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USMLE Step 1 General > Pharmacology > Flashcards

Pharmacology Flashcards

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1
Q

What needs to be given with high dose MTX to reduce side effects (aphthous ulcers and pancytopenia)?

A

Leucovorin (Folinic acid) - does not use Dihydrofolate reductase to produce THF which can then be used to for DNA, purine synthesis.

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2
Q

How is INH metabolized?

A

Acetylation. There are fast vs. slow acetylators. Slow are more susceptible to adverse se: neuro and hepatotoxicity (INH Injures Neurons and Hepatocytes)

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3
Q

Most impt acute treatment for Diphtheria?

A

Antitoxin! (passive immunity)

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4
Q

Side effects of niacin and what mediates it?

A

Flushing, Warmth, Itching. Mediated by Prostaglandins (aspirin taken before niacin can decrease the side effects)

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5
Q

Major side effect of Vancomycin and what mediates it?

A

Red Man Syndrome - Histamine

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6
Q

How does capsaicin reduce pain?

A

Dec. Substance P (polypeptide pain transmitter) in the PNS

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7
Q

Urinary retention in someone with BPH - what drug for peripheral neuropathy was he given?

A

TCA - anticholinergic

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8
Q

What drugs will decrease progression of diabetic neuropathy?

A

ACEi ARB

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9
Q

Symptoms specific for opioid withdrawal

A 
Dilated pupils
Yawning 
Lacrimation 
Hyperactive 
Bowel sounds
Piloerection 
Usually normal VS.

Will not cause seizures, tachy like withdrawal from cocaine or benzos

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10
Q

What is mechanism of Rifampin?

A

DNA dependent RNA polymerase

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11
Q

Mechanism of Theophylline? Toxicity? Treatment?

A

Phosphodiesterase inhibitor - increases cAMP - bronchodilation.

Toxicity: narrow therapeutic index
cardio: arrhythmias, tachy –> beta-block
neuro: seizures —> benzos or barbs
GI: abd pain, n, v

Treatment: Gastric Lavage + Activated Charcoal + Cathartics (stim GI)

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12
Q

How is vancomycin resistance mediated?

A

D-ala D-lac instead of D-ala D-ala (which vanco binds to) in peptidoglycan cell wall. “Pay back 2 DAL LARs for VANdalizing my wall”

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13
Q

Canagliflozin - mechanism of action and what to monitor?

A

SGLT (sodium and glucose cotransporter 2) inhibitor - decreases PT reabsorption of glucose -> more glucose lost in urineMonitor BUN/Cr. Avoid in pts with mod-severe renal impairment.

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14
Q

How does Terbinafine work?

A

Inhibits synthesis of ergosterol by inhibiting squalene epoxide

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15
Q

Entacapone and Tolcapone are what? What do we give this in combination with and why?

A

COMT inhibitors. Given in combo with Levodopa to increase the amount that reaches the brain. Levodopa can cross BBB. Dopamine can’t. But, it gets peripherally metabolized. So, we give it with
1. Carbidopa - inhibits Dopa decarboxylase
2. Entacapone - COMT inhibitor.
Tolacapone has hepatotoxicity.

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16
Q

Flutamine mechanism? used for?

A

Competitive inhibitor at testos-R Prostate carcinoma

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17
Q

What would you give pt with inferior wall MI and bradycardia (due to blockage of RCA that supplies SA and AV nodes)? What is potential side effect in the eye?

A

Atropine = muscarinic antagonist -> increase HR! Side Effect: Acute Angle Glaucoma due to mydriasis. Severe, unilateral eye pain + halos.

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18
Q

Warfarin vs. Heparin? INR, PT, PTT?

A

Warfarin = PT, INR Heparin = PTT

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19
Q

Cholestyramine does what to cholesterol synthesis? What do you need to give it in combo with then?

A

Increases cholesterol synthesis (Bile acid binding resins decrease enterohepatic bile acid circulation -> more bile acids produced -> more cholesterol) Give it in combo with statin! Block HMG CoA reductase so decrease cholesterol synthesis.

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20
Q

How are drugs that cause drug-induced SLE metabolized?

A

Phase II acetylation by liver. Slow acetylators are at greater risk .

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21
Q

What are the four cardinal symptoms of NMS? How would you distinguish NMS from Serotonin Syndrome?

