Pharmacology
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| Treatment of schistasomiasis | Praziquantel
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| Treatment of benzodiazepam (or EtOH) overdose | Flumazenil
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| Cause of cough in pt on ACE inhibitor | Bradykinin
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| Use of epinephrine in shock | 1:1000 dilation subcutaneously
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| Dantrolene | used in Tx of malignant hyperthermia after Halothane
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| Treatment of acetaminophen overdose | acetylcysteine to replace used up GSH (neutralizes acetaminophen free radicals formed in liver cytochrome system)
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| Mechanism of loop diuretic | blocks Na-K-2Cl cotransport pump in the thick ascending limb of renal medulla; also blocks Ca reabsorption
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| Cyanide poisoning treatment | Amyl nitrite and Thiosulfate
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| Thrush | may be a complication of corticosteroid inhaler
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| Isotretinoin/Accutane | always do pregnancy test on females; put them on OCPs
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| Mechanism of propylthiouracil | blocks iodination of tyrosine residues of thyroglobulin; also blocks coupling of DIT and MIT; only drug that can be used in pregnancy but may cause goiter in newborn as well as nail defects
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| P450 system in the liver | makes drugs water soluble
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| Angioedema and renal failure | side effects caused by ACE inhibitors
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| Mechanism of action of retinoic acid | behaves like a steroid (binds to receptors in nucleus w/subsequent gene transcription); ptns produced are important for growth, differentiation, reproduction and embryonic development
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| Allopurinol action in purine synthesis | blocks xanthine oxidase (identify hypoxanthine to xanthine and xanthine to uric acid on schematic)
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| Most common antibiotic used to prevent endocarditis in pts with valvular disease (all valvular dzs except asymptomatic MVP and all congenital heart dzs except asymptomatic ASD) | Amoxicillin (drug of choice)
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| Yellow coloration of skin that can be mistaken for jaundice caused by a drug | Quinacrine
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| Bluish discoloration of skin caused by a drug | Chlorpromazine and Arsenic
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| Diffuse erythema followed by separation of skin (scalded skin or toxic epidermal necrolysis) d/t drug: | Barbituates, Sulfonamides, Phenytoin, NSAIDs
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| Hair loss in a woman d/t drug: | Oral contraceptives (predictable; estrogen causes hair to be at same stage in development; may also occur after delivery)
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| Erythematous hyperpigmented plaque-like lesion that recurs at same site w/Rx use = fixed drug eruption d/t: | phenolphtalein, NSAIDs, tetracycline, Bactrim, bartbituates
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| Group of drugs w/highest a/w urticarial and maculopapular lesions | Amoxicillin, TMP/SMX, Ampicillin/PCN; they are not type I hypersensitivity histamine rxns
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| Elderly woman on thiazides is at most risk for developing | gout
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| Tardive dyskinesia, malignant syndrome (sweating, hyperpyrexia, autonomic instability) is a/w: | Neuroleptics
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| Antipsychotic drug requiring visual exam | Thioridazine (also produces heart conduction defects)
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| Drug contraindicated with MAO inhibitors | epinephrine
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| Use of Phentolamine | non-selective alpha-blocker that lowers bp during surgery for pheochromocytoma
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| Mechanism of AZT | inhibits reverse transcriptase
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| Treatment of Pb poisoning | BAL (dimercaprol )and EDTA
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| Drugs involved in folate metabolism | Phenytoin (blocks intestinal conjugase); Methotrexate/TMP-SMX (blocks dihydrofolate reductase)
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| Cromolyn sodium | stabilizes mast cell membrane preventing release of preformed mediators and release of prostaglandins/leukotrienes after the release reaction
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| Methotrexate | blocks dihydrofolate reductase and the conversion of dihydrofolate to tetrahydrofolate
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| Glucuronyl transferase in liver renders compounds | water soluble
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| Cycooxygenase | irreversibly inhibited by aspirin; reversibly by NSAIDs
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| Thromboxane A2 | synthesized by platelets; vasoconstrictor that increases platelet aggregation
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| Effect of proton blockers | blocks H+/K+/ATPase proton pump in parietal cell; not a receptor mediated event
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| H2 Blockers | blocks H2 receptor which normally activates adenyl cyclase producing cAMP which stimulates protein kinase
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| Acetylcholine | activates cholinergic receptor causing release of Ca which stimulates protein kinase
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| Misoprostol | blocks prostaglandin receptor which normally inhibits adenylate cyclase and cAMP production
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| 7-fold membrane spanning protein drug | propanolol b-blocker
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| Phase 3 clinical trials | double blind
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| Ticlopidine | substitute for aspirin in preventing strokes; CAD if pt is allergic to aspirin
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| Drug-induced SLE | procainamide, hydralazine
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| Overdose of succinylcholine | use acetylcholine blockers
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| Finasteride | blocks 5-a reductase which converts testosterone into dihydrotestosterone (testosterone will inc proximal to block and DHT will decrease)
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| Flutamide, cyproterone, spironolactone | block androgen receptor (testosterone/dihydrotestosterone increase w/o having physiologic effect)
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| Ketoconazole | inhibits testosterone synthesis; suppresses adrenal steroid synthesis
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| Leuprolide | GnRH analogue, which when given in sustained fashion, inhibits FSH and LH, hence lowering testosterone and estrogen levels
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| ACE inhibitors | inc in renin and Angiotensin-I, but a dec in AT-II and aldosterone
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| Arsenic poisoning | treat with dimercaprol
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| Chloroquine used in treatment of malaria, but malaria recurred, why? | exoerythrocytic/hepatic stage (P.vivax or P.ovale); drug kills active dz but does not eradicate hepatic stage
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| Primaquine in treatment of malaria | not good in active stage, but does kill hepatic stage of P.vivax and P. ovale
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| Dantrolene | reduces release of Ca from sarcoplasmic reticulum of skeletal muscle; antispasmodic drug; also used to treat malignant hyperthermia
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| Methanol ingestion | inc anion gap metabolic acidosis d/t conversion of methanol into formic acid; optic nerve degeneration and blindness; treat with alcohol infusion to block metabolism by alcohol dehydrogenase
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| Botulism toxin | blocks release of Ach
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| Ribavirin | used in severe RSV infxn in kids
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| Asthma | albuterol (b2-selective agonist) bronchodilator
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| Acetylcholine breakdown | occurs in synapse into choline and acetate by acetylcholinesterase in the cleft; products are recycled and not excreted
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| Amphotericin | disrupts cell membrane permeability; binds to ergosterol in membrane
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| Ketoconazole | inhibits the metabolism of nonsedating antihistamines like Seldane, leading to cardiac arrhythmias
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| Opioid toxicity | treate with Naloxone (receptor antagonist)
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| Opioids | cause constipation and miosis
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| Codeine | metabolized into morphine in small amounts; first pass metabolism of morphine in liver
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| Delerium tremens | treat with benzodiazepines
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| Lovastatin | inhibits HMG CoA reductase
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| Patent ductus arteriosus | keep open with PG-E
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| A common side effects of INF treatment is? | Neutropenia
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| Antimicrobial prophylaxis for a history of recurrent UTIs | TMP-SMZ
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| Antimicrobial prophylaxis for Gonorrhea | Ceftriaxone
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| Antimicrobial prophylaxis for Meningococcal infection | Rifampin (DOC), minocycline
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| Antimicrobial prophylaxis for Pneomocystis Carinii Pneumonia | TMP-SMZ (DOC), aerosolized pentamidine
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| Antimicrobial prophylaxis for Syphilis | Benzathine penicillin G
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| Are Aminoglycosides Teratogenic? | Yes
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| Are Ampicillin and Amoxicillin penicillinase resistant? | No
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| Are Carbenicillin, Piperacillin, and Ticarcillin penicillinase resistant? | No
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| Are Cephalosporins resistant to penicillinase? | No, but they are less susceptible than the other Beta lactams
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| Clinical use of Isoniazid (INH)? | Mycobacterium tuberculosis, the only agent used as solo prophylaxis against TB
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| Common side effects associated with Clindamycin include? | Pseudomembranous colitis (C. difficile), fever, diarrhea
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| Common toxicities associated with Fluoroquinolones? | GI upset, Superinfections, Skin rashes, Headache, Dizziness
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| Common toxicities associated with Griseofulvin are...? | Teratogenic, Carcinogenic, Confusion, Headaches
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| Describe the MOA of Interferons (INF) | Glycoproteins from leukocytes that block various stages of viral RNA and DNA synthesis
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| Do Tetracyclines penetrate the CNS? | Only in limited amounts
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| Does Ampicillin or Amoxicillin have a greater oral bioavailability? | AmOxicillin has greater Oral bioavailability
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| Does Amprotericin B cross the BBB? | No
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| Does Foscarnet require activation by a viral kinase? | No
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| Foscarnet toxicity? | Nephrotoxicity
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| Ganciclovir associated toxicities? | Leukopenia, Neutropenia, Thrombocytopenia, Renal toxicity
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| How are INFs used clinically? | Chronic Hepatitis A and B, Kaposi's Sarcoma
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| How are Sulfonamides employed clinically? | Gram +, Gram -, Norcardia, Chlamydia
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| How are the HIV drugs used clinically? | Triple Therapy' 2 Nucleoside RT Inhibitors with a Protease Inhibitor
