Treatment of Hypertension Flashcards

1
Q

risks of HTN

A

stroke, heart failure, sexual dyfx, vision loss, heart attack, kidney disease/failure

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2
Q

risk factors for HTN

A

chronic alc
smoking
stress/anxiety
sedentary
genetic
sodium
caffeine
obesity
age

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3
Q

essential hypertension cause

A

unknown

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4
Q

secondary hypertension cause

A

concurrent medical condition
renal artery constriction
pheochromocytoma on adrenal glands
primary aldosteronism

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5
Q

BP equation

A

BP = CO x TPR
CO = SV x HR

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6
Q

BP categories

A

normal: <120/80
elevated: 120-129/80
HTN I: 130-139/80-89
HTN II: >140/>90
crisis: >180/120

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7
Q

stages of HTN med care

A
  1. lifestyle changes
  2. medication management
  3. multiple medications
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8
Q

non pharmacological treatment for HTN

A

dietary salt restriction
potassium supplementation
weight loss
DASH diet
aerobic exercise

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9
Q

Diuretic general MOA

A

act on kidneys to increase sodium and water excretion

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10
Q

types of diuretics and uses

A

thiazide: mild-mod HTN
loop: reduce edema NOT HTN
potassium sparing: weak anti HTN

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11
Q

diuretics site of action

A
  1. PCT: acetazolamide
  2. PCT/descending limb: osmotic diuretics
  3. ascending limb: loop diuretic
  4. DCT: thiazide type
  5. collecting duct: potassium sparing
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12
Q

thiazide MOA

A

inhibit sodium resorption in DCT

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13
Q

loop diuretics MOA and suffix

A

inhibit sodium and chloride reabsorption in loop
-semide

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14
Q

K+ sparing MOA and suffix

A

prevent K+ secretion
-one/-ene

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15
Q

side effects of diuretics

A

fluid loss: orthostatic HTN, mental changes, confusion, irritability
electrolyte imbalance: weakness/cardiac/GI/GLC metabolism/lipid metabolism disturbances; fatigue; hyponatremia/kalemia
hyperkalemia w K sparing

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16
Q

Renin angiotensin system function

A
  1. decreased BP
  2. kidney release Renin
  3. renin converts angiotensinogen to angiotensin I
  4. travels to lungs
  5. angiotensin converting NZ converts to angiotensin II vasoconstriction
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17
Q

effects of angiotensin II

3

A

vasoconstriction
release aldosterone increasing Na retention
stim ADH causing retention
induce thirst

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18
Q

ACE inhibitor MOA

A

inhibit ang II formation to decrease vasoconstriction/lower BP
limit aldosterone secretion to decrease retention

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19
Q

ACE inhibitor suffix

A

-pril

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20
Q

ACE inhibitor side effects

A

dry cough
hyperkalemia
acute kidney damage
angioedema
fetotoxic

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21
Q

angiotensin receptor blockers MOA

A

block ang II receptors to prevent vasoconstriction and aldosterone release

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22
Q

ARB suffix

A

-sartan

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23
Q

ARB side effects

A

less than ACE
fetotoxic
acute kidney damage
hyperkalemia

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24
Q

Calcium channel blocker MOA

A

block Ca entry into vascular cells and heart, causing influx of Ca into cells to activate calmodulin - MLCK - myosin binds actin and contracts
so blocking this reduces contraction

25
CCBs side effects
dizziness flushing headache fatigue peripheral edema
26
beta blocker MOA
bind beta 1 receptor on heart to block effects of NE and epi decrease HR and CO for BP
27
betablocker suffix
-olol
28
non selective vs selective beta blockers
non selective can cause breathing issues bc active in lungs
29
beta blocker side effects
bronchoconstriction decreased HR/contractility OH depression lethargy decreased libido
30
alpha blockers suffix
-osin
31
alpha blockers MOA
block alpha 1 adrenergic receptor on vascular smooth muscle to decrease vascular resistance causes reflex tachycardia needing beta blocker
32
alpha 2 agonists drugs
clonidine methyl-DOPA
33
alpha 2 agonists MOA
stimulate alpha 2 receptors in brain to reduce sympathetic outflow decrease HR, CO, vascular resistance
34
alpha 2 agonists side effects
dry mouth dizziness sedation
35
vasodilators drugs
hydralazine minoxidil
36
vasodilator MOA
directly relax arteriolar smooth muscle to vasodilate for lower BP treat mod-servere HTN activate K channels to increase efflux, hyper polarize smooth muscle to inhibit Ca influx and muscle contraction
37
vasodilator side effects
reflex tachycardia headache OH
38
renin inhibitors
like ACE/ARB use when other drugs not working or in combo w others
39
PT considerations for HTN
monitor BP for hyper/hypo OH: monitor and be cautious w position changes fatigue/dizzy: gradual progression of exercise and monitor intensity to prevent falls exercise intensity: beta blockers blunt HR response to exercise dehydration: diuretics, impact exercise tolerance/falls/hypotension electrolyte imbalance: muscle weakness/cramp pt education: side effects
40
cardiac action potential
0: depolarization w Na channel opening influx 1: close fast Na channels for rapid repolarization 2: plateau w Ca influx and K efflux 3: repolarization K channels efflux open 4: rest
41
Class I antiarrhythmics
block fast Na channels to increase AP duration, delay repolarization
42
class I antiarrhythmics side effects
diarrhea, nausea, thrombocytopenia, torsades de pointes
43
Class IB antiarrhythmics MOA
mild block of Na channels, accelerate repolarization ventricular arrhythmics
44
Class IB antiarrhythmics side effects
CNS effects, hypotension, nausea, tremor
45
Class IC antiarrhythmics MOA
strong fast Na channel block ventricular arrhythmias
46
Class IC antiarrhythmics side effects
visual disturbances, dizziness, risk of proarrythmia, taste disturbance, constipation, headache
47
Class II antiarrhythmia drugs
beta blockers -olol block beta adrenergic receptors reducing sympathetic effects ventricular arrhythmias and atrial tachycardias
48
Class III antiarrhythmics MOA
potassium channel blockers to delay repolarization
49
Class III antiarrhythmics side effects
pulmonary toxicity, thyroid dysfunction, hepatotoxicity, corneal deposits
50
Class IV antiarrhythmics MOA
block calcium channels in cardiac tissue reduce HR by preventing next beat from firing as quickly -one -ilide
51
adenosine
inhibit AV conduction short term, IV injection for SVT
52
digoxin
reduce conduction through AV node use to control atrial flutter/fib
53
atropine
treat sinus bradycardia by blocking vagal effects on SA node
54
PT considerations for pts with arrhythmias
monitor vitals recognize side effects to avoid falls pace/progression important bc decreased exercise tolerance consider exercise type and avoid high CV load pt education: side effects knowledge of emergency procedures coordinate w healthcare providers
55
PT with Na channel blockers
monitor HR/rhythm, adapt intensity
56
PT with beta blockers
use RPE to monitor exercise intensity bc blunted HR
57
PT with K+ channel blockers
monitor EKG for torsades de pointes to respond to acute events
58
PT with Ca channel blockers
monitor for OH, positional changes