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709 Cards in this Set

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Alendronate
Alendronate - bisphosphonate - prevents bone resorption by retarding the dissolution of hydroxyapetite crystals in bone. Also increases bone formation. Used to Tx steroid-induced and postmenopausal osteoporosis, Paget's DX, and hypercalcemia. Taken orally 1x/week and the Pt must SIT UP for 1 hour to prevent reflux of the drug (~battery acid on the esophagus).
Amiloride
Amiloride - Tx lithium induced nephrogenic DI. Blocks Na channels in principle cells of LDT/CD to prevent resorption of Li. Does NOT appreciably decrease renal clearance of lithium like HCTZ.
Aminoglutethimide
Aminoglutethimide - Inhibitor of steroid synthesis - Blocks CYP450scc (stops conversion of cholesterol to pregnenolone), CYP45011B, and blocks extra-adrenal aromatase conversion of androgens to estrogens. Blocks ALL adrenal AND extra-adrenal steroid synthesis. 'Chemical adrenalectomy.' Body will respond by increasing ACTH, so usu given c a steroid to prevent it.
Beclomethasone
Beclomethasone - Inhaled cortico (asthma and nasal). REVIEW MOA p 295. Remember, because MOA involves protein synthesis, the full effect will take 2-3 days, and last 2-3 days after d/c of drug! Overall, *enhances* gene expression for lipocortin (prevents liberation of arachidonic acid), enzymes of gluconeogenesis, glycogen synthetase in liver, and IFKB (inhibiting factor kappa-beta). *Inhibit* gene expression for CRH in hypothalamus, POMC (ACTH precursor) in pit gland, COX-2 in leukocytes, IL-1/IL-6/collagenase/TNF in macrophages.
Betamethasone
Betamethasone - Systemic cortico (Long acting 36-72h). REVIEW MOA p 295. Remember, because MOA involves protein synthesis, the full effect will take 2-3 days, and last 2-3 days after d/c of drug! Overall, *enhances* gene expression for lipocortin (prevents liberation of arachidonic acid), enzymes of gluconeogenesis, glycogen synthetase in liver, and IFKB (inhibiting factor kappa-beta). *Inhibit* gene expression for CRH in hypothalamus, POMC (ACTH precursor) in pit gland, COX-2 in leukocytes, IL-1/IL-6/collagenase/TNF in macrophages.
Budesonide
Budesonide - Inhaled cortico (asthma and nasal) c low systemic absorption (20-40%) so good for use in kids! REVIEW MOA p 295 and effects listed everywhere else.
Chlorpropamide
Chlorpropamide - Sulfonylurea - First gen. T1/2 32h. Can cause dilutional hyponatremia by causing ADH release and potentiating its actio on the renal tubule (see 263).
Cortisone
Cortisone - Systemic corticosteroid (short acting 8-12h) - Converted to active hydrocortisone by hepatic 11B-OH-steroid dehydrogenase. REVIEW MOA p 295. Remember, because MOA involves protein synthesis, the full effect will take 2-3 days, and last 2-3 days after d/c of drug! Overall, *enhances* gene expression for lipocortin (prevents liberation of arachidonic acid), enzymes of gluconeogenesis, glycogen synthetase in liver, and IFKB (inhibiting factor kappa-beta). *Inhibit* gene expression for CRH in hypothalamus, POMC (ACTH precursor) in pit gland, COX-2 in leukocytes, IL-1/IL-6/collagenase/TNF in macrophages.
Demeclocycline
Demeclocycline - tetracycline antibiotic used to Tx SIADH when serum Na <120 mEq/L and Pt has severe neuro Sx.
Desmopressin
Desmopressin - long-acting synthetic analog of ADH 6-20 h (nb: AVP = ADH). Action at V2 : V1 receptors = 4000:1, so less vasoconstrictor activity (if you're like me and you have no idea what the heck a V receptor is, check p 258-9). May be administered sc, iv, or in a convenient nasal spray, but at 10x the dose! May even be used to Tx hemophillia A and type 1 VonWilli's DX.
Dexamethasone
Dexamethasone - Systemic cortico (Long acting 36-72h), also available in nasal, inhaled, otic, opthalmic preps. REVIEW MOA p 295. Remember, because MOA involves protein synthesis, the full effect will take 2-3 days, and last 2-3 days after d/c of drug! Overall, *enhances* gene expression for lipocortin (prevents liberation of arachidonic acid), enzymes of gluconeogenesis, glycogen synthetase in liver, and IFKB (inhibiting factor kappa-beta). *Inhibit* gene expression for CRH in hypothalamus, POMC (ACTH precursor) in pit gland, COX-2 in leukocytes, IL-1/IL-6/collagenase/TNF in macrophages.
Fludrocortisone
Fludrocortisone - Systemic cortico with highest MINERALocorticoid activity. Small doses have little glucocorticoid effect. Use in conjunction w/ hydrocortisone or cortisone in Addison's disease (required for life).
Flunisolide
Flunisolide - Inhaled cortico (asthma and nasal). Review other info listed on other steroids.
Fluticasone
Fluticasone - Inhaled cortico (asthma and nasal) c low systemic absorption (50%) so good for use in kids!
Glipizide
Glipizide - Sulfonylurea - 2nd gen. - Very potent, careful in elderly and Pts c CVD (possible hypoglycemia). C/I in Pts c renal or hepatic dysfx'n. Short T1/2 = 2-4h, so hypoglycemia less likely.
Glyburide
Glyburide - Sulfonylurea - 2nd gen. - Very potent, careful in elderly and Pts c CVD (possible hypoglycemia). C/I in Pts c renal or hepatic dysfx'n. Duration 24h.
Hydrochlorothiazide
HCTZ - Reduces urinary volume 25-50% in nephrogenic DI (ie no reaction to ADH). Because Pt is volume contracted from too many trips to the restroom, more absorption occurs in PCT = less volume delivered distally where urine is diluted. Also Tx of lithium induced DI, but may decrease clearance of Li (so may have to decrease dose! see p261).
Hydrocortisone
Hydrocortisone - Systemic corticosteroid (short acting 8-12h). Also available in otic and opthalmic preps. This IS cortisol. REVIEW MOA p 295. Remember, because MOA involves protein synthesis, the full effect will take 2-3 days, and last 2-3 days after d/c of drug! Overall, *enhances* gene expression for lipocortin (prevents liberation of arachidonic acid), enzymes of gluconeogenesis, glycogen synthetase in liver, and IFKB (inhibiting factor kappa-beta). *Inhibit* gene expression for CRH in hypothalamus, POMC (ACTH precursor) in pit gland, COX-2 in leukocytes, IL-1/IL-6/collagenase/TNF in macrophages.
Insulin aspart
Insulin aspart - Ultra-short-acting insulin. Kinetics similar to lispro insulin. Lispro and aspart are mo bettah than regular insulin b/c faster onset and no increase in T1/2 with higher dose.
Insulin glargine
Insulin glargine (Lantus) - Given once daily sc and goes all day long, baby (unlike bid NPH).
Iodide (Lugol's solution)
Lugol's solution - Large dose of KI. Immediately inhibits the release of T3/T4 from thyroid by preventing proteolysis of thyroglobulin. Transient inhibition of organification of iodide by preventing iodide trapping (Wolff-Chaikoff effect). After 4-7days of suppression, the thyroid 'escapes' from the supressant effect and mucho thyroid activity can happen. If a patient is going to have Iodine 131 Tx, give them Iodine to take po if they experience reactive throid storm.
Isophane insulin
Isophane insulin = NPH insulin. Intermediate-acting. Insulin complexed c arginine-rich peptides to show absorption. Onset 1-2h, peak 6-12h, lasts 18-24h.
Lente insulin
Lente insulin - Intermediate-acting insulin. Onset 1-2h, peak 6-12h, lasts 18-24h. Consists of 30% semilente insulin (relatively rapid onset), and 70% ultralente insulin (poorly soluble Zn insulin crystals, delayed onset, long duration).
Lispro Insulin
Lispro Insulin - Sold by Rx, ultra-short-acting insulin. Quick onset b/c insulin molecules cannot form hexamers. Same T1/2 as natural insulin. Can be taken 10 min ac, peak @ 1h, lasts 3-4h. Duration of action NOT prolonged by increasing dose! Lispro and aspart are mo bettah than regular insulin b/c faster onset and no increase in T1/2 with higher dose.
Lithium
Lithium - Can cause nephrogenic DI by reducing formation of cAMP from V2 stimulation by ADH in principle cells of LDT/CD. Tx c HCTZ or Amiloride.
L-thyroxine
L-thyroxine - Synthetic T4 to treat hypothyroidism (don't forget hypothyroidism can be caused by steroids, lithium and amiodarone). In initial Tx, dose is raised every 2 weeks until TSH levels are normal. Careful in Pts c CV risk factors b/c high doses can precipitate MI or a-fib.
Metformin
Metformin - Oral antihyperglycemic = drug will NOT cause hypoglycemia in euglycemic Pts or Pts c T1DM. MOA=unknown, but enhances the effect of insulin on peripheral tissues (liver, fat, muscle). Does NOT work in the absence of insulin. Poss postprandial lactic acid production by GI can precipitate lactic acidosis. C/I in renal impairment. Does NOT cause weight gain.
Methimazole
Methimazole - Thioamide for Tx hyperthyroidism. MOA=prevent organification of iodide, blocks coupling of MIT and DIT. Does NOT block peripheral conversion of T4 to T3 like PTU!
Methylprednisolone
Methylprednisolone - Systemic cortico (Int acting 12-36h). REVIEW MOA p 295. Remember, because MOA involves protein synthesis, the full effect will take 2-3 days, and last 2-3 days after d/c of drug! Overall, *enhances* gene expression for lipocortin (prevents liberation of arachidonic acid), enzymes of gluconeogenesis, glycogen synthetase in liver, and IFKB (inhibiting factor kappa-beta). *Inhibit* gene expression for CRH in hypothalamus, POMC (ACTH precursor) in pit gland, COX-2 in leukocytes, IL-1/IL-6/collagenase/TNF in macrophages.
Pioglitazone
Pioglitazone - Oral antihyperglycemic - MOA not specified, assume it works like its sister, Rosi. Also improves lipids, but can also cause wt gain.
Prednisolone
Prednisolone - Systemic cortico (Int acting 12-36h). REVIEW MOA p 295. Remember, because MOA involves protein synthesis, the full effect will take 2-3 days, and last 2-3 days after d/c of drug! Overall, *enhances* gene expression for lipocortin (prevents liberation of arachidonic acid), enzymes of gluconeogenesis, glycogen synthetase in liver, and IFKB (inhibiting factor kappa-beta). *Inhibit* gene expression for CRH in hypothalamus, POMC (ACTH precursor) in pit gland, COX-2 in leukocytes, IL-1/IL-6/collagenase/TNF in macrophages.
Prednisone
Prednisone - Systemic cortico (Int acting 12-36h). Converted to active prednisolone by liver. REVIEW MOA p 295. Remember, because MOA involves protein synthesis, the full effect will take 2-3 days, and last 2-3 days after d/c of drug! Overall, *enhances* gene expression for lipocortin (prevents liberation of arachidonic acid), enzymes of gluconeogenesis, glycogen synthetase in liver, and IFKB (inhibiting factor kappa-beta). *Inhibit* gene expression for CRH in hypothalamus, POMC (ACTH precursor) in pit gland, COX-2 in leukocytes, IL-1/IL-6/collagenase/TNF in macrophages.
Propranolol
Propranolol - Tx Sx of hyperthyroidism. Controls autonomic Sx (tachy, sweating, tremor, etc). Blocks peripheral conversion of T4 to T3!! Metabolism of propranolol very rapid in hyperthyroidism, so large doses may be needed. Tx thyroid storm with this and PTU (to block peripheral conversion of T4 to T3).
Propylthiouracil (PTU)
Propylthiouracil (PTU) - Thioamide for Tx hyperthyroidism. MOA=prevent organification of iodide, blocks coupling of MIT and DIT, *blocks peripheral conversion of T4 to T3. Remember, the major effect is blocking the SYNTHESIS, not release of thyroid hormone, so onset is slow! No 'escape' phenomenon like iodine. If Pt relapses p Tx (60-80%), I131 Tx indicated. PTU has anti-vitamin k activity that can potentiate warfarin. PTU is highly plasma protein bound than Methimazole, so not likely to cross placenta in a pregnant woman to give 10% of ze poor babies goiter. Remember this, or else you might have to learn the embryology of neonatal goiter!
Regular insulin
Regular insulin - Rapid-acting. If given sc, hexamers must disassociate before acting, so T1/2 increases with increased dose. If given iv, hexamers quickly break into 'ready to go' monomers. Taken 30-45 min ac, onset in 15 min, peak 2-4h, duration 5-8h.
Repaglinide
Repaglinide - Sulfonylurea - 2nd gen. - Same MOA as sulfonylureas, but supposedly does a good job in preventing postprandial hyperglycemia w/o much effect on fasting glucose.
Rosiglitazone
Rosiglitazone - Oral antihyperglycemic - MOA=binds to PPAR~y to cause increased expression of genes encoding for GLUT-4 in skel musc/adipose, lipoprotein lipase (good effect on lipid profile), insulin receptors in skel musc/adipose. No effect on hepatic gluconeogenesis. May prevent islet cell degen in T2DM. S/E=fluid retention (weight gain) and edema, h/a.
Tolbutamide
Tolbutamide - Sulfonylurea - First gen oral hypoglycemic. MOA=block ATP sensitive K channels in islet cells to cause increased insulin secretion. Works in non-diabetics! Does NOT sensitize periphery to insulin effects. DOA=6-10h.
Triamcinolone
Triamcinolone - Systemic cortico (Int acting 12-36h). REVIEW MOA p 295. Remember, because MOA involves protein synthesis, the full effect will take 2-3 days, and last 2-3 days after d/c of drug! Overall, *enhances* gene expression for lipocortin (prevents liberation of arachidonic acid), enzymes of gluconeogenesis, glycogen synthetase in liver, and IFKB (inhibiting factor kappa-beta). *Inhibit* gene expression for CRH in hypothalamus, POMC (ACTH precursor) in pit gland, COX-2 in leukocytes, IL-1/IL-6/collagenase/TNF in macrophages.
Alprazolam
BZ anxiolytic. MOA=potentiates effect of GABA on GABAa receptors to increase Cl conductance and hyperpolarize neurons. Short onset of action. Tx PD (b/c high potency has less CNS S/Es) to minimize 'anticipatory anxiety,' but may no prevent the actual panic attack. Action=sedative, anxiolytic, anti-convulsant, muscle relaxant, poss anterograde amnesia. NO analgesic effects.
Amantadine
Antiviral for Tx parkinson's that may stimulate release of dopamine. Wouldn't work in late stage parkinson's.
Amphetamine
Simpathiomemetic amine=Indirect CNS stimulant (nawww... really?). MOA=increases the release of catecholamines and prevents their reuptake. Anorexiant via NE release in the lateral hypothalimus. S/E=increased BP (systolic and diastolic), tachycardia. Acute tox=marked CNS stim, agitation, paranoid psychosis. Chronic tox=hallucinations, delusions, feelings of omnipotence (~ + schizophrenia Sx).
Aripiprazole
Atypical antipsychotic (5HT-2 antagonist, but PARTIAL D2 agonist).
Atomoxetine
Selective NE reuptake inhibitor for Tx of ADHD (psychomotor stimulant). Do not use c MAO-I. S/E=headache, aggression, irritability, palpitations, insomnia (ie same as med school S/E).