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| How are the Latent Hypnozoite (Liver) forms of Malaria (P. vivax, P.ovale) treated? | Primaquine
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| How can Isoniazid (INH)-induced neurotoxicity be prevented? | Pyridoxine (B6) administration
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| How can the t1/2 of INH be altered? | Fast vs. Slow Acetylators
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| How can the toxic effects fo TMP be ameliorated? | With supplemental Folic Acid
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| How can Vancomycin-induced 'Red Man Syndrome' be prevented? | Pretreat with antihistamines and a slow infusion rate
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| How do Sulfonamides act on bacteria? | As PABA antimetabolites that inhibit Dihydropteroate Synthase, Bacteriostatic
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| How do the Protease Inhibitors work? | Inhibit Assembly of new virus by Blocking Protease Enzyme
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| How does Ganciclovir's toxicity relate to that of Acyclovir? | Ganciclovir is more toxic to host enzymes
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| How does resistance to Vancomycin occur? | With an amino acid change of D-ala D-ala to D-ala D-lac
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| How is Acyclovir used clinically? | HSV, VZV, EBV, Mucocutaneous and Genital Herpes Lesions, Prophylaxis in Immunocompromised pts
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| How is Amantadine used clinically? | Prophylaxis for Influenza A, Rubella ; Parkinson's disease
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| How is Amphotericin B administered for fungal meningitis? | Intrathecally
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| How is Amphotericin B used clinically? | Wide spectrum of systemic mycoses: Cryptococcus, Blastomyces, Coccidioides, Aspergillus, Histoplasma, Candida, Mucor
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| How is Chloramphenical used clinically? | Meningitis (H. influenza, N. meningitidis, S. pneumoniae), Conserative treatment due to toxicities
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| How is Foscarnet used clinically? | CMV Retinitis in IC pts when Ganciclovir fails
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| How is Ganciclovir activated? | Phosphorylation by a Viral Kinase
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| How is Ganciclovir used clinically? | CMV, esp in Immunocompromised patients
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| How is Griseofulvin used clinically? | Oral treatment of superficial fungal infections
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| How is Leishmaniasis treated? | Pentavalent Antimony
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| How is Ribavirin used clinically? | for RSV
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| How is Rifampin used clinically? | 1. Mycobacterium tuberculosis 2. Delays resistance to Dapsone when used of Leprosy 3. Used in combination with other drugs
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| How is Trimethoprim used clinically? | Used in combination therapy with SMZ to sequentially block folate synthesis
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| How is Vancomycin used clinically? | For serious, Gram + multidrug-resistant organisms
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| How would you treat African Trypanosomiasis (sleeping sickness)? | Suramin
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| In what population does Gray Baby Syndrome occur? Why? | Premature infants, because they lack UDP-glucuronyl transferase
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| Is Aztreonam (monobactam) cross-allergenic with penicillins? | No
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| Is Aztreonam resistant to penicillinase? | Yes
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| Is Aztreonam usually toxic? | No
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| Is Imipenem resistant to penicillinase? | Yes
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| IV Penicillin | G
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| Mnemonic for Foscarnet? | Foscarnet = pyroFosphate analog
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| MOA for Penicillin (3 answers)? | 1)Binds penicillin-binding proteins 2) Blocks transpeptidase cross- linking of cell wall 3) Activates autolytic enzymes
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| MOA: Bactericidal antibiotics | Penicillin, Cephalosporins, Vancomycin, Aminoglycosides, Fluoroquinolones, Metronidazole
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| MOA: Block cell wall synthesis by inhib. Peptidoglycan cross-linking (7) | Penicillin, Ampicillin, Ticarcillin, Pipercillin, Imipenem, Aztreonam, Cephalosporins
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| MOA: Block DNA topoisomerases | Quinolones
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| MOA: Block mRNA synthesis | Rifampin
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| MOA: Block nucleotide synthesis | Sulfonamides, Trimethoprim
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| MOA: Block peptidoglycan synthesis | Bacitracin, Vancomycin
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| MOA: Block protein synthesis at 30s subunit | Aminoglycosides, Tetracyclines
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| MOA: Block protein synthesis at 50s subunit | Chloramphenicol, Erythromycin/macrolides, Lincomycin, Clindamycin, Streptogramins (quinupristin, dalfopristin)
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| MOA: Disrupt bacterial/fungal cell membranes | Polymyxins
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| MOA: Unkown | Pentamidine
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| MOA disrupt fungal cell membranes | Amphotericin B, Nystatin, Fluconazole/azoles
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| Name common Polymyxins | Polymyxin B, Polymyxin E
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| Name several common Macrolides (3) | Erythromycin, Azithromycin, Clarithromycin
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| Name some common Sulfonamides (4) | Sulfamethoxazole (SMZ), Sulfisoxazole, Triple sulfas, Sulfadiazine
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| Name some common Tetracyclines (4) | Tetracycline, Doxycycline, Demeclocycline, Minocycline
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| Name the common Aminoglycosides (5) | Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin
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| Name the common Azoles | Fluconazole, Ketoconazole, Clotrimazole, Miconazole, Itraconazole
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| Name the common Fluoroquinolones (6) | Ciprofloxacin, Norfloxacin, Ofloxacin, Grepafloxacin, Enoxacin, Nalidixic acid
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| Name the common Non-Nucleoside Reverse Transcriptase Inhibitors | Nevirapine, Delavirdine
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| Name the common Nucleoside Reverse Transcriptase Inhibitors | Zidovudine (AZT), Didanosine (ddI), Zalcitabine (ddC), Stavudine (d4T), Lamivudine (3TC)
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| Name the Protease Inhibitors (4) | Saquinavir, Ritonavir, Indinavir, Nelfinavir
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| Name two classes of drugs for HIV therapy | Protease Inhibitors and Reverse Transcriptase Inhibitors
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| Name two organisms Vancomycin is commonly used for? | Staphlococcus aureus and Clostridium difficile (pseudomembranous colitis)
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| Oral Penicillin | V
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| Resistance mechanisms for Aminoglycosides | Modification via Acetylation, Adenylation, or Phosphorylation
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| Resistance mechanisms for Cephalosporins/Penicillins | Beta-lactamase cleavage of Beta-lactam ring
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| Resistance mechanisms for Chloramphenicol | Modification via Acetylation
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| Resistance mechanisms for Macrolides | Methylation of rRNA near Erythromycin's ribosome binding site
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| Resistance mechanisms for Sulfonamides | Altered bacterial Dihydropteroate Synthetase, Decreased uptake, or Increased PABA synthesis
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| Resistance mechanisms for Tetracycline | Decreased uptake or Increased transport out of cell
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| Side effects of Isoniazid (INH)? | Hemolysis (if G6PD deficient), Neurotoxicity, Hepatotoxicity, SLE-like syndrome
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| Specifically, how does Foscarnet inhibit viral DNA pol? | Binds to the Pyrophosphate Binding Site of the enzyme
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| The MOA for Chloramphenicol is..? | Inhibition of 50S peptidyl transferase, Bacteriostatic
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| Toxic effects of TMP include? | Megaloblastic anemia, Leukopenia, Granulocytopenia
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| Toxic side effects of the Azoles? | Hormone synthesis inhibition (Gynecomastia), Liver dysfunction (Inhibits CYP450), Fever, Chills
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| Toxicities associated with Acyclovir? | Delirium, Tremor, Nephrotoxicity
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| What additional side effects exist for Ampicillin? | Rash, Pseudomembranous colitis
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| What antimicrobial class is Aztreonam syngergestic with? | Aminoglycosides
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| What are Amantadine (Parkinson's drug)-associated side effects? | Ataxia, Dizziness, Slurred speech
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| What are Aminoglycosides synergistic with? | Beta-lactam antibiotics
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| What are Aminoglycosides used for clinically? | Severe Gram - rod infections.
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| What are common serious side effects of Aminoglycosides and what are these associated with? | Nephrotoxicity (esp. with Cephalosporins), Ototoxicity (esp. with Loop Diuretics)
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| What are common side effects of Amphotericin B? | Fever/Chills, Hypotension, Nephrotoxicity, Arrhythmias
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| What are common side effects of Protease Inhibitors? | GI intolerance (nausea, diarrhea), Hyperglycemia, Lipid abnormalities, Thrombocytopenia (Indinavir)
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| What are common side effects of RT Inhibitors? | BM suppression (neutropenia, anemia), Peripheral neuropathy
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| What are common toxic side effects of Sulfonamides? (5) | -Hypersensitivity reactions -Hemolysis -Nephrotoxicity (tubulointerstitial nephritis) -Kernicterus in infants Displace other drugs from albumin (e.g., warfarin)
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| What are common toxicities associated with Macrolides? (4) | GI discomfort, Acute cholestatic hepatitis, Eosinophilia, Skin rashes
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| What are common toxicities associated with Tetracyclines? | GI distress, Tooth discoloration and Inhibition of bone growth in children, Fanconi's syndrome, Photosensitivity
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| What are common toxicities related to Vancomycin therapy? | Well tolerated in general but occasionally, Nephrotoxicity, Ototoxicity, Thrombophlebitis, diffuse flushing='Red Man Syndrome'
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| What are Fluoroquinolones indicated for? (3) | 1.Gram - rods of the Urinary and GI tracts (including Pseudomonas) 2.Neisseria 3. Some Gram + organisms
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| What are major side effects of Methicillin, Nafcillin, and Dicloxacillin? | Hypersensitivity reactions
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| What are Methicillin, Nafcillin, and Dicloxacillin used for clinically? | Staphlococcus aureus
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| What are Polymyxins used for? | Resistant Gram - infections
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| What are the Anti-TB drugs? | Rifampin, Ethambutol, Streptomycin, Pyrazinamide, Isoniazid (INH)
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| What are the clinical indications for Azole therapy? | Systemic mycoses
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| What are the clinical uses for 1st Generation Cephalosporins? | Gram + cocci, Proteus mirabilis, E. coli, Klebsiella pneumoniae (PEcK)
