Home Drug Class Flashcards
Narcotic
Opiate derived
Action: works on the MU receptors in the brain. There are also MU receptors in the abdominal.
Analgesic
for pain
narcotic
non-narcotic
Tricyclics (USES)
Used for depression (the OG of antidepressant drugs)
Other uses:
- Anticholinergic effects
- used for sleep, migraines, anti addictive disorders, and fibromyalgia.
Tricyclic (OD)
OD BLOCKS SODIUM SITES, GET WIDE QT AND TACHYCARDIA.
- have 10-15 to treat
- one pill killer
- treat with Sodium Bicarb (1mEq/kg)
MAOIs
monoamine oxidase inhibitors
treats phobias and depression.
Action: monoamine oxidase is an enzyme used in the degradation on catecholamines. when that enzyme is inhibited, catecholamines and serotonin levels increase resulting in a psychostimulation.
what should people who are on MAOIs avoid? what can you uses to treat?
- foods that have tyramine
- any sympathomimetic drugs
(both can send the patient into a hypertensive crisis)
Treat with: nitrates, CCB, and BB.
SSRI
selective serotonin reuptake inhibitor
first choice for antidepressants (the safest)
Action: keeps serotonin in the synapse longer, rather than being reuptake.
SE: headache, GI disturbances, sexual dysfunction (can get serotonin syndrome but usually from something else like St. Johns Wart – NV, tachy, agitated diarrhea, agitated)
Heterocyclic
similar to tricyclics but more stable.
Action: potentiate (increase the power) norepinephrine and block dopamine receptors and have slight anticholinergic effects.
Phenothiazines
antipsychotic medication
action: work to occupy dopamine sites resulting in decreased psychosis and sedative effect.
SE: can cause extrapyramidal side effects (EPSE)
(including tremor, slurred speech, akathesia, anxiety, distress, and can cause Tardive dyskinesia and dystonia.)
Lithium Derivatives
lithium is Greek for stone.
it was initially used as a salt substitute for cardia patients but was removed from the market with lethal side effects..
its a mood stabilizing agent. Action is not fully known but it has to do with the ability to respond to neurotransmitters by replacing the sodium ions.
Class 1a antiarrhythmic
sodium and potassium channel blockers/inhibitors
prolongs duration of action potential and increases absolute refractory period.
extends phase 2 lengthen QT interval
also block the Alpha 2 sites (helping decrease blood pressure)
Class 1b antiarrhythmic
sodium channel inhibitor (affect phase 0, not phase 2)
prophylactic (to prevent disease) use of these drugs is decreasing.
Class 1c antiarrhythmic
works on the fast sodium channels
very rare b/c they cause extreme electrical depression and decrease inotropic function and wide QRS widening
Class 2 antiarrhythmic drugs
Beta Blockers (olol)
beta 1 receptor sites (these sites in cardiac cells trigger cyclic AMP resulting in opening of calcium channels which increase HR and force of contractility)
Beta 1 blockers help to decrease the HR and force of contractility.
SE: SOB and wheezing
OD: hypotensive and Brady
Tx: glucagon, help to stimulate the cAMP and open calcium channel receptor sites
Class 3 antiarrhythmic drugs
Inhibit the potassium channels and alter phase 2
Long term use can cause long QT and TDP. And can cause pulmonary fibrosis (lung tissue will scar)
OD: very bad bc blocks everything (Na, Ca, K)
Class 4 antiarrhythmic
calcium channel blockers
help to slow cardiac conduction decreased force of cardiac contraction and vaso-dilation.
DHP- L-tracks (vascular)
Non-DHP T-Tracks (cardiac)
Cardiac Glycosides
used to increase cardiac output in pts with heart failure, and to slow conduction in the AV node.
Inhibitors Na/K pump to allow the increase in intracellular concentration of Ca.
stimulates parasympathetic system and inhibits sympathetic system.
it attaches to the lean muscle (why it is dosed on peoples lean muscle), if the decrease in lean muscle mass need to change the dose or it is very Lethal.
can be toxic to people on antibiotics cause they kill intestinal flora (it is absorbed through the intestines and are dependent on the intestinal flora)
H2 blockers
(antihistamine medicines)
can slow body from eliminating dig so pt can become toxic from normal dose
OD on cardiac Glycosides
toxic levels will have dysrhythmias, yellowed vision, and ringing in ears.
Tx: chase the rhythm and treat symptoms.
what can help with a OD cardiac glycoside overdose?
Digibind
it will remove dig from system but not off the lean muscle, so anything attached to the muscle can still release and put the pt back into toxic levels.
