Block 3 ALL Flashcards

Question

Patient presents with hot tub folliculitis, nosocomial pneumonia, nosocomial UTI Microscopy shows motile gram-negative bacteria, catalase positive, oxidase positive. What is the likely organism? & Which type of Monobactam would you give?

Answer 1

Likely organism: Pseudomonas aeruginosa infections Treatment: Give an Antipseudomonal Antibiotics like: Monobactam Aztreonam

Answer 2

Likely organism: Pseudomonas aeruginosa infections Treatment: Give an Antipseudomonal Antibiotics like: Cephalosporins 3rd gen Ceftazidime & Cefoperazone 4th gen Cefepime & Cefpirome

Answer 3

Pseudomonas aeruginosa

Answer 4

Antipseudomonal Carbapenems Imipenem Meropenem Ertapenem Doripenem MOA: Beta-lactam antibiotics (DAlaDAla analogs) that bind & block PBP to prevent cross-linking of peptidoglycans thereby inhibiting cell wall synthesis Clinical indications (broad spectrum β-lactamase resistant) **Last-resort drugs 1. Pseudomonas aeruginosa infection 2. Gram-positive cocci; except for MRSA Adverse Effects: 1) GI distress 2) Rash 3) CNS toxicity (seizures) at high plasma levels 4) confusion Mechanism of Resistance: They are inactivated by carbapenems (K. pneumonia, E. coli, E. aerogenes)

Answer 5

Antipseudomonal Carbapenems

Answer 6

Cilastatin is a renal dehydroepeptidase inhibitor to reduce inactivation of the drug in renal tubules.

Answer 7

Antipseudomonal Penicillin's are Carbenicillin, Piperacillin, & ticarcillin. MOA: They are D-Ala-D-Ala analogs (B-lactams) that block transpeptidase peptidoglycan cross-linking & they bind PBP (transpeptidases) to activate autolytic enzymes to trigger lysis Adverse Effects: 1) hypersensitivity reactions 2) Direct Coombs +ve hemolytic anemia 3) Interstitial nephritis 4) Pseudomembranous colitis

Answer 8

Cephalosporins (beta-lactam antibiotics) MOA: β-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases & they bind PBP (transpeptidases) to activate autolytic enzymes to trigger lysis Adverse Effects: 1) hypersensitivity reactions 2) autoimmune hemolytic anemia 3) disulfiram-like reaction 4) vitamin K deficiency Mechanism of Resistance: inactivated by cephalosporinases (type of β-lactamase) –– structural change in PBPs

Answer 9

There is a low rate of cross-reactivity even in penicillin-allergic patients resulting in an increase in nephrotoxicity

Answer 10

PBP/transpeptidase Inhibitor prevents cross linking of peptidoglycan to weaken the cell wall & trigger lysis

Answer 11

Piperacillin & Mezlocillin

Answer 12

Carbenicillin & Ticarcillin

Answer 13

Cephalosporins: 1st: Cefazolin 2nd: Cefotetan 3rd gen: ceftriaxone, cefotaxime, cefpodoxime, & ceftazidime 4th gen: cefepime & Cefpirome 5th: Ceftaroline & Ceftobiprole MOA: β-lactam antibiotic (transpeptidase/PBP inhibitor) that inhibits cell wall synthesis but that is less susceptible to penicillinases AE: 1) Hypersensitivity (allergy) most common with cefazolin 2) Autoimmune hemolytic anemia (+ve Coombs test) 3) Disulfiram-like reaction to alcohol 4) Vitamin K deficiency 5) Increases nephrotoxicity of aminoglycosides

Answer 14

Cephalosporins

Answer 15

Cephalosporins get inactivated by cephalosporinases (type of β-lactamase) or structural change in PBPs

Answer 16

5th: Ceftaroline & Ceftobiprole

Answer 17

2nd: Cefotetan 3rd gen: ceftriaxone, cefotaxime, cefpodoxime, & ceftazidime

Answer 18

Monobactam (Beta-lactam antibiotic) MOA: It is less susceptible to β-lactamases & it prevents peptidoglycan cross-linking by binding to penicillin-binding protein 3 (PBP3) it treats gram -ve infections (E.coli & pseudomonas) Its Synergistic with aminoglycosides Adverse Effects: 1) Gi upset 2) Phlebitis 3) Skin rash 4) Occasional liver dysfunction only good for gram -ve bacteria (E.coli & pseudomonas) & it has no cross reactivity! (good for penicillin allergies)

Answer 19

MOA: Cation polypeptides that bind to phospholipids on cell membrane of gram-negative bacteria to disrupt the cell membranes integrity leading to leakage of cellular components and subsequent cell death Adverse Effects: 1) nephrotoxicity 2) neurotoxicity (slurred speech, weakness, paresthesia) 3) respiratory failure

Answer 20

Polymyxins (Colistin [polymyxin E], polymyxin B)

Answer 21

Carbapenems, they are synthetic beta-lactam antibiotics

Answer 22

Imipenem, Meropenem, Doripenem, & Ertapenem

Answer 23

Imipenem because it is metabolized in the kidney into an inactive form which can be toxic

