Fa Pharm

Front 1

Which antibiotics block cell wall synthesis by inhibition of peptidoglycan cross-linking?

Back 1

Penicillin, ampicillin, ticarcillin, piperacillin, imipenem, aztreonam,
cephalosporins

Front 2

Which antibiotics block peptidoglycan synthesis?

Back 2

Bacitracin, vancomycin

Front 3

Which antibiotic disrupts bacterial cell membranes?

Back 3

Polymyxins

Front 4

Which antibiotics block nucleotide synthesis?

Back 4

Sulfonamides, trimethoprim

Front 5

Which antibiotic blocks D N A topoisomerases?

Back 5

Fluoroquinolones

Front 6

Which antibiotic blocks mRNA synthesis?

Back 6

Rifampin

Front 7

Which antibiotics block protein synthesis at 50S ribosomal subunit?

Back 7

Chloramphenicol, macrolides, clindamycin, streptogramins (quinupristin, dalfopristin), linezolid

Front 8

Which antibiotics block protein synthesis at 30S ribosomal subunit

Back 8

Aminoglycosides, tetracyclines

Front 9

Which antibiotics are bacteriostatic?

Back 9

"We're ECSTaTiC about bacteriostatics."

Erythromycin, Clindamycin, Sulfamethoxazole, Trimethoprim, Tetracyclines, Chloramphenicol.

Front 10

Which antibiotics are bactericidal?

Back 10

"Very Finely Proficient At Cell Murder."

Vancomycin, Fluoroquinolones, Penicillin, Aminoglycosides, Cephalosporins, Metronidazole.

Front 11

Mechanism of Penicillin? (G- IV, V-oral)

Back 11

1. Bind penicillin-binding proteins
2. Block transpeptidase cross-linking of cell wall
3. Activate autolytic enzymes

Front 12

Clinical use of penicillin?

Back 12

Mostly used for gram-positive organisms (S. pneumoniae, S.pyogenes, Actinomyces) and syphilis.

Front 13

Toxicity of penicillin?

Back 13

Hypersensitivity reactions, hemolytic anemia

Front 14

Mechanism of methicillin/nafcillin?

Back 14

Same as penicillin. Narrow spectrum; penicillinase resistant because of bulkier R group.

Front 15

Clinical use of nafcillin?

Back 15

S. aureus (except MRSA; resistant because of altered penicillin-binding protein target site).

Front 16

Toxicity of Methicillin/naficillin?

Back 16

Methicillin- interstitial nephritis
hypersensitivity

Front 17

Mechanism of ampicillin/amoxicillin?

Back 17

Wider spectrum; penicillinase sensitive. Also combine with clavulanic acid to enhance spectrum. AmOxicillin has greater Oral bioavailability than ampicillin.

Front 18

Clinical use of ampicillin/amoxicillin?

Back 18

Ampicillin HELPS kill enterococci

Extended-spectrum penicillin- certain gram-positive bacteria and gram-negative rods (Haemophilus influenzae, E. coli, Listeria monocytogenes, Proteus mirabilis, Salmonella, enterococci).

Front 19

Toxicity of ampicillin/amoxicillin?

Back 19

Hypersensitivity reactions; ampicillin rash; pseudomembranous colitis.

Front 20

Mechanism of ticarcillin, carbenicillin, piperacillin?

Back 20

Same as penicillin. Extended spectrum.

Front 21

Clinical use of ticarcillin, carbenicillin, piperacillin?

Back 21

TCP- Takes Care of Pseudomonas

Pseudomonas spp. and gram-negative rods;
susceptible to penicillinase; use with clavulanic
acid.

Front 22

Toxicity of ticarcillin, carbenicillin, piperacillin

Back 22

Hypersensitivity reaction

Front 23

What are the B-lacatamase inhibitors?

Back 23

CAST

clavulanic acid, sulbactam, tazobactam.

Front 24

Mechanism of cephalosporins?

Back 24

j3-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases. Bactericidal.

Front 25

Clinical use of 1st generation cephalosporins? (cefazolin, cephalexin)

Back 25

PEcK

gram-positive cocci, Proteus mirabilis, E. coli, Klebsiella pneumoniae.

Front 26

Clinical use of 2nd generation cephalosporins?(cefoxitin, cefaclor, cefuroxime)

Back 26

HENS PEcK

Gram-positive cocci, Haemophilus influenzae, Enterobacter aerogenes Neisseria spp., Proteus mirabilis, E. coli, Klebsiella pneumoniae, Serratia marcescens.

Front 27

Clinical use of 3rd generation cephalosporins? (ceftriaxone, cefotaxime, ceftazidime)

Back 27

Serious gram-negative infections resistant to other B lactams.
(Gonorrhea and Meningitis)

Front 28

Clinical use of 4th generation cephalosporins? Cefepime

Back 28

p for pseudomonas

Increased activity against
Pseudomonas and gram-positive organisms.

Front 29

Toxicity of cephalosporins?

Back 29

Vitamin K deficiency
Cross-hypersensitivity with penicillins occurs in 5-10% of patients.
Increased nephrotoxicity of aminoglycosides
Disulfiram-like reaction with ethanol

Front 30

Mechanism of ticarcillin, carbenicillin, piperacillin?

Back 30

Same as penicillin. Extended spectrum.

Front 31

Clinical use of ticarcillin, carbenicillin, piperacillin?

Back 31

TCP- Takes Care of Pseudomonas

Pseudomonas spp. and gram-negative rods;
susceptible to penicillinase; use with clavulanic
acid.

Front 32

Toxicity of ticarcillin, carbenicillin, piperacillin

Back 32

Hypersensitivity reaction

Front 33

What are the B-lacatamase inhibitors?

Back 33

CAST

clavulanic acid, sulbactam, tazobactam.

Front 34

Mechanism of cephalosporins?

Back 34

j3-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases. Bactericidal.

Front 35

Clinical use of 1st generation cephalosporins? (cefazolin, cephalexin)

Back 35

PEcK

gram-positive cocci, Proteus mirabilis, E. coli, Klebsiella pneumoniae.

Front 36

Clinical use of 2nd generation cephalosporins?(cefoxitin, cefaclor, cefuroxime)

Back 36

HENS PEcK

Gram-positive cocci, Haemophilus influenzae, Enterobacter aerogenes Neisseria spp., Proteus mirabilis, E. coli, Klebsiella pneumoniae, Serratia marcescens.

Front 37

Clinical use of 3rd generation cephalosporins? (ceftriaxone, cefotaxime, ceftazidime)

Back 37

Serious gram-negative infections resistant to other B lactams.
(Gonorrhea and Meningitis)

Front 38

Clinical use of 4th generation cephalosporins? Cefepime

Back 38

p for pseudomonas

Increased activity against
Pseudomonas and gram-positive organisms.

Front 39

Toxicity of cephalosporins?

Back 39

Vitamin K deficiency
Cross-hypersensitivity with penicillins occurs in 5-10% of patients.
Increased nephrotoxicity of aminoglycosides
Disulfiram-like reaction with ethanol

Front 40

Mechanism of Aztreonam?

Back 40

A monobactam resistant to B lactamases. Inhibits cell wall synthesis (binds to PBP3 ). Synergistic with aminoglycosides.

Front 41

Clinical use of Aztreonam?

Back 41

Gram-negative rods only-No activity against gram-positives or anaerobes. For penicillin-allergic patients and those with renal insufficiency who cannot tolerate aminoglycosides.

Front 42

Toxicity of Aztreonam?

Back 42

Usually nontoxic; occasional GI upset. No cross-sensitivity with penicillins or cephalosporins.

Front 43

Mechanism of lmipenem/cilastatin, meropenem?

Back 43

lmipenem is a broad-spectrum, j3-lactamase-resistant carbapenem. Always administered with cilastatin (inhibitor of renal dihydropeptidase I) to decrease inactivation of drug in renal tubules.

Front 44

Clinical use of lmipenem/cilastatin, meropenem?

Back 44

Gram-positive cocci, gram-negative rods, and anaerobes. Wide spectrum, but the significant side effects limit use to life-threatening infections, or after other drugs have failed. Meropenem, however, has a reduced risk ofseizures and is stable to dihydropeptidase I.

Front 45

Toxicity of lmipenem/cilastatin, meropenem?

Back 45

GI distress, skin rash, and CNS toxicity (seizures) at high plasma levels.

Front 46

Mechanism of Vancomycin?

Back 46

Inhibits cell wall mucopeptide formation by binding D-ala D-ala portion of cell wall precursors. Bactericidal.

Front 47

Clinical use of Vancomycin?

Back 47

Gram positive only-serious, multidrug-resistant organisms, including S. aureus, enterococci and Clostridium difficile (pseudomembranous colitis).

Front 48

Toxicity of Vancomycin?

Back 48

NOT

Nephrotoxicity, Ototoxicity, Thrombophlebitis, diffuse flushing- "red man syndrome"
(prevent with antihistamines and slow infusion rate).
Well tolerated

Front 49

What are the aminoglycosides?

Back 49

Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin

Front 50

Mechanism of Aminoglycosides?

Back 50

Bactericidal; inhibit formation of initiation complex and cause misreading of mRNA. Require oxygen for uptake; therefore ineffective against anaerobes.

Front 51

Clinical use of Aminoglycosides?

Back 51

Severe gram-negative rod infections. Synergistic with B lactam antibiotics. Neomycin for bowel surgery.

Front 52

Toxicity of Aminoglycosides?

Back 52

Nephrotoxic (esp with cephalosporins)
Ototoxicity (esp with loop diuretics)
Tertagoenic

Front 53

Resistance to Aminoglycosides?

Back 53

Transferase enzymes that inactivate the drug by acetylation, phosphorylation, or adenylation.

Front 54

Mechanism of tetracycline?

Back 54

Bacteriostatic; bind to 30S and prevent attachment of aminoacyl-tRNA; limited CNS penetration. Doxycycline is fecally eliminated and can be used in patients with renal failure. Must NOT take with milk, antacids, or iron-containing preparations because divalent cations inhibit its absorption in the gut.

Front 55

Clinical use of tetracycline?

Back 55

Borrelia burgdorferi, H. pylori, M. pneumoniae. Drug's ability to accumulate intracellularly makes it very effective against Rickettsia and Chlamydia.

Front 56

Toxicity of tetracycline?

Back 56

GI distress, discoloration of teeth and inhibition of bone growth in children, photosensitivity.

Front 57

Resistance to tetracycline?

Back 57

decrease uptake into cells or increased effiux out of cell by plasmid-encoded transport pumps.

Front 58

Mechanism of macrolides?

Back 58

Inhibit protein synthesis by blocking translocation; bind to the 23S rRNA of the 50S
ribosomal subunit. Bacteriostatic.

Front 59

Clinical use of macrolides?

Back 59

Atypical pneumonias (Mycoplasma, Chlamydia, Legionella), URis, STDs,
gram-positive cocci (streptococcal infections in patients allergic to penicillin), and Neisseria.

Front 60

Toxicity of macrolides?

Back 60

Prolonged QT interval (especially erythromycin), GI discomfort (most common cause of noncompliance), acute cholestatic hepatitis, eosinophilia, skin rashes. Increases serum concentration of theophyllines, oral anticoagulants.

Front 61

Resistance to macrolides?

Back 61

Methylation of 23S rRNA binding site.

Front 62

Mechanism of Chloramphenicol?

Back 62

Inhibits 50S peptidyltransferase activity. Bacteriostatic.

Front 63

Clinical use of Chloramphenicol?

Back 63

Meningitis (Haemophilus influenzae, Neisseria meningitidis, Streptococcus pneumoniae).
Conservative use owing to toxicities but often still used in developing countries due to
low cost.

Front 64

Toxicity of Chloramphenicol?

Back 64

Anemia (dose dependent), aplastic anemia (dose independent), gray baby syndrome (in
premature infants because they lack liver UDP-glucuronyl transferase).

Front 65

Resistance to Chloramphenicol?

Back 65

Plasmid-encoded acetyltransferase that inactivates drug.

Front 66

Mechanism of Clindamycin?

Back 66

Blocks peptide bond formation at 50S ribosomal subunit. Static

Front 67

Clinical use of Clindamycin?

Back 67

Anaerobic infections (above diaphragm)

Front 68

Toxicity of Clindamycin?

Back 68

Pseudomembranous colitis (C. difficile overgrowth), fever, diarrhea.

Front 69

Mechanism of sulfonamides?

Back 69

PABA antimetabolites inhibit dihydropteroate synthetase. Bacteriostatic.

Front 70

Clinical use of sulfonamides?

Back 70

Gram-positive, gram-negative, Nocardia, Chlamydia. Triple sulfas or SMX for simple UTI. :z:

Front 71

Toxicity of sulfonamides?

Back 71

Hypersensitivity reactions, hemolysis if G6PD deficient, nephrotoxicity (tubulointerstitial nephritis), photosensitivity, kernicterus in infants, displace other drugs from albumin "'
(e.g., warfarin).

Front 72

Mechanism of trimethoprim?

Back 72

Inhibits bacterial dihydrofolate reductase. Bacteriostatic.

Front 73

Clinical use of trimethoprim?

Back 73

Combination used for recurrent UTis, Shigella, Salmonella , Pneumocystis iiroveci pneumonia.

Front 74

Toxicity of trimethoprim?

Back 74

Megaloblastic anemia, leukopenia, granulocytopenia.

Front 75

What are the sulfa drugs?

Back 75

sulfasalazine, sulfonylureas, thiazide diuretics, acetazolamide, furosemide, celecoxib, or probenecid.

Front 76

Mechanism of Fluoroquinolones?

Back 76

Inhibit DNA gyrase (topoisomerase II). Bactericidal. Must not be taken with antacids.

Front 77

Clinical use of Fluoroquinolones?

Back 77

Gram-negative rods of urinary and GI tracts (including Pseudomonas), Neisseria, some gram- positive organisms.

Front 78

Toxicity of Fluoroquinolones?

Back 78

GI upset, superinfections, skin rashes, headache, dizziness. Contraindicated in pregnant women and in children because animal studies show damage to cartilage. Tendonitis and tendon rupture in adults; leg cramps and myalgias in kids.

Front 79

Mechanism of Metronidazole?

