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Drugs 0603 Flashcards

1
Q

Leucovorin

A

Folinic acid. Tx methotrexate overdose.

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2
Q

Filgrastim

A

G-CSF analog used to stimulate proliferation and differentiation of granulocytes in patients with neutropenia post-chemo.

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3
Q

Cyclophosphamide toxicity

A

Hemorrhagic cystitis–use mesna to bind acrolein in urine.

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4
Q

What are the following types of biological agents?
Rituximab, infliximab, certolizumab, imatinib, etanercept?

A

Rituximab: CD20 blocker for CD20+ non-Hodgkin’s lymphoma
Infliximab: TNF-a blocker for autoimmune diseases (Crohn’s, RA)
Certolizumab: pegylated humanized monoclonal Ab that targets TNF-a. Lacks Fc region (prevents complement and cell-mediated toxicity), treats autoimmune d/o associated with TNF-a
Imatinib: philadelphia chromosome + CML and kit-positive GI stromal tumors. Small-molecule tyrosine kinase receptor inhibitor.
Etanercept: TNFa inhibitor added to methotrexate for RA. Fusion protein linking soluble TNFa receptor to Fc part of human IgG1. DECOY.

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5
Q

Rituximab

A

Rituximab: CD20 blocker for CD20+ non-Hodgkin’s lymphoma

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6
Q

Infliximab

A

Infliximab: TNF-a blocker for autoimmune diseases (Crohn’s, RA)

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7
Q

Certolizumab

A

Certolizumab: pegylated humanized monoclonal Ab that targets TNF-a. Lacks Fc region (prevents complement and cell-mediated toxicity), treats autoimmune d/o associated with TNF-a

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8
Q

Imatinib

A

Imatinib: philadelphia chromosome + CML and kit-positive GI stromal tumors. Small-molecule tyrosine kinase receptor inhibitor.

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9
Q

Etanercept

A

Etanercept: TNFa inhibitor added to methotrexate for RA. Fusion protein linking soluble TNFa receptor to Fc part of human IgG1. DECOY.

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10
Q

Which drugs have 0-order elimination?

A

PEA (round, 0): phenytoin, ethanol, aspirin

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11
Q

How do you treat salicylate and amphetamine OD?

A
  1. Acidic drug OD (salicylate): NaHCO3 to trap acidic drug in basic urine
  2. Basic drug OD (amphetamines): Na4Cl to trap basic drug in acidic urine
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12
Q

Chlorpropamide, tolbutamide

A

First gen sulfonylureas. Close K+ channel in b-cell membrane –> insulin release via calcium influx. SE: disulfiram effects.

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13
Q

Glimepiride, glipizide, glyburide

A

2nd gen sulfonylureas. SE: hypoglycemia

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14
Q

Pioglitazone, rosiglitazone

A

Glitazones/thiazolidinedions. Increase insulin sensitivity in peripheral tissue. Binds to PPAR-g nuclear transcription regulator. SE: weight gain, edema, hepatotoxicity, HF, increase risk of fractures.

Adiponectins.

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15
Q

Exenatide, liraglutide

A

GLP-1 analogs. Increase insulin, decrease glucagon release. SE: N/V, pancreatitis.

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16
Q

Linagliptin, saxagliptin, sitagliptin

A

DPP-4 inhibitors. Increase insulin, decrease glucagon release. Mild urinary or respiratory infections.

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17
Q

Pramlintide

A

Amylin analogs. Decrease gastric emptying, decrease glucagon. Type 1 and type 2 DM. SE: hypoglycemia, N/D.

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18
Q

Canagliflozin

A

SGLT-2 inhibitors. Block reabs of glucose in PCT. Type 2 DM. SE: Glucosuria, UTIs, vaginal yeast infections.

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19
Q

Acarbose, miglitol

A

a-glucosidase inhibitors. Inhibit intestinal brush-border a-glucosidases. Delayed carb hydrolysis and glucose abs, decreases post prandial hyperglycemia. SE: GI.

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20
Q

Nimodipine

A

Subarachnoid hemorrhage (prevents cerebral vasospasm)

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21
Q

Clevidipine

A

HTN urgency or emergency

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22
Q

Nitroprusside

A

Releases NO, which generated cGMP in smooth muscle of arteries and veins. Reduces preload and afterload.
Use: HTN emergency, given by IV infusion
SE: rebound HTN, cyanide toxicity (co-admin with nitrates and thiosulfate to decr toxicity).

