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Basic causes of hypertension
high sodium, RAAS, aldosterone, SNS
aldosterone is made by the ___
adrenal cortex
How can SNS cause hypertension
vasoconstriction
Med classes used to treat hypertension
diuretics, ca channel blockers, alpha and beta blockers, vasodilators, ACEs, ARBs
high stroke volume usually ___ BP
increases
How do diuretics lower BP
get rid of fluids by increasing urine output (some also increase salt excretion)
What causes the RAAS system to activate
low blood flow to kidneys
What fluid retention and high sodium intake do to SV and BP
increases
The lungs are continuously releasing ___and the liver is continuously releasing ___, even when the RAAS system isn't active
ACE, angiotensiongen
When RAAS is activated, kidneys relase
renin
Renin and angiotensinogen interact to create
angiotensin 1
angiotensin 1 and ___ interact to create angiotensin 2
ACE
Drug class used to prevent the creation of angiotensin 2
ARBs
What drug class prevents ACE from creating angiotensin 2
ACE inhibitors
Angiotensin 2 causes ___ and also goes to the adrenal gland where it increases ___ production in the raas system
vasoconstriction, aldosterone
In the RAAS system, angiotensin 2 increases aldosterone production which causes
increased NaCl and H2O reabsrorption
Drug class that causes smooth muscle around blood vessels to relax
Ca channel blockers
Diuretic aimed at LoH to stop reabsorption of Na and H20
loop thiazide
diruetic aimed at getting rid of Na, while retaining K+
K+ sparing
What does SNS stimulation do to PVR (peripheral resistance)
increases
What does SNS stimulation do to BP and HR
increases
What drug classes are used to treat high PVR, HR, and BP
alpha and beta blockers
If you are on a diuretic, you are automatically a ___ risk
fall
furosemide
loop diuretic
turosemide
loop diuretic
Route used for loop diuretics
oral/IV
loop diuretic used most commonly for simple stable
turosemide
MoA for Loop diuretics
work in LoH to block reabsorption of sodium and water
Along with blocking sodium and water, loop diuretics also block reabsorption of
potassium, chloride, magnesium, and calcium
TA of loop diuretics
diuresis (decrease of edema, weight loss, low BP, increased urine output)
TU of loop diuretics
rapid mobilization of fluid, hypertension, heart failure
SE/Complications of loop diuretics
dehydration, hypotension, ototoxicity, hypokalemia, nocturia
If on a diuretic, and urine output is less than __ ml/hour, notify a provider
30
How can loop diuretics cause ototoxicity
low fluid in ear (causing difficulty balancing)
Hypokalemia is less than ___ mEq/L
3.5
Signs of hypokalemia
NV, leg cramps and weakness
Contraindications of loop diuretics
anuria
Interactions of loop diuretics
digoxin, additive hypotensive effects, NSAIDs
Why do digoxin and loop diuretics interact
hypokalemia and dysrhythmias
hydrochlorothiazide
thiazide diuretic
Route for thiazide diuretics
oral
MoA for thiazide diuretics
work in DCT to block reabsorption of sodium, water, and electrolytes
TA of thiazide diuretics
diuresis
Is the diuresis for thiazide diuretics more or less rapid that diuresis for loop diuretics
less
TU for thiazide diuretics
essential hypertension, heart failure
First choice for essential hypertension drug class
thiazide diuretics
Complications/SE of thiazide diuretics
dehydration, hypokalemia, hyperglycemia, nocturia
Why is diabetes a precaution for thiazide diuretics
hyperglycemia side effect
Contraindication of thiazide diuretic
renal impairment
Interactions of thiazide diuretic
digoxin, additive hypotensive effects, NSAIDs
Spironolactone
K sparing diuretic
Route for K sparing diuretic
oral
MoA of K sparing diuretic
block the action of aldosterone
TA of K sparing diuretic
diuresis by increasing sodium and water excretion (but holding onto potassium)
TU of K sparing diuretic
hypertension, edema, HF
Complications/SE of K sparing diuretics
hyperkalemia
hyperkalemia is greater then ___ mEq/L
5
Signs of hyperkalemia
dyspnea, dysrhythmias
How to treat hyperkalemia
insulin
Contraindications of K sparing diuretics
hyperkalemia, kidney failure w/ anuria, liver/kidney disease
Interactions of K sparing diuretics
ARBs and ACE inhibitors
Why to avoid K sparing diuretics interactions with ACE inhibitors and ARBs
increased risk of hyperkalemia
nifedipine
Ca channel blocker
amlodipine
Ca channel blocker
MoA of Ca channel blockers
blocking of Ca channels in blood vessels
TA of Ca channel blockers
vasodilation of vascular smooth muscle of the arteries/arterioles of the heart
TU of Ca channel blockers
decrease BP
Complications/SE of Ca channel blocker
reflex tachycardia, orthostatic hypotension, peripheral edema
Ca channel blockers often cause reflex tahcycardia, so a ___ is often given with it
beta blocker
Why are acute MI and hypotension precautions for Ca channel blockers
orthostatic hypotension side effect
Cardioselective beta blockers target ___ receptors
B1
Nonselective beta blockers target
B1 and B2
Where are B1 receptors
heart, kidneys
Where are B2 recptors
liver, lungs
Where are A1 receptors
arterioles
metropolol
cardioselective beta blocker
atenolol
cardioselective beta blocker
propranolol
nonselective beta blocker
carvedilol
alpha 1 and beta 1 blocker
labetalol
alpha 1 and beta 1 blocker
What type of beta blocker works the best
nonselective
MoA of beta 1 blockers on the heart
block SNS to decrease HR, contractility, CO and AV node conduction
MoA of beta 1 blockers on the kidneys
block renin to decrease BP, and sodium water reabsorption
MoA of alpha 1 blockers on the arterioles
block SNS causing vasodilation
TU of beta blockers
primary hypertension
Complications/SE of beta 1 blockers
bradycardia, low CO, orthostatic hypotension
Complications/SE of beta 2 blockers
bronchoconstriction, inhibited glycogenesis
What patient should be a SEVERE precaution for beta 2 blockers
asthma
Complications/SE Alpha 1 blocker
orthostatic hypotension
Why should diabetes patients be a precaution for beta blockers
bradycardia and inhibition of glycogenolysis
Can alpha blockers affect beta receptors
no
prazosin
peripheral alpha blocker
clonidine
central alpha blocker
MoA of alpha 1 blockers on arterioles
blocks SNS
MoA of central alpha blockers
decreases SNS outflow in brain and SC to alpha and beta receptors
TA of alpha 1 blockers
vasodilation
TA of central alpha blockers
vasodilation, decrease HR, CO
TU of alpha blocker
primary hypertension
Complications/SE of peripheral alpha blcokers
first dose orthostatic hypotension
How to administer prazosin
at night, monitor BP