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Pharmacology > Anti-Hypertensive > Flashcards

Anti-Hypertensive Flashcards

1
Q

First line drugs of choice

A 
Diuretics
Calcium Channel Blockers
ACE inhibitors
Angiotensin Receptor Blockers
(BB are not first line because they do not work well in AA populations, and cause significant side effects
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2
Q

Diuretics

A

Drugs of choice in uncomplicated hypertension

Mild/moderate hypertension with lifestyle modification

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3
Q

Thiazides

A 
Hydrochlorothiazide, Chlorthalidone
Inhibits Na/Cl cotransporter
Initial volume contraction
Decreased peripheral resistance (prostaglandins)
Mild Na excretory effects
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4
Q

Loop Diuretics

A

Furosemide (Lasix)
Blocks Na/K/2Cl co-transporter in TAL
Venous dilation from prostaglandins
Dehydration/hyponatremia, hypokalemia, impaired diabetes control, increased LDL/HDL, ototoxicity
Drug interactions: NSAIDs, Aminoglycosides

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5
Q

K Sparing Diuretics

A

Spironolactone, eplerenone, tramterene, amiloride
Aldosterone receptor blocker/prevent insertion of ENAC channels in collecting tubule
Side Effects: Hyperkalemia, gynecomastia (spironolactone)
Drug interactions: NSAIDs (block good effects of prostaglandins), ACE inhibitors and ARBs (also inhibit aldosterone)
Contraindications: RAS inhibitors (have both ACE inhibitors and ARBs)

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6
Q

Ca Channel Blockers

Nondihydropyridine

A

Can do heart and smooth muscle receptors

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7
Q

Ca Channel Blockeres

Dihydropyridines

A

More selective for vascular smooth muscle

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8
Q

Ca Channel Blockers

A

MoA: Reduce vascular resistance by reducing Ca influx

Non-dihydropyridine reduce pacemaker potentials, AV node conduction, and contractility

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9
Q

Ca Channel Blockers

Nifedipine

A

Dihydropyridine
Limited affect on pacemaker or conduction
SE: acute tachycardia, headache, peripheral edema (arteriolar dilation > venodilation), flushing

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10
Q

Ca Channel Blockers

Diltiazem

A

Non-dyhydropyridine
Reduces pacemaker and conduction current
SE: dizziness, headache, edema, bradycardia

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11
Q

Ca Channel Blockers

Verapamil

A

Non-dihydropyridine
More pronounced reduction of current
SE: dizziness, headache, edema, constipation, bradycardia

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12
Q

CCB therapeutic Notes

A

Non-dihydropyridines are contraindicated in patients with conduction disturbances
Use non-dihydropyridine with caution in patient given B-blockers
Avoid use of short acting CCBs for chronic hypertension

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13
Q

Sympatholytic Drugs

A

MOA: Reduces sympathetic-mediated vasoconstriction, Co, and renin release

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14
Q

Clonidine

A

Sympatholytic Drug
Centrally acting agent
a2 adrenergic receptor agonist in medullary CV center
Decreases sympathetic outflow from CNS
SE: sedation, dry mouth, bradycardia, dermatitis
Drug interactions: CNS depressants
Withdraw slowly to prevent rebound hypertension

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15
Q

Guanfacine

A

Longer half-life than clonidine

Less chance of rebound hypertension

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16
Q

Methyldopa

A

Sympatholytic Drug
a2-adrenergic receptor agonist (same MOA as clonidine)
Competes wtih L-DOPA for DOPA decarboxylase
Inhibits dopamine production
Drug interactions: levodopa
SE: Sedation, nightmares, movement disorders, hyperprolactinemia, anemia
Contraindications: Liver Dx
USED IN HYPERTENSION WITH PREGGOS

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17
Q

Reserpine

A

Indirect Acting Adrenergic Blocking Agent
Blocks VMAT vesicular transporter
Prevents storage of NE centerally and peripherally
Combined with diuretics for mild/moderate HTN
SE: sedation, diarrhea, depression, bradycardia, nasal congestion
Drug interactions: CNS depressant, MAOIs

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18
Q

Alpha Adrenergic Receptor Antagonists

A

Block a-adrenergic-mediated vasoconstriction at receptor

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19
Q

Phenoxybenzamine

A

Alpha adrenergic receptor antagonist
Non selective
Primary use in PHEOCHROMOCYTOMA
SE: Tachycardia

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20
Q

Prazosin

A

Alpha adrenergic receptor antagonist
Less tachycardia than direct vasodilators
Initial hypotension
Does not impair exercise tolerance
Terazosin and doxazosin have longer half-life
SE: Hypotension (first dose), dizziness, headaches, weakness
Also decreases LDL/HDL

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21
Q

Beta Blockers

A

Decrease cardiac contractility and CO
Decrease renin secretion
Decrease angiotensin II production

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22
Q

Propranolol

A

Nonselective B-blocker
Mild/moderate hypertension
Adjunct to prevent tachycardia with vasodilators
Lipophilic

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23
Q

Nadolol

A

Nonselective B-Blocker
Longer half-life than propranolol
Better compliance
Hydrophilic

