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(Other) 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
What are the SEs of loop diuretics?
Hypokalemia, hypomagnesemia, hypocalcemia, ototoxicity
26
What is dofetilide?
Class III anti-arrhythmic
27
What are the class III anti-arrhythmic?
Amiodarone, sotalol, dofetilide; K channel blockers
28
What are the SEs of protease inhibitors?
Hyperglycemia, lipodystrophy, and drug-drug interactions due ti inhibition of cytochrome P450
29
What anti-emetic is helpful when the emetogenic stimulus is due to GI irritation?
5-HT3 receptor antagonists
30
Gastrointestinal irritation causes the release of what that can lead to nausea/emesis?
Mucosal serotonin release
31
What is the MOA of ethosuxamide?
Blocks T type Ca++ channels that trigger and sustain rhythmical burst discharges in thalamic neurons
32
What is the MOA of phenytoin?
Blocks Na channels (decreases sodium current in cortical neurons) - increasing refractory period of the neuron (Carbamazepine and valproic acid are similar)
33
What is the MOA of valproic acid?
Blocks NMDA receptors, affects GABA receptors, K and Na channels as well
34
What is the MOA of bupropion?
Inhibits the reuptake of NE and DA
35
Bupropion causes increased risk for what at high doses?
Seizure
36
Bupropion is contraindicated in patients with what disorders?
Seizure disorders, anorexia, and bulimia nervosa
37
What is the MOA of dobutamine?
Beta-1 adrenergic agonist (and minimal beta 2 and alpha 1 receptors)
38
What is the MOA of trastuzumab?
Mab that binds to a portion of the extracellular domain of HER2 and prevents activation of transmembrane tyrosine kinase
39
Human epidermal growth factor receptor 2 is what type of receptor?
Tyrosine kinase receptor that is overexpressed
40
In organophosphate poisoning, atropin reverses everything except what? Why?
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
What is the MOA os colchicine?
Inhibits microtubular polymerization (binds tubulin); disrupts cytoskeletal-dependent functions such as chemotaxis, phagocytosis and degranulation
42
How is potency related to minimum alveolar concentration?
Potency is inversely proportional to Minimum alveolar concentration: the lower the MAC, the more potent the anesthetic
43
Minimum alveolar concentration is dependent on what factors?
Body temp and MAC decreases with increasing patient age
44
How does entanercept reduce the biological activity of TNF-alpha?
Acts as a decoy receptor; links a soluble TNF-alpha receptor to the Fc component of human IgG1
45
What is akathisia?
Subjective restlessness with inability to sit still
46
When does akathisia present?
Typically days to weeks after initiating antipsychotic treatment
47
What enzyme inactivates 6-mercaptopurine?
Xanthine oxidase
48
6-mercaptopurine requires activation from what enzyme?
Hypoxanthine-guanine phosphoribosyl transferase
49
What cyp enzyme is inhibited by erythromycin?
P450 3A4
50
Tamoxifen requires activation by what? What is its active metabolite?
CYP2D; endoxifen
51
What does a high arteriovenous concentration gradient of a gas anesthetic mean?
High tissue solubility; blood saturation requires more anesthetic and therefore brain saturation is delayed and onset of action is slower

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