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671 Cards in this Set
- Front
- Back
A common side effects of Interferon (INF) treatment is?
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Neutropenia
|
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Antimicrobial prophylaxis for a history of recurrent UTIs
|
TMP-SMZ
|
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Antimicrobial prophylaxis for Gonorrhea
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Ceftriaxone
|
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Antimicrobial prophylaxis for Meningococcal infection
|
Rifampin (DOC), minocycline
|
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Antimicrobial prophylaxis for PCP
|
TMP-SMZ (DOC), aerosolized pentamidine
|
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Antimicrobial prophylaxis for Syphilis
|
Benzathine penicillin G
|
|
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?
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No
|
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Are Cephalosporins resistant to penicillinase?
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No, but they are less susceptible than the other Beta lactams
|
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Are Methicillin, Nafcillin, and Dicloxacillin penicillinase resistant?
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Yes
|
|
Clinical use of Isoniazid (INH)?
|
Mycobacterium tuberculosis, the only agent used as solo prophylaxis against TB
|
|
Common side effects associated with Clindamycin include?
|
Pseudomembranous colitis (C. difficile), fever, diarrhea
|
|
Common toxicities associated with Fluoroquinolones?
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GI upset, Superinfections, Skin rashes, Headache, Dizziness
|
|
Common toxicities associated with Griseofulvin?
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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?
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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?
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No
|
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Does Foscarnet require activation by a viral kinase?
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No
|
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Foscarnet toxicity?
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Nephrotoxicity
|
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Ganciclovir associated toxicities?
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Leukopenia, Neutropenia, Thrombocytopenia, Renal toxicity
|
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How are Interferons (INF) used clinically?
|
Chronic Hepatitis A and B, Kaposi's Sarcoma
|
|
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?
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Pyridoxine (B6) administration
|
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How can the t1/2 of INH be altered?
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Fast vs. Slow Acetylators
|
|
How can the toxic effects of 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?
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As PABA antimetabolites that inhibit Dihydropteroate Synthase, Bacteriostatic
|
|
How do the Protease Inhibitors work?
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Inhibt 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
|
|
How does resistance to Vancomycin occur?
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With an amino acid change of D-ala D-ala to D-ala D-lac
|
|
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
|
|
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
|
|
How is Ganciclovir activated?
|
Phosphorylation by a Viral Kinase
|
|
How is Ganciclovir used clinically?
|
CMV, esp in Immunocompromised patients
|
|
How is Griseofulvin used clinically?
|
Oral treatment of superficial infections
|
|
How is Leishmaniasis treated?
|
Pentavalent Antimony
|
|
How is Ribavirin used clinically?
|
for RSV
|
|
How is Rifampin used clinically?
|
1. Mycobacterium tuberculosis 2. Delays resistance to Dapsone when used of Leprosy 3. Used in combination with other drugs
|
|
How is Trimethoprim used clinically?
|
Used in combination therapy with SMZ to sequentially block folate synthesis
|
|
How is Vancomycin used clinically?
|
For serious, Gram + multidrug-resistant organisms
|
|
How would you treat African Trypanosomiasis (sleeping sickness)?
|
Suramin
|
|
In what population does Gray Baby Syndrome occur? Why?
|
Premature infants, because they lack UDP-glucuronyl transferase
|
|
Is Aztreonam cross-allergenic with penicillins?
|
No
|
|
Is Aztreonam resistant to penicillinase?
|
Yes
|
|
Is Aztreonam usually toxic?
|
No
|
|
Is Imipenem resistant to penicillinase?
|
Yes
|
|
Is Penicillin penicillinase resistant?
|
No - duh
|
|
IV Penicillin
|
Penicillin-G
|
|
Mnemonic for Foscarnet?
|
Foscarnet = pyroFosphate analog
|
|
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
|
|
MOA: Block cell wall synthesis by inhib. Peptidoglycan cross-linking (7)
|
Penicillin, Ampicillin, Ticarcillin, Pipercillin, Imipenem, Aztreonam, Cephalosporins
|
|
MOA: Block DNA topoisomerases
|
Quinolones
|
|
MOA: Block mRNA synthesis
|
Rifampin
|
|
MOA: Block nucleotide synthesis
|
Sulfonamides, Trimethoprim
|
|
MOA: Block peptidoglycan synthesis
|
Bacitracin, Vancomycin
|
|
MOA: Block protein synthesis at 30s subunit
|
Aminoglycosides, Tetracyclines
|
|
MOA: Block protein synthesis at 50s subunit
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Chloramphenicol, Erythromycin/macrolides, Lincomycin, Clindamycin, Streptogramins (quinupristin, dalfopristin)
|
|
MOA: Disrupt bacterial/fungal cell membranes
|
Polymyxins
|
|
MOA: Disrupt fungal cell membranes
|
Amphotericin B, Nystatin, Fluconazole/azoles
|
|
Name common Polymyxins
|
Polymyxin B, Polymyxin E
|
|
Name several common Macrolides (3)
|
Erythromycin, Azithromycin, Clarithromycin
|
|
Name some common Sulfonamides (4)
|
Sulfamethoxazole (SMZ), Sulfisoxazole, Triple sulfas, Sulfadiazine
|
|
Name some common Tetracyclines (4)
|
Tetracycline, Doxycycline, Demeclocycline, Minocycline
|
|
Name the common Aminoglycosides (5)
|
Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin
|
|
Name the common Azoles
|
Fluconazole, Ketoconazole, Clotrimazole, Miconazole, Itraconazole
|
|
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
|
|
Name the common Nucleoside Reverse Transcriptase Inhibitors
|
Zidovudine (AZT), Didanosine (ddI), Zalcitabine (ddC), Stavudine (d4T), Lamivudine (3TC)
|
|
Name the Protease Inhibitors (4)
|
Saquinavir, Ritonavir, Indinavir, Nelfinavir
|
|
Name two classes of drugs for HIV therapy
|
Protease Inhibitors and Reverse Transcriptase Inhibitors
|
|
Name two organisms Vancomycin is commonly used for?