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23
Q

Hydralazine

A

Acts directly on arterioles (increase cGMP), resulting in decreased resistance (esp in coronary, renal and cerebral beds). Reduces afterload.
Use: severe HTN, HF, safe in pregnancy.
SE: compensatory tachycardia, HA, flushing, sweating, fluid retention, reflex tachy, lupus-like syndrome in slow acetylators.
*Treat with diuretics to counteract fluid retention and b-blockers to prevent tachy.

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24
Q

Fenoldopam

A

Dopamine D1 receptor agonist: coronary, peripheral, renal, and splanchnic vasodilation.
Decrease BP, increase natriuresis.

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25
Q

Nitrates

A

Vasodilate by increasing NO in vascular smooth muscle –> increased cGMP in smooth muscle relaxation. Decreases preload.
Increased cGMP, decrased intracellular Ca, myosin dephosphorylation.
Use: angina, acute coronary syndrome, pulmonary edema.
SE: reflex tachy (tx with b-blocker), hypotension, flushing, HA, Monday disease (tolerance during week and loss of tolerance on weekend –> tachy, dizzy, HA on reexposure).

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26
Q

HMG-CoA reductase inhibitors

A

Hepatotoxicity (LFTs), myopathy (esp with fibrates or niacin)
CI: liver dz, pregnancy

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27
Q

Cholestyramine, colestipol, colesevelam

A

Bile acid resins. Decrease LDL, increase HDL slightly, increase TG slightly
Prevent intestinal reabs of bile acids; liver must use cholesterol to make more.
SE: GI upset, decr abs of other drugs and fat-soluble vitamins, cholesterol gallstones

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28
Q

Ezetimibe

A

Decrease LDL.
Prevent cholesterol abs at small intestine brush border (block NPC1L1).
SE: rare increase LFTs, diarrhea.

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29
Q

Gemfibrozil, clofibrate, bezafibrate, fenofibrate

A

Decrease TGs!
Upregulate LPL –> increase TG clearance. Activates PPAR-a to induce HDL synthesis.
SE: myopathy (increase risk with statins), cholesterol gallstones, rash, ED, GI

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30
Q

Niacin (B3)

A

Increase HDLs. Inhibits lipolysis in adipose tissue; reduces hepatic VLDL synthesis.
SE: red, flushed face (d/t PGs, pre-tx with NSAIDs), hyperglycemia, hyperuricemia.

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31
Q

Adenosine

A

Increase K+ out of cells –> hyperpolarizing cell and decrease Ica. Drug of choice to abolish supraventricular tachycardia.
Effect blunted by theophylline and caffeine.
SE: flushing, hypotension, chest pain, sense of impending doom, bronchospasm.

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32
Q

Clozapine

A

D4 receptors? (atypical)
Use: tx-resistant schizophrenic, for positive and negative sx.
SE: agranulocytosis. Must monitor WBC. Seizures.Hypersalivation, myocarditis, weight gain.
*Must watch CLOZely

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33
Q

Mifepristone

A

Abortifacient up to 49 days after conception.
Progesterone antagonist – decidual necrosis and expulsion of products of conception. Stimulate release of endogenous PGs, sensitize myometrium to effects of hormone.

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34
Q

High potency antipsychotics/neuroleptics

A

Try Fly High: Trifuoperazine, fluphenazine, haloperidol
Block D2 (increase cAMP in CNS)
Uses: Schizo (for + sx), psychosis, acute mania, Tourette’s
Neurologic SE: Huntington, delirium, EPS symptoms
Haloperidol: NMS, tardive dyskinesia.

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35
Q

NMS–Neuroleptic malignant syndrome

A

FEVER: fever, encephalopathy, vitals unstable, elevated enzymes, rigidity of muscles.
Rigidity, myoglobinuria, autonomic instability, hyperpyrexia.
Ts: Dantrolene, D2 agonists–bromocriptine

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36
Q

Anti-psychotic SE

A

Highly lipid soluble and stored in body fat, slow to be removed.
EPS: dyskinesia, neuroleptic malignant syndrome. Tx with benztropine or diphenhydramine.
Endocrine SE: dopamine receptor antagonism –> hyperprolactinemia (galactorrhea).
Anti-muscarinic: dry mouth, constipation
Block A1: hypotension
Block Histamine: sedation
QT prolongation

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37
Q

Low potency antipsychotics/neuroleptics

A

Cheating Thieves are low: Chlorpromazine, thioridazine
Non-neurologic SE: anticholinergic, antihistamine, a-blockade effects
Chlorpromazine: Corneal deposits
Thioridazine: reTinal deposits

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38
Q

Evolution of EPS SE

A

4 hr acute dystonia (muscle spasm, stiffness, oculogyric crisis)–Tx = benztropine or diphenhydramine
4 day akathisia (restlessness, fidgetiness)–Tx = propranolol, benzodiazepines, benztropine
4 wk bradykinesia (parkinsonism)
4 mo tardive dyskinesia (involuntary writhing, mouth, tongue)–Likely due to compensatory hypersensitivity of DA receptors after long-term administration.

