Pulmonary Pharmacology Hit List Flashcards

Question

Asthma & COPD Monteleukast Class

Answer 1

Leukotriene Receptor Blocker – Anti-inflammatory

Answer 2

LTD4 activation  bronchial hyper-reactivity, bronchoconstriction, mucosal edema, increased mucus secretion

Answer 3

To reduce aspirin-related asthma

Answer 4

GIT, laryngitis, pharyngitis, nausea, otitis, sinusitis, viral infections

Answer 5

Possible association w/ suicide ideation | High doses tumorigenic in rodents

Answer 6

Leukotriene Synthesis Blocker – Anti-inflammatory

Answer 7

Inhibits leukotriene formation, decreases smooth muscle contraction and blood vessel permeability, reduces leukocytes migration to damaged areas.

Answer 8

Causes hepatic enzyme elevation – LFTs required

Answer 9

CYP1A2 interaction w/ theophylline; evaluation for other inflammation-related diseases

Answer 10

Anti-IgE antibody

Answer 11

Binds to IgE and prevents release of inflammatory mediators  decreases allergic response Reduces the frequency & severity of asthma attacks

Answer 12

Alkylating agent

Answer 13

Produces B & T cell lymphopenia, suppression of B cell activity and decreased Ig secretion; associated with neutron- thrombocytopenia, bladder cancer, myeloproliferative malignancie s

Answer 14

Hemorrhagic cystitis is a frequent complication, but this is prevented by adequate fluid intake and mesna. Can cause diarrhea.

Answer 15

Endothlin-1 Receptor Antagonist

Answer 16

Blocks smooth muscle proliferation and pulmonary artery vasoconstriction by binding to endothliun-1 type A (smooth muscle) and type B (endothelial cells)

Answer 17

Orally active

Answer 18

Teratogenic (category X)

Answer 19

Exogenous surfactant

Answer 20

Administered to preterm (<30 weeks) infants to reduce pulmonary surface tension; purified animal-derived products rich in surfactant proteins B, and C, neutral lipids, surface active PLs, and DPPC (primary surface active component)

Answer 21

Prostanoid for PAH

Answer 22

Prostanoids induce pulmonary artery vasodilation, retard smooth muscle growth and disrupt platelet aggregation.

Answer 23

Half life of 3-5 minutes, requires continuous IV infusion

Answer 24

Hypotension, muscle pains, headache, flushing

Answer 25

Phosphodieterase type 5 inhibitors

Answer 26

Tx of benign prostatic hypertension and erectile dysfunction

Answer 27

Headache is most common side effect

Answer 28

Halflife 17 hours

Answer 29

Change in color vision due to non-arteritic anterior ischemic optic neuropathy (NAION)

Answer 30

Immunosuppressent

Answer 31

DHFR inhibition, additional actions that increase adenosine-mediated immunosuppression (increase in cAMP)

Answer 32

Tx for sarcoidosis (non-caseating granulomas)

Answer 33

– NOT a front-line therapy | High-dose intravenous methotrexate chemotherapy acute kidney failure and severe and life-threatening CNS toxicity.

Answer 34

Prostanoid for PAH

Answer 35

Prostanoids induce pulmonary artery vasodilation, retard smooth muscle growth and disrupt platelet aggregation

Answer 36

Halflife of 25 minutes, requires 6-9 inhaled doses/ day (10 min per dose)

Answer 37

Cough, flushing, headache are common, hypotension, muscle cramps, bleeding, reports of hemoptysis

Answer 38

Calcium Channel Blocker (CCB)

Answer 39

CCB – prevent membrane depolarization, block the key mediator of smooth muscle contraction allowing vasodilation to endure; not all patients respond to these drugs, some develop hemodynamic decompensation

Answer 40

Halflife 3-6 h, PO TID

Answer 41

CYP3A4 | Bradycardia, headache, edema, hypotension

Answer 42

mAb against CD20 on B cells

Answer 43

mAb that binds CD20 on M cell precursors and mature B cells) Depletion lasts 6-9 months (depletion via 2 mechanisms: ACDC, complement mediated  MAC, induction of apoptosis)

