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Step 1 Drugs > General Pharm > Flashcards

General Pharm Flashcards

1
Q

a2 receptor protein class and function

A

Gi

decrease sympathetic outflow
decrease insulin release
decrease lipolysis
Increase platelet aggregation

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2
Q

B1 receptor protein class and function

A

Gs

Increase heart rate
Increase contractility
Increase renin release
Increase lipolysis

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3
Q

B2 receptor protein class and function

A

Gs

Vasodilation
Bronchodilation
Increase HR
Increase contractility
Increase lipolysis
Increase insulin release
decrease uterine tone 
Ciliary muscle relaxation
Increase aqueous humor production
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4
Q

M1 protein class and function

A

Gq

Located in CNS and enteric nervous system

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5
Q

M2 protein class and function

A

Gi

Decrease HR
Decrease contractility of atria

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6
Q

M3 protein class and function

A

Gq

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

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7
Q

D1 receptor protein class and function

A

Gs

Relaxes renal vascular smooth muscle

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8
Q

D2 protein class and function

A

Gi

Modulates transmitter release, especially in brain

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9
Q

H1 receptor protein class and function

A

Gq

Increase nasal and bronchial mucus production
Increase vascular permeability
contraction of bronchioles
pruritus
pain
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10
Q

H2 receptor protein class and function

A

Gs

increases gastric acid secretion

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11
Q

V1 receptor protein class and function

A

Gq

Increase vascular smooth muscle contractiion

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12
Q

V2 receptor protein class and function

A

Gs

Increase water permeability and reabsorption in collecting tubules of the kidney

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13
Q

Bethanechol

A

MOA: cholinomimetic
Activates bowel and bladder smooth muscle

Resistant to AChE

Clinical: postoperative ileus, neurogenic ileus, and urinary retention
Normal post void residual volume

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14
Q

Carbachol

A

MOA: Choinomimetic

Clinical: glaucoma, pupillary constriction, and relief of intraocular pressure

Watch for exacerbation of COPD, asthma, and peptic ulcers in susceptible patients

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15
Q

Pilocarpine

A

MOA: Cholinomimetic

Clinical: stimulatory of sweat, tears, and saliva
Contracts ciliary muscle of eye (open-angle glaucoma)
Pupillary sphincter (closed-angle glaucoma)

Resistant to AChE

Watch for exacerbation of COPD, asthma, and peptic ulcers in susceptible patients

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16
Q

Methacholine

A

MOA: cholinomimetic

Clinical: challenge test for asthma

Watch for exacerbation of COPD, asthma, and peptic ulcers in susceptible patients

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17
Q

Neostigmine

A

MOA: AChE inhibitor
increasing endogenous ACh

Clinical: postoperative and neurogenic ileus, urinary retention, myasthenia gravis, reversal of postoperative neuromuscular junction blockade

Due to quaternary amine structure will not cross CNS

Watch for exacerbation of COPD, asthma, and peptic ulcers in susceptible patients

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18
Q

Pyridostigmine

A

MOA: AChE inhibitor
Increases endogenous ACh
Increases strength

Clinical: Myasthenia gravis (long acting)

Does not penetrate CNS

Watch for exacerbation of COPD, asthma, and peptic ulcers in susceptible patients

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19
Q

Physostigmine

A

MOA: AChE inhibitor
Increases endogenous ACh

Clinical: Atropine or other anticholinergic toxicity
Crosses BBB

Watch for exacerbation of COPD, asthma, and peptic ulcers in susceptible patients

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20
Q

Donepezil, rivastigmine, galantamine

A

MOA: AChE inhibitor
Increases endogenous ACh

Clinical: Alzheimers

Watch for exacerbation of COPD, asthma, and peptic ulcers in susceptible patients

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21
Q

Endrophonium

A

MOA: AChE inhibitor
increases endogenous ACh

Clinical: Diagnosis of myasthenia gravis (short acting)

Quaternary amine structure does not allow CNS penetration

Watch for exacerbation of COPD, asthma, and peptic ulcers in susceptible patients

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22
Q

AChE inhibitor toxicity

A

Often due to organophosphates (parathion-insecticides)

SLUDGE: Salivation, Lacrimation, Urination, Defecation, GI distress (diarrhea), Eye Problems (miosis)

Also bronchospasm, bradycardia, Excitation of skeletal muscle, Sweating, confusion, low BP, flushing

