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USMLE Step 1 Flash Cards > Pharmacology > Flashcards

Pharmacology Flashcards

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1
Q

Effect of NSAID’s on loop diuretics. Why?

A
  • Loop diuretics▶️⬆️PG▶️dilatation of renal vasculature▶️⬆️renal blood flow▶️⬆️renal function (GFR)
  • NSAIDs ▶️⬇️PG▶️block vasodilator effect▶️⬇️diuretic response
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2
Q

What is Nesiritide? Function.

A

BNP analog▶️diuretic and vasaodilator▶️used for acute and decompensated heart failure

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3
Q

Effect of inhaled anesthetics on brain

A

⬇️Vascular resistance▶️⬆️cerebral blood flow (undesirable) ▶️⬆️intracranial pressure

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4
Q

Mechanism of action of Danosumab. Uses.

A

Monoclonal antibody treatment postmenopausal osteoporosis

Like-Osteoprotegerin ▶️ bind RANK-L ▶️ block interacion with RANK ▶️ ⬇️ Osteoclast differentiation

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5
Q

Effect on the cAMP of atenolol in heart, kidney and blood vessel

A

Atenolol - selective beta blocker

  • heart and kidney ▶️ ⬇️ cAMP ▶️ both have B1 receptor (Gs coupled)
  • blood vessel ▶️ no change cAMP ▶️ not B1, have B2
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6
Q

Which drug used for rheumatoid arthritis can cause interstitial pneumonitis and fibrosis?

A

Methotrexate

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7
Q

Treatment for restless leg syndrome. Include pharmacologic and non-pharmacologic measures.

A
  • Avoid alcohol and sleep deprivation
  • Dopamine agonists (pramipexole, ropirinole)
  • Excercise, leg massage, heating pads
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8
Q

When occur and how can you avoid the nitrate tolerance?

A
  • Chronic nitrate treatment ▶️ attenuation of blood pressure response and antianginal effects
  • Give sublingual nitroglycerin intermittent, as-needed basis, free interval
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9
Q

Differences in uses of nytroglicerin sublingual vs isosorbide dinitrate or mononitrate.

A
  • Sublingual Nitroglycerin: acute episodes of ischemia, prevention angina before strenuous exercise
  • Isosorbide: chronic stable angina - prevent recurrent anginal episodes
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10
Q

Treatment of Cataplexia. Why?

A
  • Muscarinic antagonists

-

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11
Q

Why chronic use of glucocorticoids is a major risk factor (modificable) for osteoporosis?

A
  • ⬇️ absorption of Calcium
  • Inhibit collagen synthesis by osteoblasts
  • ⬇️ GnRH ▶️ hypogonadism
  • ⬆️ urinary calcium loss
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12
Q

Mechanism of action of varenicline. Uses.

A
  • Partial agonist of nicotinic receptor (alfa4, beta2) of CNS ▶️ competes with nicotine (full agonist) ▶️ low ⬆️ dopamine ▶️ less stimulation of reward pathway that nicotine.
  • ⬇️ withdrawal cravings in cessation of tobacco
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13
Q

Mechanism of action of a substance that is low molecular weight fraction, negatively charged and stored on mast cells granules.

A

Binding and ↑ action of antithrombin III (natural anticoagulant)

*Heparin

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14
Q

Difference in action of unfractionated heparin and Low molecular weight heparin (LMWH).

A
  • LMWH ▶️ AT III(a) ▶️ bind factor Xa

- Unfractionated Heparin ▶️ (via pentasacharide in heparin chain) AT III(a) ▶️ bind factor Xa and thrombin

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15
Q

How do the PGF2alpha analogs (latanoprost, Bimatoprost) function to treat glaucoma?

A

⬇️ collagen content in the Uveosclerar outflow pathway ▶️ ⬆️ outflow of aqueous humor

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16
Q

Which glaucoma drug is contraindicated in closed-angle glaucoma? Why?

A

Alpha-1 agonist (Epiniphrine) ▶️ mydriatic effect

- mydriasis close more the iridocorneal angle ▶️ trabecular meshwork less accesible to outflow

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17
Q

Target structure of Timolol in glaucoma treatment. Mechanism of action.

A

Epithelial cells of ciliary body ▶️ ⬇️ production of aqueous humor

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18
Q

Mechanism of action of cholinomimetics in glaucoma treatment.

A
  • ciliary muscle contraction ▶️ opening trabecular meshwork
  • esphincter of iris contraction ▶️ miosis ▶️ wider anterior chamber (open angle) ▶️ trabecular meshwork more accesible to outflow
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19
Q

What could be the cause of a first-dose hypotension by ACEI?

*Which is the mechanism?

A

Volumen depletion state (diuretic use or heart failure) ▶️ ⬆️ plasma renin activity ▶️ ⬆️ Ag II effect (compensatory)

*Abrupt removal of vasoconstrictory effect of Ag II ▶️ ⬇️ peripheral vascular tone ▶️ ⬇️ BP in susceptible patients.
Prevent ▶️ start ⬇️ doses

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20
Q

How can you reverse the toxic effect in a MTX overdose?

A

Leucovorin (folinic acid) ▶️ NOT requires DHFR to become Tetrahydrofolate
Rescue bone marrow, GI tract (rapid dividing normal cells) ▶️ pancytopenia, aphtous ulcers

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21
Q

Mechanism of action of metimazole and propylthiouracil

A
  • Thioamide drug (also propylthiouracil) ▶️ ❌ thyroid peroxidase ▶️ ❌ iodine organification (MIT, DIT formation) and coupling iodotyrosines (T3, T4 formation)
  • Propylthiouracil ▶️ also ⬇️ peripheral conversion T4 ▶️ T3 (active)
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22
Q

Why you should avoid ACEI in patients with C1 esterase inhibitor deficiency? Which is this disease?

A
  • Hereditary angioedema
  • ACEI ⏩ ⬆️ Bradykinin ▶️ precipitate disease episodes

*ACE ▶️ Bradykinin ▶️ inactive products

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23
Q

When can you give Vitamin K alone?

A

Abnormal coagulation tests (PT or PTT) but NO bleeding

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24
Q

Which calcium channel blockers you must avoid in patients with conduction abnormalities (AV block) and bradycardia? Why?

A
  • Nondihydropyridines ▶️ verapamil, diltiazem ▶️ ⬇️ heart rate (negative chronotropic effect), ⬇️ contractility (negative inotropic effect)
  • worsen bradycardia and AV block.
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25
Q

Why do the proton pump inhibitors associate with higher risk of osteoporosis?

A

Long term acid supression→↓acidic environment→↓Calcium absorption (need acid environment to be absorbed)

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26
Q

Why are the class IV antiarrhythmics useful to prevent recurrent nodal arrhythmias (ex paroxysmal supraventricular tachycardia)?

A

Block Calcium channels in cardiac slow response fibers (SA and AV nodes) ▶️ ⬇️ phase 0 (conduction) and 4 (depolarization) ▶️ ⬇️ diastolic depolarization

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27
Q

Ocular side effects of first generation antihystamines (chlorpheniramine, diphenhydramine). Why do the occur?

A
  • Blurred vision for close objects (noticeable when read, no when driving), mydriasis
  • anticholinergic effect ▶️ impair accomodation (contraction of ciliary muscle ▶️ ⬆️ refractive power of lens) and contraction of pupillary sphincter (PANS control)
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28
Q

Which adverse effect is increased in a coadministration of Ganciclovir with TMP-SMX or zidovudine [AZT]? The previous is possibly treating which scenario?