Answer 44

HTN, asthenia, pruritis, urticarial, rhinitis, arthralgia

Answer 45

tx for Wegener’s granulomatosis

Answer 46

Prostanoid for PAH

Answer 47

Prostanoids induce pulmonary artery vasodilation, retard smooth muscle growth and disrupt platelet aggregation

Answer 48

Halflife of 4 hours, continuous SC or IV infusion

Answer 49

Headache, nausea, diarrhea, vasodilation, jaw pain,

Answer 50

monitor for bleeding, decreased clearance w/ gemfibrozil

Answer 51

Facilitates apoptosis of T cell populations

Answer 52

DNA, RNA synthesis inhibitor

Answer 53

associated w/ neoplastic, mutagenic, and leukopenic & thrombocytopenic toxicity; increases the risk of infection

Answer 54

Endothlin-1 Receptor Antagonist

Answer 55

Blocks smooth muscle proliferation and pulmonary artery vasoconstriction by binding to endothliun-1 type A (smooth muscle) and type B (endothelial cells)

Answer 56

Orally active | 5-8 hours; PO BID

Answer 57

Teratogenic (category X) Liver and blood toxicities Significantly elevated LFTs, anemia, naopharyngitis, interactions w/ CYP2C9 and 3A4 substrates; leading cause of drug-drug interactions

Answer 58

Calcium Channel Blockers (CCB)

Answer 59

CCB – prevent membrane depolarization, block the key mediator of smooth muscle contraction allowing vasodilation to endure;

Answer 60

Halflife 35-50 hours

Answer 61

Not all patients respond to these drugs, some develop hemodynamic decompensation

Answer 62

CYP3A4 | Edema, fatigue, hypotension

Answer 63

Calcium Channel Blockers (CCB)

Answer 64

CCB – prevent membrane depolarization, block the key mediator of smooth muscle contraction allowing vasodilation to endure

Answer 65

Headaches, facial flushing, dizziness, lightheadedness, swelling, increased urination, fatigue, nausea, ecchymosis, galactorrhea, and constipation

Answer 66

Antihistamines 1st generation Antitussive Ether/ Ethanolamine derivative

Answer 67

Based on structure of histamine – short lived, multiple dosing, H1 blockade. Antihistamine-H1 antagonist, suppresses cough by action on the respiratory center due to its anticholinergic effect

Answer 68

Side Effects – drowsiness, respiratory distress, blurred vision, dry mouth, urinary retention

Answer 69

Duration 4-6 hours

Answer 70

Antihistamines 1st generation Ether/ Ethanolamine derivative

Answer 71

Based on structure of histamine – short lived, multiple dosing, H1 blockade

Answer 72

``` Highly sedative, anticholinergic side effects Sedative Anticholinergic GI Can potentiate nasal congestion ```

Answer 73

Duration 4-6 hours

Answer 74

Antihistamines 1st generation Alklamine

Answer 75

Based on structure of histamine – short lived, multiple dosing, H1 blockade

Answer 76

``` Highly sedative, anticholinergic side effects Sedative Anticholinergic GI Can potentiate nasal congestion ```

Answer 77

Duration 4-6 hours

Answer 78

Antihistamines 1st generation Piperzine derivative – much longer duration: 4-24 hours

