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2024 - Élo - Qbank > Pharmacology Qbank > Flashcards

Pharmacology Qbank Flashcards

1
Q

How many half lives does it take to eliminate 75% of a drug?

A

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2
Q

How many half lives does it take to eliminate 50% of a drug?

A

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3
Q

How many half lives does it take to eliminate 87.5% of a drug?

A

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4
Q

What is chlordiazepoxide?

A

Long acting benzo

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5
Q

What benzos are preferred in the majority of patients with alcohol withdrawal due to the tappering effects?

A

Long acting with active metabolites; eg diazepam, chlordiazepoxide

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6
Q

In patients with liver disease and alcohol withdrawal, what drugs are the preferred choice of treatment?

A

Benzos that do not undergo oxidative metabolism in the liver and have no active metabolits (eg lorazepam, oxazepam, temazepam “LOT”)

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7
Q

What drug is added to malaria treatment to eradicate hypnozoites and therefore relapses?

A

Primaquine

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8
Q

Where are drugs with high lipohphilicity excreted? Why?

A

Liver; lipid solubility increases its tubular resorption after filtration (ie not eliminated in kidneys), also allows to cross membranes of hepatocytes

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9
Q

Drugs with high intrinsic hepatic clearance tend to have what characteristics?

A

High lipophilicity and a high volume of distribution

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10
Q

What effect does cholestyramine have on triglycerides?

A

Can cause hypertriglyceridemia

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11
Q

What is the MOA of cholestyramine?

A

Bile acid-binding resin; binds bile acids in GI, resulting in increased hepatic synthesis of bile acids (which need chol), therefore reducing LDL levels

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12
Q

What effect does niacin have on blood lipid levels?

A

Reduces TGs, increases HDL, decreases VLDL conversion to LDL (decreasing LDL)

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13
Q

What is the MOA of meglitinides?

A

Bind to and close ATP-dependent K channels, inducing depolarization and calcium channel opening; results in insulin release

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14
Q

What is the MOA of metformin?

A

Stimulates AMPK, decreasing glucose production and insulin resistance

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15
Q

What is the MOA of thiazolidinediones?

A

Activates transcription regulator PPAR-gamma, decreasing insulin resistance

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16
Q

What are the DPP4 inhibitors?

A

Sitaglitptin, saxagliptin

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17
Q

What is the MOA of sitagliptin?

A

Inhibits DPP4, increasing endogenous GLP-1 and GIP levels

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18
Q

What is a SE of DPP4 inhibitors?

A

Nasopharyngitis

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19
Q

What is the MOA of nystatin?

A

Binds to ergosterol in fungal cell membrane, causing the formation of pores and leakage of fungal cell contents

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20
Q

What is indapamide?

A

Thiazide diuretic

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21
Q

What is metalozone?

A

Thiazide diuretic

22
Q

What are the thiazide diuretics?

A

HCTZ, chlorthalidone, metalozone, indapamide

23
Q

What are the SEs of thiazide diuretics?

A

Hypokalemia, hyponatremia, hyperuricemia, and hypercalcemia

24
Q

What acid/base disorder is caused by acetazolamide?

A

Metabolic acidosis

25
Q

What are the SEs of loop diuretics?

A

Hypokalemia, hypomagnesemia, hypocalcemia, ototoxicity

26
Q

What is dofetilide?

A

Class III anti-arrhythmic

27
Q

What are the class III anti-arrhythmic?

A

Amiodarone, sotalol, dofetilide; K channel blockers

28
Q

What are the SEs of protease inhibitors?

A

Hyperglycemia, lipodystrophy, and drug-drug interactions due ti inhibition of cytochrome P450

29
Q

What anti-emetic is helpful when the emetogenic stimulus is due to GI irritation?

A

5-HT3 receptor antagonists

30
Q

Gastrointestinal irritation causes the release of what that can lead to nausea/emesis?

A

Mucosal serotonin release

31
Q

What is the MOA of ethosuxamide?

A

Blocks T type Ca++ channels that trigger and sustain rhythmical burst discharges in thalamic neurons

32
Q

What is the MOA of phenytoin?

A

Blocks Na channels (decreases sodium current in cortical neurons) - increasing refractory period of the neuron
(Carbamazepine and valproic acid are similar)

33
Q

What is the MOA of valproic acid?

A

Blocks NMDA receptors, affects GABA receptors, K and Na channels as well

34
Q

What is the MOA of bupropion?

A

Inhibits the reuptake of NE and DA

35
Q

Bupropion causes increased risk for what at high doses?

A

Seizure

36
Q

Bupropion is contraindicated in patients with what disorders?

A

Seizure disorders, anorexia, and bulimia nervosa

37
Q

What is the MOA of dobutamine?

A

Beta-1 adrenergic agonist (and minimal beta 2 and alpha 1 receptors)

38
Q

What is the MOA of trastuzumab?

A

Mab that binds to a portion of the extracellular domain of HER2 and prevents activation of transmembrane tyrosine kinase

39
Q

Human epidermal growth factor receptor 2 is what type of receptor?

A

Tyrosine kinase receptor that is overexpressed

40
Q

In organophosphate poisoning, atropin reverses everything except what? Why?

A

Paralysis; atropine reverses muscarinic effects but does not prevent the development of nicotinic effects such as muscle paralysis (pralidoxime can reverse both nicotinic and muscarinic)

41
Q

What is the MOA os colchicine?

A

Inhibits microtubular polymerization (binds tubulin); disrupts cytoskeletal-dependent functions such as chemotaxis, phagocytosis and degranulation

42
Q

How is potency related to minimum alveolar concentration?

A

Potency is inversely proportional to Minimum alveolar concentration: the lower the MAC, the more potent the anesthetic

43
Q

Minimum alveolar concentration is dependent on what factors?

A

Body temp and MAC decreases with increasing patient age

44
Q

How does entanercept reduce the biological activity of TNF-alpha?

A

Acts as a decoy receptor; links a soluble TNF-alpha receptor to the Fc component of human IgG1

45
Q

What is akathisia?

A

Subjective restlessness with inability to sit still

46
Q

When does akathisia present?

A

Typically days to weeks after initiating antipsychotic treatment

47
Q

What enzyme inactivates 6-mercaptopurine?

A

Xanthine oxidase

48
Q

6-mercaptopurine requires activation from what enzyme?

A

Hypoxanthine-guanine phosphoribosyl transferase

49
Q

What cyp enzyme is inhibited by erythromycin?

A

P450 3A4

50
Q

Tamoxifen requires activation by what? What is its active metabolite?

A

CYP2D; endoxifen

51
Q

What does a high arteriovenous concentration gradient of a gas anesthetic mean?

A

High tissue solubility; blood saturation requires more anesthetic and therefore brain saturation is delayed and onset of action is slower

2024 - Élo - Qbank (33 decks)

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