|
Staphlococcus aureus and Clostridium difficile (pseudomembranous colitis)
|
|
Oral Penicillin
|
Penicillin-V
|
|
Resistance mechanisms for Aminoglycosides
|
Modification via Acetylation, Adenylation, or Phosphorylation
|
|
Resistance mechanisms for Cephalosporins/Penicillins
|
Beta-lactamase cleavage of Beta-lactam ring
|
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Resistance mechanisms for Chloramphenicol
|
Modification via Acetylation
|
|
Resistance mechanisms for Macrolides
|
Methylation of rRNA near Erythromycin's ribosome binding site
|
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Resistance mechanisms for Sulfonamides
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Altered bacterial Dihydropteroate Synthetase, Decreased uptake, or Increased PABA synthesis
|
|
Resistance mechanisms for Tetracycline
|
Decreased uptake or Increased transport out of cell
|
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Resistance mechanisms for Vancomycin
|
Terminal D-ala of cell wall replaced with D-lac; Decreased affinity
|
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Side effects of Isoniazid (INH)?
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Hemolysis (if G6PD deficient), Neurotoxicity, Hepatotoxicity, SLE-like syndrome
|
|
Specifically, how does Foscarnet inhibit viral DNA pol?
|
Binds to the Pyrophosphate Binding Site of the enzyme
|
|
The MOA for Chloramphenicol is?
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Inhibition of 50S peptidyl transferase, Bacteriostatic
|
|
Toxic effects of TMP include?
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Megaloblastic anemia, Leukopenia, Granulocytopenia
|
|
Toxic side effects of the Azoles?
|
Hormone synthesis inhibition (Gynecomastia), Liver dysfunction (Inhibits CYP450), Fever, Chills
|
|
Toxicities associated with Acyclovir?
|
Delirium, Tremor, Nephrotoxicity
|
|
What additional side effects exist for Ampicillin?
|
Rash, Pseudomembranous colitis
|
|
What antimicrobial class is Aztreonam syngergestic with?
|
Aminoglycosides
|
|
What are Amantadine-associated side effects?
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Ataxia, Dizziness, Slurred speech
|
|
What are Aminoglycosides synergistic with?
|
Beta-lactam antibiotics
|
|
What are Aminoglycosides used for clinically?
|
Severe Gram - rod infections.
|
|
What are common serious side effects of Aminoglycosides and what are these associated with?
|
Nephrotoxicity (esp. with Cephalosporins), Ototoxicity (esp. with Loop Diuretics)
|
|
What are common side effects of Amphotericin B?
|
Fever/Chills, Hypotension, Nephrotoxicity, Arrhythmias
|
|
What are common side effects of Protease Inhibitors?
|
GI intolerance (nausea, diarrhea), Hyperglycemia, Lipid abnormalities, Thrombocytopenia (Indinavir)
|
|
What are common side effects of RT Inhibitors?
|
BM suppression (neutropenia, anemia), Peripheral neuropathy
|
|
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
|
|
What are common toxicities associated with Tetracyclines?
|
GI distress, Tooth discoloration and Inhibition of bone growth in children, Fanconi's syndrome, Photosensitivity
|
|
What are common toxicities related to Vancomycin therapy?
|
Well tolerated in general but occasionally, Nephrotoxicity, Ototoxicity, Thrombophlebitis, diffuse flushing='Red Man Syndrome'
|
|
What are Fluoroquinolones indicated for? (3)
|
1.Gram - rods of the Urinary and GI tracts (including Pseudomonas) 2.Neisseria 3. Some Gram + organisms
|
|
What are major side effects of Methicillin, Nafcillin, and Dicloxacillin?
|
Hypersensitivity reactions
|
|
What are Methicillin, Nafcillin, and Dicloxacillin used for clinically?
|
Staphlococcus aureus
|
|
What are Polymyxins used for?
|
Resistant Gram - infections
|
|
What are the Anti-TB drugs?