Benztropine
Muscarinic cholinergic antagonist for Tx parkinson's. Not dependent on D2 neurons so can use in late stage DX.
Bromocriptine
Dopamine agonist (w/ D2 preference) for use in Tx parkinson's as adjunct c levo/carb in Pts experiencing on/off or end of dose akinesia. Also Tx of NMS and hyper-PRL. S/E=ortho hypo (moreso than c levodopa), N/V and constipation early in treatment (but rarely serious), psychotic Sx more common and severe than levodopa, dyskinesias.
Bupropion
Anti-depressant. MOA unknown. Low incidence of S/Es but can lower seizure threshold.
Buspirone
Non-BZ anxiolytic. Slow onset of action (weeks). Minimal w/d potential. S/Es=dizziness and nausea (no amnesia). MOA=increase in *K* conductance to hyperpolarize neurons, probably through direct 5HT1A agonism.
BZs general
Longer acting BZs can prevent w/d Sx, shorter acting really only useful for sleep induction. Dependence seems to be an issue after Tx >8 mo. Cross tolerance c EtOH, so may be less effective in alcoholics. Note that BZs bind to an allosteric site on the GABA receptor to increase the FREQUENCY of Cl channel opening. GABA is required for their action (no GABA, no workie).
Carbamazepine
Tx epilepsy. MOA=prolong Na channel inactivation.
Chlorpromazine
Low potency typical antipsychotic (D2 antagonist). Low potency=higher incidence of ACh effects, ortho hypo, and sedation, but less incidence of EPS.
Citalopram
SSRI. S/E=N/V, sexual dysfxn, satiation/weight loss. No ACh effects, no ortho hypo, no HTN crisis (unless you forget them on the test)
Clomipramine
TCA-NE reuptake block, but very potent 5HT reuptake block. Tx OCD b/c 5HT block seems required to mitigate OCD (ex desipramine doesn't do dooky do).
Clonazepam
BZ anxiolytic. MOA=potentiates effect of GABA on GABAa receptors to increase Cl conductance and hyperpolarize neurons. Short onset of action. Tx PD (b/c high potency has less CNS S/Es) to minimize 'anticipatory anxiety,' but may no prevent the actual panic attack. Action=sedative, anxiolytic, anti-convulsant, muscle relaxant, poss anterograde amnesia. NO analgesic effects.
Clonazepam (epilepsy)
Tx epilepsy. BZ, so it increases the FREQUENCY of Cl channel opening in response to GABA.
Clozapine
Atypical antipsychotic (D2 & 5HT-2 antagonist). S/E=***agranulocytosis. Can actually decrease tardive dyskinesias in Pts who develop TD c typical antipsychotics.
Desiprimine
TCA-blocks NE reuptake. S/Es=ACh block (dry mouth, constipation, urinary retention, sexual dysfxn, memory impairment, tachycardia), H1 block (sedation, weight gain), A1 block (ortho hypo, sexual dysfxn), AV block, temor/ataxia (esp in elderly), lwered seizure threshold. Fatal arrhythmias in OD.
Dextroamphetamine
CNS stimulant (psychomotor stimulant) for Tx ADHD. Release NE and DA from neurons and prevent their reuptake. Sched II drug. Generally less peripheral effects and more prominent CNS effects vs. sympathiomemetic amines.
Diazepam
BZ anxiolytic. MOA=potentiates effect of GABA on GABAa receptors to increase Cl conductance and hyperpolarize neurons. Short onset of action. Action=sedative, anxiolytic, anti-convulsant, muscle relaxant, poss anterograde amnesia. NO analgesic effects.
Diazepam (epilepsy)
Tx epilepsy. BZ, so it increases the FREQUENCY of Cl channel opening in response to GABA.
Diphenhydramine
Antihistamine, but anti-ACh effect useful for Tx parkinson's. Not dependent on D2 neurons so can use in late stage DX.
Entacapone
COMT inhibitor for Tx parkinson's. Use c MAO-I inhibits most catecholamine degredation pathways. No mention at all in review... wouldn't waste brain space on this (or Selegiline, either).
Ethosuximide
Tx epilepsy. MOA=reduces low threshold Ca currents (T currents).
Ethotoin
Tx epilepsy. MOA=prolong Na channel inactivation.
Fenfluramine
Man in hawaiian shirt said to skip it, but to prevent gunner anxiety, it increases 5HT release and prevents reuptake.
Flumazenil
BZ antagonist.
Fluoxetine
SSRI. S/E=N/V, sexual dysfxn, satiation/weight loss. No ACh effects, no ortho hypo, no HTN crisis (unless you forget them on the test)
Flurazepam
BZ anxiolytic. MOA=potentiates effect of GABA on GABAa receptors to increase Cl conductance and hyperpolarize neurons. Short onset of action. Action=sedative, anxiolytic, anti-convulsant, muscle relaxant, poss anterograde amnesia. NO analgesic effects.
Fluvoxamine
SSRI. S/E=N/V, sexual dysfxn, satiation/weight loss. No ACh effects, no ortho hypo, no HTN crisis (unless you forget them on the test)
Gabapentin
Tx epilepsy. MOA=Promotes the release of GABA.
Haloperidol
High poteny typical antipsychotic (D2 antagonist). High potency=higher incidence of EPS (haldol shuffle), lower incidence of anti-ACh, ortho hypo, sedation.
Imipramine
TCA-blocks NE AND 5HT. S/Es=ACh block (dry mouth, constipation, urinary retention, sexual dysfxn, memory impairment, tachycardia), H1 block (sedation, weight gain), A1 block (ortho hypo, sexual dysfxn), AV block, temor/ataxia (esp in elderly), lwered seizure threshold. Fatal arrhythmias in OD.
Lamotrigine
Tx epilepsy. MOA=prolong Na channel inactivation.
Levodopa +/- carbidopa
Levodopa=precursor of dopamine used to increase levels in parkinson's Pts. Inc dopamine can cause arrhythmias and tachycardia (can prevent c B-blocker), ortho hypo via A2 stimulation of the carotid receptors, appetite supression, N/V. Dyskinesias and psychosis are dose limiting S/Es (can Tx psychosis c atypicals like clozapine or quetiapine). Carbidopa is a peripheral DOPA decarboxilase inhibitor to prevent peripheral conversion of levodopa to dopamine. Thus, the peripheral side effects are lessened, the dose of levodopa can be decreased, N/V decreased, cardiac S/Es decreased, etc.
Methylphenidate
CNS stimulant (psychomotor stimulant) for Tx ADHD. Release NE and DA from neurons and prevent their reuptake. Sched II drug. Generally less peripheral effects and more prominent CNS effects vs. sympathiomemetic amines.
Mirtazapine
Inhibitor of A2 autoreceptors on presynaptic neurons increases NE RELEASE. S/Es from 5HT-2 & H1 block=weight gain
Olanzepine
Atypical antipsychotic (D2 & 5HT-2 antagonist). S/E=super grande antihistaminic (=increased incidence of krispie kreme kraving).
Oxazepam
BZ anxiolytic. MOA=potentiates effect of GABA on GABAa receptors to increase Cl conductance and hyperpolarize neurons. Short onset of action. Action=sedative, anxiolytic, anti-convulsant, muscle relaxant, poss anterograde amnesia. NO analgesic effects. Good for use in elderly b/c metabolized by conjugation as opposed to oxidation (oxidative capacity decreases c age).
Paroxetine
SSRI. S/E=N/V, sexual dysfxn, satiation/weight loss. No ACh effects, no ortho hypo, no HTN crisis (unless you forget them on the test)
Phenezine
MAOI-Increases neuronal release of NE & 5HT (from vesicles and cytoplasm). MAO can still be inhibited 10-14 days p d/c. S/Es=Hepatotoxicity, CNS stimulation (tremors, insomnia, precip. of manic/hypomanic episode), ortho hypo. Ix c antihistamines (~pseudoephed). Tyramine or 'cheese' rxn can cause HTN crisis! Muy importante.
Phenobarbital
Tx epilepsy. MOA=enhances GABA mediated increases in Cl conductance by increasing the duration of channel opening.
Phentermine
Indirect CNS stimulant (simpathiomemetic amine), appetite suppressant. Same MOA as amphetamine (inc release of catechols and prevent reuptake). Lower abuse potential than amphetamines.
Phenytoin
Tx epilepsy. MOA=prolong Na channel inactivation.
Pramipexole
Dopamine agonist (selective for D2 and moreso D3) for use in Tx parkinson's, especially later stages. S/E=ortho hypo (moreso than c levodopa), N/V and constipation early in treatment (but rarely serious), psychotic Sx more common and severe than levodopa, dyskinesias.
Quetiapine
Atypical antipsychotic (D2 & 5HT-2 antagonist). S/E=no Anti-ACh!
Risperidone
Atypical antipsychotic (D2 & 5HT-2 antagonist). S/E=dose related EPS, possible increase in PRL, but no Anti-ACh!
Selegiline
MAO-B inhibitor to slow the degredation of dopamine (may be neuroprotective by dec oxidative stress). Does NOT inhib peripheral metabolism of dietary amines. Attenuates on/off and end of dose phenomena. Metabolized to amphetamine (which may account for S/Es of anxiety and insomnia. In late stage Pts, may exacerbate dyskinesias, confusion, and hallucinations.
Sertraline
SSRI. S/E=N/V, sexual dysfxn, satiation/weight loss. No ACh effects, no ortho hypo, no HTN crisis (unless you forget them on the test)
Sibutramine
Monoamine reuptake inhibitor-prevents reuptake of NE, DA, 5HT. No CNS depression, abuse potential, drug dependence, or valvular pathology. S/E=tachy, HTN, headache, dry mouth, insomnia, constipation, short sleep duration. No tolerance to anoriexiant effect. Not an amphetamine, but still Sched IV.
SSRIs
FF PVCS= Fluoxetine, Fluvoxamine, Paroxetine, Venlafaxine, Citalopram, Sertraline
Theophylline
Tx of neonatal apnea syndrome. MOA=Inhibits phosphodiesterase resulting in increase cAMP leading to increased Ca levels. Also antagonizes adenosine receptors. Effects=relax sm muscle (esp bronchial), CNS stim, cardiac musc stim, axn in kidney as a diuretic. Severe tox or sudden death c rapid iv infusion. Other S/E=headache, tachy, restlessness, N/V, abd pain.
Triazolam
BZ *hypnotic*. MOA=potentiates effect of GABA on GABAa receptors to increase Cl conductance and hyperpolarize neurons. Short onset of action. Used to decrease sleep latency. Don't forget it causes amnesia.
Tx PD
BZs prevent anticipatory anxiety, SSRIs prevent actual panic attack. Tx c BZ + SSRI/buspirone, taper BZ after a couple months.
Tx Tourette's
EeeeEEEeeP! Oh... sorry... use Haloperidol.
Valproate
Tx epilepsy. MOA=TONS. Prolongs Na channel inactivation, reduce low threshold Ca currents (T currents), increase GABA levels by stimulating the synthetic enzyme glutamic acid decarboxylase (this MOA is specific to valproate only, hint hint), inhibits degredation of GABA.
Venlafaxine
**Dose dependent pharmacology. Low dose ~ SSRI, higher dose prevents NE reuptake too. S/Es similar to SSRIs-N/V, sexual dysfxn, satiation/weight loss.
Zaleplon
Non-BZ hypnotic that interacts c GABA receptors. Short T1/2. Used for sleep (whatever that is). Less muscle relaxant and anti-convulsant action than BZs. Also less interaction c EtOH and less abuse potential. Still amnestic tho.
Zolpidem
Non-BZ hypnotic that interacts c GABA receptors. Short T1/2. Used for sleep (whatever that is). Less muscle relaxant and anti-convulsant action than BZs. Also less interaction c EtOH and less abuse potential. Still amnestic tho.
Zonisamide
Tx epilepsy. MOA=prolong Na channel inactivation, AND decreases low threshold Ca currents (T currents).
Clomiphene
Clomiphene - SERM - Orally active NON-steroidal compound. Think of it as the ANTI-OCP, it blocks the - feedback of E2 on the pituitary to increase GnRH secretion. Used to stimulate ovulation in women. S/E=ovarian enlargement, menopause like Sx. C/I in Pt c TE disorder, b/c acts as an estrogen on the liver.
Conjugated Estrogens
Conjugated Estrogens - Estrogens derived from equine urine containing estrone, equilin, and 17 alpha-dihydroequilin. Conjugation c straight chain fatty acids increases activity and T1/2. Also have 'synthetic' conjugated estrogen tablets composed of estrogens of plant origin. Contain same three major and six minor estrogens Premarin (the one from the horses). See E2 for use, S/E, etc.
Estradiol
Estradiol (E2) - Major estrogen product of ovaries. Review nl physio properties (p32-33). Tx of primary hypogonadism, HRT, OCPs (***used c progestins to prevent endometrial hyperplasia caused by E2), Post-coital contraception, dysmenorrhea, DUB, dec Sx of benign breast DX, hirsutism (used c finasteride/flutamide/spironolactone). Absolute C/I=Estrogen dependent breast or uterine CA, non-Dx abn genital bleeding, PHx severe thromboembolic DX, acute hepatic DX. Relative C/I=FHx breast/uterine CA, grande varicose veins, PHx hepatic DX, HTN. S/E=N/V/D, tender ta-tas, **Endometrial hyperplasia, Na/H20 retention, HTN, biliary DX, TE, postmenopausal bleeding, h/a, 'pregnancy mask' (cholasma/melasma).
Ethinyl estradiol
Ethinyl estradiol - Synthetic steroidal estrogens c an ethinyl group added @ 17 position of steroid ring to increase bioavail, potency, and T1/2 by preventing first pass metabolism. See E2 for use, S/E, etc.
Levonorgestrel
Levonorgestrel (Norplant) - Progestin from 19-nortestosterone (so still has some androgenic effects!). Used c estrogen in OCPs and HRT.
Medroxyprogesterone
Medroxyprogesterone - Progestin (Depo-provera). 150mg IM provides contraception for 3 months by causing complete amenorrhea. No increased risk of TE.
Mifepristone
Mifepristone - RU486 - Progesterone antagonist used in pregnancy termination. Also shown to prevent ovum implantation, alleviate Sx of endometriosis, treat non-resectable meningiomas and uterine leiomyomas. Can also be used in Pt c Cushing's b/c also acts as a glucocorticoid receptor antagonist.
Norelgestromin
Norelgestromin - Progestin NOT from 19-nortestosterone. No androgenic effects so doesn't antagonize the positive effect of estrogen on plasma HDLs.
Norethindrone
Norethindrone - Progestin from 19-nortestosterone (so still has some androgenic effects!). Used c estrogen in OCPs and HRT.
Norgestimate
Norgestimate - Progestin NOT from 19-nortestosterone. In OCPs like ortho-tri that are 'nice for your skin.'
Raloxifene
Raloxifene - SERM - Similar action to Tamoxifen, ie agonist on bone, lipids, liver. Antagonist on breast, CNS, skin/mucus memb. BUT… unlike Tamox, Ralox is an ANTAGONIST on uterine tissue, so no endo hyperplasia!
Tamoxifen
Tamoxifen - SERM - Orally active NON-steroidal. Used to Tx estrogen dependent breast CA. Also acts as an estrogen to improve bone density and lipids in postmenopausal women. Also acts on LIVER and UTERUS (TE, endometrial hyperplasia). In premenopausal women, will need to use GnRH analog to prevent increased GnRH/LH/FSH acting on the ovaries to produce more estrogen that interferes with estrogen blocking function of Tamox. Also antagonist on CNS and skin/mucus membranes.