Answer 24

Cilastatin

Answer 25

1st gen cephalosporin

Answer 26

2nd gen cephalosporins

Answer 27

3rd gen cephalosporins

Answer 28

4th gen cephalosporins

Answer 29

5th gen cephalosporin

Answer 30

They bind Beta-lactam enzymes & prevent them from inactivating antibiotics these include Clavulanic acid, Sulbactam & Tazobactam

Answer 31

Beta-lactam inhibitors that bind Beta-lactam enzymes & prevent them from inactivating antibiotics

Answer 32

MOA: They bind to 30S subunit of bacterial ribosomes to prevent the attachment of aminoacyl-tRNA & block bacterial protein synthesis. Treat infections like cholera, Rocky Mountain Spotted Fever, Chlamydia, & Lyme disease Adverse effects: 1) Gastric discomfort 2) Esophagitis 3) Hepatotoxicity at high doses (minocycline)

Answer 33

TCAs (30s inhibitors)

Answer 34

Bactericidal drugs that inhibit the 30S subunit to inhibit the formation of the initiation complex, translocation, & causing misreading mRNA & preventing bacterial protein synthesis. It is used for treating serious gram -ve bacilli infections (pseudomonas) Adverse effects: 1) Ototoxicity (avoid with loop diuretics) 2) Nephrotoxicity (ATN) 3) Neuromuscular paralysis (avoid in myasthenia gravis!) 4) Dermatitis (topical neomycin) 5) Teratogenic

Answer 35

Aminoglycosides Gentamycin Neomycin Amkimycin Tobramycin Streptomycin

Answer 36

Doxycycline because it is excreted in the poop

Answer 37

Avoid milk, antacids, or iron-containing preparations because things like Calcium, magnesium, and iron ions (divalent ions) bind to drug, inhibiting drug’s absorption in gut

Answer 38

Rickettsia (Rocky Mountain Spotted Fever) Borrelia burgdorferi Chlamydia spp. M. pneumoniae Acne Community-acquired MRSA

Answer 39

1) Plasmid-encoded active transport pumps will reduce the uptake or increased the efflux out of bacterial cells & 2) By making a protein that enables translation despite TCA presence

Answer 40

Treats aerobic organisms only & especially Severe gram-negative rod infections (pseudomonas)

Answer 41

Streptomycin

Answer 42

Acute tubular necrosis

Answer 43

Presents with hearing loss and tinnitus Risk compounded with loop diuretics (also cause ototoxicity) Damage to CN VIII can also lead to vestibular ataxia and vertigo

Answer 44

Through enzyme modification of the drug, bacterial transferases inactivate the drug via acetylation, phosphorylation, & adenylation. Seen with Enterococcus

Answer 45

They develop resistant against beta-lactamases (penicillinase)

Answer 46

Its a condition that is mediated by histamine (pseudo-allergic reaction) from mast cells, & it is not dependent on IgE signaling Preventable with pre-treatment with antihistamines

Answer 47

What are first generation cephalosporins? cefaZOLIN cephaLEXIN

Answer 48

They are beta lactam antibiotics highly effective against gram-positive cocci like staph and strep bacteria so they are used for preoperative antibiotic prophylaxis, to prevent wound infections caused by skin bacteria Also good against some gram -ve: H. influenzae Enterobacter aerogenes Neisseria Serratia marcescens Proteus mirabilis E. Coli Klebsiella pneumoniae

Answer 49

What are second generation cephalosporins? cefoxitin, cefaclor, cefuroxime, and cefotetan

Answer 50

They are beta-lactam antibiotics that are widely used in the hospital setting. They have broad coverage, as they are effective against both gram +ve and gram -ve bacteria. Ceftriaxone is used to treat bacterial meningitis, Lyme disease, and gonorrhea. Ceftazidime can treat pseudomonas infections.

Answer 51

What are 3rd generation cephalosporins? cefTRIAXONE cefTAZIDIME CefoTAXIME CefPODOXIME ceFIXime

Answer 52

a 3rd gen cephalosporin used to treat: 1) Meningitis: Crosses blood-brain-barrier (BBB) 2) Neisseria gonorrhoeae 3) Lyme

Answer 53

a 3rd gen cephalosporin used to treat: Pseudomonas aeruginosa

Answer 54

Ceftriaxone

Answer 55

Ceftazidime

Answer 56

beta-lactam antibiotics that are relatively newer cephalosporin drugs. Broad gram positive and negative coverage & especially used to treat Pseudomonas aeruginosa

Answer 57

What are 4th generation cephalosporins? Cefepime

Answer 58

A broad spectrum coverage against gram +ve and gram -ve bacteria, Reserved as one of the only effective treatments against MRSA, or methicillin-resistant staph aureus.\ Does NOT cover Pseudomonas aeruginosa

Answer 59

What are 5th generation cephalosporins? ceftaroline

Answer 60

Glycycline a broad-spectrum antibiotic (TCA derivative) that binds & inhibits 30S to block bacterial protein synthesis. It is used as a last resort treatment for multi-drug resistant organisms (MRSA & VRE) Adverse effects: Severe bleeding Nausea/vomiting Higher mortality rate

