Exam 2 Drug Classes Flashcards

1
Q

Rapid acting insulin

A

Onset: 15 min
Peak: 1 hr
Duration: 2-4 hrs
Given with food! Often used in conjunction with an intermediate or long acting insulin to give normal coverage

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2
Q

Short acting insulin

A

Onset: 30-60 min
Peak: 2-6 hrs
Duration: 3-8 hrs
Often given before meals, but can also be given for longer acting glucose control;
Used in insulin infusions, and those receiving tube feedings.

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3
Q

Intermediate acting insulin

A

Onset: 2-4 hours
Peak: 4-10 hours
Duration: 10-20 hours
Cloudy insulin, shake bottle;
Typically injected twice daily. Clear before cloudy!

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4
Q

Long acting insulin

A

Onset: 70 minutes
Duration: all day
NO PEAK;
Indicated for once a day dosing. Never mix with other insulins; often given at night.

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5
Q

Sulfonylureas

A

MOA: binding and closing the K-ATP channels in pancreatic beta cells, stimulation secretion of insulin. Increases sensitivity to insulin and reduces release of glucose in liver.
Side Effects: hypoglycemia
DO NOT TAKE DURING PREGNANCY, with alcohol, NSAIDs, tahamet, or sulfa asked antibiotics.
Suffix: -ide

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6
Q

Biguanides

A

MOA: lowers blood glucose by decreasing production of glucose in the liver. Enhances glucose uptake and utilization by muscle.
Side Effects: abdominal bloating, N/V/D, risk for acidosis with elevated creatinine, not used with elevated ALT.
Held for 48 hours post IV contrast.

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7
Q

DPP4 inhibitors

A

MOA: inhibits dipeptidyl peptidase 4, inactivating the incretin hormone. Causes increased insulin release, reduces glucagon release, decreases hepatic glucose production, slows down digestion and decreased appetite.
Side Effects: GI probs, skin reactions, pancreatitis risk, flu like symptoms.
Suffix: -gliptin

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8
Q

GLP-1 receptor agonists

A

MOA: enhances glucose dependent insulin secretion. Inhibits postprandial release of glucagon, suppresses appetite.
Side effects: GI symptoms, injection site reactions, weight loss, URTI. Black box warning for thyroid c-cell tumors. Not for use if history of pancreatitis or ESRD.
Short half life: 2.5 hours, peak 2 hours

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9
Q

SLG2 inhibitors

A

MOA: Prevents kidneys from reabsorbing glucose back into the blood. Excess glucose released in the urine.
Side Effects: increased risk for UTIs, genital mycotic infections, hypotension, fainting, dizziness.
PO, only for type 2 DM.
Suffix: -flozin

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10
Q

Glucagon

A

MOA: activates hepatic glucagon receptors, stimulates glycogenolysis and release of glucose.
check finger stick 15 minutes post admin, short half-life so may need multiple doses.

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11
Q

Centrally acting analgesic (atypical pain med)

A

MOA: binds weakly to mu receptors and inhibits reuptake of norepinephrine and serotonin
Side Effects: none major. drowsy, dizziness, GI symptoms, respiratory depression. Rarely may cause seizures when combined with CNS depressants.

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12
Q

Anti-convulsants (atypical pain meds)

A

MOA: unknown, thought to suppress neuronal firing.
Side Effects: drowsiness, dizziness, vision problems

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13
Q

NSAIDs (traditional,/non-selective COX inhibitors, and COX-2 selective NSAIDs)

A

MOA: decreases prostaglandins by blocking COX enzyme, crucial to production of prostaglandins.
Side Effects: GI upset, cardiovascular risk

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14
Q

Opioids

A

MOA: activate mu opioid receptors
HIGH alert meds; originally came from poppyseed plant in ancient Chinese culture; must fully assess pt before giving bc it does cause such a drastic RESP DEPRESSION; if less than 10/min reassess level of sedation; initial dose may cause MORE drowsiness than later doses, which is why so many OD’s occur - it takes more and more to get “drowsy”

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15
Q

Opioid Antagonist

A

antidote to reverse effects of morphine & morphine-like drugs (opioids); binds to opioid receptors but DOES NOT ACTIVATE, just clogs up; onset <2 min; inc BP and inc recurrent pain

IV/IM/Intranasal

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16
Q

Hydantoins

A

drug class used to treat seizures; works by targeting the sodium channel present throughout the nerves; activation of sodium channels results in the conduction of electrical impulses and the release of neurotransmitters, ultimately causing a seizure

17
Q

Cholinesterase inhibitors

A

Prevents the breakdown of acetylcholine (a chemical messenger that supports communication b/w nerve cells); acetylcholine is thought to worsen Alzheimer’s dementia; binds and reversibly inhibit acetylcholinesterase, the enzyme responsible for metabolizing acetylcholine in the synapse

18
Q

NMDA receptor antagonist

A

Blocks the N-Methyl-D-aspartate (NMDA) receptor, which is an excitatory amino acid receptor in the CNS