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Pharmacology by Somebody > Pharm USMLE Step 1.1 > Flashcards

Pharm USMLE Step 1.1 Flashcards

1
Q

A common side effects of Interferon (INF) treatment is?

A

Neutropenia

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2
Q

Antimicrobial prophylaxis for a history of recurrent UTIs

A

TMP-SMZ (Trimethoprim/sulfamethoxazole)

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3
Q

Antimicrobial prophylaxis for Gonorrhea

A

Ceftriaxone

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4
Q

Antimicrobial prophylaxis for Meningococcal infection

A

Rifampin (DOC), minocycline

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5
Q

Antimicrobial prophylaxis for PCP

A

TMP-SMZ (DOC), aerosolized pentamidine

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6
Q

Antimicrobial prophylaxis for Syphilis

A

Benzathine penicillin G

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7
Q

Are Aminoglycosides Teratogenic?

A

Yes

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8
Q

Are Ampicillin and Amoxicillin penicillinase resistant?

A

No

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9
Q

Are Carbenicillin, Piperacillin, and Ticarcillin penicillinase resistant?

A

No

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10
Q

Are Cephalosporins resistant to penicillinase?

A

No, but they are less susceptible than the other Beta lactams

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11
Q

Are Methicillin, Nafcillin, and Dicloxacillin penicillinase resistant?

A

Yes

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12
Q

Clinical use of Isoniazid (INH)?

A

Mycobacterium tuberculosis, the only agent used as solo prophylaxis against TB

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13
Q

Common side effects associated with Clindamycin include?

A

Pseudomembranous colitis (C. difficile), fever, diarrhea

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14
Q

Common toxicities associated with Fluoroquinolones?

A

GI upset, Superinfections, Skin rashes, Headache, Dizziness

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15
Q

Common toxicities associated with Griseofulvin?

A

Teratogenic, Carcinogenic, Confusion, Headaches

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16
Q

Describe the MOA of Interferons (INF)

A

Glycoproteins from leukocytes that block various stages of viral RNA and DNA synthesis

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17
Q

Do Tetracyclines penetrate the CNS?

A

Only in limited amounts

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18
Q

Does Ampicillin or Amoxicillin have a greater oral bioavailability?

A

AmOxicillin has greater Oral bioavailability

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19
Q

Does Amprotericin B cross the BBB?

A

No

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20
Q

Does Foscarnet require activation by a viral kinase?

A

No

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21
Q

Foscarnet toxicity?

A

Nephrotoxicity

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22
Q

Ganciclovir associated toxicities?

A

Leukopenia, Neutropenia, Thrombocytopenia, Renal toxicity

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23
Q

How are Interferons (INF) used clinically?

A

Chronic Hepatitis A and B, Kaposi’s Sarcoma

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24
Q

How are Sulfonamides employed clinically?

A

Gram +, Gram -, Norcardia, Chlamydia

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25
Q

How are the HIV drugs used clinically?

A

Triple Therapy’ 2 Nucleoside RT Inhibitors with a Protease Inhibitor

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26
Q

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

A

Primaquine

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27
Q

How can Isoniazid (INH)-induced neurotoxicity be prevented?

A

Pyridoxine (B6) administration

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28
Q

How can the t1/2 of INH be altered?

A

Fast vs. Slow Acetylators

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29
Q

How can the toxic effects of TMP be ameliorated?

A

With supplemental Folic Acid

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30
Q

How can Vancomycin-induced ‘Red Man Syndrome’ be prevented?

A

Pretreat with antihistamines and a slow infusion rate

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31
Q

How do Sulfonamides act on bacteria?

A

As PABA antimetabolites that inhibit Dihydropteroate Synthase, Bacteriostatic

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32
Q

How do the Protease Inhibitors work?

A

Inhibt Assembly of new virus by Blocking Protease Enzyme

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33
Q

How does Ganciclovir’s toxicity relate to that of Acyclovir?

A

Ganciclovir is more toxic to host enzymes

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34
Q

How does resistance to Vancomycin occur?

A

With an amino acid change of D-ala D-ala to D-ala D-lac

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35
Q

How is Acyclovir used clinically?

A

HSV, VZV, EBV, Mucocutaneous and Genital Herpes Lesions, Prophylaxis in Immunocompromised pts

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36
Q

How is Amantadine used clinically?

A

Prophylaxis for Influenza A, Rubella; Parkinson’s disease

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37
Q

How is Amphotericin B administered for fungal meningitis?

A

Intrathecally

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38
Q

How is Amphotericin B used clinically?

A

Wide spectrum of systemic mycoses: Cryptococcus, Blastomyces, Coccidioides, Aspergillus, Histoplasma, Candida, Mucor

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39
Q

How is Chloramphenical used clinically?

A

Meningitis (H. influenza, N. meningitidis, S. pneumoniae), Conserative treatment due to toxicities

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40
Q

How is Foscarnet used clinically?

A

CMV Retinitis in IC pts when Ganciclovir fails

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41
Q

How is Ganciclovir activated?

A

Phosphorylation by a Viral Kinase

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42
Q

How is Ganciclovir used clinically?

A

CMV, esp in Immunocompromised patients

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43
Q

How is Griseofulvin used clinically?

A

Oral treatment of superficial infections; T.capitis

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44
Q

How is Leishmaniasis treated?

A

Pentavalent Antimony

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45
Q

How is Ribavirin used clinically?

A

for RSV

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46
Q

How is Rifampin used clinically?

A
  1. Mycobacterium tuberculosis 2. Delays resistance to Dapsone when used of Leprosy 3. Used in combination with other drugs
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47
Q

How is Trimethoprim used clinically?

A

Used in combination therapy with SMZ to sequentially block folate synthesis

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48
Q

How is Vancomycin used clinically?

A

For serious, Gram + multidrug-resistant organisms

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49
Q

How would you treat African Trypanosomiasis (sleeping sickness)?

A

Suramin

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50
Q

In what population does Gray Baby Syndrome occur? Why?

A

Premature infants, because they lack UDP-glucuronyl transferase

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51
Q

Is Aztreonam cross-allergenic with penicillins?

A

No

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52
Q

Is Aztreonam resistant to penicillinase?

A

Yes

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53
Q

Is Aztreonam usually toxic?

A

No

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54
Q

Is Imipenem resistant to penicillinase?

A

Yes

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55
Q

Is Penicillin penicillinase resistant?

A

No - duh

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56
Q

IV Penicillin

A

Penicillin-G

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57
Q

Mnemonic for Foscarnet?

A

Foscarnet = pyroFosphate analog

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58
Q

MOA for Penicillin (3 answers)?

A

1)Binds penicillin-binding proteins 2) Blocks transpeptidase cross- linking of cell wall 3) Activates autolytic enzymes

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59
Q

MOA: Bactericidal antibiotics

A

Penicillin, Cephalosporins, Vancomycin, Aminoglycosides, Fluoroquinolones, Metronidazole

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60
Q

MOA: Block cell wall synthesis by inhib. Peptidoglycan cross-linking (7)

A

Penicillin, Ampicillin, Ticarcillin, Pipercillin, Imipenem, Aztreonam, Cephalosporins

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61
Q

MOA: Block DNA topoisomerases

A

Quinolones

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62
Q

MOA: Block mRNA synthesis

A

Rifampin

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63
Q

MOA: Block nucleotide synthesis

A

Sulfonamides, Trimethoprim

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64
Q

MOA: Block peptidoglycan synthesis

A

Bacitracin, Vancomycin

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65
Q

MOA: Block protein synthesis at 30s subunit

A

Aminoglycosides, Tetracyclines

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66
Q

MOA: Block protein synthesis at 50s subunit

A

Chloramphenicol, Erythromycin/macrolides, Lincomycin, Clindamycin, Streptogramins (quinupristin, dalfopristin)

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67
Q

MOA: Disrupt bacterial/fungal cell membranes

A

Polymyxins

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68
Q

MOA: Disrupt fungal cell membranes

A

Amphotericin B, Nystatin, Fluconazole/azoles

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69
Q

Name common Polymyxins

A

Polymyxin B, Polymyxin E

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70
Q

Name several common Macrolides (3)

A

Erythromycin, Azithromycin, Clarithromycin

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71
Q

Name some common Sulfonamides (4)