Answer 61

Tigecycline

Answer 62

MOA: Bacteriostatic (Bind to the 23S rRNA of the 50S ribosomal subunit to block translocation to inhibit bacterial protein synthesis Used for treating: 1) Atypical pneumonias (Legionella or Mycoplasma) 2) STI (chlamydia and gonorrhea) 3) Bordetella pertussis 4) Gram-positive cocci (streptococcal) in patients allergic to penicillin Adverse: Motility issues Arrythmias (prolonged QT) acute Cholestatic hepatitis (in patients with liver dysfunction) Rash eOsinophilia "MACRO" Complication: Torsades de Pointes Resistance: Methylation of 23S rRNA-binding site prevents binding of drug

Answer 63

adverse effects of macrolides

Answer 64

Macrolides Azithromycin Clarithromycin Erythromycin

Answer 65

Azithromycin

Answer 66

MOA: Bacteriostatic It binds the 50S subunit of bacterial ribosomes to prevent bacterial protein synthesis It is used as a second- or third-line therapy for 1) Bacterial Meningitis (H.influenzae, N. meningitis, S.pneumoniae) 2) Rickettsial diseases

Answer 67

chloramphenicol

Answer 68

Gray baby syndrome, an adverse effect of Chloramphenicol

Answer 69

MOA: Bacteriostatic It binds the 50S subunit of bacterial ribosomes to prevent bacterial protein synthesis It is used as a second- or third-line therapy for 1) Bacterial Meningitis (H.influenzae, N. meningitis, S.pneumoniae) 2) Rickettsial diseases Adverse Effects: 1) Anemia (dose dependent) 2) Leukopenia 3) Thrombocytopenia (Reversible by stopping medication) 4) Aplastic anemia (dose independent) 5) Gray-baby syndrome Premature infants lack liver UDP-glucuronosyltransferase and cannot metabolize the drug, leading to toxic accumulation Resistance: acetyltransferase to inactivate the drug

Answer 70

MOA: It targets the 50S subunit of bacterial ribosomes by blocking bacterial protein synthesis and stopping bacterial growth. Treats: 1) anaerobic bacterial infections that arise above the diaphragm e.g. Bacteroides spp., Clostridium perfringens 2) Aspiration pneumonia 3) lung abscesses 4) bacterial vaginosis 5) oral infections 6) Invasive group A streptococcal (S. pyogenes) infection Adverse effects: Pseudomembranous colitis

Answer 71

clindamycin

Answer 72

MOA: It binds the 50S subunit of bacterial ribosomes & blocks the formation of initiation complex to inhibit bacterial protein synthesis Treats: 1) Gram-positive species including MRSA and VRE (Usually as a last-resort for multi-drug resistant infections) Adverse effects: 1) Bone marrow suppression (Anemia, leukopenia, and thrombocytopenia) 2) Neuropathy optic neuritis and peripheral neuropathy) 3) Serotonin syndrome (Due to partial monoamine oxidase (MAO) inhibition A higher risk with the use of other serotonergic drugs (e.g. MAOIs, SSRIs) Resistance: A Point mutation of ribosomal RNA that changes the 50S binding site

Answer 73

MOA: Cation polypeptides that disrupts cell membrane causing leakage of cellular components and cell death Treat: colistin and other polymyxins last-resort therapy for multidrug-resistant gram-negative bacteria e.g. P. aeruginosa, E. coli, K. pneumoniae Adverse effects: 1) Nephrotoxicity 2) Neurotoxicity (slurred speech, weakness, paresthesia's) 3) Respiratory failure

Answer 74

Polymyxins Colistin (polymyxin E) Polymyxin B

Answer 75

MOA: 50S inhibitors to prevent bacterial protein synthesis

Answer 76

MOA: Inhibit topoisomerase II (DNA gyrase) and topoisomerase IV to impair bacterial DNA synthesis by preventing inhibiting DNA winding and unwinding, which causes the strand breaks avoid antacids (they reduce oral absorption of drug, reducing its efficacy) Treat: 1) Gram -ve rods in urinary and GI tracts (e.g. Pseudomonas) 2) Some gram-positive organisms 3) Otitis externa Adverse effects: 1) Tendonitis/Tendon rupture (Achilles tendon rupture) 2) Possible cartilage damage (Avoid in children) 3) Prolonged QT interval (Torsades de Pointes risk) 4) Superinfections Resistance: 1) Mutated DNA gyrase/topoisomerase genes 2) Efflux pumps

Answer 77

fluoroquinolones suffix “-floxacin” Ciprofloxacin, Moxifloxacin, or Levofloxacin

Answer 78

Ciprofloxacin Can lead to drug interactions (e.g. warfarin, theophylline)

Answer 79

Inhibit bacterial protein synthesis 30S inhibitors 50S inhibitors Folate antagonists

Answer 80

that inhibit cell wall synthesis Peptidoglycan synthesis inhibitors: 1) Glycopeptides Peptidoglycan cross-linking: 1) Penicillinase-Sensitive penicillin's 2) Penicillinase-resistant penicillin's 3) Antipseudomonal 4) Cephalosporins 5) Carbapenems 6) Monobactams

Answer 81

Inhibit topoisomerase II (DNA gyrase) and topoisomerase IV to impair bacterial DNA synthesis by preventing inhibiting DNA winding and unwinding, which causes the strand breaks