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39
Q

Atypical antipsychotics

A

Olanzapine, clozapine, quetiapine, risperidone, aripiprazole, aiprasidone
Effects on 5HT2, DA, and a and H1 receptors
Fewer extrapyramidal/anticholinergic SE.
Olanzapine: OCD

Toxicities:
Olanzapine/clozapine: weight gain
Clozapine: agranulocytosis (WBC monitoring) and seizure
RIsperidone: increase prolactin – decrease GnRH, LH, and FSH (irr menstruation and fertility)
Ziprasidone: prolong QT (the most)
Quetiapine: cataracts–periodic slit lamp exam!
All prolong QT.

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40
Q

Lithium

A

Related to inhibition of phosphoinositol cascade.
Use: Mood stabilizer and SIADH.
Toxicity: tremor, hypothyroidism, polyuria (DI), teratogenesis (Ebstein anomaly).
Excreted by kidneys. Reabsorbed at PCT with Na+.
Thiazide use makes it worse!!!

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41
Q

Buspirone

A

Stimulates 5-HT1A receptors
GAD. Does not cause sedation, addiction, or tolerance. Takes 1-2 weeks. Does not interact with alcohol.

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42
Q

SSRI

A

Fuoxetine, paroxetine, sertraline, citalopram
5HT specific reuptake inhibitors
SIADH, sexual dysfunction
Serotonin syndrome: hyperthermia, confusion, myoclonus, CV instability, flushing, diarrhea, seizures
Tx: cyproheptadine (5HT2 receptor antagonist)

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43
Q

SNRI

A

Venlafaxine, duloxetine
Inhibit 5HT and NE reuptake
Depression, GAD, panic d/o, PTSD. Duloxetine for DM peripheral neuropathy
Toxicity: increased BP, stimulant effects, sedation, N

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44
Q

TCA

A

Amitriptyline, nortriptyline, imipramine, desipramine, clomipramine (OCD), doxepin, amoxapine
Block NE and 5HT.
SE: sedation, a1-blocking effects (postural hypotension), atropine like SE (tachy, urinary retention, dry mouth). Can prolong QT.
Tri-C’s = Convulsions, Coma, Cardiotoxicity (arrhythmias). Also respiratory depression, hyperpyrexia. Confusion and hallucinations in elderly due to anticholinergic SE (use nortriptyline). Tx: NaHCO3.

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45
Q

MAOI

A

Trancylcypromine, phenelzine, isocarboxazid, selegiline (selective MAOB)
MAO Takes Pride In Shainghai.
Increase amine NTs (NE, 5HT, DA)
Atypical depression, anxiety.
Toxicity: hypertensive crisis (tyramine foods), CNS stimulation.
CI: SSRIs, TCAs, St. John’s worrt, meperidine, dextromethorphan (serotonin syndrome).

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46
Q

Bupropion

A

Atypical antidepressant, smoking sensation.
Increase NE and DA.
Toxicity: stimulant effects (tachy, insomnia), HA, seizures in anorexic/bulimic. No sexual SE.

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47
Q

Mirtazapine

A

A2 antagonist (release NE and 5HT) and potent 5HT2 and 5HT3 receptor antagonist.
Toxicity: sedation (maybe good in depressed with insomnia), increased appetite, weight gain (for anorexics), dry mouth.

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48
Q

Trazadone

A

Block 5HT2 and a1-adrenergic. For insomia.
Toxicity: sedation, N, priapism, postural hypotnesion.

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49
Q

H2 blockeres

A

Cimetidine, ranitidine, famotidine, nizatidine.
MOA: Decrease H+ decrease by parietal cells.
Use: peptic ulcer, gastritis, mild esophageal reflux.
Toxicity: Cimetidine inhibits P450 and has natiandrogenic effects. Can cross BBB (HA, confusion, dizzy), placenta. Cimetidine + ranitidine decrease renal excretion of creatinine.

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50
Q

PPI

A

Omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole.
MOA: Irr. Block H+/K+ ATPase on parietal cells.
Use: Peptic ulcer, gastritic, esophageal reflux, Zollinger-Ellison
Toxicity: risk of C. difficile, pneumonia. Decrease serum Mg2+ in long term.