|
Rifampin, Ethambutol, Streptomycin, Pyrazinamide, Isoniazid (INH)
|
|
What are the clinical indications for Azole therapy?
|
Systemic mycoses
|
|
What are the clinical uses for 1st Generation Cephalosporins?
|
Gram + cocci, Proteus mirabilis, E. coli, Klebsiella pneumoniae (PEcK)
|
|
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 )
|
|
What are the clinical uses for 3rd Generation Cephalosporins?
|
1) Serious Gram - infections resistant to other Beta lactams 2) Meningitis (most penetrate the BBB)
|
|
What are the clinical uses for Aztreonam?
|
Gram - rods: Klebsiella species, Pseudomonas species, Serratia species
|
|
What are the clinical uses for Imipenem/cilastatin?
|
Gram + cocci, Gram - rods, and Anerobes
|
|
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
|
|
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)
|
|
What are the major toxic side effects of Imipenem/cilastatin?
|
GI distress, Skin rash, and Seizures at high plasma levels
|
|
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)
|
|
What are the side effects of Polymyxins?
|
Neurotoxicity, Acute renal tubular necrosis
|
|
What are the side effects of Rifampin?
|
Minor hepatotoxicity, Drug interactions (activates P450)
|
|
What are toxic side effects for Metronidazole?
|
Disulfiram-like reaction with EtOH, Headache
|
|
What are toxicities associated with Chloramphenicol?
|
Aplastic anemia (dose independent), Gray Baby Syndrome
|
|
What conditions are treated with Metronidazole?
|
Giardiasis, Amoebic dysentery (E. histolytica), Bacterial vaginitis (Gardnerella vaginalis), Trichomonas
|
|
What do Aminoglycosides require for uptake?
|
Oxygen
|
|
What do you treat Nematode/roundworm (pinworm, whipworm) infections with?
|
Mebendazole/Thiabendazole, Pyrantel Pamoate
|
|
What drug is given for Pneumocystis carinii prophylaxis?
|
Pentamidine
|
|
What drug is used during the pregnancy of an HIV+ mother?, Why?
|
AZT, to reduce risk of Fetal Transmission
|
|
What drug is used to treat Trematode/fluke (e.g., Schistosomes, Paragonimus, Clonorchis) or Cysticercosis
|
Praziquantel
|
|
What is a common drug interaction associated with Griseofulvin?
|
Increases coumadin metabolism
|
|
What is a mnemonic to remember Amantadine's function?
|
Blocks Influenza A and RubellA; causes problems with the cerebellA
|
|
What is a prerequisite for Acyclovir activation?
|
It must be Phosphorylated by Viral Thymidine Kinase
|
|
What is a Ribavirin toxicity?
|
Hemolytic anemia
|
|
What is an acronym to remember Anti-TB drugs?
|
RESPIre
|
|
What is an additional side effect of Methicillin?
|
Interstitial nephritis
|
|
What is an occasional side effect of Aztreonam?
|
GI upset
|
|
What is Clindamycin used for clinically?
|
Anaerobic infections (e.g., B. fragilis, C. perfringens)
|
|
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
|
|
What is the major side effect for Ampicillin and Amoxicillin?
|
Hypersensitivity reactions
|
|
What is the major side effect for Carbenicillin, Piperacillin, and Ticarcillin?
|
Hypersensitivity reactions
|
|
What is the major toxic side effect of 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'
|
|
What is the memory key involving the '4 R's of Rifampin?'
|
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?
|
Same as penicillin. Extended spectrum antibiotics
|
|
What is the MOA for 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.
|
|
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)
|
|
Beta Blockers- BP?
|
decrease
|
|
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
|
|
Antiarrhythmic class IA effects?
|
increased AP duration, increased ERP increased QT interval. Atrial and ventricular.
|
|
Antiarrhythmic class IB- clinical uses?
|
post MI and digitalis induced arrhythmias
|
|
Antiarrhythmic class IB- effects?
|
decrease AP duration, affects ischemic or depolarized Purkinje and ventricular system
|
|
Antiarrhythmic class IB- toxicity?
|
local anesthetic. CNS stimulation or depression. CV depression.
|
|
Antiarrhythmic class IC- effects?
|
NO AP duration effect. useful in V-tach that progresses to V-fib and in intractable SVT LAST RESORT
|
|
Antiarrhythmic class IC- toxicity?
|
proarrhythmic
|
|
Antiarrhythmic class II- effects?
|
decrease the slope of phase 4, increase PR interval (the AV node is particularly sensitive)
|
|
Antiarrhythmic class II- mechanism?
|
blocking the beta adrenergic receptor leads to decreased cAMP, and decreased Ca2+ flux
|
|
Antiarrhythmic class II- toxicity?
|
impotence, exacerbation of asthma, CV effects, CNS effects, may mask hypoclycemia
|
|
Antiarrhythmic Class III- effects?
|
increase AP duration, increase ERP, increase QT interval, for use when other arrhythmics fail
|
|
Antiarrhythmic class IV- clinical use?