A
  • Bone marrow suppression ▶️ Neutropenia, leukopenia, thrombocytopenia.
  • CMV hemorrhagic colitis in HIV patient. Add TMP-SMX is though as prophylaxis.
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29
Q

Lipoatrophy and central fat deposition (redistribution of fat from extremities to the trunk) is a common side effect of which drugs?

A
  • Lipoatrophy ▶️ loss or wasting fat from extremities, face and buttocks ▶️ NRTI (stavudine, zidovudine), protease inhibitor
  • Central fat deposition ▶️ ⬆️ abdominal girth, buffalo hump ▶️ any HAART
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30
Q

Mechanism of action of Tacrolimus and Cyclosporine. Uses. Side effects.

A
  • Inhibition of Caclineurin
  • Normally Calcineurin [serine, threonine phosphatase] ► dephosphorylate to NAFT (transcription factor) ▶️ nucleus ➕ IL-2 promoter ▶️ ⬆️ IL-2 ▶️ differentiation and proliferation of T-cells
  • Transplant rejection and prophylaxis. Cyclo also psoriasis, RA.
  • Cyclo ▶️ bind cyclophilin
  • Tacro ▶️ bind FK506 binding protein (FKBP)
  • Highly Nephrotoxic
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31
Q

Which drug can increase the QRS duration during exercise? How does it call? Which is the normal (without drug) reaction on QRS during exercise?

A

Flecainide, Strong use-dependence ▶️ slowest to dissociate from Na channel ▶️ ⬆️ Na blocking effects in ⬆️ HR ▶️ less time between action potential for the drug to dissociate from receptor.

  • Normally Exercise ▶️ ⬆️ Heart rate ▶️ ⬆️ cardiac conduction velocity ▶️ ⬇️ QRS duration
  • Drug Exercise (test) ▶️ ⬆️ Heart rate ▶️ 🚫 fast Na channels (phase 0 depolarization of cardiac myocytes) ▶️ ⬆️ QRS duration
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32
Q

Drug of choice in a myoclonic seizure. Which type of seizure is it?

A
  • Broad spectrum anticonvulsivants ▶️ lamotrigine, levetiracetam, topiramate, valproic acid (Tx most seizures focal or generalized at onset) ⤵️ (drug of choice)
  • Generalized seizure (involve both hemispheres at onset)
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33
Q

Why do you use Rifamixin and lactulose to treat hepatic encephalopathy?

A
  • Lactulose ▶️ ⬇️ colonic pH ▶️ facilitates NH3 ⏩ NH4+

- Rifamixin ▶️ change GI bacterial flora ▶️ ⬇️ production of NH3

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34
Q

Which drug for the treatment of tuberculosis acts by disrupting the cell wall of the bacilli? What property can the mycobacterium lose?

A
  • Isoniazid ▶️ 🚫 mycolic acid synthesis

- lose acid-fastness, unable to synthesize new cell wall or multiply

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35
Q

Which site of the brain drive the nausea and vomiting reaction when give systhemic chemotherapy for cancer?

A

Area postrema (dorsal medulla, caudal fourth ventricle end)→Chemoreceptor trigger zone (CTZ)

*Recieves blood from fenestrated blood vessels (absent BBB)→sample chemicals in blood

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36
Q

What side effect of levodopa will be present although adding carbidopa?, which side effect do you avoid?

A
  • ↑Dopamine in brain→Agitation and anxiety (central side effect)
  • ↓Dopamine in periphery→Nausea and vomiting (area postrema outside BBB)→(+)emetic center at brain stem [area postrema]; ↓tachyarrhythmia, postural hypotension and hot flashes
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37
Q

Why you should replace Rifampin by Rifabutin in treatment of TB in patient HIV (+) in HAART including Protease inhibitor?

A

Rifampin ▶️ ⬆️ activity cytochrome P450 ▶️ metabolizes Protease inhbitors (really PI 🚫 C P450) ⏩ ⬇️ levels of PI

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38
Q

Contraindication of primaquine, why?

A

Glucose 6-P dehydrogenase deficiency

Can cause hemolysis

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39
Q

What drug do you use to confirm diagnosis of asthma during lung test function, and when do you use it?

A

Lung test function normal, and history suggest asthma ▶️ methacoline ▶️ muscarinic cholinergic agonist ▶️ bronchoconstriction and ⬆️ mucus production ▶️ broncoprovocation ⏩ ⬇️ FEV1 after mechacoline challenge

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40
Q

Mechanism of Jimsom weed poisoning (“Gardener mydriasis”). Treatment.

A
  • Jimsom weed ▶️ toxins (belladona alkaloids) ▶️ ❌ muscarinic cholinergic visceral receptors ▶️ atropine-like syndrome
  • Physostigmine ▶️ cholinesterase inhibitor ▶️ ⬆️ Ach in synaptic cleft
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41
Q

First line of treatment for absence seizures. Mechanism of action.

A

Ethosuximide ▶️ blocks thalamic T-type calcium channels

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42
Q

Mechanism of action of vigabatrin and uses

A
  • 🚫 GABA transminase irreversibly ▶️ ⬆️ GABA

- Treatment of resistant epilepsy

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43
Q

Risk of vertical transmision of HIV with and without HAART. Which pregannt women should take HAART?

A
  • No HAART→35%, HAART→1-2%

- All mothers regardless CD4 count or viral load until breastfeeding period

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44
Q

What antiretroviral is teratogenic and which is used to profilaxis for HIV in the newborn?

A
  • Teratogenic→Efavirenz

- Newborn prophylaxis→Zidovudine

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45
Q

What adverse effects characterized Foscarnet? why do they happen?

A
  • Hypocalcemia, hypomagnesemia→seizures

- Chelate Ca, ↓PTH release, ↑renal wasting of Mg

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46
Q

Which drug do you use to treat nausea and vomiting in diarrhea/vomiting disease (traveler diarrhea), motion sicknes disease and migraine or central nausea?

A
  • GI insults (infections, chemotherapy, distention)→↑5HT→(+)5HT3 receptors ► 5HT3 receptors antagonists (Ondansetron)
  • Central nausea (migraine)→DA2 receptor antagonists (metochlopramide, prochlorperazine)
  • Vestibular nausea→First generation H1 receptor antagonist, M1 receptor antagonists
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47
Q

How is call the pharmacologic principle when cortisol increases the response of norepinephrine?

A

Permissiveness→One hormone allows another compound exert its maximal effect

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48
Q

How does the cocaine exert its sympaticomimetic effect? Signs and symptoms that you expect to see in a intoxication.

A
  • Indirectly→Inhibit presynaptic reputake of monoamines (catecholamines - NE, DA, 5HT)
  • HTN, ↑HR, mydriasis (SANS +), CNS +→agitation, seizures, ↑arousal. Vasoconstriction→coronary vasospasm+↑platelet aggregation→myocardial ischemia; mucosal atrophy→nasal septal perforation
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49
Q

Most common situations in which ACEI can cause hyperkalemia

A
  • Renal insufficiency
  • Spare-K+ diuretics ▶️ amiloride, espironolactone, triamterene
  • K+ supplements
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50
Q

What do you suspect in a hyperthyroidism patient with fever and sore throat, oral ulcerations in treatment with antithyroid drugs? What do you do if suspect it?

A
  • Thionamide-induced agranulocyotsis (absolute neutrophil count<500/uL)
  • Suspend drug, white blood cell count with differential to confirm Dx

*In 0,5% of patients within first few months of Tx.

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51
Q

Different useful situations of antithyroid drugs

A
  • Metimazol ▶️ initially because potentially severe hepatotoxic propylthiouracil
  • Propylthiouracil ▶️ 1st trimester of pregancy because teratogenic metimazol; life-threatening thyroid storm because additional effect to 🚫 conversion T4⏩T3 in peripheral tissues
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52
Q

Common side effects of sotalol and why?

