Drugs Affecting ANS Flashcards

1
Q

Adrenergic Agonist

A
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2
Q

Branches of the ANS

A
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3
Q

Know clonidine (Catapres)

A

MOA:* MOA: activation of central alpha2 receptors results in inhibition of cardioacceleration &
vasoconstriction centers in the brain
* Leads to decreased outflow of norepinephrine
* Leading to decreases in peripheral resistance, renal vascular resistance, HR & BP by reducing sympathetic function
* Can lead to compensatory effect of retaining sodium (expand blood volume)
* Thus, sometimes given with diuretic

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4
Q

Contraindications for clonidine

A

severe coronary insuf, recent MI, renal function impairment
* Avoid clonidine if risk of depression

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5
Q

Alpha 2 Agonists - Methyldopa (Aldomet) recommendations

A

pregnant women
breastfeeding women
Children <12

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6
Q

methyldopa special requirements

A

LFT
hemolytic anemia

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7
Q

doxazosin (Cardura)
terazosin (Hytrin)

A

Selective Alpha 1 Antagonist
MOA: blocks alpha 1 receptors in smooth muscle; vasodilates arteries
B. bladder neck and prostate smooth muscle (relieve outflow obstruction)

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8
Q

Selective Alpha 1 Antagonist Adverse Effects

A

Orthostatic hypotension - known for first dose effect - give dose at bedtime
-rebound tachycardia
-nasal congestion
-fluid retention
-sexual dysfunction

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9
Q

This class of drug may reduce total cholesterol & tryglycerides and increase HDL; enhance insulin sensitivity; regress LVH

A

Selective Alpha 1 Antagonists
doxazosin and terazosin

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10
Q

Beta Adrenergic Antagonists

A

Block sympathetic (adrenergic) response by competing for beta receptors
* ***practically all therapeutic effects result from beta 1 blockade in the
heart. The major consequences/actions of blocking these receptors are:
* 1. decrease HR
* 2. decrease contractility
* 3. decrease velocity of A-V conduction
* Also prevent renin release (less water retention)

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11
Q

Beta 1 Cardioselective drugs

A

metroprolol (Lopressor)
atenolol (Tenormin)
- Children

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12
Q

Non cardioselective B 1 & 2 drugs

A

propranolol (Inderal)
- Children
labetolol (Trandate)
- Alpha & Beta blockade

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13
Q

Third Generation Beta Blockers

A

nebivolol (Bystolic)
* Block beta1 - very cardioselective
* Increases nitric oxide release
* Approved for hypertension
* Less likely to produce
problematic DM effects

carvedilol (Coreg)
* BB noncardioselective
* Vasodilation by alpha blockade
* Approved for CHF, HTN, LV
dysfunction after MI

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14
Q

Beta blocker adverse effects

A

Beta 1 blockade:
* Bradycardia
* Decreased CO
* Precipitation of CHF (in high doses)
* A-V block
* Rebound cardiac excitation

  • Beta 2 blockade:
  • Bronchospasm
  • Inhibition of glycogenolysis (breakdown of glycogen to glucose)
  • Also impaired insulin release
  • Fatigue, depression
  • Sexual dysfunction/Impotence
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15
Q

BB Teaching points

A
  • Teach patients to monitor:
  • pulse daily (call if <50 bpm)
  • blood glucose (diaphoresis is not masked)
  • BP
  • Do NOT abruptly withdraw (decrease by ½ q 4 days)
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16
Q

Angiotensin Converting Enzyme Inhibitors (ACE I)

A
  • Block the enzyme that normally converts
    angiotensin I to the potent
    vasoconstrictor angiotensin II
  • By blocking the production of angiotensin
    II, the drugs decrease vasoconstriction
    and decrease aldosterone production
    (thereby reducing retention of sodium
    and water)
  • Reduce both preload and afterload
17
Q

List ACE I

A

lisinopril (zestril)
captopril (Capoten)

18
Q

ACE I uses

A

HTN
Hypertensive Protienuric Diabetes
- renal protective (slows progression of diabetic nephropathy
Angina and ischemic heart disease
post MI
Heart failture

19
Q

ACE I Adverse Effects

A
  • Cough
  • Angioedema (swelling of face, eyes, lips, tongue)
  • Occurs within first dose - 1st month
  • Usually within 1st week
  • Hyperkalemia
  • Caution: renal impairment, salt substitutes, K-supplements, K-sparing diuretics
  • Hypotension (dizziness, HA)
  • Rash
  • Neutropenia
  • Renal insufficiency (monitor proteinuria, BUN, Creatinine)
20
Q

ACE I Absolute Contraindications

A

Bilateral Renal Artery Stenosis
Angioedema
Pregnancy

NSAIDs reduce hypotensive effect

21
Q

Angiotensin II Receptor Blockers (ARBs)

A

Instead of decreasing production of angiotensin II, these drugs compete for receptor sites.