A

Sulfamethoxazole (SMZ), Sulfisoxazole, Triple sulfas, Sulfadiazine

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72
Q

Name some common Tetracyclines (4)

A

Tetracycline, Doxycycline, Demeclocycline, Minocycline

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73
Q

Name the common Aminoglycosides (5)

A

Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin

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74
Q

Name the common Azoles

A

Fluconazole, Ketoconazole, Clotrimazole, Miconazole, Itraconazole

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75
Q

Name the common Fluoroquinolones (6)

A

Ciprofloxacin, Norfloxacin, Ofloxacin, Grepafloxacin, Enoxacin, Nalidixic acid

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76
Q

Name the common Non-Nucleoside Reverse Transcriptase Inhibitors

A

Nevirapine, Delavirdine

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77
Q

Name the common Nucleoside Reverse Transcriptase Inhibitors

A

Zidovudine (AZT), Didanosine (ddI), Zalcitabine (ddC), Stavudine (d4T), Lamivudine (3TC)

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78
Q

Name the Protease Inhibitors (4)

A

Saquinavir, Ritonavir, Indinavir, Nelfinavir

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79
Q

Name two classes of drugs for HIV therapy

A

Protease Inhibitors and Reverse Transcriptase Inhibitors

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80
Q

Name two organisms Vancomycin is commonly used for?

A

Staphlococcus aureus and Clostridium difficile (pseudomembranous colitis)

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81
Q

Oral Penicillin

A

Penicillin-V

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82
Q

Resistance mechanisms for Aminoglycosides

A

Modification via Acetylation, Adenylation, or Phosphorylation

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83
Q

Resistance mechanisms for Cephalosporins/Penicillins

A

Beta-lactamase cleavage of Beta-lactam ring

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84
Q

Resistance mechanisms for Chloramphenicol

A

Modification via Acetylation

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85
Q

Resistance mechanisms for Macrolides

A

Methylation of rRNA near Erythromycin’s ribosome binding site

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86
Q

Resistance mechanisms for Sulfonamides

A

Altered bacterial Dihydropteroate Synthetase, Decreased uptake, or Increased PABA synthesis

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87
Q

Resistance mechanisms for Tetracycline

A

Decreased uptake or Increased transport out of cell

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88
Q

Resistance mechanisms for Vancomycin

A

Terminal D-ala of cell wall replaced with D-lac; Decreased affinity

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89
Q

Side effects of Isoniazid (INH)?

A

Hemolysis (if G6PD deficient), Neurotoxicity, Hepatotoxicity, SLE-like syndrome

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90
Q

Specifically, how does Foscarnet inhibit viral DNA pol?

A

Binds to the Pyrophosphate Binding Site of the enzyme

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91
Q

The MOA for Chloramphenicol is?

A

Inhibition of 50S peptidyl transferase, Bacteriostatic

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92
Q

Toxic effects of TMP include?

A

Megaloblastic anemia, Leukopenia, Granulocytopenia

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93
Q

Toxic side effects of the Azoles?

A

Hormone synthesis inhibition (Gynecomastia), Liver dysfunction (Inhibits CYP450), Fever, Chills

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94
Q

Toxicities associated with Acyclovir?

A

Delirium, Tremor, Nephrotoxicity

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95
Q

What additional side effects exist for Ampicillin?

A

Rash, Pseudomembranous colitis

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96
Q

What antimicrobial class is Aztreonam syngergestic with?

A

Aminoglycosides

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97
Q

What are Amantadine-associated side effects?

A

Ataxia, Dizziness, Slurred speech

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98
Q

What are Aminoglycosides synergistic with?

A

Beta-lactam antibiotics

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99
Q

What are Aminoglycosides used for clinically?

A

Severe Gram - rod infections.

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100
Q

What are common serious side effects of Aminoglycosides and what are these associated with?

A

Nephrotoxicity (esp. with Cephalosporins), Ototoxicity (esp. with Loop Diuretics)

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101
Q

What are common side effects of Amphotericin B?

A

Fever/Chills, Hypotension, Nephrotoxicity, Arrhythmias

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102
Q

What are common side effects of Protease Inhibitors?

A

GI intolerance (nausea, diarrhea), Hyperglycemia, Lipid abnormalities, Thrombocytopenia (Indinavir)

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103
Q

What are common side effects of RT Inhibitors?

A

BM suppression (neutropenia, anemia), Peripheral neuropathy

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104
Q

What are common toxic side effects of Sulfonamides? (5)

A

NAME?

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105
Q

What are common toxicities associated with Macrolides? (4)

A

GI discomfort, Acute cholestatic hepatitis, Eosinophilia, Skin rashes

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106
Q

What are common toxicities associated with Tetracyclines?

A

GI distress, Tooth discoloration and Inhibition of bone growth in children, Fanconi’s syndrome, Photosensitivity

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107
Q

What are common toxicities related to Vancomycin therapy?

A

Well tolerated in general but occasionally, Nephrotoxicity, Ototoxicity, Thrombophlebitis, diffuse flushing=’Red Man Syndrome’

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108
Q

What are Fluoroquinolones indicated for? (3)

A

1.Gram - rods of the Urinary and GI tracts (including Pseudomonas) 2.Neisseria 3. Some Gram + organisms

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109
Q

What are major side effects of Methicillin, Nafcillin, and Dicloxacillin?

A

Hypersensitivity reactions

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110
Q

What are Methicillin, Nafcillin, and Dicloxacillin used for clinically?

A

Staphlococcus aureus

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111
Q

What are Polymyxins used for?

A

Resistant Gram - infections

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112
Q

What are the Anti-TB drugs?

A

Rifampin, Ethambutol, Streptomycin, Pyrazinamide, Isoniazid (INH)

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113
Q

What are the clinical indications for Azole therapy?

A

Systemic mycoses

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114
Q

What are the clinical uses for 1st Generation Cephalosporins?

A

Gram + cocci, Proteus mirabilis, E. coli, Klebsiella pneumoniae (PEcK)

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115
Q

What are the clinical uses for 2nd Generation Cephalosporins?

A

Gram + cocci, Haemophilus influenza, Enterobacter aerogenes, Neisseria species, P. mirabilis, E. coli, K. pneumoniae, Serratia marcescens ( HEN PEcKS )

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116
Q

What are the clinical uses for 3rd Generation Cephalosporins?

A

1) Serious Gram - infections resistant to other Beta lactams 2) Meningitis (most penetrate the BBB)

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117
Q

What are the clinical uses for Aztreonam?

A

Gram - rods: Klebsiella species, Pseudomonas species, Serratia species

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118
Q

What are the clinical uses for Imipenem/cilastatin?

A

Gram + cocci, Gram - rods, and Anerobes

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119
Q

What are the Macrolides used for clinically?

A

NAME?

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120
Q

What are the major structural differences between Penicillin and Cephalosporin?

A

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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121
Q

What are the major toxic side effects of Imipenem/cilastatin?

A

GI distress, Skin rash, and Seizures at high plasma levels

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122
Q

What are the major toxic side effects of the Cephalosporins?

A

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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123
Q

What are the side effects of Polymyxins?

A

Neurotoxicity, Acute renal tubular necrosis

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124
Q

What are the side effects of Rifampin?

A

Minor hepatotoxicity, Drug interactions (activates P450)

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125
Q

What are toxic side effects for Metronidazole?

A

Disulfiram-like reaction with EtOH, Headache

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126
Q

What are toxicities associated with Chloramphenicol?

A

Aplastic anemia (dose independent), Gray Baby Syndrome

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127
Q

What conditions are treated with Metronidazole?

A

Giardiasis, Amoebic dysentery (E. histolytica), Bacterial vaginitis (Gardnerella vaginalis), Trichomonas

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128
Q

What do Aminoglycosides require for uptake?

A

Oxygen

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129
Q

What do you treat Nematode/roundworm (pinworm, whipworm) infections with?

A

Mebendazole/Thiabendazole, Pyrantel Pamoate

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130
Q

What drug is given for Pneumocystis carinii prophylaxis?

A

Pentamidine

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131
Q

What drug is used during the pregnancy of an HIV+ mother?, Why?