Answer 82

Nalidixic acids

Answer 83

MOA: Folate antagonists (Impairs folate synthesis in bacteria) The drugs have chemical analogs of para-aminobenzoic acid (PABA), a folic acid precursor for bacteria which binds to and inhibits dihydropteroate synthase, preventing bacterial conversion of PABA to folic acid Clinical use (with trimethoprim): 1) Synergistic block of bacterial folate synthesis 2) Gram-positive organisms (e.g. Nocardia) 3) Gram-negative organisms Adverse effects: 1) Hypersensitivity reactions (sulfa allergy) 2)Hemolysis with G6PD deficiency 3) Nephrotoxicity (tubulointerstitial nephritis) 4) Photosensitive rash (Can develop into Stevens-Johnson syndrome) 5) Infantile kernicterus 6) Causes drug interactions (e.g. raises warfarin levels) Resistance: 1) Mutations in enzyme (bacterial dihydropteroate synthase) 2) Decreased uptake 3) Increased PABA synthesis

Answer 84

trimethoprim

Answer 85

sulfonamides

Answer 86

MOA: Folate antagonist (it inhibits bacterial folate synthesis) by blocking bacterial dihydrofolate reductase (DHFR) Broad-spectrum when used in with sulfonamides: 1) Urinary tract infections (UTIs) 2) Shigella 3) Salmonella 4) Pneumocystis jirovecii pneumonia 5) Toxoplasmosis prophylaxis 6) Community-acquired MRSA Adverse effects: 1) Hyperkalemia (high doses) 2) drug interactions (e.g. raises warfarin levels) by inhibiting CYP Enzymes 3) Displace warfarin from albumin, increasing effective dosing 4) Folate deficiency 5) Teratogenic (neural tube defects)

Answer 87

trimethoprim

Answer 88

Folate deficiency

Answer 89

MOA: Inhibits DNA-dependent RNA polymerase to reduce mRNA synthesis Used to treat: 1) Mycobacteria (M. tuberculosis (TB)) (RIPE regimen) 2) M. leprae (Delays resistance to dapsone when used for leprosy) 3) M. avium complex 4) N. meningitidis (Used for prophylaxis of close contacts) 5) H. influenzae type b (Used for prophylaxis of close contacts) Adverse effects: 1) orange body fluids 2) Induces CYP450 enzymes 3) Hepatotoxicity (Elevations of AST and ALT levels) 4) Nephrotoxicity (May cause acute interstitial nephritis) Resistance: 1) Mutations in RNA polymerase reduce drug binding 2) Monotherapy in TB rapidly leads to resistance

Answer 90

Rifampins Rifampin Rifabutin

Answer 91

Rifampin's

Answer 92

Rifabutin is favored in patients with an HIV infection because of less CYP450 induction

Answer 93

MOA: It forms toxic free radicals in the bacterial cell wall that damage DNA Bactericidal, antiprotozoal Used to treat: 1) Giardia 2) Entamoeba histolytica 3) Trichomonas vaginalis 4) Gardnerella vaginalis 5) Anaerobes (Bacteroides, C. difficile) 6) Used to treat anaerobic infections below the diaphragm (clindamycin used above) 7) H. pylori (in patients with penicillin allergies) Adverse effects: 1) Disulfiram-like reaction with alcohol (Inhibition of acetaldehyde dehydrogenase, a toxic buildup of acetaldehyde occurs) 2) GI upset (nausea, vomiting, abdominal pain) 3) Neuropathy (paresthesia's, dizziness) 4) Headache

Answer 94

Metronidazole

Answer 95

Disulfiram-like reaction with alcohol (Inhibition of acetaldehyde dehydrogenase, a toxic buildup of acetaldehyde occurs)

Answer 96

MOA: Disrupts cell membranes by creating transmembrane channels Causes intracellular leakage and membrane depolarization Ultimately inhibits DNA, RNA, and protein synthesis, leading to bacterial death Used to treat (Gram +ve bacterial infections): 1) Gram-positive cocci 2) S. aureus skin infections (esp. MRSA) 3) bacteremia 4) endocarditis 5) VRE Adverse effects: 1) Myopathy 2) Rhabdomyolysis 3) Creatinine kinase (CK) levels may rise due to release from skeletal muscle

Answer 97

Daptomycin

Answer 98

Not used for pneumonia Avidly binds to and is inactivated by alveolar surfactant

Answer 99

MOA: Makes cation glycoproteins against cell membranes A last-resort therapy for multidrug-resistant gram-negative bacteria (P. aeruginosa, E. coli, K. pneumoniae) Adverse effects: 1) Nephrotoxicity 2) Neurotoxicity (slurred speech, weakness, paresthesia's) 3) Respiratory failure

Answer 100

Colistin (polymyxin E) & Polymyxin B

Answer 101

Echinocandins: MOA: They inhibit cell wall synthesis by inhibiting the synthesis of B-glucan Used to treat: 1) Invasive aspergillus 2) Candida infection Adverse Effects: 1) Hepatotoxicity (Elevated AST and ALT) 2) GI upset (mild) 3) Infusion-associated hypersensitivity (Rash, hypotension, bronchospasm, and angioedema rarely occur due to local histamine release)