Answer 79

Based on structure of histamine – short lived, multiple dosing, H1 blockade

Answer 80

``` Highly sedative, anticholinergic side effects Sedative Anticholinergic GI Can potentiate nasal congestion ```

Answer 81

Much longer duration: 4-24 hours

Answer 82

Antihistamines | 2nd generation

Answer 83

Divergent structures, different from histamine, longer therapeutic doses,interactions H1 blockade Anti-asthmatic

Answer 84

Limited or nonsedating, enhanced safety profiles (cardiac arrhythmias, drug-drug Has only mild cognitive disturbances -adine -stine

Answer 85

Duration 8-24 hours

Answer 86

Antihistamines | 2nd generation

Answer 87

14-7x greater binding to H1 receptors than loratadine | 15-50 fold lower affinity for muscarinic receptors compared w/ H1 receptors

Answer 88

Limited or nonsedating, enhanced safety profiles (cardiac arrhythmias, drug-drug Has only mild cognitive disturbances -adine -stine

Answer 89

Long elimination halflife = 27 hours

Answer 90

Antihistamines | 2nd generation

Answer 91

Divergent structures, different from histamine, longer therapeutic doses,interactions H1 blockade Anti-asthmatic

Answer 92

Limited or nonsedating, enhanced safety profiles (cardiac arrhythmias, drug-drug Has only mild cognitive disturbances -adine -stine

Answer 93

Duration 8-24 hours

Answer 94

Antihistamines | 2nd generation

Answer 95

Divergent structures, different from histamine, longer therapeutic doses,interactions H1 blockade Anti-asthmatic

Answer 96

Limited or nonsedating, enhanced safety profiles (cardiac arrhythmias, drug-drug Has only mild cognitive disturbances -adine -stine

Answer 97

Duration 8-24 hours

Answer 98

Mild analgesic

Answer 99

Inhibition of cyclooxygenase (COX), and recent findings suggest that it is highly selective for COX-2.

Answer 100

Fever, pain, myalgia, and headache.

Answer 101

Metabolized by the liver and is hepatotoxic; side effects are multiplied when combined with alcoholic drinks.

Answer 102

The onset of analgesia is approximately 11–29.5 minutes after oral administration and its half-life is 1–4 hours.

Answer 103

Prostate hypertrophy, urinary obstruction, asthma, COPD, peptic ulcer, MAOIs

Answer 104

Antitussive

Answer 105

Suppresses cough reflex via direct action on the cough center in the medulla of the brain. Metabolized by CYP2D6 into active metabolite dextrorphan

Answer 106

MAOIs, antidepressants, respiratory insufficiency, HS White margin of safety (12-75x of TD to produce halllucinations.

Answer 107

Onset: 15-30 min, duration 3-6 hours

Answer 108

Opoid analgesic, Antitussive | 3-methylmorphine

Answer 109

Suppresses cough by action on the respiratory center | 10% is converted to morphine

Answer 110

Constipation, sedation, histamine release, vasodilation, orthostatic hypotension, dizziness

Answer 111

Topical Agent = ointment, lozenges, inhalation

Answer 112

Rub on throat and chest as a thick later, not used in nostrils or mouth

Answer 113

Topical Agent= ointment, lozenges, inhalation

Answer 114

Rub on throat and chest as a thick later, not used in nostrils or mouth

Answer 115

Nasal decongestant

Answer 116

Vasoconstricive drug that reduces nasal congestion, does not affect the release of histamine or other mediators in the allergic reaction, commonly formulated with antihistamines Alpha-adrenergic agonist Acts primarily by releasing NE from adrenergic nerves

Answer 117

Metabolized to a minor extent, 88% excreted unchanged in the urine

Answer 118

Better bioavailability – but both have a short half-life, with a peak at 0.5-2 hours

Answer 119

Side effects: CV stimulation, CNS stimulation, rebound congestion (ischemic as a result of vasoconstriction of the drug or local irritation of the drug) Behind the Counter OTC product to reduce use in meth

Answer 120

Nasal decongestant

Answer 121

Acts by directly stimulating adrenergic receptors on postsynaptic sites

Answer 122

Rapidly metabolized by MOA and COMT in the GI mucosa, liver, and other tissues

Answer 123

Topical nasal decongestant

Answer 124

Do not use for more than 3-5 days because it can cause rhinitis medicamentosa

Answer 125

Preferred agent during pregnancy