|
prevention of nodal arrhythmias (SVT)
|
|
Antiarrhythmic class IV- effects?
|
decrease conduction velocity, increase ERP, increase PR interval
|
|
Antiarrhythmic class IV- primary site of action?
|
AV nodal cells
|
|
Antiarrhythmic 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
|
|
decrease Digitoxin dose in renal failure?
|
NO
|
|
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 Antiarrhythmic drugs in class II?
|
propanolol, esmolol, metoprolol, atenolol, timolol
|
|
name four HMG-CoA reductase inhibitors.
|
Lovastatin, Pravastatin, Simvastatin, Atorvastatin
|
|
name four Antiarrhythmic drugs in class IA.
|
Quinidine, Amiodarone, Procainamide, Disopyramide
|
|
name four Antiarrhythmic drugs in class III.
|
Sotalol, Ibutilide, Bretylium, Amiodarone
|
|
name three ACE inhibitors?
|
Captopril, Enalapril, Lisinopril
|
|
name three calcium channel blockers?
|
Nifedipine, Verapamil, Diltiazem
|
|
name three Antiarrhythmic drugs in class IB.
|
Lidocaine, Mexiletine, Tocainide
|
|
name three Antiarrhythmic drugs in class IC.
|
Flecainide, Encainide, Propafenone
|
|
name three Antiarrhythmic drugs 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- site 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?
|
Acetaminophen 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 Structure
|
Large anionic polymer, acidic
|
|
For Heparin what is the Route of administration
|
Paranteral (IV, SC)
|
|
For Heparin what is the Onset of action
|
Rapid (seconds)
|
|
For Heparin what is the Mechanism of action
|
Activates antithrombin III
|
|
For Heparin what is the Duration of action
|
Acute (hours)
|
|
For Heparin what is the Ability to inhibit coagulation in vitro
|
Yes
|
|
For Heparin what is the Treatment for overdose
|
Protamine sulfate
|
|
For Heparin what is the Lab value to monitor
|
aPTT (intrinsic pathway)
|
|
For Heparin what is the Site of action
|
Blood
|
|
For Warfarin what is the Structure
|
Small lipid-soluble molecule
|
|
For Warfarin what is the Route of administration
|
Oral
|
|
For Warfarin what is the Onset of action
|
Slow, limited by half lives of clotting factors
|
|
For Warfarin what is the Mechanism of action
|
Impairs the synthesis of vitamin K-dependent clotting factors
|
|
For Warfarin what is the Duration of action
|
Chronic (weeks or months)
|
|
For Warfarin what is the Ability to inhibit coagulation in vitro
|
No
|
|
For Warfarin what is the Treatment for overdose
|
IV vitamin K and fresh frozen plasma
|
|
For Warfarin what is the Lab value to monitor
|
PT
|
|
For Warfarin what is the Site of action
|
Liver
|
|
Is toxicity rare or common whith 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.
|
|
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)?
|
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 Leuprolied?
|
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.
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|
What is are two clinical uses of Cyclosporine?
|
1. Suppresses organ rejection after transplantation 2. Selected autoimmune disorders.
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|
What is the category and mechanism of action of Zafirlukast in Asthma treatment?
|
Antileukotriene; blocks leukotriene receptors.
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|
What is the category and mechanism of action of Zileuton in Asthma treatment?
|
Antileukotriene; blocks synthesis by lipoxygenase.
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What is the category of drug names ending in -ane (e.g. Halothane)
|
Inhalational general anesthetic.
|
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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).
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|
What is the category of drug names ending in -azol (e.g. Ketoconazole)
|
Antifungal.
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|
What is the category of drug names ending in -barbital (e.g. Phenobarbital)
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Babiturate.
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What is the category of drug names ending in -caine (e.g. Lidocaine)
|
Local anesthetic.
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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.
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What is the category of drug names ending in -ipramine (e.g. Imipramine)
|
Tricyclic antidepressant.
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What is the category of drug names ending in -navir (e.g. Saquinavir)
|
Protease inhibitor.
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What is the category of drug names ending in -olol (e.g. Propranolol)
|
Beta antagonist.
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|
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).
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|
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.
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What is the category of drug names ending in -terol (e.g. Albuterol)
|
Beta-2 agonist.
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|
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.
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|
What is the category of drug names ending in -tropin (e.g. Somatotropin)
|
Pituitary hormone.
