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Thread: Quick Revision

  1. #1
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    Default Quick Revision

    PHARM_ANTIMICROBIAL
    Q: A common side effects of INF treatment is?
    A: Neutropenia

    Q: Antimicrobial prophylaxis for a history of recurrent UTIs
    A: TMP-SMZ

    Q: Antimicrobial prophylaxis for Gonorrhea
    A: Ceftriaxone

    Q: Antimicrobial prophylaxis for Meningococcal infection
    A: Rifampin (DOC), minocycline

    Q: Antimicrobial prophylaxis for PCP
    A: TMP-SMZ (DOC), aerosolized pentamidine

    Q: Antimicrobial prophylaxis for Syphilis
    A: Benzathine penicillin G

    Q: Are Aminoglycosides Teratogenic?
    A: Yes

    Q: Are Ampicillin and Amoxicillin penicillinase resistant?
    A: No

    Q: Are Carbenicillin, Piperacillin, and Ticarcillin penicillinase resistant?
    A: No

    Q: Are Cephalosporins resistant to penicillinase?
    A: No, but they are less susceptible than the other Beta lactams

    Q: Are Methicillin, Nafcillin, and Dicloxacillin penicillinase resistant?
    A: Yes

    Q: Clinical use of Isoniazid (INH)?
    A: Mycobacterium tuberculosis, the only agent used as solo prophylaxis against TB

    Q: Common side effects associated with Clindamycin include?
    A: Pseudomembranous colitis (C. difficile), fever, diarrhea

    Q: Common toxicities associated with Fluoroquinolones?
    A: GI upset, Superinfections, Skin rashes, Headache, Dizziness

    Q: Common toxicities associated with Griseofulvin are…...?
    A: Teratogenic, Carcinogenic, Confusion, Headaches

    Q: Describe the MOA of Interferons (INF)
    A: Glycoproteins from leukocytes that block various stages of viral RNA and DNA synthesis

    Q: Do Tetracyclines penetrate the CNS?
    A: Only in limited amounts

    Q: Does Ampicillin or Amoxicillin have a greater oral bioavailability?
    A: AmOxicillin has greater Oral bioavailability

    Q: Does Amprotericin B cross the BBB?
    A: No

    Q: Does Foscarnet require activation by a viral kinase?
    A: No

    Q: Foscarnet toxicity?
    A: Nephrotoxicity

    Q: Ganciclovir associated toxicities?
    A: Leukopenia, Neutropenia, Thrombocytopenia, Renal toxicity

    Q: How are INFs used clinically?
    A: Chronic Hepatitis A and B, Kaposi's Sarcoma

    Q: How are Sulfonamides employed clinically?
    A: Gram +, Gram -, Norcardia, Chlamydia

    Q: How are the HIV drugs used clinically?
    A: Triple Therapy' 2 Nucleoside RT Inhibitors with a Protease Inhibitor

    Q: How are the Latent Hypnozoite (Liver) forms of Malaria (P. vivax, P.ovale) treated?
    A: Primaquine

    Q: How can Isoniazid (INH)-induced neurotoxicity be prevented?
    A: Pyridoxine (B6) administration

    Q: How can the t1/2 of INH be altered?
    A: Fast vs. Slow Acetylators

    Q: How can the toxic effects fo TMP be ameliorated?
    A: With supplemental Folic Acid

    Q: How can Vancomycin-induced 'Red Man Syndrome' be prevented?
    A: Pretreat with antihistamines and a slow infusion rate

    Q: How do Sulfonamides act on bacteria?
    A: As PABA antimetabolites that inhibit Dihydropteroate Synthase, Bacteriostatic

    Q: How do the Protease Inhibitors work?
    A: Inhibt Assembly of new virus by Blocking Protease Enzyme

    Q: How does Ganciclovir's toxicity relate to that of Acyclovir?
    A: Ganciclovir is more toxic to host enzymes

    Q: How does resistance to Vancomycin occur?
    A: With an amino acid change of D-ala D-ala to D-ala D-lac

