Term
|
Definition
Uses: peripheral vascular disease
shock
hypertension
pheochromocytoma
urinary retention in BPH
Adverse effects: severe hypotension
tachycardia
nasal congestion
impotence
GI distrurbances |
|
|
Term
|
Definition
a-receptor antagonist
competitive and reversible |
|
|
Term
|
Definition
a-receptor antagonist
irreversible
pheochromocytoma |
|
|
Term
|
Definition
a-receptor blocker
competitive and reversible
a1 receptors
does not cause tachycardia bc specific for a1 |
|
|
Term
|
Definition
a1a receptor antagonist
alleviates urinary retention |
|
|
Term
|
Definition
Uses: cardiac arrhythmias (PAT)
myocardial ischemia ( ↓CO)
hypertension (↓SYM activity in CNS, blocks renin, ↓CO)
pheochromocytoma (not 1st line)
open angle glaucoma
Adverse effects: heart failure
hypotension
mental depression
N/V
Contraindications:
asthma (B agonists will be ineffective dilators)
diabetes (blocks symptoms of ↓BG) |
|
|
Term
|
Definition
b-antagonist
competitive, reversible
non-selective
contraindicated in asthma |
|
|
Term
|
Definition
b-antagonist
competitive, reversible
selective for b1 receptors |
|
|
Term
| Blockade of NE release drugs |
|
Definition
Guanethidine- used in hypertension and glaucoma
Doesn't cross BBB.
Adverse effects: hypotension, heart failure, impotence, diarrhea, nasal congestion
Contraindicated in pheochromocytoma bc ↑ in free catecholamines initially. |
|
|
Term
|
Definition
Blockade of NE synthesis by inhibiting tyrosine hydroxylase. Treats pheochromocytoma. Can cause depression, hypotension, nasal congestion, diarrhea, and pseudo-parkinsonism (↓ dopamine). Crosses BBB.
Blocks the effect of indirect acting adrenomimetics bc they need NE to work. |
|
|
Term
|
Definition
Blockade of NE storage leads to depletion.
Used for hypertension
Adverse effects: severe depression, hypotension, nasal congestion, diarrhea, pseudo parkinsonism (↓ dopamine in CNS), also blocks the effects of indirect acting adrenomimetics bc they need NE to work. |
|
|
Term
|
Definition
Formation of a-methylNE depletes NE. Stimulates a2 receptors to ↓sym. tone to ↓BP.
Adverse effects: depression, sedation (crosses BBB), hypotension, don't use in hemolytic anemia. |
|
|
Term
|
Definition
| Competitive blocker at NM junction. Works at Nm cholinergic receptors. Starts with small, rapid moving muscles and works its way to the mm of respiration. Used as a mm relaxant in surgery and ECT. May cause apnea, hypotension (↓ sym stimulation), and bronchospasm ( release of histamine). Use neostigmine as an antidote (AChE inhibitor). Don't use with ether or Ca chelating ABX |
|
|
Term
| Depolarizing antagonist as NM Junction (membrane becomes insensitive to ACh) |
|
Definition
Decamethonium and succinylcholine. can cause paralysis. Succ has short duration bc degraded by pseudo AChE in blood. Used in ECT and surgery (intubation or succ) Can cause apnea, hypotension and some bronchoconstriction.
Succ can cause malignant hyperthermia (genetic) by excessive Ca release. Can be treated with dantrolene. |
|
|
Term
| Classification of antiarrythmic drugs |
|
Definition
Class I= Na Channel Blockers
Class II= Delay depol
Class III= Prolong AP, ↑ Refractory Period
Class IV= Block calcium channels |
|
|
Term
|
Definition
| Class Ia antiarrhythmic. Works by blocking Na channels (slows conduction) and blocking K channels (prolongs AP duration via ↑refractory period). Adverse reactions: hypotension, arthralgia and arthritis. |
|
|
Term
|
Definition
Class Ia antiarrhythmic. Works by blocking Na channels (slows conduction), blocking K channels (prolongs AP duration), and blocks cardiac muscarinic receptors.
Adverse reactions: headache, dizziness, tinnitus (3=cinchonism) and rarely thrombocytopenia. |
|
|
Term
|
Definition
| Class Ib antiarrhythmic- blocks Na channels in Purkinge Fibers (slows conductance) and ↓ automaticity by altering threshold and↓ phase IV. |
|
|
Term
|
Definition
Class Ic antiarrhythmic drug. Works by blocking Na channels (slows conductance) binds very tightly!
