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Pharmacology II > Antihypertensives > Flashcards

Antihypertensives Flashcards

1
Q

What is the mechanism of action for the ACE-Inhibitors?

A

Angiotensin converting enzyme - Inhibitor

  • Inhibits conversion of angiotensin-1 to angiotensin-2
  • Causes vasodilation, decreased aldosterone levels, Na+ and fluid wasting and K+ retention
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2
Q

What is considered a normal BP?

A

SBP = <80

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3
Q

What BP would be considered to be prehypertension?

A 
SBP = 120 - 139    or
DBP = 80 - 89
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4
Q

What BP is considered to be Stage I HTN?

A 
SBP = 140 - 159    or 
DBP = 90 - 99
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5
Q

What BP is considered to be Stage II HTN?

A 
SBP = > or = to 160       or
DBP = > or = to 100
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6
Q

What is the BP goal for a patient without co-morbid conditions?

A

< 140/90

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7
Q

What is the BP goal for a patient with diabetes, CKD, MI, angina, stroke, or heart failure?

A

< 130/80

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8
Q

What is the goal BP for a patient with proteinuria?

A

< 125/75

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9
Q

What is the goal BP for a patient with left ventricular hypertrophy?

A

< 120/80

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10
Q

What is the goal BP for a patient with isolated systolic HTN?

A

Treat with usual BP goals…
For patients with SBP >180, first goal is to reduce to <160 and monitor closely for hypotension. Then, attempt to reduce BP to target goal.

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11
Q

What are some drugs that may worsen HTN?

A
  • Corticosteroids
  • Oral contraceptives
  • NSAIDs and COX-2 Inhibitors
  • Erythropoietin
  • Oral Decongestants
  • Some antidepressants
  • Cocaine and withdrawal from cocaine
  • Nicotine and withdrawal from nicotine
  • Amphetamines
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12
Q

What are some lifestyle modifications that can be done to reduce BP in patients?

A
  • Weight reduction
  • Dietary approaches to stop HTN
  • Physical activity
  • Dietary sodium reductions
  • Reduce consumption of alcohol
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13
Q

What is the mechanism of action for the Alpha-2 Adrenergic Agonists?

A

Stimulates Alpha-2 receptors of the brain stem associated with autonomic regulation of CV system. Activation of Alpha-2 receptors causes neurons to quit releasing norepinephrine.

  • Decreased sympathetic output
  • Decreased BP
  • Mildly decreases HR
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14
Q

What are some therapeutic uses for Alpha-2 Adrenergic Agonists?

A

Not 1st line for HTN, does not reduce M/M

  • Clonidine tabs effective for HTN urgencies
  • Clonidine used in treatment of withdrawal symptoms of nicotine, opiates, benzos, and alcohol.
  • Methyldopa is DOC in pregnancy induced HTN
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15
Q

What are some adverse effects of the Alpha-2 Adrenergic Agonists?

A
  • Orthostatic hypotension and dizziness, headache, and impaired ejaculation
  • Anticholinergic: sedation, dry mouth, constipation, urinary retention, blurred vision
  • Rebound fluid retention - add diuretic
  • WARNING: Abrupt withdrawal causes severe rebound HTN. Taper over 3 - 4 days
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16
Q

What is the mechanism of action for the Alpha-1 Blockers?

A

Competitive blocking of the alpha-1 receptors.
HTN: lowers BP by causing vasodilation. Relaxes both arterial and venous smooth muscle surrounding some blood vessels.
BPH: Relax smooth muscle of the bladder neck & prostate, which improves urine flow in BPH

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17
Q

What are some therapeutic uses for Alpha-1 Blockers?

A

Not 1st line for HTN: does not reduce M/M

  • Reduces BP well
  • BPH: treats symptoms of urinary retention
  • Raynaud’s disease
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18
Q

What are some adverse effects of Alpha-1 Blockers?

A
  • Orthostatic hypotension: FIRST DOSE EFFECT - syncope following 1st dose…give at bedtime
  • Reflex tachycardia
  • Sodium and water retention
  • Dizziness, lack of energy, drowsiness, nasal congestion, headache, decreased libido
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19
Q

What are some drug interactions of Alpha-1 Blockers?

A
  • Use with vardenafil and sildenafil causes hypotension

- Alfuzosin is contraindicated with potent CYP3A4 inhibitors

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20
Q

What are the Alpha-2 Agonist drugs?

A
  • clonidine

- methyldopa

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21
Q

What are the Alpha-1 Blocker drugs?