A

AZT, to reduce risk of Fetal Transmission

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132
Q

What drug is used to treat Trematode/fluke (e.g., Schistosomes, Paragonimus, Clonorchis) or Cysticercosis

A

Praziquantel

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133
Q

What is a common drug interaction associated with Griseofulvin?

A

Increases coumadin metabolism

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134
Q

What is a mnemonic to remember Amantadine’s function?

A

Blocks Influenza A and RubellA; causes problems with the cerebellA

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135
Q

What is a prerequisite for Acyclovir activation?

A

It must be Phosphorylated by Viral Thymidine Kinase

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136
Q

What is a Ribavirin toxicity?

A

Hemolytic anemia

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137
Q

What is an acronym to remember Anti-TB drugs?

A

RESPIre

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138
Q

What is an additional side effect of Methicillin?

A

Interstitial nephritis

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139
Q

What is an occasional side effect of Aztreonam?

A

GI upset

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140
Q

What is Clindamycin used for clinically?

A

Anaerobic infections (e.g., B. fragilis, C. perfringens)

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141
Q

What is clinical use for Carbenicillin, Piperacillin, and Ticarcillin?

A

Pseudomonas species and Gram - rods

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142
Q

What is combination TMP-SMZ used to treat?

A

Recurrent UTIs, Shigella, Salmonella, Pneumocystis carinii pneumonia

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143
Q

What is combined with Ampicillin, Amoxicillin, Carbenicillin, Piperacillin, and Ticarcillin to enhance their spectrum?

A

Clavulanic acid

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144
Q

What is Fluconazole specifically used for?

A

Cryptococcal meningitis in AIDS patients and Candidal infections of all types

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145
Q

What is Imipenem always administered with?

A

Cilastatin

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146
Q

What is Ketoconazole specifically used for?

A

Blastomyces, Coccidioides, Histoplasma, C. albicans; Hypercortisolism

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147
Q

What is Metronidazole combined with for ‘triple therapy’? Against what organism?

A

Bismuth and Amoxicillin or Tetracycline; against Helobacter pylori

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148
Q

What is Metronidazole used for clinically?

A

Antiprotozoal: Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis Anaerobes: Bacteroides, Clostridium

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149
Q

What is Niclosamide used for?

A

Cestode/tapeworm (e.g., D. latum, Taenia species Except Cysticercosis

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150
Q

What is Nifurtimox administered for?

A

Chagas’ disease, American Trypanosomiasis (Trypanosoma cruzi)

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151
Q

What is the chemical name for Ganciclovir?

A

DHPG (dihydroxy-2-propoxymethyl guanine)

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152
Q

What is the clinical use for Ampicillin and Amoxicillin?

A

Extended spectrum penicillin: certain Gram + bacteria and Gram - rods

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153
Q

What is the clinical use for Nystatin?

A

Topical and Oral, for Oral Candidiasis (Thrush)

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154
Q

What is the clinical use for Penicillin?

A

Bactericidal for: Gram + rod and cocci, Gram - cocci, and Spirochetes

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155
Q

What is the major side effect for Ampicillin and Amoxicillin?

A

Hypersensitivity reactions

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156
Q

What is the major side effect for Carbenicillin, Piperacillin, and Ticarcillin?

A

Hypersensitivity reactions

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157
Q

What is the major toxic side effect of Penicillin?

A

Hypersensitivity reactions

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158
Q

What is the memory aid for subunit distribution of ribosomal inhibitors?

A

Buy AT 30, CELL at 50’

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159
Q

What is the memory key for Isoniazid (INH) toxicity?

A

INH: Injures Neurons and Hepatocytes

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160
Q

What is the memory key for Metronidazole’s clinical uses?

A

GET on the Metro

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161
Q

What is the memory key for organisms treated with Tetracyclines?

A

VACUUM your Bed Room’

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162
Q

What is the memory key involving the ‘4 R’s of Rifampin?’

A
  1. RNA pol inhibitor 2. Revs up P450 3. Red/orange body fluids 4. Rapid resistance if used alone
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163
Q

What is the MOA for Acyclovir?

A

Inhibit viral DNA polymerase

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164
Q

What is the MOA for Amphotericin B?

A

Binds Ergosterol, forms Membrane Pores that Disrupt Homeostatis

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165
Q

What is the MOA for Ampicillin and Amoxicillin?

A

Same as penicillin. Extended spectrum antibiotics

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166
Q

What is the MOA for Carbenicillin, Piperacillin, and Ticarcillin?

A

Same as penicillin. Extended spectrum antibiotics

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167
Q

What is the MOA for Clindamycin?

A

Blocks Peptide Bond formation at the 50S subunit, Bacteriostatic

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168
Q

What is the MOA for Methicillin, Nafcillin, and Dicloxacillin?

A

Same as penicillin. Act as narrow spectrum antibiotics

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169
Q

What is the MOA for Metronidazole?

A

Forms toxic metabolites in the bacterial cell, Bactericidal

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170
Q

What is the MOA for Nystatin?

A

Binds ergosterol, Disrupts fungal membranes

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171
Q

What is the MOA for Rifampin?

A

Inhibits DNA dependent RNA polymerase

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172
Q

What is the MOA for the Aminoglycosides?

A

Inhibits formation of Initiation Complex, causes misreading of mRNA, Bactericidal

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173
Q

What is the MOA for the Azoles?

A

Inhibit Ergosterol synthesis

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174
Q

What is the MOA for the Cephalosporins?

A

Beta lactams - inhibit cell wall synthesis, Bactericidal

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175
Q

What is the MOA for the Fluoroquinolones?

A

Inhibit DNA Gyrase (topoisomerase II), Bactericidal

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176
Q

What is the MOA for the Macrolides?

A

Blocks translocation, binds to the 23S rRNA of the 50S subunit, Bacteriostatic

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177
Q

What is the MOA for the Tetracyclines?

A

Binds 30S subunit and prevents attachment of aminoacyl-tRNA, Bacteriostatic

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178
Q

What is the MOA for Trimethoprim (TMP)?

A

Inhibits bacterial Dihydrofolate Reductase, Bacteriostatic

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179
Q

What is the MOA for Vancomycin?

A

Inhibits cell wall mucopeptide formation, Bactericidal

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180
Q

What is the MOA of Amantadine?

A

Blocks viral penetration/uncoating; may act to buffer the pH of the endosome

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181
Q

What is the MOA of Aztreonam?

A

Inhibits cell wall synthesis ( binds to PBP3). A monobactam

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182
Q

What is the MOA of Foscarnet?

A

Inhibits Viral DNA polymerase

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183
Q

What is the MOA of Ganciclovir?

A

Inhibits CMV DNA polymerase

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184
Q

What is the MOA of Griseofulvin?

A

Interferes with microtubule function, disrupts mitosis, inhibits growth

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185
Q

What is the MOA of Imipenem?

A

Acts as a wide spectrum carbapenem

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186
Q

What is the MOA of Isoniazid (INH)?

A

Decreases synthesis of Mycolic Acid

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187
Q

What is the MOA of Polymyxins?

A

Bind cell membrane, disrupt osmotic properties, Are Cationc, Basic and act as detergents

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188
Q

What is the MOA of Ribavirin?

A

Inhibits IMP Dehydrogenase (competitively), and therefore blocks Guanine Nucleotide synthesis

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189
Q

What is the MOA of the RT Inhibitors?

A

Inhibit RT of HIV and prevent the incorporation of viral genome into the host DNA

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190
Q

What is the most common cause of Pt noncompliance with Macrolides?

A

GI discomfort

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191
Q

What is treated with Chloroquine, Quinine, Mefloquine?

A

Malaria (P. falciparum)

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192
Q

What microorganisms are Aminoglycosides ineffective against?

A

Anaerobes

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193
Q

What microorganisms are clinical indications for Tetracycline therapy?

A

Vibrio cholerae Acne Chlamydia Ureaplasma Urealyticum Mycoplasma pneumoniae Borrelia burgdorferi (Lyme’s) Rickettsia Tularemia

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194
Q

What microorganisms is Aztreonam not effective against?

A

Gram + and Anerobes

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195
Q

What musculo-skeletal side effects in Adults are associated with Floroquinolones?

A

Tendonitis and Tendon rupture

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196
Q

What neurotransmitter does Amantadine affect? How does it influence this NT?

