Meds On Meds Flashcards
What is pentoxifylline used for?
This agent reduces whole blood viscosity by decreasing olasma fibrinogen and platelet aggregation.
Used as Tx of intermittent claudication (lower limb occlusive disease that is not limb threatening).
What is naloxone used for?
This mu-receptor (opiod receptor) competitive ANTAGONIST with a rapid onset of action is used to treat an opiate overdose.
What is metoclopramide?
This is a dopamine antagonist that has gatric motility promoting properties.
Specifically, it lowers esophageal contraction and enhances gastric emptying.
What is Senna?
Senna glycosides are laxatives that acts by irritating the colon, leading to a laxative/mild diarrheal state.
Abuse can lead to melanosis coli.
Which antibiotic can act as a GI promotilytic agent?
Erythromycin - binds MOTILIN receptors in the gut.
What is the mechanism of action of aspirin (acetylsalicylic acid)?
Aspirin’s ability to suppress the production of prostaglandins and thromboxanes is due to its IRREVERSIBLE INACTIVATION/INHIBITION of the cyclooxygenase (COX; officially known as prostaglandin-endoperoxide synthase, PTGS) enzyme required for prostaglandin and thromboxane synthesis. Aspirin acts as an acetylating agent where an acetyl group is COVALENTLY attached to a serine residue in the active site of the PTGS enzyme. This makes aspirin different from other NSAIDs (such as diclofenac and ibuprofen), which are reversible inhibitors. Since platelets have no DNA, they are unable to synthesize new PTGS once aspirin has irreversibly inhibited the enzyme, an important difference with reversible inhibitors.
Low-dose, long-term aspirin use irreversibly blocks the formation of thromboxane A2 in platelets, producing an inhibitory effect on platelet aggregation. This antithrombotic property makes aspirin useful for reducing the incidence of heart attacks.
Which common OTC non-opiate analgesic is NOT an NSAID?
Acetaminophen (aka paracetamol) (Tylenol)
What is the mechanism by which nitric oxide (NO) vasodilates vessels?
NO stimulates the soluble form of the enzyme guanylate cyclase in the smooth muscle cells of blood vessels.
Guanylate cyclase produces cyclic guanosine monophosphate (cGMP) from guanosine triphosphate (GTP).
cGMP in turn activates cyclic nucleotide-dependent protein kinase G, which phosphorylates various proteins that play a role in DECREASING INTRACELLULAR CALCIUM levels, leading to relaxation of the muscle cells and thus to dilation of blood vessels.
(recall, muscle contraction is dependent on influx/presence of calcium in the myocyte cytoplasm).