    Q: How is Acyclovir used clinically?
    A: HSV, VZV, EBV, Mucocutaneous and Genital Herpes Lesions, Prophylaxis in Immunocompromised pts

    Q: How is Amantadine used clinically?
    A: Prophylaxis for Influenza A, Rubella ; Parkinson's disease

    Q: How is Amphotericin B administered for fungal meningitis?
    A: Intrathecally

    Q: How is Amphotericin B used clinically?
    A: Wide spectrum of systemic mycoses: Cryptococcus, Blastomyces, Coccidioides, Aspergillus, Histoplasma, Candida, Mucor

    Q: How is Chloramphenical used clinically?
    A: Meningitis (H. influenza, N. meningitidis, S. pneumoniae), Conserative treatment due to toxicities

    Q: How is Foscarnet used clinically?
    A: CMV Retinitis in IC pts when Ganciclovir fails

    Q: How is Ganciclovir activated?
    A: Phosphorylation by a Viral Kinase

    Q: How is Ganciclovir used clinically?
    A: CMV, esp in Immunocompromised patients

    Q: How is Griseofulvin used clinically?
    A: Oral treatment of superficial infections

    Q: How is Leishmaniasis treated?
    A: Pentavalent Antimony

    Q: How is Ribavirin used clinically?
    A: for RSV

    Q: How is Rifampin used clinically?
    A: 1. Mycobacterium tuberculosis
    A: 2. Delays resistance to Dapsone when used of Leprosy
    A: 3. Used in combination with other drugs

    Q: How is Trimethoprim used clinically?
    A: Used in combination therapy with SMZ to sequentially block folate synthesis

    Q: How is Vancomycin used clinically?
    A: For serious, Gram + multidrug-resistant organisms

    Q: How would you treat African Trypanosomiasis (sleeping sickness)?
    A: Suramin

    Q: In what population does Gray Baby Syndrome occur? Why?
    A: Premature infants, because they lack UDP-glucuronyl transferase

    Q: Is Aztreonam cross-allergenic with penicillins?
    A: No

    Q: Is Aztreonam resistant to penicillinase?
    A: Yes

    Q: Is Aztreonam usually toxic?
    A: No

    Q: Is Imipenem resistant to penicillinase?
    A: Yes

    Q: Is Penicillin penicillinase resistant?
    A: No - duh

    Q: IV Penicillin
    A: G

    Q: Mnemonic for Foscarnet?
    A: Foscarnet = pyroFosphate analog

    Q: MOA for Penicillin (3 answers)?
    A: 1)Binds penicillin-binding proteins
    A: 2) Blocks transpeptidase cross- linking of cell wall
    A: 3) Activates autolytic enzymes

    Q: MOA: Bactericidal antibiotics
    A: Penicillin, Cephalosporins, Vancomycin, Aminoglycosides, Fluoroquinolones, Metronidazole

    Q: MOA: Block cell wall synthesis by inhib. Peptidoglycan cross-linking (7)
    A: Penicillin, Ampicillin, Ticarcillin, Pipercillin, Imipenem, Aztreonam, Cephalosporins

    Q: MOA: Block DNA topoisomerases
    A: Quinolones

    Q: MOA: Block mRNA synthesis
    A: Rifampin

    Q: MOA: Block nucleotide synthesis
    A: Sulfonamides, Trimethoprim

    Q: MOA: Block peptidoglycan synthesis
    A: Bacitracin, Vancomycin

    Q: MOA: Block protein synthesis at 30s subunit
    A: Aminoglycosides, Tetracyclines

    Q: MOA: Block protein synthesis at 50s subunit
    A: Chloramphenicol, Erythromycin/macrolides, Lincomycin, Clindamycin, Streptogramins (quinupristin, dalfopristin)

    Q: MOA: Disrupt bacterial/fungal cell membranes
    A: Polymyxins

    Q: MOA: Unkown
    A: Pentamidine

    Q: MOAisrupt fungal cell membranes
    A: Amphotericin B, Nystatin, Fluconazole/azoles