Alendronate
Alendronate - bisphosphonate - prevents bone resorption by retarding the dissolution of hydroxyapetite crystals in bone. Also increases bone formation. Used to Tx steroid-induced and postmenopausal osteoporosis, Paget's DX, and hypercalcemia. Taken orally 1x/week and the Pt must SIT UP for 1 hour to prevent reflux of the drug (~battery acid on the esophagus).
Amiloride
Amiloride - Tx lithium induced nephrogenic DI. Blocks Na channels in principle cells of LDT/CD to prevent resorption of Li. Does NOT appreciably decrease renal clearance of lithium like HCTZ.
Aminoglutethimide
Aminoglutethimide - Inhibitor of steroid synthesis - Blocks CYP450scc (stops conversion of cholesterol to pregnenolone), CYP45011B, and blocks extra-adrenal aromatase conversion of androgens to estrogens. Blocks ALL adrenal AND extra-adrenal steroid synthesis. 'Chemical adrenalectomy.' Body will respond by increasing ACTH, so usu given c a steroid to prevent it.
Beclomethasone
Beclomethasone - Inhaled cortico (asthma and nasal). REVIEW MOA p 295. Remember, because MOA involves protein synthesis, the full effect will take 2-3 days, and last 2-3 days after d/c of drug! Overall, *enhances* gene expression for lipocortin (prevents liberation of arachidonic acid), enzymes of gluconeogenesis, glycogen synthetase in liver, and IFKB (inhibiting factor kappa-beta). *Inhibit* gene expression for CRH in hypothalamus, POMC (ACTH precursor) in pit gland, COX-2 in leukocytes, IL-1/IL-6/collagenase/TNF in macrophages.
Betamethasone
Betamethasone - Systemic cortico (Long acting 36-72h). REVIEW MOA p 295. Remember, because MOA involves protein synthesis, the full effect will take 2-3 days, and last 2-3 days after d/c of drug! Overall, *enhances* gene expression for lipocortin (prevents liberation of arachidonic acid), enzymes of gluconeogenesis, glycogen synthetase in liver, and IFKB (inhibiting factor kappa-beta). *Inhibit* gene expression for CRH in hypothalamus, POMC (ACTH precursor) in pit gland, COX-2 in leukocytes, IL-1/IL-6/collagenase/TNF in macrophages.
Budesonide
Budesonide - Inhaled cortico (asthma and nasal) c low systemic absorption (20-40%) so good for use in kids! REVIEW MOA p 295 and effects listed everywhere else.
Chlorpropamide
Chlorpropamide - Sulfonylurea - First gen. T1/2 32h. Can cause dilutional hyponatremia by causing ADH release and potentiating its actio on the renal tubule (see 263).
Cortisone
Cortisone - Systemic corticosteroid (short acting 8-12h) - Converted to active hydrocortisone by hepatic 11B-OH-steroid dehydrogenase. REVIEW MOA p 295. Remember, because MOA involves protein synthesis, the full effect will take 2-3 days, and last 2-3 days after d/c of drug! Overall, *enhances* gene expression for lipocortin (prevents liberation of arachidonic acid), enzymes of gluconeogenesis, glycogen synthetase in liver, and IFKB (inhibiting factor kappa-beta). *Inhibit* gene expression for CRH in hypothalamus, POMC (ACTH precursor) in pit gland, COX-2 in leukocytes, IL-1/IL-6/collagenase/TNF in macrophages.
Demeclocycline
Demeclocycline - tetracycline antibiotic used to Tx SIADH when serum Na <120 mEq/L and Pt has severe neuro Sx.
Desmopressin
Desmopressin - long-acting synthetic analog of ADH 6-20 h (nb: AVP = ADH). Action at V2 : V1 receptors = 4000:1, so less vasoconstrictor activity (if you're like me and you have no idea what the heck a V receptor is, check p 258-9). May be administered sc, iv, or in a convenient nasal spray, but at 10x the dose! May even be used to Tx hemophillia A and type 1 VonWilli's DX.
Dexamethasone
Dexamethasone - Systemic cortico (Long acting 36-72h), also available in nasal, inhaled, otic, opthalmic preps. REVIEW MOA p 295. Remember, because MOA involves protein synthesis, the full effect will take 2-3 days, and last 2-3 days after d/c of drug! Overall, *enhances* gene expression for lipocortin (prevents liberation of arachidonic acid), enzymes of gluconeogenesis, glycogen synthetase in liver, and IFKB (inhibiting factor kappa-beta). *Inhibit* gene expression for CRH in hypothalamus, POMC (ACTH precursor) in pit gland, COX-2 in leukocytes, IL-1/IL-6/collagenase/TNF in macrophages.
Fludrocortisone
Fludrocortisone - Systemic cortico with highest MINERALocorticoid activity. Small doses have little glucocorticoid effect. Use in conjunction w/ hydrocortisone or cortisone in Addison's disease (required for life).
Flunisolide
Flunisolide - Inhaled cortico (asthma and nasal). Review other info listed on other steroids.
Fluticasone
Fluticasone - Inhaled cortico (asthma and nasal) c low systemic absorption (50%) so good for use in kids!
Glipizide
Glipizide - Sulfonylurea - 2nd gen. - Very potent, careful in elderly and Pts c CVD (possible hypoglycemia). C/I in Pts c renal or hepatic dysfx'n. Short T1/2 = 2-4h, so hypoglycemia less likely.
Glyburide
Glyburide - Sulfonylurea - 2nd gen. - Very potent, careful in elderly and Pts c CVD (possible hypoglycemia). C/I in Pts c renal or hepatic dysfx'n. Duration 24h.
Hydrochlorothiazide
HCTZ - Reduces urinary volume 25-50% in nephrogenic DI (ie no reaction to ADH). Because Pt is volume contracted from too many trips to the restroom, more absorption occurs in PCT = less volume delivered distally where urine is diluted. Also Tx of lithium induced DI, but may decrease clearance of Li (so may have to decrease dose! see p261).
Hydrocortisone
Hydrocortisone - Systemic corticosteroid (short acting 8-12h). Also available in otic and opthalmic preps. This IS cortisol. REVIEW MOA p 295. Remember, because MOA involves protein synthesis, the full effect will take 2-3 days, and last 2-3 days after d/c of drug! Overall, *enhances* gene expression for lipocortin (prevents liberation of arachidonic acid), enzymes of gluconeogenesis, glycogen synthetase in liver, and IFKB (inhibiting factor kappa-beta). *Inhibit* gene expression for CRH in hypothalamus, POMC (ACTH precursor) in pit gland, COX-2 in leukocytes, IL-1/IL-6/collagenase/TNF in macrophages.
Insulin aspart
Insulin aspart - Ultra-short-acting insulin. Kinetics similar to lispro insulin. Lispro and aspart are mo bettah than regular insulin b/c faster onset and no increase in T1/2 with higher dose.
Insulin glargine
Insulin glargine (Lantus) - Given once daily sc and goes all day long, baby (unlike bid NPH).
Iodide (Lugol's solution)
Lugol's solution - Large dose of KI. Immediately inhibits the release of T3/T4 from thyroid by preventing proteolysis of thyroglobulin. Transient inhibition of organification of iodide by preventing iodide trapping (Wolff-Chaikoff effect). After 4-7days of suppression, the thyroid 'escapes' from the supressant effect and mucho thyroid activity can happen. If a patient is going to have Iodine 131 Tx, give them Iodine to take po if they experience reactive throid storm.
Isophane insulin
Isophane insulin = NPH insulin. Intermediate-acting. Insulin complexed c arginine-rich peptides to show absorption. Onset 1-2h, peak 6-12h, lasts 18-24h.
Lente insulin
Lente insulin - Intermediate-acting insulin. Onset 1-2h, peak 6-12h, lasts 18-24h. Consists of 30% semilente insulin (relatively rapid onset), and 70% ultralente insulin (poorly soluble Zn insulin crystals, delayed onset, long duration).
Lispro Insulin
Lispro Insulin - Sold by Rx, ultra-short-acting insulin. Quick onset b/c insulin molecules cannot form hexamers. Same T1/2 as natural insulin. Can be taken 10 min ac, peak @ 1h, lasts 3-4h. Duration of action NOT prolonged by increasing dose! Lispro and aspart are mo bettah than regular insulin b/c faster onset and no increase in T1/2 with higher dose.
Lithium
Lithium - Can cause nephrogenic DI by reducing formation of cAMP from V2 stimulation by ADH in principle cells of LDT/CD. Tx c HCTZ or Amiloride.
L-thyroxine
L-thyroxine - Synthetic T4 to treat hypothyroidism (don't forget hypothyroidism can be caused by steroids, lithium and amiodarone). In initial Tx, dose is raised every 2 weeks until TSH levels are normal. Careful in Pts c CV risk factors b/c high doses can precipitate MI or a-fib.
Metformin
Metformin - Oral antihyperglycemic = drug will NOT cause hypoglycemia in euglycemic Pts or Pts c T1DM. MOA=unknown, but enhances the effect of insulin on peripheral tissues (liver, fat, muscle). Does NOT work in the absence of insulin. Poss postprandial lactic acid production by GI can precipitate lactic acidosis. C/I in renal impairment. Does NOT cause weight gain.
Methimazole
Methimazole - Thioamide for Tx hyperthyroidism. MOA=prevent organification of iodide, blocks coupling of MIT and DIT. Does NOT block peripheral conversion of T4 to T3 like PTU!
Methylprednisolone
Methylprednisolone - Systemic cortico (Int acting 12-36h). REVIEW MOA p 295. Remember, because MOA involves protein synthesis, the full effect will take 2-3 days, and last 2-3 days after d/c of drug! Overall, *enhances* gene expression for lipocortin (prevents liberation of arachidonic acid), enzymes of gluconeogenesis, glycogen synthetase in liver, and IFKB (inhibiting factor kappa-beta). *Inhibit* gene expression for CRH in hypothalamus, POMC (ACTH precursor) in pit gland, COX-2 in leukocytes, IL-1/IL-6/collagenase/TNF in macrophages.
Pioglitazone
Pioglitazone - Oral antihyperglycemic - MOA not specified, assume it works like its sister, Rosi. Also improves lipids, but can also cause wt gain.
Prednisolone
Prednisolone - Systemic cortico (Int acting 12-36h). REVIEW MOA p 295. Remember, because MOA involves protein synthesis, the full effect will take 2-3 days, and last 2-3 days after d/c of drug! Overall, *enhances* gene expression for lipocortin (prevents liberation of arachidonic acid), enzymes of gluconeogenesis, glycogen synthetase in liver, and IFKB (inhibiting factor kappa-beta). *Inhibit* gene expression for CRH in hypothalamus, POMC (ACTH precursor) in pit gland, COX-2 in leukocytes, IL-1/IL-6/collagenase/TNF in macrophages.
Prednisone
Prednisone - Systemic cortico (Int acting 12-36h). Converted to active prednisolone by liver. REVIEW MOA p 295. Remember, because MOA involves protein synthesis, the full effect will take 2-3 days, and last 2-3 days after d/c of drug! Overall, *enhances* gene expression for lipocortin (prevents liberation of arachidonic acid), enzymes of gluconeogenesis, glycogen synthetase in liver, and IFKB (inhibiting factor kappa-beta). *Inhibit* gene expression for CRH in hypothalamus, POMC (ACTH precursor) in pit gland, COX-2 in leukocytes, IL-1/IL-6/collagenase/TNF in macrophages.
Propranolol
Propranolol - Tx Sx of hyperthyroidism. Controls autonomic Sx (tachy, sweating, tremor, etc). Blocks peripheral conversion of T4 to T3!! Metabolism of propranolol very rapid in hyperthyroidism, so large doses may be needed. Tx thyroid storm with this and PTU (to block peripheral conversion of T4 to T3).
Propylthiouracil (PTU)
Propylthiouracil (PTU) - Thioamide for Tx hyperthyroidism. MOA=prevent organification of iodide, blocks coupling of MIT and DIT, *blocks peripheral conversion of T4 to T3. Remember, the major effect is blocking the SYNTHESIS, not release of thyroid hormone, so onset is slow! No 'escape' phenomenon like iodine. If Pt relapses p Tx (60-80%), I131 Tx indicated. PTU has anti-vitamin k activity that can potentiate warfarin. PTU is highly plasma protein bound than Methimazole, so not likely to cross placenta in a pregnant woman to give 10% of ze poor babies goiter. Remember this, or else you might have to learn the embryology of neonatal goiter!
Regular insulin
Regular insulin - Rapid-acting. If given sc, hexamers must disassociate before acting, so T1/2 increases with increased dose. If given iv, hexamers quickly break into 'ready to go' monomers. Taken 30-45 min ac, onset in 15 min, peak 2-4h, duration 5-8h.
Repaglinide
Repaglinide - Sulfonylurea - 2nd gen. - Same MOA as sulfonylureas, but supposedly does a good job in preventing postprandial hyperglycemia w/o much effect on fasting glucose.
Rosiglitazone
Rosiglitazone - Oral antihyperglycemic - MOA=binds to PPAR~y to cause increased expression of genes encoding for GLUT-4 in skel musc/adipose, lipoprotein lipase (good effect on lipid profile), insulin receptors in skel musc/adipose. No effect on hepatic gluconeogenesis. May prevent islet cell degen in T2DM. S/E=fluid retention (weight gain) and edema, h/a.
Tolbutamide
Tolbutamide - Sulfonylurea - First gen oral hypoglycemic. MOA=block ATP sensitive K channels in islet cells to cause increased insulin secretion. Works in non-diabetics! Does NOT sensitize periphery to insulin effects. DOA=6-10h.
Triamcinolone
Triamcinolone - Systemic cortico (Int acting 12-36h). REVIEW MOA p 295. Remember, because MOA involves protein synthesis, the full effect will take 2-3 days, and last 2-3 days after d/c of drug! Overall, *enhances* gene expression for lipocortin (prevents liberation of arachidonic acid), enzymes of gluconeogenesis, glycogen synthetase in liver, and IFKB (inhibiting factor kappa-beta). *Inhibit* gene expression for CRH in hypothalamus, POMC (ACTH precursor) in pit gland, COX-2 in leukocytes, IL-1/IL-6/collagenase/TNF in macrophages.
Acetaminophen
Analgesic and antipyretic, but NOT anti-inflammatory. MOA unclear, poss COX3? PMN activation and platelet fxn unaltered. S/E=skin rash and hepatotoxicity. Hepatotox via MEOS dependent conversion to NABQ that reacts c sulfhydryl groups in hepatic proteins causing damage and necrosis. MEOS is induced by chronic EtOH consumption. Renal tubular necrosis can result from long term abuse of ACM.
ASA
Analgesic. Exhibits non-linear pharmacokinetics in higer doses (b/c mechanism by which salicylate is conjugated c glycine to form salicyluric acid becomes saturated). Inhibit COX1 & 2, inhibits migration of PMNs and MΦs, stabilizes lysosomal membranes, inhibits Ag/Ab aggregation. Reduces *elevated* body temp via inhib of PG synth in hypothalamus. Inhibition of platelet aggregation via COX1 production of TXA2. Acid pH in stomach promotes absorption, alkaline urine promotes excretion. 80-90% plasma protein bound (can displace drugs like warfarin). Tinnitus is a Sx of tox. Can have a hypersensitivity rxn (esp in Pts c 'toxic triad' of hypersensitivity, nasal polyps, and asthma). Caution in renal DX or dehydration (can cause dec in GFR, interstitial nephritis, edema).