Answer 102

adverse effects of Caspofungin, Micafungin, & Anidulafungin (Echinocandins)

Answer 103

MOA: Nucleoside analogs inhibit reverse transcriptase by competing with nucleosides, leading to DNA chain termination. They lack a 3'OH group, preventing synthesis of DNA from viral RNA. Activation through phosphorylation is necessary, except for tenofovir. Clinical use: 1) HIV (HIV 1 & 2) 2) ZDV (general prophylaxis and during pregnancy to reduce risk of fetal transmission) Adverse effect: 1) Hypersensitivity (Abacavir) 2) Bone marrow suppression 3) Anemia (zidovudine) 4) Pancreatitis (didanosine) 5) Lipoatrophy 6) hepatic steatosis 7) Wasting of subcutaneous fat 8) Peripheral neuropathy 9) Lactic acidosis

Answer 104

Hypersensitivity (Abacavir) it is seen in patients with HLA B*57:01 allele. It is caused by Type 4 HSR with fever, nausea, vomiting, rash

Answer 105

They can be reversed with granulocyte colony-stimulating factor (G-CSF) and erythropoietin

Answer 106

Hypersensitivity

Answer 107

Tenofovir (the rest are nucleosides)

Answer 108

Classification: NRTI MOA: Competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3’OH group). It needs to be phosphorylated to be activated. Clinical uses: 1) HIV therapy 2) General prophylaxis and during pregnancy to decrease risk of fetal transmission (ZDV) Adverse effect: 1) bone marrow suppression (reversed with G-CSF and erythropoietin) 2) peripheral neuropathy 3) lactic acidosis 4) anemia

Answer 109

Zidovudine

Answer 110

MOA: They are Guanosine analog inhibits viral DNA polymerase. They causes DNA chain termination, to prevent viral DNA replication NEED phosphorylation by HSV/VZV thymidine kinase to be activated Clinical use: 1) HSV (used for mucocutaneous and genital lesions, meningoencephalitis but they can't eliminate latent forms) 2) VZV (they can't eliminate latent forms)

Answer 111

Acyclovir, Valaciclovir, & Famciclovir

Answer 112

They are negligible activity against EBV and CMV (EBV and CMV produce different thymidine kinases with lower affinity for acyclovir, reducing phosphorylation and activation

Answer 113

MOA: A bactericidal that inhibits prokaryotic enzymes topoisomerase II (DNA gyrase) and topoisomerase IV Avoid with antacids Adverse effects: superinfections Tendonitis/rupture Resistance: chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps

Answer 114

fluroquinolones

Answer 115

Classification: rifamycin MOA: It inhibits DNA-dependant RNA polymerase Used for treating: 1) Mycobacterium tuberculosis (delay resistance to Dapsone when used for leprosy) 2) meningococcal prophylaxis 3) chemoprophylaxis in contacts of children with H. influenza type b Adverse Effects: 1) minor hepatotoxicity 2) drug interactions (increases cytochrome P450) 3) orange body fluids Resistance: mutations reduce drug binding to RNA polymerase –– monotherapy rapidly leads to resistance

Answer 116

MOA: bacteriostatic Inhibit protein synthesis by blocking translocation by binding to the 23S rRNA of the 50S ribosomal subunit Clinical Indications: 1) atypical pneumonias (Mycoplasma, Chlamydia, Legionella) 2) STIs (Chlamydia) 3) gram positive cocci (streptococcal infections in patients allergic to penicillin) 4) B. pertussis Adverse effects: MACRO: gastrointestinal Motility issues (stimulate motilin) Arrhythmia (prolonged QT interval) acute Cholestatic hepatitis Rash eOsinophilia

Answer 117

Macrolides

Answer 118

Classification: aminoglycosides MOA: bactericidal It irreversibly inhibits the initiation of the complex through binding of the 30S subunit which can cause misreading of mRNA & also block translocation. They require O2 for uptake; therefore, ineffective against anaerobes. Clinical Indications: 1) severe gram-negative rod infections (synergistic with β-lactam antibiotics) Adverse Effects: 1) nephrotoxicity (proteinuria, hypokalemia, acidosis, acute tubular necrosis) 2) neuromuscular blockage (decrease release of Ach [absolute contraindication with MG]) 3) ototoxicity (especially with loop diuretics) 4) teratogenicity Resistance: bacterial transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation MOA

Answer 119

Aminoglycosides

Answer 120

aminoglycosides

Answer 121

bacterial transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation

Answer 122

Classification: bacteriostatic antibiotic MOA: It blocks peptidyl transferase at 50S ribosomal subunit –– Clinical Indications: 1) meningitis (H. influenzae, N. meningitidis, S. pneumoniae) 2) rickettsial diseases (Rocky Mountain Spotted Fever) Adverse Effects: 1) bone marrow suppression (dose dependant) 2) anemia (dose independent) 3) aplastic anemia (dose dependant) 4) gray baby syndrome (premature infants because they lack UDP-glucuronosyltransferase) Resistance: plasmid-encoded acetyltransferase inactivates the druga