Antidote: atropine

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23
Q

homatropine

A

MOA: Muscarinic Antagonists
Act on eye

Clinical: produce mydriasis and cyclopegia

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24
Q

Benztropine

A

MOA: muscarininc antagonist
Act on CNS

Clinical: Parkinsons
Anti-psychotic overdose treatment

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25
Q

Scopolamine

A

MOA: Muscarinic Antagonist
Act on CNS

Clinical: Motion Sickness
Over treatment of myasthenia gravis side effects (also hyoscyamine can be used)

26
Q

Ipratropium, tiotropium

A

MOA: muscarinic antagonists
Act on Respiratory system

Clinical: COPD, asthma

27
Q

Oxybutynin

A

MOA: muscarinic antagonists
Act on Genitourinary system

Clinical: reduce urgency in mild cystitis and reduce bladder spasms
Urge incontinence

Also can be used with tolterodine, fesoterodine, trospium

28
Q

darifenacin and solifenacin

A

MOA: muscarinic antagonists
Act on Genitourinary system

Clinical: reduce urgency in mild cystitis and reduce bladder spasms
Urge incontinence

29
Q

tolterodine and fesoterodine

A

MOA: muscarinic antagonists
Act on Genitourinary system

Clinical: reduce urgency in mild cystitis and reduce bladder spasms
Urge incontinence

30
Q

Trospium

A

MOA: muscarinic antagonists
Act on Genitourinary system

Clinical: reduce urgency in mild cystitis and reduce bladder spasms
Urge incontinence

31
Q

Glycopyrrolate

A

MOA: muscarininc antagonist
Acts on Gastrointestinal and respiratory system

Clinical: Given parenteral for peroperative use to reduce airway secretions
Given orally for drooling, peptic ulcer

32
Q

Tropicamide

A

MOA: muscarinic antagonist
Acts on Eye

Clinical: produce mydriasis and cycloplegia

33
Q

Atropine

A 
MOA: muscarinic antagonist
eye: pupil dilation, cycloplegia
Airway: decrease secretion
Stomach: decrease acid secretion
Gut: decrease motility
Bladder: decrease urgency in cystitis

Clinical: bradycardia, produce mydriasis and cycloplegia, before bronchoscopy to decrease respiratory mucous secretions and promote bronchodilation

Organophosphate poisoning (no effect on muscle paralysis due to nicotinic receptors-use pralidoxime early on) 
Pralidoxime restores cholinesterase from its receptors

Toxicity: increase in body temperature (decreased sweating), rapid pulse, dry mouth, dry-flushed skin, cyclopegia, constipation, disorientation,

Can cause acute angle closure glaucoma in elderly due to mydriasis
Urinary retention in men with BPH
Hyperthermia in infants

1/2 life increases in elderly enhancing the chance of toxicity
Treat toxicity with physostigmine which inhibits AChE bot peripherally and centrally due to its tertiary amine properties

34
Q

Epinephrine

A

Acts on B>a

B1=Increase HR
B1 and a1=systolic BP
B2>a1 at low dose leading to decreased diastolic pressure (vasodilation)
a1>B2 at high dose leading to increased diastolic pressure

Clinical: anaphylaxis, open angle glaucoma, asthma, hypotension,

a effects predominate at high doses

35
Q

Norepinephrine

A

a1>a2>B1

Clinical: hypotension but decreased renal perfusiion

NE extravasation (induration and pallor)
a1 vasoconstriction can lead to tissue necrosis
Prevent necrosis by sodium solution of phentolamine mesylate (a1 blocker)
36
Q

Isoproterenol

A

B1=B2

Increase contractility via B1
Decreased vascular resistance via B2

Clinical: electrophysiologic evaluations of tachyarrhythmias

Can worsen ischemia

37
Q

Dopamine

A

D1=D2>B>a

Clinical: unstable bradycardia, heart failure, shock,
inotropic and chronotropic a effects predominate at high doses

Low doses: stimulates D1 receptors in renal vasculature and tubules leading to increased GFR, RBF, and Na excretion and mesenteric vasodilation

Moderate doses: Stimulates B1 receptors of heart leading to increased contractility, increased pulse pressure, and increase of systolic BP

High doses: stimulates a1 receptors leading to vasoconstriction which causes decreased CO (used for hypotension while maintaining kidney perfusion)

38
Q

Phenylephrine

A

a1>a2

Clinical: hypotension (vasoconstrictor), ocular procedures (mydriatic), rhinitis (decongestion)