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| What are the clinical uses for 2nd Generation Cephalosporins? | Gram + cocci, Haemophilus influenza, Enterobacter aerogenes, Neisseria species, P. mirabilis, E. coli, K. pneumoniae, Serratia marcescens ( HEN PEcKS )
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| What are the clinical uses for 3rd Generation Cephalosporins? | 1) Serious Gram - infections resistant to other Beta lactams 2) Meningitis (most penetrate the BBB)
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| What are the clinical uses for Aztreonam? | Gram - rods: Klebsiella species, Pseudomonas species, Serratia species
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| What are the clinical uses for Imipenem/cilastatin? | Gram + cocci, Gram - rods, and Anerobes
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| What are the Macrolides used for clinically? | -Upper respiratory tract infections -pneumonias -STDs: Gram+ cocci (streptococcal infect in pts allergic to penicillin) -Mycoplasma, Legionella,Chlamydia, Neisseria
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| What are the major structural differences between Penicillin and Cephalosporin? | Cephalosporin: 1) has a 6 member ring attached to the Beta lactam instead of a 5 member ring 2)has an extra functional group ( attached to the 6 member ring)
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| What are the major toxic side effects of Imipenem/cilastatin? | GI distress, Skin rash, and Seizures at high plasma levels
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| What are the major toxic side effects of the Cephalosporins? | 1) Hypersensitivity reactions 2) Increased nephrotoxicity of Aminoglycosides 3) Disulfiram-like reaction with ethanol (those with a methylthiotetrazole group, e.g., cefamandole)
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| What are the side effects of Polymyxins? | Neurotoxicity, Acute renal tubular necrosis
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| What are the side effects of Rifampin? | Minor hepatotoxicity, Drug interactions (activates P450)
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| What are toxic side effects for Metronidazole? | Disulfiram-like reaction with EtOH, Headache
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| What are toxicities associated with Chloramphenicol? | Aplastic anemia (dose independent), Gray Baby Syndrome
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| What conditions are treated with Metronidazole? | Giardiasis, Amoebic dysentery (E. histolytica), Bacterial vaginitis (Gardnerella vaginalis), Trichomonas
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| What do Aminoglycosides require for uptake? | Oxygen
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| What do you treat Nematode/roundworm (pinworm, whipworm) infections with? | Mebendazole/Thiabendazole, Pyrantel Pamoate
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| What drug is given for Pneumocystis carinii prophylaxis? | TMP-SMX, Pentamidine
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| What drug is used during the pregnancy of an HIV + mother?, Why? | AZT, to reduce risk of Fetal Transmission
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| What drug is used to treat Trematode/fluke (e.g., Schistosomes, Paragonimus, Clonorchis) or Cysticercosis | Praziquantel
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| What is a common drug interaction associated with Griseofulvin? | Increases coumadin metabolism
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| What is a mnemonic to remember Amantadine's function? | Blocks Influenza A and RubellA; causes problems with the cerebellA
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| What is a prerequisite for Acyclovir activation? | It must be Phosphorylated by Viral Thymidine Kinase
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| What is a Ribavirin toxicity? | Hemolytic anemia
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| What is an acronym to remember Anti-TB drugs? | RESPIre
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| What is an additional side effect of Methicillin? | Interstitial nephritis
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| What is an occasional side effect of Aztreonam? | GI upset
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| What is Clindamycin used for clinically? | Anaerobic infections (e.g., B. fragilis, C. perfringens)
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| What is clinical use for Carbenicillin, Piperacillin, and Ticarcillin? | Pseudomonas species and Gram - rods
🗑
|
||||
| What is combination TMP-SMZ used to treat? | Recurrent UTIs, Shigella, Salmonella, Pneumocystis carinii pneumonia
🗑
|
||||
| What is combined with Ampicillin, Amoxicillin, Carbenicillin, Piperacillin, and Ticarcillin to enhance their spectrum? | Clavulanic acid
🗑
|
||||
| What is Fluconazole specifically used for? | Cryptococcal meningitis in AIDS patients and Candidal infections of all types
🗑
|
||||
| What is Imipenem always administered with? | Cilastatin
🗑
|
||||
| What is Ketoconazole specifically used for? | Blastomyces, Coccidioides, Histoplasma, C. albicans; Hypercortisolism
🗑
|
||||
| What is Metronidazole combined with for 'triple therapy'? Against what organism? | Bismuth and Amoxicillin or Tetracycline; against Helobacter pylori
🗑
|
||||
| What is Metronidazole used for clinically? | Antiprotozoal: Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis Anaerobes: Bacteroides, Clostridium
🗑
|
||||
| What is Niclosamide used for? | Cestode/tapeworm (e.g., D. latum, Taenia species Except Cysticercosis
🗑
|
||||
| What is Nifurtimox administered for? | Chagas' disease, American Trypanosomiasis (Trypanosoma cruzi)
🗑
|
||||
| What is the chemical name for Ganciclovir? | DHPG (dihydroxy-2-propoxymethyl guanine)
🗑
|
||||
| What is the clinical use for Ampicillin and Amoxicillin? | Extended spectrum penicillin: certain Gram + bacteria and Gram - rods
🗑
|
||||
| What is the clinical use for Nystatin? | Topical and Oral, for Oral Candidiasis (Thrush)
🗑
|
||||
| What is the clinical use for Penicillin? | Bactericidal for: Gram + rod and cocci, Gram - cocci, and Spirochetes (Syphilis, Lyme Disease)
🗑
|
||||
| What is the major side effect for Ampicillin and Amoxicillin? Carbenicillin, Piperacillin, and Ticarcillin? Penicillin? | Hypersensitivity reactions
🗑
|
||||
| What is the memory aid for subunit distribution of ribosomal inhibitors? | Buy AT 30, CELL at 50'
🗑
|
||||
| What is the memory key for Isoniazid (INH) toxicity? | INH: Injures Neurons and Hepatocytes
🗑
|
||||
| What is the memory key for Metronidazole's clinical uses? | GET on the Metro
🗑
|
||||
| What is the memory key for organisms treated with Tetracyclines? | VACUUM your Bed Room'
🗑
|
||||
| VACUUM your Bed Room' | 1. RNA pol inhibitor 2. Revs up P450 3. Red/orange body fluids 4. Rapid resistance if used alone
🗑
|
||||
| What is the MOA for Acyclovir? | Inhibit viral DNA polymerase
🗑
|
||||
| What is the MOA for Amphotericin B? | Binds Ergosterol, forms Membrane Pores that Disrupt Homeostatis
🗑
|
||||
| What is the MOA for Ampicillin and Amoxicillin? Carbenicillin, Piperacillin, and Ticarcillin? | Same as penicillin. Extended spectrum antibiotics
🗑
|
||||
| What is the MOA for Clindamycin? | Blocks Peptide Bond formation at the 50S subunit, Bacteriostatic
🗑
|
||||
| What is the MOA for Methicillin, Nafcillin, and Dicloxacillin? | Same as penicillin. Act as narrow spectrum antibiotics
🗑
|
||||
| What is the MOA for Metronidazole? | Forms toxic metabolites in the bacterial cell, Bactericidal
🗑
|
||||
| What is the MOA for Nystatin? | Binds ergosterol, Disrupts fungal membranes
🗑
|
||||
| What is the MOA for Rifampin? | Inhibits DNA dependent RNA polymerase
🗑
|
||||
| What is the MOA for the Aminoglycosides? | Inhibits formation of Initiation Complex, causes misreading of mRNA, Bactericidal
🗑
|
||||
| What is the MOA for the Azoles? | Inhibit Ergosterol synthesis
🗑
|
||||
| What is the MOA for the Cephalosporins? | Beta lactams - inhibit cell wall synthesis, Bactericidal
🗑
|
||||
| What is the MOA for the Fluoroquinolones? | Inhibit DNA Gyrase (topoisomerase II), Bactericidal
🗑
|
||||
| What is the MOA for the Macrolides? | Blocks translocation, binds to the 23S rRNA of the 50S subunit, Bacteriostatic
🗑
|
||||
| What is the MOA for the Tetracyclines? | Binds 30S subunit and prevents attachment of aminoacyl-tRNA, Bacteriostatic
🗑
|
||||
| What is the MOA for Trimethoprim (TMP)? | Inhibits bacterial Dihydrofolate Reductase, Bacteriostatic
🗑
|
||||
| What is the MOA for Vancomycin? | Inhibits cell wall mucopeptide formation, Bactericidal
🗑
|
||||
| What is the MOA of Amantadine? | Blocks viral penetration/uncoating; may act to buffer the pH of the endosome
🗑
|
||||
| What is the MOA of Aztreonam? | Inhibits cell wall synthesis ( binds to PBP3). A monobactam
🗑
|
||||
| What is the MOA of Foscarnet? | Inhibits Viral DNA polymerase
🗑
|
||||
| What is the MOA of Ganciclovir? | Inhibits CMV DNA polymerase
🗑
|
||||
| What is the MOA of Griseofulvin? | Interferes with microtubule function, disrupts mitosis, inhibits growth
🗑
|
||||
| What is the MOA of Imipenem? | Acts as a wide spectrum carbapenem
🗑
|
||||
| What is the MOA of Isoniazid (INH)? | Decreases synthesis of Mycolic Acid
🗑
|
||||
| What is the MOA of Polymyxins? | Bind cell membrane, disrupt osmotic properties, Are Cationc, Basic and act as detergents
🗑
|
||||
| What is the MOA of Ribavirin? | Inhibits IMP Dehydrogenase (competitively), and therefore blocks Guanine Nucleotide synthesis
🗑
|
||||
| What is the MOA of the RT Inhibitors? | Inhibit RT of HIV and prevent the incorporation of viral genome into the host DNA
🗑
|
||||
| What is the most common cause of Pt noncompliance with Macrolides? | GI discomfort
🗑
|
||||
| What is treated with Chloroquine, Quinine, Mefloquine? | Malaria (P. falciparum)
🗑
|
||||
| What microorganisms are Aminoglycosides ineffective against? | Anaerobes
🗑
|
||||
| What microorganisms are clinical indications for Tetracycline therapy? | Vibrio cholerae Acne Chlamydia Ureaplasma Urealyticum Mycoplasma pneumoniae Borrelia burgdorferi (Lyme's) Rickettsia Tularemia
🗑
|
||||
| What microorganisms is Aztreonam not effective against? | Gram + and Anerobes
🗑
|
||||
| What musculo-skeletal side effects in Adults are associated with Floroquinolones? | Tendonitis and Tendon rupture
🗑
|
||||
| What neurotransmitter does Amantadine affect? How does it influence this NT? | Dopamine; causes its release from intact nerve terminals
🗑
|
||||
| What organism is Imipenem/cilastatin the Drug of Choice for? | Enterobacter
🗑
|
||||
| What organisms does Griseofulvin target? | Dermatophytes (tinea, ringworm)
🗑
|
||||
| What parasites are treated with Pyrantel Pamoate (more specific)? | Giant Roundworm (Ascaris), Hookworm (Necator/Ancylostoma), Pinworm (Enterobius)
🗑
|
||||
| What parasitic condition is treated with Ivermectin? | Onchocerciasis ('river blindness'--rIVER-mectin)
🗑
|
||||
| What populations are Floroquinolones contraindicated in? Why? | Pregnant women, Children; because animal studies show Damage to Cartilage
🗑
|
||||
| What should not be taken with Tetracyclines? / Why? | Milk or Antacids, because divalent cations inhibit Tetracycline absorption in the gut
🗑
|
||||
| What Sulfonamides are used for simple UTIs? | Triple sulfas or SMZ
🗑
|
||||
| When is HIV therapy initiated? | When pts have Low CD4+ (< 500 cells/cubic mm) or a High Viral Load
🗑
|
||||
| When is Rifampin not used in combination with other drugs? | 1. Meningococcal carrier state 2. Chemoprophylaxis in contacts of children with H. influenzae type B
🗑
|
||||
| Where does Griseofulvin deposit? | Keratin containing tissues, e.g., nails
🗑
|
||||
| Which Aminoglycoside is used for Bowel Surgery ? | Neomycin
🗑
|
||||
| Which antimicrobial classes inhibit protein synthesis at the 30S subunit? (2) | 1) Aminoglycosides = bactericidal 2) Tetracyclines = bacteriostatic
🗑
|
||||
| Which antimicrobials inhibit protein synthesis at the 50S subunit? (4) | 1) Chloramphenical = bacteriostatic 2) Erythromycin = bacteriostatic 3) Lincomycin = bacteriostatic 4)cLindamycin = bacteriostatic
🗑
|
||||
| Which individuals are predisposed to Sulfonamide-induced hemolysis? | G6PD deficient individuals
🗑
|
||||
| Which RT inhibitor causes Megaloblastic Anemia? | AZT
🗑
|
||||
| Which RT inhibitors cause a Rash? | Non-Nucleosides
🗑
|
||||
| Which RT inhibitors cause Lactic Acidosis? | Nucleosides
🗑
|
||||
| Which Tetracycline is used in patients with renal failure? / Why? | Doxycycline, because it is fecally eliminated
🗑
|
||||
| Why are Methicillin, Nafcillin, and Dicloxacillin penicillinase resistant? | Due to the presence of a bulkier R group
🗑
|
||||
| Why is Cilastatin administered with Imipenem? | To inhibit renal Dihydropeptidase I and decrease Imipenem inactivation in the renal tubules
🗑
|
||||
| List the mechanism, clinical use, & toxicity of 5 FU. | -S-phase anti-metabolite Pyr analogue -Colon, solid tumors, & BCC/ -Irreversible myelosuppression
🗑
|
||||
| List the mechanism, clinical use & toxicity of 6 MP. | -inhibits HGPRT (pur. Syn.) - Luk, Lymph,
🗑
|
||||
| List the mechanism, clinical use, & toxicity of Bleomycin. | -DNA intercalator -testicular & lymphomas -Pulmonary fibrosis mild myelosuppression.
