Pharmacology 2 Flashcards

1
Q

What is the specific clinical use of Indomethacin in neonates?

A

Indomethacin is used to close a patent ductus arteriosus.

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2
Q

What is used to reverse the action of Heparin?

A

Protamine Sulfate is used for rapid reversal of heparinization (positively charged molecule that binds to negatively charged heparin).

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3
Q

What patients are at risk for life threatening hypotension when taking Sildenafil (Viagra)?

A

Those patients who are taking nitrates.

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4
Q

What process does Zafirlukast interfere with?

A

Leukotrienes increasing bronchial tone.

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5
Q

What type of gout is treated with Allopurinol?

A

Chronic gout.

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6
Q

What type of gout is treated with Colchicine?

A

Acute gout.

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7
Q

What type of gout is treated with Probenacid?

A

Chronic gout.

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8
Q

What type of patient should not take Misoprostol and why?

A

Misoprostol is contraindicated in women of childbearing potential because it is an abortifacient.

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9
Q

Which H2 Blocker has the most toxic effects and what are they?

A

Cimetidine is a potent inhibitor of P450; it also has an antiandrogenic effect and decreases renal excretion of creatinine. Other H2 blockers are relatively free of these effects.

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10
Q

Why are the Sulfonylureas inactive in IDDM (type-1)?

A

Because they require some residual islet function.

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11
Q

Acetaldehyde is metabolized by Acetaldehyde dehydrogenase — which drug inhibs this enzyme?

A

-Disulfram & also sulfonylureas — metronidazole

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12
Q

Explain pH dependent urinary drug elimination?

A

-Weak Acids>Alkinalize urine(CN3) to remove more -Weak bases>acidify urine to remove more

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13
Q

How do you treat coma in the ER (4)?

A

-Airway -Breathing -Circulation -Dextrose (thiamine & narcan) -ABCD

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14
Q

In coma situations you rule out what (7)?

A

-Infections -Trauma -Seizures -CO -Overdose -Metabolic -Alcohol (IT’S COMA)

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15
Q

List some specifics of lead poisoning(4)?

A

-A57Blue lines in gingiva & long bones -Encephalopathy & Foot drop -Abdominal colic / -Sideroblastic anemia

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16
Q

List the specific antidote for this toxin: Acetaminophen

A

-N-acetylcystine

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17
Q

List the specific antidote for this toxin: Amphetamine

A

-Ammonium Chloride

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18
Q

List the specific antidote for this toxin: Anticholinesterases (organophosphate.)

A

-Atropine & pralidoxime

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19
Q

List the specific antidote for this toxin: Antimuscarinic (anticholinergic)

A

-Physostigmine salicylate

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20
Q

List the specific antidote for this toxin: Arsenic (all heavy metals)

A

-Dimercaprol — succimer

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21
Q

List the specific antidote for this toxin: Benzodiazepines

A

-Flumazenil

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22
Q

List the specific antidote for this toxin: Beta Blockers

A

-Glucagon

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23
Q

List the specific antidote for this toxin: Carbon monoxide

A

-100% oxygen — hyperbaric

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24
Q

List the specific antidote for this toxin: Copper

A

-Penicillamine

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25
Q

List the specific antidote for this toxin: Cyanide

A

-Nitrate — hydroxocobalamin thiosulfate

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26
Q

List the specific antidote for this toxin: Digitalis

A

-Normalize K+ — Lidocaine — & Anti-dig Mab

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27
Q

List the specific antidote for this toxin: Heparin

A

-Protamine

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28
Q

List the specific antidote for this toxin: Iron

A

-Deferoxamine

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29
Q

List the specific antidote for this toxin: Lead

A

-EDTA — dimercaprol — succimer — & penicillamine

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30
Q

List the specific antidote for this toxin: Methanol & Ethylene glycol

A

-Ethanol — dialysis — & fomepizole

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31
Q

List the specific antidote for this toxin: Methemoglobin

A

-Methylene blue

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32
Q

List the specific antidote for this toxin: Opioids

A

-B51Naloxone / naltrexone (narcan)

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33
Q

List the specific antidote for this toxin: Salicylates

A

-Alkalinize urine & dialysis

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34
Q

List the specific antidote for this toxin: TPA & Streptokinase

A

-Aminocaproic acid

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35
Q

List the specific antidote for this toxin: Tricyclic antidepressants

A

-NaHCO3

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36
Q

List the specific antidote for this toxin: Warfarin

A

-Vitamin K & fresh frozen plasma

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37
Q

What are the products and their toxicities of the metabolism of ethanol by / alcohol dehydrogenase?