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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 mecanism 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 nad 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?
|
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.
|
|
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 decresed 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
|
|
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
|
|
List the specific antidote for this toxin: Copper
|
-Penicillamine
|
|
List the specific antidote for this toxin: Cyanide
|
-Nitrate, hydroxocobalamin thiosulfate
|
|
List the specific antidote for this toxin: Digitalis
|
-Normalize K+, Lidocaine, & Anti-dig Mab
|
|
List the specific antidote for this toxin: Heparin
|
-Protamine
|
|
List the specific antidote for this toxin: Iron
|
-Deferoxamine
|
|
List the specific antidote for this toxin: Lead
|
-EDTA, dimercaprol, succimer, & penicillamine
|
|
List the specific antidote for this toxin: Methanol & Ethylene glycol
|
-Ethanol, dialysis, & fomepizole
|
|
List the specific antidote for this toxin: Methemoglobin
|
-Methylene blue
|
|
List the specific antidote for this toxin: Opioids
|
-B51Naloxone / naltrexone (Narcan)
|
|
List the specific antidote for this toxin: Salicylates
|
-Alkalinize urine & dialysis
|
|
List the specific antidote for this toxin: TPA & Streptokinase
|
-Aminocaproic acid
|
|
List the specific antidote for this toxin: Tricyclic antidepressants
|
-NaHCO3
|
|
List the specific antidote for this toxin: Warfarin
|
-Vitamin K & fresh frozen plasma
|
|
What are the products and their toxicities of the metabolism of ethanol by / alcohol dehydrogenase?
|
-Acetaldehyde -Nausea, vomiting, headache, & hypotension
|
|
What are the products and their toxicities of the metabolism of Ethylene Glycol by / alcohol dehydrogenase?
|
-Oxalic acid -Acidosis & nephrotoxicity
|
|
What are the products and their toxicities of the metabolism of Methanol by / alcohol dehydrogenase?
|
-Formaldehyde & formic acid -severe acidosis & retinal damage
|
|
Which drug(s) cause this reaction: Adrenocortical Insufficiency
|
-Glucocorticoid withdrawal
|
|
Which drug(s) cause this reaction: Agranulocytosis (3)?
|
-Cloazapine -carbamazapine -colchicine -PTU
|
|
Which drug(s) cause this reaction: Anaphylaxis?
|
-Penicillin
|
|
Which drug(s) cause this reaction: Aplastic anemia (5)?
|
-Chloramphenicol -benzene -NSAIDS -PTU -phenytoin
|
|
Which drug(s) cause this reaction: Atropine-like side effects?
|
-Tricyclic antidepressants
|
|
Which drug(s) cause this reaction: Cardiac toxicity?
|
-Daunorubicin & Doxorubicin
|
|
Which drug(s) cause this reaction: Cinchonism (2)?
|
-Quinidine -quinine
|
|
Which drug(s) cause this reaction: Cough?
|
-ACE inhibitors (Losartan>no cough)
|
|
Which drug(s) cause this reaction: Cutaneous flushing (4)?
|
-Niacin -Ca++ channel blockers -adenosine -vancomycin
|
|
Which drug(s) cause this reaction: Diabetes insipidus?
|
-Lithium
|
|
Which drug(s) cause this reaction: Disulfram-like reaction (4) ?
|
-Metronidazole -certain cephalosporins -procarbazine -sulfonylureas
|
|
Which drug(s) cause this reaction: Drug induced Parkinson's (4) ?
|
-Haloperidol -chlorpromazine -reserpine -MPTP
|
|
Which drug(s) cause this reaction: Extrapyramidal side effects (3)?
|
-Chlorpromazine -thioridazine -haloperidol
|
|
Which drug(s) cause this reaction: Fanconi's syndrome?
|
-Tetracycline
|
|
Which drug(s) cause this reaction: Focal to massive hepatic necrosis (4)?
|
-Halothane -Valproic acid -acetaminophen -Amantia phalloides
|
|
Which drug(s) cause this reaction: G6PD hemolysis(8)?
|
-Sulfonamides -INH -ASA -Ibuprofen -primaquine -nitrofurantoin /-pyrimethamine -chloramphenicol
|
|
Which drug(s) cause this reaction: Gingival hyperplasia?
|
-Phenytoin
|
|
Which drug(s) cause this reaction: Gray baby syndrome?
|
-Chloramphenicol
|
|
Which drug(s) cause this reaction: Gynecomastia (6)?
|
-Cimetidine -ketoconazole -spironolactone -digitalis -EtOH -estrogens
|
|
Which drug(s) cause this reaction: Hepatitis?
|
-Isoniazid
|
|
Which drug(s) cause this reaction: Hot flashes?
|
-Tamoxifen
|
|
Which drug(s) cause this reaction: Neuro and Nephrotoxic?
|
-polymyxins
|
|
Which drug(s) cause this reaction: Osteoporosis (2)?
|
-Corticosteroids -heparin
|
|
Which drug(s) cause this reaction: Oto and Nephrotoxicity (3)?
|
-aminoglycosides -loop diuretics -cisplatin
|
|
Which drug(s) cause this reaction: P450 induction(6)?
|
-Barbiturates -phenytoin -carbamazipine -rifampin -griseofulvin -quinidine
|
|
Which drug(s) cause this reaction: P450 inhibition(6)?
|
-Cimetidine -ketoconazole -grapefruit juice -erythromycin -INH -sulfonamides
|
|
Which drug(s) cause this reaction: Photosensitivity(3)?
|
-Tetracycline -amiodarone -sulfonamides
|
|
Which drug(s) cause this reaction: Pseudomembranous colitis?