Answer 123

Chloramphenicol

Answer 124

Classification: viral DNA/RNA polymerase inhibitor MOA: A Guanosine analog that inhibits viral DNA polymerase causing DNA chain termination & preventing viral DNA replication. It needs CMV kinase to phosphorylate it to its active triphosphate form Clinical Indications: 1) CMV (especially in immunocompromised patients) Adverse Effects: 1) hepatic and neurologic dysfunction 2) bone marrow suppression (leukopenia, neutropenia, thrombocytopenia) 3) renal toxicity 4) seizures (overdose) Resistance: through mutated viral kinase

Answer 125

Ganciclovir

Answer 126

a prodrug of ganciclovir that has better oral bioavailability

Answer 127

Classification: guanine analog MOA: monophosphorylated by HSV/VZV thymidine kinase and not phosphorylated in uninfected cells therefore few adverse effects. The triphosphate is formed by cellular enzymes & preferentially inhibits viral DNA polymerase by chain termination Clinical Indications: 1) HSV and VZV weak activity against EBV used for HSV-induced mucocutaneous and genital lesions as well as for encephalitis 2) prophylaxis in immunocompromised patients Adverse Effects: 1) nausea, diarrhea and headache (oral dosing) 2) obstructive crystalline nephropathy and acute kidney injury if not adequately hydrated Resistance: mutated viral thymidine kinase

Answer 128

Classification: NRTI MOA: It competitively inhibits nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3’OH group). It needs to be phosphorylated to be activated. Clinical Indications: 1) HIV therapy 2) general prophylaxis and during pregnancy to decrease risk of fetal transmission Adverse Effects: bone marrow suppression (reversed with G-CSF and erythropoietin), peripheral neuropathy lactic acidosis anemia

Answer 129

Zidovudine

Answer 130

Classification: integrase inhibitor MOA: It inhibits the HIV genome integration into host cell chromosome by reversibly inhibiting HIV integrase (HIV-1 and HIV-2). There are no CYP interactions making it relatively safe. It is used to treat: 1) HIV  Adverse Effects: 1) toxicity leads to increased creatine kinase

Answer 131

Raltegravir

Answer 132

Classification: viral DNA/RNA polymerase inhibitor and HIV reverse transcriptase inhibitor MOA: It binds to the pyrophosphate-binding site of enzyme & it does not require any kinase activation.  Clinical Indications: 1) CMV retinitis in immunocompromised patients when ganciclovir fails 2) acyclovir-resistant HSV  Adverse Effects: 1) nephrotoxicity 2) electrolyte abnormalities (hyper/hypocalcemia, hyper/hypophosphatemia, hypokalemia, hypomagnesemia) can lead to seizures Resistance: mutated DNA polymerase

Answer 133

They Inhibit retroviral integrase & blocks integration of HIV viral DNA (made by reverse transcriptase) into host cell chromosome to prevent viral replication Used to treat: 1) HIV They are effective againstHIV-1 and HIV-2 (they are apart of the highly-active antiretroviral therapy (HAART) Usually 3 drugs: 2 NRTIs and integrase or protease inhibitor) Myositis (myopathy) Increase creatine kinase levels

Answer 134

Integrase Inhibitors Drug Names (-tegravir ending) Raltegravir Dolutegravir Bictegravir Elvitegravir

Answer 135

Classification: NMDA receptor antagonist (antiviral) MOA: It blocks muscarinic receptors to increase DA release and decrease DA reuptake Adverse Effects: 1) insomnia 2) dizziness 3) confusion 4) ankle edema 5) atropine-like 6) livedo reticularis

Answer 136

Amantadine

Answer 137

Classification: Sialic acid analogs MOA: That bind & inhibit neuraminidase which prevents cleavage of viral progeny off of the cell surface & blocking the new viral particles to exit the cell. They may also slow the viral penetration into the airway epithelium They treat: 1) Influenza virus (flu) both influenza A and B infections Beginning within 48 hours of symptom onset can shorten course of illness Adverse effects: 1) Gastrointestinal upset 2) Zanamivir may exacerbate COPD and asthma (because it is an inhaled dry powder)

Answer 138

Oseltamivir and zanamivir

Answer 139

Classification: integrase inhibitor MOA: It inhibits HIV genome integration into host cell chromosome by reversibly inhibiting HIV integrase (HIV-1 and HIV-2). It doesn't have any CYP interactions Clinical Indications: HIV therapy Adverse Effects: toxicity leads to increased creatine kinase

Answer 140

Raltegravir

Answer 141

MOA: It inhibits synthesis of guanine nucleotide by competitively inhibiting IMP dehydrogenase Clinical Indications: 1)Hepatitis C 2)RSV Adverse Effects: 1) Hemolytic anemia 2) severe teratogen

Answer 142

Classification: cell membrane integrity inhibitor (polyene) MOA: It binds ergosterol to form membrane pores that allow leakage of electrolytes Clinical Indications: 1) serious, systemic mycoses 2) Cryptococcus 3) Blastomyces 4) Coccidiosis 5) Histoplasmosis 6) Candida 7) Mucor Adverse Effects: 1) fever/chills 2) hypotension 3) nephrotoxicity 4) arrythmias 5) anemia 6)IV phlebitis hydration helps decrease nephrotoxicity

