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Path Review Points Flashcards

0
Q

What is primary hypertension?

A

> 90% of hypertension. No underlying single cause, prob multigene controlled plus environmental factors like stress, diet, salt etc

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1
Q

What is secondary hypertension?

A

<10% of hyperT. Some identified underlying disease,most often renal is causing the hyperT

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2
Q

What are causes of secondary hypertension?

A

Renal (inc RAAS)
Adrenal (inc aldosterone, glucocorticoid and catecholamines)
Pregnancy (increase in placental sFLT-1 which is a angiogenesis inhibitor): pre-eclampsia=hyperT, peripheral edema, proteinuria . Eclampsia=with seizures.
Increased intracranial pressure

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3
Q

What is a saccular aneurysm?

A

Forms sac outside of lumen. Dilation of the wall

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4
Q

What is a fusiform aneurysm?

A

Aneurysm in the lumen of the artery

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5
Q

What is a berry aneurysm?

A

At the base of the brain, congenital defect that enlarges over time and is exaggerated by hypertension

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6
Q

What is an atherosclerotic aneurysm?

A

Weakening of the wall due to atherosclerosis leads to an aneurysm. Most common in the abdomen.

If i is thoracic, think medial degeneration that can cause inc in diameter or dissection or ectasia (involves long segment of aorta). If this process occurs in a 20y.o think marfans syndrome

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7
Q

How do aneurysms cause symptoms?

A

Mass effect (compresses things)

Distal embolization

Rupture

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8
Q

Where do intimal tears most commonly occur in aortic dissection?

A

Ascending aorta a little above aortic valve

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9
Q

What is an exit site?

A

Intimal tear in the true lumen connects to the false lumen

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10
Q

What is a reentry site?

A

False lumen reconnects with the true lumen (good thing)

–>double barrel aorta

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11
Q

What is marfan’s syndrome

A

Fibrillin defect–structural abnormality vs abnormal TGFbeta1 binding activity

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12
Q

How do you treat aortic dissection?

A
  • Replace affected area with vascular prosthesis

- Decrease BP and LV force of contraction with drugs

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13
Q

What is the role of TGF1-beta in Marfans?

A

Mutations in fibrillin-1 lead to inc activity of TGF beta (because TGF is usually inactive when bound to fibrillin)

  • abn valve dev (mitral prolapse)
  • abn alveoli
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14
Q

What is Losartan?

A

TGFbeta1 inhibitor for marfan’s

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15
Q

What are the causes of mitral stenosis?

A

Chronic rheum. heart disease

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16
Q

What are the causes of mitral regurg

A

Myxomatous degen, dilation of mitral valve ring, endocarditis (sudden due to hole or chordae rupture), MI (ruptured pap muscle)

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17
Q

Causes of aortic stenosis

A

Dystrophic (wear and tear=senile) calcification

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18
Q

Causes of aortic regurgitation

A

Dilation of aortic root (old age, hyperT, atherosclerosis, Marfans)

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19
Q

Contrast calcification on mitral valve vs aortic

A

Aortic: nodular calcification on leaflets proturding into sinuses of valsalva. No fusion of valve commissures (vs chronic rheum). usually causes stenosis

Mitral: on fibrous ring (women, elderly, elevation of LV p, myoxm degen). Can cause mitral regurg or, rarely, can erode into conduction system

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20
Q

Symptoms of aortic valve stenosis

A

Angina, syncope, congestive HF

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21
Q

What happens in myxomatous degeneration? Both grossly and clinically

A
  • Leaflets thicken, stretch, chordae elongate–>prolapse
  • Get asymptomatic systolic click, mitral regurg, thrombus formation (endocarditis or systemic embolization) or dysrhythmias

–>due to inc deposition of mucopolysaccarides in the spongiosa

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22
Q

Fish mouth orifice

A

Associated with chronic rheumatic heart disease

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23
Q

Chronic rheumatic fever heart consequences

A
  • Usually affects mitral or mitral + aortic

- valve leaflet scarring, neovascularization, fusion of commisures, shortening/thickening/fusion of chordae tendonae

