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Pharm (Geisel M2) > Term 1 Pharm - Adrenergic (NE) + Anti-HTN > Flashcards

Term 1 Pharm - Adrenergic (NE) + Anti-HTN Flashcards

1
Q

Direct acting SELECTIVE Alpha 1 agonist, cause vaso + veno constriction, pupil dilator (mydriatic), also used as a nasal decongestant, can increase BP

A

Phenylephrine (Neosynephrine)

P - pupil dilator

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2
Q

Sympatholytic agent
Directive acting SELECTIVE Alpha 2 agonist
Stimulates alpha 2 receptors in brainstem (lowering sympathetic response) & prevents release NE from nerve endings. Used as to that HTN, lower BP, and can be used as a sedative & used to prevent migraine.
SE: Can cause dry mouth, affect alertness

A

Clonidine (Catapres)

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3
Q

Direct acting Beta 1 + 2 agonist –> causes increased HR (SA), conduction (AV), and contractility (LV). SEs: vasodilation, tachycardia, tachyarrhythmia

A

Isoproterenol (Isuprel)

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4
Q

Direct acting SELECTIVE Beta 1 agonist, POTENT in heart (increasing contractility > HR). Also dilates renal and mesenteric blood vessels. Good for patients in CCU (Coronary Care Unit) who have had an M.I. but are stable –> this makes tachycardia less likely.

A

Dobutamine (Dobutrex)

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5
Q

Direct acting SELECTIVE Beta 2 agonist, bronchiole dilator, fast acting rescue inhaler. Also helps relax uterus to stop premature labor.

A

Albuterol (Ventolin)

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6
Q

Direct acting Beta3 agonist, binds to bladder: increases bladder capacity and decreases detrusor muscle tone (treatment of overactive bladder)

A

Mirabegron (Myrbetriq)

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7
Q

Direct acting DA, Beta 1, and Alpha 1 agonist that is used to treat SHOCK. At low levels binds to DA only (improved renal and mesenteric perfusion), at intermediate levels also binds to B1 (increased contractility), and at high levels also binds to A1 (increased vasoconstriction).

A

Dopamine (Intropin)

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8
Q

Indirectly stimulates adrenergic nerves to release NE, used to treat Hypotension in OR or during Surgery (controlled conditions). From plant ephedra, can also be used as nasal decongestant, is a potent CNS stimulator, can have prolonged effect, can cause HTN/insomnia.

A

Ephedrine

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9
Q

Indirectly stimulate nerves to release NE, synthetic version of ephedrine, good for nasal decongestion, used to make methampetamine

A

Pseudophedrine

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10
Q

Indirectly stimulates adrenergic nerves to release NE (similar to ephedrine & pseudopedrine). Also used in treatment of obesity, ADHD, and Narcolepsy.

A

Amphetamine

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11
Q

Natural product in red wine, old cheese, & fermented foods. Stimulates adrenergic nerves to release NE. Careful! If given with MAO inhibitor (phenelzine) it will have even greater effects “worst head ache of your life”

A

Tyramine

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12
Q

Indirectly blocks repute of NE at synapse (E + DA) and stimulates their release (CNS stimulant). Acts as a local vasoconstrictor & anesthetic, good for nose bleeds & commonly used for corneal surgery. Can cause tachy, seizure, M.I.,

A

Cocaine

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13
Q

SELECTIVE Alpha 1 antagonist, binds to alpha 1 receptors on arterioles & veins blocking binding of NE. Used to treat HTN. metabolized in liver. Start gradually & at bed time (risk of hypotension).

A

Prazosin (Minipress)

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14
Q

SELECTIVE Alpha 1 antagonist, blocks alpha 1 adrenoreceptor in prostate. Metabolized by CYP 450 enzymes. Used to treat BPH or pass kidney stones.

A

Tamulosin (Flomax)

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15
Q

NON-SELECTIVE Alpha Antagonist, inhibitor (blocks alpha 1 + 2) competitively binds to alpha 1 + 2 adrenergic receptors. Decreases preload and afterload. Used in patients with pheochromocytoma (tumor o adrenal medulla that secretes NE + E)

A

Phentalomine (phentALomine - block ALL the ALphas)

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16
Q

PURE SELECTIVE Beta 1 Antagonist (beta 1 blocker)
blocks B1 adrenoreceptor
Used to treat HTN, prevent arrhythmia, anti-angina, and prevents second M.I. (prolonged survival), decreased toxic remodeling.
Decreased CO and RAAS.
Effects start 1-2hrs after, last 12-24hrs
Excreted from renal system (longer half life).

Don’t do abrupt withdrawal
(Be careful in asthmatics, at higher levels can bind to B2 also)

A

Atenolol (Metoprolol, Toprol XL, Tenormin)

  • Atenolol is just as effective as Metoprolol
  • Metoprolol has a shorter half life since it has hepatic metabolism.