Answer 143

Amphotericin B

Answer 144

+/– flucytosine

Answer 145

Supplement K+ and Mg2+ because of altered renal tubule permeability

Answer 146

Hydration reduces nephrotoxicity

Answer 147

Classification: echinocandins (cell wall synthesis inhibitor) MOA: It inhibits cell wall synthesis by inhibiting synthesis of β-glucan Clinical Indications: 1) invasive aspergillosis 2) Candida Adverse Effects: 1) GI upset 2) flushing (r/t histamine release)

Answer 148

Caspofungin

Answer 149

Classification: ergosterol synthesis inhibitor (azoles) MOA: It inhibits fungal sterol (ergosterol) synthesis by inhibiting the cytochrome P-450 enzyme (14-α-demethylase) that converts lanosterol to ergosterol Clinical Indications: 1) alternative drugs in candidemia and infections caused by Aspergillus, Blastomyces, Cryptococcus, and Histoplasma Note ketoconazole is rarely used in systemic fungal infections Adverse Effects: 1) testosterone synthesis inhibition (gynecomastia, decreased libido) 2) liver dysfunction (increased LFTs, hepatoxicity [inhibits cytochrome P-450])

Answer 150

Ketoconazole

Answer 151

Isoniazid, sulfonamides, dapsone, primaquine, aspirin, ibuprofen, nitrofurantoin "hemolysis is D PAIN"

Answer 152

Hemolysis in G6PD deficiency

Answer 153

Chloramphenicol

Answer 154

Gray baby syndrome

Answer 155

Dapsone, clozapine, carbamazepine, propylthiouracil, methimazole, colchicine, ticlopidine, ganciclovir "Drugs Can Cause Pretty Major Collapse To Granulocytes"

Answer 156

Agranulocytosis

Answer 157

Carbamazepine, methimazole, NSAIDs, benzene, chloramphenicol, propylthiouracil "Can’t Make New Blood Cells Properly"

Answer 158

Aplastic anemia

Answer 159

Penicillin, methylDopa, Cephalosporins "P Diddy Coombs"

Answer 160

Direct Coombs ⊕ hemolytic anemia

Answer 161

Allopurinol, antiBiotics, antiConvulsants, sulfa drugs "ABCs"

Answer 162

Drug reaction with eosinophilia and systemic symptoms

Answer 163

Indinavir, heparin, quinidine, ganciclovir, vancomycin, linezolid, abciximab "I Have Quickly Gotten Very Low Amounts"

Answer 164

Thrombocytopenia

Answer 165

Anti-epileptic drugs (especially lamotrigine), allopurinol, sulfa drugs, penicillin "Steven Johnson has Epileptic Allergy to Sulfa drugs and Penicillin"

Answer 166

Rash (Stevens-Johnson syndrom

Answer 167

Fluoroquinolones

Answer 168

Tendon/cartilage damage

Answer 169

Statins, fibrates, niacin, colchicine, daptomycin, hydroxychloroquine, interferon-α, penicillamine, glucocorticoids

Answer 170

A → fusion inhibitor

Answer 171

B → NRTIs and NNRTIS

Answer 172

C → It inhibits virion release because it's a neuraminidase inhibitor

Answer 173

D → Integrase inhibitor

Answer 174

E → It inhibits uncoating of the influenza A virus only

Answer 175

Classification: NMDA receptor antagonist (antiviral) MOA: It blocks the muscarinic receptors to increase DA release and decrease DA reuptake Clinical use: HIV  Adverse Effects: 1) insomnia 2) dizziness/confusion 3) ankle edema 4) atropine-like, livedo reticularis

Answer 176

MOA: They Inhibit fungal ergosterol synthesis by inhibiting the 14-alpha-demethylase (a cytochrome P450 enzyme), thereby blocking ergosterol synthesis Inhibits formation of fungal cell membrane (note: no effect on fungal cell wall) Clinical uses: 1) Local and less serious mycoses 2) Cryptococcal meningitis in AIDS (fluconazole) 3) Candida (fluconazole) 4) Blastomyces 5) Coccidiodes 6) Histoplasma 7) Sporothrix schenckii (itraconazole) 8) Topical fungal infections (clotrimazole, miconazole) 9) Aspergillus (voriconazole, isavuconazole) Adverse effects: 1) GI upset 2) Antiandrogen (Inhibits testosterone synthesis ie. gynecomastia) 3) Inhibits CYP450 Enzymes which can lead to drug interactions (e.g. with warfarin, theophylline) 4) Hepatotoxicity (Mild hepatitis and liver dysfunction)

Answer 177

azole antifungals Fluconazole Itraconazole Ketoconazole Voriconazole Isavuconazole Clotrimazole Miconazole

Answer 178

MOA: It binds to ergosterol to form holes in fungal membranes (unique to fungal membranes) causing membrane holes/pores, allowing electrolytes that cause fungal cell lysis to leak out Clinical use: 1) Candidiasis (Swish and swallow for oral thrush) 2) Topical for diaper rash/vaginal candidiasis Adverse effect: Skin irritation or hypersensitivity

