CV- PATHOMA Flashcards

1
Q

polyarthritis nodosa is associated with what infection?

A

HepB

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2
Q

Main complication of Kawasaki disease?

A

coronary artery aneurysm

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3
Q

What abnormality in renal vasculature can cause hypertension? explain pathophysiology

A

renal artery stenosis -> decreased GFR -> increased renin -> peripheral vasoconstriction + more Na+ retention

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4
Q

Define atherosclerosis

A

INTIMAL plaque that obstructs blood flow

  • more than 70% occlusion is needed to be symptomatic
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5
Q

4 modifiable causes of atherosclerosis

it is important to memorize each of this

A
  • smoking
  • hypercholesterolemia
  • diabetes
  • hypertension (more shearing force, easy to damage endothelium)
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6
Q

Describe the mechanism of atherosclerosis formation

A

endothelium damage

  • > LDL deposited in INTIMA
  • > LDL oxidation -> oxidized LDL is consumed by macrphage, forming foam cell
  • > Foam cell becomes fatty streak, which attracts vascular SMOOTH MUSCLE CELL ( with PDGF and FGF)
  • > smooth muscle cell synthesizes extracellular matrix proteins (collagen, elastin) that form FIBROUS CAP
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7
Q

Atherosclerosis vs. Arteriolosclerorsis- what is key difference?

A

atherosclerosis- medium sized vessels

arteriolosclersis: ARTERIOLo- , thus small arterioles

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8
Q

Arteriolosclerosis: what are two types? what is cause of each type? histologic finding in each type?

A
  • hyaline arteriolosclerosis
    : caused by long standing BENIGN HTN or diabetes
    : hyalinosis of vascular wall
  • hyperplastic arteriolosclerosis
    : caused by SEVERE MALIGNANT HTN
    : hyperplasia of SMOOTH MUSCLE, onion-skin appearance on histology
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9
Q

Explain how hypertension results in weakening of intima, predisposing condition for dissection / aneurysm

A

hypertension

  • > hyaline arteriosclerosis of the vasa vasorum
  • > atrophy of media
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10
Q

Is unstable angina due to complete or incomplete occlusion?

A

incomplete occlusion
=> this may explain ST depression

vs. MI is complete occlusion => ST elevation

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11
Q

What are two possible consequences of fibrinolysis in MI?

A
  • reperfusion injury: introduction of radicals that damage myocytes
  • contraction band necrosis: introduction of Ca2+ into myocytes, resulting hypercontraction of myofibrils
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12
Q

What is heart failure cells? They are associated with what cardiac pathology?

A
  • hemosiderin laiden macrophages in alveolar sac

- left sided hear failure -> pulmonary congestion

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13
Q

most common cause of right sided HF?

A

left sided HF

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14
Q

Explain two types of ASD. which type is more common? which type is associated with Down syndrome?

A

osteum secundum: incomplete fusion of septum secundum and septum primum, majority of cases

osteum primum: opening of bottom part of septum primum, less common, associated with DOWN SYNDROME

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15
Q

Explain why tetralogy of Fellot is considered as R->L shunt

A

RV hypertrophy and overriding aorta.
RV can eject deoxygenated blood to aorta

  • this is why squatting helps. Squatting increases afterload, limiting blood going into aorta from RV (instead, it will enter pulmonary circulation)
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16
Q

Which two conditions are highly associated with coarctation of aorta?

A
  • Turner

- Bicuspid aortic valve

17
Q

What does hyper-dynamic circulation in aortic regurgitation mean?

A

increased pulse pressure,

bounding pulses, pulsating nail bed, head bobbing

18
Q

What kind of LV hypertrophy can happen as a consequence of aortic regurgitation?

A

essentric hypertrophy
: happens in volume overloaded state

vs. concentric hypertrophy: is more muscular hypertrophy, ex: HCM

19
Q

Acute rheumatic disease vs. chronic rheumatic disease: what valvular pathology is associated in each case

A

Acute: regurgitation

Chronic: stenosis

  • kinda makes sense: stenosis is due to wear and tear, thus chronic
20
Q

Compare how S.aureus and S.viridans affect different types of valves in endocarditis

A
  • S.aureus: acute, strong virulence factor, can damage previously normal valves, tricupsid (IV)
  • S.viridans: subacute, only damage PREVIOUSLY DAMAGED valves. The more valves get damaged, the more likely endocarditis develops valvular defects