricles in diastole

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8
Q

3 causes of cardiac hypertrophy

A
  • Pressure overload (HTN)
  • Volume overload
  • Sustained beta-adrenergic stimulation
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9
Q

Pathologic finding in pressure overload hypertrophy

Is this a systolic or diastolic dysfunction?

A

THICKER myocytes, concentric ventricular wall thickening

Diastolic (less filling space)

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10
Q

Pathologic finding in volume overload hypertrophy

Is this a systolic or diastolic dysfunction?

A

ELONGATED myocytes, ventricular dilation w/ thinner wall

Systolic (less contractility)

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11
Q

Potential danger in cardiac hypertrophy?

A

Lack of adequate blood supply to myocytes –> ischemia

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12
Q

Describe the pathway by which hypertrophy or dilation occurs

A

Pressure/volume overload –> increased work –> increased wall stress –> cell stretch –> hypertrophy/dilation

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13
Q

3 RESULTS of cardiac dysfunction (systolic or diastolic)

A
  • Heart failure
  • Arrhythmias
  • Neurohumoral stimulation
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14
Q

Causes of L-sided heart failure (4)

A
  • Myocardial ischemia (atherosclerosis or hypertrophy)
  • Hypertension
  • L-side valvular disease (aortic or mitral)
  • 1º myocardial disease
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15
Q

Clinical effects (seen in clinic) in L-sided failure are DUE TO what?

A
  • Congestion of pulmonary circulation

- Decreased tissue perfusion

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16
Q

Most common clinical symptoms of L-sided failure

A

Cough, dyspnea, orthopnea, paroxysmal nocturnal dyspnea

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17
Q

Potential morphologic changes in L-sided heart failure

A
  • LVH

- L atrial dilation (via L ventricular failure)

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18
Q

A patient has L-sided heart failure via chronic systemic HTN. On imaging, the L atrium is dilated. What are the clinical dangers of this finding?

A
  • A. fib –> thrombus –> embolism

- Stasis –> thrombus –> embolism

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19
Q

Lab finding in L-sided heart failure (why?)

A
  • Pre-renal azotemia (decreased renal perfusion)
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20
Q

A patient w/ L-sided heart failure is subject to what neurologic damage?

A

Hypoxic encephalopathy (decreased brain perfusion)

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21
Q

MOST COMMON cause of R-sided heart failure

A

L-sided heart failure

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22
Q

Causes of isolated R-sided heart failure

A

ANY pulmonary hypertension

- Parenchymal lung disease
- 1º Pulmonary HTN
- Pulmonary vasoconstriction
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23
Q

Systemic findings in R-sided heart failure (5)

A

Venous congestion…

- Nutmeg liver (partly congested, partly not)
- Splenomegaly (congestion)
- Body space effusions (ascites, pleural, pericardial)
- Peripheral (ANKLE) edema
- Renal congestion
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24
Q

General cause of ischemic heart disease

A

Decreased blood flow to coronary arteries –> myocardium

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25
Q

Potential RESULTS of ischemic heart disease

A
  • M.I.
  • Angina pectoris
  • Heart failure
  • Sudden cardiac death (fatal arrhythmia)
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26
Q

Most likely cause of ischemic heart disease

A

Atherosclerosis

27
Q

What is angina pectoris? Cause?

A

Transient, RECURRENT chest pain DUE TO myocardial ischemia NOT ENOUGH to cause M.I.

28
Q

3 types of angina pectoris

A
  • Stable angina (exercise/stress)
  • Prinzmetal variant
  • Unstable “crescendo” angina
29
Q

Cause of stable angina

Treatments?

A

Coronary occlusion

Rest, vasodilator

30
Q

Cause of Prinzmetal angina

Treatment?

A

Episodic coronary artery spasm

Vasodilator

31
Q

Cause of unstable “crescendo” angina

Complaint by patient?

A

Plaque rupture –> partial thrombis

Pain of increasing frequency, duration, and severity

32
Q

Which type of angina pectoris is not generally linked to atherosclerosis?

A

Prinzmetal variant

33
Q

Common morphologic finding w/ unstable angina

A

Myocardial necrosis

34
Q

Most COMMON cause of myocardial infarction

A

Atherosclerosis

35
Q

Other causes of M.I. besides atherosclerosis

A
  • Embolus
  • Vasospasm (cocaine, other)
  • Ischemia via vasculitis, shock, other
36
Q

Classic presentation of M.I.