A
  1. hyperthermia
  2. autonomic instability
  3. altered mental status
  4. muscle rigidity

Serotonin syndrome has more myoclonus instead of muscle rigidity.

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22
Q

What is toxicity of nitroprusside (given for HTN crisis)? Antidote?

A

Cyanide toxicity
Sulfur: Na thiosulfate

Nitroprusside -> NO and cyanide. Cyanide normally metabolized to thiocyanate which can be excreted by addition of sulfar group. Na thiosulfate will provide more substrate to add.

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23
Q

What are ways to give drugs that bypass first pass metabolism by liver?

A

IV, SubQ, Sublingual, Rectal

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24
Q

What does Fenoldopam do?

A

Selective dopamine-1 receptor agonist.

Arteriolar Vasodilation Improves Renal blood flow (dopamine receptors) - increased sodium and water excretion.

Only antihypertensive that does this, (other agents cause reflex sympathetic activation in the kidney) so good for ppl with HTN and renal insufficiency.

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25
Q

Side effects of Lisinopril.

A

decreased GFR and increase Cr (less constriction of efferent arteriole by angiotensin II)

hyperkalemia
cough
angioedema

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26
Q

HCTZ should be chosen in pts with ________________.

A

Osteoporosis.

HCTZ increases absorption of Ca within the distal tubules of nephron.

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27
Q

Oseltamivir mechanism of action?

A

Neuraminidase Inhibitor - inhibits viral particle release.

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28
Q

Side effect of Nitrates (NO and Isosorbide Dinitrate)

A

Headache! Cutaneous Flushing!

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29
Q

Clinical Disinfectants: Mech EtOHChlorhexidine H2O2 Iodine

A

EtOH: disrupt cell membrane, denature protein

Chlorhexidine: cell mem, coagulation of cytoplasm

H2O2: Creates destructive free radicals; YES SPORES

Iodine: Halogenation of proteins, nucleic acids; YES SPORES

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30
Q

Acute Drug Intox Q1288

A

PCP - Nystagmus
LSD - Visual hallucinations
Cocaine - CP, seizure
THC - increased appetite, impaired time perception, conjunctival injectionHeroin - miosis, resp depression

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31
Q

Why is methadone good for heroin addiction?

A

Long half life. Prolonged effects to suppress withdrawal symptoms.

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32
Q

What is a potential toxicity of mannitol?

A

pulmonary edema

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33
Q

What can increase peripheral metabolism of levodopa?

A

B6!

34
Q

Side effects of Cimetidine

A

H2-R Antagonist
Gynecomastia
Inhibits P450
Increase levels of warfarin, phenytoin, propanolol, metaprolol, quinidine, theophylline.

35
Q

How to reverse beta-blocker toxicity?

A

Glucagon (increases cAMP)

36
Q

Statins need monitoring of what?

A

LFTs Tox: Myopathy and liver toxicity.

37
Q

What meds cause fat redistribution from extremities to trunk?

A

Glucocorticoids

HIV-1 protease inhibitors (impair hepatocyte chylomicron uptake and TAG clearance)

38
Q

Side effects of thiazide diuretics

A
  1. hypoK
  2. met alkalosis
  3. hypoNa
  4. hyperuricemia - precipitate gout attack
  5. hyperlipidemia - inc. choles and LDL
  6. hyperglycemia - dec. insulin secretion and glu uptake
39
Q

What tissues are beta1-R on?

A

cardiomyocyte - heart rate, contractility JGA - renin release NOT on vascular smooth muscle.

40
Q

What characteristic would increase liver excretion of a drug rather than kidney?

A

Lipophilic (high volume of distribution) - more easily able to penetrate into hepatocytes. And when filtered by kidney, will get reabsorbed out more easily. Normally, kidney primary site of drug elimination and liver primary site of modification, but liver also excretes things thru bile and feces.

41
Q

What epileptic drug causes agranulocytosis? What is mechanism of action?

A

Carbamazepine - increases Na channel inactivation

Other toxicities: hepatotoxic, SIADH, SJS, induction of cytochrome p450.

42
Q

Administration of what drug in combo with epinephrine would cause diastolic BP to increase while not affecting HR?

A

Propranolol (nonselective B1 and B2)
diastolic BP: increase bc alpha 1 unopposed (b2 blocked)
HR: stable bc B1 blocked

43
Q

Acetazolamide acts on which part of the nephron?