Back 79

Forms free radical toxic metabolites in the bacterial cell that damage DNA. Bactericidal, antiprotozoal.

Front 80

Clinical use of Metronidazole?

Back 80

GET GAP on the Metro!

Treats Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis, Anaerobes (Bacteroides, Clostridium). Used with bismuth and amoxicillin (or tetracycline) for "triple therapy" against H. Pylori.

Front 81

Toxicity of Metronidazole?

Back 81

Disulfiram-like reaction with alcohol; headache, metallic taste.

Front 82

Mechanism of polymyxin?

Back 82

Bind to cell membranes of bacteria and disrupt
their osmotic properties. Polymyxins are cationic, basic proteins that act like detergents.

Front 83

Clinical use of polymyxin?

Back 83

Resistant gram-negative infections.

Front 84

Toxicity of polymyxin?

Back 84

Neurotoxicity, acute renal tubular necrosis.

Front 85

Treatment of M. leprae?

Back 85

Dapsone, rifampin, clofazimine

Front 86

Treatment of M. avium- intracellulare

Back 86

Azithromycin, rifampin,
ethambutol, streptomycin

Front 87

What is the mechanism of ethambutol?

Back 87

Decreased carbohydrate - "a
polymerization of mycobacterium cell wall by blocking arabinosyltransferase.

Red green color blindness

Front 88

Mechanism of isoniazid?

Back 88

Decreases synthesis of mycolic acids. Bacteria catalase- peroxidase needed to convert INH to active metabolite

Front 89

Toxicity of isoniazide?

Back 89

Neurotoxicity, hepatotoxicity, lupus. Pyridoxine (vitamin B6) can prevent neurotoxicity, lupus.

Front 90

Clinical use of rifampin?

Back 90

Mycobacterium tuberculosis; delays resistance to
dapsone when used for leprosy. Used for meningococcal prophylaxis and chemoprophylaxis in contacts of children with Haemophilus influenzae type B.

Front 91

Toxicity of Rifampin?

Back 91

Minor hepatotoxicity and drug interactions (P-450); orange body fluids (nonhazardous side effect).

Front 92

Treatment of VRE?

Back 92

Linezolid and quinupristin/dalfopristin

Front 93

Mechanism of amphotericin B?

Back 93

Binds ergosterol (unique to fungi); forms membrane pores that allow leakage of electrolytes.

Front 94

Clinical use of amphotericin B?

Back 94

Serious, systemic mycoses.
lntrathecally for fungal
meningitis; does not cross blood-brain barrier.

Front 95

Toxicity of amphotericin B?

Back 95

Fever/chills ("shake and bake"), hypotension,
nephrotoxicity, arrhythmias, anemia, IV phlebitis ("amphoterrible"). Hydration reduces nephrotoxicity. Liposomal amphotericin reduces toxicity.

Front 96

Mechanism of nystatin?

Back 96

Same as amphotericin B. Topical form because too toxic for systemic use.

Front 97

Clinical use of nystatin?

Back 97

"Swish and swallow" for oral candidiasis (thrush); topical for diaper rash or vaginal
candidiasis.

Front 98

Mechanism of Azoles?

Back 98

Inhibit fungal sterol (ergosterol) synthesis, by inhibiting the P-450 enzyme that converts
lanosterol to ergosterol.

Front 99

Clinical use of azoles?

Back 99

Systemic mycoses. Fluconazole for cryptococcal meningitis in AIDS patients (because it can cross blood-brain barrier) and candida! infections of all types.
Ketoconazole for Blastomyces, Coccidioides, Histoplasma, Candida albicans;

Front 100

Toxicity of azoles?

Back 100

Hormone synthesis inhibition (gynecomastia), liver dysfunction (inhibits cytochrome
P-450), fever, chills.

Front 101

Mechanism of flucocytosine?

Back 101

Inhibits DNA synthesis by conversion to 5-fluorouracil.

Front 102

Clinical use of flucocytosine?

Back 102

Used in systemic fungal infections (e.g., Candida, Cryptococcus) in combination with amphotericin B.

Front 103

Toxicity of flucocytosine?

Back 103

Nausea, vomiting, diarrhea, bone marrow suppression.

Front 104

Mechanism of caspfungin?

Back 104

Inhibits cell wall synthesis by inhibiting synthesis of B-glucan.

Front 105

Clinical use of caspfungin?

Back 105

Invasive aspergillosis.

Front 106

Toxicity of caspfungin?

Back 106

G l upset, flushing.

Front 107

Mechanism of Terbinafine?

Back 107

Inhibits the fungal enzyme squalene epoxidase.

Front 108

Clinical use of Terbinafine?

Back 108

Used to treat dermatophytoses (especially onychomycosis-fungal infection of finger or toe nails)

Front 109

Mechanism of Griseofulvin?

Back 109

Interferes with microtubule function; disrupts mitosis. Deposits in keratin-containing tissues (e.g., nails).

Front 110

Clinical use of Griseofulvin?

Back 110

Oral treatment of superficial infections; inhibits growth of dermatophytes (tinea, ringworm).

Front 111

Toxicity of Griseofulvin?

Back 111

Teratogenic, carcinogenic, confusion, headaches, increased P-450 and warfarin metabolism.

Front 112

Mechanism of amantadine?

Back 112

Blocks viral penetration/uncoating (M2 protein). Also causes the release of dopamine from intact nerve terminals.

Front 113

Clinical use of amantadine?

Back 113

Prophylaxis and treatment for influenza A only; Parkinson's disease.

Front 114

Toxicity of amantadine?

Back 114

Ataxia, dizziness, slurred speech.

Front 115

Resistance to amantadine?

Back 115

Mutated M2 protein. 90% of all influenza A strains are resistant to amantadine, so not used.

Rimantidine used instead- less CNS side effects

Front 116

Mechanism of oseltamivir?

Back 116

Inhibit influenza neuraminidase, decreasing the release of progeny virus.

Both influenza A and B

Front 117

Mechanism of ribavirin?

Back 117

Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase.

Front 118

Clinical use of ribavirin?

Back 118

RSV, chronic hepatitis C.

Front 119

Toxicity of ribavirin?

Back 119

Hemolytic anemia. Severe teratogen.

Front 120

Mechanism of acyclovir?

Back 120

Monophosphorylated by HSVNZV thymidine kinase. Guanosine analog. Triphosphate formed by cellular enzymes. Preferentially inhibits viral DNA polymerase by chain termination.

Front 121

Clinical use of acyclovir?

Back 121

HSV, VZV, EBV. Used for HSV-induced mucocutaneous and genital lesions as well as for encephalitis. Prophylaxis in immunocompromised patients. For herpes zoster, use a related agent, famciclovir.

Front 122

Resistance to acyclovir?

Back 122

Lack of viral thymidine kinase.

Front 123

Mechanism of ganciclovir?

Back 123

5'-monophosphate formed by a CMV viral kinase or HSVNZV thymidine kinase. Guanosine analog. Triphosphate formed by cellular kinases. Preferentially inhibits viral DNA polymerase.

Front 124

Clinical use of ganciclovir?

Back 124

CMV , especially in immunocompromised patients.

Front 125

Toxicity of ganciclovir?

Back 125

Leukopenia, neutropenia, thrombocytopenia, renal toxicity. More toxic to host enzymes
than acyclovir.

Front 126

Resistance to ganciclovir?

Back 126

Mutated CMV DNA polymerase or lack of viral kinase.

Front 127

Mechanism of foscarnet?

Back 127

Viral DNA polymerase inhibitor- does not require viral kinase

Front 128

Clinical use of foscarnet?

Back 128

CMV retinitis in immunocompromised patients when ganciclovir fails; acyclovir-resistant HSV.

Front 129

Mechanism of cyclosporine?

Back 129

Binds to cyclophilins. Complex blocks the differentiation and activation of T cells by inhibiting calcineurin, thus preventing the production of IL-2 and its receptor.

Front 130

Clinical use of cyclosporine?

Back 130

Suppresses organ rejection after transplantation; selected autoimmune disorders.

Front 131

Toxicity of cyclosporine?

Back 131

Predisposes patients to viral infections and lymphoma; nephrotoxic (preventable with
mannitol diuresis).

Front 132

Mechanism of tacrolimus?

Back 132

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

Front 133

Clinical use of tacrolimus?

Back 133

Potent immunosuppressive used in organ transplant recipients.

Front 134

Toxicity of tacrolimus?

Back 134

Significant-nephrotoxicity, peripheral neuropathy, hypertension, pleural effusion,
hyperglycemia.

Front 135

Mechanism of Sirolimus (rapamycin)?

Back 135

Binds to mTOR. Inhibits T-cell proliferation in response to IL-2.

Front 136

Toxicity of sirolimus?

Back 136

Hyperlipidemia, thrombocytopenia, leukopenia.

Front 137

Mechanism of daclizumab?

Back 137

Monoclonal antibody with high affinity for the IL-2 receptor on activated T cells.

Front 138

Mechanism of Azathioprine?

Back 138

Antimetabolite precursor of 6-mercaptopurine that interferes with the metabolism and synthesis of nucleic acids. Toxic to proliferating lymphocytes.

Front 139

Toxicity of azathioprine?

Back 139

Bone marrow suppression. Toxic effect with allopurinol.

Front 140

Mechanism of Muromonab-CD3?

Back 140

Monoclonal antibody that binds to CD3 (epsilon chain) on the surface of T cells. Blocks cellular interaction with CD3 protein responsible forT-cell signal transduction.

Front 141

Toxicity of Muromonab-CD3?

Back 141

Immunosuppression after kidney transplantation.

Front 142

Clinical use of Muromonab-CD3?

Back 142

Cytokine release syndrome, hypersensitivity reaction.

Front 143

Clinical use of aldesleukin?

Back 143

IL-2: Renal cell carcinoma, metastatic melanoma

Front 144

Clinical use of erythropoietin?

Back 144

Anemia

Front 145

Clinical use of filgrastim?

Back 145

Recovery of bone marrow- GCSF

Front 146

Clinical use of a-interferon?

Back 146

Hepatitis Band C, Kaposi's sarcoma, leukemias, malignant melanoma

Front 147

Clinical use of B-interferon?

Back 147

Multiple sclerosis

Front 148

Clinical use of gamma-interferon?

Back 148

Chronic granulomatous disease

Front 149

Clinical use of Oprelvekin?

Back 149

Il-11: Thrombocytopenia

Front 150

Clinical use of infliximab?

Back 150

TNF-alpha-Crohn's disease, rheumatoid arthritis, psoriatic arthritis

Front 151

Clinical use of abciximab?

Back 151

Glycoprotein IIb/IIIa- Prevent cardiac ischemia in unstable angina and in
patients treated with percutaneous coronary intervention

Front 152

Clinical use of trastuzumab (herceptin)?

Back 152

erb-B2- HER-2-Dverexpressing breast cancer

Front 153

Clinical use of Rituximab?

Back 153

CD20- B-cell non-Hodgkin's lymphoma

Front 154

What are the 1st generation H1 blockers?

Back 154

Diphenhydramine, dimenhydrinate, chlorpheniramine.

Front 155

Clinical uses of 1st generation H1 blockers?

Back 155

Allergy, motion sickness, sleep aid.

Front 156

Toxicity of 1st generation H1 blockers?

Back 156

Sedation, antimuscarinic, anti-a-adrenergic.

Front 157

Clinical uses of 2nd generation H1 blockers?

Back 157

Allergies

Front 158

Toxicity of 2nd generation H1 blockers?

Back 158

Far less sedating than lst generation because of decreased entry into CNS.

Front 159

What are the 2nd generation H1 blockers?

Back 159

Loratadine, fexofenadine, desloratadine, cetirizine.

Front 160

Mechanism (and type) of isoproterenol?

Back 160

Relaxes bronchial smooth muscle (B2). Adverse effect is tachycardia (B1).

Front 161

Mechanism (and type) of albuterol?

Back 161

Relaxes bronchial smooth muscle (B2). Use during acute exacerbation.

Front 162

Mechanism (and type) of albuterol?

Back 162

Long-acting agent for prophylaxis. Adverse effects are tremor and arrhythmia.

Front 163

Mechanism of theophylline?

Back 163

Likely causes bronchodilation by inhibiting phosphodiesterase, thereby .decreases cAMP hydrolysis.

Front 164

Toxicity of Theophylline?

Back 164

Narrow therapeutic index- cardiotoxic, neurotoxic, blocks actions of adenosine

Front 165

Mechanism of ipratropium?

Back 165

Muscarinic antagonist- competitive block of muscarinic receptors, preventing bronchoconstriction. Also used for COPD.

Front 166

Mechanism of Cromolyn?

Back 166

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

Front 167

Mechanism of zileuton?

Back 167

5-lipoxygenase pathway inhibitor. Blocks conversion or arachidonic acid to leukotrienes.

Front 168

Mechanism of zafirlukast/montelukast?

Back 168

Block leukotriene receptors. Especially good for aspirin-induced.

Front 169

Mechanism of Bosentan?

Back 169

Used to treat pulmonary hypertension. Competitively antagonizes endothelin-1 receptors, decreasing pulmonary vascular resistance.

Front 170

Use of Guaifenesin?

Back 170

Expectorant- removes excess sputum; does not suppress cough reflex.

Front 171

Use of N-acetylcysteine?

Back 171

Acetaminophen overdose
Mucolytic- loosen mucous plugs in CF patients

Front 172

Mechanism of sildenafil?

Back 172

Inhibit cGMP phosphodiesterase, causing increases cGMP, smooth muscle relaxation in the corpus cavernosum, I blood flow, and penile erection.

Front 173

Toxicity of sildenafil?

Back 173

Headache, flushing, dyspepsia, impaired blue-green color vision. Risk of life-threatening hypotension in patients taking nitrates.

Front 174

Mechanism of tamsulosin?

Back 174

A1-antagonist used to treat BPH by inhibiting smooth muscle contraction. Selective for a 1A,D receptors (found on prostate)

Front 175

Mechanism of Ritodrine/terbutaline?

Back 175

B2 agonists that relax the uterus; reduce premature uterine contractions.

Front 176

Mechanism and action of Dinoprostone?

Back 176

PGE2 analog causing cervical dilation and uterine contraction, inducing labor.

Front 177

Advantages of oral contraception?

