HTN Flashcards
What are the 3 major determinants of blood pressure?
Cardiac output
total blood volume
total peripheral vascular tone/resistance
Systemic BP is regulated by:
Intrarenal BP is regulated by:
Systemic BP - sympathetic nervous system, RAAS
Intrarenal BP - Angiotensin II - constricts efferent arterioles even in the face of renal hypotension (ie renal stenosis)
What are the 3 effects of angiotensin II?
ionotropy vasoconstriction Na retention (via aldosterone release)
JG cells produce renin in response to any of these 3 factors:
1) decrease stretch in the wall
2) decrease Na [ ] in the distal lumen
3) b-receptor stimulation
What is 1˚ HTN? What is 2˚ HTN?
1˚ = essential, HTN without known cause 2˚ = HTN with known, specific cause
What are causes of increased total blood volume?
What is it normally associated with?
How do you treat it?
What is its hypotension component?
causes: XS Na intake, 1˚ hyperadlosteronism, renal disease with salt retention, cushing’s syndrome
associated with: decreased renin levels
Tx: diuretics
Hypotension component: hypovolemic shock
What are causes of increased cardiac output?
How do you treat it?
What is its hypotension component?
causes: hyperthyroidism (leads to cardiac b1 stimulation), hyperkinetic heart syndrome (due to abnormal neural/catecholamine stimulation ie pheochromocytoma)
Tx: b-blockers
hypotension component: cardiogenic shocik
What are causes of increased peripheral vascular tone?
What is it normally associated with?
How do you treat it?
What is its hypotension component?
causes: renalvascular HTN, hyperthyroidism (increased catecholamine), hypothyroidism (low b2 receptors in peripheral arterioles), malignant HTN, late phase of essential HTN
associated with: increased renin levels
Tx: vasodilators
Hypotension component: distributive shock
What is 1˚ essential HTN?
no specific cause or disease, but possible mxns include:
genetic predisposition hyperactive sympathetic nervous system/stress hyperactive renin-angiotensin system increased intracellular Na vascular hypertrophy atherosclerosis
What two phases does 1˚ essential HTN progress through?
Early phase: hyperkinetic phase characterized by excess CO and increased but variable BP. Peripheral renin tends to be low
Late phase: characterized by increased peripheral vascular resistance; fixed BP, peripheral renin tends to be high.
What is 2˚ HTN?
HTN caused by specific ailments
1) Hyperaldosteroism
2) Pheochromocytoma
3) Renal artery stenosis
4) renal parenchymal disease
5) coarctation of aorta
6) Cushings
7) Thyroid dz
8) Alcohol
9) Birth control
10) pregnancy
How does hyperaldosteronism cause HTN?
What are the diagnostic features?
due to adenoma/hyperplasia of adrenal cortex
-> aldosterone secretion -> fluid expansion -> HTN
-> increased K secretion -> hypokalemia -> metabolic alkalosis
diagnostic features: low K, high aldosterone, and low renin (due to negative feedback)
How does pheochromocytoma cause HTN?
What are the diagnostic features?
tumor in adrenal medulla
NE secreting tumor -> vasoconstriction, pallor, bradycardia
Epi secreting tumor -> tachycardia, orthostatic hypotension
diagnostic features: high metanephrines and vanillymandelic acid (metabolites of NE/Epi)
How does Renal Artery Stenosis cause HTN?
What are the diagnostic features?
stenotic artery causes a fall in AFferent arteriolar pressure, which stimulates the JG apparatus to release renin, thereby causing BP to rise.
diagnostic features: abdominal bruit, low K (due to excess aldosterone secretion), high renin levels in stenotic kidney
How does coarctation of the aorta cause HTN?
What are the diagnostic features?
proximal aorta is narrowed -> diminished perfusion of the lower body + kidneys -> increased renin secretion
diagnostic features: elevated BP in the arms and lower BP in the rest of the body, rib notching, mumur (due to flow through coarctation)
How does Cushing’s disease cause HTN?
What are the diagnostic features?
hyperplasia of the pituitary gland –> increased ACTH production -> increased cortisol secretion from adrenals (cortisol has minerocorticoid properties similar to aldosterone –> HTN)
How does thyroid disease cause HTN?
What are the diagnostic features?
hyperthyroidism - induces synthesis of b1 receptors and Na/K ATPase. Results in increased CO –> HTN
hypothyroidism - reduces synthesis of b2 receptors in peripheral arterioles (b2 = results in vasodilation/decreased PVR), results in HTN
How does alcohol cause HTN?
What are the diagnostic features?
stimulates sympathetic NS, alcohol withdrawal can also stimulate sympathetic NS (leading to increase BP)
How does oral contraceptives cause HTN?
What are the diagnostic features?
estrogens stimulate angiotensinogen production by the liver -> leads to increased angiotensin II/aldosterone levels.
Angiotensin II negatively feedbacks to suppress renin secretion.
Diagnostic features: high angiotensin II, high aldosterone, low renin
What are the 3 major consequences of HTN?
development of atherosclerosis
myocardial infarcts
strokes
What are the consequences of HTN on the heart?
coronary artery disease LV hypertrophy (concentric) - S4 gallop, dyspnea, pulmonary congestion, ST depression, T inversion in lateral ventricular leads (I, aVL, V5, V6)
What are the consequences of HTN on the brain?
cerebrovascular atherosclerosis
aneurysms -> cerebral hemorrhages
What are the consequences of HTN on the kidneys?
sustained HTN causes kidneys to become diseased:
1) arteriolar sclerosis -> nephrosclerosis (thickening of the basement membrane with various degrees of hyalinization and atrophy; results in thickened glomerular capsules)
2) renal artery stenosis
3) can ultimately result in end-stage renal disease
What is aortic dissection?
blood within media layer of the blood vessel; leads to arteriolar constriction –> HTN
NOT related to atherosclerosis
What is HTN retinopathy?
patients present with arteriolar narrowing (copper lines), hemorrhage, cotton wool spots, papilledema (swelling of optic disk), which interferes with vision.
Dx: AV Nicking, copper lines, cotton wool spots
What is malignant HTN?
where renal arteries and small arteries develop hyperplastic arteriolar sclerosis with fibrinoid necrosis of arterioles and glomerular capillares, thickening of intima, and narrowing of the vascular lumen.
leads to a vicious cycle of renal arteriolar sclerosis –> increase renin levels –> increase angiotensin levels –> increase constriction/narrowing of lumens