Adverse effects include: exacerbation of vent. arrhythmias and CHF, blurred vision. |
|
|
Term
| Effects of Class II antiarrhythmic drugs |
|
Definition
| B-blockers delay development of the AP by ↑ time b/w AP. Good for treating PAT (propranolol) |
|
|
Term
|
Definition
| Class III antiarrhythmic drug. Works by: blocking K channels (prolongs AP), blocking inactivated Na channels, also has small effect as B-Blocker and CCB. Can cause pulmonary fibrosis (↓ gas exchange) |
|
|
Term
| CCB (verapamil and diltiazem) |
|
Definition
| Class IV antiarrhythmic drug. Works by blocking Ca channels which ↓ velocity of conduction as well as ↓ spontaneous depol. |
|
|
Term
|
Definition
| Antiarrhythmic- causes hyperpol by ↑K efflux and ↓ Ca AP. Increases refractory period. May cause hypotension and bronchospasm. |
|
|
Term
| Mg (as an antiarrhythmic) |
|
Definition
| can block Digitalis induced arrhythmias. (digitalis increases Ca inside cell) |
|
|
Term
| Digoxin (as antiarrhythmic) |
|
Definition
| ↓ AV conduction by ↑ vagal nerve activity. |
|
|
Term
|
Definition
Digoxin and Digitoxin. Used to ↑ force of contaction by inhibiting Na/K ATPase. It ↑ both speed and force allowing for complete systolic emptying. Results in :↑ CO, ↓ Dilation, ↓ VP, ↓ venous cardiac acceleration and venous constriction, ↑ Na and H2O excretion (Diuresis), ↓ HR, ↑ Conduction Velocity at low doses, ↓ conduction velocity at high doses, ↓ AV node conduction.
Adverse effects: bigeminy-extrasystoles (↑ Ca), ectopic foci leading to v. fib., AV block, v. tach→v. fib, a.fib., anorexia, N/V, headache, fatigue, drowsiness, confusion, hallucinations, blurred vision.
↓K= toxicity
↑Ca= arryhythmias
↓Mg= arrhythmias ( can be an antidote) |
|
|
Term
|
Definition
Relatively selective B1-agonist. At ↑ doses, agonist for B1 and B2. Isomers (-)= agonist, (+)= antagonist. for alpha so mixed has no alpha activity.
Can improve CO by ↓MAP, ↓systemic vascular resistance, therefore ↓ventricular filling pressure. Has a short half life. |
|
|
Term
|
Definition
| B1 and dopamine agonist. (↑ cAMP to ↑Ca) releases catecholamines. Produces renal dilation to increase urinary output, relieves edema ( ↓ renin is good) |
|
|
Term
|
Definition
| Milrinone and inamrinone- inhibit phosphodiesterase III, ↑cAMP and ↑ Ca, causes vasodilation. ↑CO and lowers PVR. Does have high toxicity. N/V/ thrombocytopenia. |
|
|
Term
|
Definition
amyl nitrate, glyceryl trinitrate (ng) and isosorbide dinitrate vasodilate to ↓ angina.
Form NO to relax smooth mm. ↓ preload and small↓ in afterload. Can dilate coronary arteries but usually doesnt help. Activates guanylyl cyclase. Adverse effects: headache, dizziness, flushing, syncope, tachyphylaxis |
|
|
Term
|
Definition
verapamil, diltiazem, nefedipine, bepridil. ↓Ca by blocking Ca channels. Causes arterial dilation, ↓afterload, ↓ cardiac work, coronary vascular dilation ( only helpful in Prinzmetal's)
Adverse effects: Headache, dizziness, flushing, syncope, heart failure, edema, bradycardia |
|
|
Term
|
Definition
propranolol (non-selective) and metoprolol (b1-selective). Used in exertional angina. Cause negative chronotropic and inotropic effects. ↓ Cardiac Work and systolic pressure.
Adverse effects: bradycardia, AV block, heart failure, CNS depression (fatigue, insomnia, depression). Don't use in asthma or diabetes. |
|
|
Term
|
Definition
diazepam, alprozolam, midazolam, zolipem.
Non-competitive GABAa Agonists ( Cl channels). Causes muscle relaxation, sedation and anti-anxiety.
Adverse Reactions: sedation, muscle relaxation, anterograde amnesia. Will cause withdrawal. |
|
|
Term
| Skeletal MM Relaxants (4 types) |
|
Definition
GABAa agonists= benzos GABAb agonists= baclofen
central a2 agonist= tizanidine Ca blocker= dantrolene |
|
|
Term
| Tricyclic Antidepressants |
|
Definition
| amitriptyline- nonselectively inhibits the reuptake of NE, 5HT, and DA. Many side effects: drowsiness (H1blocker), CNS stimulation |
|
|
Term
|
Definition
| No more effective, just less SE. Fluoxetine, paroxetine, citalopram, escitalopram, sertraline. Selectively inhibit the reuptake of 5-HT. |
|
|
Term
|
Definition
| ANXIETY and depression. bupropion and venlafaxine. Selectively inhibit the reuptake of 5-HT and NE. Have a ↓ incidence of AE than TCAs and are better for those with anxiety also. |
|
|
Term
|
Definition
| Used for the manic phase of bipolar disorder. Manic =↑NT. Cation that takes the place of other cations (Na, Mg, Ca, K) and slows neurotransmission. Adverse effects include: metallic taste, lethargy, cognition problems, muscle spasms. Cleared in the kidneys. |
|
|
Term
| phenytoin and carbamazepine |
|
Definition
Na channel blocker anti-epileptics. Phenytoin has tons of ADR (no warfarin) makes your gums grow. Carbamazepine is better but still lots of ADR.