(not necessarily longer 1st line of drugs for essential HTN)

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17
Q

NON-SELECTIVE Beta Antagonist (beta blocker)
Binds to Beta 1 + Beta 2 receptors, used to treat HTN, prevent arrhythmia, anti-angina, and prevents second M.I. (prolonged survival), decreased toxic remodeling. Decreases CO & RAAS. Hepatic metabolism (shorter half life). Can cause heart block if CHF is not stable. BAD FOR ASTHMATICS

A

Propranolol ( Inderal)

not necessarily longer 1st line of drugs for essential HTN

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18
Q

NON-SELECTIVE (mixed) Alpha and Beta antagonist
Blocks receptors from binding to NE. Treats HTN & to stable CHF. Usually used for HYPERTENSIVE CRISIS. Drastically lowers BP. Undergoes 1st pass metabolism. Do NOT use in patients with bradycardia, heart block, CHF, asthma, or shock. Use Low doses in patients with liver problems.

A

Labetalol = Carvedilol = Coreg (CHF)

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19
Q

Anti-HTN
ACE Inhibitor
Preserves RENAL Fx (should be used in DIABETICS)
Helps preserve LV fx after MI
Can be used for CHF
Common SE: cough, hyperkalemia angioedema in African Americans (b/c of bradykinin).
Careful w/ patients taking diuretic (aortic stenosis)
Causes fetal cartilage abnormalities if taking during pregnancy

A

Lisinopril = Captoril

*DON’T give Captopril anymore (OG) b/c causes allergic reactions.

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20
Q

Anti-HTN
ARB (blocks Ang II from binding to Ang I receptor)
Preserves renal fx (should be used in diabetics)
Can be used for CHF
Goes through 1st pass metabolism –> active metabolite is 40x more potent
Do NOT use in pregnant women
Careful w/ patients taking diuretic (aortic stenosis)

A

Lozartan (Cozaar)

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21
Q

Anti-HTN
Potent vasodilator (used for HTN CRISIS)
Used in controlled environment (OR, surgery to decrease bleeding/ magian pulmonary HTN)
Acts directly on vessels (arterioles & veins), gets broken down into NO CN- (toxic! Should never be given > 24hrs).
NO –> guanylate cyclase -> cGMP –> vasodilation (cGMP gets turned into CMP by PDE)
Liver turns CN- into SCN &then excreted in urine
Can cause headache & decreased blood flow to brain

A

Nitroprusside

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22
Q

Anti-HTN
Causes drug induced Lupus
DIRECT vasodilator, causes endothelium on arterioles to make NO –> cGMP -> vasodilation.
Metabolized in GI mucosa & in liver.
Dangerous in patients with renal disease or previous heart problems.

A

Hydralazine

23
Q

Anti-HTN
Diuretic
Usually FIRST DRUG USED
blocks Na/Cl reabsorption after filtration, lowers SVR and BP by 10-15mmHg.
ppl allergic to sulfa antibiotics shouldn’t take it.
SE: K wasting (hypokalemia, hypomagnesia) –> metabolic alkalosis –> greater chance of A fib?
More toxic in elderly. DON’T use in pregnant women

A

Hydrochlorothiazide

Chlorthalidone has proven to be better, lower SVP, better control at night, longer half life, more potent)

24
Q

Anti-HTN
Anti-Angina
Calcium channel blocker (CEB)
reduces flo of Ca through Ca slow channels –> lower BP
dilates peripheral arterioles, lower inotropy, lower after load, less O2 consumption, less spasm
Metabolized in liver, excreted as inactive metabolites
DONT use with beta blockers
Shorter acting (nifedipine –> increased risk of MI)

A

1 drug in Black patients (diuretics & CEBs)

Amlodipine Besylate (Norvasc)

25
Q

Cough is common side effect of this drug

A

ACE inhibitor (Lisinopril)

26
Q

This drug decreases BP better than Hydrochlorothiazide & prevents CV events just as well as ACE inhibitors & CEBs

A

Chlorthalidone

27
Q

Top 4 Best drug types to start with

A

1) Thiazide diuretic (e.g. HCTZ)
2) Long-acting CEB more specific for vessels (e.g. amlodipine)
3) ACE inhibitor (e.g. lisinopril)
4) ARB (e.g. losartan)

28
Q

Start Diabetics on this drug to lower BP (And ALWAYS lower their BP to less than 120/80)

A

ACE Inhibitor (Lisinopril) or ARB (Lozartan)

29
Q

Pre- HTN

A

SBP 120-139 or DBP 80-89

30
Q

HTN Stage 1

A

SBP 140-159 or DBP 90-99

31
Q

HTN Stage 2

A

SBP >160 or DBP > 100

32
Q

HTN urgency:

