Pharm Basics Review Flashcards

1
Q

Parasympathetic activation: GI, Bladder, Eye, Lung, Heart, Lacrimal glands, salivary gland, uterus, penis/clitoris

A
GI: increased digestion
Bladder: wall contraction, relax sphincter
Eye: mitosis, ciliary muscle contraction
Lung: smooth muscle contraction
Heart: decreased heart rate/contractility
Lacrimal glands: stimulate tears
Salivary gland: watery secretions
Uterus: contraction
Penis/clitoris: erection/engorgement
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2
Q

Cholinergic excess

A
Diarrhea
Urination
Miosis
Bronchospasm
Bradycardia
Excitation of skeletal muscle/CNS
Lacrimation
Salivation
Sweating
(DUMBBELSS)
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3
Q

organophosphate poisoning

A

inactivation of acetylcholinesterase -> excess cholinergic activation -> DUMBBELSS

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4
Q

Treatment of organophosphate poisoning

A

atropine - blocks muscarinic receptors

pralidoxime - regenerates acetylcholinesterase (give both)

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5
Q

Myasthenia gravis

A

Abs against acetylcholine receptor
most common presentation: ptosis & diplopia that worsens throughout the day
Tension test -> Edrophonium (autoAb test is more specific)

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6
Q

Myasthenia gravis in relation to thyroid pathology

A

50% associated with thymus hyperplasia
20% associated with thymic atrophy
15% associated with thymic tumor (thymoma)

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7
Q

What is myasthenia crisis?

A

rapidly progressing weakness especially in respiratory muscles

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8
Q

What is the treatment for myasthenia gravis?

A

indirect cholinergic agonist (acetylcholinesterase inhibitors)
immunotherapy
thymectomy
plasmapheresis

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9
Q

What are the symptoms of inhibiting parasympathetic activity?

A

Hot as a hare -> hyperpyrexia (not sweating)
Red as a beet -> flushing
Blind as a bat -> cycloplegia, mydriasis (lose accommodation)
Dry as a bone -> lack of salivation
Mad as a hatter -> delirium
Bloated as a toad -> constipation and urinary retention
Tacky as a polyester suit -> tachycardia

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10
Q

Which anticholinergics are used in the treatment of urge urinary incontinence?

A
oxybutynin
tolterodine
darifenancin
trospium
solifenacin

“Off The Darn Toilet Seat”

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11
Q

In what populations is atropine contraindicated?

A

BPH, hyperthermia, acute angle glaucoma, elderly, GI obstruction/ileus

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12
Q

What other medications have anticholinergic side effects?

A
  1. first generation H1 blockers: diphenhydramine (Benadryl), doxylamine (Unisom), chlorpheniramine
  2. Neuroleptics (thioridazine, chlorpromazine, clozapine, olanzipine)
  3. TCAs (amitriptyline)
  4. Amantadine
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13
Q

What does stimulation of the alpha1 receptors cause?

A

vascular smooth muscle contraction -> increased peripheral resistance, increased BP, mydriasis, increased bladder sphincter contraction

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14
Q

What does stimulation of the alpha 2 receptors cause?

A

stimulates beta cells of the pancreases, some smooth muscle cells, inhibits NE release

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15
Q

What does stimulation of the beta 1 receptors cause?

A

tachycardia, increased lipolysis, increased myocardial contractility, increased release of renin

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16
Q

What does stimulation of the beta 2 receptors cause?

A

vasodilation, slightly decreased peripheral resistance, brochodilation, increase lipolysis, increased insulin resistance, decreased uterine tone

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17
Q

Where does vesamicol act at the NMJ?

A

Vesamicol inhibits packaging of ACh into vesicles

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18
Q

Where does hemicholinium act at the NMJ?

A

inhibits the choline/Na+ transporter

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19
Q

Where does Black widow spider toxin act at the NMJ? What does it cause?