    Q: Name common Polymyxins
    A: Polymyxin B, Polymyxin E

    Q: Name several common Macrolides (3)
    A: Erythromycin, Azithromycin, Clarithromycin

    Q: Name some common Sulfonamides (4)
    A: Sulfamethoxazole (SMZ), Sulfisoxazole, Triple sulfas, Sulfadiazine

    Q: Name some common Tetracyclines (4)
    A: Tetracycline, Doxycycline, Demeclocycline, Minocycline

    Q: Name the common Aminoglycosides (5)
    A: Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin

    Q: Name the common Azoles
    A: Fluconazole, Ketoconazole, Clotrimazole, Miconazole, Itraconazole

    Q: Name the common Fluoroquinolones (6)
    A: Ciprofloxacin, Norfloxacin, Ofloxacin, Grepafloxacin, Enoxacin, Nalidixic acid

  2. #2
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    Default Drugs n Reactions

    Q: Which drug(s) cause this reaction: Adrenocortical Insufficiency
    A: -Glucocorticoid withdrawal

    Q: Which drug(s) cause this reaction: Agranulocytosis (3)?
    A: -Cloazapine -carbamazapine -colchicine -PTU

    Q: Which drug(s) cause this reaction: Anaphylaxis?
    A: -Penicillin

    Q: Which drug(s) cause this reaction: Aplastic anemia (5)?
    A: -Chloramphenicol -benzene -NSAIDS -PTU -phenytoin

    Q: Which drug(s) cause this reaction: Atropine-like side effects?
    A: -Tricyclic antidepressants

    Q: Which drug(s) cause this reaction: Cardiac toxicity?
    A: -Daunorubicin & Doxorubicin

    Q: Which drug(s) cause this reaction: Cinchonism (2)?
    A: -Quinidine -quinine

    Q: Which drug(s) cause this reaction: Cough?
    A: -ACE inhibitors (Losartan>no cough)

    Q: Which drug(s) cause this reaction: Cutaneous flushing (4)?
    A: -Niacin -Ca++ channel blockers -adenosine -vancomycin

    Q: Which drug(s) cause this reaction: Diabetes insipidus?
    A: -Lithium

    Q: Which drug(s) cause this reaction: Disulfram-like reaction (4) ?
    A: -Metronidazole -certain cephalosporins -procarbazine -sulfonylureas

    Q: Which drug(s) cause this reaction: Drug induced Parkinson's (4) ?
    A: -Haloperidol -chlorpromazine -reserpine -MPTP

    Q: Which drug(s) cause this reaction: Extrapyramidal side effects (3)?
    A: -Chlorpromazine -thioridazine -haloperidol

    Q: Which drug(s) cause this reaction: Fanconi's syndrome?
    A: -Tetracycline

    Q: Which drug(s) cause this reaction: Focal to massive hepatic necrosis (4)?
    A: -Halothane -Valproic acid -acetaminophen -Amantia phalloides

    Q: Which drug(s) cause this reaction: G6PD hemolysis(8)?
    A: -Sulfonamides -INH -ASA -Ibuprofen -primaquine -nitrofurantoin /-pyrimethamine -chloramphenicol

    Q: Which drug(s) cause this reaction: Gingival hyperplasia?
    A: -Phenytoin

    Q: Which drug(s) cause this reaction: Gray baby syndrome?
    A: -Chloramphenicol

    Q: Which drug(s) cause this reaction: Gynecomastia (6) ?
    A: -Cimetidine -ketoconazole -spironolactone -digitalis -EtOH -estrogens

    Q: Which drug(s) cause this reaction: Hepatitis?
    A: -Isoniazid

    Q: Which drug(s) cause this reaction: Hot flashes?
    A: -Tamoxifen

    Q: Which drug(s) cause this reaction: Neuro and Nephrotoxic?
    A: -polymyxins

    Q: Which drug(s) cause this reaction: Osteoporosis (2)?
    A: -Corticosteroids -heparin