|
-Clindamycin
|
|
Which drug(s) cause this reaction: Pulmonary fibrosis(3)?
|
-Bleomycin -amiodarone -busulfan
|
|
Which drug(s) cause this reaction: SLE-like syndrome?
|
-Hydralazine -Procainamide -INH -phenytoin
|
|
Which drug(s) cause this reaction: Stevens-Johnson syn. (3)?
|
-Ethosuxamide -sulfonamides -lamotrigine
|
|
Which drug(s) cause this reaction: Tardive dyskinesia?
|
-Antipsychotics
|
|
Which drug(s) cause this reaction: Tendonitis and rupture?
|
-Fluoroquinolones
|
|
Which drug(s) cause this reaction: Thrombotic complications?
|
-Oral Contraceptives
|
|
Which drug(s) cause this reaction: Torsade de pointes (2)?
|
-Class III antiarrhythmics (sotalol) -class IA (quinidine)
|
|
Which drug(s) cause this reaction: Tubulointerstitial Nephritis (5)?
|
-Sulfonamides -furosemide -methicillin -rifampin -NSAIDS (ex. ASA)
|
|
Describe first-order kinetics?
|
Constant FRACTION eliminated per unit time.(exponential)
|
|
Describe Phase I metabolism in liver(3)?
|
-reduction, oxy, & hydrolysis -H2O sol. Polar product -P450
|
|
Describe Phase II metabolism in liver(3)?
|
-acetylation, glucuron., & sulfation -Conjugation -Polar product
|
|
Explain differences between full and partial agonists(2).
|
- Act on same receptor - Full has greater efficacy
|
|
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.
|
|
How do spare receptors effect the Km?
|
- ED 50 is less than the Km (less than 50% of receptors)
|
|
How do you calculate maintenance dose?
|
Md= (CpxCL)/F Cp= plas. Conc. CL=clear. F=bioaval.
|
|
How does a competitive antagonist effect an agonist?
|
-Shifts the curve to the right -increases Km
|
|
How does a noncompetitive antagonist effect an agonist?
|
- Shifts the curve down -reduces Vmax
|
|
Name the steps in drug approval(4)?
|
-Phase I (clinical tests) -Phase II -Phase III -PhaseIV (surveillance)
|
|
Steady state concentration is reached in __ number of half-lifes
|
In 4 half-lifes= (94%) T1/2 = (0.7x Vd)/CL
|
|
What is the definition of zero-order kinetics? Example?
|
-Constant AMOUNT eliminated per unit time. -Etoh & ASA
|
|
What is the formula for Clearance (CL)
|
CL= (rate of elimination of drug/ Plasma drug conc.)
|
|
What is the formula for Volume of distribution (Vd)
|
Vd= (Amt. of drug in body/ Plasma drug conc.)
|
|
What is the loading dose formula?
|
Ld= (CpxVd)/F Cp=plasma conc. F= Bioaval.
|
|
A 12yo patient was treated for a reaction to a bee sting, what drug provides the best coverage of sympathomimetic receptors?
|
Epinephirine(Alpha1,2 and Beta 1,2)
|
|
A 57 yo heart failure pt develops cardiac decompensation, what drug will give you adequate perfusion of his kidneys as well as tx for his Hypotension
|
Dopamine
|
|
A fellow passenger on a Carnival cruise ship looks pale and diaphoretic, what antimuscarinic agent would you give them?
|
scopolamine
|
|
A group of pts are rushed into the ER complaining of excessive sweating, tearing, salivation, HA, N and V, muscle twitching, difficulty breathing and diarrhea. What drug would be the most effective immediate tx
|
Atropine pts are suffering from Cholinestrase inhibitor poisining (Nerve gas/Organophosphate poisining)
|
|
As an Anes you want to use a depolarizing neuromuscular blocking drug on your pt, what do you use
|
Succinylcholine
|
|
MOA of Succinylcholine
|
Prevents the release of Ca from SR of skeletal muscle
|
|
Clonidine is the preferred sym pathomimetic tx of HTN in pts with renal disease, why??
|
Centrally acting alpha agonist, thus causing a decrease in central adrenergic outflow, spairing renal blood flow
|
|
Cocaine casues vasoconstriction and local anesthesia by what mechanism
|
Indirect agonist, uptake inhibitor
|
|
Cocaine shares is mechanism of action with what antidepressant
|
TCA
|
|
Dobutamine used for the tx of shock acts on which receptors
|
Beta1 more than B2
|
|
Guanethidine enhances the release of Norepi?
|
No, it inhibits the release of Nor Epi
|
|
How does angiotensin II affect NE release?
|
It acts presynaptically to increase NE release.
|
|
How does botulinum toxin result in respiratory arrest?
|
Prevents the release of ACh, which results in muscle paralysis.
|
|
How does dantrolene work?
|
Prevents the release of calcium from the sarcoplasmic reticulum of skeletal muscle.
|
|
How does NE modulate its own release? What other neurotransmitter has this same effect?
|
NE acts presynaptically on alpha-2 receptors to inhibit its own release. ACh also acts presynaptically through M1 receptors to inhibit NE release.
|
|
How would hemicholinium treatment affect cholinergic neurons?
|
Hemicholinium inhibits the transport of choline into the nerve, thus inhibiting formation of ACh.