A

stimulates the release of ACh from the presynaptic terminal; causes spastic paralysis

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20
Q

Where does botulinum toxin act at the NMJ? What does it cause?

A

inhibits release of ACh from the presynaptic terminal; causes flaccid paralysis

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21
Q

outline the path of enzymes and cofactors required to convert phenylalanine to epinephrine.

A

phenylephrine + phenylalanine hydroxylase + BH4 -> Tyrosine + tyrosine hydroxylase + BH4 -> DOPA + DOPA decarboxylase + Vit B6 -> Dopamine + dopamine beta-hydroxyalse + Vit C -> NEpi + PNMT -> Epinephrine

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22
Q

Which enzyme is inhibited by cortisol in the conversion of phenylalanine to epinephrine?

A

PNMT (NEpi -> Epi)

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23
Q

What enzymes are responsible for metabolizing NEpi?

A

COMT (catechol-o-methyltransferases) and MAO (monoamine oxidase)

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24
Q

Where does reserpine act on the noradrenergic NMJ?

A

inhibits the packaging of NEpi into vesicles

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25
Q

Where does metyrosine act on the noradrenergic NMJ?

A

inhibits the enzyme tyrosine hydroxylase

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26
Q

What three enzymes inhibit the reuptake of NEpi?

A

cocaine, TCA’s, SNRIs

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27
Q

What three enzymes facilitate the release of NEpi?

A

amphetamines, ephedrine, tyramine

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28
Q

What two enzymes inhibit the release of NEpi?

A

guanethidine, bretylium (CCB for arrhythmia)

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29
Q

What presynaptic auto receptor stimulates the release of NEpi?

A

AT receptor (Angiotensin)

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30
Q

What two presynaptic auto receptors inhibit the release of NEpi?

A

alpha 2, M2

31
Q

What are the breakdown products of dopamine, NEpi, and Epi? When will these be elevated?

A

dopamine -> homovanillic acid (HVA)
NEpi -> vanillylmandelic acid (VMA)
Epi -> metanephrine

Elevated in tne urine of patients with phenchromocytoma

32
Q

Which receptor types use Gq signaling?

A

cutesies (q) HAVe 1 M&M

H1, alpha 1, V1, M1, M3

33
Q

Which receptor types use Gi signaling?

A

MAD 2’s

M2, alpha 2, D2

34
Q

Which receptor types use Gs signaling?

A

Gs all the rest

H2, beta 1, beta 2, V2, D1

35
Q

Outline the signaling pathway with Gq.

A

Gq -> PLC (phospholipase C) -> PIP2 -> DAG + IP3
DAG -> PKC (protein kinase C)
IP3 -> increased intracellular calcium (activates PKC)

36
Q

Outline the signaling pathway with Gs and Gi

A

Gs -> adenylyl cyclase -> ATP -> cAMP -> PKA (protein kinase A) -> increased intracellular calcium in heart & inactivation of myosin light-chain kinase (smooth muscle)

Gi does the opposite

37
Q

What four pharmacokinetics equations are most important for Step 1?

A
  1. Vd = D/C or volume of distribution = amount of drug in IV form/[drug] in plasma
  2. CL = rate of elimination/plasma concentration = 0.7 x Vd/(t1/2) (know the second one!!)
  3. LD = Css x Vd (Css = concentration at steady state)
  4. MD = Css x CL
38
Q

At 4.5 t1/2s (half-lives) what is the percentage of Css and percent eliminated?

A

94% Css and 94% eliminated at 4.5 half-lives

39
Q

What is the effect of adding a competitive antagonist to an agonist?

A

potency decreases, no change in efficacy

40
Q

What is the effect of adding a noncompetitive antagonist to an agonist?

A

potency stays the same, efficacy decreases

41
Q

What always changes with a partial agonist vs a full agonist?

A

efficacy always decreases; potency is dependent on the partial agonist

42
Q

What substances are P450 inhibitors?