A
  • Bradycardia ▶️ beta-adrenergic blocking
  • QT interval prolongation ▶️ Proarrhythmic ▶️torsades de pointes ▶️ class III (K+ channel blocking)

*Rhythm control of paroxysmal atrial fibrillation

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53
Q

Most important side effect of anthracyclines (doxorubicin, daunorubicin, epirubicin, idarubicin) and why does it occur? Treatment to it.

A
  • Oxygen free radicals in myocardium ▶️ cumulative dose-related dilated cardiomyopathy ▶️ left and right ventricular CHF
  • Desrazoxane ▶️ iron chelating agent ▶️ ⬇️ O2 free radicals
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54
Q

Treatment of inflammatory bowel disease. Mechanism of action.

A

Chron’s disease, ulcerative colitis ▶️ 5-aminosalicylates (sulfasalazine [sulfapyridine + 5-aminosalicylic acid], mesalamine) ▶️ ⬇️ CK’s, PG’s, leukotrienes during inflammation

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55
Q

Side effects of erythropoeisis-stimulating agents (ESAs) and why do they occur? Example of those agents.

A
  • Hypertension ▶️ activation of erythropoietin receptors on vascular endothelial and smooth muscle cells
  • Thromboembolic events ▶️ ⬆️ RBC mass ▶️ ⬆️ blood viscosity
  • Erythropoietin, darbepoetin
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56
Q

Mechanism of action of mifepristone. Uses.

A
  • Progesterone antagonist ▶️ apoptosis and necrosis of decidua ▶️ ❌ further development of the first trimester of pregnancy
  • With misoprostol (PGE-1 analog ▶️ softening of cervix, ⬆️ uterine contractions) to pregnancy termination
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57
Q

Why do the loop and thiazide diuretics cause hyperuricemia?

A

Hypovolemia→↑Uric acid absorption

*Potentially precipitate gout attack

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58
Q

Why do the thiazides and loop diuretics cause hypokalemia and metabolic alkalosis?

A

↓Intravascular volume→(+) aldosterone→↑secretion of H+ and K+ at collecting ducts

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59
Q

Mechanism of action of ionizing radiation in the treatment of cancer

A
  • Break double stranded DNA (both strands)

- Free radical formation→ROS formed by ionization of H2O→cellular and DNA damage

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60
Q

Which antiarrhythmic drugs that blockade Na channels have the less and higher use dependence effect?

A
  • Use dependence effect ▶️ higher rates of depolarization lead in more Na channel blockade
  • Drugs with ⬆️ use dependence effect spend more time bound to Na channel (activated-inactivated)
  • 1C>1A>1B

*Dissociation of 1B from Na channels is more rapidly and less cumulative effect over multiple cardiac cycles ▶️ little use dependence

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61
Q

Mechanism of action of thizolidinedione. Example of one of them.

A
  • Pioglitazone
  • Bind to PPAR-γ ▶️ heterodimer complex with retinoid X receptor ▶️ binds to transcriptional regulatory sequences of some genes. Ex: ⬆️ Adiponectin ▶️ ⬆️ insulin sensitivity and fatty acid oxidation
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62
Q

Mechanism of action of theophylline. Indications. Important features about it uses.

A
  • Inhibit cAMP phosphodiesterase ▶️ ↑ action of cAMP→(+)PKA→(-)myosin light chain kinase at smooth muscle (activated allow cross myosin-actin→contraction)
  • Blocks actions of adenosine (normally ↑bronchoconstriction)
  • Tx bronchial asthma; narrow therapeutic index
    (cardiotoxicity, neurotoxicity); metabolized by cytochrome P-450
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63
Q

What could occur if you give ACEI or ARB in a patient with BILATERAL renal artery stenosis? why?

A
  • Bilateral renal artery stenosis→↓RBF→↓GFR►maintain GFR►Ag II→Efferent arteriole constriction→↑GFR
  • ACEI or ARB→↓Ag II→efferent arteriolar vasodilation→↓GFR►acute renal failure
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64
Q

Treatment of choice for absence associated with tonic-clinic seizures.

A

Valproate

*Ethosuximide effective against absence seizures but not for tonic-clonic seizures

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65
Q

What drug you must avoid in a glaucoma patient?

A

Systemic or local anticholinergic (atropine, etc) ▶️ mydriasis ▶️ narrowing anterior chamber ▶️ ⬇️ outflow of aqueous humor ▶️ ⬆️ intraocular pressure ▶️ precipitate closed-angle glaucoma in patients with shallow anterior chamber or higher than normal intraocular pressure

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66
Q

Mechanism of action of meglitinide (repaglinide, nateglinide). Uses.

A
  • Inhibit the ATP-dependent K+ channels in pancreatic B cell membrane→Depolarization→open L-type calcium channel→↑calcium influx→↑insulin releasing
  • Postprandial hyperglycemias in DM

*Insulin secretagogue (sulfonylurea also)

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67
Q

What type of neuropathy can cause Isoniazid?, why?, more sensible patients.

A
  • Peripheral neuropathy
  • Vitamin B6 participate in synthesis of many neurotransmiters (DA, NE, Epi, 5TH, GABA)
  • Isoniazid similar structural to B6→↑urinary excretion, compete binding sites→B6 deficiency
  • Elderly, acoholics, liver or kidney dysfunction
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68
Q

What mechanism produce angioedema by ACEI?

A

↑↑Bradykinin (ACE→break bradykinin)→powerful vasodilator→↑vascular permeability

*Differentiate angioedema by hereditary esterase C1 inhibitor by age and history of taking ACEI

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69
Q

Long-term use of thiazolidinedione (pioglitazone) is associated with what condition?

A

Urinary bladder cancer

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70
Q

How much rectal drug administration bypass the first-pass metabolism? how does it happen?

A

Partially bypasses first-pass metabolism. Rectum drainage:

  • Superior rectal vein→inferior mesenteric vein→portal circulation (first-pass metabolism) (1/3 of drug)
  • Middle and inferior rectal vein→internal iliac and internal pudendal veins→systemic circulation (2/3 of drug)►↑bioavailability
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71
Q

Adverse effect of the mu opioids on common bile duct and gallbladder and mechanism of it.

A

Contraction of smooth muscle cells of sphincter of Oddi→spasm→↑pressure in common bile duct and gallbladder►biliary colic

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72
Q

When is useful to give pulsatile administration of GnRH?

A

Hypogonatropic hypogonadism→anovulation→infertility

*Normally from hypothalamus pulsatile→upregulation of its receptors in gonadotropin pituitary cells→↑LH and FSH►development of the dominant follicle→ovulation

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73
Q

When is useful an long-acting analog of GnRH? why?

A

Prostatic cancer, premenopausal breast cancer, endometriosis, precocious puberty

*When supression of gonadal function is desired►downregulation of GnRH receptors→↓LH and FSH

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74
Q

Major causes of death by tricyclics andtidepressants (TCA) overdose.

A
  • Inhibit fast Na+ channel conduction→↓myocardial depolarization→cardiac arrhythmias (most common cause of death)
  • Antagonist of peripheral alpha-1 adrenergic receptor→refractory hypotension
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75
Q

Side effects of selective arteriolar vasodilator (direct relaxation of smooth muscle of arterioles and no veins).

A
  • Normal effect→↓systemic vascular resistance→↓blood pressure:
    ♦ Stimulation of baroreceptors→(+) sympathetic nervous system→↑HR, contractility►↑cardiac output
    ♦ SANS→renin-angiotensin-aldosterone system→↑Na and fluid retentetion (peripheral edema)

*hydralazine, minoxidil

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76
Q

Why a calcium channel blocker (ex verapamil) affects contraction of myocyte of smooth and cardiac muscle, and not of skeletal muscle?