Back 177

Reliable
Decreased risk of endometrial and ovarian cancer
lower ectopic pregnancy
Decreased PID
Regulation of menses

Front 178

Contraindicaiton of oral contraception?

Back 178

mokers > 35 years of age (increased risk of cardiovascular events), patients with history of thromboembolism and stroke or history of estrogen-dependent tumor.

Front 179

Mechanism of Mifepristone (RU-486)

Back 179

Competitive inhibitor of progestins at progesterone receptors.

Front 180

Clinical use of Mifepristone (RU-486)?

Back 180

Termination of pregnancy. Administered with misoprostol (PGE 1) .

Front 181

Mechanism of Progestins?

Back 181

Bind progesterone receptors, reduce growth, and increase vascularization of endometrium.

Front 182

Clinical use of progestins?

Back 182

Used in oral contraceptives and in the treatment of endometrial cancer and abnormal
uterine bleeding.

Front 183

Clinical use of hormone replacement therapy?

Back 183

Used for relief or prevention of menopausal symptoms (e.g., hot flashes, vaginal atrophy) and osteoporosis (increase estrogen, decreased osteoclast activity).

Front 184

Mechanism/action of raloxifene?

Back 184

Partial estrogen agonist

Agonist on bone; reduces resorption of bone; used to treat osteoporosis.

Front 185

Mechanism/action of tamoxifen?

Back 185

Antagonist on breast tissue; used to treat and prevent recurrence of ER-positive breast cancer.

Front 186

Mechanism/action of clomiphene?

Back 186

Partial agonist at estrogen receptors in hypothalamus. Prevents normal feedback inhibition and i release of LH and FSH from pituitary, which stimulates ovulation. Used to treat infertility and PCOS. May cause hot flashes, ovarian enlargement, multiple simultaneous pregnancies, and visual disturbances.

Front 187

Clinical uses of estrogens?
(EE, DES, mestranol)

Back 187

Hypogonadism or ovarian failure, menstrual abnormalities, HRT in postmenopausal
women; use in men with androgen-dependent prostate cancer.

Front 188

Toxicity of estrogen?

Back 188

Increased risk of endometrial cancer, bleeding in postmenopausal women, clear cell adenocarcinoma of vagina in females exposed to DES in utero, increased risk of thrombi.

Front 189

Mechanism of leuprolide?

Back 189

GnRH analog with agonist properties when used in pulsatile fashion; antagonist properties when used in continuous fashion.

Front 190

Clinical use of leuprolide?

Back 190

Infertility (pulsatile), prostate cancer (continuous- use with flutamide), uterine fibroids.

Front 191

Clinical use of Testosterone?

Back 191

Treat hypogonadism and promote development of zosex characteristics; stimulation of
anabolism to promote recovery after burn or injury; treat ER-positive breast cancer

Front 192

Toxicity of Testosterone?

Back 192

Causes masculinization in females; reduces intratesticular testosterone in males by inhibiting release of LH (via negative feedback), leading to gonadal atrophy. Premature closure of epiphyseal plates. increased LDL, decreased HDL.

Front 193

Mechanism of finasteride?

Back 193

A 5a-reductase inhibitor (.!-conversion of testosterone
to dihydrotestosterone) Useful in BPH. Also promotes hair growth- used to treat male-pattern baldness.

Front 194

Mechanism of flutamide?

Back 194

A nonsteroidal competitive inhibitor of androgens at the testosterone receptor. Used in prostate carcinoma.

Front 195

Reproductive effect of ketoconazole?

Back 195

Inhibits desmolase- decreased testosterone

Front 196

Reproductive effect of spironolactone?

Back 196

Inhibits steroid binding

Front 197

Mechanism of mannitol?

Back 197

Osmotic diuretic, increased tubular fluid osmolarity, producing increased urine flow.

Front 198

Clinical use of mannitol?

Back 198

Shock, drug overdose, increased intracranial/intraocular pressure.

Front 199

Toxicity of mannitol?

Back 199

Pulmonary edema, dehydration. Contraindicated in anuria, CHF

Front 200

Mechanism of acetazolamide?

Back 200

Carbonic anhydrase inhibitor. Causes self-limited NaHC03 diuresis and reduction in total-body HC03- stores.

Front 201

Clinical use of acetazolamide?

Back 201

Glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness.

Front 202

Toxicity of acetazolamide?

Back 202

Hyperchloremic metabolic acidosis, neuropathy, NH3 toxicity, sulfa allergy.

Front 203

Mechanism of furosemide?

Back 203

Sulfonamide loop diuretic. Inhibits cotransport system (Na+, K+, 2 Cl-) of thick ascending limb of loop of Henle. Abolishes hypertonicity of medulla, preventing concentration of urine. Increased Ca2+ excretion. Loops Lose calcium.

Front 204

Clinical use of furosemide?

Back 204

Edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema), hypertension, hypercalcemia.

Front 205

Toxicity of furosemide?

Back 205

OH DANG

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

Front 206

Mechanism of Ethacrynic acid?

Back 206

Same action as furosemide.

Front 207

Clinical use of Ethacrynic acid?

Back 207

Diuresis in patients allergic to sulfa drugs.

Front 208

Toxicity of Ethacrynic acid?

Back 208

Ototoxicity, Hypokalemia, Dehydration, Nephritis (interstitial)..

Front 209

Mechanism of Hydrochlorothiazide?

Back 209

Thiazide diuretic. Inhibits NaCl reabsorption in early distal tubule, reducing diluting capacity of the nephron. .decreased Ca2+ excretion.

Front 210

Clinical use of Hydrochlorothiazide?

Back 210

Hypertension, CHF, idiopathic hypercalciuria, nephrogenic diabetes insipidus.

Front 211

Toxicity of Hydrochlorothiazide?

Back 211

Hypokalemic metabolic alkalosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, and hypercalcemia. Sulfa allergy.

Front 212

What are the Potassium sparing diuretics?

Back 212

Spironolactone, Triamterene, Amiloride, eplerenone.

Front 213

Mechanism of Potassium sparing diuretics?

Back 213

Spironolactone is a competitive aldosterone receptor
antagonist in the cortical collecting tubule. Triamterene and amiloride act at the same part of the tubule by blocking Na+channels in the CCT.

Front 214

Clinical use of K sparing diuretics?

Back 214

Hyperaldosteronism, K+ depletion, CHF

Front 215

Toxicity of K sparing diuretics?

Back 215

Hyperkalemia (can lead to arrhythmias), endocrine
effects with aldosterone antagonists (e. g., spironolactone causes gynecomastia)

Front 216

Mechanism of ACE inhibitors?
(captopril, enalapril, lisinopril)

Back 216

Inhibit angiotensin-converting enzyme, reducing
levels of angiotensin II and preventing inactivation of bradykinin, a potent vasodilator. Renin release is increased due to loss of feedback inhibition.

Front 217

Mechanism of losartan?

Back 217

Angiotensin II receptor antagonist.
(Does not cause cough)

Front 218

Toxicity of ACE inhibitors?

Back 218

Cough, Angioedema, Proteinuria, Taste changes, Hypotension, Fetal renal damage

Avoid with renal artery stenosis- ACE inhibitors significantly. decreased GFR by preventing constriction of efferent arterioles.

Front 219

What are the H2 blockers?

Back 219

Cimetidine, ranitidine, famotidine, nizatidine.

Front 220

Mechanism of H2 blockers?

Back 220

Reversible block of histamine Hz receptors~ decreased H+
secretion by parietal cells.

Front 221

Clinical use of H2 blocker?

Back 221

Peptic ulcer, gastritis, mild esophageal reflux. (esp. nocturnal)

Front 222

Toxicity of H2 blocker?

Back 222

Cimitidine (others aren't as bad)
P-450 inhibitor
Anti-androgenic effect
Confusion, headache, dizziness

Front 223

Mechanism of Proton pump inhibitors?

Back 223

Irreversibly inhibit H+fK+-ATPase in stomach parietal cells

Front 224

Clinical use of Proton pump inhibitors?

Back 224

Peptic ulcer, gastritis, esophageal reflux, Zollinger-Ellison syndrome.

Front 225

Mechanism of bismuth/ sucraflate?

Back 225

Bind to ulcer base, providing physical protection, and allow HC03secretion to reestablish pH gradient in the mucous layer.

Front 226

Clinical use of of bismuth/ sucraflate?

Back 226

Increases ulcer healing, traveler's diarrhea.

Front 227

Mechanism of misoprostol?

Back 227

A PGE 1 analog. increased production and secretion of gastric mucous barrier,decrease acid production.

Front 228

Clinical use of misoprostol?

Back 228

Prevention of NSAID-induced peptic ulcers; maintenance of a patent ductus arteriosus. Also used to induce labor.

Front 229

Toxicity of Misoprostol?

Back 229

Diarrhea. Contraindicated in women of childbearing potential (abortifacient).

Front 230

Muscarinic antagonist used in GI problems?

Back 230

Pirenzepine, propantheline.

Front 231

Mechanism of GI muscarinic antagonist?

Back 231

Block Ml receptors on ECL cells (decreased histamine secretion) and M3 receptors on parietal cells (decreased H+secretion).

Front 232

Toxicity of GI muscarinic antagonist?

Back 232

Tachycardia, dry mouth, difficulty focusing eyes.

Front 233

Mechanism of octreotide?

Back 233

Somatostatin analog

Front 234

Clinical use of octreotide?

Back 234

Acute variceal bleeds, acromegaly, VIPoma, and carcinoid tumors.

Front 235

Toxicity of octreotide?

Back 235

Nausea, cramps, steatorrhea.

Front 236

Toxicity of aluminum hydoxide antacid?

Back 236

Aluminium-minimum feces

Constipation and hypophosphatemia; proximal muscle weakness, osteodystrophy, seizures

Front 237

Toxicity of magnesium hydoxide antacid?

Back 237

Mg- must got to the bathroom

Diarrhea, hyporeflexia,
hypotension, cardiac arrest

Front 238

Toxicity of calcium carbonate antacid?

Back 238

Hypercalcemia, rebound acid

Chelates drugs like tetracycline

Front 239

Mechanism of lnfliximab?

Back 239

A monoclonal antibody to TNF

INFLIX pain on TNF

Front 240

Clinical use of lnfliximab?

Back 240

Crohn's disease, rheumatoid arthritis.

Front 241

Toxicity of lnfliximab?

Back 241

Respiratory infection (including reactivation of latent TB), fever, hypotension.

Front 242

Mechanism of sulfasalazine?

Back 242

A combination of sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflammatory). Activated by colonic bacteria.

Front 243

Clinical use of sulfasalazine?

Back 243

Ulcerative colitis, Crohn's disease.

Front 244

Toxicity of sulfasalazine?

Back 244

Malaise, nausea, sulfonamide toxicity, reversible oligospermia.

Front 245

Mechanism of ondansetron?

Back 245

5-HT3 antagonist. Powerful central-acting antiemetic.

Front 246

Clinical use of ondansetron?

Back 246

Control vomiting postoperatively and in patients undergoing cancer chemotherapy.

Front 247

Toxicity of ondansetron?

Back 247

Headache, constipation.

Front 248

Mechanism of metoclopramide?

Back 248

D2 receptor antagonist. I resting tone, contractility, LES tone, motility. Does not influence colon transport time.

Front 249

Clinical uses of metoclopramide?

Back 249

Diabetic and post-surgery gastroparesis.

Front 250

Toxicity of metoclopramide?

Back 250

Increases parkinsonian effects. Restlessness, drowsiness, fatigue, depression, nausea,
diarrhea. Drug interaction with digoxin and diabetic agents. Contraindicated in patients with small bowel obstruction.

Front 251

Mechanism of hydralazine?

Back 251

Increased cGMP ~smooth muscle relaxation. Vasodilates arterioles> veins; afterload reduction.

Front 252

Clinical use of hydralazine?

Back 252

Severe hypertension, CHF. First-line therapy for hypertension in pregnancy, with methyldopa. Frequently coadministered with a B-blocker to prevent reflex tachycardia.

Front 253

Toxicity of hydralazine?

Back 253

Compensatory tachycardia (contraindicated in angina/CAD), fluid retention, nausea, headache, angina. Lupus-like syndrome.

Front 254

What are the calcium channel blockers?

Back 254

Nifedipine, verapamil, diltiazem.
Vascular smooth muscle-nifedipine > diltiazem > verapamil (Verapamil =Ventricle).
Heart-verapamil > diltiazem > nifedipine.

Front 255

Mechanism of calcium channel blockers?

Back 255

Block voltage-dependent L-type calcium channels of cardiac and smooth muscle and thereby reduce muscle contractility.

Front 256

Clinical use of calcium channel blockers?

Back 256

Hypertension, angina, arrhythmias (not nifedipine), Prinzmetal's angina, Raynaud's.

Front 257

Toxicity of calcium channel blockers?

Back 257

Hypertension, angina, arrhythmias (not nifedipine), Prinzmetal's angina, Raynaud's.

Front 258

Mechanism of nitroglycerin/isosorbide dinitrate?

Back 258

Vasodilate by releasing nitric oxide in smooth muscle, causing I in cGMP and smooth muscle relaxation. Dilate veins>> arteries. Decreases preload.

Front 259

Clinical use of nitroglycerin/isosorbide dinitrate?

Back 259

Angina, pulmonary edema. Also used as an aphrodisiac and erection enhancer.

Front 260

Toxicity of nitroglycerin/isosorbide dinitrate?

Back 260

Reflex tachycardia, hypotension, flushing, headache, "Monday disease" in industrial
exposure; development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend, resulting in tachycardia, dizziness, and headache on reexposure.

Front 261

Mechanism/use of nitroprusside?

Back 261

Malignant hypertension

Short acting; increases cGMP via direct release of NO. Can cause cyanide toxicity (releases CN).

Front 262

Mechanism/use of fenoldopam?

Back 262

Malignant hypertension

Dopamine D 1 receptor agonist-relaxes renal vascular smooth muscle.

Front 263

Mechanism/use of diazoxide?

Back 263

Malignant Hypertension

K+ channel opener-hyperpolarizes and relaxes vascular smooth muscle. Can cause hyperglycemia (reduces insulin release).

Front 264

Mechanism of lovastatin?