A

Dopamine; causes its release from intact nerve terminals

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197
Q

What organism is Imipenem/cilastatin the Drug of Choice for?

A

Enterobacter

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198
Q

What organisms does Griseofulvin target?

A

Dermatophytes (tinea, ringworm)

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199
Q

What parasites are treated with Pyrantel Pamoate (more specific)?

A

Giant Roundworm (Ascaris), Hookworm (Necator/Ancylostoma), Pinworm (Enterobius)

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200
Q

What parasitic condition is treated with Ivermectin?

A

Onchocerciasis (‘river blindness’–rIVER-mectin)

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201
Q

What populations are Floroquinolones contraindicated in? Why?

A

Pregnant women, Children; because animal studies show Damage to Cartilage

202
Q

What should not be taken with Tetracyclines? / Why?

A

Milk or Antacids, because divalent cations inhibit Tetracycline absorption in the gut

203
Q

What Sulfonamides are used for simple UTIs?

A

Triple sulfas or SMZ

204
Q

When is HIV therapy initiated?

A

When pts have Low CD4+ (

205
Q

When is Rifampin not used in combination with other drugs?

A
  1. Meningococcal carrier state 2. Chemoprophylaxis in contacts of children with H. influenzae type B
206
Q

Where does Griseofulvin deposit?

A

Keratin containing tissues, e.g., nails

207
Q

Which Aminoglycoside is used for Bowel Surgery ?

A

Neomycin

208
Q

Which antimicrobial classes inhibit protein synthesis at the 30S subunit? (2)

A

1) Aminoglycosides = bactericidal 2) Tetracyclines = bacteriostatic

209
Q

Which antimicrobials inhibit protein synthesis at the 50S subunit? (4)

A

1) Chloramphenical = bacteriostatic 2) Erythromycin = bacteriostatic 3) Lincomycin = bacteriostatic 4)cLindamycin = bacteriostatic

210
Q

Which individuals are predisposed to Sulfonamide-induced hemolysis?

A

G6PD deficient individuals

211
Q

Which RT inhibitor causes Megaloblastic Anemia?

A

AZT

212
Q

Which RT inhibitors cause a Rash?

A

Non-Nucleosides

213
Q

Which RT inhibitors cause Lactic Acidosis?

A

Nucleosides

214
Q

Which Tetracycline is used in patients with renal failure? / Why?

A

Doxycycline, because it is fecally eliminated

215
Q

Why are Methicillin, Nafcillin, and Dicloxacillin penicillinase resistant?

A

Due to the presence of a bulkier R group

216
Q

Why is Cilastatin administered with Imipenem?

A

To inhibit renal Dihydropeptidase I and decrease Imipenem inactivation in the renal tubules

217
Q

List the mechanism, clinical use, & toxicity of 5 FU.

A

-S-phase anti-metabolite Pyr analogue -Colon, solid tumors, & BCC/ -Irreversible myelosuppression

218
Q

List the mechanism, clinical use, & toxicity of 6 MP.

A

-inhibits HGPRT (pur. Syn.) - Luk, Lymph,

219
Q

List the mechanism, clinical use, & toxicity of Bleomycin.

A

DNA intercalator -testicular & lymphomas -Pulmonary fibrosis mild myelosuppression.

220
Q

List the mechanism, clinical use, & toxicity of Busulfan.

A

Alkalates DNA -CML -Pulmonary fibrosis hyperpigmentation

221
Q

List the mechanism, clinical use, & toxicity of Cisplatin.

A

-Alkalating agent -testicular,bladder,ovary,& lung -Nephrotoxicity & CN VIII damage.

222
Q

List the mechanism, clinical use, & toxicity of Cyclophosphamide.

A

-Alkalating agent -NHL, Breast, ovary, & lung. - Myelosuppression, & hemorrhagic cystitis.

223
Q

List the mechanism, clinical use, & toxicity of Doxorubicin.

A

-DNA intercalator -Hodgkin’s, myeloma, sarcoma, and solid tumors -Cardiotoxicity & alopecia

224
Q

List the mechanism, clinical use, & toxicity of Etoposide.

A

-Topo II inhibitor(GII specific) -Oat cell of Lung & prostate, & testicular -Myelosuppression & GI irritation.

225
Q

List the mechanism, clinical use, & toxicity of Methotrexate.

A

-S-phase anti-metabolite folate analogue -Luk, Lymp, sarc, RA, & psoriasis / -Reversible myelosuppression

226
Q

List the mechanism, clinical use, & toxicity of Nitrosureas.

A

Alkalate DNA -Brain tumors -CNS toxicity

227
Q

List the mechanism, clinical use, & toxicity of Paclitaxel.

A

MT polymerization stabilizer -Ovarian & breast CA -Myelosupperession & hypersensitivity.

228
Q

List the mechanism, clinical use, & toxicity of Prednisone.

A

-Triggers apoptosis -CLL, Hodgkin’s in MOPP -Cushing-like syndrome

229
Q

List the mechanism, clinical use, & toxicity of Tamoxifen.

A

Estrogen receptor antagonist -Breast CA -increased endometrial CA risk

230
Q

List the mechanism, clinical use, & toxicity of Vincristine.

A

-MT polymerization inhibitor(M phase) -MOPP, lymphoma, Willm’s & choriocarcinoma -neurotoxicity and myelosuppression

231
Q

Which cancer drugs effect nuclear DNA (4)?

A

Alkalating agents+cisplatin -Doxorubicin+Dactinomycin -Bleomycin -Etoposide

232
Q

Which cancer drugs inhibit nucleotide synthesis(3)?

A
  • Methotrexate - 5 FU - 6 mercaptopurine
233
Q

Which cancer drugs work at the level of mRNA(2)?

A

Steroids -Tamoxifen

234
Q

Which cancer drugs work at the level of proteins(2)?

A

Vinca alkaloids(inhibit MT) -Paclitaxel

235
Q

ACE inhibitors- clinical use?

A

hypertension, CHF, diabetic renal disease

236
Q

ACE inhibitors- mechanism?

A

reduce levels of Angiotensin II, thereby preventing the inactivation of bradykinin (a potent vasodilator); renin level is increased

237
Q

ACE inhibitors- toxicity?

A

fetal renal damage, hyperkalemia, Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems, Rash, Increased renin, Lower Angiotensin II (CAPTOPRIL)

238
Q

Acetazolamide- clinical uses?

A

glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness

239
Q

Acetazolamide- mechanism?

A

acts at the proximal convoluted tubule to inhibit carbonic anhydrase. Causes self-limited sodium bicarb diuresis and reduction of total body bicarb stores.

240
Q

acetazolamide- site of action?

A

proximal convoluted tubule

241
Q

Acetazolamide- toxicity?

A

hyperchloremic metabolic acidosis, neuropathy, NH3 toxicity, sulfa allergy

242
Q

Acetazolamide causes?

A

ACIDazolamide’ causes acidosis

243
Q

Adenosine- clinical use?

A

DOC in diagnosing and abolishing AV nodal arrhythmias

244
Q

ADH antagonists- site of action?

A

collecting ducts

245
Q

adverse effect of Nitroprusside?

A

cyanide toxicity (releases CN)

246
Q

adverse effects of beta-blockers?

A

impotence, asthma, CV effects (bradycardia, CHF, AV block), CNS effects (sedation, sleep alterations)

247
Q

adverse effects of Captopril?

A

fetal renal toxicity, hyperkalemia, Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems, Rash, Increased renin, Lower Angiotensin II (CAPTOPRIL)

248
Q

adverse effects of Clonidine?

A

dry mouth, sedation, severe rebound hypertension

249
Q

adverse effects of ganglionic blockers?

A

severe orthostatic hypotension, blurred vision, constipation, sexual dysfunction

250
Q

adverse effects of Guanethidine?

A

orthostatic and exercise hypotension, sexual dysfunction, diarrhea

251
Q

adverse effects of Hydralazine?

A

nausea, headache, lupus-like syndrome, reflex tachycardia, angina, salt retention

252
Q

adverse effects of Hydrochlorothiazide?

A

hypokalemia, slight hyperlipidemia, hyperuricemia, lassitude, hypercalcemia, hyperglycemia

253
Q

adverse effects of Loop Diuretics?

A

K+ wasting, metabolic alkalosis, hypotension, ototoxicity

254
Q

adverse effects of Losartan?