A

Proximal tubule - blocks carbonic anhydrase - decrease NaHCO3 resorption and water resorption. results in urinary bicarb wasting and alkaline urine.

44
Q

How do beta-blockers help treat hyperthyroidism?

A
  1. inhibit peripheral conversion2. block symp effects
45
Q

Side effect of: ThioridazineChlorpromazineHaloperidol ZiprasidoneOlanzapine Clozapine

A

Thioridazine - retinal deposits that resemble retinitis pigmentosa

Chlorpromazine - corneal depositsHaloperidol - extrapyramidal symptoms

Ziprasidone - prolonged QT

Olanzapine - weight gainClozapine - agranulocytosis, seizures

46
Q

*How warfarin related to cytochrome p450? How do levels change gradually or abruptly?

A

Warfarin metabolized by cytochrome p450. p450 inducers - decrease activity p450 inhibitors - increase activity Levels change gradually.

47
Q

p450 Inducers*

A 
"Coronas, Guinness, PBRS induce Chronic Alcoholism" Carbamazepine
Griseofulvin
Phenytoin
Barb 
Rifampin 
St. John's Wart
Chronic Alcoholism
48
Q

p450 inhibitors*

A 
"CRACK AMIGOS" 
Cimetidine 
Ritonavir
 Amiodarone
Ciprofloxacin 
Ketoconazole
Acute alcohol
Macrolides INH Grapefruit juice, Gemfibrozil Omeprazole Sulfa
49
Q

p450 substrates

A 
"Always, Always, Always, Always Think When Starting Others" 
Anti-depressants
Antiepileptics
Antipsychotics
Anesthestics
Theophylline
Warfarin
Statin
OCP
50
Q

How does morphine work?

A

mu opioid receptor -> G protein coupled activation of K channels -> K influx -> hyperpolarization

51
Q

What drugs when administered with phenytoin would decrease it’s levels?

A

p450 inducers: Coronas, Guinness, PBRS induce Chronic Alcoholism. CarbamazepineGriseofulvinPhenytoinBarbsRifampinSt Johns Wart Chronic alcohol.

52
Q

What alpha blocker is reversible vs. irreversible?***

A

Phenoxybenzamine - irreversible, half life longer. Phentolamine - reversible.

53
Q

What cumulative dose dependent adverse effect associated with Doxorubicin?

A

Dilated Cardiomyopathy

54
Q

Majority of overdose deaths are caused by?

A

Prescription drugs - opioid analgesics!

55
Q

What adverse effect do selective arteriolar vasodilators (hydralazine, minoxidil) have?

A

Reflex sympathetic activity -> tachycardia, sodium and water retention and edema Often given with sympatholytics or diuretics.

56
Q

Angioedema assoc. with ACEi is due to what?

A

Kinin accumulation.

57
Q

Pro-carcinogens are converted into active metabolites by?

A

Cytochrome p450 oxidase system (microsomal monooxygenase)

58
Q

Dopamine effects at low dose vs. high dose.

A

Low = Dopa = renal vasodilation

High = B1 = inc. HR, cont = inc. CO

Higher = A1 = vasoconstriction = more afterload, so CO goes down

59
Q

Depolarizing vs. Non-depolarizing NMJ blocking agents

A

Depolarinzing = succinylcholine = Ach-R agonist

phase 1 = sustained depol - no antidote

phase 2 = repolarized, but blocked (looks like non-depol on train of four response) - neostigmine reverses

Nondepolarizing = “curarine, curium” = competitive antagonist - reversed with neostigmine

60
Q

Two conditions associated with SVC syndrome. Which one more common, what other sx?

A

Mediastinal mass > Pancoast tumor

Pancoast tumor more commonly presents with - shoulder pain due to brachial plexus compression - Horner’s syndrome (PAM) due to symp cervical ganglia compression

61
Q

DRESS syndrome

A

“Drug rxn with eosinophilia and systemic sx” adverse rxn 2-8 wks after exposure to anticonvulsant, allopurinol, sulfonamides, or certain antibiotics

fever, generalized LAD, facial edema
morbiliform rash that colaesce
eosinophilia
liver (hepatitis, jaundice)
kidney (acute interstitial nephritis) 
lung (cough, dypsnea) Sx improve weeks after withdrawal of drug.
62
Q

What form of nitrate when given orally is nearly 100% bioavailable?