🗑
|
||||
| List the mechanism, clinical use, & toxicity of Busulfan. | -Alkalates DNA -CML -Pulmonary fibrosis hyperpigmentation
🗑
|
||||
| List the mechanism, clinical use, & toxicity of Cisplatin. | -Alkalating agent -testicular,bladder,ovary,& lung -Nephrotoxicity & CN VIII damage.
🗑
|
||||
| List the mechanism, clinical use, & toxicity of Cyclophosphamide. | -Alkalating agent -NHL, Breast, ovary, & lung. - Myelosuppression, & hemorrhagic cystitis.
🗑
|
||||
| List the mechanism, clinical use, & toxicity of Doxorubicin. | -DNA intercalator -Hodgkin's, myeloma, sarcoma, and solid tumors -Cardiotoxicity & alopecia
🗑
|
||||
| List the mechanism, clinical use, & toxicity of Etoposide. | -Topo II inhibitor(GII specific) -Oat cell of Lung & prostate, & testicular -Myelosuppression & GI irritation.
🗑
|
||||
| List the mechanism, clinical use, & toxicity of Methotrexate. | -S-phase anti-metabolite folate analogue -Luk, Lymp, sarc, RA, & psoriasis / -Reversible myelosuppression
🗑
|
||||
| List the mechanism, clinical use, & toxicity of Nitrosureas. | -Alkalate DNA -Brain tumors -CNS toxicity
🗑
|
||||
| List the mechanism, clinical use, & toxicity of Paclitaxel. | -MT polymerization stabilizer -Ovarian & breast CA -Myelosupperession & hypersensitivity.
🗑
|
||||
| List the mechanism, clinical use, & toxicity of Prednisone. | -Triggers apoptosis -CLL, Hodgkin's in MOPP -Cushing-like syndrome
🗑
|
||||
| List the mechanism, clinical use, & toxicity of Tamoxifen. | -Estrogen receptor antagonist -Breast CA -increased endometrial CA risk
🗑
|
||||
| List the mechanism, clinical use, & toxicity of Vincristine. | -MT polymerization inhibitor(M phase) -MOPP, lymphoma, Willm's & choriocarcinoma -neurotoxicity and myelosuppression
🗑
|
||||
| Which cancer drugs effect nuclear DNA (4)? | -Alkalating agents+cisplatin -Doxorubicin+Dactinomycin -Bleomycin -Etoposide
🗑
|
||||
| Which cancer drugs inhibit nucleotide synthesis(3)? | - Methotrexate - 5 FU - 6 mercaptopurine
🗑
|
||||
| Which cancer drugs work at the level of mRNA(2)? | -Steroids -Tamoxifen
🗑
|
||||
| Which cancer drugs work at the level of proteins(2)? | -Vinca alkaloids(inhibit MT) -Paclitaxel
🗑
|
||||
| ACE inhibitors- clinical use? | hypertension, CHF, diabetic renal disease
🗑
|
||||
| ACE inhibitors- mechanism? | reduce levels of Angiotensin II, thereby preventing the inactivation of bradykinin (a potent vasodilator); renin level is increased
🗑
|
||||
| ACE inhibitors- toxicity? | fetal renal damage, hyperkalemia, Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems, Rash, Increased renin, Lower Angiotensin II (CAPTOPRIL)
🗑
|
||||
| Acetazolamide- clinical uses? | glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness
🗑
|
||||
| Acetazolamide- mechanism? | acts at the proximal convoluted tubule to inhibit carbonic anhydrase. Causes self-limited sodium bicarb diuresis and reduction of total body bicarb stores.
🗑
|
||||
| acetazolamide- site of action? | proximal convoluted tubule
🗑
|
||||
| Acetazolamide- toxicity? | hyperchloremic metabolic acidosis, neuropathy, NH3 toxicity, sulfa allergy
🗑
|
||||
| Acetazolamide causes…? | ACIDazolamide' causes acidosis
🗑
|
||||
| Adenosine- clinical use? | DOC in diagnosing and abolishing AV nodal arrhythmias
🗑
|
||||
| ADH antagonists- site of action? | collecting ducts
🗑
|
||||
| adverse effect of Nitroprusside? | cyanide toxicity (releases CN)
🗑
|
||||
| adverse effects of beta-blockers? | impotence, asthma, CV effects (bradycardia, CHF, AV block), CNS effects (sedation, sleep alterations)
🗑
|
||||
| adverse effects of Captopril? | fetal renal toxicity, hyperkalemia, Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems, Rash, Increased renin, Lower Angiotensin II (CAPTOPRIL)
🗑
|
||||
| adverse effects of Clonidine? | dry mouth, sedation, severe rebound hypertension
🗑
|
||||
| adverse effects of ganglionic blockers? | severe orthostatic hypotension, blurred vision, constipation, sexual dysfunction
🗑
|
||||
| adverse effects of Guanethidine? | orthostatic and exercise hypotension, sexual dysfunction, diarrhea
🗑
|
||||
| adverse effects of Hydralazine? | nausea, headache, lupus-like syndrome, reflex tachycardia, angina, salt retention
🗑
|
||||
| adverse effects of Hydrochlorothiazide? | hypokalemia, slight hyperlipidemia, hyperuricemia, lassitude, hypercalcemia, hyperglycemia
🗑
|
||||
| adverse effects of Loop Diuretics? | K+ wasting, metabolic alkalosis, hypotension, ototoxicity
🗑
|
||||
| adverse effects of Losartan? | fetal renal toxicity, hyperkalemia
🗑
|
||||
| adverse effects of Methyldopa? | sedation, positive Coombs' test
🗑
|
||||
| adverse effects of Minoxidil? | hypertrichosis, pericardial effusion, reflex tachycardia, angina, salt retention
🗑
|
||||
| adverse effects of Nifedipine, verapamil? | dizziness, flushing, constipation (verapamil), nausea
🗑
|
||||
| adverse effects of Prazosin? | first dose orthostatic hypotension, dizziness, headache
🗑
|
||||
| adverse effects of Reserpine? | sedation, depression, nasal stuffiness, diarrhea
🗑
|
||||
| Amiodarone- toxicity? | pulmonary fibrosis, corneal deposits, hepatotoxicity, skin deposits resulting in photodermatitis, neurologic effects, consitpation, CV (bradycardia, heart block, CHF), and hypo- or hyperthyroidism.
🗑
|
||||
| Digoxin antidote? | slowly normalize K+, lidocaine, cardiac pacer, and anti-Dig Fab fragments
🗑
|
||||
| Beta Blockers- CNS toxicity? | sedation, sleep alterations
🗑
|
||||
| Beta Blockers- CV toxicity? | bradycardia, AV block, CHF
🗑
|
||||
| Beta Blockers- site of action? | Beta adrenergic receptors and Ca2+ channels (stimulatory)
🗑
|
||||
| Bretyllium- toxicity? | new arrhythmias, hypotension
🗑
|
||||
| Ca2+ channel blockers- clinical use? | hypertension, angina, arrhythmias
🗑
|
||||
| Ca2+ channel blockers- mechanism? | block voltage dependent L-type Ca2+ channels of cardiac and smooth muscle- decreasing contractility
🗑
|
||||
| Ca2+ channel blockers- site of action? | Cell membrane Ca2+ channels of cardiac sarcomere
🗑
|
||||
| Ca2+ channel blockers- toxicity? | cardiac depression, peripheral edema, flushing, dizziness, constipation
🗑
|
||||
| Ca2+ sensitizers'- site of action? | troponin-tropomyosin system
🗑
|
||||
| Cautions when using Amiodarone? | check PFTs, LFTs, and TFTs
🗑
|
||||
| class IA effects? | increased AP duration, increased ERP increased QT interval. Atrial and ventricular.
🗑
|
||||
| class IB- clinical uses? | post MI and digitalis induced arrhythmias
🗑
|
||||
| class IB- effects? | decrease AP duration, affects ischemic or depolarized Purkinje and ventricular system
🗑
|
||||
| class IB- toxicity? | local anesthetic. CNS stimulation or depression. CV depression.