A
CRACK AMIGOS
Ciprofloxacin
Ritonavir (protease inhibitors)
Amiodarone
Cimetidine
Ketoconazole
Acute alcohol
Macrolides 
Isoniazid
Grapefruit juice
Omeprazole
Sulfonamides
43
Q

What substances are P450 inducers?

A
Guiness, Coronas, PBRs Induce Chronic Alcohol use
Griseofulvin
Carbamazepine
Phenytoin
Barbiturates
Rifampin
St. John's wort
chronic alcoholism
44
Q

Outline the pathway of ethanol breakdown

A

ethanol + alcohol dehydrogenase + NAD+ -> Acetaldehyde + acetaldehyde dehydrogenase + NAD+ -> Acetate

45
Q

What drug inhibits alcohol dehydrogenase?

A

fomepizole
used to Tx methanol (-> formaldehyde) and ethylene glycol (-> oxalic acid) toxicity
(prevents the formation of the toxic breakdown products)

46
Q

What drug inhibits acetaldehyde dehydrogenase?

A

disulfiram

used to Tx alcoholism

47
Q

What hepatic phase of metabolism is lost first by geriatric patients? Which phase is mediated by cytochrome P450?

A
  1. Phase I is lost first in geriatric patients

2. Phase I is mediated by CYP450s

48
Q

What types of reactions occur during phase 1 of drug metabolism?

A

Reduction, oxidation, hydrolysis with cytochrome P450

usually yield slightly polar, water-soluble metabolites

49
Q

What types of reactions occur during phase 2 of drug metabolism?

A

conjugation (methylation, glucuronidation, acetylation, sulfating)
usually yields very polar, inactive metabolites

50
Q

What do you treat an acidic drug overdose with and why? (ex: salicylates)

A

Treat with NaHCO3 -> traps the acidic drug in the basic urine

51
Q

What do you treat a basic drug overdose with and why? (ex: amphetamines)

A

Treat with NH4Cl -> traps the basic drug in the acidic urine

52
Q

What is the antidote to acetaminophen?

A

N-acetylcystein

53
Q

What is the antidote to salicylates?

A

NaHCO3, dialysis

54
Q

What is the antidote to amphetamines?

A

ammonium chloride

55
Q

What is the antidote to anticholinesterases, organophosphates?

A

pralidoxime, atropine

56
Q

What is the antidote to antimuscarinic, anticholinergic agents?

A

physostigmine

57
Q

What is the antidote to digoxin?

A

anti-dig fragments, atropine if HR is decreased; K+, Mg2+

58
Q

What is the antidote to Iron?

A

deferoxamine

59
Q

What is the antidote to lead?

A

EDTA, succorer, dimercaprol

60
Q

What is the antidote to arsenic, mercury, gold?

A

dimercaprol, succimer

61
Q

What is the antidote to copper, arsenic, gold?

A

penicillamine

62
Q

What is the antidote to cyanide?

A

nitrite + thiosulfate, hydroxocaobalamin

63
Q

What is the antidote to methemoglobin?

A

methylene blue, VitC

64
Q

What is the antidote to carbon monoxide?

A

100% O2

65
Q

What is the antidote to methanol, ethylene glycol (antifreeze)

A

fomeprizole, ethanol, dialysis

66
Q

What is the antidote to opioids?

A

Naloxone, naltrexone

67
Q

What is the antidote to benzodiazepines?

A

flumazenil

68
Q

What is the antidote to TCAs?

A

NaHCO3

69
Q

What is the antidote to Heparin?

A

Protamine sulfate

70
Q

What is the antidote to warfarin?

A

VitK

71
Q

What is the antidote to t-PA, streptokinase?

A

aminocaproic acid

72
Q

What is the antidote to theophylline?

A

beta blocker

73
Q

What is the mechanism of action of dantrolene?

A

prevents the release of Ca2+ from the sarcoplasmic reticulum of skeletal m.

74
Q

What substances inhibit the reuptake of norepinephrine?

A
  1. cocaine
  2. TCAs
  3. SNRIs