A
  • Smooth and cardiac muscle need influx of extracellular calcium through L-type Ca channel (blocked CCB) to activate RyR receptor at sarcoplasmic reticulum and release more Ca to contraction
  • Skeletal muscle is not dependent of extracellular influx of Ca. Depolarized receptor activate RyR without Ca influx.
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77
Q

Mechanism of action and most important side effects of carbamazepine

A
  • ⬇️ Na channel ability to recover from inactivation
  • Bone marrow suppression ▶️ thromobocytopenia, anemia, agranulocytosis
  • Syndrome of inappropiate ADH secretion ▶️ hyponatremia
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78
Q

Treatment and prevention of gynecomastia in patient receiving androgen depriving therapy (ADT). What ADT are possible and in what case in men?

A
  • Tamoxifen ▶️ selective estrogen receptor modulator ▶️ inhibit effect of estrogen in breast
  • ADT ▶️ orchiectomy, long-acting GnRH agonists therapy, androgen receptor inhibitors
  • Prostate cancer
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79
Q

Treatment for enterobiasis (pinworm) in pregnant women. First line in non-pregnant individuals.

A
  • Pregnant→pyrantel pamoate

- Non-pregnant and others→albendazol

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80
Q

Uses and mechanism of action of Naltrexone

A
  • Block mu-opioid receptors
  • Alcohol dependence→Block rewarding and reinforcing, ↓craving, can be initiated while still drinking

*Use long-acting depot form (monthly) for risk of non-adherence to dialy administration

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81
Q

Treatment options for clostridium difficile infection. Which of them inhibits the sigma subunit of RNA polymerase and what is its proper use?

A
  • Metronidazol, Vancomycin
  • Fidaxomicin→macrocyclic (related to macrolides), inhibit the sigma subunit of RNA polymerase→impairment protein synthesis→cell death (bacteriocidal)

*Useful in recurrent infection and ↑risk recurrence (recent antibiotic use, gastric acid supression)

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82
Q

Manifestations of acute dystonia as adverse effect of antipsychotics. Which type of antipsychotics can cause them and how?

A
  • 4 hours to 4 days after initiate drug
  • Muscle spasm (acute torticolis), stiffness, oculogyric crisis, opisthotonus, laryngospasm (rare)
  • 1st generation High-potency antipsychotics→D2 antagonism in nigrostriatal pathway►predominates excess action of M1
83
Q

How do you treat acute dystonia as a side effect of antipsychotic therapy?

A

Block excess action of M1 (cholinergic muscarinic neurons)►Benztropine, diphenhydramine→re-establish dopaminergic-cholinergic balance

84
Q

Most common adverse effects of psychostimulants for treatment of ADHD.

A

Decreased appetite, weight loss and insomnia

*Less common→↑ HR and blood pressure►monthly follow up

85
Q

Most important side effect of lamotrigine. Uses.

A
  • Stevens-Johnson syndrome (life-threatening rash)

- Anticonvulsivant, bipolar disorders

86
Q

Drugs that impair periphery conversion of T4 to T3

A

Amiodarone, non-selective ß-blockers, propylthiouracil, glucocorticoids, iopanoic acid

87
Q

How do you measure the solubility of an gas anesthetics and determine a high or low solubility? What is the consequence in the onset of action?

A

Blood/gas partition coefficient

  • ↓coefficient►low solubility→blood saturates quickly→fast↑ in partial pressure→fast brain saturation→↓onset of time→rapid onset of action
  • ↑coefficient►high solubility→blood saturates slowly→delayed↑ in partial pressure→slow brain saturation→↑onset of time→slow onset of action
88
Q

How do you measure potency in a gas anesthetics?

A

Minimal alveolar concentration→concentration of gas in the lungs that produces the desired effect in 50% patients

*Potent anesthetics→lower partial pressure to be effective

89
Q

Treatment of Beta-blocker overdose. Mechanism of action.

A

Glucagon→↑intracellular cAMP→→↑Ca during muscle contraction→↑HR, cardiac contractility, blood pressure in minutes

90
Q

Why if manitol is a diuretic can worsen pulmonary edema? What is its mechanism of action?

A
  • Causes initial intravascular volume expansion

- Osmotic diuretic inhibit water and NaCl reabsorption in the PT and descending limb of loop of henle

91
Q

Mechanism of action of Oseltamivir

A
  • Sialic acid analogue▶️competitively inhibits influenza neuraminidase▶️❌release of viral progeny
  • Neuraminidase cleaves terminal acid residues on glyconjugate receptors▶️release of attached influenza virions from infected cells
92
Q

Mechanism of action of Oseltamivir

A
  • Sialic acid analogue▶️competitively inhibits influenza neuraminidase▶️❌release of viral progeny
  • Neuraminidase cleaves terminal acid residues on glyconjugate receptors▶️release of attached influenza virions from infected cells
93
Q

What is cinacalnet and what is used for?

A
  • Calcimimetic allosterically activates calcium-sensing receptor in parathyroid gland▶️⬇️PTH release
  • Secondary hyperparathyroidism in dialysis
94
Q

What is the sevelamer and what is used for?

A
  • Non-absorbable phosphate-binding polymer▶️⬇️absorption of PO4 in GI tract
  • Hyperphosphatemia in dialysis
95
Q

How do you distinguish a neuroleptic malignant syndrome and serotonin syndrome?

A

Both▶️mental status change, autonomic instability, hyperthermia

  • Serotonin▶️neuromuscular hyperactivity▶️shivering, clonus, hyperreflexia (vomiting and diarrhea most common than NMS)
  • NMS▶️diffuse rigidity and hyporreflexia
96
Q

Which compounds rise and decrease in blood the thiazide diuretics?

A

⬆️ glucose, lipids (cholesterol LDL), uric acid, calcium

⬇️ sodium, magnesium, potassium (metabolic alkalosis)

97
Q

Mechanism of action of opiates

A
  • High affinity for the mu receptor▶️coupled to inhibitory G proteins and higher analgesic effects
  • Primary afferent neuron▶️activation of mu R▶️close voltage-gated calcium channel▶️⬇️ neurotransmitter release (Ach, NE, Epi, Substance P, etc) from presynaptic membrane
  • Postsynaptic membrane ▶️bind to mu R▶️open potassium channels▶️K efflux▶️membrane hyperpolarization

*Opiated-induced inhibition of synapse activity in CNS▶️attenuated pain

98
Q

Mechanism of action of flutamide. Common use in a prostate cancer.

A
  • Competitive testosterone receptor inhibitor
  • Sometimes prescribed concurrently with long-acting GnRH agonist▶️initial and transient ⬆️LH and testosterone (avoid the androgen effect▶️worst symptoms)
99
Q

Indication and mechanism of action of Diphenoxylate. How do you avoid the abuse of it?

A
  • Low-potency opioid agonist▶️bind mu receptor at GI tract▶️⬇️ motility
  • Empiric symptomatic therapy for uncomplicated diarrhea▶️Ex; inflammatory bowel disease, functional diarrhea. (Must be avoided in diarrhea due toxin, invasive organism or clostridium difficile).
  • Combined with atropine▶️if take higher doses▶️adverse effects of atropine (dry mouth, tachycardia, blurry vision) would decrease subsequent increase doses by abuse
100
Q

What oral anti-diabetic agent can cause as side effect, exacerbation of heart failure (and why) and hepatotoxicity?

A

Thiazolidinediones (ex, pioglitazone, rosiglitazone)

  • Fluid retention→exacerbate HF→assess risk and signs of HF
  • Hepatotoxicity→periodic liver function tests (with troglitazone, no longer available)
101
Q

Mechanism of action of biphosphonate. Effects bone metabolism.