A

fetal renal toxicity, hyperkalemia

255
Q

adverse effects of Methyldopa?

A

sedation, positive Coombs’ test

256
Q

adverse effects of Minoxidil?

A

hypertrichosis, pericardial effusion, reflex tachycardia, angina, salt retention

257
Q

adverse effects of Nifedipine, verapamil?

A

dizziness, flushing, constipation (verapamil), nausea

258
Q

adverse effects of Prazosin?

A

first dose orthostatic hypotension, dizziness, headache

259
Q

adverse effects of Reserpine?

A

sedation, depression, nasal stuffiness, diarrhea

260
Q

Amiodarone- toxicity?

A

pulmonary fibrosis, corneal deposits, hepatotoxicity, skin deposits resulting in photodermatitis, neurologic effects, consitpation, CV (bradycardia, heart block, CHF), and hypo- or hyperthyroidism.

261
Q

Beta Blockers- CNS toxicity?

A

sedation, sleep alterations

262
Q

Beta Blockers- CV toxicity?

A

bradycardia, AV block, CHF

263
Q

Beta Blockers- site of action?

A

Beta adrenergic receptors and Ca2+ channels (stimulatory)

264
Q

Beta Blockers- BP?

A

decrease

265
Q

Bretyllium- toxicity?

A

new arrhythmias, hypotension

266
Q

Ca2+ channel blockers- clinical use?

A

hypertension, angina, arrhythmias

267
Q

Ca2+ channel blockers- mechanism?

A

block voltage dependent L-type Ca2+ channels of cardiac and smooth muscle- decreasing contractility

268
Q

Ca2+ channel blockers- site of action?

A

Cell membrane Ca2+ channels of cardiac sarcomere

269
Q

Ca2+ channel blockers- toxicity?

A

cardiac depression, peripheral edema, flushing, dizziness, constipation

270
Q

Ca2+ sensitizers’- site of action?

A

troponin-tropomyosin system

271
Q

Cautions when using Amiodarone?

A

check PFTs, LFTs, and TFTs

272
Q

Antiarrhythmic class IA effects?

A

increased AP duration, increased ERP increased QT interval. Atrial and ventricular.

273
Q

Antiarrhythmic class IB- clinical uses?

A

post MI and digitalis induced arrhythmias

274
Q

Antiarrhythmic class IB- effects?

A

decrease AP duration, affects ischemic or depolarized Purkinje and ventricular system

275
Q

Antiarrhythmic class IB- toxicity?

A

local anesthetic. CNS stimulation or depression. CV depression.

276
Q

Antiarrhythmic class IC- effects?

A

NO AP duration effect. useful in V-tach that progresses to V-fib and in intractable SVT LAST RESORT

277
Q

Antiarrhythmic class IC- toxicity?

A

proarrhythmic

278
Q

Antiarrhythmic class II- effects?

A

decrease the slope of phase 4, increase PR interval (the AV node is particularly sensitive)

279
Q

Antiarrhythmic class II- mechanism?

A

blocking the beta adrenergic receptor leads to decreased cAMP, and decreased Ca2+ flux

280
Q

Antiarrhythmic class II- toxicity?

A

impotence, exacerbation of asthma, CV effects, CNS effects, may mask hypoclycemia

281
Q

Antiarrhythmic Class III- effects?

A

increase AP duration, increase ERP, increase QT interval, for use when other arrhythmics fail

282
Q

Antiarrhythmic class IV- clinical use?

A

prevention of nodal arrhythmias (SVT)

283
Q

Antiarrhythmic class IV- effects?

A

decrease conduction velocity, increase ERP, increase PR interval

284
Q

Antiarrhythmic class IV- primary site of action?

A

AV nodal cells

285
Q

Antiarrhythmic class IV- toxicity?

A

constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression), and torsade de pointes (Bepridil)

286
Q

classes of antihypertensive drugs?

A

diuretics, sympathoplegics, vasodilators, ACE inhibitors, Angiotensin II receptor inhibitors

287
Q

decrease Digitoxin dose in renal failure?

A

NO

288
Q

decrease Digoxin dose in renal failure?

A

YES

289
Q

Digitalis- site of action?

A

Na/K ATPase

290
Q

Digoxin v. Digitoxin: bioavailability?

A

Digitoxin>95% Digoxin 75%

291
Q

Digoxin v. Digitoxin: excretion?

A

Digoxin=urinary Digitoxin=biliary

292
Q

Digoxin v. Digitoxin: half life?

A

Digitoxin 168hrs Digoxin 40 hrs

293
Q

Digoxin v. Digitoxin: protein binding?

A

Digitoxin 70% Digoxin 20-40%

294
Q

Esmolol- short or long acting?

A

very short acting

295
Q

Ethacrynic Acid- clinical use?

A

Diuresis in pateints with sulfa allergy

296
Q

Ethacrynic Acid- mechanism?

A

not a sulfonamide, but action is the same as furosemide

297
Q

Ethacrynic Acid- toxicity?

A

NO HYPERURICEMIA, NO SULFA ALLERGY; same as furosemide otherwise

298
Q

Furosemide- class and mechanism?

A

Sulfonamide Loop Diuretic. Inhibits ion co-transport system of thick ascending loop. Abolishes hypertonicity of the medulla, thereby preventing concentration of the urine.

299
Q

Furosemide- clinical use?

A

edematous states (CHF, cirrhosis, nephrotic syndrome, pulm edema), HTN, hypercalcemia

300
Q

Furosemide- toxicity? (OH DANG)

A

Ototoxicity, Hypokalemia, Dehydration, Allergy (sulfa), Nephritis (interstitial), Gout

301
Q

Furosemide increases the excretion of what ion?

A

Ca2+ (Loops Lose calcium)

302
Q

how do we stop angina?

A

decrease myocardial O2 consumption by: 1-decreasing end diastolic volume 2- decreasing BP 3- decreasing HR 4-decreasing contractility 5-decreasing ejection time

303
Q

Hydralazine- class and mechanism?

A

vasodilator- increases cGMP to induce smooth muscle relaxation (arterioles>veins; afterload reduction)

304
Q

Hydralazine- clinical use?

A

severe hypertension, CHF

305
Q

Hydralazine- toxicity?

A

compensatory tachycardia, fluid retention, lupus-like syndrome

306
Q

Hydrochlorothiazide- clinical use?

A

HTN, CHF, calcium stone formation, nephrogenic DI.

307
Q

Hydrochlorothiazide- mechanism?

A

Inhibits NaCl reabsorption in the early distal tubule. Decreases Ca2+ excretion.

308
Q

Hydrochlorothiazide- toxicity? (hyperGLUC, plus others)

A

Hypokalemic metabolic alkalosis, hyponatremia, hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia, sulfa allergy.

309
Q

Ibutilide- toxicity?

A

torsade de pointes

310
Q

K+- clinical use?

A

depresses ectopic pacemakers, especially in digoxin toxicity

311
Q

K+ sparing diuretics- clinical use?

A

hyperaldosteronism, K+ depletion, CHF

312
Q

K+ sparing diuretics- site of action?

A

cortical collecting tubule

313
Q

K+ sparing diuretics- toxicity?

A

hyperkalemia, endocrine effects (gynecomastia, anti-androgen)

314
Q

loop diuretics (furosemide)- site of action?

A

thick ascending limb

315
Q

Mannitol- clinical use?

A

ARF, shock, drug overdose, decrease intracranial/intraocular pressure

316
Q

Mannitol- contraindications?

A

anuria, CHF

317
Q

Mannitol- mechanism?

A

osmotic diuretic- increase tubular fluid osmolarity, thereby increasing urine flow

318
Q

mannitol- site of action?

A

proximal convoluted tubule, thin descending limb, and collecting duct

319
Q

Mannitol- toxicity?

A

pulmonary edema, dehydration

320
Q

Mg+- clinical use?

A

effective in torsade de pointes and digoxin toxicity

321
Q

name five Antiarrhythmic drugs in class II?

A

propanolol, esmolol, metoprolol, atenolol, timolol

322
Q

name four HMG-CoA reductase inhibitors.

A

Lovastatin, Pravastatin, Simvastatin, Atorvastatin

323
Q

name four Antiarrhythmic drugs in class IA.