No cough or angioedema

Still contraindicated in pregnancy

22
Q

Losartan (Cozar)
valsartan (Diovan)

A

ARBs

23
Q

Renin Inhibitor

A

aliskerin (Tekturna)

Direct renin inhibitor: decreases the conversion of
angiotensinogen to angiotensin I
* Plasma renin activity is not increased
* Use: HTN
* Adverse Effects:
* Angioedema, cough
* Hyperkalemia
* Substrate CYP 3A4
* Contraindication: pregnancy

24
Q

Calcium Channel Blockers MOA

A

Block the influx of calcium which results in: * 1. relaxes arterial smooth muscle (decrease afterload)
* 2. decreases cardiac contractility (negative inotrope)
* 3. decreases sinoatrial (SA) and atrioventricular (AV) nodal conduction
* ***blocking action of CCBs occurs via different receptors

25
Q

Non-Dihyropyridines MOA and Use

A

Calcium Channel Blocker

Primary site is heart * Decrease contractility
* Decrease conduction
* Dilate coronary arterioles
* Best choice for CAD * ***avoid in HF
* verapamil (Calan)
* diltiazem (Cardizem)

26
Q

Dihydropyridines

A

Calcium Channel Blocker

Primary site is arterial smooth muscle * Thus, greater degree of vasodilation
* Best choice for hypertension * ***avoid in unstable angina (tachycardia)
and with significant peripheral edema
* amlodipine (Norvasc)
* nicardipine (Cardene)
* nifedipine (Procardia)

27
Q

Calcium Channel Blockers Adverse Effects and concerns

A

Adverse Effects:
* HA, dizziness, hypotension
* Bradycardia (verapamil & diltiazem) – call if HR <50 bpm
* Peripheral edema
* Constipation (more with verapamil)
* Contraindications:
* 2nd or 3rd degree AV block
* Severe HF
* Aortic stenosis
* Work well in Black population
* All CCBs are on CYP 3A4 substrate * Careful with grapefruit juice (3A4 inhibitor)

28
Q

hydralazine (Apresoline)

A

direct arterial vasodilator (decrease afterload)
* Limited effect on HTN when used alone B/C vasodilating action that decreases BP also stimulates compensatory
mechanisms:
* Increased HR (SNS)
* Sodium & water retention (RAAS)
* May take with beta-blocker (prevent the tachycardia) and diuretic (prevent sodium & water retention)

29
Q

hydrochlorothiazide
chlorthalidone

A

Thiazide DiureticsMOA: Decrease reabsorption of Na & Chloride in the distal tubule; exert effect on luminal surface of the tubule; requires adequate renal perfusion
* Ex: hydrochlorothiazide (HCTZ)
chlorthalidone
* Uses: * Ineffective when immediate diuresis is required
* Primary use is long-term management of hypertension and HF
* Relatively ineffective with decreased renal function
* Assess for allergies to sulfonamides (chemically related)

30
Q
  • Orthostatic hypotension
  • Electrolyte imbalances:
  • Hypokalemia
  • Hypercalcemia
  • Hyponatremia
  • Hypomagnesium
  • Glucose intolerance (may impair pancreatic release of insulin & diminish tissue utilization of
    glucose)
  • Dry mouth
  • Potentiate uric acid retention
  • Transient increases in chol, LDL, triglycerides
A

Adverse effects of thiazide diuretics

31
Q

Loop Diuretic - Name two

A

furosemide (Lasix)
torsemide (Dermadex)

32
Q

Loop Diuretics MOA

A
  • MOA: Block reabsorption of Na and Chloride in the ascending loop of Henle, where the greatest Na reabsorption occurs
  • Ex: furosemide (Lasix)
    torsemide (Demadex)
  • Use:
  • Hypertension
  • HF
  • Diuretic of choice when more rapid or potent effects are needed (pulm edema)
  • Their sodium losing effect is up to 10X greater than thiazide diuretics
  • May use with renal insufficiency (Creatinine clearance <25 mL/min)
  • Schedule last dose early enough to prevent nocturia (4:00 pm)
33
Q

Loop Diuretic Adverse Effects

A

Electrolyte imbalances:
* Hypokalemia
* Hypercalcemia
* Hyponatremia
* Hypomagnesium
* Excessive diuresis
* Orthostatic hypotension
* Glucose intolerance
* High doses = transient hearing loss
* Hyperuricemia

34
Q

Loop Diuretics Teaching

A
  • Maintain potassium levels in cardiac patients at 4-4.5 mEq/L
  • Potassium supplement:
  • PO – give with meals to decrease GI distress
  • Liquid – mix with juice to improve taste
  • Teach patient:
  • Consume diet with potassium rich foods
  • Report muscle cramps, irregular heart beat, weakness
35
Q

K sparing diuretics

A
  • MOA: Promote Na excretion but retain potassium in the distal tubule
  • Ex: spironolactone (Aldactone)
  • Aldactone antagonizes aldosterone (aldosterone promotes retention of sodium & water & excretion of K)
  • Uses:
  • Not used as often as primary diuretic (typically used in combo with K-losing diuretic)
  • Primary utility is to block aldosterone action in HF
  • Hypertension
  • Good choice in pregnancy
  • Contraindication: impaired renal function (due to risk of hyperkalemia)
  • Adverse Effects:
  • Hyperkalemia (teach pt to avoid high K diet; avoid salt substitutes that contain K chloride)
  • Hypotension
  • Hyperuricemia
  • Gynecomastia
36
Q

JNC VIII HTN Guidelines

A

First Line Classes:
* 1. Thiazides
* 2. ACE Inhibitors
* 3. ARBs (Angiotensin Receptor Blockers)
* 4. CCB (Calcium Channel Blockers)

No beta blocker

37
Q

Initiating HTN Treatment

A
    1. > 60 yo <150/90
    1. <60 yo <140/90
    1. All ages with Diabetes <140/90
  • **Non-Black
  • Thiazides, ACEI, ARB, CCB
  • **Black
  • Thiazides, CCB
    1. All ages chronic kidney disease
      (CKD) <140/90
  • **treat with ACEI or ARB
38
Q

Can you use ACEI and ARB together?

A

No