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M1 Spring Block 1 > PDA Drugs > Flashcards

PDA Drugs Flashcards

1
Q

Sympathomimetic

A

Drugs that mimic agonists of the sympathetic system.

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2
Q

What are the mechanisms of action of sympathomiemetics?

A

Act at the postganglionic terminal - directly activate receptors, block breakdown/reuptake, stimulate production and release of catecholamines

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3
Q

Sympatholytics

A

Generally competitive antagonists that inhibit effects of the SNS.

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4
Q

Where are α1 receptors located?

A
  1. Eye
  2. Arteries
  3. Veins,
  4. GU smooth muscle (male)
  5. Vas deferens (male)
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5
Q

Where are α2 receptors located?

A

Presynaptic nerve terminals and CNS

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6
Q

Where are β1 receptors located?

A

Heart and kidney

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7
Q

Where are β2 receptors located?

A
  1. Arteries (skeletal, cardiac muscle)
  2. Bronchi
  3. Skeletal muscle
  4. Liver
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8
Q

What 6 drugs are considered direct-acting catecholamines?

A
  1. Norepinephrine
  2. Epinephrine
  3. Isoproterenol
  4. Dopamine
  5. Dobutamine
  6. Methydopa
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9
Q

What are the direct-acting catecholamines used for and what are they metabolized by?

A
  1. Cardiovascular actions
  2. MAO and catechol-O-Metransferase
    * Must be given parenterally, short half life
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10
Q

Norepinephrine

A

Receptor: α1, α2, β1
Cardio thru α1
Increases PVR, mean BP
Can cause reflexes bradycardia

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11
Q

Epinephrine

A

Receptor: α1, α2, β1, β2

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12
Q

What CV, respiratory, and metabolic effects does epinephrine cause?

A 
1. Increases HR, contractile force, CO, 
systolic BP-decrease diastolic BP (dose)
constrict most vascular beds except sk muscle (dose)
2. Bronchodilation
3. Hyperglycemia, inc in FFA
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13
Q

At low concentrations epinephrine will cause blood vessels in skeletal muscle to _______ and at high concentrations it will cause them to ___________.

A
  1. Dilate ( β2)

2. Constrict α1

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14
Q

Isoproterenol

A

Receptor: β1, β2

Therapeutic use: Emergency use for treatment of bradycardia or heart block

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15
Q

What are the effects of isoproterenol on the CV and respiratory systems??

A
  1. Decrease PVR and mean BP, Inc HR, contractile force, CO

2. Bronchodilation

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16
Q

Dopamine

A

Low: “Renal dose” decrease PVR, inc. renal blood flow, dilation of renal/mesenteric a. (D1)
Intermediate dose: “cardiac” inc. HR, contractile force, CO (D1 + β1)
High dose: “pressor dose” vasoconstriction, inc. PVR (D1+β1+α1)

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17
Q

Dobutamine

A

β1 agonist

Inc. HR, contract, CO - minimal change in PVR and BP

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18
Q

What are therapeutic uses of dobutamine?

A
  1. Short-term treatment of cardiac decompensation - following cardiac surgery, heart failure, MI
  2. Cardiac stress testing
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19
Q

Methydopa

A

Pro-drug
α2 agonist (centrally reduces sympathetic outflow)
Treats HTN
SE: sedation, dry mouth, edema, rebound HTN w/ sudden discontinuation

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20
Q

What is an indirect sympathomimetic and when do you need to worry about it?

A

Tryamine - patients on MAOIs

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21
Q

Phenylephrine

A

α1 agonist

Vasoconstriction, dilate eye - nasal decongestant

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22
Q

Clonidine

A

α2 agonist - decrease sympathetic outflow

SE: Sedation, dry mouth, edema, rebound HTN

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23
Q

Albuterol

A

β2 agonist: Short duration bronchodilator - asthma

SE: Tremor, anxiety

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24
Q

Salmeterol

A

β2 agonist: Long duration bronchodilator - COPD, persistant asthma

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25
Q

Pseudoephedrine

A

α1 agonist - used as a nasal decongestant

26
Q

Guanadrel

A

Inhibits NE release/depletes neuronal amine stores - Essential HTN
SE: Orthostatic hypotension, male sexual dysfunction, diarrhea, muscle weakness, edema

27
Q

Guanethidine

A

Inhibits NE release/depletes neuronal amine stores - Essential HTN
SE: Orthostatic hypotension, male sexual dysfunction, diarrhea, muscle weakness, edema

28
Q

Reserpine

A

Blocks VMAT, inhibits NE release - active in CNS

Depression, sedation, suicidal tendencies

29
Q

Cocaine

A

Blocks NET - increases duration of NE in synaptic cleft

30
Q

Phenoxybenzoine

A

Irreversible blocks α receptors - vasodilation proportional to sympathetic tone - pheochromocytoma
SE: Tachycardia, salt/water retention, o. hypotension