A

Quinidine, Amiodarone, Procainamide, Disopyramide

324
Q

name four Antiarrhythmic drugs in class III.

A

Sotalol, Ibutilide, Bretylium, Amiodarone

325
Q

name three ACE inhibitors?

A

Captopril, Enalapril, Lisinopril

326
Q

name three calcium channel blockers?

A

Nifedipine, Verapamil, Diltiazem

327
Q

name three Antiarrhythmic drugs in class IB.

A

Lidocaine, Mexiletine, Tocainide

328
Q

name three Antiarrhythmic drugs in class IC.

A

Flecainide, Encainide, Propafenone

329
Q

name three Antiarrhythmic drugs in class IV.

A

Verapamil, Diltiazem, Bepridil

330
Q

name three K+ sparing diuretics?

A

Spironolactone, Triamterene, Amiloride (the K+ STAys)

331
Q

name two bile acid resins.

A

cholestyramine, colestipol

332
Q

name two LPL stimulators.

A

Gemfibrozil, Clofibrate

333
Q

Nifedipine has similar action to?

A

Nitrates

334
Q

preferential action of the Ca2+ channel blockers at cardiac muscle?

A

cardiac muscle: Verapamil>Diltiazem>Nifedipine

335
Q

preferential action of the Ca2+ channel blockers at vascular smooth muscle?

A

vascular sm. Mus.: Nifedipine>Diltiazem>Verapamil

336
Q

Procainamide- toxicity?

A

reversible SLE-like syndrome

337
Q

Quinidine- toxicity?

A

cinchonism: HA, tinnitus, thrombocytopenia, torsade de pointes due to increased QT interval

338
Q

Ryanodine- site of action?

A

blocks SR Ca2+ channels

339
Q

Sotalol- toxicity?

A

torsade de pointes, excessive Beta block

340
Q

Spironolactone- mechanism?

A

competitive inhibirot of aldosterone in the cortical collecting tubule

341
Q

thiazides- site of action?

A

distal convoluted tubule (early)

342
Q

Triamterene and amiloride- mechanism?

A

block Na+ channels in the cortical collecting tubule

343
Q

Verapamil has similar action to?

A

Beta Blockers

344
Q

what two vasodilators require simultaneous treatment with beta blockers to prevent reflex tachycardia and diuretics to prevent salt retention?

A

Hydralazine and Minoxidil

345
Q

which diuretics cause acidosis?

A

carbonic anhydrase inhibitors, K+ sparing diuretics

346
Q

which diuretics cause alkalosis?

A

loop diuretics, thiazides

347
Q

which diuretics decrease urine Ca2+?

A

thiazides, amiloride

348
Q

which diuretics increase urine Ca2+?

A

loop diuretics, spironolactone

349
Q

which diuretics increase urine K+?

A

all except the K+ sparing diuretics Spironolactone, Triamterene, Amiloride

350
Q

which diuretics increase urine NaCl?

A

all of them

351
Q

Acetaminophen has what two clinical uses and lacks what one clinical use of the NSAIDs?

A

Acetaminophen has antipyretic and analgesic properties, but lacks anti-inflammatory properties.

352
Q

Can Heparin be used during pregnancy?

A

Yes, it does not cross the placenta.

353
Q

Can Warfarin be used during pregnancy?

A

No, warfarin, unlike heparin, can cross the placenta.

354
Q

Does Heparin have a long, medium, or short half life?

A

Short.

355
Q

Does Warfarin have a long, medium, or short half life?

A

Long.

356
Q

For Heparin what is the Structure

A

Large anionic polymer, acidic

357
Q

For Heparin what is the Route of administration

A

Paranteral (IV, SC)

358
Q

For Heparin what is the Onset of action

A

Rapid (seconds)

359
Q

For Heparin what is the Mechanism of action

A

Activates antithrombin III

360
Q

For Heparin what is the Duration of action

A

Acute (hours)

361
Q

For Heparin what is the Ability to inhibit coagulation in vitro

A

Yes

362
Q

For Heparin what is the Treatment for overdose

A

Protamine sulfate

363
Q

For Heparin what is the Lab value to monitor

A

aPTT (intrinsic pathway)

364
Q

For Heparin what is the Site of action

A

Blood

365
Q

For Warfarin what is the Structure

A

Small lipid-soluble molecule

366
Q

For Warfarin what is the Route of administration

A

Oral

367
Q

For Warfarin what is the Onset of action

A

Slow, limited by half lives of clotting factors

368
Q

For Warfarin what is the Mechanism of action

A

Impairs the synthesis of vitamin K-dependent clotting factors

369
Q

For Warfarin what is the Duration of action

A

Chronic (weeks or months)

370
Q

For Warfarin what is the Ability to inhibit coagulation in vitro

A

No

371
Q

For Warfarin what is the Treatment for overdose

A

IV vitamin K and fresh frozen plasma

372
Q

For Warfarin what is the Lab value to monitor

A

PT

373
Q

For Warfarin what is the Site of action

A

Liver

374
Q

Is toxicity rare or common whith Cromolyn used in Asthma prevention?

A

Rare.

375
Q

List five common glucocorticoids.

A
  1. Hydrocortisone 2. Predisone 3. Triamcinolone 4. Dexamethasone 5. Beclomethasone
376
Q

Secretion of what drug is inhibited by Probenacid used to treat chronic gout?

A

Penicillin.

377
Q

The COX-2 inhibitors (celecoxib, rofecoxib) have similar side effects to the NSAIDs with what one exception?

A

The COX-2 inhibitors should not have the corrosive effects of other NSAIDs on the gastrointestinal lining.

378
Q

What are are the Sulfonylureas (general description) and what is their use?

A

Sulfonylureas are oral hypoglycemic agents, they are used to stimulate release of endogenous insulin in NIDDM (type-2).

379
Q

What are five advantages of Oral Contraceptives (synthetic progestins, estrogen)?

A
  1. Reliable (
380
Q

What are five disadvantages of Oral Contraceptives (synthetic progestins, estrogen)?

A
  1. Taken daily 2. No protection against STDs 3. Raises triglycerides 4. Depression, weight gain, nausea, HTN 5. Hypercoagulable state
381
Q

What are five possible toxic effects of Aspirin therapy?

A
  1. Gastric ulceration 2. Bleeding 3. Hyperventilation 4. Reye’s syndrome 5. Tinnitus (CN VIII)
382
Q

What are five toxicities associated with Tacrolimus (FK506)?

A
  1. Significant: nephrotoxicity 2. Peripheral neuropathy 3. Hypertension 4. Pleural effusion 5. Hyperglycemia.
383
Q

What are four advantages of newer low-molecular-weight heparins (Enoxaparin)?

A
  1. Better bioavailability 2. 2 to 4 times longer half life 3. Can be administered subcutaneously 4. Does not require laboratory monitoring
384
Q

What are four clinical activities of Aspirin?

A
  1. Antipyretic 2. Analgesic 3. Anti-inflammatory 4. Antiplatelet drug.
385
Q

What are four clinical uses of glucocorticoids?

A
  1. Addison’s disease 2. Inflammation 3. Immune suppression 4. Asthma
386
Q

What are four conditions in which H2 Blockers are used clinically?

A
  1. Peptic ulcer 2. Gastritis 3. Esophageal reflux 4. Zollinger-Ellison syndrome
387
Q

What are four H2 Blockers?

A
  1. Cimetadine 2. Ranitidine 3. Famotidine 4. Nizatidine
388
Q

What are four Sulfonylureas?

A
  1. Tolbutamide 2. Chlorpropamide 3. Glyburide 4. Glipizide
389
Q

What are four thrombolytics?

A
  1. Streptokinase 2. Urokinase 3. tPA (alteplase), APSAC (anistreplase)
390
Q

What are four unwanted effects of Clomiphene use?

A
  1. Hot flashes 2. Ovarian enlargement 3. Multiple simultaneous pregnancies 4. Visual disturbances
391
Q

What are nine findings of Iatrogenic Cushing’s syndrome caused by glucocorticoid therapy?

A
  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
392
Q

What are signs of Sildenafil (Viagra) toxicity?

A

Headache, flushing , dyspepsia, blue-green color vision.

393
Q

What are the clinical uses for Ticlopidine, Clopidogrel?