A

-Acetaldehyde -Nausea — vomiting — headache — & hypotension

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38
Q

What are the products and their toxicities of the metabolism of Ethylene Glycol by / alcohol dehydrogenase?

A

-Oxalic acid -Acidosis & Nephrotoxicity

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39
Q

What are the products and their toxicities of the metabolism of Methanol by / alcohol dehydrogenase?

A

-Formaldehyde & formic acid -severe Acidosis & retinal damage

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40
Q

Which drug(s) cause this reaction: Adrenocortical Insufficiency

A

-Glucocorticoid withdrawal

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41
Q

Which drug(s) cause this reaction: Agranulocytosis (3)?

A

-Cloazapine -carbamazapine -colchicine -PTU

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42
Q

Which drug(s) cause this reaction: Anaphylaxis?

A

-penicillin

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43
Q

Which drug(s) cause this reaction: Aplastic anemia (5)?

A

-Chloramphenicol -benzene -NSAIDS -PTU -phenytoin

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44
Q

Which drug(s) cause this reaction: Atropine-like side effects?

A

-Tricyclic antidepressants

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45
Q

Which drug(s) cause this reaction: Cardiac toxicity?

A

-Daunorubicin & Doxorubicin

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46
Q

Which drug(s) cause this reaction: Cinchonism (2)?

A

-Quinidine -quinine

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47
Q

Which drug(s) cause this reaction: Cough?

A

-ACE inhibitors (Losartan>no cough)

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48
Q

Which drug(s) cause this reaction: Cutaneous flushing (4)?

A

-Niacin -CA++ channel blockers -adenosine -vancomycin

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49
Q

Which drug(s) cause this reaction: Diabetes insipidus?

A

-Lithium

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50
Q

Which drug(s) cause this reaction: Disulfram-like reaction (4) ?

A

-metronidazole -certain cephalosporins -procarbazine -sulfonylureas

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51
Q

Which drug(s) cause this reaction: Drug induced Parkinson’s (4) ?

A

-Haloperidol -chlorpromazine -reserpine -MPTP

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52
Q

Which drug(s) cause this reaction: Extrapyramidal side effects (3)?

A

-chlorpromazine -thioridazine -Haloperidol

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53
Q

Which drug(s) cause this reaction: Fanconi’s syndrome?

A

-Tetracycline

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54
Q

Which drug(s) cause this reaction: Focal to massive hepatic necrosis (4)?

A

-Halothane -Valproic acid -acetaminophen -Amantia phalloides

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55
Q

Which drug(s) cause this reaction: G6PD hemolysis(8)?

A

-Sulfonamides -INH -ASA -Ibuprofen -primaquine -nitrofurantoin /-pyrimethamine -Chloramphenicol

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56
Q

Which drug(s) cause this reaction: Gingival hyperplasia?

A

-phenytoin

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57
Q

Which drug(s) cause this reaction: Gray baby syndrome?

A

-Chloramphenicol

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58
Q

Which drug(s) cause this reaction: Gynecomastia (6)?

A

-Cimetidine -ketoconazole -spironolactone -digitalis -EtOH -estrogens

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59
Q

Which drug(s) cause this reaction: Hepatitis?

A

-Isoniazid

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60
Q

Which drug(s) cause this reaction: Hot flashes?

A

-Tamoxifen

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61
Q

Which drug(s) cause this reaction: Neuro and Nephrotoxic?

A

-polymyxins

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62
Q

Which drug(s) cause this reaction: Osteoporosis (2)?

A

-Corticosteroids -heparin

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63
Q

Which drug(s) cause this reaction: Oto and Nephrotoxicity (3)?

A

-aminoglycosides -loop diuretics -cisplatin

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64
Q

Which drug(s) cause this reaction: P450 induction(6)?