A
  • doxazosin HTN/BPH
  • alfuzosin BPH
  • terazosin HTN/BPH
  • tamsulosin BPH
  • prazosin HTN
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22
Q

What are the Beta-1 Blocker drugs?

A

A - O in alphabet

  • acebutolol
  • atenolol
  • betaxolol
  • bisoprolol
  • metoprolol
  • nebivolol
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23
Q

What is the mechanism of action for the Beta-1 Blockers?

A
  • Selectively block the Beta-1 receptors
  • Higher affinity for Beta-1 receptors than Beta-2 receptors
  • Decreased HR, decreased force of contraction
  • Block juxtaglomerular cells - block renin release
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24
Q

What are the therapeutic uses for Beta-1 Blockers?

A

Preferred drug for HTN in pts. with cardiac co-morbidities such as:

  • chronic unstable angina
  • acute coronary syndrome
  • post-MI
  • systolic and diastolic CHF to improve M/M
  • Atrial fibrillation and tachycardia
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25
Q

What are some other, non-cardiac therapeutic uses for Beta-1 Blockers?

A
  • Hyperthyroidism to protect heart from excess adrenaline in patients with poorly controlled hyperthyroidism.
  • Essential tremor
  • Autonomic nervous system overload (stage fright; PTSD)
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26
Q

What are some adverse effects of Beta-1 Blockers?

A
  • Hypotension
  • sexual impairment
  • nightmares
  • Transient decreased HDL & increased Tg
  • Acute heart failure, reduced cardiac output
  • Bradycardia and AV block
  • May mask S/S or hypoglycemia in diabetics
  • WARNING: risk of fatal rebound HTN, tachycardia, angina, and MI with abrupt withdrawal. Taper over 1 - 2 weeks
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27
Q

Which patients must you use caution in when prescribing Beta-1 blockers in?

A
  • Uncompensated heart failure
  • AV block
  • Diabetes
  • Cardioselective Beta-blockers are safer than non-selective agents in pts with diabetes, peripheral vascular disease, asthma, and COPD
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28
Q

What are some drug interactions of Beta-1 Blockers?

A
  • Additive AV blocking when given with digoxin, verapamil, or diltiazem
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29
Q

Which drugs may have intrinsic sympathomimetic activity?

A

Beta-1 blockers

  • These have partial agonist activity
  • Have little effect on resting HR, cardiac output, and Tg levels.
  • Do not reduce CV risk like other Beta-blockers and may be detrimental post-MI.
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30
Q

What are the non-selective Beta-blockers?

A

Pinched Paul’s Nads

  • propanolol
  • nadolol
  • pindolol
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31
Q

What is the mechanism of action for the non-selective Beta-blockers?

A

Same as Beta-blockers

  • Selectively block the Beta-1, Beta-2, receptors
  • Decreased HR, decreased force of contraction
  • Block juxtaglomerular cells - block renin release
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32
Q

What are some therapeutic uses for the non-selective beta-blockers?

A
  • chronic unstable angina
  • acute coronary syndrome
  • post-MI
  • systolic and diastolic CHF to improve M/M
  • Atrial fibrillation and tachycardia Cartelol and timolol are used as eye drops to treat glaucoma
  • Hyperthyroidism to protect heart from excess adrenaline in patients with poorly controlled hyperthyroidism.
  • Essential tremor
  • Autonomic nervous system overload (stage fright; PTSD)
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33
Q

Which class of drugs may be used for migraine prophylaxis?

A

Non-selective beta-blockers

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34
Q

Which drugs may treat the following conditions?

  • Hyperthyroidism to protect heart from excess adrenaline in patients with poorly controlled hyperthyroidism.
  • Essential tremor
  • Autonomic nervous system overload (stage fright; PTSD)
  • chronic unstable angina
  • acute coronary syndrome
  • post-MI
  • systolic and diastolic CHF to improve M/M
  • Glaucoma
A
  • Beta-1 Blockers

- non-selective Beta-blockers

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35
Q

What are some adverse effects that may be seen with Non-selective beta-blockers?

A
  • Hypotension
  • sexual impairment
  • nightmares
  • Transient decreased HDL & increased Tg
  • Acute heart failure, reduced cardiac output
  • Bradycardia and AV block
  • May mask S/S or hypoglycemia in diabetics
  • WARNING: risk of fatal rebound HTN, tachycardia, angina, and MI with abrupt withdrawal. Taper over 1 - 2 weeks
  • Peripheral vasoconstriction
  • Bronchoconstriction
  • Hypoglycemia
  • USE CAUTION: in asthma, COPD, PVD, decompensated heart failure, AV-block or fragile diabetes
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36
Q

What are some drug interactions associated with non-selective beta-blockers?

A
  • Additive AV blocking when given with digoxin, verapamil, or diltiazem
  • May blunt the response to albuterol and other Beta-2 agonists
37
Q

What are the alpha-1, beta-1, and beta-2 blocker drugs?

A
  • carvedilol
38
Q

What is the mechanism of action for the alpha-1, beta-1, and beta-2 blocker drugs?

A
  • Selectively block the Beta-1, Beta-2, and alpha-1 receptors
39
Q

What are the therapeutic uses for the alpha-1, beta-1, and beta-2 blocker drugs?

A
  • Improves M/M in patients with CHF and post-MI
40
Q

What are the adverse effects of the alpha-1, beta-1, and beta-2 blocker drugs?

A
  • Similar to cardioselective Beta-1 blockers (except no change in lipid levels) plus…
  • Similar to non-selective Beta-blockers plus…
  • Similar to Alpha-1 blockers (except will not cause reflex tachycardia)
41
Q

What are the therapeutic uses for ACE-I drugs?

A
  • DOC for managing hypertension to improve M/M
  • Diabetic neuropathy or persons with proteinuria: slows progression of renal failure in diabetics, even in diabetics without HTN
  • Stroke prevention
  • Improved M/M when administered with Beta-blocker in pts. with chronic stable angina, MI, and systolic heart failure
  • Slows the progression of CHF and improves quality of life
  • Acute MI
42
Q

What are some dosing recommendations for patients taking ACE-I drugs?

A
  • Test dose of captopril appropriate in pts with high level of RAA activity e.g.. hyponatremia, diuretic use, heart failure
  • Reduce starting dose in pts. who are on diuretic, volume depleted, or at risk of orthostatic HTN, or elderly.
43
Q

What are some adverse effects of ACE-I drugs?

A
  • Hypotension
  • Bradykinin related side effects:
    • Dry, hacking cough
    • Non-allergic rash
    • Angioedema - immediately Dx use
  • Hyperkalemia
  • Acute reversible renal insufficiency: more likely to occur in people with renal artery stenosis, preexisting renal dx, or taking NSAIDs.
  • Contraindicated in pregnancy.
44
Q

What are some drug interactions of ACE-I drugs?

A
  • Co-admin of NSAIDs in persons with underlying renal compromise may worsen renal function
  • NSAIDs may diminish BP lowering effects of ACE-I
  • Concurrent use with K+ sparing diuretics, ARBs, or K+ supplements may lead to hyperkalemia
  • May cause alterations in lithium levels
45
Q

Which molecule is the primary afferent vasodilator in the kidney?

A

Prostaglandin

46
Q

Which molecule is a potent vasoconstrictor of the efferent arteriole in the kidney?

A

Angiotensin-2

47
Q

What is the role of an ACE-I in regulation of kidney function?

A
  • ACE-I will reduce ANG-2 levels, thus causing the efferent arteriole to vasodilate, which reduces the glomerular filtration pressure.
  • In persons with bilateral stenosis or on NSAIDs, they may not be able to compensate for the reduction in pressure and suffer a dramatic decrease in glomerular filtration
  • NSAIDs produce prostaglandins
48
Q

What are the Angiotensin-2 Receptor Blocker (ARB) drugs?

A
  • candesartan
  • irbesartan
  • olmesartan
  • valsartan
  • eprosartan
  • losartan
  • telmisartan
49
Q

What is the mechanism of action for the ARBs?

A
  • directly bind and block the angiotensin-2-receptor
  • ACE-I block only one pathway of Ang-2 production, but reduce angiotensin-2 levels at all receptor sites.
  • ARBs block only one type of angiotensin-2-receptor, but block it more completely
  • Above is the difference between ACEs and ARBs
50
Q

What are some therapeutic uses for ARBs?

A

Same as ACE-Is

  • Where ACE-I are preferred, ARBs are an acceptable alternative in a pt. who cannot tolerate bradykinin-related side effects of an ACE-I
  • May be equal to or superior to ACE-I in preventing diabetic nephropathy.
51
Q

What are some adverse effects of the ARBs?

A
  • Similar ADRs as ACE-I except…
  • Less likely to cause cough and rash due to their lack of effects on bradykinin levels
  • Hx of angioedema is a precaution rather than contraindication
  • Contraindicated in pregnancy
52
Q

What are some drug interactions associated with ARBs?

A
  • Co-admin of NSAIDs in persons with underlying renal compromise may worsen renal function
  • NSAIDs may diminish BP lowering effects of ACE-I
  • Concurrent use with K+ sparing diuretics or K+ supplements may lead to hyperkalemia
  • May cause alterations in lithium levels
53
Q

What are the Calcium Channel Blocking (CCB) drugs?

A 
Pines
- amlodipine
- felodipine
- isradipine
- nicardipine
- nifedipine
Cardiac
- diltiazem
- verapamil
54
Q

What is the mechanism of action for the CCB drugs?

A
  • Inhibits the entrance of Ca++ into the smooth muscle cells of the coronary and arterial vessels.
  • All CCBs are vasodilators
  • diltiazem and verapamil also act on the calcium channels of the heart causing them to have some Beta-1 blocker properties - negative inotropes and negative chronotrope
55
Q

What are some therapeutic uses for CCBs?

A
  • DOC for managing HTN to improve M/M
  • Angina (chronic or exertional)
  • Long-term benefits in diabetes have been shown
  • Effective for isolated systolic HTN in elderly and in african americans
  • Raynaud’s
  • Cardiac CCBs can be used to treat a-fib and tachycardia; however they are NOT cardioprotective in same way beta-blockers are in post-MI and heart failure
56
Q

What are some adverse effects of CCBs?

A

All CCBs:
- vasodilators: dizziness, hypotension, flushing, peripheral edema, and headache
- especially verapamil: constipation
- Except amlodipine: have negative inotropic effect
- gingival enlargement
Pine CCBs:
- especially nifedipine & nicardipine: reflex tachy,
Cardiac CCBs:
- DO NOT cause reflex tachy

57
Q

Why should immediate release nifedipine not be administered in patients?

A
  • It is associated with dangerous, ping-ponging BP, relfex tachy, arrhythmias, MI, and death.
  • Do NOT prescribe
58
Q

What are some drug interactions associated with CCBs?

A
  • Especially verapamil and diltiazem: cytochrome p450 interactions
  • verapamil and diltiazem may also cause AV block if given with Beta-blockers
59
Q

What is the mechanism of action by which the diuretics work within the kidneys?

A
  • Block tubular reabsorption of Na+ and fluid at different sites within the nephron
  • Water follows sodium: water passively follows Na+ concentration
60
Q

At what location within the nephron do thiazide diuretics act?

A

distal convoluted tubule

61
Q

How do thiazide and loop diuretics induce hypokalemia and acid/base imbalance?

A
  • Urine that hits the Na/K/H channels at the end of the distal convoluted tubule is full of Na+
  • Na/K/H channels sense increase and rev up to compensate
  • When the channels absorb Na+, they must do so in exchange for either a K+ or H+ molecule
  • Channels are not active enough to counteract diuretic, but active enough to cause hypokalemia or acid/base imbalance
62
Q

What are the thiazide diuretic drugs?

A
  • chlorothiazide
  • chlorthalidone
  • hydrochlorothiazide
  • metolazone - thiazide like
  • indapamide
63
Q

What is the mechanism of action of the thiazide diuretics?

A
  • Enter nephron via organic acid secretory pathway of proximal tubule and block tubular reabsorption of Na+ at early part of distal convoluted tubule
  • Also posses some vasodilatory effects
64
Q

Why are thiazides more effective than loop diuretics for chronic HTN?

A
  • Thiazides do not cause rebound vasoconstriction as loops sometimes do.
  • They also have direct acting vasodilatory properties
65
Q

What are some therapeutic uses for thiazide diuretics?

A
  • DOC for management of HTN to improve M/M
  • Offer synergy when combined with and other antihypertensive
  • Treat mild to moderate edema
  • Minor uses: reduce amount of Ca++ excreted into urine; thus useful in tx of calcium-based kidney stones and reduction of risk of osteoporosis
66
Q

What are some adverse effects associated with thiazide diuretics?

A
  • Dehydration and electrolyte balance
  • Hypokalemia
  • May increase Tg & LDL
  • Hypeeruricemia may produce Gout attacks
  • High doses may cause hyperglycemia in some diabetics
67
Q

What are some drug interactions associated with thiazide diuretics?

A
  • Beta-blockers may increase hyperglycemic effects of thiazides in type II diabetics
  • synergistic hypotension may occur when used with ACE-I or any other hypertensive
68
Q

What are the loop diuretics?

A

Torch Fur with Butane

  • furosemide
  • bumetanide
  • torsemide
69
Q

What is the mechanism of action for the loop diuretics?

A
  • Act in ascending limb of loop of hence
  • Secreted into urine by organic acid pathway of proximal tubule
  • Pts. with renal failure will require larger doses to be effective.
70
Q

What are the therapeutic uses for loop diuretics?

A
  • Edema associated with CHF or renal failure
  • IV for acute pulmonary edema or acute decompensated heart failure
  • Tx of HTN due to fluid overload in pts. with reduced ClCr
71
Q

What are some adverse effects of loop diuretics?

A
  • Orthostatic hypotension, dizziness, photosensitivity, rash, and hyperuricemia (gout)
  • dehydration, hypokalemia, and electrolyte imbalance (pts. usually require K+ supplement)
  • Ototoxicity- hearing can be affected, especially when used with aminoglycosides
  • Prerenal azotemia- decreased kidney function due to over-depletion of blood volume
72
Q

What are some dosing recommendations for loop diuretics?

A
  • Dose at night when dosing twice daily
  • Higher doses might be needed in patients with renal failure and heart failure to overcome diuretic resistance
  • synergy with thiazides
73
Q

What are some drug interactions that may be associated with loop diuretics?

A
  • Hypokalemia; if pt becomes hypokalemic while on digoxin, toxicity may occur
    Synergistic hypotension may occur with concomitant use of ACE-I or other anti-HTN
74
Q

What are the potassium sparing diuretics?

A
  • spironolactone

- eplerenone

75
Q

What is the mechanism of action for the potassium sparing diuretics?

A
  • Synthetic aldosterone agonists. Competes with aldosterone at renal receptor sites.
  • Aldosterone normally stimulates Na+ reabsorption and K+ elimination at the distal tubule
  • Causes Na+ elimination and K+ reabsorption
76
Q

What are the therapeutic uses of the Potassium sparing diuretics?

A
  • Not powerful enough as a diuretic to be used alone to treat edema
  • Improves M/M in left vent. systolic dysfunction
  • Reduce portal vein HTN in liver failure pts. with ascites
  • Used in combo with thiazides or loops to help retain K+ and prevent hypokalemia
  • Resistant HTN, where pts. are already on 3 or more drugs
77
Q

What are some adverse effects that may be associated with potassium sparing diuretics?

A
  • Hyperkalemia: may be life threatening

- Spironolactone - may cause gynecomastia in men and menstrual irregularities and deepening of the voice in women.

78
Q

What are the contraindications and precautions associated with potassium sparing diuretics?

A
  • Serum K+ > 5.5 at initiation or ClCr less than or equal to 30 ml/min
  • Use EXTREME CAUTION in pts taking K+ supplements, ACE-Is, ARBs, or using salt substitutes
  • Eplerenone use contraindicated with powerful CYP3A4 inhibitors, such as macrolides and azoles
79
Q

What are some medications that may be used to treat orthostatic hypotension?

A
  • midodrine: alpha-1 agonist

- fludrocortisone: increases salt and water retention

80
Q

What are some tips for preventing orthostatic hypotension in pts?

A
  • Get up slowly from lying or seated position.
  • Exercise calf muscles before sitting up
  • Avoid bending at waist to pick stuff up
  • Sit or lie down immediately after feeling light-headed
  • Avoid alcohol
81
Q

How should most patients with stage 1 HTN be treated initially?

A
  • With a thiazide diuretic
82
Q

How should patients with stage 2 HTN be treated initially?

A
  • With combination therapy with one of the agents preferably being a thiazide diuretic
83
Q

How should a patient with isolated Systolic HTN be treated initially?

A
  • thiazide diuretics and CCBs seem to work well
84
Q

What drugs are the drugs of choice in the management of HTN with or without compelling indications as they have the best evidence supporting benefits on Mortality and Morbidity

A
  • Diuretics
  • ACE-Inhibitors
  • Angiotensin-2-Receptor Blockers (ARBs)
  • Calcium Channel Blockers (CCBs)
85
Q

What would be the best management of HTN in a patient with systolic heart failure / left vent. hypertrophy?

A
  • ACE-I + diuretic (loop or thiazide depending on fluid issues)
  • Also, beta-blockers, ARB, aldosterone agonist
86
Q

What would be the best management of HTN in a patient who is post-MI?

A
  • Beta-blocker + ACE-I
  • Also aldosterone antagonist
  • Propanolol, timolol, carvediolol, and metoprolol have all been proven beneficial in post-MI studies.
87
Q

What would be the best management of HTN in a patient who have angina or acute coronary syndrome?

A
  • Beta-blocker
88
Q

What would be the best management of HTN in a patient who has diabetes?

A
  • ACE-Is or ARBs

- Also, thiazide diuretics

Pharmacology II (9 decks)

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