Back 264

HMG CoA reductase inhibitor

Inhibit cholesterol precursor, mevalonate

Front 265

Side effects of statins?

Back 265

Hepatotoxic
Rhabdomyolisis

Front 266

Mechanism of niacin?

Back 266

Inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation

Increases HDL!!!!

Front 267

Side effects of niacin?

Back 267

Redness and flushing (give aspirin)
Hyperglycemia
Hyperuricemia (gout worsened)

Front 268

Mechanism of cholestyramine/ colestipol/ colesevelam?

Back 268

Prevent intestinal
reabsorption of bile acids; liver must use cholesterol
to make more (can increase TGs)

Front 269

Toxicity of cholestyramine/ colestipol/ colesevelam?

Back 269

Tastes bad and causes GI discomfort, decreases absorption of fat-soluble vitamins
Cholesterol gallstones

Front 270

Mechanism of ezetimibe?

Back 270

Prevent cholesterol reabsorption at small intestine brush border

Front 271

Mechanism of fibrates?

Back 271

Upregulates LPL leading to increased TG clearance

Major effect is on TGs

Front 272

Mechanism of digoxin?

Back 272

Direct inhibition ofNa+fK+ATPase leads to indirect inhibition ofNa+JCa2+ exchanger/
antiport. Increases [Ca2+L positive inotropy. Stimulates vagus nerve

Front 273

Clinical use of digoxin?

Back 273

CHF (increases contractility); atrial fibrillation (decreases conduction at AV node and depression of SA node).

Front 274

Cholinergic toxicity of digoxin?

Back 274

Cholinergic-nausea, vomiting, diarrhea, blurry yellow vision (think Van Gogh).

Front 275

ECG toxicity of digoxin

Back 275

Increased PR, Decreased QT, T wave inversion, arrhythmia, hyperkalemia

Worsened by renal failure (decreased excretion), hypokalemia, quinidine

Front 276

Antidote for digoxin?

Back 276

Slowly normalize K+, lidocaine, cardiac pacer, anti-dig Fab fragments, Mg2+.

Front 277

Mechanism of fibrates?

Back 277

Upregulates LPL leading to increased TG clearance

Major effect is on TGs

Front 278

Mechanism of digoxin?

Back 278

Direct inhibition ofNa+fK+ATPase leads to indirect inhibition ofNa+JCa2+ exchanger/
antiport. Increases [Ca2+L positive inotropy. Stimulates vagus nerve

Front 279

Clinical use of digoxin?

Back 279

CHF (increases contractility); atrial fibrillation (decreases conduction at AV node and depression of
SA node).

Front 280

Cholinergic toxicity of digoxin?

Back 280

Cholinergic-nausea, vomiting, diarrhea, blurry yellow vision (think Van Gogh).

Front 281

ECG toxicity of digoxin

Back 281

Increased PR, Decreased QT, T wave inversion, arrhythmia, hyperkalemia

Worsened by renal failure (decreased excretion), hypokalemia, quinidine

Front 282

Antidote for digoxin?

Back 282

Slowly normalize K+, lidocaine, cardiac pacer, anti-dig Fab fragments, Mg2+.

Front 283

Mechanism of fibrates?

Back 283

Upregulates LPL leading to increased TG clearance

Major effect is on TGs

Front 284

Mechanism of digoxin?

Back 284

Direct inhibition ofNa+fK+ATPase leads to indirect inhibition ofNa+JCa2+ exchanger/
antiport. Increases [Ca2+L positive inotropy. Stimulates vagus nerve

Front 285

Clinical use of digoxin?

Back 285

CHF (increases contractility); atrial fibrillation (decreases conduction at AV node and depression of
SA node).

Front 286

Cholinergic toxicity of digoxin?

Back 286

Cholinergic-nausea, vomiting, diarrhea, blurry yellow vision (think Van Gogh).

Front 287

ECG toxicity of digoxin

Back 287

Increased PR, Decreased QT, T wave inversion, arrhythmia, hyperkalemia

Worsened by renal failure (decreased excretion), hypokalemia, quinidine

Front 288

Antidote for digoxin?

Back 288

Slowly normalize K+, lidocaine, cardiac pacer, anti-dig Fab fragments, Mg2+.

Front 289

What are the rapid acting insulins?

Back 289

Lispro, Aspart

Front 290

Toxicity of insulin?

Back 290

Hypoglycemia, hypersensitivity reaction (very rare).

Front 291

What are the long acting insulin?

Back 291

Glargine, detemir

Front 292

Mechanism of sulfonylureas?

Back 292

C lose K+ channel in
B cell membrane, so
cell depolarizes, triggering of insulin release via increased Ca influx

Front 293

Clinical use of sulfonylureas?

Back 293

Stimulate release of endogenous insulin in type 2 DM. Require some islet function, so useless in type l DM

Front 294

Toxicity of sulfonylureas?

Back 294

First generation: disulfiram-like effects.
Second generation: hypoglycemia.

Front 295

What is the mechanism of metformin?

Back 295

Decreased gluconeogenesis, increased glycolysis, increased peripheral glucose uptake (insulin sensitivity)

Front 296

Toxicity of metformin?

Back 296

Most grave adverse effect is lactic acidosis (contraindicated in renal failure).

Front 297

Mechanism of rosiglitazone?

Back 297

Increased insulin sensitivity in peripheral tissue. Binds to PPAR -y nuclear transcription regulator.

Front 298

Toxicity of rosiglitazone?

Back 298

Weight gain, edema. Hepatotoxicity,
CV toxicity.

Front 299

Mechanism of acarbose/ miglitol?

Back 299

Inhibit intestinal brush- border a-glucosidases. Delayed sugar hydrolysis and glucose absorption lead to decreased postprandial hyperglycemia.

Front 300

Mechanism of Pramlintide?

Back 300

Decreased glucagon

Front 301

Toxicity of Pramlintide?

Back 301

Hypoglycemia, nausea, diarrhea.

Front 302

Mechanism of exenatide?

Back 302

GLP-1 analog
Increases insulin, decrease glucagon post meal

Front 303

Mechanism of propylthiouracil and methimazole?

Back 303

Inhibit organification of iodide and coupling of thyroid hormone synthesis. Propylthiouracil also decreases peripheral conversion ofT4 to T 3.

Front 304

Clinical use of propylthiouracil and methimazole?

Back 304

Hyperthyroidism

Front 305

Toxicity of propylthiouracil and methimazole?

Back 305

Skin rash, agranulocytosis (rare), aplastic anemia. Methimazole is a possible teratogen.

Front 306

Clinical use of GH?

Back 306

GH deficiency, Turner syndrome

Front 307

Clinical use of somatostatin (octreolide)?

Back 307

Acromegaly, carcinoid, gastrinoma, glucagonoma

Front 308

Clinical use of oxytocin?

Back 308

Stimulates labor, uterine contractions, milk let-down; controls uterine hemorrhage

Front 309

AOH (desmopressin)

Back 309

Pituitary (central, not nephrogenic) 0I

Front 310

Mechanism of demeclocycline?

Back 310

AOH antagonist (member of the tetracycline family).

Front 311

Clinical use of demeclocycline?

Back 311

SIADH

Front 312

Toxicity of demeclocycline?

Back 312

Nephrogenic DI, photosensitivity, abnormalities of bone and teeth.

Front 313

Mechanism of glucocorticoids?

Back 313

Decrease the production ofleukotrienes and prostaglandins by inhibiting phospholipase A2
and expression of COX-2.

Front 314

Toxicity of glucocorticoids?

Back 314

Iatrogenic Cushing's syndrome-buffalo hump, moon facies, truncal obesity, muscle
wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic
ulcers, diabetes (if chronic). Adrenal insufficiency when drug stopped after chronic use.

Front 315

Mechanism of aspirin?

Back 315

Irreversibly inhibits cyclooxygenase by covalent binding, which decreases synthesis of both thromboxane and prostaglandins. A type of NSAID.

Front 316

Clinical use of aspirin?

Back 316

Low dose (< 300 mg/day): .!-platelet aggregation. Intermediate dose (300-2400 mg/day): antipyretic and analgesic. High dose (2400-4000 mg/day): anti-inflammatory.

Front 317

Toxicity of aspirin?

Back 317

Gastric upset. Chronic use can lead to acute renal failure, interstitial nephritis, and upper GI bleeding. Reye's syndrome in children with viral infection.

Front 318

What are the important NSAIDs?

Back 318

Ibuprofen, naproxen, indomethacin, ketorolac.

Front 319

Mechanism of NSAIDs?

Back 319

Reversibly inhibit cyclooxygenase (both COX-1 and COX-2). Block prostaglandin
synthesis.

Front 320

Clinical use of NSAIDs?

Back 320

Antipyretic, analgesic, anti-inflammatory. Indomethacin is used to close a PDA.

Front 321

Toxicity of NSAIDs?

Back 321

Renal damage, fluid retention, aplastic anemia, GI distress, ulcers.

Front 322

Mechanism of celecoxib?

Back 322

Reversibly inhibit specifically the cyclooxygenase (COX) isoform 2, which is found in inflammatory cells and vascular endothelium and mediates inflammation and pain; spares COX-1, which helps maintain the gastric mucosa. Thus, should not have the corrosive effects of other NSAIDs on the GI lining.

Front 323

Toxicity of celecoxib?

Back 323

Increased risk of thrombosis. Sulfa allergy. Less toxicity to GI mucosa (lower incidence of ulcers,
bleeding than NSAIDs).

Front 324

Mechanism of acetaminophen?

Back 324

Reversibly inhibits cyclooxygenase, mostly in CNS. Inactivated peripherally.

Front 325

Clinical use of celecoxib?

Back 325

Rheumatoid and osteoarthritis; patients with gastritis or ulcers.

Front 326

Clinical use of acetaminophen?

Back 326

Antipyretic, analgesic, but lacking anti-inflammatory properties. Use in children.

Front 327

Toxicity of acetaminophen?

Back 327

Overdose produces hepatic necrosis; acetaminophen metabolite depletes glutathione
and forms toxic tissue adducts in liver. N-acetylcysteine is antidote-regenerates glutathione.

Front 328

Mechanism of bisphosphonates? (dronate)

Back 328

Inhibit osteoclastic activity; reduce both formation and resorption of hydroxyapatite.

Front 329

Clinical use of bisphosphonates?

Back 329

Malignancy-associated hypercalcemia, Paget's disease of bone, postmenopausal
osteoporosis.

Front 330

Toxicity of bisphosphonates?

Back 330

Corrosive esophagitis (except zoledronate), nausea, diarrhea, osteonecrosis of the jaw.

Front 331

Mechanism of colchicine?

Back 331

Acute gout (with NSAIDs). Binds and stabilizes tubulin to inhibit polymerization, impairing leukocyte chemotaxis and degranulation. GI side effects, especially if given orally.

Front 332

Mechanism of probenecid?

Back 332

Chronic gout. Inhibits reabsorption of uric acid in PCT (also inhibits secretion of penicillin).

Front 333

Mechanism of allopurinol?

Back 333

Chronic gout. Inhibits xanthine oxidase, decreased conversion of xanthine to uric acid. Also used in lymphoma and leukemia to prevent tumor lysis-associated urate nephropathy. increased concentrations of azathioprine and 6-MP

Front 334

Mechanism of Etanercept?

Back 334

Recombinant form of human TNF receptor that binds TNF

Front 335

Mechanism of adalimumab?

Back 335

Anti-TNF antibody

Front 336

Mechanism of heparin?

Back 336

Cofactorfortheactivationofantithrombin,decrease thrombin,and Xa.Short half-life.

Front 337

Clinical use of heparin?

Back 337

Immediate anticoagulation for pulmonary embolism, stroke, acute coronary syndrome, MI, DVT. Used during pregnancy (does not cross placenta). Follow PTT.

Front 338

Toxicity of heparin?

Back 338

Bleeding, thrombocytopenia (HIT), osteoporosis, drug-drug interactions. For rapid
reversal (antidote), use protamine sulfate (positively charged molecule that
binds negatively charged heparin).

Front 339

Mechanism of Heparin-induced thrombocytopenia?

Back 339

Act more on Xa, have better
bioavailability and 2-4 times longer half-life. Can be administered subcutaneously
and without laboratory monitoring. Not easily reversible.

Front 340

Mechanism of low-molecular weight heparin?

Back 340

Heparin binds to platelet factor IV, causing
antibody production that binds to and activates platelets leading to their clearance and resulting in a thrombocytopenic, hypercoagulable state.

Front 341

Mechanism of lepirudin/ bivalirudin?

Back 341

Hirudin derivatives; directly inhibit thrombin. Used as an alternative to heparin for anticoagulating patients with HIT.

Front 342

Mechanism of warfarin?

Back 342

Interferes with normal synthesis and y-carboxylation of vitamin K-dependent clotting factors II, VII, IX, and X and protein C and S. Metabolized by the cytochrome P-450 pathway. In laboratory assay, has effect on EXtrinsic pathway and increase PT. Long half-life.

Front 343

Clinical use of warfarin?

Back 343

Chronic anticoagulation. Not used in pregnant women (because warfarin, unlike heparin, can cross the placenta). Follow PT/INR values.

Front 344

Toxicity of warfarin?

Back 344

Bleeding, teratogenic, skin/tissue necrosis, drug-drug interactions.

Front 345

Mechanism of alteplase?

Back 345

Directly or indirectly aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots. increases PT, increases PTT, no change in platelet count.

Front 346

Toxicity of alteplase?

Back 346

Bleeding. Contraindicated in patients with active bleeding, history of intracranial
bleeding, recent surgery, known bleeding diatheses, or severe hypertension. Treat toxicity with aminocaproic acid, an inhibitor of fibrinolysis.

Front 347

Mechanism of clopidogrel/ ticlopidine?

Back 347

Inhibit platelet aggregation by irreversibly blocking ADP receptors. Inhibit fibrinogen binding by preventing glycoprotein lib/Ilia expression.

Front 348

Clinical use of clopidogrel?

Back 348

Acute coronary syndrome; coronary stenting, decreases incidence or recurrence of thrombotic stroke.

Front 349

Mechanism of abciximab?

Back 349

Monoclonal antibody that binds to the glycoprotein receptor IIb/IIIa on activated platelets, preventing aggregation.