Baclofen
Sk musc relaxant (central acting). Although agonist @ GABAb receptors, questionable if this is the MOA. End result, however, is a reduction in glutamate release from spinal neuronal circuits. Particularly effective in hypertonic d/os like MS and spinal cord injury. S/E include sedation, confusion, weakness, and sudden w/d can lead to hallucinations.
Botulinum toxin
Skeletal muscle relaxant. MOA=Presynaptic block by cleaving proteins in the presynaptic neuron involved in exocytosis of ACh containing vesicles. Relaxes muscles currently contracted as well as non-contracted muscle.
Buprenorphine
Narc analgesic. Partial agonist @ Mu. Partial agonist activity and long T1/2 make it useful to decrease opiate craving in addicts.
Cisatracurium
Skeletal muscle relaxant. MOA=Postsynaptic block via non-depolarizing (competitive) block of ACh receptors on postsynaptic neuron. Increasing [ACh] can reverse the block, ie use of AChase inhibitors like neostigmine. Recent studies suggest possible action
Dantrolene Na
Peripheral acting muscle relaxant. Direct effects on excitation-contraction coupling mechanism by decreasing Ca release from the SR thereby allowing relaxation of *hypertonic skel musc. Esp useful PRO for anesthetic-induced malignant hyperthermia.
Desflurane
Inhalational anesthetic. Rapid increases in concentration (ex 1 MAC to 1.5 MAC) produces SNS activation that transiently increases HR & BP. High incidence of airway irritation when used as single agent (can decrease c pretreatment w/ narcotics). Can react c CO2 absorber to form CO (prevent by keeping absorber moist, esp 1st case in morning).
Diazepam
Skeletal musc relaxant (central acting). BZs increase GABA xmission to decrease interneuronal signaling. Effects reduce hypertonicity and rigidity (ie currently contracted muscle is relaxed). Used primarily to reduce spasticity.
Etomidate
IV anesthetic. Rapid onset of sleep and recovery. NO analgesic properties (use c narcs or N2O). MOA=increase in inhibitory synaptic xmission via GABAa receptors. High incidence of exitatory phenomenon (involuntary movement & myoclonus). Minimal effects on CV and respiratory systems (good for use in little old ladies). Pts can exhibit marked adrenocortical suppression esp c continuous infusion (can last 4 days). Relatively high incidence of N/V.
Fentanyl
Narc analgesic. Full agonist @ Mu receptors. Will wait for Pt to urinate p Tx c Fentanyl b/c urinary retention more prominent.
Halothane
Inhalational anesthetic. At 1 MAC, can increase cerebral blood flow by 60-70%. Decreases dp/dt and CO, poss changes in cardiac rhythm and conduction. BP lowering effect appears to be due more to decreased CO. Post-op hapatic necrosis has been reported. Can cause inc in vagal tone to dec HR, and sensitizes heart to exogenous catecholamines.
Ibuprofen
Propionic acid derivative analgesic. Inhibit COX1 & 2, inhibits migration of PMNs and MΦs, stabilizes lysosomal membranes, inhibits Ag/Ab aggregation. Reduces *elevated* body temp via inhib of PG synth in hypothalamus. 95% plasma protein bound. Caution in renal DX or dehydration (can cause dec in GFR, interstitial nephritis, even *nephrotic synd), esp in chronic use. Less gastric irritation then ASA. Poss hypersens rxn similar to ASA (esp urticaria).
Inhalational anesthetics
Lipid solubility=potency. Blood:gas coeff inversely proportional to rate of onset/offset. All decrease exitatory xmission and increase inhibitory xmission. Produce irregularly descending depression of CNS (higher cortical centers, ascending RAS and spinal cord affected first). All decrease vasc sm tone for a dose related drop in BP. Dose related respiratory depression, decrease in tidal volume. Dose dependent relaxation of skeletal musc. N/V.
Isoflurane
Inhalational anesthetic. No specifics given.
Ketamine
IV anesthetic. Produces a cataleptic trance-like state, Pt may appear awake c open eyes aka 'dissociative anesthesia.' Pt maintains protective reflexes (ie cough and gag). Relatively rapid acting w/ a return of conciousness in 15 min, but complete recovery can be slow. Profound analgesia. MOA=non-competative inhibition of NMDA subtype of glutamate receptor (acts to control signal strength), decreases excitatory xmission by reducing Ca conduction. S/E=CV system stimulation (PRO c BZs), inc cerebral blood flow and pressure, funky dreams can occur days or weeks p d/c (PRO c BZs). Good drug for use in quick, painful procedures (like setting a Fx) or in repeat procedures like burns and debridement.
Lidocaine
Amide local anesthetic. Blocks Na channels in the inactivated-closed state (rapidly firing axons exibit a higher affinity). Degraded by hepatic CYP450 (so lookout for tox in hepatic DX or reduced hepatic blood flow). Toxicity Sx=initial CNS stimulation (apprehension, salivation, tremor) followed by convulsions & CNS mediated HTN and tachy, followed by hypotension. Tx c BZs.
Meperidine
Narc analgesic. Exact receptor effects not listed. Concommittant Tx c MAOIs can produce excitation, convulsions, hyperpyrexia, rep depression, and hypoTN. No miosis (pinpoint pupils) in tox c meperidine!
Midazolam
Used to reduce anxiety and sedate patient as adjunct to anesthesia. Minimal CV and resp depression. Do NOT cause analgesia.
Morphine
Narc analgesic. Full agonist @ Mu, kappa, and delta receptors. Higher levels of histamine release S/E. A&V dilation can cause ortho hypo.
Nalbuphine
Narc analgesic. Partial agonist @ Mu, full agonist @ kappa.
Naloxone
Opiate antagonist.
Naltrexone
Opiate antagonist.
Narcotic analgesics
All actions mediated by binding to opiate receptors at pre or postsynaptic sites in the CNS or peripheral tissues that are coupled to various GTP-dependent proteins (G proteins). Presynaptic actions decrease voltage-gated Ca influx that reduces exitatory neurtransmitter release. Postsynaptic effects produce increased K efflux via activation of receptor mediated K channels leading to hyperpolarization (ie reduction in signal strength). Inhibit nociceptive reflexes (spinal & supraspinal sites) to raise threshold of pain perception and diminish rxn to pain (even though pain is still perceived) via Mu receptors (continuous dull pain reduced better than intermittant sharp pain). S/E of drowsiness and anti-anxiety quite variable. Cause euphoria or feeling of detachment. Dose-dependent respiratory depression (decrease respiratory center sensitivity to CO2). N/V by direct axn on CTZ. Can cause histamine release (itchiness). Intestinal tone increased, motility decreased as well as miosis effects not effected by tolerance (that can develop over 1-3w). Toxicity triad=depressed respiration, miosis (pinpoint pupils xcept meperidine), coma.
Nitrous Oxide
Inhalational *analgesic. Rapid onset/offset (low blood:gas coeff). Used in combo w/ inhalational anesthetics to lower the concentration required for same level of anesthesia. MOA unknown. Hypoxia w/ concentrations over 80%. Diffusion hypoxia possible if administration rapidly terminated w/o supplemental oxygen. High diffusion can exacerbate pneumothorax, cause tympanic membrane rupture, and increased gastric volume/pressure. Chronic exposure show to dec fertility in women, can also cause a peripheral neuropathy.
Pancuronium
Skeletal muscle relaxant. MOA=Postsynaptic block via non-depolarizing (competitive) block of ACh receptors on postsynaptic neuron. Increasing [ACh] can reverse the block, ie use of AChase inhibitors like neostigmine. Recent studies suggest possible action on presynaptic Na channels to also decrease ACh release.
Procaine
Ester local anesthetic. Blocks Na channels in the inactivated-closed state (rapidly firing axons exibit a higher affinity). Degraded by pseudocholinesterase in plasma, so short doa. Possible anaphylaxis to ester anesthetics. Toxicity Sx=initial CNS stimulation (apprehension, salivation, tremor) followed by convulsions & CNS mediated HTN and tachy, followed by hypotension. Tx c BZs. For you history buffs, this was the first synthetic local ever synthesized!
Propofol
Careful, he loves this drug. IV anesthetic, but must use c narcotics, N2O, or regional anesthetic b/c propofol DOES NOT cause analgesia. Induction and recovery rapid, less 'hang over' than thiopental. MOA=appears to be via GABAa receptors. S/E=dose dependent depression of respiration c possible apnea. HypoTN due to reduced vascular resistance. 15-30% decrease in cardiac indices. REDUCTION in N/V from anti-emetic properties. Injection site irritation and burning, possible hypersensitivity to egg albumin used in preparation.
Sevoflurane
Inhalational anesthetic. Under low flow conditions, can react c CO2 absorber to form 'Compound A,' although not shown to cause tox in humans.
Succinylcholine
Skeletal muscle relaxant. MOA=Postsynaptic block via depolarizing (non-competitive) block. Binding to postsynaptic Na channels induces a 'flickering' of ion conductance. Initial block c depolarization=Phase 1 block which can be potentiated c AChase inhibitors. Continued occupancy of receptors induces desensitization and eventually the membrane repolarizes. Succinylcholine is still occupying the receptor, however, acting like a competitive inhibitor (thus characteristics are just like the other competitive inhibs)=Phase 2 block, which can be overcome via increased [ACh]. Pts c atypical AChase (or on AChase inhibitors) exhibit a prolonged block. Pts c burn injuries or trauma (esp CNS) can experience marked hyperkalemia that can cause MI.
5-HT1 receptor effects
Vascular 5-HT1 receptors mediate vasodilation-direct stimulation vascular sm, stimulation of endothelial cells which produce EDRF (endo-derived relaxation factor), pre-junctional inhib. NE release from sympathetic fibers. 5-HT1B receptors constricts large extracerebral arteries and A/V anastamoses as well as coronary arteries. Presynaptic 5-HT1B & D inhibits proinflammatory peptide release from CN5. 5-HT1A involved in behavior (large concentration in hippocampus).
5-HT2 receptor effects
Increase IP3 and intracellular calcium to mediate vasoconstriction, PGI2 synthesis by vasc endo cells, platelet aggregation, bronchoconstriction, GI motility and secretion. Central 5-HT2 receptors (in cerebral cortex) are the major 5-HT receptor involved in depression.
5-HT3 receptor effects
Stim of prejunctional 5-HT3 receptors increases ACh release in GI tract. Sensory effects: Bezold-Jarisch chemoreceptor reflex, stim of dermal afferent pain fibers, stim of visceral sensory fibers (afferent vagal fibers to vomiting center), stim of CTZ (aka cookie tossing control center).
5-HT4 receptor effects
Stimulation of prejunctional 5-HT4 receptors increases ACh release from intramural cholinergic neurons in the GI tract.
Al & Mg hydroxides
Antacids-Weak water soluble bases. Al compounds can cause constipation, Mg compounds can cause diarrhea (Mg effect predominates in mixed Al/Mg compounds). "All stopped up vs. Oh My God."
Almotriptan
5-HT1B & D agonist for Tx of migraine and cluster headache. If 1 dose didn't work, subsequent doses are not likely to be any more effective. S/E=rebound headache, 'atypical' sensations, dizziness/vertigo, ***severe coronary vasospasms in Pts c CAD. Do not use w/in 24 hours of injestion of ergot-type drugs.
Anti-ACh effects of antihistamines
CNS depression (sedation), inhibition of nasopharyngeal secretion, prevention of motion sickness (action in vestibular nuclei), anti-emetic effect. Especially in older Pts-dry mouth, dry cough, urinary retention (c BPH), exacerbation of glaucoma.
Bisacodyl
Laxative-irritant action increases accumulation of water and electrolytes in the lumen of the colon (6-12 h c po dosing, 15-60 min c suppository). Can cause GI colic, laxative dependence, dehydration, and electrolyte imbalance. Used for bowel evacuation prior to exam.
Bismuth compunds
Coating agent-Antiulcer effects via contraction of surface layer of mucus in GI to protect mucosa as well as coating it. Increases PG synthesis and alkali secretion. Antiproteolytic counteracts breakdown of mucus coat by pepsin and bacterial proteases. Anti-bacterial effects by binding to -SH groups of bacterial proteins which destroys tertiary structure as well as prevention of bacterial binding to mucosa by decreasing their adherent properties. Can have salicylate toxicity c bismuth salicylate. Stool becomes radio-opaque with all bismuth compounds.
Bromopheniramine
H1 receptor antagonist
Cetirizine
Newer H1 antagonist (*decreased anticholinergic effects) for Tx of allergies.
Chlorpheniramine
H1 receptor antagonist
Cimetidine
H2 receptor antagonist for Tx of GERD, ulcers, Zollinger-Ellison (gastrinoma). Inhibits hepatic cyP-450 (which breaks down estrogen) and can cause gynecomastia, azospermia, dec libido. Increases T1/2 of B agonists, warfarin, diazepam. Can cause CNS effects-confusion to overs psychosis.
Cisapride
5-HT4 receptor agonist to enhance ACh release in GI. Enhances esophageal clearance of gastric acid, elevates lower esoph sphincter tone, accelerates gastric emptying, decreases small bowel transit time. Tx gastric reflux, promote gastric and duodenal emptying pre-op or pre-endoscope. S/E-abd cramping & diarrhea.
Cromolyn (sodium)
Inhibits mast cell degranulation by preventing increase in intercellular calcium caused by sIgE bridges.
Cyproheptadine
H1, ACh, 5-HT1 & 2 receptor antagonist (crosses BBB). Tx allergic DX, appetite stimulation, migrane, carcinoid synd, PTSD. S/E=exacerbation of glaucoma, BPH, GI/GU obstruction. CNS depression additive c other drugs (poss paradoxical exitation in kids). Dry mouth, nose, throat.
Dimenhydrinate
H1 receptor antagonist. Used PRO for motion sickness and vertigo of vestibular origin (Meniere's DX).
Diphenhydramine
H1 receptor antagonist. Also exibits local anesthetic effect. Can be used in Parkinson's to Tx the central motor d/o caused by anti-psychotic drugs.
Diphenoxylate
Antidiarrheal-opiate that slows colonic transit rate by direct/indirect inhibition of GI motility (but tone increases). Contains atropine to prevent abuse.
Docusate sodium
Laxative-anionic surfactant that lowers surface tention of feces to allow penetration by water. No laxative dependence.
Dronabinol
Antiemetic-THC
Effects of H1 receptor block
Prevents smooth muscle constriction (bronchial and GI), inhibit pain and itching at sensory nerve endings, antagonize the increase in capillary permiability.
Famotidine
H2 receptor antagonist for Tx of GERD, ulcers, Zollinger-Ellison (gastrinoma).
Fexofenadine
Newer H1 antagonist (*decreased anticholinergic effects) for Tx of allergies.
H. pylori Tx
Say ciao to H. pylori' - clarithromycin, amoxacillin, omeprazole
Hydrocortizone
Corticosteroid (enema, foam, suppository) for Tx of inflam. bowel DX (IBD). Given po for extensive colonic DX or small intestine DX.
Infliximab
MAB against TNF for use in IBD.
Ipecac
Emetic-stimulates CTZ. CI c injestion of petrolium distillates or corrosive chemicals, CNS depressants can cause aspiration of vomitus, can precipitate seizures in Pts poisoned by CNS stimulants.