A
  • Similar structure to pyrophosphate→attach to hydroxyapatite binding sites→Osteoclast take up the biphosphonate→unable to continue resorption►↓osteoclast activity
  • Induce osteoclast apoptosis, ↓development/recruitment of osteoclast precursors cells
102
Q

Mechanism of action of Teriparatide

A

Similar 34 amino acid sequence at N-terminal of PTH

  • Maturation of pre-osteoblasts into bone-forming osteoblasts
  • ↑Ca intestinal absorption, renal reabsorption
103
Q

What drug can elevate the concentration of statins and increase risk of myopathy and why? What is statin exception?

A
  • CYP450 inhibitors→Cimetidine, erythromycin (also claritromycin, No azitromycin), ciprofloxacin, azole antifungals, Isoniazid, Ritonavir, grapefuit juice
  • Statins are metabolized by the liver cytochrome P-450 3A4, except pravastatin. Atorvastatin can ↑40%.
104
Q

Mechanism of action of Lumacaftor and Ivacaftor. Indications.

A

CFTR-modulating medications

  • Lumacaftor→restoring CFTR proteins to the membrane
  • Ivacaftor→enhancing protein function (ex, chloride transport) at the membrane
  • Improve predicted forced expiratory volume (FEV) and ↓rates of pulmonary exacerbations in Cystic Fibrosis
105
Q

Side effects of ACEIs

A
  • ↓GFR→not concerned unless ↓>30% (long-term benefits well known)
  • Hypokalemia
  • Cough
  • Angioedema
106
Q

How much time must patient wait when switch from MAOI to SSRI and why?

A
  • 2 weeks→regeneration of MAO

- Contraindicated coadministration of SSRI and MAOI→↑↑risk of serotinin syndrome

107
Q

Why are long-acting nitrates provided with free-interval dosing?

A

Decrease tolerance development

*Night▶️sleep and cardiac work is least

108
Q

Which opoids side effects persist with higher doses of them, when tolerance have developed for analgesic effects and most side effects?

A

Constipation and miosis

109
Q

Non-systemic treatment for postherpetic neuralgia (PHN)

A
  • Lidocaine patches→↓depolarization of neurons in peripheral nerves
  • Topical Capsaicin→Loss of membrane potential in nociceptive fibers, ↓substance P
110
Q

Which are the compartments of the multi-compartment model of distribution of a drug?

*To what drugs apply this model?

A
  • Central compartment→plasma
  • Well-vascularized peripheral compartment→brain, liver, kidney, lung►quickly distributed
  • Poorly-vascularized peripheral compartment→skeletal muscle, fat, bone►redistribution

*Accounts for the short duration of action of many commonly anesthetics (propofol - highly lipophilic)

111
Q

What type of heparin is most effective innactivating thrombin?

A
  • Unfractionated heparin→pentasaccharide sequence long enough→binds to antithrombin►conformational change→inactivate factor Xa, and thrombin
  • unlike LMWH→ inactivate factor Xa>thrombin
112
Q

Mechanism of action argatroban, dabigatran, bivalirudin, hirudin, lepirudin. Drug of choice of which condition?

A
  • Binding to thrombin active site▶️direct thrombin inhibitors (don’t need antithrombin III)
  • Heparin induced thrombocytopenia (HIT) [antibodies to heparin and platelet factor IV▶️unfractionated heparin>LMWH]▶️paradoxical thrombosis

*Suspect HIT▶️suspend all forms of heparin

113
Q

Mechanism of action and adverse effect of daptomycin.

A
  • Creates transmembrane channels▶️intracellular ion leakage▶️disrupt bacterial membrane (cellular membrane depolarization), inhibition of macromolecules synthesis (DNA, RNA, proteins)
  • Myopathy, ⬆️Creatinphosphokinase (CPK)▶️disrupt muscle fiber membrane [most with other drugs myopathy associated - statin]

*Limited to gram (+) infections

114
Q

In what cases is daptomycin ineffective?

A
  • No penetrate outer membrane of gram (-)▶️innecfetive treating gram (-) infections
  • Innactivated by pulmonary surfactant▶️innecfective to treat penumonia
115
Q

Which antibiotic can increase the risk of serotonin syndrome? In what case?

A
  • Linezolid

- Concomitant use with proserotoninergic drugs (ex,SSRI)

116
Q

Treatment for intractable parkinson symptoms (bradykinesia, rigidity). Why target those structures?

A

High frequency deep brain stimulation of globus pallidus internus or subthalamic nucleus▶️🚫them▶️thalamo-cortical desinhibition▶️improve motility

*Nigrostriatal degeneration in parkinson▶️➕subthalamic nucleus▶️⬆️➕globus pallidus internus▶️🚫thalamus

117
Q

What drug inhibit the action of a enzyme induced by IL-1 and TNF-alpha during inflammation by inflammatory cells and no by normal surrounding tissue? Advantage of those drugs.

A
  • Selective COX-2 inhibitors
  • Spares COX-1→maintain gastric mucosa
  • Spares platelet function as TXA2 production is dependent on COX-1
118
Q

Mechanism of action of antibiotics which side effect is ototoxicity (tinnitus, hearing loss) and nephrotoxicity. In which infections they are not effective?

A
  • Aminoglycosides▶️bactericidal▶️irreversible inhibition of initiation complex▶️binds to 30S ribosomal subunit▶️misreading of mRNA▶️🚫Protein synthesis
  • Requiere O2 for uptake▶️ineffective against anaerobes

*Useful for severe gram (-) infections. Synergistic with B-lactams (affect cell wall synthesis)

119
Q

Mechanism of action of Entacapone, Tolcapone

A

⬇️ Peripheral degradation of levodopa

🚫Catechol-O-methyltransferase (COMT)⏩Levodopa▶️3-O-methyldopa

120
Q

Indication of treatment of hepatitis C infection.

A

Rivabirin and interpheron alpha▶️virologic and histologic evidence of chronic infection▶️HCV RNA in serum, chronic inflammation with fibrosis in liver Bx

121
Q

Mechanism of action, uses and characteristic feature of Buspirone.

A
  • Partial agonists of 5TH1A receptors
  • Generalized anxiety disorders
  • Slow onset of action (1-2 weeks). No cause sedation, addiction, tolerance or withdrawal
122
Q

Mechanism of action and uses of Bosentan.

A
  • Endothelin-receptor antagonist→block endothelin►potent vasoconstrictor, endothelial proliferation activator
  • ↓Pulmonary arterial pressure, ↓progression of vascular and right ventricular hypertrophy
123
Q

Mechanism of action of selective estrogen receptor modulators. Examples and differences between them.

A
  • Mixed agonist/antagonists depending on tissue
  • Tamoxifen:
  • Breast►antiestrogenic effect (adjuvant tx of positive estrogen receptor breast cancer)→↓recurrence Ca, ↓estrogen-dependent benign breast lesions (fibroadenoma, cystic changes)
  • Endrometrial tissue►endometrial hyperplasia and cancer (No risk with Raloxifen)
  • Bone►agonist estrogen receptor→↑bone mineral density after menopause
124
Q

Target of monoclonal antibody used for HER2 positive invasive ductal breast carcinoma

A

Trastuzumab→binds extracellular portion of HER2→prevents activation of transmembrane tyrosin kinase receptor►↓proliferation and ↑apoptosis

*HER2(+)→20% of invasive breast cancers

125
Q

Treatment of hormone receptor positive breast cancer (ER and/or PR) in premenopausal and postmenopausal women

A
  • Premenopausal→selective estrogen receptor modulator (Tamoxifen)
  • Postmenopausal→aromatase inhibitors (anastrozole, letrozole)
126
Q

Treatment of wilson disease

A

D-penicillamine→free sulfhydryl group→copper chelator

127
Q

Which diuretic is recommended by some experts when associated high risk of osteoporotic fracture? why? what other benefit respect this effect is seen?