Front 350

Clinical use of abciximab?

Back 350

Acute coronary syndromes, percutaneous transluminal coronary angioplasty.

Front 351

Toxicity of abciximab?

Back 351

Bleeding, thrombocytopenia.

Front 352

What phase of the cell cycle does bleomycin effect?

Back 352

G2 (synthesis of components needed for mitosis)

Front 353

What phase of the cell cycle does Vinca alkaloids and taxols effect?

Back 353

Mitosis

Front 354

What phase of the cell cycle does antimetabolites effect?

Back 354

Synthesis

Front 355

What phase of the cell cycle does etoposide effect?

Back 355

Synthesis and G2

Front 356

Mechanism of Methotrexate (MTX)?

Back 356

Folic acid analog that inhibits dihydrofolate reductase-> decreases dTMP ~> decreases DNA and
J- protein synthesis.

Front 357

Clinical use of Methotrexate (MTX)?

Back 357

Cancers: Leukemias, lymphomas, choriocarcinoma, sarcomas.
Non-neoplastic: Abortion, ectopic pregnancy, rheumatoid arthritis, psonas1s.

Front 358

Toxicity of Methotrexate (MTX)?

Back 358

Myelosuppression, which is reversible with leucovorin (folinic acid) "rescue." Macrovesicular fatty change in liver. Mucositis. Teratogenic.

Front 359

Mechanism of 5-fluorouracil (5-FU)?

Back 359

Pyrimidine analog bioactivated to 5F-dUMP, which covalently complexes folic acid.
This complex inhibits thymidylate synthase ~> decrease dTMP -> decreased DNA and decreased protein synthesis.

Front 360

Clinical use of 5-fluorouracil (5-FU)?

Back 360

Colon cancer and other solid tumors, basal cell carcinoma (topical).
Synergy with MTX.

Front 361

Toxicity of 5-fluorouracil (5-FU)?

Back 361

Myelosuppression, which is not reversible with leucovorin. Overdose: "rescue" with thymidine. Photosensitivity.

Front 362

Mechanism of 6-mercaptopurine (6- MP)?

Back 362

Purine (thiol) analog ~> decreased de novo purine synthesis.
Activated by HGPRTase.

Front 363

Clinical use of 6-mercaptopurine (6- MP)?

Back 363

Leukemias, lymphomas (not CLL or Hodgkin's).

Front 364

Toxicity of 6-mercaptopurine (6- MP)?

Back 364

Bone marrow, GI,liver. Metabolized by xanthine oxidase; thus increased toxicity with allopurinol.

Front 365

Mechanism of 6-thioguanine (6-TG)?

Back 365

Purine (thiol) analog ~> decreased de novo purine synthesis.
Activated by HGPRTase.

Front 366

Clinical use of 6-thioguanine (6-TG)?

Back 366

Acute lymphoid leukemia.

Front 367

Toxicity of 6-thioguanine (6-TG)?

Back 367

Bone marrow depression, liver.
Can be given with allopurinol.

Front 368

Mechanism of Cytarabine (ara-C)

Back 368

Pyrimidine antagonist ~> inhibition of DNA polymerase.

Front 369

Clinical use of Cytarabine (ara-C)?

Back 369

AML, ALL, high- grade non-Hodgkin's lymphoma.

Front 370

Toxicity of Cytarabine (ara-C)?

Back 370

Leukopenia,
thrombocytopenia, megaloblastic anemia.

Front 371

Mechanism of Dactinomycin?

Back 371

Intercalates in DNA.

Front 372

Clinical use of Dactinomycin?

Back 372

Wilms' tumor, Ewing's sarcoma, rhabdomyosarcoma. Used for childhood tumors (children ACT out).

Front 373

Toxicity of Dactinomycin?

Back 373

Myelosuppression.

Front 374

Mechanism of Doxorubicin?

Back 374

Generate free radicals. Noncovalently intercalate
in DNA ---> breaks in DNA ---> decreased replication.

Front 375

Clinical use of Doxorubicin?

Back 375

Hodgkin's lymphomas; also for myelomas, sarcomas, and solid tumors (breast, ovary, lung).

Front 376

Toxicity of Doxorubicin?

Back 376

Cardiotoxicity, myelosuppression, and alopecia. Toxic to tissues with extravasation.

Front 377

Mechanism of Bleomycin?

Back 377

Induces free radical formation, which causes breaks in DNA strands.

Front 378

Clinical use of Bleomycin?

Back 378

Testicular cancer,
Hodgkin's lymphoma.

Front 379

Toxicity of Bleomycin?

Back 379

Pulmonary fibrosis, skin changes. Minimal myelosuppression.

Front 380

Mechanism of Etoposide/teniposide?

Back 380

Inhibits topoisomerase II ---> increased DNA degradation.

Front 381

Clinical use of Etoposide/teniposide?

Back 381

Small cell carcinoma of the lung and prostate, testicular carcinoma.

Front 382

Toxicity of Etoposide/teniposide?

Back 382

Myelosuppression, Gl irritation, alopecia.

Front 383

Mechanism of Cyclophosphamide?

Back 383

Covalently X-link (interstrand) DNA at guanine N-7. Require bioactivation by liver.

Front 384

Clinical use of Cyclophosphamide?

Back 384

Non-hodgkin's lymphoma
Breast cancer
Ovarian cancer
Immunosuppressant

Front 385

Toxicity of Cyclophosphamide,?

Back 385

Myelosuppression; hemorrhagic cystitis, partially prevented with mesna (thiol group of mesna binds toxic metabolite).

Front 386

Mechanism of Nitrosoureas (carmustine, lomustine)?

Back 386

Require bioactivation. Cross blood-brain barrier
---7 CNS.

Front 387

Clinical use o Nitrosoureas
(carmustine, lomustine)f?

Back 387

Brain tumors (including glioblastoma multiforme).

Front 388

Toxicity of Nitrosoureas
(carmustine, lomustine)?

Back 388

CNS toxicity (dizziness, ataxia).

Front 389

Mechanism of busulfan?

Back 389

Alkylates DNA

Front 390

Clinical use of bulsufan?

Back 390

CML. Also used to ablate patient's bone marrow before bone marrow transplantation.

Front 391

Toxicity of busulfan?

Back 391

Pulmonary fibrosis, hyperpigmentation.

Front 392

Mechanism of Vincristine/ vinblastin?

Back 392

Alkaloids that bind to tubulin in M-phase and block polymerization of microtubules so that mitotic spindle cannot form. Microtubules are the vines of your cells.

Front 393

Clinical use of Vincristine/ vinblastin?

Back 393

Hodgkin's lymphoma, Wilms' tumor, choriocarcinoma.

Front 394

Toxicity of Vincristine/ vinblastin?

Back 394

V incristine- neurotoxicity (areflexia, peripheral neuritis), paralytic ileus.
VinBLASTine BLASTs Bone marrow (suppression).

Front 395

Mechanism of Paclitaxel?

Back 395

Hyperstabilize polymerized microtubules in M-phase so that mitotic spindle cannot break down (anaphase cannot occur).
It is TAXing to stay polymerized.

Front 396

Clinical use of Paclitaxel?

Back 396

Ovarian and breast cancer

Front 397

Toxicity of Paclitaxel?

Back 397

Myelosuppression and hypersensitivity.

Front 398

Mechanism of Cisplatin, carboplatin?

Back 398

Cross-link DNA.

Front 399

Clinical use of Cisplatin, carboplatin?

Back 399

Testicular, bladder, ovary, and lung carcinomas.

Front 400

Toxicity of Cisplatin, carboplatin?

Back 400

Nephrotoxicity and acoustic nerve damage.

Front 401

Mechanism of Hydroxyurea?

Back 401

Inhibits Ribonucleotide Reductase ~ decreases DNA Synthesis (S-phase specific).

Front 402

Clinical use of Hydroxyurea?

Back 402

Melanoma, CML, sickle cell disease (increases HbF).

Front 403

Toxicity of Hydroxyurea?

Back 403

Bone marrow suppression, GI upset.

Front 404

Mechanism of Prednisone (in cancer)?

Back 404

May trigger apoptosis. May even work on nondividing cells.

Front 405

Clinical use of Prednisone (in cancer)?

Back 405

Most commonly used glucocorticoid in cancer chemotherapy. Used in CLL, Hodgkin's lymphomas (part ofthe MOPP regimen).

Front 406

Mechanism of Tamoxifen, raloxifene?

Back 406

SERMs-receptor antagonists in breastand agonists in bone. Block the binding ofestrogen to estrogen receptor-positive cells.

Front 407

Toxicity of Tamoxifen, raloxifene?

Back 407

Tamoxifen-may incr. the risk of endometrial carcinoma via partial agonist effects; "hot
flashes." Raloxifene-no incr. in endometrial carcinoma because it is an endometrial antagonist.

Front 408

Clinical use of Tamoxifen, raloxifene?

Back 408

Breast cancer. Also useful to prevent osteoporosis.

Front 409

Mechanism of Trastuzumab (Herceptin)?

Back 409

Monoclonal antibody against HER-2 (erb-B2 ). Helps kill breast cancer cells that overexpress HER-2, possibly through antibody-dependent cytotoxicity.

Front 410

Clinical use of Trastuzumab (Herceptin)?

Back 410

Metastatic breast cancer.

Front 411

Toxicity of Trastuzumab (Herceptin)?

Back 411

Cardiotoxicity.

Front 412

Mechanism of lmatinib (Gieevec)?

Back 412

Philadelphia chromosome bcr-abl tyrosine kinase inhibitor.

Front 413

Clinical use of lmatinib (Gieevec)?

Back 413

CML, GI stromal tumors.

Front 414

Toxicity of lmatinib (Gieevec)?

Back 414

Fluid retention.

Front 415

Mechanism of Rituximab?

Back 415

Monoclonal antibody against CD20, which is found on most B-cell neoplasms.

Front 416

Clinical use of Rituximab?

Back 416

Non-Hodgkin's lymphoma, rheumatoid arthritis (with methotrexate).

Front 417

Mechanism of Trastuzumab (Herceptin)?

Back 417

Monoclonal antibody against HER-2 (erb-B2 ). Helps kill breast cancer cells that overexpress HER-2, possibly through antibody-dependent cytotoxicity.

Front 418

Clinical use of Trastuzumab (Herceptin)?

Back 418

Metastatic breast cancer.

Front 419

Toxicity of Trastuzumab (Herceptin)?

Back 419

Cardiotoxicity.

Front 420

Mechanism of lmatinib (Gieevec)?

Back 420

Philadelphia chromosome bcr-abl tyrosine kinase inhibitor.

Front 421

Clinical use of lmatinib (Gieevec)?

Back 421

CML, GI stromal tumors.

Front 422

Toxicity of lmatinib (Gieevec)?

Back 422

Fluid retention.

Front 423

Mechanism of Rituximab?

Back 423

Monoclonal antibody against CD20, which is found on most B-cell neoplasms.

Front 424

Clinical use of Rituximab?

Back 424

Non-Hodgkin's lymphoma, rheumatoid arthritis (with methotrexate).

Front 425

Antiarrhythmic effect of adenosine?

Back 425

Increases K+ out of cells ~> hyperpolarizingthe cell+ decreases Ica. Drug of choice in diagnosing/ abolishing supraventricular tachycardia. Very short acting (~ 15 sec). Toxicity includes flushing, hypotension, chest pain. Effects blocked by theophylline.

Front 426

Antiarrhythmic effect of K+?

Back 426

Depresses ectopic pacemakers in hypokalemia (e.g., digoxin toxicity).

Front 427

Antiarrhythmic effect of Mg2+?

Back 427

Effective in torsades de pointes and digoxin toxicity.

Front 428

Mechanism of Ca blocker antiarrhythmic effect?

Back 428

Decreased conduction velocity, Increased ERP, Increased PR interval.
Used in prevention of nodal arrhythmias (e.g. SVT)

Front 429

What are the important class III antiarrhythmics?

Back 429

Sotalol, ibutilide, bretylium, dofetilide, amiodarone.

Front 430

Mechanism of class III antiarrhythmics?

Back 430

Increased AP duration, Increased ERP. Used when other antiarrhythmics fail. Increased QT interval.

Front 431

Toxicity of amiodarone?

Back 431

Pulmonary fibrosis
Hepatoxicity
Hyporthyroidism/hyperthyroidism
Skin deposits (blue/gray)- photodermitis
Corneal deposits
Bradycardia, heartblock, CHF

Front 432

What are the Class II antiarrhythmics?

Back 432

Beta blockers
Propranolol, esmolol, metoprolol, atenolol, timolol.

Front 433

Mechanism of Class II antiarrhythmics?

Back 433

Decreased cAMP, decr. Ca2+ currents. Suppress abnormal pacemakers by decr. slope of phase 4. AV node particularly sensitive- incr. PR interval. Esmolol very short acting.

Front 434

Clinical use of Class II antiarrhythmics?

Back 434

V-tach, SVT, slowing ventricular rate during atrial fibrillation and atrial flutter.

Front 435

Toxicity of Beta blockers?

Back 435

Impotence, exacerbation of asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations).

Metoprolol can cause dyslipidemia. Treat overdose with glucagon.

Front 436

Mechanism of Class I antiarrhythmics?

Back 436

Slow or block conduction (especially in depolarized cells). decr. slope of phase 0 depolarization and incr. threshold for firing in abnormal pacemaker cells. Are state dependent (selectively depress tissue that is frequently depolarized, e.g., fast tachycardia).

Front 437

Action of of Class IA antiarrhythmics?

Back 437

Increases AP duration, Decr. ERP, Incr. QT interval.

Affect both atrial and ventricular arrhythmias, especially reentrant and ectopic supraventricular and ventricular tachycardia.

Front 438

What are the Class IA antiarrhythmics?

Back 438

"The Queen Proclaims Diso's pyramid."

Quinidine, Procainamide, Disopyramide.

Front 439

Toxicity of Class IA antiarrhythmics?

Back 439

quinidine (cinchonism-headache, tinnitus); thrombocytopenia; torsades de pointes due to incr. QT interval; procainamide (reversible SLE-like syndrome).

Front 440

Action of Class IB antiarrhythmics?

