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Drugs Flashcards

1
Q

Drug that exacerbates hypoglycemia and masks its adrenergic symptoms

A

beta-blockers

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2
Q

What reflects affinity of enzymes for substrates?

A

Km
cannot be altered by enzyme or substrate concentration
independent of Vmax

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3
Q

What reflects enzyme concentration

A

Vmax
can be changed by enzyme concentration
independent of Km

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4
Q

How long does it take for a drug eliminated by first-order kinetics to achieve a 95% steady state concentration?

A 
4 to 5 half lives
zero half-life = 0% elim
1 half-life = 50% elim
2 half-life = 75% elim
3 half-life = 87.5% elim
4 half-life = 93.75% elim
5 half life = 96.875% elim
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5
Q

List high blood flow organs.

Will lipophilic drugs be rapidly or slowly distributed to these organs?

A

Brain, liver, kidneys, lungs

Rapidly

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6
Q

List low blood flow organs.

Will lipophilic drugs be rapidly or slowly distributed to these organs?

A

Skeletal mm, fat, bone

Slowly

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7
Q

What does each part of Medicare cover? (A-D)

A

A - inpatient care, SNFs, hospice, homehealth
B - Physician services, labs, tests, preventive, therapies, select prescription drugs
C - All benefits and services under A and B, HMO, PPO, PFFS
D - outpatient prescription drugs

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8
Q

What drugs can cause serum sickness?
Type of HS rxn?
Sx?

A

cephalosporin (esp cefaclor), penicillin, trimethoprim-sulfamethoxazole, vaccines, antitoxins, tetracyclines, cipro.
Type III HS rxn
Sx - rash, fever, polyarthralgias or polyarthritis

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9
Q

What characteristics of a drug tend to trap the drug in the plasma compartment resulting in a low Volume Distribution (eg Vd = 3-5L)

A

High molecular weight
High plasma protein binding
High charge
Hydrophilicity

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10
Q

What characteristics of a drug tend to resulting in a high Volume Distribution (eg Vd = 41L)?

A

Low molecular weight
Avidly bind tissues
Does not bind albumin
Lipophilic

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11
Q

Antipsychotic side effect: subjective restlessness with inability to sit still

A

akathisia

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12
Q

Antipsychotic side effect: tremor, rigidity, bradykinesia, masked facies

A

Drug-induced parkinsonism

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13
Q

Antipsychotic side effect: sudden-onset, sustained mm contractions

A

Acute dystonic reaction

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14
Q

Antipsychotic side effect: involuntary movements (eg lip smacking, choreoathetoid movements)

A

Tardive dyskinesia

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15
Q

Antipsychotic side effect: fever, rigidity, mental status changes, autonomic instability

A

NMS

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16
Q

Fraction of administered drug that reaches the systemic circulation in a chemically unchanged form
IV vs oral?

A

Bioavailability (F)
IV (F=1)
Oral (F<1)
F = (area under oral curve x IV dose)/(area under IV curve x oral dose)

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17
Q

[substrate] at 1/2 Vmax

A

Km

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18
Q

How do K wasting drugs (loop diuretics, thiazides) contribute to digoxin toxicity?

A

Hypokalemia allows digoxin to inhibit the Na+-K+ ATPase more effectively

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19
Q

Hepatic necrosis with marked elevations of AST and ALT without concomitant elevation of alk phos or amylase is caused by OD of what?

A

Acetaminophen

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20
Q

What receptor results in influx of Ca, Na, and K outflux after binding?

A

Nicotinic receptors. Ach binds, then opens these ligand-gated ion channels.

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21
Q

Half life: how long will it take for a drug to reach 87.5% of final steady state level?

A

1 half-life = 50%
2 half lives = 75%
3 half lives = 87.5%
4 half lives = 93.75%

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22
Q

Why doesnt morphine provide good pain relief if used after buprenorphine?

A

Buprenorphene = partial agonist; long half life.
Morphine = full agonist
Partial agonist prevents full agonist from exerting full effects.

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23
Q

What is Trimethaphan and hexamethonium’s MOA?

A

Ganglionic blocker that blocks baroreceptor-mediated changes in HR

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24
Q

Dihydroergotamine is what kind of drug? Why is it contraindicated in Raynaud?

A

Ergot alkaloid used for migraines

Causes intense vasoconstriction so contraindicated

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25
Q

What type of anesthetics are prone to cause allergic reactions?

A

Ester-type (eg tetracaine) bc they are metabolized to para-aminobenzoic acid derivatives.
Note: Amide-type anesthetics are not metabolized to these derivatives and are less likely to cause reactions

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26
Q

What intracellular organelle has increased activity if a patient ODs on drugs?

A

Smooth ER - involved in detoxification of drugs and other toxic substances

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27
Q

How does quinidine cause digoxin toxicity if administered together?

A

Decreases clearance of digoxin –> inc serum digoxin levels

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28
Q

What is the risk of taking BB and non-dihydropyridine type Ca channel blockers together?