39
Q

Albuterol

A

B2>B1

Clinical: acute asthma

40
Q

Salmeterol

A

B2>B1

Clinical: long acting asthma or COPD control

41
Q

Terbutaline

A

B2>B1

Clinical: reduce premature uterine contractions

42
Q

Amphetamine

A

MOA: Indirect sympathomimetic
Reuptake inhibitor and releases stored catecholamines

Clinical: narcolepsy, obesity, attention deficit disorder

43
Q

Ephedrine

A

MOA: indirect sympathomimetic
releases stored catecholamines

Clinical: nasal decongestion, urinary incontinence, hypotension

44
Q

Cocaine

A

MOA: indirect sympathomimetic
Reuptake inhibtor

Clinical: causes vasoconstriction and local anesthesia
Never give B blockers if cocaine Intoxication is suspected

45
Q

Dobutamine

A

B1 effects (increase cAMP)

Passive inotropic effect increasing contractility and CO decreased ventricular filling pressures

Weakly positive chonotropic effect leading to Increased HR and increased myocardial oxygen consumption

increased conduction velocity leading to arrhythmias

46
Q

Clonidine

A

MOA: a2 agonist

Clinical: hypertensive urgency (doesn’t decrease renal flow)
ADHD, severe pain
Off label-ethanal and opioid withdrawal

Toxicity: CNS depression, bradycardia, hypotension, respiratory depression and small pupil size

47
Q

a-methyldopa

A

MOA: a2 agonist

Clinical: hypertension in pregnancy

toxicity: direct Coombs + hemolytic anemia, SLE-like syndrome

48
Q

Phenoxybenzamine

A

MOA: irreversible a-blocker

Clinical: pheochromocytoma preoperatively to prevent catecholamine crisis

Toxicity: orthostatic hypotension, reflex tachycardia

49
Q

Prazosin, terazosin, doxazosin, tamsulosin

A

MOA: a1 selective blockers
Relaxation of smooth muscle in arterial and venous walls decreasing TPR

Clinical: urinary symptoms of BPH, PTSD (prazosin)
Hypertension (not tamsulosin)

Toxicity: 1st dose othostatic hypotension, dizziness, headache, vertigo

50
Q

Mirtazapine

A

MOA: a2 selective blocker

Clinical: depression

Toxicity: sedation, increased serum cholesterol, increased appetite

51
Q

-olols and carvedilol, labetalol

A

MOA: Beta Blockers

Clinical:
Angina pectoris: decreased HR, contractility leading to less O2 consumption
MI: metoprolol, carvedilol and bisoprolol lead to decreased mortality
SVT: metoprolol and esmolol lead to decreased AV conduction velocity (class II antiarrythmics)
Hypertension: decreased CO, decreased renin secretion (due to B1 receptor blockade on JGA cells)
CHF: slow progression of chronic failure
Glaucoma: timolol decreased secretion of aqueous humor

Toxicity: impotence, bradycardia, AV block, CHF, Seziures, sedation, sleep alterations, dyslipidemia (metoprolol), asthmatics/COPD may exacerbate

Avoid in cocaine users
May block hypoglycemia symptoms in diabetes but no Contraindicated

Selectivity: B1=A through M
Nonselective: M through Z,
Nonselective a and B antagonists: carvedilol and labetaolol

Nebivolol can stimulate B3 receptors which activate NO synthase in vasculature

52
Q

CYP inducers

A 
Chronic Alcohol
Modafinil
St. John's Wort
Phenytoin
Phenoarbital
Nevirapine
Rifampin
Griseolfulvin
Carbamazepine
53
Q

CYP substrates

A 
Anti-epileptics
Antidepressants
Antipsychotics
Anesthetics
Theophylline
Warfarin
Statins
OCPs
54
Q

CYP inhibitors

A 
Acute alcohol abuse
Gemfibrozil
Ciprofloxacin
Isoniazid
Grapefruit Juice
Quinidine
Amiordarone
Ketoconazole (all azoles)
Macrolides
Sulfonamides
Cimetidine
Ritonavir
55
Q

a1 receptor protein class and function

A

Gq

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

56
Q

Hemicholinium

A

Blocks Choline uptake into axon

57
Q

Vesamicol

A

Block ACH intake into vesicles

58
Q

Metyrosine

A

Blocks tyrosine to DOPA

59
Q

Reserpine

A

Blocks Dopamine into vesicles

60
Q

Bretylium

A

NE release from axon

61
Q

Guanethidine

A

blocks NE release

Step 1 Drugs (15 decks)

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