51
Q

Bismuth, sucralfate

A

MOA: Bind to ulcer base, physicial protection, allows bicarb secretion to reestablish pH in mucous layer.
Use: ulcer healing and travers’ diarrhea.

52
Q

Misoprostol

A

MOA: PGE1 analog. Increase secretion of gastric mucous barrier, decrease acid production.
Use: prevent NSAID induced peptic ulcers, maintain PDA, ripens cervix.
Toxicity: diarrhea, abortifacient (CI in childbearing age W)

53
Q

Octreotide

A

MOA: long-acting somatostatin analog, inhibig splanchnic vasoconstriction homrones.
Use: acute variceal bleeds, acromegaly, VIPoma, carcinoid tumors
Toxicity: N, cramps, steatorrhea.

54
Q

Antacid use

A

All: can affect absorption, bioavailability, or urinary excretion of other drugs by changing gastric and urinary pH or delay gastric emptying. Hypokalemia.
1. Aluminum hydroxide: constipation, hypophosphatemia, proximal muscle weakness, osteodystrophy, seizures.
2. Calcium carbonate: hypercalcemia (increases gastrin), rebound acid increases. Can chelate and decr effectives of other drugs (tetracycline).
3. Magnesium hydroxide: diarrhea, hyporeflexia, hypotension, cardiac arrest (MG is a smooth muscle relaxer). MG=must go to bathroom.

55
Q

Osmotic laxatives

A

Magnesium hydroxide, magnesium citrate, polyethylene glycol, lactulose
MOA: osmotic load to draw water
Use: constipation. Lactulose: hepatic enceph since gut flora degrades it into metabolites (lactic acid and acetic acid) that promote nitrogen excretion as NH4+.
Toxicity: diarrhea, dehydration, abused by bulimics.

56
Q

Sulfasalazine

A

MOA: combo of sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflammatory). Activated by colonic bacteria.
Use: UC, Crohns (colitis part)
Toxicity: malaise, nausea, sulfonamide toxicity, reversible oligospermia. Blocks IL-1, TNF, lipooxygenase, free radical scavaging.

57
Q

Ondansetron

A

MOA: 5HT3 blocker, decrease vagal stimulation, powerful central-acting antiemetic.
Use: Control vomiting postop and in chemo
Toxicity: HA, constpiation, QT prolongation.
* Too much serotonin – diarrhea, not enough serotonin – constipation!

58
Q

Metoclopramide

A

MOA: D2 receptor blocker. Increases resting tone, contractility, LES tone, motility. Does not influence colon trasnport time.
Use: Diabetic and postsurgery gastroparesis, antiemetic, GERD
Toxicity: Increase Parkinsonian effects, tardive dyskinesia, restlessness, drowsiness, fatigue, depression, diarrhea. Drug intxn with digoxin and diabetic agents.
CI: patients with SBO or Parkinson disease (D1 receptor blockage)–seizrue

59
Q

Orlistat

A

MOA: inhibit gastric and pancreatic lipase – decrease breakdown and absorption of dietary fats.
Use: weight loss
Toxicity: steatorrhea, decrease absorption of fat-soluble vitamins.

60
Q

Heparin

A

MOA: Activates AT, decr thrombin and factor Xa. Short half-life. PTT*
Use: PE, acute coronary syndrome, MI, DVT. PREGNANCY.
Toxicity: Bleeding, HIT, osteoporosis, drug-drug intxn.
Antidote: protamine sulfate (+ charged)

61
Q

HIT

A

IgG abs against heparin-bound platelet factor 4 (PF4). Ab-heparin-PF4 complex activates platelets –> thrombosis and thrombocytopenia.
*Switch to direct thrombin inhibitors! Argatroban, bivalirudin, dabigatran

62
Q

Low molecular-weight heparins

A

Enoxaparin, dalteparin, fondaparinaux (indirect, best for hepatic dysfxn)
More on factor Xa, better bioavailability, 2-4x longer half-life, SQ and no monitoring. Not easily reversible.

63
Q

Argatroban, bivalirudin, dabigatran

A

Bivalirudin–related to hirudin (leeches)
Inhibit thrombin directly. Alternative for HIT.