🗑
|
||||
| class IC- effects? | NO AP duration effect. useful in V-tach that progresses to V-fib and in intractable SVT LAST RESORT
🗑
|
||||
| class IC- toxicity? | proarrhythmic
🗑
|
||||
| class II- effects? | decrease the slope of phase 4, increase PR interval (the AV node is particularly sensitive)
🗑
|
||||
| class II- mechanism? | blocking the beta adrenergic receptor leads to decreased cAMP, and decreased Ca2+ flux
🗑
|
||||
| class II- toxicity? | impotence, exacerbation of asthma, CV effects, CNS effects, may mask hypoclycemia
🗑
|
||||
| Class III- effects? | increase AP duration, increase ERP, increase QT interval, for use when other arrhythmics fail
🗑
|
||||
| class IV- clinical use? | prevention of nodal arrhythmias (SVT)
🗑
|
||||
| class IV- effects? | decrease conduction velocity, increase ERP, increase PR interval
🗑
|
||||
| class IV- primary site of action? | AV nodal cells
🗑
|
||||
| class IV- toxicity? | constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression), and torsade de pointes (Bepridil)
🗑
|
||||
| classes of antihypertensive drugs? | diuretics, sympathoplegics, vasodilators, ACE inhibitors, Angiotensin II receptor inhibitors
🗑
|
||||
| Digoxin clinical use? | CHF, atrial fibrillation
🗑
|
||||
| Digoxin effect on contractility? | increase (reflex response)
🗑
|
||||
| Digoxin contraindications? | renal failure, hypokalemia, pt on quinidine
🗑
|
||||
| decrease Digitoxin dose in renal failure? | No, hepatic clearance
🗑
|
||||
| decrease Digoxin dose in renal failure? | YES
🗑
|
||||
| Digitalis- site of action? | Na/K ATPase
🗑
|
||||
| Digoxin v. Digitoxin: bioavailability? | Digitoxin>95% Digoxin 75%
🗑
|
||||
| Digoxin v. Digitoxin: excretion? | Digoxin=urinary Digitoxin=biliary
🗑
|
||||
| Digoxin v. Digitoxin: half life? | Digitoxin 168hrs Digoxin 40 hrs
🗑
|
||||
| Digoxin v. Digitoxin: protein binding? | Digitoxin 70% Digoxin 20-40%
🗑
|
||||
| Esmolol- short or long acting? | very short acting
🗑
|
||||
| Ethacrynic Acid- clinical use? | Diuresis in pateints with sulfa allergy
🗑
|
||||
| Ethacrynic Acid- mechanism? | not a sulfonamide, but action is the same as furosemide
🗑
|
||||
| Ethacrynic Acid- toxicity? | NO HYPERURICEMIA, NO SULFA ALLERGY; same as furosemide otherwise
🗑
|
||||
| Furosemide- class and mechanism? | Sulfonamide Loop Diuretic. Inhibits ion co-transport system of thick ascending loop. Abolishes hypertonicity of the medulla, thereby preventing concentration of the urine.
🗑
|
||||
| Furosemide- clinical use? | edematous states (CHF, cirrhosis, nephrotic syndrome, pulm edema), HTN, hypercalcemia
🗑
|
||||
| Furosemide- toxicity? (OH DANG) | Ototoxicity, Hypokalemia, Dehydration, Allergy (sulfa), Nephritis (interstitial), Gout
🗑
|
||||
| Furosemide increases the excretion of what ion? | Ca2+ (Loops Lose calcium)
🗑
|
||||
| how do we stop angina? | decrease myocardial O2 consumption by: 1-decreasing end diastolic volume 2- decreasing BP 3- decreasing HR 4-decreasing contractility 5-decreasing ejection time
🗑
|
||||
| Hydralazine- class and mechanism? | vasodilator- increases cGMP to induce smooth muscle relaxation (arterioles>veins; afterload reduction)
🗑
|
||||
| Hydralazine- clinical use? | severe hypertension, CHF
🗑
|
||||
| Hydralazine- toxicity? | compensatory tachycardia, fluid retention, lupus-like syndrome
🗑
|
||||
| Hydrochlorothiazide- clinical use? | HTN, CHF, calcium stone formation, nephrogenic DI.
🗑
|
||||
| Hydrochlorothiazide- mechanism? | Inhibits NaCl reabsorption in the early distal tubule. Decreases Ca2+ excretion.
🗑
|
||||
| Hydrochlorothiazide- toxicity? (hyperGLUC, plus others) | Hypokalemic metabolic alkalosis, hyponatremia, hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia, sulfa allergy.
🗑
|
||||
| Ibutilide- toxicity? | torsade de pointes
🗑
|
||||
| K+- clinical use? | depresses ectopic pacemakers, especially in digoxin toxicity
🗑
|
||||
| K+ sparing diuretics- clinical use? | hyperaldosteronism, K+ depletion, CHF
🗑
|
||||
| K+ sparing diuretics- site of action? | cortical collecting tubule
🗑
|
||||
| K+ sparing diuretics- toxicity? | hyperkalemia, endocrine effects (gynecomastia, anti-androgen)
🗑
|
||||
| loop diuretics (furosemide)- site of action? | thick ascending limb
🗑
|
||||
| Mannitol- clinical use? | ARF, shock, drug overdose, decrease intracranial/intraocular pressure
🗑
|
||||
| Mannitol- contraindications? | anuria, CHF
🗑
|
||||
| Mannitol- mechanism? | osmotic diuretic- increase tubular fluid osmolarity, thereby increasing urine flow
🗑
|
||||
| mannitol- site of action? | proximal convoluted tubule, thin descending limb, and collecting duct
🗑
|
||||
| Mannitol- toxicity? | pulmonary edema, dehydration
🗑
|
||||
| Mg+- clinical use? | effective in torsade de pointes and digoxin toxicity
🗑
|
||||
| name five in class II? | propanolol, esmolol, metoprolol, atenolol, timolol
🗑
|
||||
| name four HMG-CoA reductase inhibitors. | Lovastatin, Pravastatin, Simvastatin, Atorvastatin
🗑
|
||||
| name four in class IA. | Quinidine, Amiodarone, Procainamide, Disopyramide
🗑
|
||||
| name four in class III. | Sotalol, Ibutilide, Bretylium, Amiodarone
🗑
|
||||
| name three ACE inhibitors? | Captopril, Enalapril, Lisinopril
🗑
|
||||
| name three calcium channel blockers? | Nifedipine, Verapamil, Diltiazem
🗑
|
||||
| name three in class IB. | Lidocaine, Mexiletine, Tocainide
🗑
|
||||
| name three in class IC. | Flecainide, Encainide, Propafenone
🗑
|
||||
| name three in class IV. | Verapamil, Diltiazem, Bepridil
🗑
|
||||
| name three K+ sparing diuretics? | Spironolactone, Triamterene, Amiloride (the K+ STAys)
🗑
|
||||
| name two bile acid resins | cholestyramine, colestipol
🗑
|
||||
| name two LPL stimulators. | Gemfibrozil, Clofibrate
🗑
|
||||
| Nifedipine has similar action to? | Nitrates
🗑
|
||||
| preferential action of the Ca2+ channel blockers at cardiac muscle? | cardiac muscle: Verapamil>Diltiazem>Nifedipine
🗑
|
||||
| preferential action of the Ca2+ channel blockers at vascular smooth muscle? | vascular sm. Mus.: Nifedipine>Diltiazem>Verapamil
🗑
|
||||
| Procainamide- toxicity? | reversible SLE-like syndrome
🗑
|
||||
| Quinidine- toxicity? | cinchonism: HA, tinnitus, thrombocytopenia, torsade de pointes due to increased QT interval
🗑
|
||||
| Ryanodine- stie of action? | blocks SR Ca2+ channels
🗑
|
||||
| Sotalol- toxicity? | torsade de pointes, excessive Beta block
🗑
|
||||
| Spironolactone- mechanism? | competitive inhibirot of aldosterone in the cortical collecting tubule
🗑
|
||||
| thiazides- site of action? | distal convoluted tubule (early)
🗑
|
||||
| Triamterene and amiloride- mechanism? | block Na+ channels in the cortical collecting tubule
🗑
|
||||
| Verapamil has similar action to? | Beta Blockers
🗑
|
||||
| what two vasodilators require simultaneous treatment with beta blockers to prevent reflex tachycardia and diuretics to prevent salt retention? | Hydralazine and Minoxidil
🗑
|
||||
| which diuretics cause acidosis? | carbonic anhydrase inhibitors, K+ sparing diuretics
🗑
|
||||
| which diuretics cause alkalosis? | loop diuretics, thiazides
🗑
|
||||
| which diuretics decrease urine Ca2+? | thiazides, amiloride
🗑
|
||||
| which diuretics increase urine Ca2+? | loop diuretics, spironolactone
🗑
|
||||
| which diuretics increase urine K+? | all except the K+ sparing diuretics Spironolactone, Triamterene, Amiloride
🗑
|
||||
| which diuretics increase urine NaCl? | all of them
🗑
|
||||
| Acetaminophen has what two clinical uses and lacks what one clinical use of the NSAIDs? | It has antipyretic and analgesic properties, but lacks anti-inflammatory properties.
🗑
|
||||
| Can Heparin be used during pregnancy? | Yes, it does not cross the placenta.
🗑
|
||||
| Can Warfarin be used during pregnancy? | No, warfarin, unlike heparin, can cross the placenta.
🗑
|
||||
| Does Heparin have a long, medium, or short half life? | Short.
🗑
|
||||
| Does Warfarin have a long, medium, or short half life? | Long.
🗑
|
||||
| For Heparin what is the 1. Structure 2. Route of administration 3. Onset of action 4. Mechanism of action 5. Duration of action 6. Ability to inhibit coagulation in vitro 7. Treatment for overdose 8. Lab value to monitor 9. Site of action | 1. Large anionic polymer, acidic 2.Paranteral (IV, SC) 3. Rapid (seconds) 4. Activates antithrombin III 5. Acute (hours) 6. Inhibits coagulation 7. Overdose Tx = Protamine 8. Monitor aPTT (intrinsic) 9. Acts on blood
🗑
|
||||
| For Warfarin what is the 1. Structure 2. Route of administration 3. Onset of action 4. Mechanism of action 5. Duration of action 6. Ability to inhibit coagulation in vitro 7. Treatment for overdose 8. Lab value to monitor 9. Site of action | 1. Small lipid-soluble 2. Oral 3. Slow, limited by t1/2 of clotting factors 4. Impairs synthesis of vit K-dependent clotting factors 5. Chronic (weeks or months) 6. Can’t inhibit coagulation 7. Overdose Tx = IV vit K & FFP 8. Monitor PT 9. Acts on liver
🗑
|
||||
| Is toxicity rare or common with Cromolyn used in Asthma prevention? | Rare
🗑
|
||||
| List five common glucocorticoids. | 1. Hydrocortisone 2. Predisone 3. Triamcinolone 4. Dexamethasone 5. Beclomethasone
🗑
|
||||
| Secretion of what drug is inhibited by Probenacid used to treat chronic gout? | Penicillin; it’s concentration is increased and action is prolonged
🗑
|
||||
| The COX-2 inhibitors (celecoxib, rofecoxib) have similar side effects to the NSAIDs with what one exception? | The COX-2 inhibitors should not have the corrosive effects of other NSAIDs on the gastrointestinal lining.
