Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiology > Path Review Points > Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

What is secondary hypertension?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is a saccular aneurysm?

A

Forms sac outside of lumen. Dilation of the wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is a fusiform aneurysm?

A

Aneurysm in the lumen of the artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How do aneurysms cause symptoms?

A

Mass effect (compresses things)

Distal embolization

Rupture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where do intimal tears most commonly occur in aortic dissection?

A

Ascending aorta a little above aortic valve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is an exit site?

A

Intimal tear in the true lumen connects to the false lumen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a reentry site?

A

False lumen reconnects with the true lumen (good thing)

–>double barrel aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is marfan’s syndrome

A

Fibrillin defect–structural abnormality vs abnormal TGFbeta1 binding activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do you treat aortic dissection?

A
  • Replace affected area with vascular prosthesis

- Decrease BP and LV force of contraction with drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is Losartan?

A

TGFbeta1 inhibitor for marfan’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the causes of mitral stenosis?

A

Chronic rheum. heart disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Causes of aortic stenosis

A

Dystrophic (wear and tear=senile) calcification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Causes of aortic regurgitation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Symptoms of aortic valve stenosis

A

Angina, syncope, congestive HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Fish mouth orifice

A

Associated with chronic rheumatic heart disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What do you think of when you see right sided endocarditis?

A

IV drug user

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Pathogenesis of bacterial endocarditis and possible consequence

A
  • 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How does non-bacterial thrombotic endocarditis occur?

A

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
Q

List the earliest changes due to ischemic injury to the myocardium

A
  • 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
Q

List 4 clinical consequences of myocardial ischemia

A
  1. Silent
  2. Stable
  3. Prinzmetal’s variant angina (coronary artery spasm with ST segment elevation)
  4. Acute coronary syndromes
29
Q

How long until myocytes die without reperfusion in acute myocardial infarction?

A

within 20 min

30
Q

How long until cell death reaches its max extent?

A

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
Q

What does total occlusion of an artery result in vs less than total occlusion?

A

Transmural myocardial infarction –>total occlusion

Subendocardial infarction –>partial or total occlusion that was quickly revascularized

32
Q

When does coagulative necrosis occur?

A

12 hrs-3 days (doomed to occur if ischemia happens for more than 20-40minutes)

33
Q

What happens microscopically minutes after an acute MI?

A

Thin wavy stretched myocytes

34
Q

What happens microscopically 6-24hrs after an acute MI?

A

Coagulative necrosis (loss of nuclei, cross striations and hypereosinophilia

35
Q

What happens microscopically 6hrs-3days after an acute MI?

A

Infiltration by polys then macrophages

36
Q

What happens microscopically 7-10days after an acute MI?

A

clearance of debris by macrophages

37
Q

What happens microscopically 2-4wks after an acute MI?

A

Ingrowth of granulation tissue

38
Q

What happens microscopically 8-10wks after an acute MI?

A

Collagenized scar forms

39
Q

What happens grossly for 6-12 hrs after an acute MI?

A

Nothing, can only be detected by TTC stains

40
Q

What happens grossly 12-24hrs after an acute MI?

A

Dark mottling (trapped deoxy blood)

41
Q

What happens grossly 1-3days after an acute MI?

A

Progressive tan-yellow pallor of necrosis

42
Q

What happens grossly 3-10days after an acute MI?

A

Hyperemic border with progressively depressed necrotic center

43
Q

What happens grossly 10-14days after an acute MI?

A

Grey-red depressed area due to advanced granulation tissue

44
Q

What happens grossly 2-8wks after an acute MI?

A

Grey-white scar from periphery to center

45
Q

Contraction band necrosis

A

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
Q

What is a hemorrhagic infarct a marker of?

A

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
Q

3 consequences of reperfusion after ischemic injury

A
  1. Rescue non lethally injured myocytes
  2. Alter pattern of necrosis of dying cells (contraction band)
  3. Cause additional injury
48
Q

Pericarditis

A

Can be a complication of transmural MI or can occur 10 days later as an autoimmune issue

49
Q

How long after MI do we expect to see ruptures in the heart if they occur?

A

After 3-5 days because that is max acute inflammation, softening and necrosis

50
Q

How do ventricular aneurysms form?

A

Scar stretches. Can lead to thrombus due to stasis and emboli
problems with conduction through that part as well

51
Q

Gross heart changes in restrictive cardiomyopathy

A

Dilated atria with normal sized ventricles

52
Q

Microscopic changes in DCM

A

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
Q

Complications of DCM

A
  • Progressive HF (death w/o transplant or can resolve in pregnancy)
  • Mitral Regurg (annulus dilation)
  • Dysrhythmias
  • Emboli from mural thrombi
54
Q

Banana shaped compressed ventricles

A

HOCM (obstructive)

–hypercontractility

55
Q

Myofibril disarray associated with?

A

HCM

56
Q

HCM murmur

A

Systolic

57
Q

Complications of HCM?

A
  • Outflow obstruction (1/3)
  • Mitral endocarditis
  • Emboli from mural thrombosis
58
Q

Treatment of HCM

A

Drugs to reduce contraction strength or surgery/ablation for outflow obstruction

59
Q

Causes of HCM

A

ALL genetic defects in sarcomere proteins

60
Q

Congo red stain

A

stains for amyloid (think restrictive CM)

61
Q

Difference between HCM and RCM?

A

stiffness of ventricles without hypercontractility

62
Q

3 forms of amyloid affecting the heart

A
  1. Immunoglobulin light chain derived (mult myeloma)
  2. Soluble amyloid associated protein (rheumatoid arthritis)
  3. Transthyretin (senile cardiac amyloid)
63
Q

Lymphocytic myocarditis associated with?

A
  • viral (coxsackievirus A/B
  • Protozoa (Chagas’ disease)
  • transplant rejection
  • Bacteria (lyme)
  • Autoimmune, (lupus)
  • subacute presentation, can dev DCM
64
Q

Eosinophilic myocarditis associated with?

A

-drug hypersensitivity

65
Q

Granulomatous myocarditis associated with?

A
  • Sacoidosis disease–systemic

- if just in heart, giant cell myocarditis=terrible fulminant disease, req transplant but can recur

66
Q

Clinical presentation of myocarditis

A
  • 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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions