Antihypertensives Flashcards

0
Q

what is increased cardiac output in blood pressure?

A
  • Increased fluid volume, excess sodium intake & sodium renal retention
  • Excess stimulation of the RAAS (Renin-Angiotensin-Aldosterone System)
  • Over-activity of the SNS
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1
Q

what are some factors influencing blood pressure?

A
  • Increased cardiac output

* Increased peripheral resistance

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2
Q

what increased peripheral resistance?

A
  • excess stimulation of the RAAS
  • Over-activity of the SNS
  • Genetic alterations in cell membranes, e.g. increased intracellular Na/Ca which alters vascular smooth muscle tone.
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3
Q

What are the blood pressure goals?

A
  • treat to BP < 140/90 in most patients
  • treat to BP < 130/80 in pts with diabetes or chronic kidney disease, MI, angina, stroke.
  • treat to BP < 125/75 in patients with proteinuria
  • treat to BP , 140/90 for isolated systolic HTN also. For patients with SBP > 180, the first goal is to reduce SBP to <160. Monitor closely for hypotension: dizziness, sweating, tachycardia, falls, fatigue, etc. Then attempt to reduce BP to the target goal as long as the patient tolerates this reduction.
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4
Q

what are some cardiovascular risks and blood pressure?

A
  • HTN increased the risk of stroke, transient ischemic attacks, dementia, retinopathy, myocardial infarction (MI), angina, heart failure, left ventricular hypertrophy, chronic kidney disease (esp. African American, Hispanic, & Native American), peripheral arterial disease, and early death from a cardiovascular cause.
  • Starting at BP of 115/75, risk of CV disease doubles with every 20/10 increase.
  • SBP is a stronger predictor of CV disease than DBP
  • Isolated systolic HTN may result from pathophysiologic changes in arterial vasculature consistent with aging. These changes decrease the compliance of the arterial wall.
  • Pulse pressure (SSBP-DBP) may reflect the extent of atherosclerotic disease and measure arterial stiffness. Higher pulse pressure values are correlated with an increased risk of CV mortality
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5
Q

what are some drugs that worsen hypertension?

A
  • corticosteroids
  • Oral contraceptives
  • NSAIDs and COX-II inhibitors
  • oral decongestants
  • Erythropoietin
  • Some antidepressants
  • Cocaine and cocaine withdrawal
  • Ephedra, ma huang
  • Nicotine and nicotine withdrawal
  • Anabolic steroids
  • Narcotic/opioid withdrawal
  • Amphetamines
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6
Q

What are some complications of HTN?

A
  • eye damage & blindness
  • heart failure, MI, angina, CAD
  • chronic kidney disease, failure
  • stroke (hemorrhagic or ischemic)
  • TIA (mini stroke), dementia
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7
Q

what drugs make up alpha 2 adrenergic agonists?

A

clonidine (Catapres)

methyldopa (Aldomet)

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8
Q

What are alpha 2 adrenergic agonists (clonidine & methyldopa) mechanism of action?

A
  • preferentially stimulates the alpha 2 receptors of the brain stem associated with autonomic regulation of the cardiovascular system. Remember that activation of the alpha 2 receptor will cause neurons to quit releasing norepinephrine. Thus, alpha 2 receptors are inhibitory in nature. this will result in decreased sympathetic output, decreased blood pressure, & decreased heart rate.
  • Clonidine comes in a patch form that is changed weekly. This may be a good option for patients with compliance problems.
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9
Q

What are the alpha 2 adrenergic agonists therapeutic uses? (clonidine & methyldopa)

A
  • Main use is treatment of chronic hypertension.
  • Clonidine tabs chewed & swallowed are effective for hypertensive urgecies.
  • Clonidine has been used in the treatment of withdrawal symptoms of nicotine, opiates, benzodiazepines, & alcohol.
  • Methyldopa is a drug of choice in pregnancy induced hypertension.
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10
Q

What are the adverse effects of Alpha 2 Adrenergic Agonists? (Clonidine & methyldopa)

A
  • drowsiness (35%)
  • dry mouth (40%)
  • constipation
  • headache
  • impaired ejaculation
  • **avoid abrupt withdrawal- will cause severe rebound HTN
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11
Q

What drugs are included in the alpha 1 blockers (antagonists)?

A
"zosin" drugs
doxazosin 
prazosin
Silodosin
terazosin
tamsulosin
alfuzosin
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12
Q

what are the alpha 1 blockers (antagonists) mechanism of action?

A
  • competitive blocking of the alpha 1 receptors
  • HTN: lowers blood pressure by causing vasodilation. Relaxes both arterial and venous smooth muscle surrounding some blood vessels.
  • BPH: These drugs also relax the smooth muscle of the bladder neck & prostate, which improves urine flow in BPH
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13
Q

what are the alpha 1 blockers (antagonists) therapeutic uses?

A
  • HTN

* urinary retention associated with benign prostatic hyperplasia (BPH), & Raynaud’s disease (vasoconstriction disease)

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14
Q

what are the adverse effects of alpha 1 blockers (antagonists)?

A
  • Orthostatic hypotension (>10%) warn patient about this!!! FIRST DOSE EFFECT- syncope (fainting) following the 1st dose. To minimize falls, instruct patient about orthostatic hypotension, give at bedtime, and initiate therapy with dosage titration. The BPH selective alpha 1 blockers are less likely to cause orthostatic hypotension.
  • reflex tachycardia
  • dizziness, lack of energy, drowsiness, nasal congestion, headache, decreased libido, and inhibition of ejaculation.
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15
Q

What drugs are included in the First-Generation: Non-selective Beta blockers?

A

“olol” drugs

  • propranolol
  • Sotalol
  • Timolol
  • nadolol
  • carteolol
  • pindolol
  • penbutolol
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16
Q

what are First-Generation: non-selective Beta blockers mechanism of action?

A
  • competitive blocking of the beta 1 & beta 2 receptors
  • Cardiovascular effects (beta 1 mediated): decreased hear rate (negative chronotrope); decreased force of contraction (negative inotrope); decreased cardiac workload & oxygen demand.
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17
Q

What are the First-Generation: non-selective Beta blockers therapeutic uses?

A
  • Cardiac: Hypertension, angina, post MI, heart failure, atrial fibrilation, & tachycardia.
  • Some, carteolol & timolol, are used as eye drops to treat glaucoma.
  • Other: Hyperthyroidism, migraine prophylaxis, essential tremor, stage fright.
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18
Q

What are the adverse effects of First-Generation: non-selective beta blockers?

A
  • Beta 1: hypotension, sexual impairment, nightmares, some lower HDL & higher Tg (minor with chronic use). Heart failure, reduced cardiac output (fatigue) arrhythmias, & bradycardia (beta 1 mediated).
  • Beta 2: Peripheral vasoconstriction (beta 2 mediated): not a problem for most people unless there is a history of peripheral vascular disease (PVD), Reynaud’s, or non-healing ulcers where there is already some decreased peripheral blood flow.
  • bronchoconstriction (beta 2 mediated): This bronchoconstriction is not a problem for most patients. However, patients with COPD or asthma may be adversely affected.
  • May mask signs & symptoms of hypoglycemia in diabetics (beta 2)
  • Metabolism disturbances (beta 2 mediated): lead to decreased release of glucagon & decreased liver glycogenolysis (decreased conversion of glycogen to glucose). This can decrease a diabetic’s ability to correct hypoglycemia. Again, this is normally not a problem for most people, but can cause prolonged hypoglycemia in diabetics.
  • Do not stop abruptly!!! May cause rebound angina, arrhythmias, heart attack, & DEATH.
19
Q

What drugs are included in the group Second-Generation: Cardioselective Beta 1 blockers?

A
"olol" 
acebutolol
metoprolol
atenolol
bisoprolol
betaxolol
esmolol
20
Q

What are the mechanism of action for the group Second-Generation: Cardioselective beta 1 blockers?

A
  • selectively blocks beta 1 receptors
  • These agents have a higher affinity for the beta 1 receptors than the beta 2 receptors. They can lose their selectivity at higher doses.
21
Q

What are the therapeutic uses of Second-Generation: Cardioselective Beta 1 Blockers?

A
  • Same cardiac therapeutic uses as the non-selective beta blockers
  • Cardiac: Hypertension, angina, post MI, heart failure, atrial fibrillation, & tachycardia.
  • Hyperthyroidism, migraine prophylaxis, essential tremor, stage fright
  • *less effective for stage fright and migraine prophylaxis.
22
Q

What are the adverse effects of Second-Generation: Cardioselective Beta 1 Blockers?

A
  • Same hypotensive, cardia, and sexual side effects as the non-selective beta blockers.
  • *hypotension, sexual impairment, heart failure, reduced cardiac output (fatigue) arrhythmias, & bradycardia.
  • They are less likely to cause peripheral vasoconstriction, bronchoconstriction, or hypoglycemia, but can still mask hypoglycemia.
  • They should also NOT be stopped abruptly
23
Q

What are the drugs included in the group Third-Generation: Beta Blockers with Vasodilating Actions? what receptors??

A

carvedilol (alpha 1, beta 1, beta 2)
labetalol (alpha 1, beta 1, beta 2)
nebivolol (beta 1)

24
Q

What are the therapeutic uses for carvedilol? (Third-Generation: Beta blockers with vasodilating actions)

A

Hypertension and heart failure

25
Q

what are the side effects of carvedilol?

A

*it has similar side effects to the alpha 1 blockers (except will not cause reflex tachycardia) & the same side effects as the non-selective beta blockers.

26
Q

What are the uses and effects of labetalol?

A

It is not used for CHF. It is most commonly used for hypertensive emergencies. It has similar side effects to carvedilol.
Same side effects as non-selective beta blockers and alpha 1 blockers

27
Q

what are the uses and side effects of nebivolol?

A

Uses: to treat hypertension

  • promotes synthesis and release of nitric oxide causing vasodilation.
  • beta 2 blockers increase the release of nitric oxide.
28
Q

what drugs make up the group ACE-inhibitors?

A
"pril"
captopril
benazepril
fosinopril
enalapril
ramipril
trandolapril
lisinopril
quinapril
moexipril
29
Q

give an overview of the RAAS.

A

Angiotensin-2 is a potent vasoconstrictor. Angiotensin-2 also stimulates synthesis of other vasoconstrictors, inhibits the synthesis of bradykinin (a vasodilator) & stimulates the secretion of aldosterone, which causes the kidneys to retain Na+ & fluid to waste K+

30
Q

what is the mechanism of action for ACE-inhibitors?

A
  • ACE-inhibitors inhibit the conversion of angiotensin-1 to its more active form, angiotensin-2.
  • ACE-inhibitors counteract or inhibit all of the pharmacological effects of angiotensin-2. Thus, ACE-inhibitors cause vasodilation, decrease aldosterone levels, Na+ & fluid wasting K+ retention.
31
Q

What are the therapeutic uses of ACE-inhibitors?

A
  • Chronic Hypertension
  • Chew & swallow oral tablets for hypertensive urgencies
  • Congestive heart failure: slows the progression of CHF & improves the patient’s quality of life.
  • Diabetes: slows the progression of renal failure in diabetics, even without HTN.
32
Q

What are the adverse effects of ACE-inhibitors?

A

*Hypotension (especially with the first dose- give a test dose of captopril to be safe)
*Hyperkalemia (elevated serum K+) - due to aldosterone effects
*Bradykinin related side effects
»dry hacky cough (can reduce dose & retry) [5%]
»non-allergic rash
»rarely angioedema (swelling of lips & face) - immediately discontinue
*Contraindicated in pregnancy

33
Q

what drugs are included in the group Angiotensin-2 receptor blockers? (ARBs)

A
"sartan"
losartan
candesartan
valsartan
irbesartan
telmisartan
olmesartan
eprosartan
34
Q

What is the mechanism of action for ARBs? (Angiotensin-2 Receptor Blockers)

A

Directly bind & block the angiotensin-2 receptors

35
Q

What are the therapeutic uses of ARBs?

A
  • Same therapeutic uses as the ACE-inhibitors
  • Chronic Hypertension
  • Chew & swallow oral tablets for hypertensive urgencies
  • Congestive heart failure
  • Diabetes
  • Good choice as an alternative to an ACE-I in atients who cannot tolerate ACE-I side effects.
36
Q

What are the adverse effects of ARBs?

A
  • May cause hyperkalemia & hypotension
  • Less likely to cause cough, rash, & angioedema due to their lack of efforts on bradykinin.
  • also contraindicated in pregnancy
37
Q

What drugs are included in the group direct renin inhibitor?

A

aliskiren

38
Q

What is the mechanism of action for Direct renin inhibitor?

A
  • Binds tightly with renin and inhibits cleavage of angiotensinogen into angiotensin-1
  • Reduces influence of entire RAAS
39
Q

what are the therapeutic uses of direct renin inhibitors?

A

Chronic hypertension

40
Q

what are the adverse effects of direct renin inhibitors?

A

Generally well tolerated, diarrhea, contraindicated in pregnancy.

41
Q

what drugs are included in the group Calcium Channel Blockers?

A
"zem" "amil" "dipine"
diltiazem
verapamil
nifedipine
nicardipine
amlodipine
isradipine
felodipine
nimodipine
nisoldipine
42
Q

what is the mechanism of action for calcium channel blockers?

A
  • All inhibit entrance of Ca++ into smooth muscle cells of coronary and arterial vessels. Calcium is necessary for strength of muscle contraction & tone.
  • *All these drugs are vasodilators
  • Calcium channels are also present on the heart, coupled with beta 1 receptors. Diltiazem and verapamil also act on the calcium channels of the heart which causes them to have some effects similar to the selective beta 1 blockers.
43
Q

what are the therapeutic uses of calcium channel blockers.

A
  • Most can be used to treat chronic hypertension & angina
  • Like the beta 1 blockers, verapamil & diltiazem can also be used for arrhythmias such as atrial-fibrillation & tachycardia.
44
Q

what are the adverse effects of CCBs.

A
  • flushing, peripheral edema, headache, and reflex tachycardia are common side effects.
  • Verapamil & Diltiazem also have side effects similar to the selective beta 1 blockers. They can slow the S-A node & A-V node conduction, causing bradycardia. They can also have negative inotropic effects.
  • All CCBs can cause peripheral edema & constipation. Constipation is caused by relaxation of the smooth muscle of the GI tract.
  • Gingival enlargement.- gingival hypoplasia.
  • Immediate-release/ short-acting nifedipine (10 mg cap) is associated with dangerous ping-ponging blood pressure, reflex tachycardia, arrhythmias, myocardial infarction, & death. Not recommended for PRN use. Sustained-release nifedipine is perfectly safe.