A
  • Prolonged (> 30 min) chest pain, radiates down L arm

- Sweating

37
Q

Determinants of M.I. presentation

A
  • Site, degree, rate, duration of arterial occlusion
  • Size of perfused area
  • Metabolic demands of at-risk area
  • Available collateral blood flow
  • Arterial spasm or not
38
Q

Where are the first areas of ischemia/necrosis in an M.I.?

These areas are also the ______

A

Sub-endocardial myocardium FARTHEST from the artery and NOT able to get oxygen via diffusion from chamber

LAST to heal (if at all)

39
Q

How long can it take for necrosis to be seen?
How long can it take for the WHOLE wall to be necrotic?
How long can it take for irreversible injury to result?

A

2 hours
6 hours
20 minutes

40
Q

In ischemic damaged myocardium, levels of ___ drop while levels of ___ rise

A

ATP; Lactate

41
Q

Most commonly affected arteries in M.I.

A

1) LAD (anterior interventricular)
2) R coronary
3) L circumflex

42
Q

A patient has an M.I. due to LAD occlusion. Where will the areas of myocardial damage be?

A

Apex, LV anterior wall, anterior 2/3 of septum

43
Q

A patient has an M.I. due to RCA occlusion. Where will the areas of myocardial damage be?

A

RV free wall, LV posterior wall, posterior 1/3 of septum

44
Q

A patient has an M.I. due to LCX occlusion. Where will the area of myocardial damage be?

A

LV lateral wall

45
Q

General morphologic progression of M.I. (5 “stages”)

A

Dark mottling (hemorrhage) –> yellow-tan center (necrosis) –> Red-grey (granulation tissue, vessels) –> grey-white (scarring) –> full white (dense collagen)

46
Q

Nearby myocardial cells that did NOT die during an M.I. will look how?

A

Hypertrophic and spaced out (to cover dead area)

47
Q

An M.I. has been reperfused following partial necrosis/death of the myocardium. What pathologic feature will be seen within that area? Why?

A

CONTRACTION BANDS - living myocytes exposed to calcium from blood (reperfusion) –> contraction

48
Q

How does myocyte functionality relate to viability (alive) during an M.I.?

A

They are non-functional within a few minutes, but still completely living for 20 min (at least)

49
Q

Why do myocytes continue to die slightly after being reperfused (after an M.I.)?

A

Sudden O2 causes ROS creation by damaged cells

50
Q

While parts of the myocardium remain alive after a reperfused M.I., what continues to increase?

A

Ventricular dysfunction

51
Q

Fastest lab findings in an M.I.
Intermediate lab finding in an M.I. (timing-wise)
Last and longest lab finding in an M.I. (BEST)

A

Myoglobin (disappears in hours)
CK-MB (stays for a few days)
Troponin I and T (stays for many days)

52
Q

Most common cause of death following a treated M.I.

A

Fatal arrhythmia (50%)

53
Q

An arrrhythmia following an M.I. is most likely to occur following what type of M.I.? Why?

A

RCA - conducting system is in posterior of heart

54
Q

A patient has an M.I. and later shows progressive heart failure. Why?

A

Contractile dysfunction due to dead myocardium

55
Q

A patient has an M.I. and later shows chest discomfort and a friction rub. Imaging shows dark red around damaged myocardium. Why?

A

Fibrinous pericarditis due to attempted healing

56
Q

A patient has an M.I. and later dies acutely w/ severe chest pain. Why?

A

Myocardial rupture via weakened, necrotic wall

57
Q

Risk factors for a myocardial rupture following an M.I. (4)

A
  • Older
  • Transmural, anterior M.I.
  • First M.I. (less protective scar tissue)
  • No preceding LV hypertrophy
58
Q

3 types of myocardial rupture post-M.I.

A
  • External (anterior)
  • Septal (L to R shunt)
  • Papillary muscle (valvular dysfunction)
59
Q

Commonly seen formation on imaging following an M.I.

A

Mural thrombus

60
Q

An M.I. is large and transmural, and shows signs of early expansion to surrounding myocardium. Most likely complication?

A

Ventricular aneurysm

61
Q

What makes a “sudden cardiac death”?

Most common cause?

A

Unexpected death of cardiac cause due to NO symptoms or within 1 day of symptoms starting

Coronary artery disease (sub-clinical level –> occlusion)

62
Q

Most literal cause of the sudden cardiac death from CAD?

A

Fatal V fib arrhythmia due to ischemic myocardium

63
Q

Progression of heart morphologic changes in chronic systemic HTN

A

Pressure overload –> L ventricular hypertrophy –> L atrial enlargement –> A. fib, CHF, maybe sudden death

Cardiovascular 2 (20 decks)

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