Kaopectate
Antidiarrheal-hydrated Al silicate clay c pectin. Negatively charged clay absorbes bacterial toxins. Pectin becomes hydrated to form a viscous colloidal solution which helps to consolidate the stool.
Lactulose
Laxative-synthetic disaccharide not absorbed in the GI. Converted to lactic, acetic, and organic acids by enterobacteria which exerts an osmotic effect. Acidification of colonic contents causes ammonia trapping to Tx PSE in hepatic DX. No laxative dependence.
Loperamide
Antidiarrheal-opiate that slows colonic transit rate by direct/indirect inhibition of GI motility (but tone increases).
Loratadine
Newer H1 antagonist (*decreased anticholinergic effects) for Tx of allergies. Now OTC (claritin).
Magnesium compounds
Laxative-Hypertonic solutions create osmotic draw. Can cause GI colic, laxative dependence, dehydration and electrolyte dependence. Used for bowel evacuation prior to exam.
Meclizine
H1 receptor antagonist. Used PRO for motion sickness and vertigo of vestibular origin (Meniere's DX).
Methylcellulose
Laxative-bulk laxative made from indigestible components that attract H2O to form a hydrogel. Increased bulk stimulates stretch receptors to increase peristalsis. No laxative dependence.
Methylprednisone
Corticosteroid (enema, foam, suppository) for Tx of inflam. bowel DX (IBD). Given po for extensive colonic DX or small intestine DX.
Metoclopramide
5-HT3 antagonist, D2 antagonist, 5-HT4 agonist. MOA=GI stim via 5-HT4 receptors, antiemetic effects via 5-HT3 & D2 receptor block in CTZ. Tx GERD (inc in LES tone), pre-op/endoscope GI clearing, prevent N/V c gastric CA, UC, PUD, and Pts receiving chemo/radiation treatment. S/E=sedation and fatigue, altered GI absorption of other drugs, D2 block can cause galactorrhea, amenorrhea, gynecomastia, dystonias, tardive dyskinesia.
Misoprostol
Antacid-Stable analog of PGE1, stimulation of gastric parietal cell PGE1 receptors inhibits acid secretion. No effect on basal acid secretion, but blocks acid increase in response to histamine, pentagastrin, aspirin, food and coffee. Also exerts a protective effect on gastric mucosa. S/E=diarrhea in 5-15% of Pts. DO NOT USE IN WOMEN WITHOUT CONTRACEPTION-Misoprostol is a potent abortifacient.
Nedocromil (sodium)
Inhibits mast cell degranulation by preventing increase in intercellular calcium caused by sIgE bridges.
Octreotide
Antidiarrheal-somatostatin agonist. Reduces diarrhea/flushing associated c metastatic carcinoid syndrome and VIPomas. Used to stop bleeding of esophageal varices c less S/E than AVP. Decreases spanchnic blood flow and lower portal venous pressure.
Olopatadine
Opthalmic-Inhibits mast cell degranulation by preventing increase in intercellular calcium caused by sIgE bridges AND blocks H1 histamine receptors.
Olsalazine
NSAID-two 5-ASA molecules joined by an azo bond which is cleaved in the large bowel by enterics.
Omeprazole
Antacid-inhibits gastric H-K ATPase to block acid secretion for 1-3 days. Inhibits both basal and nocturnal acid secretion as well as acid secretion by other stimuli. Causes a reactive increase in plasma gastrin concentration. Tx of Z-E syndrome.
Ondansetron
Selective 5-HT3 antagonist. MOA=5-HT3 block at CTZ and vagal afferents. Tx N/V from chemo/radiation or post-op. More effective than metoclopramide and no movement d/os, as effective as dexamethazone (can be combined for added efficacy). S/E=constipation.
Polyethylene glycols (PEGS)
Laxative-Hypertonic solutions create osmotic draw. Can cause GI colic, laxative dependence, dehydration and electrolyte dependence. Used for bowel evacuation prior to exam.
Prochlorperazine
Antiemetic-Blocks D2 receptors in CTZ.
Promethazine
H1 receptor antagonist. Used for TREATMENT of CURRENT Sx of motion sickness (suppository or im), also pre-op sedation.
Psyllium
Laxative-bulk laxative made from hydrophyllic mucilloid from seed coats, forms hydrogel. Tx of hyperlipoproteinemia. No laxative dependence.
Ranitidine
H2 receptor antagonist for Tx of GERD, ulcers, Zollinger-Ellison (gastrinoma).
Scopolamine
Antiemetic-blocks ACh receptors in vestibular nuclei and reticular formation. S/E=dry mouth, sedation, inability to concentrate, amnesia, and fatigue.
Sucralfate
Coating agent-water insoluble complex of Al hydroxide and sucrose sulfate which polymerizes when pH < 4 to form a sticky viscous gel that coats/protects the mucosa. Gel binds tightly to ulcerated gastric mucosa, and refluxes into esophagus in GERD. Does not dissolve in duodenum despite rise in pH. Does NOT neutralize acid or inhibit its secretion. More effective on duodenal ulcers, not effected by cigarette smoking, good for intubated Pts to prevent INF. Do NOT use c H2 antagonists (b/c acidic pH required for polymerization).
Sulfasalazine
NSAID-65% reaches distal ileum and large bowel where it is degraded to sulfasalazine and 5-ASA that blocks production of PGs and LTs (inhibits cyclooxygenase and lipooxygenase). S/E=hepatic damage and bone marrow depression esp in slow acetylators. Can interfere with folate absorption so must give folate supplements.
Sumatriptan
5-HT1B & D agonist for Tx of migraine and cluster headache. Short T1/2, so Sx may recur after 1 dose. If 1 dose didn't work, subsequent doses are not likely to be any more effective. S/E=rebound headache, 'atypical' sensations, dizziness/vertigo, ***severe coronary vasospasms in Pts c CAD. Do not use w/in 24 hours of injestion of ergot-type drugs.
Tegaserod
5-HT4 receptor agonist to enhance ACh release in GI. Enhances esophageal clearance of gastric acid, elevates lower esoph sphincter tone, accelerates gastric emptying, decreases small bowel transit time. Tx gastric reflux, promote gastric and duodenal empt
Tx of carcinoid tumor
Cyproheptadine (blocks 5-HT1 or 2 receptors) or Octreotide (somatostatin agonist that inhibits 5-HT release).
Tx of GERD
Omeprazole, H2 antagonists, Sucralfate, Cisapride
Tx of IBS
Bulk laxatives, dicyclomine (ACh antagonist), tegaserod (for constipation predominant IBS).
Ursodiol
Tx of gallstones and primary biliary cirrhosis. Trace constituent of the normal bile acids that undergoes enterohepatic recirculation. Increases bile acid/cholesterol ratio by decreasing cholesterol synthesis (inhib HM CoA reductase), reducing GI absorption of cholesterol, and decreases biliary secretion of cholesterol. Prevents gallstone formation and solubilizes existing gallstones. Also appears to slow progression of primary biliary cirrhosis thus increasing the time before hepatic transplant is required.
Cyclophosphamide
Alkylating agent, not cycle specific, DLT-Myelosup. (but platelets relatively spared), ***also toxic to bladder (hemorrhagic cystitis, etc)
Thiotepa
Alkylating agent, not cycle specific, DLT-Myelosup.
Busulfan
Alkylating agent, not cycle specific, DLT-Myelosup.
Carmustine
Alkylating agent, not cycle specific, DLT-Myelosup.
Lomustine
Alkylating agent, not cycle specific, DLT-Myelosup.
Semustine
Alkylating agent, not cycle specific, DLT-Myelosup.
Temozolamide
Alkylating agent, not cycle specific, DLT-Myelosup.
Procarbazine
Alkylating agent, not cycle specific, DLT-Myelosup.
Cisplatin
Alkylating agent, not cycle specific, DLT-***Nephrotoxicity (can mitigate by hydration c NS a & p infusion)
Carboplatin
Alkylating agent, not cycle specific, DLT-**Myelosup.
Oxaliplatin
Alkylating agent, not cycle specific, DLT-***Neurotoxicity
Methotrexate
Binds Dihydrofolate Reductase (DHFR) so no makie purines/pyrimidines, S cycle specific, DLT-Myelo (prolonged c effusions) - BM rescue c leucovorin
Leucovorin
BM rescue in Methotrexate usage
5-Fluorouracil
Uracil analog that inhibits thymidylate synthase to prevent THYMINE synthesis, S cycle specific, DLT-Myelo, also causes tear duct stenosis (epiphora)
Capecitabine
Converted intracellularly to 5-FU by thymidine phosphorylase (but administered PO!), S cycle specific, Derm toxicity (hand-foot Synd) (p 198 lists the derm S/E of this drug, but tear duct one for 5-FU... Go figure)
Cytarabine
Phosphorylated inhibitor of DNA polymerase, S cycle specific, central CNS toxicity
6-Mercaptopurine
Converted by hypoxanthine guanine phosphoribosyl transferase to 6MP nucleotide that inhibits DNA/RNA formation, S cycle specific, DLT-Myelo
Vinblastine
Vinca alkaloid inhibits microtubule assembly, M phase specific, DLT-Myelo (WBCs>platelets), also a vesicant (Tx c heat & intradermal hyaluronidase)
Vincristine
Vinca alkaloid inhibits microtubule assembly, M phase specific, Non-myelosuppressive! DLT-Neurotoxicity (Paresthesias, los of DTRs & GI motility), also a vesicant (Tx c heat & intradermal hyaluronidase)
Estramustine
Inhibits microtubule assembly, M phase specific, DLT-Myelo
Paclitaxel
Promotes microtubule assembly & *stabilizes against depolymerization, M phase specific, DLT-Myelo but also peripheral neurotoxic ~vincristine
Etoposide
Topoisomerase II inhibitor (causes double stranded breaks in DNA), G2 phase specific, DLT-Myelo
Teniposide
Topoisomerase II inhibitor (causes double stranded breaks in DNA), G2 phase specific, DLT-Myelo
Topotecan
Topoisomerase I inhibitor (single stranded DNA breaks), G2 phase specific, DLT-Myelo
Irinotecan
Topoisomerase I inhibitor (single stranded DNA breaks), G2 phase specific, DLT-delayed diarrhea ~ 24h p infusion
Doxorubicin
Anthracycline (topoisomerase II inhibitor), not cycle specific, DLT-Myelo but also CARDIOTOXIC! Must keep total dose <550mg/m²
Bleomycin
Intercalates (inserts in) DNA causing strand breaks c Oxygen free radicals, G2 phase specific, DLT-***Pulmonary Fibrosis (do NOT forget this one)
L-asparaginase
Causes hydrolysis of serum asparagine (essential amino acid for leukemia cells), G1 cycle specific, DLT-Hepatotoxicity (decreased K dependent clotting factors & albumin)
Imatinib
Inhibits ATP binding to Bcr-Abl tyrosine kinase (product of t9:22 philly chromosome in CML), ? Cycle specific, no specific tox
Raloxifene
Estrogen receptor antagonist, can cause hot flashes, fluid retention, poss endometrial CA
Tamoxifen
Estrogen receptor antagonist, can cause hot flashes, fluid retention, poss endometrial CA
Anastrozole
Aromatase inhibitor (blocks conversion of androstenedione to estrone), few S/Es
Bicalutamide
Androgen receptor antagonist, S/E=gynecomastia, hot flashes, impotence, diarrhea
Leuprolide
GnRH agonist (overstimulation of receptors causes downregulation, thus decreases FSH/LH by 90% in 2 weeks), S/E=hot flashes, impotence, tumor flare up (can prevent tumor flare c bicalutamide)
Levamisole
Potentiates action of 5-FU
Thalidomide
Inhibits TNF-alpha preventing angiogenesis necessary for tumor blood supply, S/E=TERATOGENIC(phocomelia=no limbs), drowsiness, peripheral neuropathy, constipation
Trastuzumab
Binds epidermal growth factor receptor (Her 2/neu), S/E=chills, fever during 1st infusion.***Also cardiotoxic!
5-Fluorouracil
Uracil analog that inhibits thymidylate synthase to prevent THYMINE synthesis, S cycle specific, DLT-Myelo, also causes tear duct stenosis (epiphora)
6-Mercaptopurine
Converted by hypoxanthine guanine phosphoribosyl transferase to 6MP nucleotide that inhibits DNA/RNA formation, S cycle specific, DLT-Myelo
Anastrozole
Aromatase inhibitor (blocks conversion of androstenedione to estrone), few S/Es
Bicalutamide
Androgen receptor antagonist, S/E=gynecomastia, hot flashes, impotence, diarrhea
Bleomycin
Intercalates (inserts in) DNA causing strand breaks c Oxygen free radicals, G2 phase specific, DLT-***Pulmonary Fibrosis (do NOT forget this one)
Busulfan
Alkylating agent, not cycle specific, DLT-Myelosup.
Capecitabine
Converted intracellularly to 5-FU by thymidine phosphorylase (but administered PO!), S cycle specific, Derm toxicity (hand-foot Synd) (p 198 lists the derm S/E of this drug, but tear duct one for 5-FU... Go figure)
Carboplatin
Platinum Alkylating agent, not cycle specific, DLT-**Myelosup.
Carmustine
(BCNU) IV Nitrosurea Alkylating agent, not cycle specific, DLT-Myelosup.
Cisplatin
Platinum Alkylating agent, not cycle specific, DLT-***Nephrotoxicity (can mitigate by hydration c NS a & p infusion)
Cyclophosphamide
Alkylating agent, not cycle specific, DLT-Myelosup. (but platelets relatively spared), ***also toxic to bladder (hemorrhagic cystitis, etc)
Cytarabine
Phosphorylated inhibitor of DNA polymerase, S cycle specific, central CNS toxicity
Doxorubicin
Anthracycline (topoisomerase II inhibitor), not cycle specific, DLT-Myelo but also CARDIOTOXIC! Must keep total dose <550mg/m²
Estramustine
Inhibits microtubule assembly, M phase specific, DLT-Myelo
Etoposide
Topoisomerase II inhibitor (causes double stranded breaks in DNA), G2 phase specific, DLT-Myelo
Imatinib
Inhibits ATP binding to Bcr-Abl tyrosine kinase (product of t9:22 philly chromosome in CML), ? Cycle specific, no specific tox
Irinotecan
Topoisomerase I inhibitor (single stranded DNA breaks), G2 phase specific, DLT-delayed diarrhea ~ 24h p infusion
L-asparaginase
Causes hydrolysis of serum asparagine (essential amino acid for leukemia cells), G1 cycle specific, DLT-Hepatotoxicity (decreased K dependent clotting factors & albumin)
Leucovorin
BM rescue in Methotrexate usage
Leuprolide
GnRH agonist (overstimulation of receptors causes downregulation, thus decreases FSH/LH by 90% in 2 weeks), S/E=hot flashes, impotence, tumor flare up (can prevent tumor flare c bicalutamide)
Levamisole
Potentiates action of 5-FU
Lomustine
(CCNU) PO Nitrosurea Alkylating agent, not cycle specific, DLT-Myelosup.
Methotrexate
Binds Dihydrofolate Reductase (DHFR) so no makie purines/pyrimidines, S cycle specific, DLT-Myelo (prolonged c effusions) - BM rescue c leucovorin
Oxaliplatin
Platinum Alkylating agent, not cycle specific, DLT-***Neurotoxicity
Paclitaxel
Promotes microtubule assembly & *stabilizes against depolymerization, M phase specific, DLT-Myelo but also peripheral neurotoxic ~vincristine
Procarbazine
Alkylating agent, not cycle specific, DLT-Myelosup.