🗑
|
||||
| What are are the Sulfonylureas (general description) and what is their use? | Sulfonylureas are oral hypoglycemic agents, they are used to stimulate release of endogenous insulin in NIDDM (type-2).
🗑
|
||||
| What are five advantages of Oral Contraceptives (synthetic progestins, estrogen)? | 1. Reliable (1% failure) 2. Lowers risk of endometrial and ovarian cancer 3. Decreased incidence of ectopic pregnancy 4. Lower risk of pelvic infections 5. Regulation of menses
🗑
|
||||
| What are five disadvantages of Oral Contraceptives (synthetic progestins, estrogen)? | 1. Taken daily 2. No protection against STDs 3. Raises triglycerides 4. Depression, weight gain, nausea, HTN 5. Hypercoagulable state
🗑
|
||||
| What are five possible toxic effects of Aspirin therapy? | 1. Gastric ulceration 2. Bleeding 3. Hyperventilation 4. Reye's syndrome 5. Tinnitus (CN VIII)
🗑
|
||||
| What are five toxicities associated with Tacrolimus (FK506) used to prevent liver transplant rejection? | 1. Significant: nephrotoxicity 2. Peripheral neuropathy 3. Hypertension 4. Pleural effusion 5. Hyperglycemia.
🗑
|
||||
| What are four advantages of newer low-molecular-weight heparins (Enoxaparin)? | 1. Better bioavailability 2. 2 to 4 times longer half life 3. Can be administered subcutaneously 4. Does not require laboratory monitoring
🗑
|
||||
| What are four clinical activities of Aspirin? | 1. Antipyretic 2. Analgesic 3. Anti-inflammatory 4. Antiplatelet drug.
🗑
|
||||
| What are four clinical uses of glucocorticoids? | 1. Addison's disease 2. Inflammation 3. Immune suppression 4. Asthma
🗑
|
||||
| What are four conditions in which H2 Blockers are used clinically? | 1. Peptic ulcer 2. Gastritis 3. Esophageal reflux 4. Zollinger-Ellison syndrome
🗑
|
||||
| What are four H2 Blockers? | 1. Cimetadine 2. Ranitidine 3. Famotidine 4. Nizatidine
🗑
|
||||
| What are four Sulfonylureas? | 1. Tolbutamide 2. Chlorpropamide 3. Glyburide 4. Glipizide
🗑
|
||||
| What are four thrombolytics? | 1. Streptokinase 2. Urokinase 3. tPA (alteplase), APSAC (anistreplase)
🗑
|
||||
| What are four unwanted effects of Clomiphene use? | 1. Hot flashes 2. Ovarian enlargement 3. Multiple simultaneous pregnancies 4. Visual disturbances
🗑
|
||||
| What are nine findings of Iatrogenic Cushing's syndrome caused by glucocorticoid therapy? | 1. Buffalo hump 2. Moon facies 3. Truncal obesity 4. Muscle wasting 5. Thin skin 6. Easy bruisability 7. Osteoporosis 8. Adrenocortical atrophy 9. Peptic ulcers
🗑
|
||||
| What are signs of Sildenafil (Viagra) toxicity? | Headache, flushing , dyspepsia, blue-green color vision.
🗑
|
||||
| What are the clinical uses for Ticlopidine, Clopidogrel? | Acute coronary syndrome; coronary stenting. Decreases the incidence or recurrence of thrombotic stroke.
🗑
|
||||
| What are the four conditions in which Omeprazole, Lansoprazole is used? | 1. Peptic ulcer 2. Gastritis 3. Esophageal reflux 4. Zollinger-Ellison syndrome
🗑
|
||||
| What are three clinical uses of the Leuprolide? | 1. Infertility (pulsatile) 2. Prostate cancer (continuous: use with flutamide) 3. Uterine fibroids
🗑
|
||||
| What are three clinical uses of the NSAIDs? | 1. Antipyretic 2. Analgesic 3. Anti-inflammatory
🗑
|
||||
| What are three common NSAIDS other than Aspirin? | Ibuprofen, Naproxen, and Indomethacin
🗑
|
||||
| What are three complications of Warfarin usage? | 1. Bleeding 2. Teratogenicity 3. Drug-drug interactions
🗑
|
||||
| What are three possible complications of Heparin therapy? | 1. Bleeding 2. Thrombocytopenia 3. Drug-drug interactions
🗑
|
||||
| What are three possible toxicities of NSAID usage? | 1. Renal damage 2. Aplastic anemia 3. GI distress
🗑
|
||||
| What are three toxicities of Leuprolide? | 1. Antiandrogen 2. Nausea 3. Vomiting
🗑
|
||||
| What are three toxicities of Propylthiouracil? | 1. Skin rash 2. Agranulocytosis (rare) 3. Aplastic anemia
🗑
|
||||
| What are three types of antacids and the problems that can result from their overuse? | 1. Aluminum hydroxide: constipation and hypophosphatemia 2. Magnesium hydroxide: diarrhea 3. Calcium carbonate: Hypercalcemia, rebound acid increase - All may cause hypokalemia
🗑
|
||||
| What are three unwanted effects of Mifepristone? | 1. Heavy bleeding 2. GI effects (n/v, anorexia) 3. Abdominal pain
🗑
|
||||
| What are two Alpha-glucosidase inhibitors? | 1. Acarbose 2. Miglitol
🗑
|
||||
| What are two clinical uses of Azathioprine? | 1. Kidney transplantation 2. Autoimmune disorders (including glomerulonephritis and hemolytic anemia)
🗑
|
||||
| What are two conditions in which COX-2 inhibitors might be used? | Rheumatoid and osteoarthritis.
🗑
|
||||
| What are two Glitazones? | 1. Pioglitazone 2. Rosiglitazone.
🗑
|
||||
| What are two mechanisms of action of Propythiouracil? | Inhibits organification and coupling of thyroid hormone synthesis. Also decreases peripheral conversion of T4 to T3.
🗑
|
||||
| What are two processes Corticosteroids inhibit leading to decreased inflammation? | 1. Phospholipase A2 is prevented from releasing arachidonic acid 2. Decreases protein synthesis thus lowering amount of Cyclooxygenase enzymes
🗑
|
||||
| What are two toxicities associated with Cyclosporine? | 1. Predisposes to viral infections and lymphoma 2. Nephrotoxic (preventable with mannitol diuresis)
🗑
|
||||
| What are two toxicities of the Glitazones? | 1. Weight gain 2. Hepatotoxicity (troglitazone)
🗑
|
||||
| What are two toxicities of the Sulfonylureas? | 1. Hypoglycemia (more common with 2nd-generation drugs: glyburide, glipizide) 2. Disulfiram-like effects (not seen with 2nd-generation drugs).
🗑
|
||||
| What are two types of drugs that interfere with the action of Sucralfate and why? | Sucralfate cannot work in the presence of antacids or H2 blockers because it requires an acidic environment to polymerize.
🗑
|
||||
| What can result due to antacid overuse? | Can affect absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying.
🗑
|
||||
| What enzyme does Zileuton inhibit? | Lipoxygenase
🗑
|
||||
| What enzymes are inhibited by NSAIDs, acetaminophen and COX II inhibitors? | Cyclooxygenases (COX I, COX II).
🗑
|
||||
| What is a common side effect of Colchicine used to treat acute gout, especially when given orally? | GI side effects. (Note: Indomethacin is less toxic, more commonly used.)
🗑
|
||||
| What is a common side effect of Misoprostol? | Diarrhea
🗑
|
||||
| What is a possible result of overdose of Acetaminophen? | Overdose produces hepatic necrosis; acetaminophen metablolite depletes glutathione and forms toxic tissue adducts in liver.
🗑
|
||||
| What is a possible toxicity of Alpha-glucosidase inhibitors used in type-2 diabetes? | GI disturbances.
🗑
|
||||
| What is a possible toxicity of Ticlopidine, Clopidogrel usage? | Neutropenia (ticlopidine); reserved for those who cannot tolerate aspirin.
🗑
|
||||
| What is a sign of toxicity with the use of thrombolytics? | Bleeding
🗑
|
||||
| What is action of insulin in the liver, in muscle, and in adipose tissue? | 1. In liver, increases storage of glucose as glycogen. 2. In muscle, stimulates glycogen and protein synthesis, and K+ uptake. 3. In adipose tissue, facilitates triglyceride storage.
🗑
|
||||
| What is are two clinical uses of Cyclosporine? | 1. Suppresses organ rejection after transplantation 2. Selected autoimmune disorders.
🗑
|
||||
| What is the category and mechanism of action of Zafirlukast in Asthma treatment? | Antileukotriene; blocks leukotriene receptors.
🗑
|
||||
| What is the category and mechanism of action of Zileuton in Asthma treatment? | Antileukotriene; blocks synthesis by lipoxygenase.
🗑
|
||||
| What is the category of drug names ending in -ane (e.g. Halothane) | Inhalational general anesthetic.
🗑
|
||||
| What is the category of drug names ending in -azepam (e.g. Diazepam) | Benzodiazepine.
🗑
|
||||
| What is the category of drug names ending in -azine (e.g. Chlorpromazine) | Phenothiazine (neuroleptic, antiemetic).
🗑
|
||||
| What is the category of drug names ending in -azol (e.g. Ketoconazole) | Antifungal.
🗑
|
||||
| What is the category of drug names ending in -barbital (e.g. Phenobarbital) | Babiturate.
🗑
|
||||
| What is the category of drug names ending in -caine (e.g. Lidocaine) | Local anesthetic.
🗑
|
||||
| What is the category of drug names ending in -cillin (e.g. Methicillin) | Penicillin.
🗑
|
||||
| What is the category of drug names ending in -cycline (e.g. Tetracycline) | Antibiotic, protein synthesis inhibitor.
🗑
|
||||
| What is the category of drug names ending in -ipramine (e.g. Imipramine) | Tricyclic antidepressant.
🗑
|
||||
| What is the category of drug names ending in -navir (e.g. Saquinavir) | Protease inhibitor.
🗑
|
||||
| What is the category of drug names ending in -olol (e.g. Propranolol) | Beta antagonist.