A

-Barbiturates -phenytoin -carbamazipine -rifampin -griseofulvin -Quinidine

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65
Q

Which drug(s) cause this reaction: P450 inhibition(6)?

A

-Cimetidine -ketoconazole -grapefruit juice -erythromycin -INH -Sulfonamides

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66
Q

Which drug(s) cause this reaction: Photosensitivity(3)?

A

-Tetracycline -amiodarone -Sulfonamides

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67
Q

Which drug(s) cause this reaction: Pseudomembranous colitis?

A

-Clindamycin

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68
Q

Which drug(s) cause this reaction: Pulmonary fibrosis(3)?

A

-Bleomycin -amiodarone -busulfan

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69
Q

Which drug(s) cause this reaction: SLE-like syndrome?

A

-Hydralazine -Procainamide -INH -phenytoin

70
Q

Which drug(s) cause this reaction: Stevens-Johnson syn. (3)?

A

-Ethosuxamide -Sulfonamides -lamotrigine

71
Q

Which drug(s) cause this reaction: Tardive dyskinesia?

A

-Antipsychotics

72
Q

Which drug(s) cause this reaction: Tendonitis and rupture?

A

-Fluoroquinolones

73
Q

Which drug(s) cause this reaction: Thrombotic complications?

A

-Oral Contraceptives

74
Q

Which drug(s) cause this reaction: Torsade de pointes (2)?

A

-Class III antiarrhythmics (sotalol) -Class IA (Quinidine)

75
Q

Which drug(s) cause this reaction: Tubulointerstitial Nephritis (5)?

A

-Sulfonamides -furosemide -methicillin -rifampin -NSAIDS (ex. ASA)

76
Q

Describe first-order kinetics?

A

Constant FRACTION eliminated per unit time.(exponential)

77
Q

Describe Phase I metabolism in liver(3)?

A

-reduction — oxy — & hydrolysis -H2O sol. Polar product -P450

78
Q

Describe Phase II metabolism in liver(3)?

A

-acetylation — glucuron. — & sulfation -Conjugation -Polar product

79
Q

Explain differences between full and partial agonists(2).

A
  • Act on same receptor - Full has greater efficacy
80
Q

Explain potency in relation to full and partial agonists(2).

A
  • partial agonist can have increased — decreased — /A21or equal potency as full agonist. - Potency is an independent factor.
81
Q

How do spare receptors effect the Km?

A
  • ED 50 is less than the Km (less than 50% of receptors)
82
Q

How do you calculate maintenance dose?

A

Md= (CpxCL)/F Cp= plas. Conc. CL=clear. F=bioaval.

83
Q

How does a competitive antagonist effect an agonist?

A

-Shifts the curve to the right -increases Km

84
Q

How does a noncompetitive antagonist effect an agonist?

A
  • Shifts the curve down -reduces Vmax
85
Q

Name the steps in drug approval(4)?

A

-phase I (clinical tests) -phase II -phase III -PhaseIV (surveillance)

86
Q

Steady state concentration is reached in __ number of half-lifes

A

In 4 half-lifes= (94%) T1/2 = (0.7x Vd)/CL

87
Q

What is the definition of zero-order kinetics? Example?

A

-Constant AMOUNT eliminated per unit time. -EtOH & ASA

88
Q

What is the formula for Clearance (CL)

A

CL= (rate of elimination of drug/ Plasma drug conc.)

89
Q

What is the formula for Volume of distribution (Vd)

A

Vd= (Amt. of drug in body/ Plasma drug conc.)

90
Q

What is the loading dose formula?

A

Ld= (CpxVd)/F Cp=plasma conc. F= Bioaval.

91
Q

A 12yo patient was treated for a reaction to a bee sting — what drug provides the best coverage of sympathomimetic receptors?

A

Epinephirine(Alpha1 —2 and Beta 1 —2)

92
Q

A 57 yo heart failure pt develops cardiac decompensation — what drug will give you adequate perfusion of his kidneys as well as tx for his Hypotension

A

Dopamine

93
Q

A fellow passenger on a Carnival cruise ship looks pale and diaphoretic — what antimuscarinic agent would you give them?

