Antihypertensives Flashcards

1
Q

3 main factors affecting blood pressure

A

CO
Blood volume
Resistance
- artery walls flexibility
- artery diameter
- blood viscosity or thickness

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2
Q

Causes of HTN

A

essential HTN is UNKNOWN

psychological and physiological stress
High Na and low K and Ca - facilitates RAAS increasing BP
metabolic syndrome - obesity, dyslipidaemia, diabetes - mainly affects afterload/SVR since larger body mass (excess fat and sugar) the longer the blood vessels, in response, the heart has to pump harder to get the same amount of pressure getting into the tissues putting a strain in the heart overtime increasing chance of having CADs
smoking - excess vasoconstriction
environmental factors - eg. pollution as air pollutants enter the systemic circulation and causes vasoconstriction
genetic factors

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3
Q

long-term consequences of HTN

A

heat performance gets overused leading to several CADs:

Heart failure - when RAAS gets overused causing blood retention in the systemic circulation (pulmonary/ peripheral oedema)
Accelerated atherosclerosis > MI
Renal failure - renal arteries are damaged overtime and narrows causing insufficient bladder perfusion in the kidneys
Stroke - blood vessels in the brain gets damaged
Weakened blood vessel walls > aortic/ cerebral aneurysms

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4
Q

Classes of Antihypertensive meds

A

ACE inhibitors
ARBs - ACE II receptor blockers
Beta-blockers
Calcium channel blockers
Diuretics

Centrally acting antihypertensives (methyldopa)
Peripheral vasodilators (hydralazine)

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5
Q

Pharmacodynamics of ACE inhibitors

A

inhibits conversion of ACE I to ACE II causing:
decreased vasoconstriction > decreased SVR
decreased aldosterone production > increasing Na+ and H2O excretion
decreased BP
increased renal blood pressure

indications: HTN, heart failure and nephropathy

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6
Q

Ace inhibitor meds

A

quinapril
lisinopril
enalapril
captropril
fosinopril

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7
Q

adverse effects of Ace inhibitors

A

Hypotension (monitor for orthostatic hypotension and dizziness)
Hyperkalaemia (since aldosterone is inhibited K+ are retained)
Angioedema (blocks airway, swelling underneath the skin)
Cough (ACE inactivates bradykinin - which mediates inflammation causing vasodilation)

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8
Q

Nursing considerations for Ace inhibitors

A

monitor hypotension
monitor K+ levels - avoid diet rich in K and Na
assess angiodema (swelling of the face and mouth)
educate NOT TO SUDDENLY STOP ACEIs as it causes REBOUND HTN

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9
Q

ACE inhibitors contradictions

A

pregnancy - teratogenic effects on foetus

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10
Q

Pharmacodynamics of ARBs/ Angiotensin II receptor blockers

A

Blocks angiotensin II receptors in the smooth muscles of the arteries inhibiting vasoconstriction
High affinity to AT II receptors causing vasodilation
Lowers BP and increase blood volume to the heart

Indicators:
HTN
alternative to ACE inhibitors to manage HF and diabetic nephropathy

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11
Q

AT II receptor blocker/ ARB meds

A

losartan
candesartan

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12
Q

adverse effects of ARBs

A

Hypotension
Hyperkalaemia

DO NOT CAUSE COUGH as it does not accumulate bradykinin

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13
Q

Pharmacodynamics of beta-blockers

A

Antagonist at sympathetic (noradrenaline) beta receptors
Blocks:
alpha-1 receptors: decreased SVR
beta-1 receptors:
- decreased HR and myocardial contractility > reduced myocardial O2 demand
- inhibits renin release > inhibit Na+ and H2O retention > reduce preload and decrease SVR
- slows development of atherosclerotic plaques

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14
Q

Indicators of beta blockers

A

HTN
Stable angina
Cardiac dysrhythmias after MI
HF
secondary prevention after MI

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15
Q

Beta blocker meds

A

Cardioselective Beta-1 blockers:
metoprolol
celiprolol
bisoprolol

Beta and Alpha-1 blockers:
labetalol
carvedilol
sotalol

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16
Q

Adverse effects of Beta blockers

A

Bradycardia
Bronchospasm
Drowsiness and fatigue
Worsen CHF

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17
Q

Contradictions for beta blockers

A

Pts with asthma/COPD - beta blockers can block beta-2 receptors in the lungs causing bronchospasm
Pts with DM - beta blockers inhibits beta cells in the pancreas preventing glycogenolysis causing hypoglycaemia

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18
Q

Nursing considerations for beta blockers

A

DO NOT STOP ABRUPTLY - risk of rebound HTN, instead decrease dose slowly
monitor hypotension - risk of falling from orthostatic hypotension
educate to change position slowly
monitor S&S of HF - wet lung sounds, weight gain, oedema

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19
Q

Pharmacodynamics of calcium channel blockers/ CCBs

A

blocks Ca channels by inhibiting Ca influx into smooth muscles and myocardial cells
- smooth muscle relaxation> vasodilation including coronary blood vessels
- reduce AV conduction
- decrease heart workload

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20
Q

CCB meds

A

3 classes:
Verapamil - myocardium
Nifedipine - smooth muscle
Diltiazem - myocardium & smooth muscle

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21
Q

CCBs indicators

A

HTN
Angina
Dysrhythmias

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22
Q

CCBs adverse effects

A

Constipation
Nocturia (waking up during the night and urinate)
Headache (cerebral vasodilation)
Hypotension, postural hypotension and fatigue (risk of falls)