Answer 126

Expectorants | Mucinex

Answer 127

Symptomatic relief of ineffective productive coughs, not used for chronic coughs, loosens and thins lower respiratory tract secretions by increasing volume and reducing volume of secretions.

Answer 128

In veterinary medicine, used to induce and maintain anesthesia in horses

Answer 129

Use in diseases with increased mucus production – cystic fibrosis, COPD, Bronchiectasis, Respiratory infections, TB. Break H bonds by substituting a sulfhydryl radical-HS

Answer 130

Given aerosol or by direct instillation into the ET tube

Answer 131

Given orally to reduce liver injury w/ acetoaminophen (Tylenol) overdose

Answer 132

Side effects – bronchospasm (asthma) – if used with asthma, use 10% with bronchodilator Side Effects – increase mucus production (be prepared to suction a patient who cannot cough), do not mix with antibiotics in the same nebulizer, disagreeable odor due to the hydrogen sulfide, N/V

Answer 133

Aersolized Diuretic/ sodium channel blocker

Answer 134

Diuretic that can be given by aerosol to patients w/ CF, sodium channel blocker. In CF, sodium is absorbed into the epithelium along with water, leaving the mucus thick and dehydrated – but by blocking the absorption, dehydration of the mucus is prevented

Answer 135

The drug is dissolved in 0.3% NaCl solution and nebulized

Answer 136

Inhibition of RNA synthesis, binds the beta subunits of RNA polymerase Bactericidal for IC and EC bacteria Resistance – DNA dependent RNA polymerase does not bind drug Never given as a single agent due to resistance

Answer 137

Abs – oral, impaired by food & para-aminosalicylic acid (admin 8-12 hours apart)

Answer 138

Penetrates all tissues well including CSF (meningitis) Metabolized – de-acetylated in liver (halflife increased by hepatic dysfunction/ de-acetylated rifampin still has full antibacterial activity but is not resorbed Excreted primarily in bile, small amount renal tubular secretion, but no adjustment w/ renal failure

Answer 139

Discolors body fluids – orange/red tears, urine, saliva), GI disturbances, CND complains, Hepatotoxic (more relevant in slow acetylators);

Answer 140

Induces P450 (within 2 weeks of drug use), reduces the halflife of prednisone, BBs, suldonamides, dapsone, NNRTIs Probenecid increases serum levels of rifampin Rifabutin has less effect on the metabolism of HIV protease inhibitors

Answer 141

MRSA, MRSE, prophylaxis of household members exposed to memingococci or H. influenza, eradication of staph in nasal carriers

Answer 142

Interferes w/ mycolic acid synthesis – disrupts cell wall synthesis; cidal for rapidly dividing bacilli; extracellular cavitary lesions; static for slowly growing lesions; penetrates host cells – effective for intracellular bacilli

Answer 143

Inability to take up the drug, alteration of target enzyme, overproduction of target enzyme, emerges rapidly (INH is never used as a single agent in active infections) – 1/10^6 will develop resistance, and the average cavitary lesion has 100 million bacteria

Answer 144

Absorbed rapidly from the GI tract with oral dose or can be given IM. Distributed to all tissues/ fluids (including placenta, meninges in meningitis, breast milk)

Answer 145

Acetylated via N-acetyl transferase (some people are fast metabolizers, some are slow – slow metabolizers have levels 2-3 times higher)- determines halflife of 1-5 hours

Answer 146

Drug and inactive metabolites excreted in the urine (~75%) – no adjustment w/ renal failure

Answer 147

Peripheral neuropathy due to competition w/ pyridoxical phosphate (corrected w/ B6 admin) – more frequent in malnourishment Hepatotoxic (2% major toxic rxn to metabolite)

Answer 148

Antacids w/ Al3+ salts decrease absorption; administer 1h before any antacids Corticosteroids decrease efficacy Inhibits P450 that metabolizes phenytoin, diazepam, fluoxentine, nelfinavir

Answer 149

Bacilli convert pyrazinamide to pyrazinoic acid, decreasing pH and inhibiting growth; resistant strains may lack pyrazinamidase/ cidal or static depending onconcentration in infected site

Answer 150

