101314 path of HTN Flashcards

1
Q

HTN effects on morphology of small arteries or arterioles

A

hyaline arteriolosclerosis

hyperplastic arteriolosclerosis

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2
Q

hyaline arteriolosclerosis

A

benign
with age
seen in also benign nephrosclerosis

homogeneous pink, thickening of vessels with narrowing of lumen (due to leakage of plasma across endothelium as a result of HTN-when this leakage occurs, sm musc cells produce excess matrix)

(when you increase pres, the endothelial barrier fails)

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3
Q

hyperplastic arteriolosclerosis

A

characteristic of malignant HTN

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4
Q

what is a characteristic feature of hyperplastic arteriolosclerosis

A

onion skinning, concentric laminated walls with luminal narrowing due to reduplicated basement membrane and sm musc cells

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5
Q

necrotizing arteriolitis

A

term used when malignant HTN is associated with fibrinoid necrosis

bad, end stage of arterioles

irregular fibrin deposition as cells die in the wall

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6
Q

systemic hypertensive heart disease

A

concentric left ventricular hypertrophy IN THE ABSENCE of other cardiovascular pathology

history of pathologic evidence of HTN

affects 25% of US population

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7
Q

morphology of systemic hypertensive heart disease

A

cardiomegaly-concentric hypertrophy w/o dilatation (greater than 1.5 cm wall thickness)

myocyte HYPERTROPHY (increase myocyte size and nuclear enlargement)

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8
Q

systemic hypertensive heart disease possible outcomes

A
normal longevity
progressive ischemic heart disease
progressive renal damage
stroke
progressive heart failure
sudden cardiac death
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9
Q

effects of systemic hypertensive heart disease on brain

A

cerebral vessels affected by arteriolosclerosis are weakane and more likely to rupture, causing intracerebral hemorrhage

infarcts

hypertensive encephalopathy (headaches, confusion, vomiting, convulsions)

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10
Q

systemic hypertensive heart disease effects on kidney

A

benign HTN (gradual)-common in older pts. kidneys usually atrophic. granular, pitted surfaces. hyaline arteriolosclerosis of vessels results in ischemia and atrophy. glomeruli may become sclerosed.

in malignant HTN-see pinpoint petechial hemorrhages on surface. fibrinoid necrosis of arterioles. hyperplastic arteriolosclerosis and microthrombi lead to global ischemia.

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11
Q

cor pulmonale

A

pulmonary hypertensive heart disease

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12
Q

causes of cor pulmonale

A

acute-massive pulmonary embolism, resulting in RV dilatation w/o hypertrophy (b/c hypertrophy takes TIME)

chronic-caused by primary pulmonary or secondary pulmonary HTN due to chronic lung diseases. you see RV hypertrophy.

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13
Q

CHF pathogenesis

A

usually fromt a slowly developing intrinsic deficit in contraction (but occasionally can be acute)

mechanisms:

  • abnormal load presented to heart
  • impaired ventricular filling
  • osbruction due to valve stenosis
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14
Q

compensatory mechanisms for CHF-acute

A

frank starling mechanism

activation of neurohumoral (NE, renin angiotensin aldosterone, release of ANP for atrium)

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15
Q

compensatory mechanisms for CHF-non acute

A

cardiac hypertrophy

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16
Q

what kinds of hypertrophy are there for the cardiac muscle?

A

pressure overload-causing concentric hypertrophy (HTN, aortic stenosis)

volume overload-causing eccentric hypertrophy. hypertrophy accompanied by dilatation (mitral or aortic regurg)

17
Q

left ventricular hypertrophy is an independent risk factor for sudden death: true of false?

A

true

18
Q

heart failure cells

A

hemosiderin laden macrophages that you see in pulmonary edema

19
Q

prerenal azotemia

A

impaired kidney fxn due to severe perfusion deficit. can occur with left sided heart failure that results in severe perfusion deficit.

20
Q

how does R sided heart failure occur USUALLY?

A

secondary to left sided failure

21
Q

when you have an obstruction, ventricles respond by?

A

acutely-dilatation

chronic-hypertrophy

22
Q

azotemia is more significiant with which sided heart failure?

A

right sided