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Pharmacology > Antihypertensives > Flashcards

Antihypertensives Flashcards

1
Q

Epidemiology of hypertension (HTN)

A
  • ~50% of adults in the US
  • Increasing prevalence globally
  • ~$131 billion/year & 670,00
  • “Silent Killer”
  • Leading cause of cardiovascular disease/death globally
  • Increased risk for heart disease & stroke: leading causes of death in US
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2
Q

Describe normal blood pressure (BP)

A
  • Systolic BP <120; Diastolic BP <80
  • Must be maintained for organ perfusion
  • Affected by age, weight, sex, race
  • Depends on cardiac output (CO) and total peripheral resistance (TPR)
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3
Q

What variables do antihypertensive medications work on the affect BP

A
  • Heart rate (HR)
  • Stroke Volume (SV)
  • Total peripheral resistance (TPR)
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4
Q

Describe short term BP regulation (seconds-minutes)

A
  • Barorecptor reflex: stretch receptors in large arteries of thorax/neck
  • Humoral factors: catecholamines (adrenal), arginine-vasopressin (pituitary), and angiotensin II (kidneys)
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5
Q

Describe long term BP regulation (hours-days)

A
  • Kidneys: Renin-angiotensin system (RAAS)
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6
Q

Describe how baroreceptors work in BP regulation

A
  • Posture change -> venous pooling -> drop in BP -> postural baroreflex activated
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7
Q

Describe orthostatic hypotension

A
  • AKA postural hypotension
  • Abnormal drop in BP when changing positions: ≥20 mmHg systolic and/or ≥10 mmHg diastolic
  • Due to delayed/inadequate baroreceptor reflex
  • Risk factors: Age >60, Parkinson’s disease, medications
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8
Q

Describe hypertension

A
  • regulation of BP is the same
  • Setpoint of baroreceptors & blood volume is changed
  • Diagnosed by 2 or more BP checks at separate visits
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9
Q

Describe essential hypertension

A
  • ~95%
  • AKA primary HTN
  • gradual onset
  • lifelong
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10
Q

Describe secondary HTN

A
  • ~5%
  • early childhood/later in life
  • dramatic onset
  • may be related to treatable condition
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11
Q

Classes of antihypertensives

A
  • Diuretics
  • Sympatholytics
  • Vasodilators
  • Renin-Angiotensin System (RAS) Inhibitors
  • Calcium channel blockers (CCB)
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12
Q

Describe diuretics

A
  • increased renal excretion of water & sodium, decreased plasma volume
  • decreased blood volume = decreased stroke volume = decreased cardiac output
  • 3 groups based on where they act win nephron: Thiazides (first line therapy), Loop, and Potassium sparing
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13
Q

Describe differences between Thiazides, Loop, and Potassium sparing diuretics

A
  • Thiazides: act on distal tubule, less potent than loop diuretics
  • Loop: act on the loop of Henle, more potential for side effects
  • Potassium sparing: act in collecting duct, mild diuretic effect, “spare” potassium
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14
Q

Lists diuretic drugs

A
  • Chlorthalidone
  • Hydrochlorothiazide
  • Bumetanide
  • Spironolactone
  • Metolazone
  • Furosemide
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15
Q

Adverse effects of diuretics

A
  • Hypokalemia: weakness, fatigue, confusion; often requires supplementation to prevent
  • Hyperkalemia (potassium sparing): muscle cramps, weakness, paresthesia
  • Hyponatremia: confusion, lethargy, seizures
  • Electrolyte imbalances may be fatal if not addressed
  • Fluid depletion: tachycardia, increased CO & TPR (baroreceptor), may activate RAAS
  • Impaired glucose & lipid metabolism
  • Orthostatic hypotension: take early in the day
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16
Q

Describe sympatholytics

A
  • Generally work to descries sympathetic drive
  • Classified based on where they work: Beta blockers, Alpha blockers, Presynaptic adrenergic inhibitors, Centrally acting agents, Ganglionic blockers
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17
Q

Describe beta blockers

A
  • MOA: bind to beta receptors in heart/lungs blocking binding of catecholamines
  • decrease renin = decrease blood volume = SV = decrease CO
  • decrease contractility = decrease SV = decrease CO
  • decrease HR = decrease CO
  • Adjunct therapy
18
Q

Considerations in beta blocker drug selection

A
  • Cardioselectivity
  • Intrinsic sympathomimetic activity (ISA)
  • Membrane stabilization activity
  • Lipophilicity
  • “Newer” generation
19
Q

Describe cardioselectivity and ISA

A
  • Cardioselectivity: non-selective (preferred in other conditions) and selective ( less bronchoconstriction; beta 1>beta 2)
  • ISA: maintain HR
20
Q

Describe membrane stabilization

A
  • Normalize excitability of cardiac cell membrane
  • Propranolol, metoprolol
21
Q

Describe lipophilicity and 3rd generation beta blockers

A
  • Lipophilicity: alters CNS effects (Propranolol)
  • 3rd generation: vasodilation due to alpha1 blockade (Antioxidant effects)
22
Q

Adverse effects of beta blockers

A
  • Generally well tolerated
  • Bronchoconstriction. (asthma)
  • Excessive HR/myocardial depression
  • Impaired glucose & lipid metabolism
  • Orthostatic hypotension
  • Mask hypoglycemia
  • Fatigue/depression
  • Decreased HR
  • Increased rate of perceived exertion (RPE)
  • If abruptly stopped: MI, arrhythmia, sudden death
23
Q