A

scopolamine

94
Q

A group of pts are rushed into the ER complaining of excessive sweating — tearing — salivation — HA — N and V — muscle twitching — difficulty breathing and diarrhea. What drug would be the most effective immediate tx

A

Atropine pts are suffering from Cholinestrase inhibitor poisining (Nerve gas/Organophosphate poisining)

95
Q

As an Anes you want to use a depolarizing neuromuscular blocking drug on your pt — what do you use

A

Succinylcholine

96
Q

MOA of Succinylcholine

A

Prevents the release of Ca from SR of skeletal muscle

97
Q

Clonidine is the preferred sym pathomimetic tx of HTN in pts with renal disease — why??

A

Centrally acting alpha agonist — thus causing a decrease in central adrenergic outflow — spairing renal blood flow

98
Q

Cocaine casues vasoconstriction and local anesthesia by what mechanism

A

Indirect agonist — uptake inhibitor

99
Q

Cocaine shares is mechanism of action with what antidepressant

A

TCA

100
Q

Dobutamine used for the tx of shock acts on which receptors

A

Beta1 more than B2

101
Q

Guanethidine enhances the release of Norepi?

A

No — it inhibits the release of Nor Epi

102
Q

How does angiotensin II affect NE release?

A

It acts presynaptically to increase NE release.

103
Q

How does botulinum toxin result in respiratory arrest?

A

Prevents the release of ACh — which results in muscle paralysis.

104
Q

How does dantrolene work?

A

Prevents the release of calcium from the sarcoplasmic reticulum of skeletal muscle.

105
Q

How does NE modulate its own release? What other neurotransmitter has this same effect?

A

NE acts presynaptically on alpha-2 receptors to inhibit its own release. ACh also acts presynaptically through M1 receptors to inhibit NE release.

106
Q

How would hemicholinium treatment affect cholinergic neurons?

A

Hemicholinium inhibits the transport of choline into the nerve — thus inhibiting formation of ACh.

107
Q

How would you reverse the effect of a neuromuscular blocking agent?

A

Give an antichloinesterase - neostigmine — edrophonium — etc

108
Q

If a patient is given hexamethonium — what would happen to his/her heart rate?

A

It would increase to ~ 100 beats/min. Both sympathetic and vagal stimulation would be knocked out — but the SA node has an intrinsic pace of 100 beats/min — which is normally checked by vagal stimulation.

109
Q

Isopoterenol was given to a patient with a developing AV block — why?

A

Stimulates beta adrenergic receptors

110
Q

Norepi feedbacks and inhibits the presynaptic receptor by what mechanism

A

Binding to the presynaptic alpha 2 release modulating receptors

111
Q

Reserpine will block the syntheis of this drug and but not its precursor.

A

Blocks Norepi — but not Dopamine

112
Q

These drugs acts indirectly by releasing strored catecholamines in the presynaptic terminal

A

Amphetamine and Ephedrine

113
Q

What anticholinesterase crosses the blood-brain-barrier?

A

physostigmine

114
Q

What antimuscarinic agent is used in asthma and COPD?

A

Ipratropium

115
Q

What antimuscarinic drug is useful for the tx of asthma

A

Ipratropium

116
Q

What are the classic symptoms of cholinesterase inhibitor poisoning (parathion or other organophosphates)?

A

Diarrhea — Urination — Miosis — Bronchospasm — Bradycardia — Excitation of skeletal muscle and CNS — Lacrimation — Sweating — and Salivation = DUMBBELS; also abdominal cramping

117
Q

What are the clinical indications for bethanechol?

A

Activates cholinergic receptors on bladder and bowel smooth muscle — alleviating post-op and neurogenic ileus and urinary retention.

118
Q

What are the clinical indications for neostigmine?

A

Post-op and neurogenic ileus and urinary retention — myasthenia gravis — and reversal of neuromuscular junction blockade (post-op) through anticholinesterase activity.

119
Q

What are the indications for using amphetamine?

A

narcolepsy — obesity — and attention deficit disorder (I wouldn’t recommend this)

120
Q

What are the nondepolarizing neuromuscular blocking drugs?

A

Tubocurarine — atracurium — mivacurium — pancuronium — vecuronium — rapacuronium

121
Q

What are the phases of succinylcholine neuromuscular blockade?

