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Pharmacology > Pharmacokinetics and Autonomic Drugs > Flashcards

Pharmacokinetics and Autonomic Drugs Flashcards

1
Q

What is Bioavailability

A

Bioavailability (F) = % drug administered that reaches systemic circulation unchanged

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2
Q

In what instances is Bioavailability (F) 100%

A

IV administration, and in kids: interosseous

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3
Q

What is Volume of Distribution (Vd)

A

Vd = amount of drug in body / [drug] in plasma

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4
Q

What can change Volume of Distribution (Vd)?

A

kidney and liver diseases can change the Vd of protein bound drugs

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5
Q

What is the equation for half-life?

A

t1/2 = 0.7xVd/CL

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6
Q

What is clearance (Cl)

A 
Clearance = rate of elimination / [drug] in plasma
Clearance = Vd x Ke (Ke= elimination constant)
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7
Q

What is Loading Dose

A

Loading Dose = Cp x Vd/F where Cp = target [drug] in plasma

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8
Q

What is Maintenance Dose and what causes it to decrease

A

Maintenance Dose = Cp x Cl/F where Cp = target [drug] in plasma
Decreases in liver and kidney diseases because of decreased clearance

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9
Q

What is Steady State?

A

Depends on half-life of drug.
Most drugs require 4-5 half-lifes to reach steady state.
Not effected by frequency or amount of dosing

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10
Q

What is the difference between Zero and First order elimination?

A

0 order = constant amount is eliminated
eg: start 100, 80, 60, 40, 20, 0
1st order = constant fraction is eliminated
eg: start 100, 50, 25, 12.5, 6.25 etc

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11
Q

Which drugs are Zero order?

A

“Zero PEAs for me”

Phenytoin, Ethanol, Aspirin

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12
Q

What are weak acid drugs, where do they get trapped and how do you treat overdose?

A

Aspirin, Methotrexate, Phenobarbital
Trapped in basic environments
Use bicarbonate to treat overdose by ionizing, and trapping in urine

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13
Q

What are weak base drugs, where do they get trapped and how do you treat overdose?

A

Amphetamines
Trapped in acidic environments
Use ammonium chloride to treat overdose and trap in urine

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14
Q

What are Phase 1 types of drug metabolism? Which enzyme do they require? What do they yield? What occurs in Geriatric patients?

A

Reduction, Oxidation, Hydrolysis
Require cytochrome P450
Yield slightly polar, water-soluble, usually active metabolites
Phase 1 is lost first in geriatric patients

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15
Q

What are Phase 2 types of drug metabolism? What do they yield?

A

Glucuronidation, Acetylation, Conjugation

Yield very polar, inactive metabolites which are renally excreted

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16
Q

What occurs in slow acetylators?

A

increased side effects of drugs due to slower metabolism

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17
Q

Receptor a1: what g-protein class, and what are its functions

A

Gq,

Increase contraction of: vascular SmM, pupillary dilator muscle (mydriasis), intestinal and bladder sphincter muscle

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18
Q

Receptor a2: what g-protein class, and what are its functions

A

Gi,
Decrease sympathetic outflow, insulin release, lipolysis
increase platelet aggregation

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19
Q

Receptor b1: what g-protein class, and what are its functions

A

Gs,

Increase heart rate, contractility, renin release, lipolysis

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20
Q

Receptor b2: what g-protein class, and what are its functions

A

Gs,
Vasodilation, bronchodilation
Increased heart rate, contractility, lipolysis, insulin release, aqueous humor production
Decreased uterine tone, ciliary muscle relaxation

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21
Q

Receptor M1: what g-protein class, and what are its functions

A

Gq,

CNS, enteric nervous system

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22
Q

Receptor M2: what g-protein class, and what are its functions

A

Gi,

decrease heart rate, contractility of atri

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23
Q

Receptor M3: what g-protein class, and what are its functions

A

Gq,
Increased exocrine gland secretion (lacrimal, gastric etc), gut peristalsis, contraction of bladder, bronchioles, pupillary sphincter muscle (miosis), ciliary muscle (acommodation)