Back 440

Decreases AP duration
Preferentially affect ischemic or depolarized Purkinje and ventricular tissue. Useful in acute ventricular arrhythmias (especially post-MI) and in digitalis-induced arrhythmias.

Front 441

What are the Class IB antiarrhythmics?

Back 441

''I'd Buy Lidy's Mexican Tacos."

Lidocaine, Mexiletine, Tocainide.

Front 442

Toxicity of Class IB antiarrhythmics?

Back 442

Local anesthetic. CNS stimulation/depression, cardiovascular depression.

Front 443

Action of of Class IC antiarrhythmics?

Back 443

No effect on AP duration. Useful in V-tachs that progress to VF and in intractable SVT. Usually used only as last resort in refractory tachyarrhythmias. For patients without structural abnormalities.

Front 444

What are the Class IC antiarrhythmics?

Back 444

"Chipotle's Food has Excellent Produce."

Flecainide, Encainide, Propafenone.

Front 445

Toxicity of Class IC antiarrhythmics?

Back 445

proarrhythmic, especially post-MI (contraindicated). Significantly prolongs refractory period in AV node.

Front 446

What is the volume of distribution? Calculation?

Back 446

Vd=amount of drug/plasma drug concentration

Relates the amount ofdrug in the body to the plasma concentration. Vd ofplasma protein-bound drugs can be altered by liver and kidney disease.

Front 447

How would drugs with low/ medium/ high Vd distribute?

Back 447

Low Vd (4-8 L) distribute in blood.
Medium Vd distribute in extracellular space or body water.
High Vd (>body weight) distribute into all tissues.

Front 448

What is the clearance? Calculation?

Back 448

CL= rate of elimination/ plasma concentration
CL=Vd* Ke (elimination constant)
Relates the rate of elimination to the plasma concentration.

Front 449

Calculation for Half-life?

Back 449

t(1/2)= (0.7*Vd)/CL

Drugs infused at a constate rate take 4-5 half lives to reach steady state

Front 450

Calculation for Loading dose?

Back 450

LD= Cp*Vd/F (F=bioavaliability)

Front 451

Calculation for maintenance dose?

Back 451

MD= Cp*CL/F (F=bioavaliability)

Front 452

What is a physiologic antagonist?

Back 452

Substance that produces the opposite physiologic effect of an agonist but does not act at the same receptor.

Front 453

Major function of A1 receptor?

Back 453

Incr. vascular smooth muscle contraction, Incr. pupillary dilator muscle contraction (mydriasis), Incr. intestinal and bladder sphincter muscle contraction

Front 454

Major function of A2 receptor?

Back 454

Decreases sympathetic outflow
Decreases insulin release

Front 455

Major function of B1 receptor?

Back 455

Increases heart rate
Increases contractility
Increases renin release
Increases lipolysis

Front 456

Major function of B2 receptor?

Back 456

Vasodilation, bronchodilation, incr. heart rate, incr. contractility, incr. lipolysis, incr. insulin release, incr. uterine tone

Front 457

Major function of M1 receptor?

Back 457

CNS, enteric nervous system

Front 458

Major function of M2 receptor?

Back 458

Decreases heart rate and contractility of atria

Front 459

Major function of M3 receptor?

Back 459

Incr. excrine gland secretion (e.g. sweat, gastric acid) Incr. gut peristalsis, Incr. bladder contraction Bronchoconstriction, pupillary constriction, ciliary contraction (accommodation)

Front 460

Major function of D1 receptor?

Back 460

Relaxes renal vascular smooth muscle

Front 461

Major function of Ds receptor?

Back 461

Modulates transmitter release, especially in brain

Front 462

Major function of H1 receptor?

Back 462

Increases nasal and bronchial mucus production, contraction of bronchioles, pruritus, and pain

Front 463

Major effect of H2 receptor?

Back 463

Increases gastric acid secretion

Front 464

Major effect of V1 receptor?

Back 464

Increases vascular smooth muscle contraction

Front 465

Major effect of V2 receptor?

Back 465

Increases H20 permeability and reabsorption in the collecting tubules of the kidney

Front 466

Which receptors are Gq (Phospolipase C, PKC)?

Back 466

H1, A1, V1, M1, M3

HAVe 1 M&M

Front 467

Which receptors are Gs (Adenylyl cyclase, cAMP)?

Back 467

B1, B2, D1, H2, V2

Front 468

Which receptors are Gi (Adenylyl cyclase, cAMP)?

Back 468

M2, A2, D2

MAD 2's

Front 469

Mechanism of hemicholinium?

Back 469

Blocks reuptake of choline

Front 470

Major effect of H2 receptor?

Back 470

Increases gastric acid secretion

Front 471

Major effect of V1 receptor?

Back 471

Increases vascular smooth muscle contraction

Front 472

Major effect of V2 receptor?

Back 472

Increases H20 permeability and reabsorption in the collecting tubules of the kidney

Front 473

Which receptors are Gq (Phospolipase C, PKC)?

Back 473

H1, A1, V1, M1, M3

HAVe 1 M&M

Front 474

Which receptors are Gs (Adenylyl cyclase, cAMP)?

Back 474

B1, B2, D1, H2, V2

Front 475

Which receptors are Gi (Adenylyl cyclase, cAMP)?

Back 475

M2, A2, D2

MAD 2's

Front 476

Mechanism of hemicholinium?

Back 476

Blocks reuptake of choline

Front 477

What are important sulfa drugs?

Back 477

Celecoxib, furosemide, probenecid, thiazides, TMP-SMX, sulfasalazine, sulfonylureas, acetazolamide, sulfonamide antibiotics.

Front 478

Toxicity of sulfa drugs?

Back 478

Patients with sulfa allergies may develop fever, pruritic rash, Stevens-Johnson syndrome, hemolytic anemia, thrombocytopenia, agranulocytosis, and urticaria

Front 479

Mechanism of alcohol toxicity

Back 479

lcohol metabolism depletes NAD+, which is needed for fatty acid oxidation in the liver and conversion of pyruvate to lactate-> fatty liver and lactic acidosis

Front 480

Important Inducers of P-450?

Back 480

Queen Barb Steals Phen-phen and Refuses Greasy Carbs Chronically.

Quinidine, Barbiturates, St. John's wort, Phenytoin, Rifampin, Griseofulvin, Carbamazepine, Chronic alcohol use

Front 481

Important inhibitors of P-450?

Back 481

Inhibit yourself from drinking
beer from a KEG because it makes you Acutely SICk.

HIV protease inhibitors Ketoconazole Erythromycin Grapefruit juice Acute alcohol use Sulfonamides Isoniazid Cimetidine

Front 482

What drugs cause disulfram-like reaction?

Back 482

Metronidazole, certain cephalosporins, procarbazine, 1st-generation sulfonylureas

Front 483

What drug causes nephrotoxicity and neurotoxicity?

Back 483

Polymyxins

Front 484

What drug causes nephrotoxicity and ototoxicity?

Back 484

Aminoglycosides, vancomycin, loop diuretics, cisplatin

Front 485

What drugs causes cinchonism?

Back 485

Quinidine, quinine

Front 486

What drugs cause diabetes insipidus?

Back 486

Lithium, demeclocycline

Front 487

What drugs cause parkinson-like syndrome?

Back 487

Haloperidol, chlorpromazine, reserpine, metoclopramide

Front 488

What drugs cause seizures?

Back 488

Bupropion, imipenem/cilastatin, isoniazid

Front 489

What drug cause tardive dyskinesia?

Back 489

Antipsychotics

Front 490

What drug causes fanconi's syndrome?

Back 490

Expired tetracycline

Front 491

What drugs causes interstitial nephritis?

Back 491

Methicillin, NSAIDs, furosemide

Front 492

What drugs causes hemorrhagic cystitis?

Back 492

Cyclophosphamide, ifosfamide (prevent by coadministering with mesna)

Front 493

What drugs causes tendonitis?

Back 493

Fluoroquinolones

Front 494

What drugs causes

Back 494

Hydralazine, INH, Procainamide, Phenytoin (it's not HIPP to have lupus)

Front 495

What drugs causes Stevens Johnson syndrome?

Back 495

Ethosuximide, lamotrigine, carbamazepine, phenobarbital, phenytoin, sulfa drugs,
penicillin, allopurinol

Front 496

What drugs causes photosensitivity?

Back 496

Sulfonamides, Amiodarone, Tetracycline (SAT for a photo)

Front 497

What drugs cause osteoporosis?

Back 497

Corticosteroids, heparin

Front 498

What drugs cause gout?

Back 498

Furosemide, thiazides

Front 499

What drugs cause gingival hyperplasia?

Back 499

Phenytoin

Front 500

What drugs cause hypothyroidism?

Back 500

Lithium, amiodarone

Front 501

What drugs cause hot flashes?

Back 501

Tamoxifen, clomiphene

Front 502

What drugs cause gynecomastia?

Back 502

Spironolactone, Digitalis, Cimetidine, chronic Alcohol use, estrogens, Ketoconazole (Some Drugs Create Awesome Knockers)

Front 503

What drugs cause pseudomembranous colitis?

Back 503

Clindamycin, ampicillin

Front 504

What drugs cause hepatitis?

Back 504

INH

Front 505

What drugs cause hepatic necrosis?

Back 505

Halothane, valproic acid, acetaminophen, Amanita phalloides

Front 506

What drugs cause acute cholestatic?

Back 506

Macrolides

Front 507

What drugs cause cough?

Back 507

ACE inhibitors (note: ARBs like losartan-no cough)

Front 508

What drugs cause pulmonary fibrosis?

Back 508

BLeomycin, Amiodarone, Busulfan (it's hard to BLAB when you have pulmonary
fibrosis )

Front 509

What drugs cause thrombotic complications?

Back 509

OCPs (e.g., estrogens and progestins)

Front 510

What drugs cause megaloblastic anemia?

Back 510

Phenytoin, Methotrexate, Sulfa drugs (having a blast with PMS)

Front 511

What drugs cause hemolysis in G6PD deficient patients?

Back 511

Isoniazid (INH), Sulfonamides, Primaquine, Aspirin, Ibuprofen, Nitrofurantoin
(hemolysis IS PAIN)

Front 512

What drugs cause Gray baby syndrome?

Back 512

Chloramphenicol

Front 513

What drugs cause direct coombs positive hemolytic anemia?

Back 513

Methyldopa

Front 514

What drugs cause Aplastic anemia?

Back 514

Chloramphenicol, benzene, NSAIDs, propylthiouracil, methimazole

Front 515

What drugs cause agrunolcytosis?

Back 515

Clozapine, carbamazepine, colchicine, propylthiouracil, methimazole, dapsone

Front 516

What drugs cause torsades de pointes?

Back 516

Class III (sotalol), class lA (quinidine) antiarrhythmics

Front 517

What drugs cause Dilated cardiomyopathy?

Back 517

Doxorubicin (Adriamycin), daunorubicin

Front 518

What drugs cause cutaneous flushing?

Back 518

VANC: Vancomycin, Adenosine, Niacin, Ca2+ channel blockers

Front 519

What drugs cause coronary vasospasm?

Back 519

Cocaine, sumatriptan

Front 520

What drugs cause atropine-like side effects?

Back 520

TCAs

Front 521

What is the antidote for acetaminophen?

Back 521

N-acetylcysteine

Front 522

What is the antidote for Salicylates?

Back 522

NaHC03 (alkalinize urine), dialysis

Front 523

What is the antidote for Amphetamines (basic)?

Back 523

NH4Cl (acidify urine)

Front 524

What is the antidote for Acetylcholinesterase inhibitors,
organophosphates?

Back 524

Atropine, pralidoxime

Front 525

What is the antidote for antimuscarinic, anticholinergic agents?

Back 525

Physostigmine salicylate

Front 526

What is the antidote for Beta blockers?

Back 526

Glucagon

Front 527

What is the antidote for iron?

Back 527

Deferoxamine

Front 528

What is the antidote for lead?

Back 528

CaEDTA, dimercaprol,
succimer, penicillamine

Front 529

What is the antidote for mercury, arsenic, gold?

Back 529

Dimercaprol (BAL),
Succimer

Front 530

What is the antidote for copper, arsenic, gold?

Back 530

Penicillamine

Front 531

What is the antidote for cyanide?

Back 531

Nitrite, hydroxocobalamin, thiosulfate

Front 532

What is the antidote for methemoglobin?

Back 532

Methylene blue, vitamin C

Front 533

What is the antidote for methanonl, ethylene glycol?

Back 533

Ethanol, dialysis, fomepizole

Front 534

What is the antidote for opioid?

Back 534

Naloxone/naltrexone

Front 535

What is the antidote for benzodiazepine?

Back 535

Flumazenil

Front 536

What is the antidote for TCAs?

Back 536

NaHC03 (plasma
alkalinization)

Front 537

What is the antidote for heparin?

Back 537

Protamine

Front 538

What is the antidote for warfarin?

Back 538

Vitamin K, fresh frozen
plasma

Front 539

What is the antidote for tPA, streptokinase?

Back 539

Aminocaproic acid

Front 540

What is the antidote for theophylline?

Back 540

Beta blocker

Front 541

Action of Bethanechol?

Back 541

Postoperative and neurogenic ileus and urinary retention

Front 542

Clinical application of Bethanechol?

Back 542

Activates Bowel and Bladder
smooth muscle; resistant to AChE.
Beth Anne, call (bethanechol) me if you want to activate your Bowels and Bladder.

Front 543

Toxicity of cholinesterase inhibitors or direct agonist?

Back 543

DUMBBELSS.
Causes Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation ofskeletal muscle and CNS, Lacrimation, Sweating, and Salivation.

Front 544

Action of Carbachol?

Back 544

CARBon copy of acetylcholine.

Front 545

Clinical application of Carbachol?

Back 545

Glaucoma, pupillary contraction, and relief of intraocular pressure

Front 546

Action of Pilocarpine?

Back 546

Contracts ciliary muscle of eye (open angle), pupillary sphincter (narrow angle); resistant to AChE. PILE on the sweat and tears.

Front 547

Clinical application of Pilocarpine?

Back 547

Potent stimulator of sweat, tears, saliva

Front 548

Action of Methacholine

Back 548

Stimulates muscarinic receptors in airway when inhaled.

