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General Pharm Flashcards

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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
Scopolamine
MOA: Muscarinic Antagonist Act on CNS Clinical: Motion Sickness Over treatment of myasthenia gravis side effects (also hyoscyamine can be used)
26
Ipratropium, tiotropium
MOA: muscarinic antagonists Act on Respiratory system Clinical: COPD, asthma
27
Oxybutynin
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
darifenacin and solifenacin
MOA: muscarinic antagonists Act on Genitourinary system Clinical: reduce urgency in mild cystitis and reduce bladder spasms Urge incontinence
29
tolterodine and fesoterodine
MOA: muscarinic antagonists Act on Genitourinary system Clinical: reduce urgency in mild cystitis and reduce bladder spasms Urge incontinence
30
Trospium
MOA: muscarinic antagonists Act on Genitourinary system Clinical: reduce urgency in mild cystitis and reduce bladder spasms Urge incontinence
31
Glycopyrrolate
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
Tropicamide
MOA: muscarinic antagonist Acts on Eye Clinical: produce mydriasis and cycloplegia
33
Atropine
``` 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
Epinephrine
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
Norepinephrine
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
Isoproterenol
B1=B2 Increase contractility via B1 Decreased vascular resistance via B2 Clinical: electrophysiologic evaluations of tachyarrhythmias Can worsen ischemia
37
Dopamine
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
Phenylephrine
a1>a2 Clinical: hypotension (vasoconstrictor), ocular procedures (mydriatic), rhinitis (decongestion)
39
Albuterol
B2>B1 Clinical: acute asthma
40
Salmeterol
B2>B1 Clinical: long acting asthma or COPD control
41
Terbutaline
B2>B1 Clinical: reduce premature uterine contractions
42
Amphetamine
MOA: Indirect sympathomimetic Reuptake inhibitor and releases stored catecholamines Clinical: narcolepsy, obesity, attention deficit disorder
43
Ephedrine
MOA: indirect sympathomimetic releases stored catecholamines Clinical: nasal decongestion, urinary incontinence, hypotension
44
Cocaine
MOA: indirect sympathomimetic Reuptake inhibtor Clinical: causes vasoconstriction and local anesthesia Never give B blockers if cocaine Intoxication is suspected
45
Dobutamine
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
Clonidine
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
a-methyldopa
MOA: a2 agonist Clinical: hypertension in pregnancy toxicity: direct Coombs + hemolytic anemia, SLE-like syndrome
48
Phenoxybenzamine
MOA: irreversible a-blocker Clinical: pheochromocytoma preoperatively to prevent catecholamine crisis Toxicity: orthostatic hypotension, reflex tachycardia
49
Prazosin, terazosin, doxazosin, tamsulosin
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
Mirtazapine
MOA: a2 selective blocker Clinical: depression Toxicity: sedation, increased serum cholesterol, increased appetite
51
-olols and carvedilol, labetalol
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
CYP inducers
``` Chronic Alcohol Modafinil St. John's Wort Phenytoin Phenoarbital Nevirapine Rifampin Griseolfulvin Carbamazepine ```
53
CYP substrates
``` Anti-epileptics Antidepressants Antipsychotics Anesthetics Theophylline Warfarin Statins OCPs ```
54
CYP inhibitors
``` Acute alcohol abuse Gemfibrozil Ciprofloxacin Isoniazid Grapefruit Juice Quinidine Amiordarone Ketoconazole (all azoles) Macrolides Sulfonamides Cimetidine Ritonavir ```
55
a1 receptor protein class and function
Gq Increase vascular smooth muscle contraction Increase pupillary dilator muscle contraction (mydriasis) Increase intestinal and bladder sphincter muscle contraction
56
Hemicholinium
Blocks Choline uptake into axon
57
Vesamicol
Block ACH intake into vesicles
58
Metyrosine
Blocks tyrosine to DOPA
59
Reserpine
Blocks Dopamine into vesicles
60
Bretylium
NE release from axon
61
Guanethidine
blocks NE release

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