Active against tubercle bacilli in acid environment of lysosome & macrophage (most significant effect at intracellular sites where MTB replicates slowly)

Answer 151

Well/ rapidly absorbed within 2 hours & widely distributed- including to CSF

Answer 152

Metabolized in liver, excreted in urine via glomerular filtration

Answer 153

Dose related hepatotoxicity (most severe rxn), mild non gouty arthalgias, hyperuricemia is usually asymptomatic

Answer 154

Inhibition of RNA synthesis. Disrupts cell wall synthesis – inhibits arabinosyl transferase, necessary for peptidoglycan units of cell wall resulting in increased cell wall permeability Static, possibly cidal at high levels Bacilli must be actively dividing

Answer 155

Slow development of resistance | No cross resistance

Answer 156

Absorption of 75% dose, concentrates in kidneys, lungs, saliva, therapeutic levels in CSF with inflamed meninges , placenta, breast milk. Elimination – partly metabolized in the liver, excreted in the urine, T1/2 of 3.5 hours

Answer 157

Optic neuritis, dose related, decreased visual acuity, loss of color discrimination – monthly visual exams- reversible weeks to months after therapy, can cause allergic rxns, hyperuricemia, drug interactions (Al3+ containing antacids reduce absorption

Answer 158

Antiobiotic Second line drub TB

Answer 159

Blocks cell wall synthesis; structural analog of D-alaninel can block enzymes, L-alanine racemase & D-alanine synthetase/ enzymes for D-alanine incorporation into pentapeptide or peptidoglycan strands Depending on conc – cidal or static

Answer 160

Effective in resistant organisms – no cross-resistance | Broad spectrum, second-line agent, active against pulmonary and extra-pulmonary TB

Answer 161

Only used when other treatments fail – MDR-TB (INH, RIF-R) Used against mycobacterium avium Used to treat UTIs

Answer 162

Administered orally w/ good absorption (70-90%) Distributed widely & not protein bound Lungs, pleura, synovial fluid, CSF more when inflamed/ excreted unchanged –renal – dose adjustment in renal failure

Answer 163

Adverse effects – involve CNS – reversible when therapy is discontinued- Headache, tremor, vertigo, confusion, psychotic states w/ suicidal tendencies, paranoia, seizures (not for use in epileptic pts) – risk of suicide increased w/ depression / manifest within first 2 weeks

Answer 164

Aminopenicillins | Cell wall

Answer 165

Can be taken with food unlike other penicillins | =dose is affected by the state of the kidneys or admin of other organic acids

Answer 166

Aminopenicillins | Cell wall

Answer 167

MSSA, anaerobes | Can cause N/V in children

Answer 168

Aminopenicillins | Cell wall

Answer 169

Amp-R H influenza, mixed gram positive and anaerobic infections (CAP)

Answer 170

B-lactam | Cell wall

Answer 171

Small hydroxyethyl side chain makes it easier for B lactam to move through complex outer membrane of GN bacteria.

Answer 172

High resistance to beta-lactamases | Broadest spectrum of the B-lactams

Answer 173

Give IV Excreted by glomerular filtration and secretion Drug formulated w/ cilastatin to inhibit hydrolysis in brush border

Answer 174

Active against GN and GP, not as a monotherapy for P aeruginosa/ resistant nosocomial gram-negative (Enterobacter) / Combine w/ aminoglycoside to tx actinobacter

Answer 175

Contra-indicated in patients w/ CNS seizures/ expensive

Answer 176

(Cell wall) B-lactam 3rd generation cephalopsporin

Answer 177

Same 4 membered B-lactam ring as penicillins w/ a 6 membered dihydrothizide ring – more chemical binding sites More resistant to B-lactamases Broader spectrum

Answer 178

Effective in pts allergic to penicillin

Answer 179

1st  3rd = greater GN less GP / more resistance to B-lactamases / increased ability to enter CSF

Answer 180

Used for active infections – bacteremia, severe pulmonary infections use w/ aminoglycosidases, do not work against enterococci

Answer 181

Mostly IV/ IM (can be oral) | Renal Excretion

Answer 182

Binds to 50S ribosomal subunit / Static

Answer 183

More acid stable, rapid first pass metabolism (primary metabolite is still active), eliminated by kidney & liver Absorption increases w/ food Inhibits CYP P450 but not as much as erythromycin

Answer 184