🗑
|
||||
| What is the category of drug names ending in -operidol (e.g. Haloperidol) | Butyrophenone (neuroleptic).
🗑
|
||||
| What is the category of drug names ending in -oxin (e.g. Digoxin) | Cardiac glycoside (inotropic agent).
🗑
|
||||
| What is the category of drug names ending in -phylline (e.g. Theophylline) | Methylxanthine.
🗑
|
||||
| What is the category of drug names ending in -pril (e.g. Captopril) | ACE inhibitor.
🗑
|
||||
| What is the category of drug names ending in -terol (e.g. Albuterol) | Beta-2 agonist.
🗑
|
||||
| What is the category of drug names ending in -tidine (e.g. Cimetidine) | H2 antagonist
🗑
|
||||
| What is the category of drug names ending in -triptyline (e.g. Amitriptyline) | Tricyclic antidepressant.
🗑
|
||||
| What is the category of drug names ending in -tropin (e.g. Somatotropin) | Pituitary hormone.
🗑
|
||||
| What is the category of drug names ending in -zosin (e.g. Prazosin) | Alpha-1 antagonist
🗑
|
||||
| What is the category, desired effect, and adverse effect of Isoproterenol in the treatment of Asthma? | Nonspecific beta-agonist; desired effect is the relaxation of bronchial smooth muscle (Beta 2). Adverse effect is tachycardia (Beta 1).
🗑
|
||||
| What is the category, desired effect, and period of use of albuterol in the treatment of Asthma? | Beta 2 agonist; desired effect is the relaxation of bronchial smooth muscle (Beta 2). Use during acute exacerbation
🗑
|
||||
| What is the category, desired effect, and possible mechanism of Theophylline in treating Asthma? | Methylzanthine; desired effect is bronchodilation, may cause bronchodilation by inhibiting phosphodiesterase, enzyme involved in degrading cAMP (controversial).
🗑
|
||||
| What is the category, mechanism of action, and effect of Ipratroprium in Asthma treatment? | Muscarinic antagonist; competatively blocks muscarinic receptors, preventing bronchoconstriction.
🗑
|
||||
| What is the category, mechanism of action, and particular use of beclomethasone and prednisone in Asthma treatment? | Corticosteroids; prevent production of leukotrienes from arachodonic acid by blocking phospholipase A2. Drugs of choice in a patient with status asthmaticus (in combination with albuterol.)
🗑
|
||||
| What is the category, method of use, and adverse effects of Salmeterol in Asthma treatment? | Beta 2 agonist; used as a long-acting agent for prophylaxis. Adverse effects are tremor and arrhythmia
🗑
|
||||
| What is the clincial use for Misoprostol? | Prevention of NSAID-induced peptic ulcers, maintains a PDA.
🗑
|
||||
| What is the clinical use for Clomiphene? | Treatment of infertility.
🗑
|
||||
| What is the clinical use for Heparin? | Immediate anticoagulation for PE, stroke, angina, MI, DVT.
🗑
|
||||
| What is the clinical use for Sildenafil (Viagra)? | Erectile dysfunction.
🗑
|
||||
| What is the clinical use for Sucralfate? | Peptic ulcer disease.
🗑
|
||||
| What is the clinical use for Warfarin? | Chronic anticoagulation.
🗑
|
||||
| What is the clinical use of Mifepristone (RU486)? | Abortifacient.
🗑
|
||||
| What is the clinical use of Tacrolimus (FK506)? | Potent immunosuppressive used in organ transplant recipients.
🗑
|
||||
| What is the effect of the Glitazones in diabetes treatment? | Increase target cell response to insulin.
🗑
|
||||
| What is the enzyme inhibited, the effect of this inhibition, and the clinical use of the antiandrogren Finasteride? | Finasteride inhibits 5 Alpha-reductase, this decreases the conversion of testosterone to dihydrotestosterone, useful in BPH
🗑
|
||||
| What is the lab value used to monitor the effectiveness of Heparin therapy? | The PTT.
🗑
|
||||
| What is the lab value used to monitor the effectiveness of Warfarin therapy? | The PT.
🗑
|
||||
| What is the main clinical use for the thrombolytics? | Early myocardial infarction.
🗑
|
||||
| What is the mechanism of action of Sucralfate? | 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.
🗑
|
||||
| What is the mecanism of action of the COX-2 inhibitors (celecoxib, rofecoxib)? | Selectively inhibit cyclooxygenase (COX) isoform 2, which is found in inflammatory cells and mediates inflammation and pain; spares COX-1 which helps maintain the gastric mucosa.
🗑
|
||||
| What is the mecanism of action, effective period, and ineffective period of use for Cromolyn in treating Asthma? | Prevents release of mediators from mast cells. Effective only for the prophylaxis of asthma. Not effective during an acute attack.
🗑
|
||||
| What is the mechanism of action and clinical use of the antiandrogen Flutamide? | Flutamide is a nonsteroidal competitive inhibitor of androgens at the testosterone receptor, used in prostate carcinoma.
🗑
|
||||
| What is the mechanism of action and clinical use of the antiandrogens Ketoconazole and Spironolactone? | Inhibit steroid synthesis, used in the treatment of polycystic ovarian syndrome to prevent hirsutism.
🗑
|
||||
| What is the mechanism of action of Acetaminophen? | Reversibly inhibits cyclooxygenase, mostly in CNS. Inactivated peripherally.
🗑
|
||||
| What is the mechanism of action of Allopurinol used to treat chronic gout? | Inhibits xanthine oxidase, decresing conversion of xanthine to uric acid.
🗑
|
||||
| What is the mechanism of action of Aspirin? | Acetylates and irreversibly inhibits cyclooxygenase (COX I and COX II) to prevent the conversion of arachidonic acid to prostaglandins.
🗑
|
||||
| What is the mechanism of action of Clomiphene? | It 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.
🗑
|
||||
| What is the mechanism of action of Colchicine used to treat acute gout? | Depolymerizes microtubules, impairing leukocyte chemotaxis and degranulation.
🗑
|
||||
| What is the mechanism of action of Cyclosporine? | 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.
🗑
|
||||
| What is the mechanism of action of Heparin? | Heparin catalyzes the activation of antithrombin III.
🗑
|
||||
| What is the mechanism of action of Mifepristone (RU486)? | Competitive inibitor of progestins at progesterone receptors.
🗑
|
||||
| What is the mechanism of action of Misoprostol? | Misoprostol is a PGE1 analog that increases the production and secretion of the gastic mucous barrier.
🗑
|
||||
| What is the mechanism of action of NSAIDs other than Aspirin? | Reversibly inhibit cyclooxygenase (COX I and COX II). Block prostaglandin synthesis.
🗑
|
||||
| What is the mechanism of action of Omeprazole, Lansoprazole? | Irreversibly inhibits H+/K+ ATPase in stomach parietal cells.
🗑
|
||||
| What is the mechanism of action of Probenacid used to treat chronic gout? | Inhibits reabsorption of uric acid.
🗑
|
||||
| What is the mechanism of action of Sildenafil (Viagra)? | Inhibits cGMP phosphodiesterase, casuing increased cGMP, smooth muscle relaxation in the corpus cavernosum, increased blood flow, and penile erection.
🗑
|
||||
| What is the mechanism of action of the Alpha-glucosidase inhibitors? | Inhibit intestinal bursh border Alpha-glucosidases; delayed hydrolysis of sugars and absorption of sugars leading to decreased postprandial hyperglycemia.
🗑
|
||||
| What is the mechanism of action of the glucocorticoids? | Decrease the production of leukotrienes and protaglandins by inhibiting phospholipase A2 and expression of COX-2.
🗑
|
||||
| What is the mechanism of action of the H2 Blockers? | Reversible block of histamine H2 receptors
🗑
|
||||
| What is the mechanism of action of the Sulfonylureas? | Close K+ channels in Beta-cell membrane leading to cell depolarization causing insulin release triggered by increase in Calcium ion influx.
🗑
|
||||
| What is the mechanism of action of the thrombolytics? | 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.)
🗑
|
||||
| What is the mechanism of action of Ticlopidine, Clopidogrel | Inhibits platelet aggregation by irreversibly inhibiting the ADP pathway involved in the binding of fibrinogen.
🗑
|
||||
| What is the mechanism of action of Warfarin (Coumadin)? | 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.
🗑
|
||||
| What is the mechanism of Azathioprine? | Antimetabolite derivative of 6-mercaptopurine that interferes with the metablolism and synthesis of nucleic acid.
🗑
|
||||
| What is the mechanism of Leuprolide? | 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
🗑
|
||||
| What is the mechanism of Tacrolimus (FK506)? | Similar to cyclosporine; binds to FK-binding protein, inhibiting secretion of IL-2 and other cytokines.
🗑
|
||||
| What is the memory key for the action of Sildenafil (Viagra)? | Sildenafil fills the penis
🗑
|
||||
| What is the memory key for the effect of aluminum hydroxide overuse? | AluMINIMUM amount of feces.
🗑
|
||||
| What is the memory key for the effect of magnesium hydroxide overuse? | Mg = Must go to the bathroom.
🗑
|
||||
| What is the memory key to remember which pathway (extrinsic vs. intrinsic) and which lab value Warfarin affects? | WEPT: Warfarin affects the Extrinsic pathway and prolongs the PT.
🗑
|
||||
| What is the possible mechanism and effect of Metformin in treating diabetes? | Mechanism unknown; possibly inhibits gluconeogenesis and increases glycolysis; effect is to decrease serum glucose levels
🗑
|
||||
| What is the specific clinical use of Indomethacin in neonates? | Indomethacin is used to close a patent ductus arteriosus.
🗑
|
||||
| What is used to reverse the action of Heparin? | Protamine Sulfate is used for rapid reversal of heparinization (positively charged molecule that binds to negatively charged heparin).
🗑
|
||||
| What patients are at risk for life threatening hypotension when taking Sildenafil (Viagra)? | Those patients who are taking nitrates.
🗑
|
||||
| What process does Zafirlukast interfere with? | Leukotrienes increasing bronchial tone.
🗑
|
||||
| What type of gout is treated with Allopurinol? | Chronic gout.
🗑
|
||||
| What type of gout is treated with Colchicine? | Acute gout.
🗑
|
||||
| What type of gout is treated with Probenacid? | Chronic gout.
🗑
|
||||
| What type of patient should not take Misoprostol and why? | Misoprostol is contraindicated in women of childbearing potential because it is an abortifacient.