64
Q

Warfarin

A

MOA: blocks g-carboxylation of vitamin K (factors, 2, 7, 9, 10, proteins C, S). Metabolism affected by polymorphisms of gene for vitamin K epoxide reductase complex (VKORC1). Affects extrinsic pw and PT. Long half-life.
Use: chronic anti-coag (DVT prophylaxis, prevent stroke in afib). Not for pregnant wome.
Toxicity: Bleeding, teratogenic, skin/tissue necrosis, drug-drug intxn. Protein C/S have shorter half-lives–start tx with heparin!
*Skin/tissue necrosis: due to small vessel microtromboses.
Reversal: vitamin K or FFP (rapid).

65
Q

Direct factor Xa inhibitors

A

Apixaban, rivaroxaban
MOA: bind to/directly block factor Xa.
Use: Tx and proph for DT and PE (rivaroxaban); stroke prophylaxis in afib. No monitoring.
Toxicity: bleeding, no reversal agent

66
Q

Thrombolytics

A

Alteplase (tPA), reteplase, streptokinase, tenecteplase
MOA: directly or indirectly convert plasminogen to plasmin, which cleaves thrombin and fibrin clots. **Increases PT, PTT, no change in platelets.
Use: Early MI or stroke, direct thrombolysis of severe PE.
Toxicity: Bleeding. CI in active bleeding, hx of intracranial bleeding, recent surgery, known bleeding diatheses, or severe HTN.
Reversal: aminocaproic acid (blocks fibrinolysis), FFP, and cryoprecipitate to replace factors.

67
Q

Asprin

A

MOA: irr blocks COX1+2 by covalent acetylation. Lasts until new platelet is produced. Increases bleedint time, decreases TXA2 and PGs, no effect on PT/PTT.
Use: antipyretic, analgesic, anti-inflammatory, antiplatelet
Toxicity: GI ulceration, tinnitus (CN8), acute renal failure, interstitial nephritis, upper GI bleeding, Reye syndrome.
Overdose: hyperventilation but becomes mixed metabolic acidosis-resp alkalosis.

68
Q

ADP receptor inhibitors

A

Clopidogrel, prasugrel, ticagrelor (reversible), ticlopidine.
MOA: block platlet aggregation by irr. Blocking ADP receptors. Prevents expression of glycoproteins Iib/IIIa on platelet surface.
Use: Acute coronary sydnrome, coronary stenting, decreases incidence or recurrent of thrombotic stroke.
Toxicity: Neutropenia (ticlopidine), TTP

69
Q

PDEIII Inhibitors

A

Cilostazol, dipyridamole
MOA: increase cAMP in platelets, inhibits platelet aggregation, vasodilators.
Use: intermittent claudication, coronary vasodilation, prevention of stroke or TIAs (with aspirin), angina proph
Toxicity: N/HA, facial flushing, hypotension, abd pain

70
Q

GPIIb/IIIa Inhibitors

A

Abciximab, eptifibatide, tirofiban
MOA: Bind to Iib/IIIa on activated platelets, prevent agg. Abciximab is made from monoclonal ab Fab fragments.
Use: unstable angina, percutaneous transluminal coronary angioplasty.
Toxicity: Bleeding, thrombocytopenia

71
Q

Azathioprine, 6MP, 6TG

A

MOA: Purine analogs–decerase de novo purine synthesis. Activated by HGPRT. Azathioprine –> 6MP.

Use: Prevent organ rejection, RA, IBD, SLE, wean pt off steroids

Toxicity: Myelosuppression, GI, liver.
*Azothioprine and 6MP: metabolized by XO. Allopurinol/feboxustat incr toxicity.

72
Q

Cladribine (2CDA)

A

MOA: Purine analog–inhibtion of DNA pol, DNA strand breaks
Use: Hairy cell leukemia
Toxicity: Myelosuppresion, nephrotoxicity, neurotoxicity

73
Q

Cytarabine (arabinofuranosyl cytidine)

A

MOA: Pyrimidine analog–blocks DNA pol
USE: Leukemias (AML), lymphomas
Toxicity: Leukopenia, thrombocytopenia, megaloblastic anemia.
*CYTarabine causes panCYTopenia

74
Q

5-FU

A

MOA: Pyrimidine analog bioactivated to 5F-dUMP–covalently complexes folic acid. Inhibits thymidylate synthase –> decr dTMP, DNA synth.

Use: Colon cancer, pancreatic cancer, basal cell carcinoma (topical)

Toxicity: Myelosuppression (not reversible with leucovorin)

75
Q

MTX

A

MOA: folic acid analog that competitively inhibits dihydrofolate reductase –> decr dTMP, DNA synth.

Use: 1. Cancers: leukemias (ALL), lymphomas, choriocarcinoma, sarcomas. 2. Non-neoplastic: ectopic pregnancy, medical aborption (w misoprostol), RA, psoriasis, IBD, vasculitis.

