101314 path of HTN Flashcards
HTN effects on morphology of small arteries or arterioles
hyaline arteriolosclerosis
hyperplastic arteriolosclerosis
hyaline arteriolosclerosis
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)
hyperplastic arteriolosclerosis
characteristic of malignant HTN
what is a characteristic feature of hyperplastic arteriolosclerosis
onion skinning, concentric laminated walls with luminal narrowing due to reduplicated basement membrane and sm musc cells
necrotizing arteriolitis
term used when malignant HTN is associated with fibrinoid necrosis
bad, end stage of arterioles
irregular fibrin deposition as cells die in the wall
systemic hypertensive heart disease
concentric left ventricular hypertrophy IN THE ABSENCE of other cardiovascular pathology
history of pathologic evidence of HTN
affects 25% of US population
morphology of systemic hypertensive heart disease
cardiomegaly-concentric hypertrophy w/o dilatation (greater than 1.5 cm wall thickness)
myocyte HYPERTROPHY (increase myocyte size and nuclear enlargement)
systemic hypertensive heart disease possible outcomes
normal longevity progressive ischemic heart disease progressive renal damage stroke progressive heart failure sudden cardiac death
effects of systemic hypertensive heart disease on brain
cerebral vessels affected by arteriolosclerosis are weakane and more likely to rupture, causing intracerebral hemorrhage
infarcts
hypertensive encephalopathy (headaches, confusion, vomiting, convulsions)
systemic hypertensive heart disease effects on kidney
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.
cor pulmonale
pulmonary hypertensive heart disease
causes of cor pulmonale
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.
CHF pathogenesis
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
compensatory mechanisms for CHF-acute
frank starling mechanism
activation of neurohumoral (NE, renin angiotensin aldosterone, release of ANP for atrium)
compensatory mechanisms for CHF-non acute
cardiac hypertrophy