31
Q

Phentolamoine

A

Blocks α receptors - reverse/shorten DOA of anesthesia

SE: Tachycardia, salt/water retention, o. hypotension

32
Q

Prazosin

A

α1 antagonist - decreases PVR, favorable effect on lipid profile - (short term) congestive heart failure, HTN, BPH
*First dose phenomenon (hypotension)
SE: alt/water retention, o. hypotension

33
Q

Tamsulosin

A

α1a antagonist - decreases tone in GU tract, little BP effects - BPH

34
Q

Propranolol

A

β blocker - HTN, angina, cardiac arrhythmias, acute MI, pheochromocytoma, migrane prophylaxis
SE: Cardiac depression, bradycardia, bronchoconstriction, impotence, sedation, nightmares

35
Q

Timolol

A

β blocker - Glaucoma, HTN, angina, cardiac arrhythmias, acute MI, pheochromocytoma, migrane prophylaxis
SE: Cardiac depression, bradycardia, bronchoconstriction, impotence, sedation, nightmares

36
Q

Metoprolol

A

(β1 > β2) blocker - Chronic Heart Failure, HTN, angina, cardiac arrhythmias, acute MI
SE: Cardiac depression, bradycardia, impotence, sedation, nightmares, hypotension

37
Q

Atenolol

A

β1 blocker - not in CNS - HTN, angina, cardiac arrhythimas, acute MI, pheochromocytoma
SE: Cardiac depression, bradycardia, impotence hypotension

38
Q

Carvedilol

A

βα1 blocker - cardio effects, PVR, has some antioxidant properteis and Ca channels - Chronic Heart Failure, HTN, acute MI

39
Q

Labetalol

A

βα1 blocker - Essential HTN
Oral: Essential HTN
IV: Hypertensive Emergencies

40
Q

What are the two most important enzymes for NE metabolism?

A
  1. Catechol-O-methyltransferase

2. Monoamine oxidase

41
Q

What is botulinum toxins mechanism of action?

A

Cleaves snares in the presynaptic nerve at the NMJ - can’t release ACh - skeletal muscle paralysis

42
Q

What enzyme is the rate limiting step for NE synthesis?

A

Tyrosine hydroxylase - converts tyrosine -> DOPA

43
Q

Bethanechol

A

Muscarinic agonist (orally/SQ) Void bladder

44
Q

Pilocarpine

A

Muscarinic agonist (orally/SQ) - Salivation, open up angle in eye - glaucoma

45
Q

What are side the side effects of the cholinergic agonists and AChE inhibitors?

A 
S: Salivation
L: Lacrimation
U: Urination
D: Defecation
G: GI upset
E:  emesis
Bradycardia, hypotension, blurred vision
46
Q

What two drugs are irreversible AChE substrate inhibitors?

A

Sarin and Malathion

47
Q

Edrophonium

A

AChE inhibitor - reverse paralysis, diagnosis of myasthenia gravis

48
Q

Physostigmine

A

AChE inhibitor (Active in CNS): Treats wide angle glaucoma

49
Q

Neostigmine

A

AChE inhibitor (Periphery): Treats myasthenia gravis, urinary and GI motility issues

50
Q

Atropine

A

Muscarinic antagonist (some CNS) Bradyarrhthmias, dilates eye, blocks vagal reflexes - treats AChE and muscarinic toxicity i.e. Sarin

51
Q

Scopolamine

A

Muscarinic antagonist (More CNS penetration) treats motion sickness and vestibular disease

52
Q

Ipratropium

A

Muscarinic antagonist (inhaled no CNS) - bronchodilation, treats COPD

53
Q

Tropicamide

A

Muscarinic antagonist - Dilates eyes

54
Q

Oxygutynin

A

Muscarinic antagonist (Bladder, some CNS) - Overactive bladder, incontinence (women)

55
Q

Darifenacin

A

Muscarinic antagonist (some M3, less CNS) Overactive bladder, incontinence (women)

56
Q

Glycopyrrolate

A

Muscarinic antagonist (NMJ no CNS) - reverse sk muscle paralysis

57
Q

Rocuronium

A

(Competitive NMJ Blocker) Adjuvent during surgery - metabolized by liver

58
Q

Atracurium

A

(Competitive NMJ Blocker) Adjuvent during surgery - spontaneously degrades in blood, slight histamine release

59
Q

Vecuronium

A

(Competitive NMJ Blocker) Adjuvent during surgery - metabolized by liver

60
Q

Pancuronium

A

(Competitive NMJ Blocker) Adjuvent during surgery - metabolized by kidney, slight increase in HR, BP, and histamine release

61
Q

Succinylcholine

A

(Depolarizing NMJ Blocker) Flaccid paralysis Allows tracheal intubation

62
Q

Pralidoxime

A

(Depolarizing NMJ Blocker)

M1 Spring Block 1 (10 decks)

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