Toxicity: Myelosuppresion (rev with leucovorin), hepatotoxicity, mucositis (mouth ulcers), pulmonary fibrosis.

76
Q

Bleomycin (antitumor)

A

MOA: free radical formation, DNA strand breaks

Use: Testicular cancer, Hodgkin lymphoma

Toxicity: Pulmonary fibrosis, skin hyperpigmentation, mucositis, minimal myelosuppresion.

77
Q

Dactinomycin/actinomycin D (antitumor)

A

MOA: Intercalates in DNA.

Use: Wilms tumor, Ewing sarcoma, rhabdomyosarcoma. Childhood tumors. Children’s ACT out.

Toxicity: Myelosuppression.

78
Q

Doxorubicin, daunorubicin (antitumor)

A

MOA: Generates free radicals. Intercalates in DNA, DNA breaks, decr replication.

Use: Solid tumors, leukemias, lymphomas.

Toxicity: Cardiotoxicity (dilated), myelosuppression, alopecia. Toxic to tissues following extravasation. Dexrazoxane (iron chelating agent) used to prevent cardiotoxicity.

79
Q

Busulfan (alkylating agent)

A

MOA: Cross-links DNA.

Use: CML. Used to ablate bone marrow before transplant.

Toxicity: Severe myelosuppression, pulmonary fibrosis, hyperpigmentation.

80
Q

Cyclophosphamide, ifosfamide (alkylating agent)

A

MOA: Cross links DNA at guanine N7. Requires bioactivation by liver.

Use: Solid tumors, leukemia, lymphomas.

Toxicity: Myelosuppression, hemorrhagic cystitis, partially prevented with mesna (thiol group of mesna binds toxic metabolites).

81
Q

Nitrosoureas (carmustine, lomustine, semustine, streptozocin) (alkylating agents)

A

MOA: requires bioactivation. Crosses BBB – CNS. Cross links DNA.

Use: Brain tumors (including glioblastoma multiforme).

Toxicity: CNS toxicity (convulsions, dizziness, ataxia).

82
Q

Paclitaxel (MT inhib)

A

MOA: Hyperstabilize polyermized MTs in M phase, mitotic spindle can’t break down (no anaphase)
*Taxing to stay polymerized!

Use: Ovarian and breast carcinomas

Toxicity: Myelosuppression, alopecia, HSN, peripheral neuropathy

83
Q

Vincristine, vinblastine (MT inhib)

A

MOA: Vinca alkaloids, bind b-tubulin and block polymerization into MT, prevent mitotic spindle formation, M-phase arrest.

Use: Solid tumors, leukemias, Hodgkin (vinblastine), and nonhodgkin (vincristine). Also Wilms, Ewing, choriocarinoma.

Toxicity: Neurotoxicity (areflexia, peripheral neuritis), paralytic ileus
*Vinblastine blasts bones (suppression).

84
Q

Cisplatin, carboplatin

A

MOA: Cross-link DNA (platinum coord complex)

Use: Testicular, bladder, ovary, lung carcinomas

Toxicity: Nephrotoxicity, ototoxicity. Prevent nephrotoxicity with amifostine (free radical scavenger) and chloride (saline) diuresis.

85
Q

Etoposide, teniposide

A

MOA: Etoposide inhibits topoisomerase II – increase DNA degradation

Use: Solid tumors (testicular and small cell lung), leukemias, lymphomas

Toxicity: Myelosuppression, GI upset, alopecia

86
Q

Irinotecan, topotecan

A

MOA: Inhibit topoisomerase I and block DNA unwinding and rep.

Use: Colon cancer (irinotecan), ovarian, small cell lung cancer (topotecan)

Toxicity: Severe myelosuppression, diarrhea.

87
Q

Hydroxyurea

A

MOA: Block rionucleotide reductase –> decrease DNA synthesis (S-specific).

Use: Melanoma, CML, sickle cell disease (increase HbF)

Toxicity: Severe myelosuppression, GI upset.

88
Q

Eradicate ball cancer

A

Etoposide, bleomycin (or ifosfamide), cisplatin

89
Q

Predisone, prednisolone

A

MOA: bind intracytoplasmic receptor, alter gene transcription

Use: MC used glucocorticoids in chemo. CLL, non-Hodgkin lymphoma, immunosuppression

Toxicity: Cushing

90
Q

Bevacizumab

A

MOA: monoclonal ab against VEGF, block angiogenesis

Use: Solid tumors (colorectal cancer, RCC)

Toxicity: Hemorrhage, blood clots, imparied wound healing

91
Q

Erlotinib

A

MOA: EGFR tyrosine kinase inhibitor

Use: Non-small cell lung carcinoma

Toxicity: Rash

92
Q

Imatinib

A

MOA: Tyrosine kinase inhibitor of BCR-ABL and c-kit (common in Gi stromal tumors).