A

Phase 1 = prolonged depolarization — no antidote — effect potentiated by anticholinesterase; Phase 2 = repolarized but blocked — an anticholinesterase is the antidote for this phase.

122
Q

What are two indirect acting adrenergic agonists?

A

amphetamine and ephedrine

123
Q

What beta 2 agonist will help your 21yo Astma pt?

A

Albuterol — tertbutaline

124
Q

What cholinergic inhibitor acts by directly inhibiting Ach release at the presynaptic terminal

A

Botulinum

125
Q

What cholinomimetic is useful in the diagnosis of Myasthenia Gravis

A

Edrophonium

126
Q

What cholinomimetics might your pt be taking for his glaucoma

A

Carbachol — pilocarpine — physostigmine — echothiophate

127
Q

What class of drug is echothiophate? What is its indication?

A

anticholinesterase glaucoma

128
Q

What conditions would you use dantrolene?

A

In treatment of malignant hyperthermia — due to concomitant use of halothane and succinylcholine. Also in neuroleptic malignant syndrome — a toxicity of antipsychotic drugs.

129
Q

What drug is used to diagnose myasthenia gravis?

A

edrophonium (extremely short acting anticholinesterase)

130
Q

What drugs target anticholinesterase

A

Neostigmine — pyridostigmine edrophonium — physostigmine echothiophate

131
Q

What effect would atropine have on a patient with peptic ulcer disease?

A

Theoretically it could be used to block the cephalic phase of acid secretion (vagal stimulation).

132
Q

What effect would atropine have on the preganglionic sympathetic activation of sweat glands? Would this person sweat?

A

None. No — because atropine would block the postganglionic muscarinic receptors involved in sweat gland stimulation.

133
Q

What enzyme is responsible for the breakdown of ACh in the synaptic cleft?

A

Acetylcholinesterase; ACh is broken down into choline and acetate.

134
Q

What enzyme is responsible for the degredation of Ach

A

Acetylcholine esterase

135
Q

What enzyme is responsible for the production of Ach from Acetyl CoA and Choline

A

Choline acetyltransferase

136
Q

What is the clinical utility of clonidine?

A

Treatment of hypertension — especially with renal disease (lowers bp centrally — so flow is maintained to kidney).

137
Q

What is the clinical utility of cocaine?

A

The only local anesthetic with vasoconstrictive properties.

138
Q

What is the difference between the affinity for beta receptors between albuterol/terbutaline and dantroline?

A

Dobutamine has more of an affintiy for beta-1 than beta-2 — and is used for treating heart failure and shock. Albuterol and terbutaline is the reverse — and is used in treatment of acute asthma.

139
Q

What is the difference in receptor affinity of epinephrine at low doses? High doses?

A

Prefers beta’s at low doses — but at higher doses alpha agonist effects are predominantly seen.

140
Q

What is the effect of epinephrine infusion on bp and pulse pressure?

A

Increased systolic and pulse pressure — decreased diastolic pressure — and little change in mean pressure.

141
Q

What is the effect of guanethidine on adrenergic NE release?

A

It inhibits release of NE.

142
Q

What is the effect of norepinephrine on bp and pulse pressure?

A

Increases mean — systolic — and diastolic bp — while there is little change in pulse pressure.

143
Q

What is the effect of TCA’s on the adrenergic nerve?

A

They inhibit reuptake of NE at the nerve terminal (as does cocaine).

144
Q

What is the only depolarizing neuromuscular blocking agent?

A

Succinylcholine

145
Q

What is the receptor affinity and clinical use of isoproterenol?

A

It affects beta receptors equally and is used in AV heart block (rare).

146
Q

What physiological effects was the Anes using Atropine to tx

A

SLUD (salivation — Lacrimation — urination — Defecation)as well as airway secretion — GI motility — acid secretions

147
Q

What reversal agent could a Anes give to reverse the effects of Atropine

A

Bethanechol — Neostigmine — physostigmine

148
Q

What side effect of using atropine to induce pupillary dilation would you expect?

A

Atropine would also block the receptors in the ciliary muscle — causing an impairment in accommodation (cycloplegia).