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23
Q

Nursing considerations for CCBs

A

Orthostatic hypotension (risk of falls) - encourage to sit in the side of the bed for few minutes then rise up slowly
Change positions slowly when lying

DO NOT STOP MEDS ABRUPTLY! it can cause rebound HTN/ Angina
DO NOT DRINK GRAPEFRUIT JUICE - can cause severe hypotension
ELEVATE leg to reduce oedema
ENCOURAGE fluids, fruits, and fibre rich diet for CONSTIPATION

24
Q

Pharmacodynamics of Diuretics

A

act to reduce Na reabsorption in the kidneys
reduce H20 retention
decrease blood volume and plasma Na

25
Q

4 main classes of Diuretics

A

Loop diuretics
Thiazide diuretics
K sparring diuretics
Osmotic diuretics

26
Q

Pharmacodynamics of Loop diuretics

A

Acts on loop of henley
Inhibit Na+ & Cl- reabsorption (25%) > Na+ loss > decreased reabsorption of H20 > increase UO and decrease blood volume
VERY STRONG DIURESIS

27
Q

Loop diuretic meds

A

Furosemide

28
Q

Loop diuretics indicators:

A

HTN
HF or CHF
renal disease
Pulmonary and Peripheral oedema

29
Q

Loop diuretics adverse effects

A

HYPOKALAEMIA - highest risk (< 3 mmol/L)
Dehydration
Hypotension
Hyponatraemia
Hyperglycaemia

30
Q

Nursing considerations for Loop diuretics

A

obtain and monitor vitals
monitor input and ouput
Replace K+ if below normal

31
Q

Pharmacodynamics of Thiazide diuretics

A

acts on DCT/ distal convoluted tubule
inhibit reabsorption of Na+ & Cl- (5%) > decreasing reabsorption of water > increase UO and decrease blood volume
LESS DIURESIS compared to Loop diuresis

32
Q

Thiazide diuretic meds

A

bendroflumethiazide
chlortalidone
indapamide

33
Q

Thiazide diuretics adverse effects

A

HYPOKALAEMIA - less intense compared to loop diuretics (< 3mmol/L)
Hypotension
Hyperglycaemia
Hyponatraemia
Dehydration

34
Q

Thiazide diuretics indicators

A

HTN
HF
renal disease
Oedema

35
Q

Nursing considerations for thiazide diuretics

A

obtain and monitor vitals
monitor input and output
replace K+ if levels below normal
daily weights
AVOID for pts with GOUT
AVOID this meds for pts with SULFA ALLERGY

36
Q

Pharmacodynamics of K+ sparring diuretics

A

Aldosterone antagonist
increase Na+ & H20 excretion > reabsorb K+

37
Q

K+ sparring diuretic meds

A

Spironolactone

38
Q

K+ sparring diuretics indicators

A

HTN
Oedema
Hypokalaemia

39
Q

K+ sparring diuretics adverse effects

A

HYPERKALAEMIA (> 5 mmol/L)
hypotension
diarrhoea
gastritis
drowsiness
erectile dysfunction

40
Q

Nursing considerations for K+ sparring diuretics

A

AVOID FOODS HIGH IN K
monitor K+ levels (risk of hyperkalaemia)

41
Q

Pharmacodynamics of osmotic diuretics

A

increase viscosity of the filtrate H20 can’t be reabsorbed
increase excretion of Na+ & Cl-

42
Q

Osmotic diuretics indicators:

A

Cerebral oedema
Decreased intraocular pressure (fluid inside the eyes)

43
Q

osmotic diuretics adverse effects

A

Oedema
blurred vision
N&V, diarrhoea
urinary retention

44
Q

Nursing considerations for osmotic diuretics

A

IV ONLY!
perform neuro assessment and LOC (lvl of consciousness) for cerebral oedema

45
Q

adverse effects of diuretics to older adults

A

DEHYDRATION
POSTURAL HYPOTENSION
ELECTROLYTE IMBALANCES

RISK FOR: falls, incontinence, confusion, constipation and fever

46
Q

what is “triple whammy” when taking antihypertensives

A

a combination of ACE inhibitors, ARBs, diuretics and NSAIDs

47
Q

adverse effects of “triple whammy”

A

decrease renal function

48
Q

Pharmacodynamics of methyldopa

A

a prodrug converted into methylnoradrenaline
active metabolite that binds to alpha-2 receptors in the brain stem
reducing sympathetic stimulation > decrease SVR > slows HR

49
Q

adverse effects of methyldopa

A

postural hypotension
mental clouding (less wakeful or aware)
GI upsets

50
Q

nursing considerations for methyldopa

A

AVOID ALCOHOL (increase sedation effects)
TAKE IT WITH FOOD if feeling nauseated

51
Q

Pharmacodynamics of Hydralazine

A

direct acting vasodilator
selective arterioles dilator > decrease SVR > increases HR and myocardial contractility

52
Q

Hydralazine indicators

A

HTN (especially for pregnant mothers)
HF

53
Q

hydralazine adverse effects

A

Tachycardia
hypotension
fluid retention
GI upset
headache
dizziness

54
Q

Pharmacodynamics of Glyceryl Trinitrate/ GTN

A

decreases smooth muscle contractility
act mainly on veins and arterioles
reduces preload and some afterload > decreases BP

55
Q

GTN indicators

A

HTN prior to STEMI and stroke clot retrieval