Raloxifene
Estrogen receptor antagonist, can cause hot flashes, fluid retention, poss endometrial CA
Semustine
(CCNU/Methyl) PO Nitrosurea Alkylating agent, not cycle specific, DLT-Myelosup.
Tamoxifen
Estrogen receptor antagonist, can cause hot flashes, fluid retention, poss endometrial CA
Temozolamide
Alkylating agent, not cycle specific, DLT-Myelosup.
Teniposide
Topoisomerase II inhibitor (causes double stranded breaks in DNA), G2 phase specific, DLT-Myelo
Thalidomide
Inhibits TNF-alpha preventing angiogenesis necessary for tumor blood supply, S/E=TERATOGENIC(phocomelia=no limbs), drowsiness, peripheral neuropathy, constipation
Thiotepa
Alkylating agent, not cycle specific, DLT-Myelosup.
Topotecan
Topoisomerase I inhibitor (single stranded DNA breaks), G2 phase specific, DLT-Myelo
Trastuzumab
Binds epidermal growth factor receptor (Her 2/neu), S/E=chills, fever during 1st infusion.***Also cardiotoxic!
Vinblastine
Vinca alkaloid inhibits microtubule assembly, M phase specific, DLT-Myelo (WBCs>platelets), also a vesicant (Tx c heat & intradermal hyaluronidase)
Vincristine
Vinca alkaloid inhibits microtubule assembly, M phase specific, Non-myelosuppressive! DLT-Neurotoxicity (Paresthesias, los of DTRs & GI motility), also a vesicant (Tx c heat & intradermal hyaluronidase)
Milrinone
Tx s/p MI. Inhibits type III PDEase > increases cAMP in cardiomyocytes = inc dp/dt, faster relaxation in diastole, balanced vasodilation (dec pre/afterload), dec pulm vasc resistance. SV increases via inc dp/dt and decreased pre/afterload. Tx doesn't decrease cardiovascular mortality.
Carvedilol
Tx HF via ß1, ß2, α1 block. Tx of Pt NYHA II & III and ejection fract <35% also taking ACE-I and diuretic (and possibly digoxin). Takes months (during which EF is less and Pt feels like crap). Eventually EF improves above baseline. Start low, go slow, but build to highest tolerable dose (beneficial effects directly dose-related).
Valsartan
AntiHTN-ARB-balanced vasodilators. Essentially same as ACE inhibitors. Do not inhibit metabolism of bradykinin or increase synth of prostaglandins. Approved for HT, but dose response shallow (use thiazide to inc efficacy). Use if ACE inhib not tollerated by Pt (ex cough). NO NO in pregnancy or breast feeding. S/E=angioedema (esp if ACE inhib did), HypoTN, HyperK.
Diltiazam
Antidysrhythmic-Ca blocker (Class IV) in slow fibers esp. AV node. Decrease HR, contractility (dec CO), AV conduction (=inc P-R). Inc ERP in AV node. Tx Afib/flutter to control vent rate, cardioverts AV re-entry tach (PSVT). S/E=HypoTN, heart block, sinus bradycardia.
ARBs in HF
-sartan drugs. Almost same effects as ACE-I, but not yet approved for Tx of HF. Can be substituted for ACE-I if Pt does not tolerate ACE-I well (ex dry cough).
Diazoxide
AntiHTN (*only in HTN emergency)-reduce availability of intercellular Ca in arteries (dunno how) > Arteriodilator. Reserved for Pts c severe HTN refractory to first-line drugs. Lower TPR > dec BP but there is a baroreflexive increase in SNS tone = all that you think it would. Possible to use c ß blocker.
Procainamide
Antidysrhythmic-Na, K block (Class IA). Similar to Quinidine but no block ACh/α, small ganglionic antinicotinic effect > hypoTN. Tx Vtach in Afib/flutter, PVCs, seldom used outPt due to toxicity (one of SHIP drugs). S/E=HypoTN, Torsade, SLE like Synd.
Eplerenone
Aldo receptor antagonist (also spironolactone). Prevents/reverses cardiac remodeling. Decreases Sx, hospitalizations, and death ~30% Pts. S/E=Hyperkalemia (incidence increases with higher dose), esp in use c ACE-I (except daily captopril b/c short T1/2). Eplerenone does not have partial agonist activity at aldo receptors like spironolactone > no gynecomastia or breast pain! Yay!
Sotalol
Antidysrhythmic-Nonselective B block (l isomer=class II), K block (d & l isomer-class III) > inc APD/ERP via BOTH methods. Delay conduction in AV node. Inc ERP in ventricles > inc Q-T. Cardioversion of Afib/flutter to sinus rhythm. Dec vent rate in Afib. Cx Tx Vtach/fib instead of amiodarone b/c less S/E. S/E=torsade, dec vent contractility in HF, AV block.
Tx of diastolic HF
Diuretics and nitrate venodilators to dec left vent filling pressure. B-blockers to dec HR and prolong filling time. CCA will probably also work.
Minoxadil
AntiHTN-reduce availability of intercellular Ca in arteries (dunno how) > Arteriodilator. Reserved for Pts c severe HTN refractory to first-line drugs. Lower TPR > dec BP but there is a baroreflexive increase in SNS tone = all that you think it would. Possible to use c ß blocker. Leads to late night infomercials.
Adenosine
Antidysrhythmic-inc K conduction to hyperpolarize AV node (thus decrease AV conduction). T1/2 10 seconds. 'Stuns' the heart momentarily in the hope it will start up again in sinus rhythm. DIAGNOSIS of AV node re-entry tach (PSVT) as well as Tx. S/E=trasient asystole, short-lived intense burning, flushing, dyspnea.
Isosorbide mono/dinitrate
Nitrate vasodilators given PO selectively venodilate > decrease cardiac preload.
Nifedipine
AntiHTN-DHP CCA (read mech p 185-6). Arteriodilation > dec TPR/DBP and inc coronary blood flow. Inc compliance of muscular arteries > dec SBP. No effect on venules, so no effect on venous return. Dec contractility, but CO no change or inc. Do not cause Na retention. Best for systolic HTN.Good for Pt c asthma, DM, renal dysfxn, gout, hyperlipidemia. S/E=mucho vasodilation, pedal edema, GERD, coronary steal. See p 186+
Dobutamine in Tx of MI
ß1/2 agonist. + inotropic effect of B1 inc SV. Arterio/vasodilation via B2 stim > dec TPR, SBP, DBP. Little effect on HR. Inc in GFR solely via inc in CO. Dobutamine>Dopamine b/c: Dob doesn't inc DBP (afterload), less likely to cause tachycardia, venodilation decreases venous return so filling pressure decreased.
Dopamine in Tx of MI
Low dose=renal dose (inc RBF only via D1). Intermed dose= D1 + B1 > inc dp/dt, SV, CO (small inc HR). Large dose (>10μg/kg/min) includes α1 agonism > inc TPR, DBP, SBP > dec SV, CO! Can be reversed c iv dobutamine or sodium nitroprusside.
Digoxin
Antidysrhythmic-acts centrally to inc vagal tone, dec symp tone, increase dp/dt via partial inhib Na/K pump. Dec HR, AV conduction, inc ERP in AV node via inc vagal tone. Inc stroke volume via inc dp/dt. Tx Afib/flutter, inc dp/dt in Pt c HF c systolic dysfxn. S/E c OD=PAC/PVC (via Na/K block), inc SNS activity, AV block.
α-methyldopa
AntiHTN-converted to NE in brain > stimulates α2 receptors > dec SNS tone. Normally need to use c diuretic. Limited clinical use, but ok in PEDS and Pregnancy! S/E=sedation, dry mouth, rebound HTN, fatigue, flu-like symptoms, + Coomb's test, hepatitis, and a condition known as hot dog fingers (well maybe not that one).
Digoxin in HF
Review p 218+. Good effects: direct= + inotropic, indirect= + vagal tone, - SNS tone. Bad direct effect= inhib of Na/K pump decreases phase 4 membrane potential difference > increased automaticity. Inc intercellular Ca also inc possibility of delayed after-depolarizations which trigger dysrhythmias. Tx HF in Pt c systolic dysfxn on ACE and diuretic. Tx Pt c Afib b/c increase in vagal tone controls vent rate. I'm serious, look over p 218-221.
Dofetilide
Antidysrhythmic-PO-similar to sotalol (K block), no B block (PURE class III). Inc Q-T, no effect QRS, P-R, AV conduction. More efficacious than sotalol and amiodarone, but more torsade. No effect on BP or contractility.
Sodium Nitroprusside
AntiHTN (emergency only)-Makes NO when contacts RBCs > vasodilation (dunno why balanced) & platelet inhib. ONLY IN SUPINE PTs! Controlled HypoTN during surgery or acute dissecting Ao. T1/2=30s. S/E=tachycardia, palpitations, *thiocyanate intox!!
Labetalol
Tx Hypertensive *emergency*-α & ß blocker-Dec MAP via dec TPR (balanced vasodilation). CO, PRA, ATII unch. Basal HR falls, exercise tachy attenuated. Fall in renal perfusion press > inc FF = slow Na retention (correct c dose of thiazide). Effect c IV dose is smooth-onset 2-4 min, peak 10-15 min, duration 2-4h. Little fetal tox in preeclampsia.
Esmolol
Antidysrhythmic-Selective B1 block (class II). Especially used to control vent rate in Pt c Afib/flutter or sinus tach during cardiac cath b/c of short T1/2 (9 min).
Tx thiocyanate intoxication
Toxicity usually several days p Tx c Na nitropruss. Give furosemide to inc renal fxn. Thiosulfate + CN > thiocyanate (excreted by kidneys). OR nitrite + thiosulfate + meth blue to: hemoglobin > methemoglobin... methemoglobin binds CN... Reacts c thiosulfate > hemoglobin + thiocyanate > renal ex. (meth blue converts metHgb > Hgb).
Hydrochlorothiazide (HCTZ)
AntiHTN-thiazide diuretic. MOA for fall in BP not known, but dependent on maintaining negative Na balance. Anti-HTN effect occurs in small doses causing only a mild natriuresis. S/E=Hypokalemia, inc RAA axis, hyperlipidemia (mitigated if hypokalemia controlled).
Morphine
Tx Pt s/p MI. Dec SNS tone from analgesic effect (pain=inc SNS) and inhibition of carotid baroreflex > dec pre/afterload, HR, automaticity, cardiac O2 demand, and increases SV.
Lisinopril
AntiHTN-ACE inhibitor-balanced vasodilation, also increases compliance of large arteries (only ACE inhib and CCA do this) > decrease SBP, DBP, MAP. CO, HR, SV little changed. Inc RBP, dec FF (ie no Na retention). Reverse cardiac remodeling from ATII. Plasma ATII dec, but aldo maintained by ACTH and plasma K. Add thiazide to increase efficacy. S/E=cough (preventable c ASA) or switch to ARB, angioedema. PRC-X!! ok in 1st trimester tho.
ß blockers in HTN
Often used c thiazides. Decrease TPR by unknown mechanism. Often used in young patients with no $$ (ie those with Megalife insurance), because often cheaper.
Verapamil
Antidysrhythmic-Ca blocker (Class IV) in slow fibers esp. AV node. Decrease HR, contractility (dec CO), AV conduction (=inc P-R). Inc ERP in AV node. Tx Afib/flutter to control vent rate, cardioverts AV re-entry tach (PSVT). S/E=HypoTN, heart block, sinus bradycardia.
Atenolol
Antidysrhythmic-Selective B1 block (class II). Inc ERP induced by Epi/NE. Dec rate of SA node, AV conduction. Inc P-R on EKG. Tx PVCs, Vtach (via Afib/flut, AV node re-entry, hyperthyroid). DOC in congenital Q-T elongation. S/E neg inotropic, bradycard, AV block.
Lidocaine
Antidysrhythmic-Class IB, only effects ventricles. Na blocker. Dec ERP/APD of FAST fibers (dunno why). Supresses automaticity in ischemic/digoxin tox tissue, stops re-entry dysrhythm by 2way block of area c retrograde xmission. IV b/c high 1st pass. No effect on EKG. Tx PVC S/P MI (but not PRO!). S/E=CNS - seizures Tx c diazepam.
Captopril
AntiHTN-ACE inhibitor-balanced vasodilation, also increases compliance of large arteries (only ACE inhib and CCA do this) > decrease SBP, DBP, MAP. CO, HR, SV little changed. Inc RBP, dec FF (ie no Na retention). Reverse cardiac remodeling from ATII. Plasma ATII dec, but aldo maintained by ACTH and plasma K. Add thiazide to increase efficacy. S/E=cough (preventable c ASA) or switch to ARB. PRC-X!! ok in 1st trimester tho.
Losartan
AntiHTN-ARB-balanced vasodilators. Essentially same as ACE inhibitors. Do not inhibit metabolism of bradykinin or increase synth of prostaglandins. Approved for HT, but dose response shallow (use thiazide to inc efficacy). Use if ACE inhib not tollerated by Pt (ex cough). NO NO in pregnancy or breast feeding. S/E=angioedema (esp if ACE inhib did), HypoTN, HyperK.
Quinidine
Antidysrhythmic-Blocks Na, K, α, ACh. Class IA. Dec AV conduction (K block). Dilates arteri/venules (α block) > baroreflex mediated tachycardia. Tx ventricular rate in Afib/flutter, supress PVCs. S/E=AV block, Vtach (c OD), HypoTN, syncope, torsade, GI, headache, tinnitus. Reduces clearance of digoxin.
Furosemide
Loop Diuretic-Tx of congestive Sx in HF (but do NOT improve survival!). Decrease in ECF volume > dec venous return = dec left vent filling pressure. Must dose b-tid. Use smallest dose possible. Should be given c K sparing diuretic to prevent HypoKalemia.
Prazosin
AntiHTN-α blocker (can use c thiazide)-small dec in MAP via dec in TPR (may initially be accompanied by tachycardia). Inc FF > Na retention. Dec insulin resistance. PRA and plasma aldo unchanged. Balanced vasodilation. Only in mild-mod HTN. S/E=first dose ortho hypo, Na/H20 retention. GOOD effect on lipid profile! Dec LDL, TGs, inc HDL even c thiazide or B blocker.
Bumetanide
Loop Diuretic-Tx of congestive Sx in HF (but do NOT improve survival!). Decrease in ECF volume > dec venous return = dec left vent filling pressure. Must dose b-tid. Use smallest dose possible. Should be given c K sparing diuretic to prevent HypoKalemia.
Terazosin
AntiHTN-α blocker (can use c thiazide)-small dec in MAP via dec in TPR (may initially be accompanied by tachycardia). Inc FF > Na retention. Dec insulin resistance. PRA and plasma aldo unchanged. Balanced vasodilation. Only in mild-mod HTN. S/E=first dose ortho hypo, Na/H20 retention. GOOD effect on lipid profile! Dec LDL, TGs, inc HDL even c thiazide or B blocker.
Balanced vasodilation in HF
isosorbide dinitrate + hydralazine. Decreases mortality but does NOT reverse cardiac remodeling. 2 major problems: venodilation lost via tolerance to nitrate, and prolonged Tx c hydralizine causes SLE-like syndrome.
Sodium Nitroprusside s/p MI
Converted to NO to cause balanced vasodilation. Dec SBP/DBP decreases filling pressure & afterload. Inc CO b/c dec DBP. Dilation of pulmonary arterioles decreases RV afterload. A large fall in DBP can inc SNS tone via baroreflex and/or comprimise myocardial perfusion.