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24
Q

Receptor D1: what g-protein class, and what are its functions

A

Gs,

relaxes renal vascular SmM

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25
Q

Receptor D2: what g-protein class, and what are its functions

A

Gi,

Modulates transmitter release, especially in brain

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26
Q

Receptor H1: what g-protein class, and what are its functions

A

Gq,

increased nasal, bronchial mucus production, contraction of bronchioles, puritis, pain

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27
Q

Receptor H2: what g-protein class, and what are its functions

A

Gs,

Increased gastric acid secretion

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28
Q

Receptor V1: what g-protein class, and what are its functions

A

Gq,

Increased vascular SmM contraction

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29
Q

Receptor V2: what g-protein class, and what are its functions

A

Gs,

Increased H2O permeability, reabsorption in collecting tubules of kidney

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30
Q

Hemicholinium: Site of action,

A

Inhibits choline reuptake on presynaptic cholinergic neuron

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31
Q

Vesamicol: Site of action

A

Cholinergic neuron: Inhibits intracellular transportation of Acetyl-CoA and Choline via ChAT into secretory vessicle for assembly into ACh

32
Q

Botulinum: site of action

A

Cholinergic neuron: Inhibits release of ACh into synaptic cleft

33
Q

Metyrosine: Site of action

A

Noradrenergic neuron: inhibits conversion of tyrosine into dopa, therefore decreasing production of dopamine and NE

34
Q

Reserpine: Site and mechanism of action

A

Noradrenergic neuron: irreversibly blocks VMAT (vesiclular monoamine transporter) so that NE, 5HT3, and Dopamine cannot enter secretory vesicles for exocytosis. They are degraded by MAO and COMT in the cytoplasm, and [monoamine] in the synapse is depeated, leading to depression

35
Q

Guanethidine, Bretylium: site of action

A

inhibit release of NE into synapse

36
Q

Amphetamine: site of action

A

increases release of NE into synase

37
Q

Cocaine, TCAs, Amphetamines

A

inhibit reuptake of NE into presynaptic neuron

38
Q

Bethanechol: Direct or Indirect agonist? Clinical application? Action?

A

Direct agonist (cholinomimetic)
Application: Postoperative ileus, neurogenic ileus (constipation), urinary retention
Action: (+) bowel and bladder SmM, resistant to AChE
“BETHANy, CHOL me if you want to activate your bowels and bladder”

39
Q

Carbachol: Direct or Indirect agonist? Clinical application? Action?

A 
Direct agonist (cholinomimetic)
Application: glaucoma, pupillary contraction, relief of intraocular pressure
Action: "CARBon copy of ACh"
40
Q

Pilocarpine: Direct or Indirect agonist? Clinical application? Action?

A

Direct agonist (cholinomimetic)
Application: open-angle and closed-angle glaucoma
Action: potent stimulator of sweat, tears, saliva.
Contracts ciliary muscle of eye for open-angle, and pupillary sphinter for closed angle. resistant to AChE
“Cry, Drool, Sweat on your PILOw”

41
Q

Methacholine: Direct or Indirect agonist? Clinical application? Action?

A

Direct agonist (cholinomimetic)
Application: challenge test for asthma
Action: (+) M receptors in airway

42
Q

Neostigmine: Direct or Indirect agonist? Clinical application? Action?

A 
Indirect Agonist (anti-AChE)
Application: same as Bethanechol (postoperative neurogenic ileus and urinary retention) + myasthenia gravis, reversal of neuromuscular junction blockade (postop)
Action: increase endogenous ACh,
"Neo CNS = No CNS penetration"
43
Q

Pyridostigmine: Direct or Indirect agonist? Clinical application? Action?

A 
Indirect agonist (anti-AChE)
Application: Myasthenia gravis (long acting), does not penetrate CNS
Action: same as neostigmine. Increase endogenous ACh so increase strength
"pyRIDostiGMine gets RID of Myasthenia Gravis"
44
Q

Edrophonium: Direct or Indirect agonist? Clinical application? Action?

A 
Indirect agonist (anti-AChE)
Application: diagnosis of myasthenia gravis (extremely short acting)
Action: increases endogenous ACh
45
Q

Physostigmine: Direct or Indirect agonist? Clinical application? Action?