A
  • Hydroclorothiazide→↑Calcium reabsorption in distal tubule→↑bone mineral density→↓risk of fracture for osteoporosis
  • Hypocalciuria→↓recurrent renal stones
128
Q

What mutation make anti-EGFR (epidermal growth factor receptor) therapy resistant? which are those drugs?

A
  • Mutation of KRAS (proto-oncogen)→GTP binding protein→transduce signals from some receptors (EGFR)→cell proliferation and growth
  • Activating Mutation→resistant to Tx→cetuximab, panitumumab→metastatic colon cancers (Stage IV wild-type KRAS)

*Genetic testing to identify wild-type and mutated KRAS prior Tx

129
Q

What antibiotic can precipitate serotonin syndrome if combined with SSRI? Why?

A

Linezolid▶️has MAOI activty

*Gram (+), vancomycin resistant enterococcus, MRSA

130
Q

Potential ocular adverse effect of oxygen therapy

A

Retinopathy of prematurity or retrolental fibroplasia: ⬆️⬆️O2▶️⬆️VEGF⬆️neovascularization and retinal detachment with blindness

131
Q

Mechanism of action of arterial vasodilator used for hypertensive emergency crisis with effect on renal arterial vascular bed. What is its renal effect?

A
  • Fenoldopan▶️short acting, selective, peripheral Dopamine-1 receptor agonist (no effect on alpha or beta)▶️➕adenyl cyclase▶️⬆️cAMP▶️vasodilation in most arterial beds
  • Renal vasodilation▶️⬆️renal perfusion, diuresis, natriuresis (beneficial specially for acute renal failure)

*Remember hydralazine also arterial vasodilator but NO renal effect▶️no used in HTN crisis▶️reflex sympathetic➕▶️⬆️HR, contractility; fluid, Na retention

132
Q

Treatment of nephrogenic diabetes insipidus

A
  • Thiazide diuretics▶️induce mild hypovolemia▶️⬆️Na and water reabsorption at proximal tubules
  • Indomethacin▶️⬇️PG synthesis▶️normally 🚫ADH
133
Q

Treatment of central diabetes insipidus

A

Desmopressin (synthetic ADH)

134
Q

Effect of benzodiazepines and barbiturates on GABA receptor

A

Positive allosteric modulation. In respondo to GABA stimulation:

  • BZD▶️⬆️frequency of open the chloride channel of the GABA A receptor
  • Barbiturates▶️⬆️time of open the chloride channel of GABA A receptor
135
Q

Mechanism of action of baclofen, uses.

A
  • GABA B receptor agonist▶️G-protein pathway

- Muscle relaxant

136
Q

Why dextrose infusion and heme can improve acute intermittent porphyria symptoms?

A

Downregulates expression of ALA synthase▶️⬇️ALA▶️⬇️PBG which is ⬆️⬆️ by PBG deaminase deficiency

137
Q

Uses and mechanism of action of vitamin D analogs.

A
  • Psoriaris▶️topical⏩calciprotiene (calcipotriol), calcitriol, tacalcitol
  • 🚫(Vitamin D receptor) nuclear transcription factor▶️❌keratinocyte proliferation; ➕keratinocyte differentiation
  • 🚫 T cell proliferation and other inflammatory mediators
138
Q

Mechanism of action of Oseltamivir

A

🚫Neuraminidase▶️❌release of new virus attached to cellular surface▶️new formed virions remain adherent to infected cells▶️❌viral spread

*Neuraminidase cleave at sialyc acid residues of host cell glycoconjugate receptors that bind Hemaglutunin of virus▶️release attached virions from infected cells

139
Q

Uses and mechanism of action of Bevacizumab and Trastuzumab

A
  • Bevacizumab→anti-VEGF►Tx Ovarian cancer

- Trastuzumab→anti-HER2►Tx Breast cancer

140
Q

Immediate reverse of anticoagulation in patient in treatment with Dabigatran

A

Idarucizumab→atracts dabigatran 350x more than thrombin (binds free and thrombin bound)

141
Q

Uses and mechanism of action of Natalizumab and Vedolizumab

A
  • Natalizumab→alpha-4-beta-1 integrin cell adhesion molecule inhibitor (CNS)►Tx Multiple sclerosis; alpha-4-beta-7 integrin cell adhesion molecule inhibitor (Gut)►Tx Crohn’s disease
  • Associated with progressive leukoencephalopathy, reactivation of JC virus
  • Vedolizumab→alpha-4-beta-7 integrin cell adhesion molecule inhibitor only (Not associated with PML)
142
Q

Uses and mechanism of action of Secukinumab

A

IL-17 inhibitor→Tx Psoriasis

143
Q

What is Romiplostin and its uses?

A
  • Fusion antibody peptide
  • Thrompoetin agonist→megakaryocytic proliferation and stimulation►Tx Idiopathic thrombocytopenic purpura in patients with no response to splenectomy
144
Q

Uses and mechanism of action of Sacubitril

A
  • Neprilysin Inhibitor [member of Angiotensin Receptor Neprilysin Inhibitor (ARNI)]→↑Bradikynin→cardiac muscle relax; ↑Natriuretic peptides
  • Tx Congestive heart failure, NYHA II-IV with ↓ejection fraction
  • Neprilysin→zinc-dependent metalloprotease→ breakdown bradikynin and natriuretic peptides
  • Is a prodrug activated by plasma esterase
145
Q

Uses and mechanism of action of Patiromer. Possible side effects and contraindication.

A
  • Non-absorbed cation exchange polymer with calcium as a counter ion
  • Chronic hyperkalemia in CKD on RAAS inhibition (ACEI or ARB) and ↑risk of hyperkalemia and arrhythmia. NOT for acute hyperkalemia.
  • Contraindication: Avoid in mechanical bowel obstruction
  • Side effects: Hypomagnesemia, hypercalcemia

*Allow use ARB and ACEI and delay progression of renal injury

146
Q

Treatment of primary myelofibrosis, why?

A
  • Ruxolitinib▶️JAK2 inihibitor
  • Associated with V617F JAK2 mutation →oncogene (Gain of function)►myeloproliferative disorders: polycythemia vera, essential thrombocythemia, myelofibrosis, except CML (philadelphia chromosome)
147
Q

Principal target of nitroglycerin

A

Large veins▶️venodilator

*larger dosis▶️arteriolar dilation▶️headache, flushing

148
Q

A positive test of HLA-B*57:01 is relevant in a HIV patient considering treatment with which drug?

A
  • Abacavir (NRTI)
  • 2-8% patients▶️abacavir hypersensitivity reaction (AHR): strongly associated with the allele▶️bind abacavir to HLA-B*57:01▶️alter self-peptide presentation▶️delayed hypersensitivity reaction (type IV)
149
Q

Which type of insulin would be more appropriate to control postprandial high blood glucose levels?

A
  • Lispro, Aspartat, Glulisine (monomeric insulins)▶️mean peak 45 to 75 minutes. Before each meal.
  • Regular▶️dimeric and hexameric▶️⬆️time to dissociate and absorb▶️peak 2-4 hours▶️after postprandial glucose peak▶️inadequate control of Glc following meals
150
Q

What antiarrhythmic can increase the QRS (phases 0) and have minimal effect on QTc?

A

Class IC▶️Na channel blocker at myocyte▶️⬇️initial depolarization, ⬆️QRS; little effect on QTc▶️lack K channel blocking activity [Flecainide, propafenone]

151
Q

Treatment of VIPoma

A

Somatostatin (octreotide)▶️⬇️production of many GI hormones (VIP, gastrin, glucagon, CCK)

152
Q

How do the Beta-blockers affect the RAAS system? what is the effect on each component?