Doxazosin
AntiHTN-α blocker (can use c thiazide)-small dec in MAP via dec in TPR (may initially be accompanied by tachycardia). Inc FF > Na retention. Dec insulin resistance. PRA and plasma aldo unchanged. Balanced vasodilation. Only in mild-mod HTN. S/E=first dose ortho hypo, Na/H20 retention. GOOD effect on lipid profile! Dec LDL, TGs, inc HDL even c thiazide or B blocker.
Clonidine
AntiHTN-Used c diuretic-Direct α2 stim in brain > dec SNS tone. Similar effects as methyldopa, but more S/E including vivid dreams, restlessness, depression. Withdrawal syndrome = apprehension, tremor, headache, sweating, tachycardia, etc.
Felodipine
AntiHTN-DHP CCA (read mech p 185-6). Arteriodilation > dec TPR/DBP and inc coronary blood flow. Inc compliance of muscular arteries > dec SBP. No effect on venules, so no effect on venous return. Dec contractility, but CO no change or inc. Do not cause Na retention. Best for systolic HTN.Good for Pt c asthma, DM, renal dysfxn, gout, hyperlipidemia. S/E=mucho vasodilation, pedal edema, GERD, coronary steal. See p 186+
Propranolol
Antidysrhythmic-Nonselective B block (class II). Inc ERP induced by Epi/NE. Dec rate of SA node, AV conduction. Inc P-R on EKG. Tx PVCs, Vtach (via Afib/flut, AV node re-entry, hyperthyroid). DOC in congenital Q-T elongation. S/E neg inotropic, bradycard, AV block.
Ibutilide
Antidysrhythmic-IV-activates a slow inward Na current, possibly inhibit K channel a bit. Delays repolarization in fast fibers. Dose related inc in Q-T, no effect on AV conduction, P-R, or QRS. Tx cardioversion Afib/flutter (of short duration) better than amiodarone. S/E=torsade, *dysrhythmogenic!
Amlodipine
AntiHTN-DHP CCA (read mech p 185-6). Arteriodilation > dec TPR/DBP and inc coronary blood flow. Inc compliance of muscular arteries > dec SBP. No effect on venules, so no effect on venous return. Dec contractility, but CO no change or inc. Do not cause Na retention. Best for systolic HTN.Good for Pt c asthma, DM, renal dysfxn, gout, hyperlipidemia. S/E=mucho vasodilation, pedal edema, GERD, coronary steal. See p 186+
Hydralazine
AntiHTN-reduce availability of intercellular Ca in arteries (dunno how) > Arteriodilator. Reserved for Pts c severe HTN refractory to first-line drugs. Lower TPR > dec BP but there is a baroreflexive increase in SNS tone = all that you think it would. Possible to use c ß blocker.
Nitroglycerine
IV infusion. Small doses selectively dilate veins to dec filling pressure > dec wall stress and inc subendocardial perfusion in diastole. Larger doses will arteriodilate to dec afterload. Tolerance a problem.
Enalapril
AntiHTN-ACE inhibitor-balanced vasodilation, also increases compliance of large arteries (only ACE inhib and CCA do this) > decrease SBP, DBP, MAP. CO, HR, SV little changed. Inc RBP, dec FF (ie no Na retention). Reverse cardiac remodeling from ATII. Plasma ATII dec, but aldo maintained by ACTH and plasma K. Add thiazide to increase efficacy. S/E=cough (preventable c ASA) or switch to ARB. PRC-X!! ok in 1st trimester tho.
ACE inhibitors in HF
-pril drugs. Larger doses than in HTN. Balanced vasodilation. ALL Pts c HF should be on an ACE-I to: prevent cardiac remodeling via ATII, improve functional status and quality of life, dec hospitalization and mortality. Must monitor plasma K and Cr esp c
Amiodarone
Antidysrhythmic-blocks Na, K, α, ß (Class III). Prolongs ERP/APD in fast fibers. Dec conduction in AV node. Slows SA firing. Prolongs P-R, Q-T, QRS intervals. Tx cardioversion Afib/flut, vent rate in Afib/flut, IV to stop emergent Vtach (Cx Tx sotalol better). S/E=Red man, bradycardia, AV block, hyper/po thyroid due to 37% Iodine content, pulm fibrosis. Less torsade despite Q-T elongation. Dec hepatic/renal clearance of other drugs.
Gemfibrozil
Antilipemic (esp to dec TGs)-activates lipoprotein lipase, esp in skel musc-can use alone or c statin, ok in T2DM. S/E=GI, myopathy, gallstones, CI in renal/hepatic DX
Aspirin
PO Antiplatelet-suicide inhibits COX-1 so platelets cannot produce TXA2 > inc bleeding time, no effect on aPTT or PT.
Streptokinase
Fibrinolytic-binds plasminogen (doesn't act as a kinase!) inducing conf. change so it can cleave another plasminogen>plasmin to degrade factors 5,8 and fibrinogen. Large doses needed if Pt has Abs to Strep.
Propranolol
Antianginal - B-blocker (O-Z are non-selective B blockers)
Eptifibatide
IV Antiplatelet-irrev binds IIb/IIIa receptor (so cannot bind fibrinogen!), immediate effect lasts 24h. Ind=PTCA, stenting, acute coronary synd. (MI, unstable angina - chest pain, depressed S-T seg, elevated cardiac enzymes) S/E=bleeding
Niacin
Antilipemic-MOA unknown, esp dec TGs and inc HDLs (larger the starting level, larger the inc). S/E=pruritis, GI Sx, bad 4 T2DM, gout
Enoxaparin
LMW Heparin - Binds activated factor 10, no change in aPTT, only partially reversed by protamine sulfate. Benefits=no need to monitor levels, inc bioavail, only cleared by kidney, less S/Es, but expensive and not covered by medicare! See p 96
Danaproid
s.c. anticoag-nonheparin GAG heparan from pig-promotes binding of AntiTh3, but no effect on aPTT or PT. Use in Pts c heparin induced thrombocytopenia. T1/2=24h and inc in renal failure. NO ANTIDOTE.
Inositol hexanicotinate
Antilipemic-Formulation of niacin-MOA unknown, esp dec TGs and inc HDLs (larger the starting level, larger the inc). S/E=GI Sx, bad 4 T2DM, gout, but NOT pruritis/flushing!
Ardeparin
LMW Heparin - Binds activated factor 10, no change in aPTT, only partially reversed by protamine sulfate. Benefits=no need to monitor levels, inc bioavail, only cleared by kidney, less S/Es, but expensive and not covered by medicare! See p 96
Abciximab
IV Antiplatelet-Mono Ab that irrev binds IIb/IIIa receptor (so cannot bind fibrinogen!), immediate effect lasts 24h. Ind=PTCA, stenting, acute coronary synd. (MI, unstable angina - chest pain, depressed S-T seg, elevated cardiac enzymes) S/E=bleeding
Reteplase
IV Fibrinolytic-slightly modified t-PA from recombinant tech- massively activates plasmin causing systemic fibrinolysis due to degredation of factors 5, 8 and fibrinogen see 104-105
Warfarin
PO anticoag-prevents post-xlational carboxylation of factors 2,7,9,10 (in vivo ONLY). T1/2 of factor 7 shortest @ 6h so effect measured by PT (measure of extrinsic path) but aPTT and PT can inc in OD. Reversal c iv/sc/po phytonadione. Must see p 99+
Isosorbide dinitrate
PO Antianginal - converted to NO in vasc smooth musc to cause relaxation (venodilation much longer than arterio). Dec preload dec LV wall tention, inc blood flow to endocardium. Tolerance develops!
Tirofiban
IV Antiplatelet-irrev binds IIb/IIIa receptor (so cannot bind fibrinogen!), immediate effect lasts 24h. Ind=PTCA, stenting, acute coronary synd. (MI, unstable angina - chest pain, depressed S-T seg, elevated cardiac enzymes) S/E=bleeding
Phytonadione
Reduced Vitamin K (iv/sc/po)-Reversal of Warfarin - takes several hours, up to 24h for full reversal. Repeated doses of vit K required after warfarin OD. 2 other methods=iv fresh frozen plasma (b/c provides clotting factors), or iv factor 9 concentrate (large amounts of clotting factors 2,7,9,10).
Colesevelan
Antilipemic-Binds bile acids, PRC-B, S/E=GI Sx, binds other drugs (but not statins, digoxin, or warfarin)
Clopidogrel
PO Antiplatelet-Blocks ADP stim of P2Y(12) > + adenyl cyclase > inc cAMP > lower intracel Ca > dec platelet fxn. Can be used c or instead of ASA. S/E = less neutropenia and agranulocytosis than Ticlopidine.
Anistreplase
Fibrinolytic-anisoylated strep-plasminogen activator complex-attempt to make more clot specific (not very good).
Dalteparin
LMW Heparin - Binds activated factor 10, no change in aPTT, only partially reversed by protamine sulfate. Benefits=no need to monitor levels, inc bioavail, only cleared by kidney, less S/Es, but expensive and not covered by medicare! See p 96
Fenofibrate
Antilipemic (esp to dec TGs)-activates lipoprotein lipase, esp in skel musc-can use alone or c statin, ok in T2DM. S/E=GI, myopathy, gallstones, CI in renal/hepatic DX
Lovastatin
Antilipemic-Inhibits HMGCoA Reductase, S/E=myopathy, AST/ALT (baseline then p 6&12 wk, then 2x/yr), rhabdo, PRC-X
Heparin (Unfractioned)
IV Antiplatelet-increases rate of activated clotting factors (2,9,10,11,12) binding (irreversibly) to antithrombin III by enzymatic binding to AntiTh3. Effect guaged by intrinsic pathway aPTT (doesn't change extrinsic time-PT). Works in vitro/in vivo. Effects reversed by protamine sulfate. See p94
Felodipine
PO Antianginal-block L-type Ca channels in ARTERIOLES > dec DBP(afterload), inc cardiac blood flow. S/E=Bradycardia, paradoxical angina, MIs. See p. 64
Nitroglycerin
TD or sl Antianginal - converted to NO in vasc smooth musc to cause relaxation (venodilation much longer than arterio). Dec preload dec LV wall tention, inc blood flow to endocardium. Tolerance develops!
Colestipol
Antilipemic-Binds bile acids, PRC-C, S/E=GI Sx, bind almost any other drug! (must take other meds 1h a or 4h p po dosing c resin)
S/E of CCA
Severe bradycardia (may respond to IV CaCl), SA nodal failure or AV block, HF in Pt c systolic dysfxn, HypoTN, Paradoxical angina (DBP too low to perfuse heart, coronary steal-healthy vessels dilate > atherosclerotic ones, inc O2 demand - esp c A&F), GER
Atorvastatin
Antilipemic-Inhibits HMGCoA Reductase, S/E=myopathy, AST/ALT (baseline then p 6&12 wk, then 2x/yr), rhabdo, PRC-X
Cholestyramine
Antilipemic-Binds bile acids, PRC-C, S/E=GI Sx, bind almost any other drug! (must take other meds 1h a or 4h p po dosing c resin)
Isosorbide mononitrate
PO Antianginal - converted to NO in vasc smooth musc to cause relaxation (venodilation much longer than arterio). Dec preload dec LV wall tention, inc blood flow to endocardium. Tolerance develops!
Diltiazem
IV/PO Antianginal-block L-type Ca channels in ARTERIOLES (V&D heart too) > dec DBP(afterload), inc cardiac blood flow. S/E=Bradycardia, paradoxical angina, MIs. See p. 64
Ezetimibe
Antilipemic-Blocks cholesterol receptor in GI - add to Tx c statins to achieve LDL goal (& decrease statin dose to avoid myopathy)
Lepirudin
IV anticoag-direct inhib of thrombin (IIa) from salivary gland of leeches. Used in Pt c hep induced thrombocytopenia. Dosed to inc aPTT to 1.5-2.5x normal. T1/2 = 1.3h and inc in renal failure. NO ANTIDOTE.
Verapamil
IV/PO Antianginal-block L-type Ca channels in ARTERIOLES (V&D heart too) > dec DBP(afterload), inc cardiac blood flow. S/E=Constipation!, Bradycardia, paradoxical angina, MIs. See p. 64
Amlodipine
PO Antianginal-block L-type Ca channels in ARTERIOLES > dec DBP(afterload), inc cardiac blood flow. S/E=Bradycardia, paradoxical angina, MIs. See p. 64
Aminocaproic acid
Antagonist of plasmin-lysine analog that binds to plasmin and plasminogen preventing their binding to fibrin in thrombi. Used to prevent bleeding caused by thrombolytic therapy (but no work so good).
Alteplase
IV Fibrinolytic-unmod t-PA from recombinant tech- massively activates plasmin causing systemic fibrinolysis due to degredation of factors 5, 8 and fibrinogen see 104-105
Pravastatin
Antilipemic-Inhibits HMGCoA Reductase, S/E=myopathy, AST/ALT (baseline then p 6&12 wk, then 2x/yr), rhabdo, PRC-X
Atenolol
Antianginal - B-blocker (A-N are selective B1 blockers)
Ticlopidine
PO Antiplatelet-Blocks ADP stim of P2Y(12) > + adenyl cyclase > inc cAMP > lower intracel Ca > dec platelet fxn. Can be used c or instead of ASA. Must give 10d for full effect. S/E=neutropenia, thrombocytopenia, agranulocytosis. Clopidogrel prob better.
Abacavir
NRTI - Nucleoside analog phosphorylated to ZTP that inhib viral RT
Acyclovir
Guanosine analog-activated by viral kinases (2nd & 3rd phosphorylation by host kinases) - *HSV1&2, severe VSV, EBV (oral hairy leukoplakia)
Alendazole
Well absorbed GI - Roundworm (Echinococcus) & neurocysticercosis - Inhibits microtubule synth
Amphotericin B
↑ memb permiability (afinity for fungal ergosterol) - Antifungal - IV & topical
Chloroquine
Inhib malarial heme polymerase - P. malaria & non-R P. falciparum - vivax & ovale will relapse (use primaquine)
Cidofovir
Inh DNA polymerase (activated by HOST kinases to diphosphate form) - R CMV, Acyclo R HSV & VZV
Clotrimazole
Azole-Inhibit fungal CYP450-Antifungal - Oral troche & topical
Cromolyn Sodium
Alters Cl channels to stabilize mast cell/eosinophil membrane & prevent egranulation - Bronchial Asthma PRO
Efavirenz
NNRTI - NOT a nucleoside! Binds directly to HIV RT
Fluconazole
Azole-Inhibit fungal CYP450-Antifungal - PRO vaginal candidiasis c Abx use
Fomivirisen
antisense oligonuc binds to mRNA and blocks translation to protein - CMV retinitis
Foscarnet
Directly inhibits viral DNA polymerase - R CMV & HSV - Dose related nephrotox!
Griseofulvin
Inhibit mitotic spindle formation - PO antifungal - DOC ringworm (tinea)
Itraconazole
Azole-Inhibit fungal CYP450-Antifungal - PO
Ivermectin
↑ GABA neuroxmission->death, threadworm & roundworm
Lamivudine
NRTI - Nucleoside analog phosphorylated to ZTP that inhib viral RT
Lopinavir
HIV PI - Prevents cleavage of the two polyprotein products of HIV mRNA (Virions cannot mature)
Mebendazole
Pinworm INF (Enterobius) - Inhibits microtubule synth
Mefloquine
Inhib malarial heme polymerase - *R P. falciparum - vivax & ovale will relapse (use primaquine)
Metronidazole
cidal anaero (B. fragilis!) - DOC C. diff collitis - Giard, amebiasis, trich - No EtOH, monitor AST/ALT
Miconazole
Azole-Inhibit fungal CYP450-Antifungal - IV & topical
Montelukase
LTD4 receptor blocker - chronic maintenance therapy for Asthma
Niclosamide
Activate ATPase or uncouple ox phos - Tapeworm (flatworm) - Flat like a nickle!