Front 549

Clinical application of Methacholine?

Back 549

Challenge test for diagnosis of asthma

Front 550

Action of Neostigmine?

Back 550

Increased endogenous ACh; no CNS penetration.
NEO CNS =NO CNS penetration.

Front 551

Clinical use of neostigmine?

Back 551

Postoperative and neurogenic ileus and urinary retention, myasthenia gravis, reversal of neuromuscular junction blockade (postoperative)

Front 552

Clinical use of Pyridostigmine?

Back 552

Myasthenia gravis (long acting); does not penetrate CNS

Front 553

Action of Pyridostigmine?

Back 553

Anticholinesterases

Front 554

Clinical use of Edrophonium?

Back 554

Diagnosis of myasthenia gravis (extremely short acting)

Front 555

Action of Edrophonium?

Back 555

Anticholinesterases

Front 556

Clinical use of Physostigmine?

Back 556

Glaucoma (crosses blood-brain barrier ~> CNS) and atropine overdose

Front 557

Action of Physostigmine?

Back 557

Anticholinesterases

Front 558

Clinical use of Echothiophate

Back 558

Glaucoma

Front 559

Action of Echothiophate?

Back 559

Irreversible Anticholinesterases

Front 560

Action of atropine/ tropicamide?

Back 560

Muscuranic Antagonist

Produce mydriasis and
cycloplegia

Front 561

Action of benztropine?

Back 561

Muscuranic Antagonist

PARKinson's disease-PARK my BENZ

Front 562

Action of scopolamine?

Back 562

Muscuranic Antagonist

Motion sickness

Front 563

Action of ipratropium?

Back 563

Muscuranic Antagonist

Asthma, COPD (I pray I can
breathe soon!)

Front 564

Action of Oxybutynin/ glycopyrolate?

Back 564

Muscuranic Antagonist

Reduce urgency in mild
cystitis and reduce bladder
spasms

Front 565

Action of methscopolamine, pirenzepine, propantheline?

Back 565

Muscuranic Antagonist

Peptic Ulcer treatment

Front 566

Systemic action of atropine?

Back 566

Incr. pupil dilation, cycloplegia.
Decr. secretions.
Decr. acid secretion.
Decr. motility
Decr. urgency in cystitis.

Front 567

Toxicity of atropine?

Back 567

Incr. body temperature (due to decr. sweating); rapid pulse; dry mouth; dry, flushed skin; cycloplegia; constipation; disorientation.
Acute-closure glucoma, BPH

Front 568

Action of hexamethonium?

Back 568

Ganglionic blocker. Used in experimental models
to prevent vagal reflex responses to changes in blood pressure-e.g., prevents reflex bradycardia caused by NE.

Front 569

Toxicity of hexamethonium?

Back 569

Severe orthostatic hypotension, blurred vision, constipation, sexual dysfunction.

Front 570

Mechanism/selectivity of epinephrine?

Back 570

Sympathomimetics
a 1, a2, B1, B2, low doses selective for B1

Front 571

Application of epinephrine?

Back 571

Anaphylaxis, glaucoma (open angle), asthma, hypotension

Front 572

Mechanism/selectivity of norepinephrine?

Back 572

Sympathomimetics
a1, a2> B1

Front 573

Application of norepinephrine?

Back 573

Hypotension (but decr. renal perfusion )

Front 574

Mechanism/selectivity of Isoproterenol?

Back 574

Sympathomimetics
B1=B2

Front 575

Application of Dopamine?

Back 575

Shock (increases renal perfusion), heart failure

Front 576

Mechanism/selectivity of Dobutamine?

Back 576

Sympathomimetics
D1=D2>B>a, inotropic but not chronotropic

Front 577

Application of Dobutamine?

Back 577

B1>B2, inotropic but not chronotropic

Front 578

Mechanism/selectivity of Phenylephrine?

Back 578

Sympathomimetics
A1>A2

Front 579

Application of Phenylephrine?

Back 579

Pupillary dilation,
vasoconstriction, nasal
decongestion

Front 580

Mechanism/selectivity of Metaproterenol, albuterol, salmeterol, terbutaline?

Back 580

Selective B2 agonist

Front 581

Clinical use of Metaproterenol, albuterol, salmeterol, terbutaline?

Back 581

MAST: Metaproterenol and
Albuterol for acute asthma; Salmeterol for long-term treatment; Terbutaline to reduce premature uterine contractions

Front 582

Action of ritodrine?

Back 582

B2 agonist
Reduces premature uterine contractions

Front 583

Mechanism of amphetamine?

Back 583

Indirect general agonist, releases stored catecholamines

Front 584

Clinical use of amphetamine?

Back 584

Narcolepsy, obesity, attention deficit disorder

Front 585

Mechanism of ephedrine?

Back 585

Indirect general agonist, releases stored catecholamines

Front 586

Clinical use of ephedrine?

Back 586

Nasal decongestion, urinary incontinence, hypotension

Front 587

Mechanism of cocaine?

Back 587

Indirect general agonist, uptake inhibitor

Front 588

Clinical use of cocaine?

Back 588

Causes vasoconstriction and local anesthesia

Front 589

Mechanism of clonidine/ methyldopa?

Back 589

Centrally acting A2-agonist, decreases central adrenergic outflow

Front 590

Clinical use of clonidine/ methyldopa?

Back 590

Hypertension, especially with renal disease (no decreased blood flow to kidneys)

Front 591

Application/selectivity of Phenoxybenzamine (irreversible) and phentolamine (reversible)?

Back 591

Nonselective A blocker

Pheochromocytoma (use phenoxybenzamine
before removing tumor, since high levels of released catecholamines will not be able to overcome blockage)

Front 592

Toxicity of alpha blocker?

Back 592

Orthostatic hypotension, reflex tachycardia

Front 593

Application/selectivity of prazosin?

Back 593

A1 blocker

Hypertension, urinary retention in BPH

Front 594

Toxicity of prazosin?

Back 594

1st-dose orthostatic hypotension, dizziness, headache

Front 595

Application/selectivity of mirtazapine?

Back 595

A2 blocker
Depression

Front 596

Toxicity of mirtazapine?

Back 596

Sedation, increased serum cholesterol, increased appetite

Front 597

Clinical use of Beta blockers?

Back 597

Hypertension
Angina pectoris
MI
SVT
CHF
Glaucoma
Migranes

Front 598

Effects of Beta blockers?

Back 598

Decr. cardiac output ( decr. heart rate, contractility) decr. renin secretion, decr. AV conduction velocity, slows chronic failure, decrease secretion of aqueous humor

Front 599

Toxicity of Beta blockers?

Back 599

Impotence, exacerbation of asthma, cardiovascular
adverse effects (bradycardia, AV block, CHF), CNS adverse effects (sedation, sleep alterations); use with caution in diabetics

Front 600

What are the nonselective Beta antagonist?

Back 600

ropranolol, timolol, nadolol, and pindolol

Front 601

What are the Beta 1 antagonist?

Back 601

Acebutolol (partial agonist), Betaxolol, Esmolol (short acting), Atenolol, Metoprolol

Cardioselective
A BEAM of B1 blockers. Advantageous in patients with comorbid pulmonary disease and diabetes

Front 602

What are the nonselective alpha-1 and beta antagonist?

Back 602

Carvedilol, labetalol

Hypertension

Front 603

What are the partial B- agonist?

Back 603

Pindolol, Acebutolol

Front 604

Mechanism of epinephrine in glaucoma?

Back 604

A agonist

Decrease aqueous humor synthesis due to vasoconstriction

Front 605

Mechanism of brimonidine in glaucoma?

Back 605

Decreased aqueous humor synthesis

Front 606

Mechanism of timolol in glaucoma?

Back 606

Decreased aqueous humor secretion

Front 607

Mechanism of acetazolamide in glaucoma?

Back 607

Decreased aqueous humor secretion due to decrease HCO3 via inhibition of carbonic anhydrase

Front 608

Mechanism of cholinomimentics in glaucoma?

Back 608

Decreased outflow of aqueous humor; contract ciliary muscle and open trabecular meshwork; use pilocarpine in emergencies; very effective at opening meshwork into canal of Schlemm

Front 609

Side effect of epinephrine in glaucoma?

Back 609

Mydriasis, stinging; do not use in closed-angle glaucoma

Front 610

Side effect of brimonidine in glaucoma?

Back 610

No pupillary or vision changes

Front 611

Side effect of timolol in glaucoma?

Back 611

No pupillary or vision changes

Front 612

Side effect of acetazolamide in glaucoma?

Back 612

No pupillary or vision changes

Front 613

Side effect of cholinomimetics in glaucoma?

Back 613

Miosis, cyclospasm

Front 614

Mechanism of latanoprost? Side effect?

Back 614

PGF(2A) Increased outflow of aqueous humor

Darkens color of iris (browning)

Front 615

What are the opioid analgesics?

Back 615

Morphine, fentanyl, codeine, heroin, methadone, meperidine, dextromethorphan.

Front 616

Mechanism of opioid analgesics?

Back 616

Act as agonists at opioid receptors to modulate synaptic transmission-open K+ channels, close Ca2+ channels-> Decreased synaptic transmission. Inhibit release of ACh, NE, 5-HT, glutamate, substance P.

Front 617

Clinical use of opioid analgesics?

Back 617

Pain, cough suppression (dextromethorphan), diarrhea (loperamide and diphenoxylate), acute pulmonary edema, maintenance programs for addicts (methadone).

Front 618

Toxicity of opioid analgesics?

Back 618

Addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation.

Front 619

Mechanism of butorphanol?

Back 619

Partial agonist at opioid mu receptors, agonist at kappa receptors.

Front 620

Clinical use of butorphanol?

Back 620

Pain; causes less respiratory depression than full agonists.

Front 621

Toxicity of butorphanol?

Back 621

Causes withdrawal if on full opioid agonist.

Front 622

Mechanism of Tramadol?

Back 622

Very weak opioid agonist; also inhibits serotonin and NE reuptake (works on multiple neurotransmitters- "tram it all" in).

Front 623

Clinical use of Tramadol?

Back 623

Chronic pain
(Can decrease seizure threshold)

Front 624

Mechanism of Phenytoin?

Back 624

Increase Na channel inactivation

Front 625

Clinical use of Phenytoin?

Back 625

1st line treatment of tonic clonic seizures
Also for simple and partial
Fosphenytoin for parenteral use

Front 626

Mechanism of carbamazepine?

Back 626

Increase Na channel inactivation

Front 627

Clinical use of carbamazepine?

Back 627

1st line treatment of tonic clonic seizures

Trigeminal neuralgia

Front 628

Mechanism of Lamotrigine?

Back 628

Blocks voltage gated Na channels

Front 629

Clinical use of Lamotrigine?

Back 629

Tonic clonic, simple, and partial

Front 630

Mechanism of Gabapentin?

Back 630

Designed as GABA analog, but primarily inhibits HVA Ca2+ channels

Front 631

Clinical use of Gabapentin?

Back 631

Adjuvant seizure treatment

Also used for peripheral
neuropathy, bipolar disorder

Front 632

Mechanism of Topiramate?

Back 632

Blocks Na channels, Increase GABA action

Front 633

Clinical use of Topiramate?

Back 633

Tonic clonic, simple, and partial

Front 634

Mechanism of phenobarbital?

Back 634

Increases GABA(A) action
1st line in pregnant, children

Front 635

Clinical use of phenobarbital?

Back 635

Tonic clonic,simple and partial seizures

Front 636

Mechanism of Valproic acid?

Back 636

Increases Na+ channel inactivation, Increases GABA concentration

Front 637

Clinical use of Valproic acid?

Back 637

Tonic clonic, absence, simple, and partial seizures

Myoclonic seizures

Front 638

Mechanism of Ethosuximide?

Back 638

Blocks thalamic T-type Ca2+ channels

Front 639

Clinical use of Ethosuximide?

Back 639

Absence seizures (1st line)

Front 640

Mechanism of tiagabine?

Back 640

Inhibits GABA re-uptake

Front 641

Clinical use of tiagabine?

Back 641

Simple and partial seizures

Front 642

Mechanism of Vigabatrin?

Back 642

Irreversibly inhibits GABA transaminase --> Increase GABA

Front 643

Clinical use of Vigabatrin?

Back 643

Simple and partial seizures

Front 644

Mechanism of phenytoin?

Back 644

Use-dependent blockade of Na+ channels; Increases refractory period; inhibition of glutamate release from excitatory presynaptic neuron.

Front 645

Toxicity of carbamazepine?

Back 645

Diplopia, ataxia, blood dyscrasias (agranulocytosis,
aplastic anemia), liver toxicity, teratogenesis, induction of cytochrome P-450, SIADH, Stevens-Johnson syndrome.

Front 646

Toxicity of ethosuximide?

Back 646

GI distress, fatigue, headache, urticaria, Stevens- Johnson syndrome.

Front 647

Toxicity of phenobarbital?

Back 647

Sedation, tolerance, dependence, induction of cytochrome P-450.

Front 648

Toxicity of phenytoin?

Back 648

Nystagmus, diplopia, ataxia, sedation, gingival hyperplasia, hirsutism, megaloblastic anemia, teratogenesis (fetal hydantoin syndrome), SLE-like syndrome, induction of cytochrome P-450 .

Front 649

Toxicity of valproic acid?

Back 649

GI distress, rare but fatal hepatotoxicity (measure LFTs), neural tube defects in fetus (spina bifida), tremor, weight gain. Contraindicated in pregnancy.

Front 650

Toxicity of lamotrigine?

Back 650

Stevens-Johnson syndrome.

Front 651

Toxicity of gabapentin?

Back 651

Sedation, ataxia.

Front 652

Toxicity of topiramate?

Back 652

Sedation, mental dulling, kidney stones, weight loss.

Front 653

Mechanism of barbiturates?

Back 653

Facilitate GABAA action by Increase duration o f Cl- channel opening, thus decreases neuron firing.

Front 654

Clinical use of barbiturates?

Back 654

Sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental).

Front 655

Mechanism of benzodiazepines?

Back 655

Facilitate GABAA action by Increasing frequency of Cl- channel opening decreases REM sleep. Most have long half-lives and active metabolites.

Front 656

Clinical use of benzodiazepines?