    Q: Which drug(s) cause this reaction: Oto and Nephrotoxicity (3)?
    A: -aminoglycosides -loop diuretics -cisplatin

    Q: Which drug(s) cause this reaction: P450 induction(6)?
    A: -Barbiturates -phenytoin -carbamazipine -rifampin -griseofulvin -quinidine

    Q: Which drug(s) cause this reaction: P450 inhibition(6)?
    A: -Cimetidine -ketoconazole -grapefruit juice -erythromycin -INH -sulfonamides

    Q: Which drug(s) cause this reaction: Photosensitivity(3)?
    A: -Tetracycline -amiodarone -sulfonamides

    Q: Which drug(s) cause this reaction: Pseudomembranous colitis?
    A: -Clindamycin

    Q: Which drug(s) cause this reaction: Pulmonary fibrosis(3)?
    A: -Bleomycin -amiodarone -busulfan

    Q: Which drug(s) cause this reaction: SLE-like syndrome
    A: -Hydralazine -Procainamide -INH -phenytoin

    Q: Which drug(s) cause this reaction: Stevens-Johnson syn. (3) ?
    A: -Ethosuxamide -sulfonamides -lamotrigine

    Q: Which drug(s) cause this reaction: Tardive dyskinesia?
    A: -Antipsychotics

    Q: Which drug(s) cause this reaction: Tendonitis and rupture?
    A: -Fluoroquinolones

    Q: Which drug(s) cause this reaction: Thrombotic complications?
    A: -Oral Contraceptives

    Q: Which drug(s) cause this reaction: Torsade de pointes (2) ?
    A: -Class III antiarrhythmics (sotalol) -class IA (quinidine)

    Q: Which drug(s) cause this reaction: Tubulointerstitial Nephritis (5)?
    A: -Sulfonamides -furosemide -methicillin -rifampin -NSAIDS (ex. ASA)

  3. #3
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    Default Antidotes

    Q: List some specifics of lead poisoning(4)?
    A: -A57Blue lines in gingiva& long bones -Encephalopathy & Foot drop -Abdominal colic / -Sideroblastic anemia

    Q: List the specific antidote for this toxin: Acetaminophen
    A: -N-acetylcystine

    Q: List the specific antidote for this toxin: Amphetamine
    A: -Ammonium Chloride

    Q: List the specific antidote for this toxin: Anticholinesterases (organophosphate.)
    A: -Atropine & pralidoxime

    Q: List the specific antidote for this toxin: Antimuscarinic (anticholinergic)
    A: -Physostigmine salicylate

    Q: List the specific antidote for this toxin: Arsenic (all heavy metals)
    A: -Dimercaprol, succimer

    Q: List the specific antidote for this toxin: Benzodiazepines
    A: -Flumazenil

    Q: List the specific antidote for this toxin: Beta Blockers
    A: -Glucagon

    Q: List the specific antidote for this toxin: Carbon monoxide
    A: -100% oxygen, hyperbaric

    Q: List the specific antidote for this toxin: Copper
    A: -Penicillamine

    Q: List the specific antidote for this toxin: Cyanide
    A: -Nitrate, hydroxocobalamin thiosulfate

    Q: List the specific antidote for this toxin: Digitalis
    A: -Normalize K+, Lidocaine, & Anti-dig Mab

    Q: List the specific antidote for this toxin: Heparin
    A: -Protamine

    Q: List the specific antidote for this toxin: Iron
    A: -Deferoxamine

    Q: List the specific antidote for this toxin: Lead
    A: -EDTA, dimercaprol, succimer, & penicillamine

    Q: List the specific antidote for this toxin: Methanol & Ethylene glycol
    A: -Ethanol, dialysis, & fomepizole

    Q: List the specific antidote for this toxin: Methemoglobin
    A: -Methylene blue

