HTN pathopharm (325E1) Flashcards
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
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
what are potassium rich you should eat when on a thiazide & loop diuretics
avocado, spinach, watermelon, banana, beans, tomatoes, sweet potatoes, beets
what should you monitor in a pt on hydrochlorothiazide & furosemide
potassium labs
what is the loop diuretic we will be tested on
furosemide
where do loop diuretics work
loop of henle
what does loop diuretics cause
profound diuresis (so used for HTN & fluid overload)
what can indicate kidney dysfunction
low urine output in a pt taking a loop diuretic
normal K+ range
3.5-5
what is the potassium sparing diuretics diuretic we will be tested on
spironolactone
what diuretic is usually given with another class of diuretics
potassium sparing
what should you monitor in a person taking spironolactone
+K because of hyperkalemia
classes of sympatholytics
-alpha adrenergic blockers
-centrally acting alpha2 agonists
-beta adrenergic blockers
what do sympatholytics all impact
the SNS (fight or flight response) which causes vasoconstriction which is usually good unless chronically wrongly activated then we need these drugs to turn it off
what beta adrenergic blockers do we need to know for the exam
-metoprolol (selective)
-propranolol (non selective)
-carvedilol (alpha & beta)
two types of beta receptors
-beta 1: found in the heart (cardioselective)
-beta 2: found in the lung (usually we do not want to block this)
what pts should not take propranolol & carvedilol
pt’s with lung disease, asthma or COPD bc it is non selective and will block beta 2
blocking beta 1 receptors does what
decrease heart rate and contractility
increasing nitric oxide does what
causes vasodilation
what can beta blockers mask
hypoglycemia bc it prevents tachycardia which is a main sign of low BG
what happens if you do not wean a pt off of beta blockers
possible rebound HTN which causes critical rise in BP and puts pt at high risk for CV event/stroke/death
when do we hold beta blockers
HR is less than 60 or systolic BP is less than 100
what alpha 2 adrenergic antagonist do we need to know for the exam
clonidine
what selective alpha 1 blocker do we need to know for the exam
doxazosin
what are the classes of RAAS blockers
-ace inhibitors
-ARBs
-Renin inhibitors
what conversion in RAAS do ace inhibitors stop
A1 to A2
what conversion in RAAS do ARBs stop
A2 to aldosterone
what ace inhibitors do we need to know for the exam
-captopril
-lisinopril
what is a first line therapy for hypertension and heart failure
ace inhibitors
what is the HTN drug of choice for pts w/ DM
ace inhibitors (captopril & lisinopril)
what is the biggest complaint from pts to switch from an ace inhibitor
dry, nonproductive persistent cough
what is the biggest fear when giving ACE inhibitors
angioedema -> rare but most common in African Americans, it is the swelling of your larynx
what drugs can pregnant women not take
-ace inhibitors
-ARBs
what should you monitor if a pt is on captopril or lisinopril
K+ level due to risk of hyperkalemia
what angiotensin receptor blocker do we need to know for the exam
Iosartan
what is the difference in angioedema risk between ARBs and ACE
ARBs do not have the racial disparity seen in ACE
what renin inhibitor do we need to know for the exam
aliskiren
what RAAS blockers cannot be given together
ACE and ARBs
what calcium channel blockers do we need to know for the exam
-nifedipine (HTN)
-nicardipine (HTN)
-diltiazem (rhythm disturbances)
-verapamil (rhythm disturbances)
what drug should be given for refractive hypertension in an IV
nicardipine
who are calcium channel blockers best for
elderly and African Americans
what vasodilators do we need to know for the exam
hydralazine
PO hydralazine is usually seen
in combination w/ other anti HTN agents
IV hydralazine is usually seen
in emergent settings or when PO cannot be tolerated
why do we care about low potassium
K+ works on our heart and if low can cause cardiac rhythm problem
MOA for all diuretics
-increased urinary output
-decreased circulating volume
-decreased arterial resistance