A

Both have additive neg effects on HR –> sinus bradycardia

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29
Q

Co-admin of what drugs can cause theophylline toxicity?

A

Theophylline is metabolized by hepatic cytochrome oxidases.

Illness, cimetidine, ciprofloxacin, macrolides, verapamil can inc serum conc

30
Q

Baclofen MOA?

A

agonist at GABA-B receptor - effective for tx of spasticity secondary to both brain and spinal cord disease (eg MS)

31
Q

Define potency of an inhaled anesthetic?

A

determined by the minimum conc in the brain to achieve an adequate level of anesthesia.
Potency is inversely proportional to the Minimal alveolar conc (MAC)

32
Q

Minimal alveolar concentration definition?

A

% of anesthetic in the inspired gas mixture that renders 50% of patients unresponse to stimuli.

33
Q

What CHF drug slows HR and has no effect on cardiac contractility and/or relaxation ? MOA?

A

Ivabradine
Slows rate of SA node firing by selective inhibition of funny sodium channels (If), prolonging the slow depol phase (phase 4)

34
Q

When one hormone allows another to exert its maximal effect. (eg cortisol improves response of NE, but has no direct vasoactive properties of its own)

A

permissiveness

35
Q

Patient on amphotericin B with premature atrial and ventricular contractions is due to what?

A

Renal tubular dysfunction due to amphotericin B nephrotoxicity. Hypokalemia and hypomagnesemia seen. HypoK causes U waves, premature atrial and ventricular contractions

36
Q

Ptosis seen in Graves disease cannot be improved with conventional antithyroid drugs. What drug can decrease the extraocular volume?

A

high dose glucocorticoids since inflammatory infiltration and accumulation of GAGs are responsible

37
Q

How do PPIs reduce histamine, vagal stimulation, and gastrin?

A

PPIs block H+/K+-ATPase proton pump, which is the final common pathway for HCL secretion (stim by Ach, histamine and gastrin)

38
Q

MOA of topical capsaicin for postherpetic neuralgia?

A

Defunctionalizes afferent pain fibers and depletes SUBSTANCE P.

39
Q

Neuropeptide Y plays a role in what, and may be found in what type of drugs?

A

Appetite and pain perception

Antiobesity drugs

40
Q

Endorphins and dynorphins have what function?

A

Help with pain relief by activating u-opioid (endorphins) and k-opioid (dynorphins) receptors.

41
Q

The human multidrug resistance gene codes for what? How does it function and what does it do?

A

P-glycoprotein
Transmembrane ATP-dependent efflux pump w/broad specificity for hydrophobic compounds.
Reduces influx of drugs into the cytosol and increases efflux from the cytosol –> prevent chemo drugs from working

42
Q

MOA of gabapentin vs levetiracetam

A

Anticonvulsants
Gabapentin - inhibits presynaptic voltage-gated Ca channels (prevents fusion and release of NT)
Levetiracetam - disrupts vesicle fusion

43
Q

What processes results in a bimodal distribution of the speed of isoniazid metabolism

A

Acetylation - isoniazid is metabolized by acetylation.

Some people are fast vs slow acetylators

44
Q

Halogenated inhaled anesthetics (eg halothane, desflurane) has a complication of what?

A

metabolized by hepatic cyt P450 –> hepatocellular damage (HALOTHANE HEPATITIS)
Present with acute hepatitis days after exposure. Liver bx shows centrilobular hepatic necrosis

45
Q

What diuretic, if given aggresively, can cause pulmonary edema?

A 
Osmotic diuretics (eg mannitol)  
Use cautiously in high-risk patients (eg CHF or preexisting pulm edema)
46
Q

MOA of rasburicase in patients with cancer?

A

Protects organs from rapid lysis of neoplastic cells by converting uric acid into more soluble metabolites (DEGRADES URIC ACID)
Note: allopurinol inhibits uric acid formation

47
Q

Where do BB act?

A

Inhibit the neurotransmitter-receptor interaction in adrenergic synapses

48
Q

Corticosteroids do what to:

neutrophils, lymphocytes, monocytes, basophils and eosinophils

A

Decreases all except neutrophils

Inc neutrophils due to demargination of neutrophils previously attached to the vessel wall

49
Q

Opioid peptides are derived from what? This can be a precursor to what other proteins?

A

POMC - precursor to beta-endorphins (opioid), ACTH, and MSH

50
Q

Intracellular signaling of sildenafil is similar to what other substance?

A

BNP, ANP, NO
Activate guanylyl cyclase and inc conversion of GTP to cGMP
Sildenafil dec degradation of cGMP. Inc cGMP –> inc relaxation of vascular smooth mm

51
Q

What characteristic of drugs allow them to be preferentially processed by the liver into more polar compounds?

A

High Vd, Good penetration into CNS = high lipophilicity

52
Q

What drugs target an enzyme that is IL-1 inducible that is highly expressed by inflammatory cells and undetectable in surrounding normal tissue?