    Q: List the specific antidote for this toxin: Opioids
    A: -B51Naloxone / naltrexone (Narcan)

    Q: List the specific antidote for this toxin: Salicylates
    A: -Alkalinize urine & dialysis

    Q: List the specific antidote for this toxin: TPA & Streptokinase
    A: -Aminocaproic acid

    Q: List the specific antidote for this toxin: Tricyclic antidepressants
    A: -NaHCO3

    Q: List the specific antidote for this toxin: Warfarin
    A: -Vitamin K & fresh frozen plasma

    Q: What are the products and their toxicities of the metabolism of ethanol by / alcohol dehydrogenase?
    A: -Acetaldehyde -Nausea, vomiting, headache, & hypotension

    Q: What are the products and their toxicities of the metabolism of Ethylene Glycol by / alcohol dehydrogenase?
    A: -Oxalic acid -Acidosis & nephrotoxicity

  4. #4
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    Default Moa

    Q: What is the mecanism of action of Sucralfate?
    A: Aluminum sucrose sulfate polymerizes in the acid environment of the stomach and selectively binds necrotic peptic ulcer tissue. Acts as a barrier to acid, pepsin, and bile.

    Q: What is the mecanism of action of the COX-2 inhibitors (celecoxib, rofecoxib)?
    A: Selectively inhibit cyclooxygenase (COX) isoform 2, which is found in inflammatory cells nad mediates inflammation and pain; spares COX-1 which helps maintain the gastric mucosa.

    Q: What is the mecanism of action, effective period, and ineffective period of use for Cromolyn in treating Asthma?
    A: Prevents release of mediators from mast cells. Effective only for the prophylaxis of asthma. Not effective during an acute attack.

    Q: What is the mechanism of action and clinical use of the antiandrogen Flutamide?
    A: Flutamide is a nonsteroidal competitive inhibitor of androgens at the testosterone receptor, used in prostate carcinoma.

    Q: What is the mechanism of action and clinical use of the antiandrogens Ketoconazole and Spironolactone?
    A: Inhibit steroid synthesis, used in the treatment of polycystic ovarian syndrome to prevent hirsutism.

    Q: What is the mechanism of action of Acetaminophen?
    A: Reversibly inhibits cyclooxygenase, mostly in CNS. Inactivated peripherally.

    Q: What is the mechanism of action of Allopurinol used to treat chronic gout?
    A: Inhibits xanthine oxidase, decresing conversion of xanthine to uric acid.

    Q: What is the mechanism of action of Aspirin?
    A: Acetylates and irreversibly inhibits cyclooxygenase (COX I and COX II) to prevent the conversion of arachidonic acid to prostaglandins.

    Q: What is the mechanism of action of Clomiphene?
    A: Clomiphene is a partial agonist at estrogen receptors in the pituitary gland. Prevents normal feedback inhibition and increses release of LH and FSHfrom the pituitary, which stimulates ovulation.

    Q: What is the mechanism of action of Colchicine used to treat acute gout?
    A: Depolymerizes microtubules, impairing leukocyte chemotaxis and degranulation.

    Q: What is the mechanism of action of Cyclosporine?
    A: Binds to cyclophilins (peptidyl proline cis-trans isomerase), blocking the differentiation and activation of T cells mainly by inhibiting the production of IL-2 and its receptor.

    Q: What is the mechanism of action of Heparin?
    A: Heparin catalyzes the activation of antithrombin III.

    Q: What is the mechanism of action of Mifepristone (RU486)?
    A: Competitive inibitor of progestins at progesterone receptors.

    Q: What is the mechanism of action of Misoprostol?
    A: Misoprostol is a PGE1 analog that increases the production and secretion of the gastic mucous barrier.

    Q: What is the mechanism of action of NSAIDs other than Aspirin?
    A: Reversibly inhibit cyclooxygenase (COX I and COX II). Block prostaglandin synthesis.

    Q: What is the mechanism of action of Omeprazole, Lansoprazole?
    A: Irreversibly inhibits H+/K+ ATPase in stomach parietal cells.