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How would you reverse the effect of a neuromuscular blocking agent?
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Give an antichloinesterase - neostigmine, edrophonium, etc
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If a patient is given hexamethonium, what would happen to his/her heart rate?
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It would increase to ~ 100 beats/min. Both sympathetic and vagal stimulation would be knocked out, but the SA node has an intrinsic pace of 100 beats/min, which is normally checked by vagal stimulation.
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Isopoterenol was given to a patient with a developing AV block, why?
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Stimulates beta adrenergic receptors
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Norepi feedbacks and inhibits the presynaptic receptor by what mechanism
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Binding to the presynaptic alpha 2 release modulating receptors
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Reserpine will block the syntheis of this drug and but not its precursor.
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Blocks Norepi, but not Dopamine
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These drugs acts indirectly by releasing strored catecholamines in the presynaptic terminal
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Amphetamine and Ephedrine
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What anticholinesterase crosses the blood-brain-barrier?
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physostigmine
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What antimuscarinic agent is used in asthma and COPD?
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Ipratropium
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What antimuscarinic drug is useful for the tx of asthma
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Ipratropium
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What are the classic symptoms of cholinesterase inhibitor poisoning (parathion or other organophosphates)?
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Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of skeletal muscle and CNS, Lacrimation, Sweating, and Salivation = DUMBBELS; also abdominal cramping
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What are the clinical indications for bethanechol?
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Activates cholinergic receptors on bladder and bowel smooth muscle, alleviating post-op and neurogenic ileus and urinary retention.
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What are the clinical indications for neostigmine?
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Post-op and neurogenic ileus and urinary retention, myasthenia gravis, and reversal of neuromuscular junction blockade (post-op) through anticholinesterase activity.
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What are the indications for using amphetamine?
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narcolepsy, obesity, and attention deficit disorder (I wouldn't recommend this)
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What are the nondepolarizing neuromuscular blocking drugs?
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Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rapacuronium
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What are the phases of succinylcholine neuromuscular blockade?
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Phase 1 = prolonged depolarization, no antidote, effect potentiated by anticholinesterase; Phase 2 = repolarized but blocked, an anticholinesterase is the antidote for this phase.
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What are two indirect acting adrenergic agonists?
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amphetamine and ephedrine
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What beta 2 agonist will help your 21yo Astma pt?
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Albuterol, tertbutaline
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What cholinergic inhibitor acts by directly inhibiting Ach release at the presynaptic terminal
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Botulinum
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What cholinomimetic is useful in the diagnosis of Myasthenia Gravis
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Edrophonium
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What cholinomimetics might your pt be taking for his glaucoma
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Carbachol, pilocarpine, physostigmine, echothiophate
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What class of drug is echothiophate? What is its indication?
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anticholinesterase glaucoma
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What conditions would you use dantrolene?
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In treatment of malignant hyperthermia, due to concomitant use of halothane and succinylcholine. Also in neuroleptic malignant syndrome, a toxicity of antipsychotic drugs.
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What drug is used to diagnose myasthenia gravis?
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edrophonium (extremely short acting anticholinesterase)
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What drugs target anticholinesterase
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Neostigmine, pyridostigmine edrophonium, physostigmine echothiophate
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What effect would atropine have on a patient with peptic ulcer disease?
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Theoretically it could be used to block the cephalic phase of acid secretion (vagal stimulation).
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What effect would atropine have on the preganglionic sympathetic activation of sweat glands? Would this person sweat?
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None. No, because atropine would block the postganglionic muscarinic receptors involved in sweat gland stimulation.
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What enzyme is responsible for the breakdown of ACh in the synaptic cleft?
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Acetylcholinesterase; ACh is broken down into choline and acetate.
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What enzyme is responsible for the degredation of Ach
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Acetylcholine esterase
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What enzyme is responsible for the production of Ach from Acetyl CoA and Choline
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Choline acetyltransferase
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What is the clinical utility of clonidine?
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Treatment of hypertension, especially with renal disease (lowers bp centrally, so flow is maintained to kidney).
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What is the clinical utility of cocaine?
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The only local anesthetic with vasoconstrictive properties.
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What is the difference between the affinity for beta receptors between albuterol/terbutaline and dantroline?
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Dobutamine has more of an affintiy for beta-1 than beta-2, and is used for treating heart failure and shock. Albuterol and terbutaline is the reverse, and is used in treatment of acute asthma.
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What is the difference in receptor affinity of epinephrine at low doses? High doses?
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Prefers beta's at low doses, but at higher doses alpha agonist effects are predominantly seen.
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What is the effect of epinephrine infusion on bp and pulse pressure?