A

COX-2 inhibitors (eg celecoxib)

53
Q

Nitroprusside toxicity can result in what? Tx?

A

Cyanide toxicity - altered mental status, seizures, CV collapse, lactic acidosis, bight red venous blood
Tx -
Detoxifying sulfur donors (eg sodium thiosulfate)
Direct binding of cyanide (hydrocobalamin)
induction of methemoglobinemia (sodium nitrite)

54
Q

Patients who have OD’d on BB should be treated with what? MOA?

A

Glucagon

Activates G-protein-coupled receptors –> Increases cAMP in cardiac myocytes (inc HR and contractility)

55
Q

Drug metabolism:

  1. Dec activity of hepatic N-acetyltransferase results in what?
  2. Def in Thiopurine methyltransferase results in what?
  3. Polymorphisms of cyt p450 causes what?
A
  1. Diminished ability to metabolize drugs (eg isoniazide and sulfonamides)
  2. Inc drug toxicity of 6-MP
  3. Cyp p450 in the liver is responsible for the majority of drug metabolism. Polymorphisms results in diff phenotypes that differ in rates of metabolism. Alters tx efficacy and drug toxicity
56
Q

What are the major cause of morbidity and mortality from theophylline intoxication?

A

Seizures

Tachyarrhythmias are another major concern

57
Q

What intracellular event is responsible for the beneficial effects of nitroglycerin?

A

Myosin dephosphorylation

Nitrates –> NO –> activate GC –> inc cGMP –> myosin light-chain dephosphorylation –> vascular smooth mm relaxation

58
Q

Differentiate efficacy vs potency

A

Efficacy: intrinsic ability of a drug to elicit an effect (measures max ceiling of activity)
Potency: dose of drug required to produce a given effect (affected by drug affinity for its receptor and amt of drug able to reach target tissues).

59
Q

Why should all patients beginning treated with TNF-a inhibitors be evaluated for latent Tb?

A

TNF-a inhibitors (eg etanercept, infliximab, adalimumab)
impairs cell-mediated immunity.
TNF-a is necessary for effective sequestration of mycobacteria within granulomas.

60
Q

Medication that inhibits neprilysin (metalloprotease) does what?

A

Prevents inactivation of bradykinin, glucagon, enkephalins, and natriuretic peptides

61
Q

Drug that destroys an inflammatory mediator produced by macrophages

A

Infliximab - TNF a inhibitor

Note: prone to Tb reactivation bc TNFa is needed for macrophages

62
Q

What causes an obese patient to have a lower steady state plasma concentration of a drug initially compared to a patient with normal BMI.

A

Greater volume distribution

63
Q

What is a known side effect of nitric oxide overdose?

A

Methemoglobinemia

64
Q

MOA of orlistat?

A

Weight loss drug
Orlistat works by inhibiting gastric and pancreatic lipases, the enzymes that break down triglycerides in the intestine. When lipase activity is blocked, triglycerides from the diet are not hydrolyzed into absorbable free fatty acids, and instead are excreted unchanged.
Decreases total cholesterol, inc HDL, dec LDL, dec triglycerides
Note: phentermine is another weight loss drug that has MOA like amphetamine

65
Q

Why does taking Gemfibrozil after statins cause increase myalgia?

A

Gemfibrozil increased the blood concentration of most statins by partially inhibit the metabolism or glucorinidation of the statin acid byproduct.
INHIBITS CYT P450 metabolism

66
Q

Compare codeine to dextromethorphan in terms of analgesia, constipation, and abuse potential

A

Codeine

  • analgesia: increased
  • Constipation: increased
  • Abuse - increased
67
Q

How does prednisone cause increased risk of osteoporosis?

A

Inhibit osteoblast function

Enhances bone resorption due to decreased calcium absorption

68
Q

A drug that has rapid increase in plasma concentration initially, then increase slows down is due to what?

A

This drug is a rapidly redistributed drug.
At first the drug is rapidly redistributed so the plasma level falls suddenly. This is followed by normal elimination which causes the characteristic change in the slope.

69
Q

MOA of baclofen?

A

Baclophen is an agonist for the GABAB receptors. Its beneficial effects in spasticity result from actions at spinal and supraspinal site.

70
Q

MOA of neomycin?

A

Killing of bacteria in the gut that generate ammonia
Wiki: killing bacteria in the intestinal tract, it keeps ammonia levels low and prevents hepatic encephalopathy, especially prior to GI surgery

71
Q

How can chronic use of morphine result in toxicity?

A

Morphine is metabolized to active metabolites that accumulate - esp problematic in kidney disease

72
Q

What is magnesium trisilicate and what side effects can it cause?

A

Magnesium trisilicate is an inorganic compound that is used as a food additive.
It can also be used in oral pharmaceutical formulations and food products as a glidant. It is also used therapeutically as an antacid, and also for the treatment of ciprofloxacin overdose or toxic
SE: moderately severe diarrhea

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