Use: CML, GI stromal tumors

Toxicity: Fluid retention

93
Q

Rituximab

A

MOA: monoclonal ab against CD20 (most B cell neoplasms)

Use: Non-hodgkin lymphoma, CLL, IBD, rheumatoid arthritis

Toxicity: Increase risk of progressive multifocal leukoencephaloapthy

94
Q

Tamoxifen, raloxifene

A

MOA: SERMs–antagonists in breast and agonists in bone. Block binding of estrogen to ER+ cells.

Use: Breast cancer (tamoxifen only) and prevention. Raloxifene useful to prevent ostoeporosis

Toxicity: Tamoxifen–partial agonist in endometrium (increase cancer risk), hot flashes. Raloxifen: no incr in endometrial CA, partial antagonist in endometrial tissue.

95
Q

Trastuzumab (herceptin)

A

MOA: Monoclonal ab against HER-2 (c-erbB2), tyrosine kinase receptor. Helps kill cancer cells that overexpress HER-2, through inhibition of HER2-initiated cellular signaling and ab-depedent cytotoxicity.

Use: HER-2+ breast cancer and gastric cancer (tras2zumab)

Toxicity: Cardiotoxicity–heartceptin

96
Q

Vemurafenib

A

MOA: small molecule inhibitor of BRAF oncogene + melanoma

Use: Mets melanoma

97
Q

Interferons

A

MOA: Glycoproteins normally made by virus-infected cells, exhibit wide range of antiviral and antitumor properties.

IFNa: chronic hep B and C, kaposi, hairy cell leukemia, condyloma acuminatum, RCC, malignant melanoma
IFNb: multiple sclerosis
IFNg: chronic granulomatous disease

Toxicity:

98
Q

Hep C therapy

A

Ribavirin: block guanine nucleotides by inhibiting IMP dehydrogenase. Chronic HCV, RSV (palivizumab for kids). Toxicity: hemolytic anemia, severe teratogen

Simeprevir: HCV protease inhibitor, prevents viral replication. Chronic HCV in combo wtih ribavirin and peginterferon-a. NOT monotherapy. Toxicity: photosensitivity, rash

Sofosbuvir: inhibitos HCV RNA-dep RNA pol, chain terminator. Chronic HCV via combo with ribavirin and pegifnA. NOT monotherpay. Toxicity: fatigue, HA, nausea

99
Q

Abx to avoid in pregnancy

A

Sulfonamides: kernicterus
Aminoglycosides: ototoxicity
FQ: cartilage damage
Clarithromycin: embryotoxic
Tetracyclines: discolored teeth, inhibition of bone growth
Ribavirin (antiviral): teratogenic
Griseofulvin (antifungal): teratogenic
Chloramphenicol: Gray baby

100
Q

Epinephrine, brimonidine

A

Glaucoma drugs
Epinephrine (a1): decrease aqueous humor synthesis via vasoconstriction. *This causes mydriasis–DO NOT use in closed angle
Brimonidine (a2): decrease aqueous humor synthesis
*Both can cause blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, ocular pruritis

101
Q

Timilol, betaxolol, carteolol

A

Glucoma drugs
Decrease aqueous humor synthesis, no pupillary or vision changes

102
Q

Acetazolamide

A

Glucoma drugs
Decrease aqueous humor synthesis via inhibition of CA. No pupillary or vision changes.

103
Q

Pilocarpine, carbachol

A

Glucoma drugs, Direct cholinomimetics
Increase outflow of aquous humor via contraction of ciliary muscle and opening of trabecular meshwork. Use pilocarpine in emergencies–opens meshwork into canal
*Miosis and cyclospasm (contraction of ciliary muscle).

104
Q

Physostigmine, echothiophate

A

Glucoma drugs, Indirect cholinomimetics
*Miosis and cyclospasm (contraction of ciliary muscle).

105
Q

Latanoprost

A

Glucoma drugs, PGF2a
Increase outflow of aqueous humor
*Darkens color of iris (browning)

106
Q

Pentazocine

A

Partial opioid, lower abuse potential. Can cause withdrawal sx if using full opioid agonist.