A

Acute coronary syndrome; coronary stenting. Decreases the incidence or recurrence of thrombotic stroke.

394
Q

What are the four conditions in which Omeprazole, Lansoprazole is used?

A
  1. Peptic ulcer 2. Gastritis 3. Esophageal reflux 4. Zollinger-Ellison syndrome
395
Q

What are three clinical uses of the Leuprolide?

A
  1. Infertility (pulsatile) 2. Prostate cancer (continuous: use with flutamide) 3. Uterine fibroids
396
Q

What are three clinical uses of the NSAIDs?

A
  1. Antipyretic 2. Analgesic 3. Anti-inflammatory
397
Q

What are three common NSAIDS other than Aspirin?

A

Ibuprofen, Naproxen, and Indomethacin

398
Q

What are three complications of Warfarin usage?

A
  1. Bleeding 2. Teratogenicity 3. Drug-drug interactions
399
Q

What are three possible complications of Heparin therapy?

A
  1. Bleeding 2. Thrombocytopenia 3. Drug-drug interactions
400
Q

What are three possible toxicities of NSAID usage?

A
  1. Renal damage 2. Aplastic anemia 3. GI distress
401
Q

What are three toxicities of Leuprolied?

A
  1. Antiandrogen 2. Nausea 3. Vomiting
402
Q

What are three toxicities of Propylthiouracil?

A
  1. Skin rash 2. Agranulocytosis (rare) 3. Aplastic anemia
403
Q

What are three types of antacids and the problems that can result from their overuse?

A
  1. Aluminum hydroxide: constipation and hypophosphatemia 2. Magnesium hydroxide: diarrhea 3. Calcium carbonate: Hypercalcemia, rebound acid increase - All may cause hypokalemia
404
Q

What are three unwanted effects of Mifepristone?

A
  1. Heavy bleeding 2. GI effects (n/v, anorexia) 3. Abdominal pain
405
Q

What are two Alpha-glucosidase inhibitors?

A
  1. Acarbose 2. Miglitol
406
Q

What are two clinical uses of Azathioprine?

A
  1. Kidney transplantation 2. Autoimmune disorders (including glomerulonephritis and hemolytic anemia)
407
Q

What are two conditions in which COX-2 inhibitors might be used?

A

Rheumatoid and osteoarthritis.

408
Q

What are two Glitazones?

A
  1. Pioglitazone 2. Rosiglitazone.
409
Q

What are two mechanisms of action of Propythiouracil?

A

Inhibits organification and coupling of thyroid hormone synthesis. Also decreases peripheral conversion of T4 to T3.

410
Q

What are two processes Corticosteroids inhibit leading to decreased inflammation?

A
  1. Phospholipase A2 is prevented from releasing arachidonic acid 2. Decreases protein synthesis thus lowering amount of Cyclooxygenase enzymes
411
Q

What are two toxicities associated with Cyclosporine?

A
  1. Predisposes to viral infections and lymphoma 2. Nephrotoxic (preventable with mannitol diuresis)
412
Q

What are two toxicities of the Glitazones?

A
  1. Weight gain 2. Hepatotoxicity (troglitazone)
413
Q

What are two toxicities of the Sulfonylureas?

A
  1. Hypoglycemia (more common with 2nd-generation drugs: glyburide, glipizide) 2. Disulfiram-like effects (not seen with 2nd-generation drugs).
414
Q

What are two types of drugs that interfere with the action of Sucralfate and why?

A

Sucralfate cannot work in the presence of antacids or H2 blockers because it requires an acidic environment to polymerize.

415
Q

What can result due to antacid overuse?

A

Can affect absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying.

416
Q

What enzyme does Zileuton inhibit?

A

Lipoxygenase

417
Q

What enzymes are inhibited by NSAIDs, acetaminophen and COX II inhibitors?

A

Cyclooxygenases (COX I, COX II).

418
Q

What is a common side effect of Colchicine used to treat acute gout, especially when given orally?

A

GI side effects. (Note: Indomethacin is less toxic, more commonly used.)

419
Q

What is a common side effect of Misoprostol?

A

Diarrhea

420
Q

What is a possible result of overdose of Acetaminophen?

A

Overdose produces hepatic necrosis; acetaminophen metablolite depletes glutathione and forms toxic tissue adducts in liver.

421
Q

What is a possible toxicity of Alpha-glucosidase inhibitors used in type-2 diabetes?

A

GI disturbances.

422
Q

What is a possible toxicity of Ticlopidine, Clopidogrel usage?

A

Neutropenia (ticlopidine); reserved for those who cannot tolerate aspirin.

423
Q

What is a sign of toxicity with the use of thrombolytics?

A

Bleeding.

424
Q

What is action of insulin in the liver, in muscle, and in adipose tissue?

A
  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.
425
Q

What is are two clinical uses of Cyclosporine?

A
  1. Suppresses organ rejection after transplantation 2. Selected autoimmune disorders.
426
Q

What is the category and mechanism of action of Zafirlukast in Asthma treatment?

A

Antileukotriene; blocks leukotriene receptors.

427
Q

What is the category and mechanism of action of Zileuton in Asthma treatment?

A

Antileukotriene; blocks synthesis by lipoxygenase.

428
Q

What is the category of drug names ending in -ane (e.g. Halothane)

A

Inhalational general anesthetic.

429
Q

What is the category of drug names ending in -azepam (e.g. Diazepam)

A

Benzodiazepine.

430
Q

What is the category of drug names ending in -azine (e.g. Chlorpromazine)

A

Phenothiazine (neuroleptic, antiemetic).

431
Q

What is the category of drug names ending in -azol (e.g. Ketoconazole)

A

Antifungal.

432
Q

What is the category of drug names ending in -barbital (e.g. Phenobarbital)

A

Babiturate.

433
Q

What is the category of drug names ending in -caine (e.g. Lidocaine)

A

Local anesthetic.

434
Q

What is the category of drug names ending in -cillin (e.g. Methicillin)

A

Penicillin.

435
Q

What is the category of drug names ending in -cycline (e.g. Tetracycline)

A

Antibiotic, protein synthesis inhibitor.

436
Q

What is the category of drug names ending in -ipramine (e.g. Imipramine)

A

Tricyclic antidepressant.

437
Q

What is the category of drug names ending in -navir (e.g. Saquinavir)

A

Protease inhibitor.

438
Q

What is the category of drug names ending in -olol (e.g. Propranolol)

A

Beta antagonist.

439
Q

What is the category of drug names ending in -operidol (e.g. Haloperidol)

A

Butyrophenone (neuroleptic).

440
Q

What is the category of drug names ending in -oxin (e.g. Digoxin)

A

Cardiac glycoside (inotropic agent).

441
Q

What is the category of drug names ending in -phylline (e.g. Theophylline)

A

Methylxanthine.

442
Q

What is the category of drug names ending in -pril (e.g. Captopril)

A

ACE inhibitor.

443
Q

What is the category of drug names ending in -terol (e.g. Albuterol)

A

Beta-2 agonist.

444
Q

What is the category of drug names ending in -tidine (e.g. Cimetidine)

A

H2 antagonist

445
Q

What is the category of drug names ending in -triptyline (e.g. Amitriptyline)

A

Tricyclic antidepressant.

446
Q

What is the category of drug names ending in -tropin (e.g. Somatotropin)

A

Pituitary hormone.

447
Q

What is the category of drug names ending in -zosin (e.g. Prazosin)

A

Alpha-1 antagonist

448
Q

What is the category, desired effect, and adverse effect of Isoproterenol in the treatment of Asthma?

A

Nonspecific beta-agonist; desired effect is the relaxation of bronchial smooth muscle (Beta 2). Adverse effect is tachycardia (Beta 1).

449
Q

What is the category, desired effect, and period of use of albuterol in the treatment of Asthma?

A

Beta 2 agonist; desired effect is the relaxation of bronchial smooth muscle (Beta 2). Use during acute exacerbation.

450
Q

What is the category, desired effect, and possible mechanism of Theophylline in treating Asthma?

A

Methylzanthine; desired effect is bronchodilation, may cause bronchodilation by inhibiting phosphodiesterase, enzyme involved in degrading cAMP (controversial).

451
Q

What is the category, mechanism of action, and effect of Ipratroprium in Asthma treatment?