24
Q

Pindolol

A 
Non-selective B-Blocker
Partial agonist
Less bradycardia
Lipophilic
Good for patients who still want to exercise
25
Q

Metoprolol

A

B1-Selective
Fewer respiratory side effects
Lipophilic

26
Q

Atenolol

A

B1-Selective
Hydrophilic
Excreted by kidney

27
Q

Labetolol

A 
B-Blocker
Has some a-blocker capacity
Orthostatic hypotension and sexual dysfunction
Used for pheochromocytoma
Lipophilic
28
Q

Carvedilol

A 
Nonselective B-Blocker
a-receptor antagonist
vasodilator
Lipophilic
Increases NO
29
Q

BB SE

A 
Bradycardia
Impotence
Increased TG
Decreased HDLs
Hyperglycemia
Impaired exercise tolerance
30
Q

BB Drug Interactions

A

CCB

Reduced contractility and conduction

31
Q

BB Contraindication

A

Cardiogenic shocks
Sinus bradycardia
Asthma
Severe Heart Failure

32
Q

BB and Diabetics

A

Can mask insulin-induced hypoglycemia

Give them ACEI instead

33
Q

Vasodilators

A

Vasodilation of arterioles

34
Q

Hydralazine

A

Vasodilator
Orally effective
Used in drug resistant hypertension and emergency
Long term use is poor
SE: Tachycardia, angina aggravation, fluid retention, nausea, vomiting, sweating, flushing, lupus-like symptoms
NSAIDs can reduce effectiveness

35
Q

Minoxidil

A

Vasodilator
Used in drug resistant hypertension
SE: Same as hydralazine including hypertrichosis (werewolf syndrome)

36
Q

Nitroprusside

A 
Vasodilator
Used in emergencies (BP > 200)
Immediate onset
Brief duration
Promotes arterial and venous dilation
SE: Nausea, vomiting, muscle twitch, cyanide poisoning (from metabolites in long-term usage)
37
Q

ACE Inhibitors

A

Blocks production of angiotensin II and ATII-mediated vasoconstriction
ATII causes growth and aldosterone release
ACE inhibitors prevent breakdown of bradykinin so it can go on and increase prostaglandins and NO

38
Q

Catopril

A

ACEI
Short half life
Multiple daily doses
Active metabolites

39
Q

Enalapril

A 
ACEI
Converted to active metabolite enalaprilat
Longer onset of action
Longer half life
Dose 1-2xday
40
Q

Lisinopril

A 
ACEI
Water soluble
Excreted unchanged by kidney
Longer half-life
Allows 1x daily dosing
More predicitable onset and duration of action
41
Q

ACEI SE

A

Hyperkalemia
Rash
Dry cough
Angioedema

42
Q

ACEI Drug Interactions

A

Exacerbates hyperkalemic effect of K sparing drugs

43
Q

ACEI Contraindications

A

PREGGOS

Bilat renal stenosis

44
Q

ACEI Notes

A

Prolongs survival in pts with HF or LV dysfunction after MI (ATII promotes growth/inflammation so if we prevent that the heart wont get more damaged)
Preserves renal function in diabetic patients

45
Q

Angiotensin II Receptor Blockers (ARBs)

A

Mediate vasoconstriction and Na retention
Less effective in Na-sensitive hypertensiv epatients (AA_
Reduce dose in hypovolemia or live disease
Better results with diuretic combo
Effect takes 1 week

46
Q

Losartan

A

Selective ARB
SE: Hyperkalemia
Contraindications: PREGGOS (cause renal failure)
Drug interactions: exacerbates hyperkalemia in K sparing drugs

47
Q

Good Combos

A

Thiaxaide or loop diurteic with K sparing diuretic
Thiazide with BB
CCB with ACEI

48
Q

Bad Combos

A

ACEI with K sparing diuretics (exacerbate hyperkalemia)
ACEI and ARBs (no advantage in diuretics, but increased risk of hyperkalemia)
Don’t mix drugs with same MOA, efficacy won’t increase

49
Q

Diabetes mellitus

A

ACEI (delay loss of renal function)
a-blockers
CCBs (limited effects on carbohydrate metabolism)

50
Q

Hearth Failure

A

ACEIs (reduce mortality and recurrent MI)

Combine with diuretics for congestion

51
Q

MI

A

ACEIs reduce remodeling
ACEIs reduce subsequent MI
BBs (but not the partial agonist pindolol) reduce arrhythmia and remodeling

52
Q

Pregnancy

A

Avoid ACEI or ARBs and BBs (inhibits renin)

Methyldopa is widely used

53
Q

African Americans

A

Monotherapy with diuretics, CCBs most efficacious

Monotherapy with BBs and ACEIs not as effective though good control can be done through combined diuretics

54
Q

Elderly

A

Small doses with small increments
Simple regimens
Monitor side effects closely

55
Q

Diabetes mellitis

A

ACEI
A-blockers
CCBs have some effects on carbohydrate metabolism

56
Q

Hyperlipidemia

A

Low dose diuretics have little effects on cholesterol and TG
BB can raise TG
A-blockers can decrease LDL/HDL ration
CCBs, ACEIs, ARBs have little effect on lipid profile

57
Q

Obstructive Airway Disease

A

Avoid BBs

Pharmacology (44 decks)

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