🗑
|
||||
| Which H2 Blocker has the most toxic effects and what are they? | Cimetidine is a potent inhibitor of P450; it also has an antiandrogenic effect and decreases renal excretion of creatinine. Other H2 blockers are relatively free of these effects.
🗑
|
||||
| Why are the Sulfonylureas inactive in IDDM (type-1)? | Because they require some residual islet function.
🗑
|
||||
| Acetaldehyde is metabolized by Acetaldehyde dehydrogenase, which drug inhibs this enzyme? | Disulfram & also sulfonylureas, metronidazole
🗑
|
||||
| Explain pH dependent urinary drug elimination? | -Weak Acids>Alkinalize urine(CO3) to remove more -Weak bases>acidify urine to remove more
🗑
|
||||
| How do you treat coma in the ER (4)? | Airway -Breathing -Circulation -Dextrose(thiamine & narcan) -ABCD
🗑
|
||||
| In coma situations you rule out what (7)? | -Infections -Trauma -Seizures -CO -Overdose -Metabolic -Alcohol (IT'S COMA)
🗑
|
||||
| List some specifics of lead poisoning(4)? | -A57Blue lines in gingiva& long bones -Encephalopathy & Foot drop -Abdominal colic / -Sideroblastic anemia
🗑
|
||||
| List the specific antidote for this toxin: Acetaminophen | -N-acetylcystine
🗑
|
||||
| List the specific antidote for this toxin: Amphetamine | -Ammonium Chloride; acidifies urine to increase elimination
🗑
|
||||
| List the specific antidote for this toxin: Anticholinesterases (organophosphate.) | -Atropine & pralidoxime
🗑
|
||||
| List the specific antidote for this toxin: Antimuscarinic (anticholinergic) | -Physostigmine salicylate
🗑
|
||||
| List the specific antidote for this toxin: Arsenic (all heavy metals) | -Dimercaprol, succimer
🗑
|
||||
| List the specific antidote for this toxin: Benzodiazepines | -Flumazenil
🗑
|
||||
| List the specific antidote for this toxin: Beta Blockers | -Glucagon
🗑
|
||||
| List the specific antidote for this toxin: Carbon monoxide | -100% oxygen, hyperbaric
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| List the specific antidote for this toxin: Copper | -Penicillamine
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| List the specific antidote for this toxin: Cyanide | -Nitrate, hydroxocobalamin thiosulfate
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| List the specific antidote for this toxin: Digitalis | -Normalize K+, Lidocaine, & Anti-dig Mab
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| List the specific antidote for this toxin: Heparin | -Protamine
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| List the specific antidote for this toxin: Iron | -Deferoxamine
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| List the specific antidote for this toxin: Lead | -EDTA, dimercaprol, succimer, & penicillamine
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| List the specific antidote for this toxin: Methanol & Ethylene glycol | -Ethanol, dialysis, & fomepizole
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| List the specific antidote for this toxin: Methemoglobin | -Methylene blue
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| List the specific antidote for this toxin: Opioids | -B51Naloxone / naltrexone (Narcan)
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| List the specific antidote for this toxin: Salicylates | -Alkalinize urine & dialysis
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| List the specific antidote for this toxin: TPA & Streptokinase | -Aminocaproic acid
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| List the specific antidote for this toxin: Tricyclic antidepressants | -NaHCO3
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| List the specific antidote for this toxin: Warfarin | -Vitamin K; fresh frozen plasma
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| What are the products and their toxicities of the metabolism of ethanol by / alcohol dehydrogenase? | -Acetaldehyde -Nausea, vomiting, headache, & hypotension
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| What are the products and their toxicities of the metabolism of Ethylene Glycol by / alcohol dehydrogenase? | -Oxalic acid -Acidosis & nephrotoxicity
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| What are the products and their toxicities of the metabolism of Methanol by / alcohol dehydrogenase? | -Formaldehyde & formic acid -severe acidosis & retinal damage
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| Which drug(s) cause this reaction: Adrenocortical Insufficiency | -Glucocorticoid withdrawal
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| Which drug(s) cause this reaction: Agranulocytosis (3)? | -Cloazapine -carbamazapine -colchicine -PTU (propylthiouracil)
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| Which drug(s) cause this reaction: Anaphylaxis? | -Penicillin
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| Which drug(s) cause this reaction: Aplastic anemia (5)? | -Chloramphenicol -benzene -NSAIDS -PTU (propylthiouracil) -phenytoin
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| Which drug(s) cause this reaction: Atropine-like side effects (lowers parasym “rest/digest” activity of muscles and glands)? | -Tricyclic antidepressants
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| Which drug(s) cause this reaction: Cardiac toxicity? | - Doxorubicin, Daunorubicin
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| Which drug(s) cause this reaction: Cinchonism (HA, tinnitus, vertigo)(2)? | -Quinidine -quinine
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| Which drug(s) cause this reaction: Cough? | -ACE inhibitors (Losartan>no cough)
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| Which drug(s) cause this reaction: Cutaneous flushing (4)? | -Niacin -Ca++ channel blockers -adenosine -vancomycin
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| Which drug(s) cause this reaction: Diabetes insipidus? | -Lithium
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|
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| Which drug(s) cause this reaction: Disulfram-like reaction (4) ? | -Metronidazole -certain cephalosporins -procarbazine -sulfonylureas
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| Which drug(s) cause this reaction: Drug induced Parkinson's (4) ? | -Haloperidol -chlorpromazine -reserpine -MPTP
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|
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| Which drug(s) cause this reaction: Extrapyramidal side effects (3)? | -Chlorpromazine -thioridazine -haloperidol
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|
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| Which drug(s) cause this reaction: Fanconi's (proximal tubule kidney dysfxn) syndrome? | outdated Tetracycline and gentamycin
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|
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| Which drug(s) cause this reaction: Focal to massive hepatic necrosis (4)? | -Halothane -Valproic acid -acetaminophen -Amantia phalloides
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|
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| Which drug(s) cause this reaction: G6PD hemolysis(8)? | -Sulfonamides -INH -ASA -Ibuprofen -primaquine -nitrofurantoin /-pyrimethamine -chloramphenicol
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| Which drug(s) cause this reaction: Gingival hyperplasia? | -Phenytoin
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|
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| Which drug(s) cause this reaction: Gray baby syndrome? | -Chloramphenicol
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|
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| Which drug(s) cause this reaction: Gynecomastia (6) ? | -Cimetidine -ketoconazole -spironolactone -digitalis -EtOH -estrogens
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|
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| Which drug(s) cause this reaction: Hepatitis? | -Isoniazid
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|
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| Which drug(s) cause this reaction: Hot flashes? | -Tamoxifen
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|
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| Which drug(s) cause this reaction: Neuro and Nephrotoxic? | -polymyxins
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|
||||
| Which drug(s) cause this reaction: Osteoporosis (2)? | -Corticosteroids -heparin
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|
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| Which drug(s) cause this reaction: Oto and Nephrotoxicity (3)? | -aminoglycosides -loop diuretics -cisplatin
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|
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| Which drug(s) cause this reaction: P450 induction(6)? | -Barbiturates -phenytoin -carbamazipine -rifampin -griseofulvin -quinidine
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|
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| Which drug(s) cause this reaction: P450 inhibition(6)? | -Cimetidine -ketoconazole -grapefruit juice -erythromycin -INH -sulfonamides
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|
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| Which drug(s) cause this reaction: Photosensitivity(3)? | -Tetracycline -amiodarone -sulfonamides
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|
||||
| Which drug(s) cause this reaction: Pseudomembranous colitis? | -Clindamycin, Ampicillin
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|
||||
| Which drug(s) cause this reaction: Pulmonary fibrosis(3)? | -Bleomycin -amiodarone -busulfan
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|
||||
| Which drug(s) cause this reaction: SLE-like syndrome | -Hydralazine -Procainamide -INH -phenytoin
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|
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| Which drug(s) cause this reaction: Stephen-Johnson syn. (3) ? | -Ethosuxamide -sulfonamides -lamotrigine
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|
||||
| Which drug(s) cause this reaction: Tardive dyskinesia? | -Antipsychotics
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|
||||
| Which drug(s) cause this reaction: Tendonitis and rupture? | -Fluoroquinolones
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|
||||
| Which drug(s) cause this reaction: Thrombotic complications? | -Oral Contraceptives
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|
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| Which drug(s) cause this reaction: Torsade de pointes (2) ? | -Class III antiarrhythmics (sotalol) -class IA (quinidine)
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|
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| Which drug(s) cause this reaction: Tubulointerstitial Nephritis (5)? | -Sulfonamides -furosemide -methicillin -rifampin -NSAIDS (ex. ASA)
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|
||||
| Describe first-order kinetics | Constant FRACTION eliminated per unit time.(exponential)
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|
||||
| Describe Phase I metabolism in liver(3)? | -reduction, oxy, & hydrolysis -H2O sol. Polar product -P450
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|
||||
| Describe Phase II metabolism in liver(3)? | -acetylation, glucuron.,& sulfation -Conjugation -Polar product
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|
||||
| Explain differences between full and partial agonists(2). | - Act on same receptor - Full has greater efficacy
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|
||||
| Explain potency in relation to full and partial agonists(2). | - partial agonist can have increased, decreased, /A21or equal potency as full agonist. - Potency is an independent factor.
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|
||||
| How do spare receptors effect the Km? | - ED 50 is less than the Km (less than 50% of receptors)
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|
||||
| How do you calculate maintenance dose? | Md= (CpxCL)/F Cp= plas. Conc. CL=clear. F=bioaval.
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|
||||
| How does a competitive antagonist effect an agonist? | -Shifts the curve to the right -increases Km
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|
||||
| How does a noncompetitive antagonist effect an agonist? | - Shifts the curve down -reduces Vmax
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|
||||
| Name the steps in drug approval(4)? | -Phase I (clinical tests) -Phase II -Phase III -PhaseIV (surveillance)
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|
||||
| Steady state concentration is reached in __#half-lifes | In 4 half-lifes= (94%) T1/2 = (0.7x Vd)/CL
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|
||||
| What is the definition of zero-order kinetics? Example? | -Constant AMOUNT eliminated per unit time. -Etoh & ASA
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|
||||
| What is the formula for Clearance (CL) | CL= (rate of elimination of drug/ Plasma drug conc.)
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|
||||
| What is the formula for Volume of distribution (Vd) | Vd= (Amt. of drug in body/ Plasma drug conc.)
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|
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