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USMLE Pharmacology > Autonomic > Flashcards

Autonomic Flashcards

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USMLE® Step 1 flashcards
1
Q

Pharmacokinetics

A 
Effects of body on drug
Absorption
Distribution
Metabolism
Excretion
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2
Q

Pharmacodynamics

A 
Effects of drug on body 
Receptor binding
Drug efficacy
Drug potency
Toxicity
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3
Q

a1 receptors

A

Gq (phospholipase C)

Increase vascular smooth muscle contraction
Increase pupillary dilator muscle contraction (mydriasis)
Increase intestinal and bladder sphincter muscle contraction

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4
Q

a2 receptors

A

Gi (inhibitory; adenylyl cyclase)

Decrease sympathetic outflow
Decrease insulin release
Decrease lipolysis
Increase platelet aggregation

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5
Q

B1 receptors

A

Gs (excitatory; adenylyl cyclase)

Increase HR, contractility, renin release, and lipolysis

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6
Q

B2 receptors

A

Gs (excitatory; adenylyl cyclase)

Vasodilation, bronchodilation
Increase HR, contractility, lypolysis, insulin release, and aqueous humor production
Decrease uterine tone (tocolysis)
Ciliary muscle relaxation

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7
Q

M1

A

Gq (phospholipase C)

CNS
Enteric nervous system

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8
Q

M2

A

Gi (inhibitory; adenylyl cyclase)

Decrease HR and contractility of atria

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9
Q

M3

A

Gq (phopholipase C)

Increase exocrine gland secretions (lacrimal, salivary, gastric acid), gut peristalsis, bladder contraction, pupillary sphincter muscle contraction (miosis)
Bronchoconstriction
Ciliary muscle contraction (accommodation)

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10
Q

D1

A

Gs (adenylyl cyclase)

Relaxes renal vascular smooth muscle

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11
Q

D2

A

Gi (inhibitory; adenylyl cyclase)

Modulates transmitter release, especially in brain

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12
Q

H1

A

Gq (phospholipase C)

Increase nasal and bronchial mucus production
Increase vascular permeability
Contraction of bronchioles
Pruritus
Pain
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13
Q

H2

A

Gs (adenylyl cyclase)

Increase gastric acid secretion

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14
Q

V1

A

Gq (phospholipase C)

Increase vascular smooth muscle contraction

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15
Q

V2

A

Gs (adenylyl cyclase)

Increase H2O permeability and reabsorption in the collecting tubules of the kidney (V2 is found in the 2 kidneys)

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16
Q

Phospholipase C pathway (Gq)

A

Converts PIP2 –> DAG + IP3
DAG –> Protein kinase C
IP3 –> Increased [Ca2+] = smooth muscle contraction

H1, a1, V1
M1, M3
“HaVe 1 M&M”

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17
Q

Adenylyl cyclase pathway (Gs)

A

Converts ATP –> cAMP
cAMP activates protein kinase A = increases [Ca2+] in heart and inhibits myosin light-chain kinase in smooth muscle

B1, B2, D1
H2, V2

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18
Q

Adenylyl cyclase pathway (Gi)

A

INHIBITORY
Blocks conversion of ATP to cAMP, PKA, etc.

M2, a2, D2
“MAD 2’s”

19
Q

Drugs blocking cholinergic synthesis

A

Hemicholinium
Vesamicol
Botulinum
AChE inhibitors

20
Q

Drugs blocking noradrenergic synthesis

A 
Metyrosine
Reserpine
Bretylium, guanethidine
Amphetamine
Cocaine, TCAs, amphetamines
21
Q

Fraction of administered drug that reaches systemic circulation unchanged

A

Bioavailability (F)

22
Q

Volume of distribution

A

Amount of drug in body/plasma drug concentration
Volume occupied by total absorbed drug amount at plasma concentration
Altered by liver and kidney disease

23
Q

Low Vd

A

Blood (4-8 L)

Large/charged molecules; plasma protein bound

24
Q

Medium Vd

A

ECF

Small hydrophilic molecules

25
Q

High Vd

A

All tissues including fat

Small lipophilic molecules, especially if bound to tissue protein

26
Q

Half life

A

T1/2 = (0.693 x Vd)/Cl

Property of first order elimination

27
Q

A drug infused at a constant rate takes how long to reach steady state?

A

4-5 half lives

28
Q

Clearance

A

Volume of plasma cleared of drug per unit time

Cl = rate of elimination of drug/plasma drug concentration
Cl = Vd x Ke (elimination constant)

Impaired with cardiac, hepatic, or renal dysfunction

29
Q

Loading dose

A

Loading dose = (Cp x Vd)/F

Cp = target plasma concentration at steady state

30
Q

Maintenance dose

A

Maintenance dose = (Cp x Cl x dosage interval)/F

In renal or liver disease, maintenance dose decreases and loading dose is unchanged

31
Q

Does time to steady state depend on dose and dosing frequency?

A

NO = time to steady state depends primarily on T1/2 and is independent of dose and dosing frequency

32
Q

Zero order elimination

A

Rate of elimination constant = constant AMOUNT eliminated per unit time
“Capacity-limited”
Decreases linearly with time

33
Q

Zero order elimination examples (3)

A

Phenytoin
Ethanol
Aspirin (at high or toxic concentrations)
“PEA” = round like 0 in zero order

34
Q

First order elimination

A

Rate of elimination directly proportional to drug concentration = constant FRACTION eliminated per unit time
Plasma concentration decreases EXPONENTIALLY with time
“Flow dependent”

35
Q 
Weak acids (3)
Overdose treatment?
A 
Phenobarbital
Methotrexate
Aspirin
Trapped in basic environments
Treat overdose with bicarbonte!!!
36
Q 
Weak bases (1)
Overdose treatment?
A

Amphetamines
Trapped in acidic environment
Treat overdose with ammonium chloride

37
Q

Phase I metabolism

A

Reduction
Oxidation
Hydrolysis with CYP450

Yields slightly polar/water soluble metabolites (still active)
Lost first by geriatric patients

38
Q

Phase II metabolism

A

Conjugation:
Glucuronidation
Acetylation
Sulfation

Yields very polar, inactive metabolites (renal excretion)
Retained by geriatric patients
Slow acetylators have greater side effects from certain drugs due to decreased rate of metabolism

39
Q

Therapeutic index

A

TD50/ED50

Median toxic dose/median effective dose = measures safety of drug

40
Q

Safer drugs have higher/lower TI?

A

HIGHER!!!

41
Q

Examples of low therapeutic index drugs? (4)

A

Digoxin
Lithium
Theophylline
Warfarin

42
Q

S/sx of organophosphate/cholinesterase inhibitor poisoning

A 
"DUMBBELSS"
Diarrhea
Urination
Miosis
Bronchospasm
Bradycardia
Excitation of skeletal muscle/CNS
Lacrimation
Sweating
Salivation
43
Q

Antidote for organophosphate/cholinesterase inhibitor poisoning

A

Atropine (competitive inhibitor) + pralidoxime (regenerates AChE if given early)

USMLE Pharmacology (15 decks)

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