A

DBP usually >120, no sx, no damage

33
Q

HTN emergency

A

DBP usually >120 w/acute end-organ damage and symptoms

34
Q

Resistant HTN

A

BP not controlled despite an appropriate 3-drug regimen, dosed to >50% of maximum FDA-recommended dose

35
Q

Essential HTN & Risk Factors

A

Unknown origin

Risk factors: age, black race, family history, high Na intake, excess EtOH, excess weight, physical inactivity

36
Q

Secondary HTN

A

usually caused by renal disease, renovascular disease, sleep apnea, endocrine disorders, certain drugs

37
Q

Serious target-organ damaging effects

A

CAD, CHF, stroke (ischemic or hemorrhagic), CKD, (encephalopathy, aortic dissection)

38
Q

How to look for extent of organ damage

A

Careful Hx, PE, UA (look for microabluminuria), BM, BUN/Cr, fasting glucose, lipid panel, ECG; usually not CXR

39
Q

All patients with HTN should try what first

A

non-drug (lifestyle) modification

Weight loss, low-Na diet, exercise, smoking, EtOH, etc

40
Q

Antihypertensive meds should be started if:

A

SBP>140 (in patients 150 (patients >60) or
DBP >90.

Usually start with just one drug
Consider starting with two drugs if BP>160/100

41
Q

What drugs can be used for monotherapy (double-duty)

A
  • Atrial fib may be on CEB for rate control
  • CHF may be on ACE inhibitor or beta-blocker for survival
  • Post-MI should be on beta-blocker for improved survival
42
Q

Be careful in patients >65 yo with isolated systolic HTN (DBP

A

don’t lower DBP below 60

43
Q

General goals for BP based on age

A

General population 80 years old

- Goal is

44
Q

Name 4 Drug Classes for treating HTN

A

1) Diuretics
2) Inhibitors of the RAA System
3) Vasodilators
4) Sympatholytic agents

45
Q

Anti-HTN
for BRIEF use in OR of ICU via IV (during anesthesia) for HTN crisis or controlled hypotension during cardiovascular surgery
NOT used for long term HTN control (too many adverse effects, rarely used)
Sympatholytic agent
Ganglionic transmission blocker (Ach), blocks Nn at sympathetic AND parasympathetic ganglia but NOT Nm (doesn’t affect muscle)
Causes vaso and veno-dilation
Can cause sever drop in BP in minutes (possibly HR) & reduction in any para- and sym- responses

A

Trimethaphan (Arfonad)

46
Q

Anti-HTN
binds to vesicles that containNE and prevent their uptake –> depletes neurons of NE (or serotonin) at alpha 1 and beta 1
takes 2-3 weeks to get effects
SE: DEPRESSION! (depletes brain of NE), dizziness, hypotentsion
FDA approved in 1953 but been around for 2,000yrs (ppl used to chew leaves) –> this plus diuretic used to be standard treatment in the 50s

A

Reserpine

2,000 years old!
Cheap! No brand name

47
Q

A 52-yo executive with IDDM and asthma has a history of moderate hypertension in the past, but has not paid much attention to treating it. He presents to the ER with severe head ache, blurred vision, and shortness of breath. BP is 220/130. He has retinal hemorrhages on exam.

1) What drug is most important to give now for rapid control of his blood pressure
2) What drugs would you prescribe as you switch patient to chronic oral therapy?
3) Are any specific drugs contra-indicated for use in this patient?

A

1) Nitroprusside: He’s in HTN emergency/HTN crisis. Want to lower MAP
2) Lisinopril
3) Propranolol: Propranolol is BAD here b/c it blocks beta 2 receptors (he’s SOB

48
Q

Which HTN medication causes fetal abnormalities in cartilage?

A

Lisinopril

49
Q

A 62-yo man has just been admitted to the hospital to treat an acute but small STEMI. He is comfortable, without CHF but with some PVCs, and has already begun daily aspirin and atorvastatin. He has had mild HTN for several years, responding well (BP 138/88) to HCTZ 25 mg per day. You are planning his discharge medications. Which antihypertensive makes the most sense for this patient?

A) Continue hydrochlorothiazide
B) Switch to metoprolol
C) Switch to verapamil
D) Switch to prazosin
E) Switch to lisinopril
A

B) Switch to metoprolol

Beta blocker helps with preventing dangerous remodeling while also controlling HTN & improving survival & preventing 2nd heart attack

50
Q

What kinds of diuretics are there?

A
  • Thiazides
  • Loop Diuretics
  • K sparing diuretics
51
Q

What kinds of inhibitors of RAAS are there?

A
  • ACE inhibitors

- Angiotensin receptor blockers

52
Q

What kinds of vasodilators are there?

A
  • Direct acting

- Calcium entry blockers

53
Q

What kinds of sympatholytic agents are there?

A
  • Act within CNS
  • Act on autonomic ganglia
  • Act on post-ganglionic neurons
  • Block peripheral adrenergic receptors

Pharm (Geisel M2) (15 decks)

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