A

Muscarinic antagonist; competatively blocks muscarinic receptors, preventing bronchoconstriction.

452
Q

What is the category, mechanism of action, and particular use of beclomethasone and prednisone in Asthma treatment?

A

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.)

453
Q

What is the category, method of use, and adverse effects of Salmeterol in Asthma treatment?

A

Beta 2 agonist; used as a long-acting agent for prophylaxis. Adverse effects are tremor and arrhythmia.

454
Q

What is the clincial use for Misoprostol?

A

Prevention of NSAID-induced peptic ulcers, maintains a PDA.

455
Q

What is the clinical use for Clomiphene?

A

Treatment of infertility.

456
Q

What is the clinical use for Heparin?

A

Immediate anticoagulation for PE, stroke, angina, MI, DVT.

457
Q

What is the clinical use for Sildenafil (Viagra)?

A

Erectile dysfunction.

458
Q

What is the clinical use for Sucralfate?

A

Peptic ulcer disease.

459
Q

What is the clinical use for Warfarin?

A

Chronic anticoagulation.

460
Q

What is the clinical use of Mifepristone (RU486)?

A

Abortifacient.

461
Q

What is the clinical use of Tacrolimus (FK506)?

A

Potent immunosuppressive used in organ transplant recipients.

462
Q

What is the effect of the Glitazones in diabetes treatment?

A

Increase target cell response to insulin.

463
Q

What is the enzyme inhibited, the effect of this inhibition, and the clinical use of the antiandrogren Finasteride?

A

Finasteride inhibits 5 Alpha-reductase, this decreases the conversion of testosterone to dihydrotestosterone, useful in BPH

464
Q

What is the lab value used to monitor the effectiveness of Heparin therapy?

A

The PTT.

465
Q

What is the lab value used to monitor the effectiveness of Warfarin therapy?

A

The PT.

466
Q

What is the main clinical use for the thrombolytics?

A

Early myocardial infarction.

467
Q

What is the mecanism of action of Sucralfate?

A

Aluminum sucrose sulfate polymerizes in the acid environment of the stomach and selectively binds necrotic peptic ulcer tissue. Acts as a barrier to acid, pepsin, and bile.

468
Q

What is the mecanism of action of the COX-2 inhibitors (celecoxib, rofecoxib)?

A

Selectively inhibit cyclooxygenase (COX) isoform 2, which is found in inflammatory cells nad mediates inflammation and pain; spares COX-1 which helps maintain the gastric mucosa.

469
Q

What is the mecanism of action, effective period, and ineffective period of use for Cromolyn in treating Asthma?

A

Prevents release of mediators from mast cells. Effective only for the prophylaxis of asthma. Not effective during an acute attack.

470
Q

What is the mechanism of action and clinical use of the antiandrogen Flutamide?

A

Flutamide is a nonsteroidal competitive inhibitor of androgens at the testosterone receptor, used in prostate carcinoma.

471
Q

What is the mechanism of action and clinical use of the antiandrogens Ketoconazole and Spironolactone?

A

Inhibit steroid synthesis, used in the treatment of polycystic ovarian syndrome to prevent hirsutism.

472
Q

What is the mechanism of action of Acetaminophen?

A

Reversibly inhibits cyclooxygenase, mostly in CNS. Inactivated peripherally.

473
Q

What is the mechanism of action of Allopurinol used to treat chronic gout?

A

Inhibits xanthine oxidase, decresing conversion of xanthine to uric acid.

474
Q

What is the mechanism of action of Aspirin?

A

Acetylates and irreversibly inhibits cyclooxygenase (COX I and COX II) to prevent the conversion of arachidonic acid to prostaglandins.

475
Q

What is the mechanism of action of Clomiphene?

A

Clomiphene is a partial agonist at estrogen receptors in the pituitary gland. Prevents normal feedback inhibition and increses release of LH and FSHfrom the pituitary, which stimulates ovulation.

476
Q

What is the mechanism of action of Colchicine used to treat acute gout?

A

Depolymerizes microtubules, impairing leukocyte chemotaxis and degranulation.

477
Q

What is the mechanism of action of Cyclosporine?

A

Binds to cyclophilins (peptidyl proline cis-trans isomerase), blocking the differentiation and activation of T cells mainly by inhibiting the production of IL-2 and its receptor.

478
Q

What is the mechanism of action of Heparin?

A

Heparin catalyzes the activation of antithrombin III.

479
Q

What is the mechanism of action of Mifepristone (RU486)?

A

Competitive inibitor of progestins at progesterone receptors.

480
Q

What is the mechanism of action of Misoprostol?

A

Misoprostol is a PGE1 analog that increases the production and secretion of the gastic mucous barrier.

481
Q

What is the mechanism of action of NSAIDs other than Aspirin?

A

Reversibly inhibit cyclooxygenase (COX I and COX II). Block prostaglandin synthesis.

482
Q

What is the mechanism of action of Omeprazole, Lansoprazole?

A

Irreversibly inhibits H+/K+ ATPase in stomach parietal cells.

483
Q

What is the mechanism of action of Probenacid used to treat chronic gout?

A

Inhibits reabsorption of uric acid.

484
Q

What is the mechanism of action of Sildenafil (Viagra)?

A

Inhibits cGMP phosphodiesterase, casuing increased cGMP, smooth muscle relaxation in the corpus cavernosum, increased blood flow, and penile erection.

485
Q

What is the mechanism of action of the Alpha-glucosidase inhibitors?

A

Inhibit intestinal bursh border Alpha-glucosidases; delayed hydrolysis of sugars and absorption of sugars leading to decresed postprandial hyperglycemia.

486
Q

What is the mechanism of action of the glucocorticoids?

A

Decrease the production of leukotrienes and protaglandins by inhibiting phospholipase A2 and expression of COX-2.

487
Q

What is the mechanism of action of the H2 Blockers?

A

Reversible block of histamine H2 receptors

488
Q

What is the mechanism of action of the Sulfonylureas?

A

Close K+ channels in Beta-cell membrane leading to cell depolarization causing insulin release triggered by increase in Calcium ion influx.

489
Q

What is the mechanism of action of the thrombolytics?

A

Directly of indirectly aid conversion of plasminogen to plasmin which cleaves thrombin and fibrin clots. (It is claimed that tPA specifically converts fibrin-bound plasminogen to plasmin.)

490
Q

What is the mechanism of action of Ticlopidine, Clopidogrel

A

Inhibits platelet aggregation by irreversibly inhibiting the ADP pathway involved in the binding of fibrinogen.

491
Q

What is the mechanism of action of Warfarin (Coumadin)?

A

Warfarin interferes with the normal synthesis and gamma-carboxylation of vitamin K-dependent clotting factors II, VII, IX, and X, Protein C and S via vitamin K antagonism.

492
Q

What is the mechanism of Azathioprine?

A

Antimetabolite derivative of 6-mercaptopurine that interferes with the metablolism and synthesis of nucleic acid.

493
Q

What is the mechanism of Leuprolide?

A

GnRH analog with agonist properties when used in pulsatile fashion and antagonist properties when used in continuous fashion, causing a transient initial burst of LH and FSH

494
Q

What is the mechanism of Tacrolimus (FK506)?

A

Similar to cyclosporine; binds to FK-binding protein, inhibiting secretion of IL-2 and other cytokines.

495
Q

What is the memory key for the action of Sildenafil (Viagra)?

A

Sildenafil fills the penis

496
Q

What is the memory key for the effect of aluminum hydroxide overuse?

A

AluMINIMUM amount of feces.

497
Q

What is the memory key for the effect of magnesium hydroxide overuse?

A

Mg = Must go to the bathroom.

498
Q

What is the memory key to remember which pathway (extrinsic vs. intrinsic) and which lab value Warfarin affects?

A

WEPT: Warfarin affects the Extrinsic pathway and prolongs the PT.

499
Q

What is the possible mechanism and effect of Metformin in treating diabetes?

A

Mechanism unknown; possibly inhibits gluconeogenesis and increases glycolysis; effect is to decrease serum glucose levels

500
Q

What is the specific clinical use of Indomethacin in neonates?

A

Indomethacin is used to close a patent ductus arteriosus.

Pharmacology by Somebody (25 decks)

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