A

Isosorbide Mononitrate

63
Q

First Order vs. Zero Order kinetics.

A

First Order: Constant FRACTION metabolized

Zero Order: Constant AMOUNT metabolized.

64
Q

Ending associated with First gen vs. Second gen Antihistamines?

A

First gen: -amine or -ateSecond gen: -adine + cetirizine

65
Q

Pharmacokinetic Equations

A

Vd = Drug in the body/Plasma
Concentration CL = 0.7 x Vd / t1/2
LD = Css x Vd
MD = Cxx x CL

66
Q

Isoproterenol does what to cardiac contractility and vascular resistance?

A 
B1 = inc. cardiac contractility 
B2 = dec. vascular resistance
67
Q

Pralidoxime vs. Atropine

A

Atropine = Muscarinic antagonist.Pralidoximine = antidote to organophosphate poisoning - reactivates cholinesterases by dephosphorylating them

68
Q

What are the Gq, Gs, and Gi receptors?

A

Gq = HAV M&M = H1, A1, V1, M1, M3 - Phospholipase C: PIP2 -> DAG (Protein Kinase C) and IP3 (Ca++)

Gi = MAD2s = M2 A2 D2 - Inhibit Adenylyl cyclase -> dec. cAMP -> Protein Kinase A (inhibits myosin light chain kinase in smooth muscle, inc. Ca++ in the heart)

Gs = everything else = B1, B2, D1, V2, H2

69
Q

PIlocarpine

A

Direct Ach agonist. Potent stimulator of sweat, tears, and saliva. Contracts ciliary muscle of eye and pupillary sphincter.

70
Q

Autonomic effects on insulin secretion? Overall what is sympathetic vs. parasympathetic effect?

A 
Increased Insulin Secretion: 
M3 (Gq)*
Beta2 (Gs)* 
Glucagon (Gs, Gq) 
GLP1 (Gs)

Decreased Insulin Secretion:
A2 (Gi)*
Somatostatin 2 (Gi)

Overall, PNS Stimulates; Symp Inhibits (A2 predominates)

71
Q

Administering what with Epinephrine would increase insulin secretion?

A

Alpha blocker

72
Q

Minimal Alveolar Concentration

A

Concentration of the anesthetic in the alveoli at which 50% of patients are unresponsive to painful stimuli. Inversely proportional to the potency of the anesthetic

73
Q

What agonist/antagonists would cause pupillary dilation and uterine muscle relaxation?

A

Alpha1 agonist = pupillary dilation

b2 agonist = uterine Muscle Relaxation

74
Q

Nasal decongestants used for over a few days, they stop working and return of symptoms/rhinorrhea. Why? How to tx? What other drug is associated with this phenomenon?

A

Tachyphylaxis. Use of exogenous alpha1 agonists -> negative feedback -> less NE -> relative vasodilation. Return of nasal congestive symptoms.

Stop use of meds for normal feedback pathways to normalize.

Other drug: Nitrates. Need drug free intervals of 8-10 hours.

75
Q

Dantrolene

A

Blocks ryanodine-R and prevents release of Ca into cytoplasm of skeletal muscle fibers. Used for malignant hyperthermia.

76
Q

Warfarin vs. Heparin - why can only 1 of them cross placenta?

A

Heparin - water soluble
Warfarin - lipophilic - can cross the placenta
Other ex: Conjugated bilirubin - charged - cannot cross placenta.

77
Q

Clonidine

A

Alpha-2 agonist. Decreases BP by decreasing CNS outflow.

78
Q

Patient on furosemide, simvastatin, metoprolol, aspirin, hydralazine, and isosorbide dinitrate. Sx: weakness, LE cramping, “almost fall” over the last weekWhat is this due to?

A

HypoK from furosemide.

Sx: muscle weakness, cramps, myalgias, fatigue

Note: NOT rhabdomyolysis from statins. This would be more acute in presentation, with muscle pain, generalized weakness, myoglobinuria and dark urine.

79
Q

Flumazenil inhibits _______, but does not inhibit ______.

A

Inhibits benzodiazepine - competitive inhibitor

Does NOT inhibit barbiturates.

80
Q

Pt is on clopidogrel. Treating him with omeprazole, a CYPC19 inhibitor, results in increased risk of recurrent thrombose. What explains this

A

CYPC19 activates clopidogrel.

USMLE Step 1 General (7 decks)

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