``` Legionnaire’s disease Mycoplasma pneumonia Chlamydia pneumonia H influenza Strep pneumo & GAS Moraxella ```

Answer 185

Tetracycline | 30S – protein synthesis

Answer 186

First broad spectrum (GN & GP) Bacteriostatic – binding to the ribosome 30s is reversible Enters cell through porin channels

Answer 187

Resistance occurs slowly – can develop if the efflux pump is induced Inhibited by di & tri-valent cations

Answer 188

Best absorbed in acidic conditions of the stomach | Hepatic elimination

Answer 189

Adverse – N/V – less w/ doxy Superinfections, chelation of calcium (teeth discoloration/ depression of bone growth) Some vestibular toxicity (minoclycine), photosensitivity (doxy)

Answer 190

Used for Atypical pneumonia (Mycoplasma, Legionells, Chlamydia), Lyme disease, acne, periodontal disease

Answer 191

Binds to 50S ribosomal subunit / Static | Narrow spectrum

Answer 192

Admin orally, but increased acidity may inactivate Well –distributed but not to CSF Concentrates in liver (check liver functions) Excreted in bile/ feces Placenta/ breast milk

Answer 193

One of few drugs to cross into prostatic fluid and accumulates in macrophages

Answer 194

``` Legionnaire’s disease Mycoplasma pneumonia Chlamydia pneumonia GP & GN atypical organisms Can be used to eliminate the carrier state w/ corynebacterium diphtheria ```

Answer 195

Epigastric distress is the most common side effect Transient deafness Big time inhibitor of CYP P450 Cholestatic hepatitis

Answer 196

B-lactam | Cell wall

Answer 197

Not used in patients w/ seizures | Does not need co-admin of cilastatin

Answer 198

Best outcomes for Extended Spectrum Beta-lactam (ESBL) E coli & Klebsiella

Answer 199

Newer Fluoroquinolone

Answer 200

Analog of quinolone nalidixic acid Inhibition of bacterial DNA gyrase Bactericidal

Answer 201

Resistance via alterations in DNA gyrase enzyme (increases in SA and PA) = quinolone resistance-determining region (QRDR) Resistance – not plasmid mediated – decreased porins, energy-dependent efflux

Answer 202

Good oral absorption, wide distribution, decreased abs w/ antacids, poor CSF penetration, renal & liver excretion

Answer 203

Strep pneumo, Legionella, GN coverage similar to aminoglycosides – synergism w/ B-lactams

Answer 204

(Cell wall) | B-lactam

Answer 205

Does not need co-admin of cilastatin Less G+ activity Less CNS px

Answer 206

Best outcomes for Extended Spectrum Beta-lactam (ESBL) E coli & Klebsiella

Answer 207

Newer Fluoroquinolone

Answer 208

Analog of quinolone nalidixic acid Inhibition of bacterial DNA gyrase Bactericidal

Answer 209

Mostly hepatic clearance Not used for UTIs Hepatic elimination

Answer 210

(Cell wall) | B-lactam

Answer 211

An acid administered as a salt w/ high doses – evaluate pt w/ HTN CHF exists as a non-absorble anion, K+ moves into the tubule in exchange for H+  hypokalemic alkylosis

Answer 212

Can cause HS rxns, delayed allergic rxns, >2 days rash, more common with ampicillin & amoxicillin Hives/ uticaria Most life-threatening responses are caused by peritoneal drug admin

Answer 213

Adenocarcinoma | Non-squamous NSCLC

Answer 214

Humanized antibody, binds VEGF, given IV Inhibition promotes non-physiologic apoptosis of endothelial cells and decreases deposition of subendothelial matric making the vasculature more susceptible to severe bleeding

Answer 215

Risk of bleeding in squamous lung cancers – not approved | Can cause HTN

Answer 216

Forms DNA intra-strand cross-links and adducts

Answer 217

Allergic (platinum rxns) Dose-related myelosuppression; cumulative anemia Dose-related N/V Blood chemistry dyscrasia, increase in hepatic enzymes, BUN & creatinine

Answer 218

SCLC/ NSCLC

Answer 219

Forms DNA intra-strand cross-links and adducts

Answer 220

Dose-related severe nephrotoxicity, myelosuppression, N/V | Significant ototoxicity

Answer 221

Adenocarcinoma

Answer 222

Reversible multi-kinase inhibitor, ALK | CYP3A4 inhibitor

Answer 223

Oral on empty stomach

Answer 224

Visual disorders are common

Answer 225

Pro-drug of active alkylating moiety

Answer 226