A 
Indirect agonist (anti-AChE)
**do not confuse with pyridostigmine for myasthenia
Application: Anticholinergic toxicity ( x BBB into CNS)
Action: increase endogenous ACh **FOR ATROPINE OD
"Physostigmine Phyxes atropine OD"
46
Q

Donepezil: Direct or Indirect agonist? Clinical application? Action?

A 
Indirect agonist (Anti-AChE)
Application: Alzheimer's
Action: increase endogenous ACh
47
Q

Cholinesterase Inhibitor Poisoning: Causes, effects, antidote

A

Causes: organophosphates (Parathion) found in insecticides, which irreversibly (-) AChE
Effects: Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of skeletal musc and cns, Lacrimation, Sweating, Salivation
Antidote: atropine + pralidoxime (regenerates AChE)

48
Q

Atropine, Homatropine, Tropicamide: Drug type, Organ system, Application

A

Muscarinic antagonist
Eye
Produce mydriasis and cycloplegia

49
Q

Benztropine: Drug type, Organ system, Application

A

Muscarinic antagonist
CNS
Parkinsons “Park my Benz”

50
Q

Scopolamine: Drug type, Organ system, Application

A

Muscarinic antagonist
CNS + auditory nerve
Motion sickness

51
Q

Ipratropium, Tiotropium: Drug type, Organ system, Application

A

Muscarinic antagonist
Respiratory
COPD, Asthma “IPRAy i can breathe soon”

52
Q

Oxybutynin: Drug type, Organ system, Application

A

Muscarinic antagonist
Genitourinary
Reduce urgency in mild cystitis and reduce bladder spasms

53
Q

Glycopyrrolate: Drug type, Organ system, Application

A

Muscarinic antagonist
GI, Respiratory
Parenteral: preop for reducing airway secretions; Oral: drooling, peptic ulcer

54
Q

Atropine: Drug type, Main Use, Action, Toxicity, Side Effects

A

Muscarinic antagonist
Main use: bradycardia and ophthalmic
Action:
- increase pupil dilation and cycloplegia,
- decrease airway secretions, stomach acid secretions, gut motility, bladder urgency in cystitis
- BLOCKS DUMBBeLSS but not excitation of CNS and SkM because that is mediated by nicotinic receptors
Toxicity:
- increase body temp (since decr sweating), rapid pulse, dry mouth, dry flushed skin, cycloplegia, constipation, disorientation (“hot as a hare, dry as a bone, red as a beet, blind as a bat, mad as a hatter”)
- acute-CLOSURE glaucoma in elderly due to mydriasis, urinary retention in men w/ BPH, and hyperthermia in infants
- Jimson Weed

55
Q

Epinephrine: Drug type, Receptor affinity, Application

A

Direct Sympathomimetic
b > a, no affinity for D1
Application: anaplylaxis, open angle glaucoma, asthma, hypotension

56
Q

Norepinephrine: Drug type, Receptor affinity, Application, Cardiovascular effects

A

Direct Sympathomimetic
a > b1, no affinity for b2 or D1
Application: hypotension (but decrease renal perfusion)
CV effects: a1 mediated increase in systolic and diastolic pressures due to vasoconstriction, incr MAP, leading to bradycardia

57
Q

Isoproterenol: Drug type, Receptor affinity, Application, Cardiovascular effects

A

Direct Sympathomimetic
b1 and 2, no affinity for a or D
Application: Torsade de pointes (tachycardia decreases QT interval), bradyarrhythmias (but may worsen ischemia)
CV effects: b2 mediated vasodilation leading to decreased MAP and increased HR through b1 reflex

58
Q

Dopamine: Drug type, Receptor affinity, Application

A

Direct Sympathomimetic
D1 at low dose, b1 and b2 at medium dose, a1 and a2 at high dose
Application: Shock (renal perfusion), HF, inotropic and chronotropic

59
Q

Dobutamine: Drug type, Receptor affinity, Application

A

Direct Sympathomimetic
b1&raquo_space; b2 or a1, a2
Application: HF, cardiac stress testing, inotropic and chronotropic

