Overview of HTN: Epidemiology and Consequences AND Pathology of HTN Flashcards
T/F Hypertension encompasses a large group of disorders.
T
Two broad groups of htn
- primary/essential: resistance or compliance htn
2. secondary
What is the underlying abnormal regulation that contributes to htn?
drysregulated svr supplemented by abnormal regulation of sodium/fluid and abnormal fibrosis of tissues
Consequences of htn: left ventricle
higher systolic pressure, higher systolic wall stress, hypertrophy, fibrosis of myocardium leading to impaired diastolic relaxation
Consequences of htn: arterial system
increased wall stress, arterial vascular disease (aneurysms, atherosclerosis), arteriolar disease (obliterative destruction of systemic arterioles) leading to even more increased SVR
Consequences of htn: kidney
destruction of kidney due to arteriolar destruction leading to even more reduced ability to excrete sodium –> nephroarteriolosclerosis
Why is htn regarded the “silent killer”?
leads to conditions that actually have lots of symptoms and damage
- cardiac dysfunction secondary to progressive lvh and myocardial fibrosis –> increased frequency of systolic/diastolic chf
- accelerated atherosclerotic disease in large/small arteries –> MI, stroke, aneurysm
- renal dysnfucntion secondary to progressive renal destruction –> chronic renal failure
What is secondary htn and how common is it?
5-10% of pts –> due to underlying disease process, most often renal or adrenal
What is primary htn?
multigene controlled plus environmental factors leading to htn syndrome
What is benign htn?
adaptive: any most people have this: diastolic bp>90 or systolic > 140 –> clinically silent until later in course
What is malignant htn?
5% of pts –> usually follows benign ht –> diastolic bp>120, systolic>210 w/clinical symptoms that will be lethal if not treated rapidly
What vascular diseases can be accelerated by htn but may exist otherwise?
- atherosclerosis
2. hyaline arteriolosclerosis
What vascular disease are the consequence of htn?
- adaptive: vasoconstriction, hypertrophy, fibroelastic intimal hyperplasia
destructive: fibrinioid necrosis, hyperplastic arteriolitis, microangiopathic hemolytic anemia
What is the difference between adaptive and destructive htn w/regards to their according causative htn?
adaptive: any htn
destructive: only malignant htn
What kinds of vascular changes are irreversible?
arterial fibroelastic intimal hyperplasia, hyalin arteriosclerosis, advanced atherosclerosis
vs reversible vasoconstriction, medial hypertrophy
What is hte consequence of irreversible change
fixed increase in vascular resistance causing difficulty to treat
What hypothesis explains destructive vascular changes w/htn?
upregulation of RAAS –> toxic effects on blood vessels as in fibrinoid necrosis or hyperplastic intimal arteriolitis
Consequences of htn: cardiac (not just left ventricle)
coronary atherosclerosis leading to CHF, angina, MI
Consequences of htn: cerebral
microaneurysms, rupture of berry, lacunae, charcot-bourchard aneurysms leading to intracerebral hemorrhage, white infarcts from ischemia due to emboli from larger cerebral vessels
Which effects of nephroarteriolosclerosis are aggravators of htn?
- decreased GFR, decreased Na excretion
- activation of RAA
- loss of urodilatin/natriuretic peptides from kidney
loss of renal excretory function produces chronic renal failure
Risk factors for malignant htn?
men, smokers, African Americans, low SES status
Mortality associated with malignant htn?
90% in 1 year untreated
75% in 5 years if treated
Clinical presentation of malignant htn
headache, nausea, vomiting, visual, papilledema, retinal flame-shaped hemorrhage, hematuria, proteinuria, MAHA, activation of RAAS, azotemia
Causes of death in malignant htn
- acute renal failure
- stroke
- acute congestive heart failure w/wo MI