``` Blood dyscrasias  anemia Hemorrhagic cystitis (mesna) Infertility Monitor for 2ndary malignancies Pulmonary fibrosis ```

Answer 227

Intercalator, free radical generator, topo II inhibitor (DNA STRUCTURE)

Answer 228

``` Myelosuppresion, Cumulative dose cause CHF Hepatic disease 2ndary malignancies Extravasational necrosis N/V ```

Answer 229

Adenocarcinoma

Answer 230

EGFR kinase inhibition (lung cx) – most never smokers Mutations high in Asian populations

Answer 231

Oral, few side effects

Answer 232

DNA-topo II complex stabilizer

Answer 233

Myelosuppression, infection N/V Diarrhea, alopecia

Answer 234

DNA polymerase inhibitor via incorpotation of triphosphate form during DNA synthesis (DNA SYNTHESIS)

Answer 235

Myelosuppression, arthralgia, sensory peripheral neuropathy

Answer 236

Intra- and Inter- strand cross-linker

Answer 237

Alopecia, N/V, blood dyscrasia  infection

Answer 238

Hemorrhagic cystitis is rare when ifosfamide is given together with mesna. Dose-limiting side effect is encephalopathy

Answer 239

SCLC Myelosuppression and GI toxicity | Elevated liver functions and serum creatinine

Answer 240

Prevents DNA from unwinding by inhibition of topoisomerase 1.

Answer 241

Myelosuppression and GI toxicity | Elevated liver functions and serum creatinine

Answer 242

Folic Acid analog Dihydrofolate reductase inhibition (universal) Folic acid essential dietary factor Polyglutamation (which traps drug) also inhibits thymidylate synthase (TS) and 2 early enzymes in purine biosynthesis Rescue other cells with Leucovorin

Answer 243

Methotrexate is a highly teratogenic drug and categorized in pregnancy category X

Answer 244

Micro tubule (MT) stabilizer inhibiting depolymerization (MT)

Answer 245

``` Inhibiting dihydrofolate reductase (DHFR) DHFR inhibitor (DNA SYNTHESIS) ```

Answer 246

Low blood cell counts, as measured by a Complete Blood Count. This is a dose-limiting toxicity.

Answer 247

DNA topo I complex stabilizer

Answer 248

Myelosuppression and GI toxicity | Hyperbilirubinemia

Answer 249

MT inhibitor, tubules disintegrate into spiral aggregates/ protofilaments

Answer 250

Peripheral neuropathy, hyponatremia, constipation, and hair loss. First symptoms of peripheral neuropathy is foot drop:

Answer 251

MT inhibitor, tubules disintegrate into spiral aggregates/ protofilaments

Answer 252

Neutropenia, (peripheral neuropathy)

Pulmonary Pharmacology Hit List Flashcards

(295 cards)