A
  • Block B1 receptor in juxtaglomerular cells→↓renin

- ↓Renin, ↓Angiotensin I, ↓Angiotensin II, ↓Aldosterone, no affect Bradykinin

153
Q

How much time would a drug metabolized by first order kinetcs require to achieve a 95% plasma steady state concentration during continous infusion?

A

4 to 5 half-lifes

154
Q

Treatment for congenital adrenal hyperplasia

A

Low doses of exogenous corticosteroids→supress ACTH secretion→↓androgen by adrenal cortex

155
Q

Mechanism of action of Bupropion, potential side effect and which patients are at higher risk of it?

A
  • Norepinephrine/dopamine reuptake inhibitor (amphetamine-like effect)
  • Seizures→eating disorders (anorexia and bulimia nervosa), previous seizure disorders►contraindicated

*No sexual dysfunction or weight gain

156
Q

Potential consequence of use ACEI and ARBs during pregnancy, why?

A
  • Fetal low angiotensin II→fetal renal maldevelopment (required for normal renal development)►↓diuresis→oligohydramnios→pulmonary hypoplasia, skeletal defects (limb deformities)
  • ↓AgII→impaired cranial vascularization→hypocalvaria (hypoplasia of skull bones)

*Potter sequence

157
Q

Mechanism of action of adenosine on myocardial cells and uses.

A

A1 receptor▶️⬆️K+ out of cells▶️hyperpolarization and ⬇️ICa▶️transient conduction delay at AV node⏩Dx/terminating certain forms of SVT

158
Q

Anticonvulsivants associated with Steven-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN)

A

Lamotrigine
Carbamazepine
Phenobarbital
Phenytoin

159
Q

Mechanism of action of cromolyn and negocio mil (cromoglycate) and indication

A
  • 🚫Mast cell degranulation▶️❌release of preformed inflammatory mediators
  • Do not influence bronchial constriction directly, used to prevent acute attacks of asthma

*Good prophylaxis for exercise induced attack, aspirin hypersensitivity, seasonal symptoms

160
Q

Mechanism of action of Triptans. For what are they used?

A
  • Serotonin 5HT1B/5HT1D agonist→↓release of vasoactive peptides (substance P, calcitonin gene-related peptide [CGRP] - vasodilation, plasma protein extravasation►neurogenic inflammation)→vasoconstriction, block pain pathways in brainstem
  • Abortive therapy for the outpatient acute migraines
161
Q

Why are the selective COX-2 inhibitors associated with increased risk of cardiovascular events?

A

COX-2 in vascular endothelial cells and vascular smooth cells→prostacyclin synthesis→anticoagulant and vasodilatory
- Selective COX-2 inhibitors→↓Prostacyclin

162
Q

Treatment of serotonin syndrome

A
  • Supportive→airway maintenance, hydration, temperature maintenance
  • Cyproheptadine→1st generation histamine antagonist with nonspecific 5HT1, 5HT2 receptor antagonist
163
Q

Why amphotericin B can cause premature ventricular beats, presented as palpitations and weakness?

A

Renal tubular dysfunction▶⬆membrane permeability of distal tubule▶hypokalemia, hypomagnesemia▶arrhythmia and weakness

*if profound hypokalemia▶ventricular tachycardia or fibrillation

164
Q

Cause of acyclovir nephrotoxicity and how can be prevented?

A
  • Acyclovir concentration in collecting duct exceeds its solubility→crystallization, crystalluria, renal tubular damage
  • Transient, prevented and treated→adequate hydration, dosage adjustment, slow rate of infusion
165
Q

Which is the only antiarrhythmic that slows the heart rate (negative chronotropic) with no effect on cardiac contractility (inotropy) and/or relaxation (lusitropy)? Mechanism of action.

A
  • Ivabradine→inhibition of funny sodium channels (If)→slows the rate of sinoatrial node firing►prolong the slow depolarization phase (phase 4)
166
Q

Why do thiazolidinediones cause water weight gain, peripheral edema and adipose weight gain?

A
  • ↑Na reabsorption in renal collecting ducts→may decompensate congestive heart failure
  • ↑Storgae in adipocytes and ↑number of adipocytes
167
Q

Major side effect of nondihydropyridine CCB

A

Constipation

Verapamil, Diltiazem, also bradycardia, AV block (negative chronotropy), worse HF (negative inotropic)

168
Q

Major side effect and mechanism of action of Vincristine.

A
  • Neurotoxicity→peripheral neuropathy►disruption of neuronal microtubules
  • Inhibit microtubule formation on M phase of cell cycle→replicated chromosomes are unable to align and segregate into the daughter cells
169
Q

What is the difference between glyburide and glimeperide vs glipizide?

A

All are second generation sulfonylurea

  • Glyburide and glimepiride→long acting►higher incidence of hypoglycemia
  • Glipizide→short acting►lower incidence of hypoglycemia
170
Q

What is the rinitis medicamentosa and why may it occur?

A

Rebound rinorrhea (no cough, sneezing or postnasal drip)→tachyphylaxis by topical alpha-adrenergic agonists descongestants (>3 days of use)→negative feedback in norepinephrine synthesis and release→remove normal vasoconstrictive tone

*Similar effect with Nitroglycerine

171
Q

Special indications of use class IB antiarrhythmics. Which are they?

A
  • Acute ventricular arrhythmias (specially post-MI), digitalis-induced arrhythmias
  • Lidocaine, Mexiletine
  • Phenytoin also fall in this category
172
Q

What properties of penicillins allow them to inhibit the transpeptidase?

A

Structurally similar to D-alanine-D-alanine→bind convalently to the active site of transpeptidase

*Transpeptidase→final cross-linking step in peptidoglycan cell wall formation→joining of amino acid in third position of a peptidoglycan molecule to the terminal D-alanine D-alanine of another peptidoglycan molecule

173
Q

Which is the main difference between dihydripyridine and non-dihydropyridine calcium channel blockers?

A
  • Dihydropyridine (amlodipine, clevidipine, nicardipine, etc)→act on vascular smooth muscle►vasodilator
  • Non-dihydropyridine (verapamil, diltiazem)→act on heart►↓muscle contractility, ↓conduction velocity. Rate control in atrial fibrilation
174
Q

What would be the effect to take cimetidine and warfarine simultaneously? Why?

A

Cimetidine potent (-) cytochrome P450→↓warfarin metabolism►↑↑warfarin blood levels→↑effects or toxic→risk of bleeding

175
Q

Major adverse effect of clozapine

A

Neutropenia and potential life-threatening agranulocytosis

176
Q

Why aromatase inhibitors may work for treatment of breast cancer? in which case?

A
  • Breast cancer Estrogen receptor (+)
  • Anastrazole, letrozole, exemestane→↓synthesis of estrogen from androgens→↓estrogen in postmenopausal►slow progression of ER (+) tumors

*Less effective as monotherapy in premenopausal→ovarian aromatase is upregulated by gonadotropins

177
Q

How can be accomplished the resistance to isoniazid by mycobacterium tuberculosis?

A
  • Non-expression of catalase peroxidase (needed to activate INH)
  • Mutation of INH binding site on mycolic acid synthesis enzyme (target of INH)
178
Q

Uses of Vemurafenib. Mechanism of action.

A
  • BRAF V600E (+) Melanoma

- Inibitor of mutated BRAF→↑activation on the signaling pathways for melanocyte growth, survival and metastasis

179
Q

Why do phenytoin cause gingival hyperplasia?