149
Q

What sympathomimetic would you not prescribe for hypotension in a pt with renal artery sclerosis.

A

Norepinephrine (Alpha1 —2 and beta 1)

150
Q

What type of neurological blockade would hexamethonium create?

A

Hexamethonium is a nicotinic antagonist — and thus is a ganglionic blocker.

151
Q

What would be the effect on blood pressure with infusion of the alpha -2 agonist clonidine?

A

Initially vasoconstriction would increase bp — but then it acts on central alpha-2 receptors to decrease adrenergic outflow resulting in decreased bp.

152
Q

Which antimuscarinic agents are used in producing mydriasis and cycloplegia?

A

atropine — homatropine — tropicamide

153
Q

Which drug increases Sys BP w/o affecting Pulse Pressure

A

Epinephrine

154
Q

Which of epi — norepi — or isoproterenol results in bradycardia?

A

Norepinephrine

155
Q

Which of the following would atropine administration cause? Hypothermia — bradycardia — excess salivation — dry flushed skin — or diarrhea

A

Dry flushed skin — due to inhibition of sympathetic post-ganglionic blockade on muscarinic receptors of sweat glands. All others are opposite of what would be expected.

156
Q

Which of these three drugs will cause a reflex bradycardia in your pt (Norepi — Epi — or Isoporterenol)

A

Norepinephrine

157
Q

Which receptors does phenylephrine act upon?

A

alpha-1 > alpha-2; used as a pupil dilator — vasoconstrictor — and for nasal decongestion

158
Q

While at a tail gait party — you bite into a sandwich that a yellow jacket is also enjoying. Knowing your allergy to this creature — what should you do?

A

Epinephrine to treat anaphylaxis. Also useful if you have open angle glaucoma — asthma — or hypotension.

159
Q

Why are albuterol and terbutaline effective in tx of acute asthmatic attacks?

A

These B-2 agonists cause respiratory smooth muscle to relax.

160
Q

Why does atropine dilate the pupil?

A

Blocking muscarinic receptors in the circular fibers of the eye — results in unopposed action of radial muscles to dilate.

161
Q

Why does NE result in bradycardia?

A

NE increases bp — which stimulates baroreceptors in the carotid sinus and the aorta. The CNS signals through vagal stimulation to decrease heart rate.

162
Q

Why is carbachol and pilocarpine useful in treatment of glaucoma?

A

They activate the ciliary muscle of the eye (open angle) and pupillary sphincter (narrow angle).

163
Q

Why is pyridostigmine effective in the treatment of myasthenia gravis?

A

As an anticholinesterase it increases endogenous ACh and thus increases strength.

164
Q

Why is reserpine effective in treating HTN?

A

Reserpine inhibits dopamine transport into vesicles — attenuating its conversion to NE by dopamine beta-hydroxylase.

165
Q

Why is there a drop in systolic — mean — and diastolic bp with infusion of isoproterenol?

A

Stimulating beta receptors stimulates heart rate — but beta receptor induced vasodilation reduces peripheral resistance.

166
Q

Why would a patient with cog-wheel rigidity and a shuffling gait be given benztropine?

A

Parkinson patients benefit from antimuscarinic agents through its inhibitory action within the indirect pathway.

167
Q

Why would dopamine be useful in treating shock?

A

Receptors = D1=D2>beta>alpha — thus increasing heart rate (beta) and blood pressure (alpha vasoconstriction) while maintaining kidney perfusion (dopamine receptors)

168
Q

Why would you give a drug like pancuronium or succinylcholine?

A

Useful in muscle paralysis during surgery or mechanical ventilation.

169
Q

Why would you use pralidoxime after exposure to an organophosphate?

A

Pralidoxime regenerates active cholinesterase.

170
Q

Will Hemicholinum affect the release of stored Ach during Cholinergic Stimulation

A

No — hemicholinum block the uptake of Choline and thus Ach synthesis

171
Q

Would blockade of muscarininc receptors in the bladder be useful in treating urinary retention?

A

No. Atropine is used to reduce urgency in mild cystitis. So it would aggravate the urinary retention.

172
Q

Your patient wants an effective drug to treat his motion sickness — what would you prescribe

A

Scopolamine