HTN pathopharm (325E1) Flashcards
(67 cards)
what is the primary driver of BP
the sympathetic nervous system
what are the two ways RAAS affects BP
1) Na & H2O retention (fluid volume)
2) Vasoconstrictor & H2O retention (tighter/smaller passage)
how much volume is on board in blood vessels to keep normal BP
RAAS system
drop in BP and/or changes in Na levels -> release of angiotensinogen (A) by liver -> kidneys release renin which combines w/ A to make angiotensin 1 -> in the lung A1 is converted to A2 by ace -> A2 + adrenal glands release aldosterone to increase Na & H20 retention or combines w/ ADH to cause vasoconstriction
what is pathological reason for hypertension
chronic stress that stimulates RAAS so RAAS is constantly running, not just when it is actually needed to maintain or hypersensitivity to angiotensin 2 or high secretors of renin
other mechanisms that affect blood pressure
1) arterial baroreceptors: receptors in the heart that sense BP and can alter by altering HR
2) vascular auto-regulation: regulates based on mean arterial pressure (MAP) so alters the resistance (diameter) in the arterioles consistent BP at tissue level
blood pressure categories
normal: <120 & <80
elevated: 120-129 & <80
HTN 1: 130-139 or 80-89
HTN 2: 140+ or 90+
HTN crisis: >180 &/or >120
primary HTN
“no known cause”
complicated interactions of genetics, environment & several neurohormonal effects
SNS, RAAS, Natriuretic peptides
what causes an overactive SNS that then leaves to increased BP/HTN
systemic inflammation, endothelial disfunction, obesity related hormones, insulin resistance which leads to systemic vasoconstriction, overactive raas -> overtime remodels blood vessels & damages which leads to permeant increase of peripheral vascular resistance
natriuretic peptides
chemical and hormones that helps control renal sodium excretion interruptions in these can cause increased BP by holding onto more Na & H2O causing increased BP
risk factors for primary hypertension
-insulin resistance
-age: M >55, F>60
-smoking
-salt intake
-low activity
-stress
-obesity
-African Americans
-high Alc consumption
-hyper lip
-genetics
secondary hypertension
known cause -> treat underlying condition
-renal disorder: kidneys not sensing BP prop
-adrenomedullary tumors: constant secretion of aldosterone or release of angiotension
-adrenomedullary tumors: release epinephrine & stims SNS
-Drugs (meds)
-pregnancy
what medications can lead to secondary hypertension
-oral contraceptives
-corticosteroids
-antihistamines
-cocaine
-amphetamines
Signs and Symptoms of HTN
silent killer, usually no signs
look for end organ damage (chest pain, headache, visual changes, weakness/pain in extremeities)
what is HTN highly correlated with
CAD bc of high demand the left ventricle causing hypertrophy -> accelerates progression of atherosclerosis and increases risk for aortic aneurysm weakened vessel walls)
long term outcomes of HTN
-cardiac: CAD
-Kidneys: ESRD (inc raas & sns)
-brain: stroke/aneurysm/hemorrhage (dec blood flow & O2)
-eyes: retinopathy & blindness (leading cause, inc pressure)
-gangrene, intermittent claudication
HTN crisis
-rapidly progression htn
-occurs more common in primary htn
-2 types: urgency & emergency (more serious)
HTN crisis: urgency
-no S/s of end stage organ damage
-BP >180/120
-treat w/ oral agents & gradually reduce
-causes: anxiety, pain, abrupt withdrawal
HTN crisis: emergency
-uncontrolled BP that leads to end organ damage
-BP: >180/120
-S/s: headache, blurred vision, stroke, brain hem, chest pain, acute coronary syndrome, heart dysry
-aggressively lower BP in mins to hours w/ IV meds (labetalol)
classes of diuretics
-potassium sparing
-thiazide
-loop
MOA for all diuretics
-increased urinary output
-decreased circulating volume
-decreased arterial resistance
how do diuretics lower BP
decreasing cardiac output by lowering stroke volume (block sodium & chloride reabsorption)
what is the first line management of HTN
thiazide diuretics
what is the thiazaide diuretic we will be tested on
hydrochlorothiazide
where do thiazide diuretics work
distal tubule