A

↑Platelet-derived growth factor (PDGF)→Gingival macrophages (+) proliferation of gingival cells and alveolar bone

*Regress after discontinuation

180
Q

For what you can give aspirin previously to Niacin?

A

Avoid flushing, warmth, itching→mediated by release of prostaglandins (PGD2, PGE2)

181
Q

Mechanism of action of niacin.

A
  • Inhibit lipolysis (hormone sensitive lipase) in adipose tissue
  • ↓Hepatic TG syntesis→↓VLDL (subsequently metabolized to LDL in circulation)→↓LDL
  • Most effective ↑HDL (Reduce the clearance)
182
Q

Which are the PCSK9 inhibitors and mechanism of action?

A
  • Proprotein convertase subtilisin kexin 9 (PCSK9)→↑degradation of LDL receptors
  • PCSK9 inhibitor→monoclonal antibody (alirocumab, evolocumab)→↑availability of LDL receptor on hepatocyte→↑clearance of LDL from blood
183
Q

What could happen if patient take together cyclosporine and grapefruit juice?

A

Grapefruit juice (furocoumarins)→inhibit liver and GI tract cytochrome P450 (CYP3A isoenzymes)►metabolizes cyclosporine→↑levels►dose dependent renal vasoconstriction and tubular cell damage→acute renal failure→Nephrotoxicity (↑creatinine), hypertension

184
Q

Which laboratory finding may suggest digitalis toxicity? Clinical presentation.

A
  • Block Na-K-ATPase→↑extracellular K→Hyperkalemia
  • Cardiac arrhytmias→bradycardia, junctional scape beats (↑AV nodal block)
  • GI→Nausea, abdominal pain, vomiting
  • Neurologic→fatigue, confusion, weakness, color vision alteration
185
Q

Mechanism of rate lowering effect of digoxin.

A

↑Parasympathetic tone→(-) AV nodal conduction

  • Block Na/K ATPase pump:
  • In vagal afferent fibers→sensitizes arterial baroreceptors, cardiac receptors→↑afferent input from CV system to brain
  • ↑Efferent parasympathetic ganglionic transmission
  • Potentiate end organ responde to Ach→↑vagal output
186
Q

Mechanism of action and uses of Sirolimus

A

mTOR inhibitor
Binds FKBP (FK506 binding protein)
- Block T cell activation and B cell differentiation by preventing reponse to IL-2

187
Q

What means an increased or decreased arteriovenous concentration gradient of a gas anesthetic?

A

Reflects the overall solubility of an anesthetic→rate of of induction

  • High solubility→large amount of anesthetic is taken from arterial blood, low venous concentration►large AV gradient→slow onset of action
  • Low solubility→less peripheral uptake►small AV gradient (blood saturation is rapid)→fast onset of action
188
Q

Why do Fibrates can predispose the formation of cholesterol gallstones?

A

Inhibition of cholesterol 7 alpha hydroxylase→rate limiting step in synthesis of bile acids→↓cholesterol solubility

189
Q

Side effects of Niacin

A
  • Flushing, hyperglycemia, hepatotoxicity

- ↓Renal excretion of uric acid→↑risk for acute gouty arthritis

190
Q

How do you distinguish side effects by amiodarone and digoxin if both cause vague symptoms, arrhythmias and color visions alterations?

A

Hyperkalemia is sign of digoxin toxicity (Na/K ATPase pump inhibition)

*Amiodarone doesn’t cause hyperkalemia

191
Q

What is the anti-PD1 therapy and its uses?

A
  • Monoclonal antibody against PD1→block inhibition of T-lymphocyte by tumor cells►restore cytotoxic T cell response→promote apoptosis of tumor cells
  • Melanoma, some types of lung cancer
    +Nivolumab

*PD1 (programmed death receptor 1) of cytotoxic T-lymphocyte binds to PD1L (PD1 ligand) of tumor cells (↑ in tumor cells)►Inhibition of T-lymphocytes (similar to CTLA4)→evasion of immune system

192
Q

Mechanism of tricyclic antidepressant overdose that can cause death

A
  • Cardiac fast sodium channel inhibition (myocytes and His-Purkinje system)→arrhythmias
  • Refractory hypotension→↓cardiac contractility and direct peripheral vasodilation (alpha-1 antagonist)
193
Q

Mechanism of action of hydroxyurea to treat sickle cell disease

A

↑ Fetal Hemoglobin (HbF) (incompletely understood mechanism)→protection against polymerization of sickle cells

*Originally to treat neoplasia

194
Q

Mechanism of Gardos channel blocker to treat sickle cell disease

A

Calcium-dependent (Gardos) potassium channel→efflux of K and H2O from RBC→block it to ↓efflux and avoid dehydration→↓polymerization of HbS

195
Q

Treatment of tricyclic antidepressant overdose and when do you use it?

A
  • Sodium bicarbonate:
  • ↑serum pH→non-ionized (neutral) form of drug→less accesible to bind Na channel
  • ↑Na→overcome the competitive, rapid Na channel blockade
  • Widened QRS interval or ventricular arrhythmias
196
Q

Which organisms based in their structure can be resistant to antibiotics that inhibit peptidoglycan cell wall synthesis? What antibiotics can be used to kill them?

A
  • Mycoplasma, Ureaplasma urealyticum→lack peptidoglycan cell wall
  • Anti-ribosomal agents (tetracycline, macrolides)
197
Q

Mechanism of action of Ramelteon and its uses?

A
  • Melatonin agonist→high affinity binding to melatonin receptors in suprachiasmatic nucleus
  • Insomnia treatment in elderly patients (few side effects)

*Avoid benzo, antihistamines, sedating antidepressants in Tx insomnia in elderly

198
Q

How can be induced apoptosis in malignant plasma cells of multiple myeloma?

A

Bortezomib (boronic acid containing dipeptide)→proteasome inhibitor►accumulation of toxic intracellular proteins, excess of proapoptotic proteins►Apoptosis

199
Q

In which situation does Buprenorphine precipitate opioid withdrawal?

A
  • Partial opioid agonist with low intrinsic activity (efficacy) for opioid mu receptors
  • Binds with high affinity (potency)→prevent binding or displaces other opioids►opioid receptor antagonist in the presence of full opioid agonists
200
Q

What is the coronary steal phenomenon and which drugs can cause it? Uses of it.

A
  • Blood flow in ischemic areas is reduced due arteriolar dilation in nonischemic areas→hypoperfusion, worsening of existing ischemia
  • Adenosin, Dipyridamole→selective vasodilators of coronary vessels►used in myocardial perfusion studies→detection of ischemic areas
201
Q

What drug is used to avoid reccurent calcium oxalate urinary stones formation and which is its mechanism for it?

A
  • Tiazide diuretics (ex, Hydrochlorotiazide)→↓urinary calcium excretion, ↑calcium absorption:
  • Block Na/Cl cotransporter at DCT→↓Na absorption→(+) basolateral Na/Ca antiporter→out Ca, in Na►↑Ca luminal reabsorption
  • Hypovolemia induced→↑Na and H2O absoprtion at PT!→passive ↑paracellular Ca reabsorption

**Indication→Hypercalciuria, Contraindicated→hypercalcemia

202
Q

Use and mechanism of action of Fomepizole.

A
  • Methanol or ethylene glycol poisoning

- Inhibits alcohol dehydrogenase→Ex, methanol poisoning►block methanol→Formaldehyde (toxic)

203
Q

Which property must have a substance or drug to cross the placenta?

A
  • Hydrophilic→Don’t cross the placenta (Ex, conjugated bilirrubin, fractionated and no fractionated heparin)
  • Lipophilic→Cross the placenta (Ex, unconjugated bilirrubin, warfarin)

USMLE Step 1 Flash Cards (9 decks)

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