Describe alpha blockers

A
  • MOA: bind to alpha1 receptors on vascular smooth muscle, blocking binding of catecholamines
  • decrease vasoconstriction = decreased TPR
  • Adjunct therapy
  • Commonly used in: benign prostatic hyperplasia, post-traumatic stress disorder (PTSD)
24
Q

Adverse effects of alpha blockers

A
  • Reflex tachycardia: caused by neg. feedback mechanism; caution in pts with cardiac disease
  • Orthostatic hypotension: take at night to lower risk
25
Q

Describe presynaptic adrenergic inhibitors

A
  • MOA: inhibit presynaptic norepinephrine release in peripheral adrenergic neurons
  • decrease sympathetic mediated excitation of heart & peripheral vasculature (decrease CO/TPR)
  • not first line for anything
26
Q

Adverse effects of presynaptic adrenergic inhibitors

A
  • orthostatic hypotension
  • bradycardia
  • tardive dyskinesia
27
Q

Adverse effects on centrally acting agents

A
  • Dry mouth
  • Dizziness
  • Sedation
  • Rebound hypertension/tachycardia: due to rebound sympathetic activity
28
Q

Describe ganglionic blockers

A
  • MOA: affect pre/post synaptic neurons in sympathetic & parasympathetic pathways
  • decrease HR/SV = decrease CO
  • not first line for anything
29
Q

Adverse effects of ganglionic blockers

A
  • Profound hypotension
  • Constipation, urinary retention
  • Dry mouth, blurred vision
30
Q

Describe vasodilators

A
  • MOA: vasodilator the peripheral vasculature directly at cell
  • decrease cGMP = decrease contractility of smooth muscle cells = decrease TPR
  • Adjunct therapy: nitric oxide being studied is used in COVID patients
31
Q

Adverse effects of vasodilators

A
  • Headache
  • Reflex tachycardia: baroreceptor reflex compensation
  • Orthostatic hypotension
  • Unwanted hair growth: face, ears, forehead
32
Q

Describe RAS inhibitors

A
  • Inappropriate activation of renin-angiotensin system -> Angiotensin II
  • Stimulates vascular tissue growth, thickening, & hypertrophy of vascular walls
  • Vasoconstriction
  • Sympathetic nervous system activation
  • Aldosterone release -> Sodium/water retention
  • Self perpetuating cycle
33
Q

MOA of RAS inhibitors

A
  • ACE inhibitors: inhibit enzyme converts angiotensin I to angiotensin II
  • ARBs: block angiotensin II receptors in tissues
  • Renin inhibitors: inhibit renin conversion of angiotensin to angiotensin I
  • decrease fluid/sodium retention = decrease SV = decrease CO
  • decrease angiotensin II = decrease vasoconstriction = decrease TPR
  • First line therapy (ACE inhibitorsARBs)
34
Q

Adverse effects of RAS inhibitors

A
  • Generally well tolerated
  • Hyperkalemia (ARBs/ACE inhibitors)
  • Dry cough (ACE/Renin inhibitors)
  • Angioedema (ACE inhibitors)
  • Kidney injury
35
Q

Describe calcium channel blockers (CCB)

A
  • MOA: blocks calcium entry into vascular smooth muscle
  • decrease HR/SV = decrease CO
  • vasodilation = decrease TPR
  • First line therapy
36
Q

Adverse effects of calcium channel blockers (CCB)

A
  • Peripheral edema
  • Orthostatic hypotension
37
Q

Treatment principles of antihypertensives

A
  • Dietary modifications: dietary approaches to stop HTN (DASH) diet; moderate alcohol & tobacco use
  • Decrease body weight
  • Increase physical activity
  • Behavior modification & stress management
38
Q

Antihypertensives implications for physical therapy

A
  • Underrated patients: increased risk for CV events/stroke
  • Reinforce: lifestyle modifications, dietary modifications, & importance of medication compliance
39
Q

Antihypertensives impact on physical therapy

A
  • Orthostatic hypotension can lead to fainting/falls: changing positions, exiting warm pools
  • With beta blockers: delayed hypoglycemia symptoms, dyspnea, fatigue, unable to use HR to monitor exertion
  • Depressed HR & contractility can decrease exercise tolerance
  • Electrolyte abnormalities can cause paresthesia, muscle cramps, weakness, increase risk of cardiac dysfunction
40
Q

Physical therapy modifications with antihyptensives

A
  • Check BP before & after activities
  • Assist patients when changing positions or exiting heated pool
  • Use caution with activities that cause widespread vasodilation: widespread application of heat (Hubbard tank, whirlpool)
  • Ask patients to check blood glucose prior to activities if on glucose lowering therapies
  • Use RPE to gauge activity level in pts especially with beta blockers
  • Allow for cool down periods after exercise
  • Monitor for signs of electrolyte abnormalities: check for high risk medications
41
Q

Take home points for antihypertensives

A
  • HTN is common & increases risk of heart disease & stroke
  • Variety of treatments exis
  • PT’s play a role in: reinforcing appropriate treatment; helping patients increase physical activity; making modifications to therapy to reduce risk adverse effects

Pharmacology (12 decks)

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