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Increased systolic and pulse pressure, decreased diastolic pressure, and little change in mean pressure.
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What is the effect of guanethidine on adrenergic NE release?
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It inhibits release of NE.
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What is the effect of norepinephrine on bp and pulse pressure?
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Increases mean, systolic, and diastolic bp, while there is little change in pulse pressure.
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What is the effect of TCA's on the adrenergic nerve?
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They inhibit reuptake of NE at the nerve terminal (as does cocaine).
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What is the only depolarizing neuromuscular blocking agent?
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Succinylcholine
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What is the receptor affinity and clinical use of isoproterenol?
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It affects beta receptors equally and is used in AV heart block (rare).
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What physiological effects was the Anes using Atropine to tx
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SLUD (salivation, Lacrimation, urination, Defecation)as well as airway secretion, GI motility, acid secretions
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What reversal agent could a Anes give to reverse the effects of Atropine
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Bethanechol, Neostigmine, physostigmine
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What side effect of using atropine to induce pupillary dilation would you expect?
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Atropine would also block the receptors in the ciliary muscle, causing an impairment in accommodation (cycloplegia).
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What sympathomimetic would you not prescribe for hypotension in a pt with renal artery sclerosis.
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Norepinephrine (Alpha1,2 and beta 1)
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What type of neurological blockade would hexamethonium create?
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Hexamethonium is a nicotinic antagonist, and thus is a ganglionic blocker.
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What would be the effect on blood pressure with infusion of the alpha -2 agonist clonidine?
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Initially vasoconstriction would increase bp, but then it acts on central alpha-2 receptors to decrease adrenergic outflow resulting in decreased bp.
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Which antimuscarinic agents are used in producing mydriasis and cycloplegia?
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atropine, homatropine, tropicamide
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Which drug increases Sys BP w/o affecting Pulse Pressure
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Epinephrine
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Which of epi, norepi, or isoproterenol results in bradycardia?
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Norepinephrine
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Which of the following would atropine administration cause? Hypothermia, bradycardia, excess salivation, dry flushed skin, or diarrhea
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Dry flushed skin, due to inhibition of sympathetic post-ganglionic blockade on muscarinic receptors of sweat glands. All others are opposite of what would be expected.
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Which of these three drugs will cause a reflex bradycardia in your pt (Norepi, Epi, or Isoporterenol)
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Norepinephrine
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Which receptors does phenylephrine act upon?
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alpha-1 > alpha-2; used as a pupil dilator, vasoconstrictor, and for nasal decongestion
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While at a tail gait party, you bite into a sandwich that a yellow jacket is also enjoying. Knowing your allergy to this creature, what should you do?
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Epinephrine to treat anaphylaxis. Also useful if you have open angle glaucoma, asthma, or hypotension.
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Why are albuterol and terbutaline effective in tx of acute asthmatic attacks?
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These B-2 agonists cause respiratory smooth muscle to relax.
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Why does atropine dilate the pupil?
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Blocking muscarinic receptors in the circular fibers of the eye, results in unopposed action of radial muscles to dilate.
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Why does NE result in bradycardia?
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NE increases bp, which stimulates baroreceptors in the carotid sinus and the aorta. The CNS signals through vagal stimulation to decrease heart rate.
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Why is carbachol and pilocarpine useful in treatment of glaucoma?
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They activate the ciliary muscle of the eye (open angle) and pupillary sphincter (narrow angle).
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Why is pyridostigmine effective in the treatment of myasthenia gravis?
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As an anticholinesterase it increases endogenous ACh and thus increases strength.
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Why is reserpine effective in treating HTN?
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Reserpine inhibits dopamine transport into vesicles, attenuating its conversion to NE by dopamine beta-hydroxylase.
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Why is there a drop in systolic, mean, and diastolic bp with infusion of isoproterenol?
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Stimulating beta receptors stimulates heart rate, but beta receptor induced vasodilation reduces peripheral resistance.
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Why would a patient with cog-wheel rigidity and a shuffling gait be given benztropine?
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Parkinson patients benefit from antimuscarinic agents through its inhibitory action within the indirect pathway.
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Why would dopamine be useful in treating shock?
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Receptors = D1=D2>beta>alpha, thus increasing heart rate (beta) and blood pressure (alpha vasoconstriction) while maintaining kidney perfusion (dopamine receptors)
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Why would you give a drug like pancuronium or succinylcholine?
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Useful in muscle paralysis during surgery or mechanical ventilation.
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Why would you use pralidoxime after exposure to an organophosphate?
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Pralidoxime regenerates active cholinesterase.
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Will Hemicholinum affect the release of stored Ach during Cholinergic Stimulation
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No, hemicholinum block the uptake of Choline and thus Ach synthesis
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Would blockade of muscarininc receptors in the bladder be useful in treating urinary retention?
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No. Atropine is used to reduce urgency in mild cystitis. So it would aggravate the urinary retention.
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Your patient wants an effective drug to treat his motion sickness, what would you prescribe
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Scopolamine
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