60
Q

Phenylephrine: Drug type, Receptor affinity, Application

A

Direct Sympathomimetic
a1 > a2, no affinity for b or D1
Application: hypotension (vasoconstriction), occular procedures (mydriatic), rhinitis (decongestant)

61
Q

Metaproterenol, Albuterol, salmeterol, terbutaline: Drug type, Receptor affinity, Application

A

Direct Sympathomimetic
b2&raquo_space; b1, no affinity for a or D1
Application:
- metaproterenol and albuterol for acute asthma
- salmeterol for long-term asthma or COPD
- terbutaline to reduce premature uterine contractions

62
Q

Ritodrine: Drug type, Receptor affinity, Application

A

Direct Sympathomimetic
b2 only
Application: reduces premature uterine contractions

63
Q

Amphetamine: Drug type, Mechanism, Application

A

Indirect Sympathomimetic
releases stored catecholamines
Application: narcolepsy, obesity, ADD

64
Q

Ephedrine: Drug type, Mechanism, Application

A

Indirect Sympathomimetic
releases stored catecholamines
Application: Nasal decongestion, urinary incontinence, hypotension

65
Q

Cocaine: Drug type, Mechanism, Application, Contraindication

A

Indirect Sympathomimetic
Reuptake inhibitor
Application: Vasoconstriction and local anesthesia
Contraindication: Never give b-blocker if cocaine intoxication is suspected (lead to unopposed a1 activation, extreme htn)

66
Q

Clonidine, a-methyldopa: Drug type, Mechanism, Application

A

Sympathoplegics
Centrally acting a2-agonist, decrease central sympathetic outflow
Application: HTN (especially w/ renal dz)

67
Q

Phenoxybenzamine: Drug type, Application, Toxicity

A

Irreversible Nonselective a-blocker
Pheochromocytoma – used before removing tumor to irreversibly block a-receptors since it won’t be overcome by the high levels of released catecholamines
Toxicity: orthostatic hypotension, reflex tachycardia

68
Q

Phentolamine: Drug type, Application

A

Reversible Nonselective a-blocker

For patients on MAO inhibitors who eat tyramine-containing foods (red wine, cheese, fish)

69
Q

(Praz/Teraz/Doxaz/Tamsul)-osin: Drug type, Application, Toxicity

A

“-osin” = a1-selective blocker
For htn, urinary retention in BPH
Toxicity: first dose orthostatic hypotension, dizziness, headache

70
Q

Mirtazapine: Drug type, Application, Toxicity

A

a2-selective blocker
For depression
Toxicity: sedation, increased serum cholesterol and appetite

71
Q

(Acebut-, betax-, esm-, aten-, metopr-, propran-, tim-, pind-, labet-)-olol: Drug type, Application and effect, Toxicity, Use with caution in…

A

b-blockers
Angina pectoris – decrease HR, contractility, so less O2 consumption
MI – decrease mortality
Hypertension – decrease CO and renin secretion (because JGA cell b1 blockade!!)
CHF – slow progression of chronic failure

Toxicity: impotence, exacerbation of asthma, cardiovasc (bradycardia, AV block, CHF), CNS (seizures, sedation, sleep alterations)

Caution in diabetics because b2 receptors increase insulin release so inhibiting b will decrease insulin leading to hyperglycemia

72
Q

b-blockers for SVT

A

metoprolol, esmolol (class II antiarrhythmic)

73
Q

b-blocker for glaucoma

A

timolol

decrease secretion of aqueous humor

74
Q

Name the b1-selective antagonists, and use

A

Acebutalol (partial agonist), Betaxolol, Esmolol (short acting), Atenolol, Metoprolol
Advantageous in pts w/ comorbid pulmonary disease

75
Q

Name the non-selective b antagonists

A

Propranolol, Timolol, Nadolol, Pindolol

76
Q

Name the non-selective vasodilatory a- and b-antagonists

A

Carvedilol, Labetalol

77
Q

Name the partial b-agonists

A

Pindolol and acebutalol
Partial Agonist Pindolol Acebutalol (PAPA)
note: pindolol is also non-selective antagonist, and acebutalol is b1 selective antagonist)

Pharmacology (12 decks)

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