Nystatin
↑ memb permiability (afinity for fungal ergosterol) - Antifungal - PO (but not absorbed for oral candidiasis) & topical
Permethrin
DOC lice!
Praziquantel
↑ Ca perm=tetanic contractions/death - Flukes (fluke to have q&z in a word!)
Primaquine
Liver stages P vivax & ovale (use c blood schizonticide like chloroquine)
Pyrantel Pamoate
ACh (neuromuscular) blockade - Pin (Enterobius) & roundworm (Echinococcus)
Pyrimethamine-sulfadoxine
DiHfolate reductase I - selective for malarial & toxoplasmodial DHFR - chloroquine R malaria
Revirapine
NNRTI - NOT a nucleoside! Binds directly to HIV RT
Rimantadine
Prevents viral uncoating @ flu A M2 proton channel - PRO Flu A (esp in elderly)- NOT flu B!!!!!
Ritonavir
HIV PI - Prevents cleavage of the two polyprotein products of HIV mRNA (Virions cannot mature)
Saquinavir
HIV PI - Prevents cleavage of the two polyprotein products of HIV mRNA (Virions cannot mature)
Stavudine
NRTI - Nucleoside analog phosphorylated to ZTP that inhib viral RT
Tenofovir
NRTI combination
Terbinafine
Inh squalene epoxidase - ↑ squalene kills fungus - DOC Fungal nail INF PO - PO&top for tinea
Valacyclovir
Precursor to Acyclovir c ↑ Bioavail. - *HSV1&2, severe VSV, EBV (hairy leukoplakia)
Vidarabine
Inh viral DNA polymerase - Herpes keratitis
Voriconazole
Azole-Inhibit fungal CYP450-Antifungal - PO & IV
Zafirlukast
LTD4 receptor blocker - chronic maintenance therapy for Asthma
Zidovudine
NRTI - Nucleoside analog phosphorylated to ZTP that inhib viral RT
Zileuton
5-lipoxygenase inhibitor to prevent LT formation - Asthma
Amikacin
Aminoglyco - cidal @ 30s - Serious G- INF, synergy c Vanc for G+, Ototox & Nephrotox!
Amoxacillin
Aminopenicillin PO - DOC Otitis Media
Ampicillin
Aminopenicillin IV - DOC Otitis Media
Azithromycin
Macrolide - 50s - DOC CAP (esp myco&legion) - Staph/Strep in Pt c PCN ALL
Aztreonam
ßL - Monobactam - cidal for G(-), NO G(+) - Rx for Pt c PCN allergy
Benzathine Penicillin G
Orig. IM PCN
Cefazolin
ßL -1st Gen Ceph - +++ G(+) (Staph/Strep) NOT Entero - Surg PRO
Cefepime
ßL -4th gen Ceph - xtra ßLase R - +++ G+/-
Cefotaxime
ßL -3rd gen Ceph - +++ G-, ++ G+, Good CSF penitration
Cefotetan
ßL -2nd gen Ceph - ++ G+/- & anaerobe - ABD Surg PRO
Cefoxitin
ßL -2nd gen Ceph - ++ G+/- & anaerobe - ABD Surg PRO
Ceftazidime
ßL -3rd gen Ceph - +++ G-, ++ G+, Good CSF - Only Ceph vs. Pseudo
Ceftriaxone
ßL -3rd gen Ceph - +++ G-, ++ G+, Good CSF penetration
Ciprofloxacin
Fluro - cidal (inhibits topoisomerase) - +++ G-, some G+, mycobac & atypicals, NOT c arrythmics!
Clarithromycin
Macrolide - 50s - DOC CAP (esp myco&legion) - Staph/Strep in Pt c PCN ALL
Clavulanate
Clavaulanic acid - BLase Inhibitor
Clindamycin
Bacteriostatic - Binds 50s - G+ and Anaerobe (not C. diff so collitis poss SE) good bone penetration - NO G-
Cloxacillin
Penicillinase resistant PCN
Dicloxacillin
Penicillinase resistant PCN
Doxycycline
static - Binds 30s - Rikettsia & chlamydia (+++intracellular) - cheap Rx atypical PN
Erythromycin
Macrolide - 50s - DOC CAP (esp myco&legion) - Staph/Strep in Pt c PCN ALL
Gatifloxacin
Fluro - cidal (inhibits topoisomerase) - +++ G-, better G+, mycobac & atypicals, NOT c arrythmics!
Gemifloxacin
Fluro - cidal (inhibits topoisomerase) - +++ G-, some G+, mycobac & atypicals, NOT c arrythmics!
Gentamycin
Aminoglyco - cidal @ 30s - Serious G- INF, synergy c Vanc for G+, Ototox & Nephrotox!
Imipenem
ßL (ßLase R)Carbapenem - BROAD spec S-MRSA & VRE (used c cilastatin aka seizurecillin) MDR pathogens & polymicrobial life threatening INF!
Levofloxacin
Fluro - cidal (inhibits topoisomerase) - +++ G-, some G+, mycobac & atypicals, NOT c arrythmics!
Linezolid
50s - high R G+ ie. MRSA & VRE
Meropenem
ßL (ßLase R) - Carbapenem - BROAD spec S-MRSA & VRE - MDR pathogens & polymicrobial life threatening INF!
Minocycline
static - Binds 30s - Rikettsia & chlamydia (+++intracellular) - cheap Rx atypical PN
Moxifloxacin
Fluro - cidal (inhibits topoisomerase) - +++ G-, better G+, mycobac & atypicals, NOT c arrythmics!
Nafcillin
Penicillinase resistant PCN
Nitrofurantoin
Urinary antiseptic - UTIs esp E. coli & entero - Brown urine!
Oxacillin
Penicillinase resistant PCN
Penicillin G
Orig. IV PCN
Penicillin VK
Orig. PO PCN
Piperacillin
IV PCN for Gram (-) esp. Pseudomonas (use c ßLase I)
Procaine Penicillin G
Orig. IM PCN
Quinupristin/Dalfopristin
50s - high R G+ ie. MRSA & VRE
Sulbactam
ßLase Inhibitor
Tazobactam
ßLase Inhibitor
Tetracycline
static - Binds 30s - Rikettsia & chlamydia (+++intracellular) - cheap Rx atypical PN
Ticarcillin
IV PCN for Gram (-) esp. Pseudomonas (use c ßLase I)
Tobramycin
Aminoglyco - cidal @ 30s - Serious G- INF, synergy c Vanc for G+, Ototox & Nephrotox!
Trimethoprim-Sulfamethoxazole
inhibits dihydrofolate reductase - UTIs, PCP
Tx of TB c +PPD & neg CXR
6-9 months daily isoniazid (INH)
Tx of TB c +PPD & TB in sputum
9 mo Isoniazid, Rifampin, Ethambutol, Pyrazinamide (INH, RIF, PZA, EMB)
Tx of TB in Pt c HIV taking PI and NNRTI
9 mo Isoniazid, RIFABUTIN (NOT Rifampin), Ethambutol, Pyrazinamide
Vancomycin
G+ ONLY - MRSA - Serious INF in Pt c PCN ALL - 2nd line for C. diff collitis
methscopolamine
muscarinic antagonist (4º)
tyramine
indirect adrenergic agonist
mecamylamine
N1 receptor antagonist: [autonomic hyperreflexia]
caffeine
PDEase inhibitor
ammonium chloride
decreases pH in urine
latanoprost
glaucoma (PGF-2α analog): [> UVEOSCLERAL outflow]
echothiophate
glaucoma (organophosphate inhibitor): [>AH outflow]
tacrolimus
immunosuppressive: [inhibit Tcell (via calcineurin)]
succinylcholine
cholinergic agonist; nicotinic agonist: [non-compet. NMJ block]
carbachol (carbamylcholine)
cholinergic agonist: [long term miosis]
5-aminosalicylic acid
NSAID: [inhibit COX1/2 & lipoxygenase: Tx inflam bowel dz
mannitol
glaucoma (osmotic diuretic)
acetazolamide
CA inhibitor; increases pH in urine: [<AH prod in glauc.]
aspirin
NSAID: [irreversible COX1/2]
terbutaline
adrenergic agonist: [β2>>β1]
dicyclomine
muscarinic antagonist: [irritable bowel synd]
ephedrine
mixed adrenergic agonist: [pressor agent in anesthesia]
oxymetazoline
adrenergic agonist: [α only = nasal decongest - Afrin]
flunisolide
corticosteroid
norepinephrine
adrenergic agonist: [mostly α… α>β1>β2]
bretylium
sympatholytic: [inhibit NE release]
timolol
glaucoma; β-adrenoreceptor antagonist: [β1&β2]
guanethidine
sympatholytic: [inhibit NE release]
betaxolol
glaucoma (β-adrenoreceptor antagonist): [β1]
phenoxybenzamine
α-adrenoreceptor antagonist: [covalent, non-competitive]
botulinum toxin
affects ACh synthesis/release
N-methylatropine
muscarinic antagonist (4º)
a-methyldopa
sympatholytic: [hypertension in kids and pregnant]
tolterodine
muscarinic antagonist: [urinary incont.]
pyridostigmine
carbamate inhibitor
physostigmine
carbamate inhibitor: [non-competitive]
cyclopentolate
muscarinic antagonist: {mydriasis]
tropicamide
muscarinic antagonist: [DOC mydriasis - eye exam]
dorzolamide
glaucoma (CA inhibitor): [<AH prod]
pseudoephedrine
mixed adrenergic agonist: [nasal decongestant - Sudafed]
epinephrine
glaucoma; adrenergic agonist: [mydriasis,incr. outflow α1… β2>β1>α]
yohimbine
α-adrenoreceptor antagonist: [α2 in baroreflex -- >HR]
propranolol
β-adrenoreceptor antagonist: [β1&β2]
scopolamine
muscarinic antagonist
parathion
organophosphate inhibitor
OKT-3 (muromonab-CD3)
immunosuppressive: [monoclonal Ab vs CD3 - inactivate Tcell]
tamsulosin
α-adrenoreceptor antagonist: [ α1A--DOC Prostatic Hypertrophy = FloMax]
phenylephrine
adrenergic agonist: [pure α1]
celecoxib
NSAID: [reversible COX2]
atropine
muscarinic antagonist : [Parkinsons]
pirbuterol
adrenergic agonist: [β2>β1]
sirolimus (rapamycin)
immunosuppressive: [cell cycle arrest - block B/Tcells]
cyclophosphamide
immunosuppressive
dexamethasone
corticosteroid
alprostadil
Tx of impotence
apraclonidine
glaucoma (α2-agonist): [<AH prod]
ergotamine, dihydroergotamine
partial α-adrenoreceptor agonist: [migraines]
isofluophate (DFP)
glaucoma; organophosphate inhibitor: [>AH outflow]
carbaryl
carbamate inhibitor
labetalol
α1-adrenoreceptor antagonist; β-adrenoreceptor antagonist
pilocarpine
glaucoma; cholinergic agonist: [>AH outflow]
metoprolol
β-adrenoreceptor antagonist: [β1]
ibuprofen
NSAID: [reversible COX1/2]
trimethaphan
N1 receptor antagonist: [hypotens. During head/neck surg.]
amphetamine
indirect adrenergic agonist
cyclosporine
immunosuppressive
bethanechol
cholinergic agonist: [musc. GU,GI - bowel stasis/urinary ret]
benztropine
muscarinic antagonist: [Parkinsons]
triamcinolone
corticosteroid
glycopyrrolate
muscarinic antagonist (4º): [< saliva perioperatively]
dipivefrin
glaucoma: [to Epi.. >AH outflow α1]
reserpine
sympatholytic: [inhibit NE storage]
prazosin (terazosin, doxazosin)
α-adrenoreceptor antagonist: [α1 - mild hypertension]
cortisone
corticosteroid: [mostly Cellular immunity]
donepezil
carbamate inhibitor: [DOC Alzheimers]
cocaine
alters NE metabolism: [blocks Na+ chan, Uptake1]
ipratropium
muscarinic antagonist (4º): [COPD - relax bronch. Sm. Musc.]
papaverine
PDEase inhibitor, Tx of impotence
dobutamine
adrenergic agonist: [β1=β2]
propantheline
muscarinic antagonist (4º)
oxybutynin
muscarinic antagonist: [urinary incont.]
dimpylate
organophosphate inhibitor
indomethacin
NSAID: [reversible COX1]
albuterol
adrenergic agonist : [β2>>β1]
salicylate
NSAID: [reversible COX1/2]
beclomethasone
corticosteroid
edrophonium
carbamate inhibitor: [Dx Myas. Gravis, direct N2 stim]
acetylcholine
cholinergic agonist
prednisolone
corticosteroid; immunosuppressive
phentolamine
α-adrenoreceptor antagonist; Tx of impotence
cevimeline
cholinergic agonist: [Sjogrens]
prednisone
corticosteroid; immunosuppressive
pralidoxime
Tx of organophosphate poisoning: [hydrolysis of Pi]
dopamine
adrenergic agonist: [D1>β1>β2>α1]
methacholine
cholinergic agonist: [Dx bronchial asthma]
azathioprine
immunosuppressive
hydrocortisone
corticosteroid
ritodrine
adrenergic agonist: [β2>>β1…delay parturition]
phenylpropanolamine
indirect adrenergic agonist
hyoscyamine
muscarinic antagonist: [irritable bowel synd]
diphenhydramine
muscarinic antagonist: [antihistamine - Benadryl]
salmeterol
adrenergic agonist: [β2>>β1… relieve bronchoconstr. w/o >HR -- asthma]
malathion
organophosphate inhibitor: [insecticide]
atenolol
β-adrenoreceptor antagonist: [β1]
nicotine
nicotinic agonist
isoproterenol
adrenergic agonist: [β only]
trihexyphenidyl
muscarinic antagonist: [Parkinsons]
theophylline
PDEase inhibitor
mycophenolate
immunosuppressive: [block inosin mono-P dehydrog. = no Guanine in B/T cells]
sildenafil
PDEase inhibitor; Tx of impotence
corticosteroids
immunosuppressive
neostigmine
carbamate inhibitor: [also N2 agonist-- Tx Myas. Gravis]
esmolol
β-adrenoreceptor antagonist: [i.v. - quick acting]
5-aminosalicylic acid
NSAID
acetazolamide
CA inhibitor; increases pH in urine
acetylcholine
cholinergic agonist
albuterol
adrenergic agonist
alprostadil
Tx of impotence
a-methyldopa
sympatholytic
ammonium chloride
decreases pH in urine
amphetamine
indirect adrenergic agonist
apraclonidine
glaucoma (α2-agonist)
aspirin
NSAID
atenolol
β-adrenoreceptor antagonist
atropine
muscarinic antagonist
azathioprine
immunosuppressive
beclomethasone
corticosteroid
benztropine
muscarinic antagonist
betaxolol
glaucoma (β-adrenoreceptor antagonist)
bethanechol
cholinergic agonist
botulinum toxin
affects ACh synthesis/release
bretylium
sympatholytic
caffeine
PDEase inhibitor
carbachol (carbamylcholine)
cholinergic agon