107
Q

Tramadol

A

Weak opioid, also inhibits 5HT and NE reuptake. “tram it all”–works on multiple NTs.
Use: chornic pain.
*Decreases seizure threshold, serotonin syndrome.

108
Q

Local anesthetics–Esters

A

Procaine, cocaine, tetracaine

109
Q

Local anesthetics–Amides

A

All have 2 I’s
Lidocaine, mepivacain, bupivacaine (cardiovascular toxicity)

110
Q

Order of nerve blockade (local anesthetic)

A

Small-diameter fibers > large
Myelinated fibers > unmyelinated fibers

111
Q

Order of nerve sensation loss (local anesthetic)

A

Pain, temp, touch, pressure

112
Q

Local anesthetics

A

Block Na+ channels, bind to inner part of channel when it’s activated (most effective in rapidly firing neurons).

113
Q

Depolarizing NM blocking drugs

A

Succinylcholine: strong Ach receptor agonist, produces sustained depolarization and prevents muscle contraction.
Reversal of blockage: Phase I–prolonged depolarization/NO ANTIDOTE. Block potentiated by cholinesterase inhibitors. Phase II–repolarized but blocked/ACh receptors are available, but desensitized. Antidote: cholinesterase inhibitors.
Complications: hypercalcemia, hyperkalemia, malignant hyperthermia

114
Q

Nondepolarizing NM blocking drugs

A

Tubocurarine, atracurium, mivacurium, pancuronium: all are competitive antagonists and compete with ACh for receptors. *Can release histamine and cause fall in BP, flushing, bronchoconsriction.
Reversal of blockage: neostigmine (must be given with atropine to prevent muscarinic effects like bradycardia), edrophonium, other cholinesterase inhibitors.

115
Q

Zolpiedem, zaleplon, eszopiclone

A

BZ1 subtype of GABA receptor, reversed by flumazenil
Use: insomnia
SE: ataxia, HA, confusion. Short duration because of rapid metabolism by liver. Only modest day-after psychomotor depression and few amnestic effects. Less dependence.

116
Q

Halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, N2O

A

Effects: myocardial depression, respiratory depression, N/emesis, increased cerebral blood flow (decreased cerebral metabolic demand).

Toxicity: hepatotoxicity (halothane), nephrotoxicity (methoxyflurane), proconvulsant (enflurane), expansion of trapped gas in body (N2O).

Can cause malignant hyperthermia–inhaled anesthetics (except N2O) and succinylcholine induce fever and severe muscle contractions. Tx with dantrolene.

117
Q

Midazolam

A

MC drug used for endoscopy. Short acting benzo. Can cause severe post op resp depression, decrease in BP, anterograde amnesia

118
Q

Ketamine

A

PCP analogs that act as dissociative anesthetics. Block NMDA receptors. CV stimulants. Cause disorientation, hallucination, bad dreams, increases cerebral blood flow.

119
Q

Propofol

A

Sedation in ICU, rapid anesthesia induction, short procedures. Less postop N than thiopental. Potentiates GABAa.

120
Q

Baclofen

A

Inhibits GABAb receptors at the spinal cord level, inducing skeletal muscle relxation.
Use: muscle spasms

121
Q

Cyclobenzprine

A

Centrally acting skeletal muscle relaxant. Structurally related to TCAs, similar anticholinergic side effets.
Use: muscle spasms

122
Q

Parkinson drugs

A

BALSA
-Bromocriptine: ergot, DA agonist
-Amantadine: incr DA release and decr reuptake, also antiviral for influenza A and rubella. Toxicity = ataxia, livedo reticularis.
-L-dopa/carbidopa: carbidopa blocks peripheral conversion to dopamine by blocking DOPA decarboxylase. Reduces SE of peripheral L-dopa conversion too (N/V). Also entacapone/tolcapone block COMT.
-Selegiline (and COMT inhibitors): blocks breakdown centrally to increase DA. Selegiline blocks MAO-B, Tolcapone blocks COMT.
-Antimuscarinics: Benztropine–improves tremor and rrigidity but little effect on bradykinesia.

123
Q

Alzheimer drugs

A

Memantine: NMDA receptor antagonist, prevent excitotoxicity (Ca). SE: Dizziness, confusion, hallucinations.

Donepezil, galantamine, rivastigmine, tacrine: AChE inhibitors. SE: N/dizziness, insomnia

124
Q

Huntington disease drugs

A

NT changes in Huntington: decr GABA, Ach, incr DA
Tetrabenazine and reserpine: inhibit VMAT
Haloperidol: D2 receptor blocker

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