Other Drugs Flashcards

1
Q

Pyrantel pamoate

A

Neuromuscular blocking agent. Prolongs nicotine receptor activation resulting in paralysis. Anti-parasitic.

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2
Q

Ivermectin

A

Hyperpolarises cell membranes via glutamate gated chloride channels. Can’t cross BBB

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3
Q

Albendazole/Mebendazole

A

inhibition of tubulin polymerisation that leads to impaired glucose uptake.

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4
Q

QT prolonging antibiotics

A

Erythromycin, Clarithromycin, Cotrim

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5
Q

QT prolonging antipsychotics

A

Handover, TCAs, Fluoxetine

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6
Q

Anti arrhythmics contraindicated in Long QT syndrome

A

Quinine. Flecainide, Amiodarone, Sotalol

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7
Q

Cisapride

A

Motility stimulant, selective ACH release at level of myenteric plexus (gastroparesis, gord), results in increase esophageal peristalsis, LES pressure

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8
Q

How do opioid work in tet spells?

A

Reduced respiratory drive and reduced hyperpnoea and tachycardia to improve pulmonary blood flow and reduce O2 demand

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9
Q

What is cholestyramine?

A

Cholestyramine is the chloride salt of a basic anion exchange resin that combines with bile acids in the intestine to form an insoluble complex excreted in feces.

It results in continuous removal of bile acids from the enterohepatic circulation, leading to increased oxidation of cholesterol to bile acids and lowering LDL and serum cholesterol.

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10
Q

What is the mechanism of action of clofibrate?

A

Clofibrate is a fibric acid derivative that activates lipoprotein lipase to promote the conversion of VLDL to LDL, increasing lipolysis and clearance of triglyceride-rich particles.

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11
Q

What is colestipol?

A

Colestipol is an insoluble, high molecular weight basic anion exchange copolymer with the same mechanism of action as cholestyramine.

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12
Q

What is nicotinic acid?

A

Nicotinic acid, also known as niacin (B3), is used for the treatment of pellagra and can lower levels of lipids in large doses.

The exact mechanism is not specified.

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13
Q

What is the mechanism of action of simvastatin?

A

Simvastatin inhibits coenzyme A (HMG-CoA) reductase, the rate-limiting step in cholesterol biosynthesis, decreasing VLDL-C concentration and inducing LDL receptors, resulting in decreased production and increased catabolism of LDL-C.

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