Back 656

Anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification (especially alcohol withdrawal-DTs), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia).

Front 657

What are the most addictive benzodiazepine?

Back 657

Short acting= TOM- Triazolam, Oxazepam, Midazolam.

Front 658

Toxicity of benzodiazepine?

Back 658

Dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates.
Treat overdose with flumazenil (competitive antagonist at GABA benzodiazepine receptor).

Front 659

What are the nonbenzodiazepine hypnotics?

Back 659

Zolpidem (Ambien), zaleplon, eszopiclone.

Front 660

Mechanism of nonbenzodiazepine hypnotics?

Back 660

Act via the BZl receptor subtype and is reversed by flumazenil.

Front 661

Toxicity of nonbenzodiazepine hypnotics?

Back 661

Ataxia, headaches, confusion. Short duration because of rapid metabolism by liver ..
enzymes. Unlike older sedative-hypnotics, cause only modest day-after psychomotor depression and few amnestic effects. Lower dependence risk than benzodiazepines.

Front 662

Which anesthetics act most rapidly?

Back 662

Those with decreased solubility in the blood

Front 663

What is the toxicity of inhaled anesthetics?

Back 663

Hepatotoxicity (halothane), nephrotoxicity (methoxyflurane), proconvulsant
(enflurane), malignant hyperthermia (rare), expansion of trapped gas (nitrous oxide)

Front 664

Mechanism of sumatriptan?

Back 664

5-HT(lB/ID) agonist. Causes vasoconstriction, inhibition of trigeminal activation and vasoactive peptide release. Half-life < 2 hours.

Front 665

Clinical use of sumatriptan?

Back 665

Acute migraine, cluster headache attacks.

Front 666

Toxicity of sumatriptan?

Back 666

Coronary vasospasm (contraindicated in patients
with CAD or Prinzmetal's angina), mild tingling.

Front 667

Mechanism/ use of memantine?

Back 667

NMDA receptor antagonist; helps prevent excitotoxicity (mediated by Ca2+).

Alzheimer's disease

Front 668

Mechanism/ use of donepezil?

Back 668

Acetylcholinesterase inhibitor

Alzheimer's disease

Front 669

Mechanism of selegiline?

Back 669

Parkinson's disease

Selectively inhibits MAO-B, which preferentially metabolizes dopamine over NE and 5-HT, thereby increasing the availability of dopamine.

Front 670

Mechanism of L-dopa/carbidopa?

Back 670

Increases level of dopamine in brain. Unlike dopamine, L-dopa can cross blood-brain barrier and is converted by dopa decarboxylase in the CNS to dopamine.

Front 671

Toxicity of L-dopa/carbidopa?

Back 671

Arrhythmias from peripheral conversion to dopamine. Long-term use can -> dyskinesia following administration, akinesia between doses. Carbidopa, a peripheral decarboxylase inhibitor, is given with L-dopa in order to 1' the bioavailability of L-dopa in the brain and to limit peripheral side effects.

Front 672

Mechanism of tolcapone?

Back 672

COMT inhibitors-prevent L-dopa degradation, thereby increasing dopamine availability

Front 673

Mechanism of bromocriptine?

Back 673

Dopamine receptor Agonist

Front 674

Action of dantrolene?

Back 674

Used in the treatment of malignant hyperthermia, which is caused by inhalation anesthetics (except N20) and succinylcholine. Also used to treat neuroleptic malignant syndrome.

Prevents the release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle.

Front 675

Mechanism of succinylcholine?

Back 675

Depolarizing
Phase I (prolonged depolarization)-no antidote. Block potentiated by cholinesterase inhibitors.
Phase II (repolarized but blocked)-antidote consists of cholinesterase inhibitors (e.g., neostigmine ).

Front 676

Mechanism of tubocurarine (and other curiums)?

Back 676

Antagonist of acetylcholine receptor

Front 677

What are the local anesthetics?

Back 677

Esters-procaine, cocaine, tetracaine;
amides-lldocalne, meplvacalne, buplvacalne (amldes have 2 I's in name).

Front 678

Mechanism of local anesthetics?

Back 678

Block Na+ channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na+ channels, so most effective in rapidly firing neurons. 3° amine local anesthetics penetrate membrane in uncharged form, then bind to ion channels as charged form.

Front 679

Does infected tissue require more or less local anesthetics?

Back 679

More.

Alkaline anesthetics are charged and cannot penetrate membrane effectively. More anesthetic is needed in these cases.

Front 680

What is the order of nerve blockade for local anesthetics?

Back 680

Small-diameter fibers> large diameter. Myelinated fibers > unmyelinated fibers.
pain (lose first)> temperature> touch> pressure (lose last).

Front 681

Toxicity of local anesthetics?

Back 681

CNS excitation, severe cardiovascular toxicity (bupivacaine), hypertension,
hypotension, and arrhythmias (cocaine).

Front 682

Clinical use of propofol?

Back 682

Used for rapid anesthesia induction and short procedures. Less postoperative nausea than thiopental. Potentiates GABA(A).

Front 683

Clinical use of Arylcyclohexylamines (Ketamine)?

Back 683

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

Front 684

Clinical use of thiopental?

Back 684

Thiopental-high potency, high lipid solubility, rapid entry into brain. Used for induction of anesthesia and short surgical procedures. Effect terminated by rapid redistribution into tissue and fat.

Front 685

Drug used for alcohol withdrawal?

Back 685

Benzodiazepines

Front 686

Drug used for anorexia/bulemia

Back 686

SSRIs

Front 687

Drug used for anxiety?

Back 687

Benzodiazepines Buspirone
SSRis

Front 688

Drug used for ADHD?

Back 688

Methylphenidate (Ritalin) Amphetamines (Dexedrine)

Front 689

Drug used for atypical depression?

Back 689

MAO inhibitors SSRis

Front 690

Drug used for bipolar disorder?

Back 690

"Mood stabilizers":
Lithium Valproic acid Carbamazepine
Atypical antipsychotics

Front 691

Drug used for depression?

Back 691

SSRis, SNRis TCAs

Front 692

Drug used for depression with insomnia?

Back 692

Mirtazapine

Front 693

Drug used for obessive-compulsive disorder?

Back 693

SSRis Clomipramine

Front 694

Drug used for panic disorder?

Back 694

SSRis TCAs Benzodiazepines

Front 695

Drug used to treat PTSD?

Back 695

SSRIs

Front 696

Drug used to treat schizophrenia?

Back 696

Antipsychotics

Front 697

Drug used to treat tourette's syndrome?

Back 697

Antipsychotics (haloperidol)

Front 698

Drug used to treat social phobias?

Back 698

SSRIs

Front 699

Mechanism/action of Trazodone?

Back 699

Primarily inhibits serotonin reuptake. Used for atypical depression, insomnia, as high doses are needed for antidepressant effects. Toxicity: sedation, nausea, priapism, postural hypotension.

Front 700

Mechanism/action of maprotiline?

Back 700

Blocks NE reuptake.
Atypical depression
Toxicity: sedation, orthostatic hypotension.

Front 701

Mechanism/action of mirtazapine?

Back 701

A2 antagonist (incr. release of NE and 5HT) and potent 5-HT2 and 5-HT3 receptor antagonist
Atypical depression
Toxicity: sedation, orthostatic hypotension.

Front 702

Mechanism/action of buproprion?

Back 702

Also used for smoking cessation. Incr. NE and dopamine via unknown mechanism. Toxicity: stimulant effects (tachycardia, insomnia), headache, seizure in bulimic patients. No sexual side effects.

Front 703

What are the monoamine oxidase inhibitors?

Back 703

Phenelzine, tranylcypromine, isocarboxazid, selegiline (selective MAO-B inhibitor).

Front 704

Clinical use of MAOIs?

Back 704

Atypical depression, anxiety, hypochondriasis.

Front 705

Toxicity of MAOIs?

Back 705

Hypertensive crisis with tyramine ingestion (in many foods, such as wine and cheese) and B-agonists; CNS stimulation. Contraindicated with SSRis or meperidine (to prevent serotonin syndrome).

Front 706

What are the SNRIs?

Back 706

Venlafaxine, duloxetine.

Front 707

Mechanism of SNRIs?

Back 707

Inhibit serotonin and NE reuptake.

Front 708

Clinical use of SNRIs?

Back 708

Depression. Venlafaxine is also used in generalized anxiety disorder; duloxetine is also indicated for diabetic peripheral neuropathy. Duloxetine has greater effect on NE.

Front 709

Toxicity of SSRIs?

Back 709

Fewer than TCAs. Gl distress, sexual dysfunction
(anorgasmia). "Serotonin syndrome" with any drug that Incr. serotonin (e.g., MAO inhibitors) hyperthermia, muscle rigidity, cardiovascular collapse, flushing, diarrhea, seizures. Treatment: cyproheptadine (5-HT2 receptor antagonist).

Front 710

Clinical use of SSRIs?

Back 710

Depression, OCD, bulimia, social phobias.

Front 711

What are the SSRIs?

Back 711

Fluoxetine, paroxetine, sertraline, citalopram.

Front 712

Mechanism of buspirone?

Back 712

Stimulates 5-HT lA receptors (partial agonist)

Front 713

What are the TCAs?

Back 713

Imipramine, amitriptyline, desipramine, nortriptyline, clomipramine, doxepin, amoxapme.

Front 714

Mechanism of TCAs?

Back 714

Block reuptake of NE and serotonin.

Front 715

Side effects of TCAs?

Back 715

Sedation, a-blocking effects, atropine-like (anticholinergic) side effects (tachycardia,
urinary retention). 3° TCAs (amitriptyline) have more anticholinergic effects than do zoTCAs (nortriptyline). Desipramine is the least sedating and has lower seizure threshold.

Front 716

Toxicity of TCAs?

Back 716

Convulsions, Coma, Cardiotoxicity (arrhythmias); also respiratory depression, hyperpyrexia. Confusion and hallucinations in elderly due to anticholinergic side effects (use nortriptyline).

Front 717

Mechanism of Lithium?

Back 717

Not established; possibly related to inhibition of phosphoinositol cascade.

Front 718

Clinical use of Lithium?

Back 718

Mood stabilizer for bipolar disorder; blocks relapse and acute manic events. Also SIADH.

Front 719

Toxicity of lithium?

Back 719

Movement (tremor) Nephrogenic diabetes insipidus, Hypothyroidism Pregnancy problems (Ebstein anomaly and malformation of the great vessels.)

Front 720

What are the atypical antipsychotics?

Back 720

It's atypical for old closets to quietly risper from A to Z.

Olanzapine, clozapine, quetiapine, risperidone, aripiprazole, ziprasidone.

Front 721

Mechanism of atypical antipsychotics?

Back 721

Block 5-HT2, dopamine, A, and H1 receptors.

Front 722

Clinical use of atypical antipsychotics?

Back 722

Schizophrenia- both positive and negative
symptoms. Olanzapine is also used for OCD, anxiety disorder, depression, mania, Tourette's syndrome.

Front 723

Toxicity of atypical antipsychotics?

Back 723

Fewer extrapyramidal and anticholinergic side effects than traditional antipsychotics. Olanzapine/clozapine may cause significant weight gain. Clozapine may cause agranulocytosis (requires weekly WBC monitoring).

Front 724

What are the typical (neuroleptic) antipsychotics?

Back 724

Haloperidol, trifluoperazine, fluphenazine, thioridazine, chlorpromazine (haloperidol + "-azine"s).

Front 725

What are the high and low potency antipsychotics?

Back 725

High potency: haloperidol, trifluoperazine, fluphenazine -neurologic side effects (extrapyramidal symptoms).

Low potency: thioridazine, chlorpromazine- non-neurologic side effects (anticholinergic, antihistamine, and A blockade effects)

Front 726

Clinical use of antipsychotics?

Back 726

Schizophrenia (primarily positive symptoms), psychosis, acute mania, Tourette's syndrome.

Front 727

Mechanism of antipsychotics?

Back 727

All typical antipsychotics block dopamine D2 receptors (Incr. [cAMP]).

Front 728

Toxicity of neuroleptics

Back 728

Highly lipid soluble and stored in body fat; thus, very slow to be removed from body 2. Extrapyramidal system (EPS) side effects
3. Endocrine side effects (e.g., dopamine receptor antagonism -> hyperprolactinemia -> galactorrhea)
4. Side effects arising from blocking muscarinic (dry mouth, constipation), a (hypotension), and histamine (sedation) receptors

Hint 728

Neuroleptic malignant syndrome (NMS)-rigidity, myoglobinuria, autonomic instability, hyperpyrexia. Treatment: dantrolene, agonists (e.g., bromocriptine).

Tardive dyskinesia- stereotypic oral-facial movements due to long-term antipsychotic use. Often irreversible.

Front 729

What are the typical (neuroleptic) antipsychotics?

Back 729

Haloperidol, trifluoperazine, fluphenazine, thioridazine, chlorpromazine (haloperidol + "-azine"s).

Front 730

What are the high and low potency antipsychotics?

Back 730

High potency: haloperidol, trifluoperazine, fluphenazine -neurologic side effects (extrapyramidal symptoms).

Low potency: thioridazine, chlorpromazine- non-neurologic side effects (anticholinergic, antihistamine, and A blockade effects)

Front 731

Clinical use of antipsychotics?

Back 731

Schizophrenia (primarily positive symptoms), psychosis, acute mania, Tourette's syndrome.

Front 732

Mechanism of antipsychotics?

Back 732

All typical antipsychotics block dopamine D2 receptors (Incr. [cAMP]).

Front 733

Toxicity of neuroleptics

Back 733

1. Highly lipid soluble and stored in body fat; thus, very slow to be removed from body
2. Extrapyramidal system (EPS) side effects
3. Endocrine side effects (e.g., dopamine receptor antagonism -> hyperprolactinemia -> galactorrhea)
4. Side effects arising from blocking muscarinic (dry mouth, constipation), a (hypotension), and histamine (sedation) receptors

Hint 733

Neuroleptic malignant syndrome (NMS)-rigidity, myoglobinuria, autonomic instability, hyperpyrexia. Treatment: dantrolene, agonists (e.g., bromocriptine).

Tardive dyskinesia- stereotypic oral-facial movements due to long-term antipsychotic use. Often irreversible.