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24
What do you think of when you see right sided endocarditis?
IV drug user
25
Pathogenesis of bacterial endocarditis and possible consequence
- Requires pre-existing fibrin deposition on the heart followed by bacteremia allowing the bacteria to enter fibrin deposit - Shedding of antigens into the blood and dev of antibodies->intravascular immune complex formation causing glomerulonephritis or small vessel vasculitis - Valvular regurge (perforation or ruptured cordae) - Embolism (septic emboli can lead to abscesses elsewhere)
26
How does non-bacterial thrombotic endocarditis occur?
Occurs in pts with injury to endocardium often due to turbulent blood flow and in the setting of hypercoaguability like low grade DIC or mucin producing adenocarcinomas
27
List the earliest changes due to ischemic injury to the myocardium
- Switch from aerobic to anaerobic glycolysis - Cessation of contraction - Altered electrical activity - Relaxation of myofibrils allowing for stretch of myocytes due to contraction of adj myocytes - Reversible by reperfusion for 20-40 min
28
List 4 clinical consequences of myocardial ischemia
1. Silent 2. Stable 3. Prinzmetal's variant angina (coronary artery spasm with ST segment elevation) 4. Acute coronary syndromes
29
How long until myocytes die without reperfusion in acute myocardial infarction?
within 20 min
30
How long until cell death reaches its max extent?
Not all cells die at once. Start in subendocardium and go in wavelike fashion towards the epicardium, taking 4-6 hours to reach its max extent
31
What does total occlusion of an artery result in vs less than total occlusion?
Transmural myocardial infarction -->total occlusion Subendocardial infarction -->partial or total occlusion that was quickly revascularized
32
When does coagulative necrosis occur?
12 hrs-3 days (doomed to occur if ischemia happens for more than 20-40minutes)
33
What happens microscopically minutes after an acute MI?
Thin wavy stretched myocytes
34
What happens microscopically 6-24hrs after an acute MI?
Coagulative necrosis (loss of nuclei, cross striations and hypereosinophilia
35
What happens microscopically 6hrs-3days after an acute MI?
Infiltration by polys then macrophages
36
What happens microscopically 7-10days after an acute MI?
clearance of debris by macrophages
37
What happens microscopically 2-4wks after an acute MI?
Ingrowth of granulation tissue
38
What happens microscopically 8-10wks after an acute MI?
Collagenized scar forms
39
What happens grossly for 6-12 hrs after an acute MI?
Nothing, can only be detected by TTC stains
40
What happens grossly 12-24hrs after an acute MI?
Dark mottling (trapped deoxy blood)
41
What happens grossly 1-3days after an acute MI?
Progressive tan-yellow pallor of necrosis
42
What happens grossly 3-10days after an acute MI?
Hyperemic border with progressively depressed necrotic center
43
What happens grossly 10-14days after an acute MI?
Grey-red depressed area due to advanced granulation tissue
44
What happens grossly 2-8wks after an acute MI?
Grey-white scar from periphery to center
45
Contraction band necrosis
Reperfusion of dead cells (no nuclei) that had an influx of Ca2+ that caused hypercontraction. Marker of reperfusion, not a marker of reperfusion injury
46
What is a hemorrhagic infarct a marker of?
Reperfusion injury -mediated by oxygen derived free radicals that can kill additional myocytes and injure microvessels, resulting in interstitial hemorrhage. Leads to red infarct and contraction band necrosis
47
3 consequences of reperfusion after ischemic injury
1. Rescue non lethally injured myocytes 2. Alter pattern of necrosis of dying cells (contraction band) 3. Cause additional injury
48
Pericarditis
Can be a complication of transmural MI or can occur 10 days later as an autoimmune issue
49
How long after MI do we expect to see ruptures in the heart if they occur?
After 3-5 days because that is max acute inflammation, softening and necrosis
50
How do ventricular aneurysms form?
Scar stretches. Can lead to thrombus due to stasis and emboli problems with conduction through that part as well
51
Gross heart changes in restrictive cardiomyopathy
Dilated atria with normal sized ventricles
52
Microscopic changes in DCM
Hypertrophied myocytes, stretched thin myocytes, interstitial fibrosis leading to reduced contractility (1/3-1/2 have underlying genetic defects, or myocarditis, infectious autoimmune, alcohol, pregnancy, drugs etc)
53
Complications of DCM
- Progressive HF (death w/o transplant or can resolve in pregnancy) - Mitral Regurg (annulus dilation) - Dysrhythmias - Emboli from mural thrombi
54
Banana shaped compressed ventricles
HOCM (obstructive) --hypercontractility
55
Myofibril disarray associated with?
HCM
56
HCM murmur
Systolic
57
Complications of HCM?
- Outflow obstruction (1/3) - Mitral endocarditis - Emboli from mural thrombosis
58
Treatment of HCM
Drugs to reduce contraction strength or surgery/ablation for outflow obstruction
59
Causes of HCM
ALL genetic defects in sarcomere proteins
60
Congo red stain
stains for amyloid (think restrictive CM)
61
Difference between HCM and RCM?
stiffness of ventricles without hypercontractility
62
3 forms of amyloid affecting the heart
1. Immunoglobulin light chain derived (mult myeloma) 2. Soluble amyloid associated protein (rheumatoid arthritis) 3. Transthyretin (senile cardiac amyloid)
63
Lymphocytic myocarditis associated with?
- viral (coxsackievirus A/B - Protozoa (Chagas' disease) - transplant rejection - Bacteria (lyme) - Autoimmune, (lupus) - subacute presentation, can dev DCM
64
Eosinophilic myocarditis associated with?
-drug hypersensitivity
65
Granulomatous myocarditis associated with?
- Sacoidosis disease--systemic | - if just in heart, giant cell myocarditis=terrible fulminant disease, req transplant but can recur
66
Clinical presentation of myocarditis
- Mild flu-like illness+palpitations+ chest pain that progresses to fulminant HF - CAn have lethal dysrhythmias or cause sudden death in young athletes - can diagnose with endomyocardial biopsy

Cardiology (16 decks)

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