    Q: What is the mechanism of action of Probenacid used to treat chronic gout?
    A: Inhibits reabsorption of uric acid.

    Q: What is the mechanism of action of Sildenafil (Viagra)?
    A: Inhibits cGMP phosphodiesterase, casuing increased cGMP, smooth muscle relaxation in the corpus cavernosum, increased blood flow, and penile erection.

    Q: What is the mechanism of action of the Alpha-glucosidase inhibitors?
    A: Inhibit intestinal bursh border Alpha-glucosidases; delayed hydrolysis of sugars and absorption of sugars leading to decresed postprandial hyperglycemia.

    Q: What is the mechanism of action of the glucocorticoids?
    A: Decrease the production of leukotrienes and protaglandins by inhibiting phospholipase A2 and expression of COX-2.

    Q: What is the mechanism of action of the H2 Blockers?
    A: Reversible block of histamine H2 receptors

    Q: What is the mechanism of action of the Sulfonylureas?
    A: Close K+ channels in Beta-cell membrane leading to cell depolarization causing insulin release triggered by increase in Calcium ion influx.

    Q: What is the mechanism of action of the thrombolytics?
    A: Directly of indirectly aid conversion of plasminogen to plasmin which cleaves thrombin and fibrin clots. (It is claimed that tPA specifically converts fibrin-bound plasminogen to plasmin.)

    Q: What is the mechanism of action of Ticlopidine, Clopidogrel
    A: Inhibits platelet aggregation by irreversibly inhibiting the ADP pathway involved in the binding of fibrinogen.

    Q: What is the mechanism of action of Warfarin (Coumadin)?
    A: Warfarin interferes with the normal synthesis and gamma-carboxylation of vitamin K-dependent clotting factors II, VII, IX, and X, Protein C and S via vitamin K antagonism.

    Q: What is the mechanism of Azathioprine?
    A: Antimetabolite derivative of 6-mercaptopurine that interferes with the metablolism and synthesis of nucleic acid.

    Q: What is the mechanism of Leuprolide?
    A: GnRH analog with agonist properties when used in pulsatile fashion and antagonist properties when used in continuous fashion, causing a transient initial burst of LH and FSH

    Q: What is the mechanism of Tacrolimus (FK506)?
    A: Similar to cyclosporine; binds to FK-binding protein, inhibiting secretion of IL-2 and other cytokines.

  5. #5
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    Default Clinical Use

    Q: What is the clincial use for Misoprostol?
    A: Prevention of NSAID-induced peptic ulcers, maintains a PDA.

    Q: What is the clinical use for Clomiphene?
    A: Treatment of infertility.

    Q: What is the clinical use for Heparin?
    A: Immediate anticoagulation for PE, stroke, angina, MI, DVT.

    Q: What is the clinical use for Sildenafil (Viagra)?
    A: Erectile dysfunction.

    Q: What is the clinical use for Sucralfate?
    A: Peptic ulcer disease.

    Q: What is the clinical use for Warfarin?
    A: Chronic anticoagulation.

    Q: What is the clinical use of Mifepristone (RU486)?
    A: Abortifacient.

    Q: What is the clinical use of Tacrolimus (FK506)?
    A: Potent immunosuppressive used in organ transplant recipients.

    Q: What is the effect of the Glitazones in diabetes treatment?
    A: Increase target cell response to insulin.

    Q: What is the enzyme inhibited, the effect of this inhibition, and the clinical use of the antiandrogren Finasteride?
    A: Finasteride inhibits 5 Alpha-reductase, this decreases the conversion of testosterone to dihydrotestosterone, useful in BPH

    Q: What is the lab value used to monitor the effectiveness of Heparin therapy?
    A: The PTT.

    Q: What is the lab value used to monitor the effectiveness of Warfarin therapy?
    A: The PT.

    Q: What is the main clinical use for the thrombolytics?
    A: Early myocardial infarction.

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