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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
Where does metyrosine act on the noradrenergic NMJ?
inhibits the enzyme tyrosine hydroxylase
26
What three enzymes inhibit the reuptake of NEpi?
cocaine, TCA's, SNRIs
27
What three enzymes facilitate the release of NEpi?
amphetamines, ephedrine, tyramine
28
What two enzymes inhibit the release of NEpi?
guanethidine, bretylium (CCB for arrhythmia)
29
What presynaptic auto receptor stimulates the release of NEpi?
AT receptor (Angiotensin)
30
What two presynaptic auto receptors inhibit the release of NEpi?
alpha 2, M2
31
What are the breakdown products of dopamine, NEpi, and Epi? When will these be elevated?
dopamine -> homovanillic acid (HVA) NEpi -> vanillylmandelic acid (VMA) Epi -> metanephrine Elevated in tne urine of patients with phenchromocytoma
32
Which receptor types use Gq signaling?
cutesies (q) HAVe 1 M&M | H1, alpha 1, V1, M1, M3
33
Which receptor types use Gi signaling?
MAD 2's | M2, alpha 2, D2
34
Which receptor types use Gs signaling?
Gs all the rest | H2, beta 1, beta 2, V2, D1
35
Outline the signaling pathway with Gq.
Gq -> PLC (phospholipase C) -> PIP2 -> DAG + IP3 DAG -> PKC (protein kinase C) IP3 -> increased intracellular calcium (activates PKC)
36
Outline the signaling pathway with Gs and Gi
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
What four pharmacokinetics equations are most important for Step 1?
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
At 4.5 t1/2s (half-lives) what is the percentage of Css and percent eliminated?
94% Css and 94% eliminated at 4.5 half-lives
39
What is the effect of adding a competitive antagonist to an agonist?
potency decreases, no change in efficacy
40
What is the effect of adding a noncompetitive antagonist to an agonist?
potency stays the same, efficacy decreases
41
What always changes with a partial agonist vs a full agonist?
efficacy always decreases; potency is dependent on the partial agonist
42
What substances are P450 inhibitors?
``` CRACK AMIGOS Ciprofloxacin Ritonavir (protease inhibitors) Amiodarone Cimetidine Ketoconazole Acute alcohol Macrolides Isoniazid Grapefruit juice Omeprazole Sulfonamides ```
43
What substances are P450 inducers?
``` Guiness, Coronas, PBRs Induce Chronic Alcohol use Griseofulvin Carbamazepine Phenytoin Barbiturates Rifampin St. John's wort chronic alcoholism ```
44
Outline the pathway of ethanol breakdown
ethanol + alcohol dehydrogenase + NAD+ -> Acetaldehyde + acetaldehyde dehydrogenase + NAD+ -> Acetate
45
What drug inhibits alcohol dehydrogenase?
fomepizole used to Tx methanol (-> formaldehyde) and ethylene glycol (-> oxalic acid) toxicity (prevents the formation of the toxic breakdown products)
46
What drug inhibits acetaldehyde dehydrogenase?
disulfiram | used to Tx alcoholism
47
What hepatic phase of metabolism is lost first by geriatric patients? Which phase is mediated by cytochrome P450?
1. Phase I is lost first in geriatric patients | 2. Phase I is mediated by CYP450s
48
What types of reactions occur during phase 1 of drug metabolism?
Reduction, oxidation, hydrolysis with cytochrome P450 | usually yield slightly polar, water-soluble metabolites
49
What types of reactions occur during phase 2 of drug metabolism?
conjugation (methylation, glucuronidation, acetylation, sulfating) usually yields very polar, inactive metabolites
50
What do you treat an acidic drug overdose with and why? (ex: salicylates)
Treat with NaHCO3 -> traps the acidic drug in the basic urine
51
What do you treat a basic drug overdose with and why? (ex: amphetamines)
Treat with NH4Cl -> traps the basic drug in the acidic urine
52
What is the antidote to acetaminophen?
N-acetylcystein
53
What is the antidote to salicylates?
NaHCO3, dialysis
54
What is the antidote to amphetamines?
ammonium chloride
55
What is the antidote to anticholinesterases, organophosphates?
pralidoxime, atropine
56
What is the antidote to antimuscarinic, anticholinergic agents?
physostigmine
57
What is the antidote to digoxin?
anti-dig fragments, atropine if HR is decreased; K+, Mg2+
58
What is the antidote to Iron?
deferoxamine
59
What is the antidote to lead?
EDTA, succorer, dimercaprol
60
What is the antidote to arsenic, mercury, gold?
dimercaprol, succimer
61
What is the antidote to copper, arsenic, gold?
penicillamine
62
What is the antidote to cyanide?
nitrite + thiosulfate, hydroxocaobalamin
63
What is the antidote to methemoglobin?
methylene blue, VitC
64
What is the antidote to carbon monoxide?
100% O2
65
What is the antidote to methanol, ethylene glycol (antifreeze)
fomeprizole, ethanol, dialysis
66
What is the antidote to opioids?
Naloxone, naltrexone
67
What is the antidote to benzodiazepines?
flumazenil
68
What is the antidote to TCAs?
NaHCO3
69
What is the antidote to Heparin?
Protamine sulfate
70
What is the antidote to warfarin?
VitK
71
What is the antidote to t-PA, streptokinase?
aminocaproic acid
72
What is the antidote to theophylline?
beta blocker
73
What is the mechanism of action of dantrolene?
prevents the release of Ca2+ from the sarcoplasmic reticulum of skeletal m.
74
What substances inhibit the reuptake of norepinephrine?
1. cocaine 2. TCAs 3. SNRIs

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