cognition problems, hypersensitivity, and teratogenesis, PP binding and P450s. ( NO WARFARIN) |
|
|
Term
|
Definition
| Ca blocker antiepileptic. Used for absense seizures. |
|
|
Term
|
Definition
| GABA antiepileptic. Used as pain modulator |
|
|
Term
| Lamotrigine and valproate |
|
Definition
| Lamotrigine blocks Na and Glu, used in bipolar disorder. Valproate is broad spectrum used in bipolar and pain. Has severe Gi effects. |
|
|
Term
|
Definition
Mesolimbic-reward
Mesocortical- cognition and proccessing
Nigrostriatal- movement
Tuberoinfundibular- ADR |
|
|
Term
|
Definition
| Since ↓ in dopamine in nigrostriatal tract, L-DOPA enters CNS but is broken down. Carbidopa is a DOPA decarboxylase inhibitor. Tolcapone is a COMT inhibitor. Selegeline is an MAO inhibitor. |
|
|
Term
|
Definition
Treat schizophrenia by ↓ DA. Phenothiazines- chlorpromazine is a non-specific D2 receptor blocker. Tons of bad ADRs- Parkinson's syndrome, dry mouth, sedation, hypotension.
Haloperidol is ↑↑ D2 blocking, however it is non selective in nigrostriatal tract (pseudoparkinsons). |
|
|
Term
|
Definition
| Clozapine and piserdone are 5HT2 and D2 antagonists. Much less ADRs. |
|
|
Term
| Ideal general anesthetics |
|
Definition
Rapid and pleasant induction and emergence.
Easily identified changes in depth of anesthesia.
Muscle relaxation.
Absence of toxicity and adverse effects.
Highly specific.
Rapid recovery with no SE.
Amnesia.
Easy to administer.
Useful for all ages. |
|
|
Term
|
Definition
| not metabolized, low potency, good analgesic but but must be used with other anesthetics, minimal effects on heart and BP and respiration. Inhibits methionine synthetase and B12 metabolism. Can be abused. |
|
|
Term
|
Definition
| high potency, poor analgesia so good for maintenance, good in kids, bronchodilation, ↓BP, dilates vasculature (↑ risk of arrhythmias), sensitizes heart to catecholamines, relaxes skeletal mm and potentiates NM blockers, can trigger malignant hyperthermia. Inhibits uterine contraction, causes hepatic toxicity. |
|
|
Term
|
Definition
| Rapid recovery and induction, excreted unchanged via lungs, ↓BP, tachycardia, relaxes muscles and potentiates NM blockers, dilates vasculature (but not as much), bronchodilation, cough, uterine relaxation. |
|
|
Term
|
Definition
| Slow induction and recovery, 2-8% metabolized,↓BP, ↑ cranial pressure, bronchodilation, skeletal mm relaxation, enhances NM blockers, uterine relaxation |
|
|
Term
|
Definition
| rapid induction and recovery, maintenance bc of cough and salivation,eliminated unchanged via lungs, ↓BP, ↑ Cerebral BF, bronchodilation, Skeletal mm relaxation and enhance NM blockers. |
|
|
Term
|
Definition
| Rapid induction and recovery, 3% metabolized, ↓ BP, increases cerebral BF, most effective bronchodilator, skeletal mm relaxation and enhances NM blockers. |
|
|
Term
|
Definition
| IV, hepatic metabolism and renal excretion, ↓BP, causes respiratory distress (barb), occasional histamine release. |
|
|
Term
|
Definition
| IV, rapid onset and recovery, hepatic metabolism and renal+biliary excretion, pain on injection and involuntary motor movements, easy on BP and heart, no histamine release, N/V, ↓corticosteroid production |
|
|
Term
|
Definition
| Rapid onset and recovery, IM, oral and rectal, hepatic metabolism and renal+biliary excretion, DISSOCIATIVE AMNESIA (analgesia, amnesia, unresponsiveness, eyes open, spontaneous respiration, involuntary movements) ↑ BP, ↓ reuptake of catecholamines. Increase cerebral BF, bronchodilation (indirect), hallucinations |
|
|
Term
|
Definition
| rapid onset and recovery, hepatic and extra hepatic metabolism, renal excretion, ↓BP, antiemetic, possible histamine release. |
|
|
Term
|
Definition
| LA ester prototype: metabolized by plasma esterases, allergic rxns, needs to be injected, for infiltration nerve block or spinal, hydrolysis produces PABA (interacts with sulfas). |
|
|
Term
|
Definition
| short half life, safe locally but not for IV bc may induce thrombosis in regional block. |
|
|
Term
|
Definition
| LA amide prototype: longer lasting and more intense than procaine, also ↓ allergic rxns. All routes except eyes!, metabolized by hepatic enzymes. |
|
|
