Cardiac Pathology 1 - HF, IHD, HTN HD,

Question 1

What 3 changes occur in an aging heart?

Answer 1

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

Question 2

What myocardial changes occur with aging?

Answer 2

• Lipofuscin and basophilic degneration

- Fewer myocytes, increased collagen fibers

Question 3

What valvular changes occur with age?

Answer 3

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

Question 4

What happens to LA with age?

Answer 4

Increases in size due to MV leaflets bucking toward left artrium

Question 5

What vascular changes occur with age?

Answer 5

Coronary atherosclerosis

Stiffening of the aorta

Question 6

What is congestive heart failure?

Answer 6

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

Question 7

What does CHF result from (2)?

Answer 7

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

Question 8

What 2 settings do cardiac myocytes become hypertrophic?

Answer 8

1) Sustained pressure or volume overload

2) Sustained trophic signals (b-adrenergic stim)

Question 9

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

Answer 9

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

Question 10

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

Answer 10

Myocytes elongate and VENTRICULAR DILATION is seen.

Systolic dysfunction - insufficient expelling capacity.

Question 11

What is a hypertrophic heart vulnerable to?

Answer 11

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

Question 12

What is the best measure of hypertrophy?

Answer 12

Heart weight!

Question 13

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

Answer 13

Either!

Question 14

What are 4 things that commonly result in L-HF

Answer 14

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

Question 15

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

Answer 15

1) Congestion in pulmonary circulation (then edematous).

2) Decreased tissue perfusion.

Question 16

What is the clinical presentation of L-HF?

Answer 16

Cough, dyspnea, orthopnea, paroxysmal nocturnal dyspnea.

Question 17

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

Answer 17

Left ventricular hypertrophy.

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

Question 18

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

Answer 18

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

Question 19

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

Answer 19

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

Question 20

What are signs of PRIMARY R-HF?

Answer 20

Minimal pulm congestion, but marked venous congestion

Question 21

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

Answer 21

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

Question 22

What causes ischemic heart disease (IHD)?

Answer 22

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

Question 23

What are consequences of IHD?

Answer 23

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

Question 24

What is the leading cause of death in the US?

Answer 24

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

Question 25

Definition of angina pectoris.

Answer 25

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

Question 26

What are the three clinical variants of angina?

Answer 26

1) Stable angina 2) Prinzmetal variant angina 3) Unstable ("crescendo") angina

Question 27

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

Answer 27

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

Question 28

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

Answer 28

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

Question 29

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.

Answer 29

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

Question 30

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

Answer 30

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)

Question 31

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

Answer 31

Classic presentation of an MI

Question 32

Do all MIs present with the typical symptoms?

Answer 32

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

Question 33

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

Answer 33

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

Question 34

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

Answer 34

Approx 20-30min for complete recovery.

Question 35

What 3 coronary vessels are at highest risk of infarct?

Answer 35

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

Question 36

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

Answer 36

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

Question 37

What does triphenltetrazolium chloride stain and what does it show?

Answer 37

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

Question 38

Evolution of MI (gross and micro)

Answer 38

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)

Question 39

What is the goal of reperfusion?

Answer 39

Limit the infarct size by rescuing the at risk myocardium.

Question 40

What are four methods of reperfusion?

Answer 40

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

Question 41

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

Answer 41

NECROSIS occurs and CONTRACTION BANDS form.

Question 42

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

Answer 42

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

Question 43

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?

Answer 43

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.

Question 44

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

Answer 44

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

Question 45

What are 5 complications of MI?

Answer 45

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

Question 46

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

Answer 46

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.

Question 47

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

Answer 47

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

Question 48

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

Answer 48

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

Question 49

What precipitates Sudden Cardiac Death and what is SCD?

Answer 49

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.

Question 50

What are characteristics of L-sided Hypertensive disease?

Answer 50

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

Question 51

What can L-sided Hypertensive disease lead to?

Answer 51

CHF and risk factor for SCD

Question 52

What are characteristics of R-sided Hypertensive disease? | Most common cause?

Answer 52

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

Question 53

What can cause an acute cor pulmonale?

Answer 53

A large pulmonary embolus.

Question 54

Cor pulmonale definition

Answer 54

RV failure due to increased vascular resistance or pulmonary HTN.

Question 55

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

Answer 55

Sudden Cardiac Death