Answer 179

Antimetabolite: A fungal DNA polymerase and RNA polymerase inhibitor MOA: Flucytosine is converted into 5-fluorouracil (5-FU) by cytosine deaminase a Fluorinated analog of cytosine which inhibits fungal DNA and RNA polymerase thereby blocking DNA replication and fungal protein synthesis Clinical use: Used in combination with amphotericin B to treat 1) Cryptococcal meningitis Adverse effects: 1) Bone marrow suppression (anemia, thrombocytopenia, or leukopenia) 2) Nephrotoxicity 3) Hepatotoxicity 4) Nausea/vomiting

Answer 180

It is cleared renally so avoid in patients with renal failure

Answer 181

Flucytosine

Answer 182

A squalene oxidase inhibitor (fungal enzyme) MOA: It inhibits the synthesis of lanosterol, a precursor to ergosterol, which forms fungal cell membrane (Cleared via liver metabolism) Clinical use: 1) Dermatophytosis (tinea) Especially onychomycosis - fungal infections of nails 2) Paracoccidioidomycosis 3) Seborrheic dermatitis Adverse effects: 1) Headache 2) Loss of taste (dysgeusia) can lead to weight loss, 3) depression/anxiety 4) Hepatotoxicity 5) GI upset

Answer 183

Terbinafine?

Answer 184

First line drugs -RIPES 1) ISONIAZID (H) 2) RIFAMPICIN (R) 3) PYRAZINAMIDE (Z) 4) ETHAMBUTOL (E) 5) STREPTOMYCIN (S)

Answer 185

MOA: It impairs the synthesis of mycolic acid (a key component of mycobacterial cell wall) that must be activated by bacterial catalase-peroxidase (encoded by KatG). It is an inactive pro-drug that must be converted into its active drug by an mycobacterial enzyme Clinical use: 1) Mycobacteria (especially M. tuberculosis, RIPE therapy for active TB & a Monotherapy for latent TB, TB prophylaxis Adverse effects: 1) Vitamin B6 (pyridoxine) deficiency (Isoniazid inhibits pyridoxine phosphokinase, which normally activates vitamin B6 into its active form (PLP)) 2) Inhibits CYP450 Enzymes it can lead to drug interactions (e.g. warfarin, theophylline) 3) Drug-induced lupus-like reaction 4) Hepatotoxicity 5) Anion gap metabolic acidosis

Answer 186

Isoniazid (INH)

Answer 187

an antibiotic used to treat active tuberculosis MOA: Exact mechanism is unknown but it is activated by the conversion to pyrazinoic acid by the mycobacterial enzyme pyrazinamidase (more active at acidic pH (e.g. in macrophage phagolysosomes)) Clinical use: Active Mycobacterium tuberculosis (Part of RIPE regimen of rifamycin, isoniazid, pyrazinamide, and ethambutol) Adverse effects: 1) Hepatotoxicity (Dose-dependent that is synergistic with rifampin’s hepatotoxic effect (also in RIPE treatment for TB)) 2) Hyperuricemia/Gout (Pyrazinamide competes with uric acid for secretion by the kidneys, resulting in increased uric acid levels) 3) Arthralgias8

Answer 188

Pyrazinamide (PZA)

Answer 189

MOA: It blocks the breakdown of heme to hemozoin by inhibiting heme polymerase it can also cause Heme accumulation is toxic to plasmodia Treats: 1) Plasmodium spp. (Malaria) Adverse effects: 1) Retinopathy (Rare chronic use) 2) Myopathy 3) Pruritus (Occurs more commonly in dark-skinned individuals) 4) GI upset 5) Headaches/dizziness Resistance: Membrane efflux pump

Answer 190

Chloroquine

Answer 191

artemisinins atovaquone-proguanil mefloquine (quinidine analog)

Answer 192

MOA: It inhibits arabinosyltransferase which prevents the production of arabinogalactan, a key component of mycobacterial cell wall Clinical uses: 1) Mycobacterium tuberculosis (Part of RIPE regimen of rifamycin, isoniazid, pyrazinamide, and ethambutol) 2) mycobacterium avium complex (MAC) Adverse effects: 1) Optic neuropathy Clinically manifests as red-green color blindness, decreased visual acuity, and central scotoma Reversible with discontinuation of the drug

Answer 193

Ethambutol

Answer 194

Capreomycin?

Answer 195

Ethionamide

Answer 196

Kanamycin Amikacin

Answer 197

Fluoroquinolone Ciprofloxacin

Answer 198

Streptomycin IM, IV

Answer 199

Cycloserine

Answer 200

MOA: Inhibits folic acid synthesis of bacteria Treats: Bacteriostatic Highly specific to M. TB Adverse effects: GI intolerance HS reactions Hematological Abnormalities

Answer 201

diarylquinoline MOA: It targets C subunit of mycobacterial ATP synthase to Inhibit of proton pump activity. It is good for shortening the duration of treatment without any increased risk of relapse Used to treat: MDR-TB Adverse effects: 1) AST and/or ALT elevations 2) Amylase and/or lipase elevation 3) Musculoskeletal system abnormalities- myalgia 4) Cardiac rhythm disturbances (prolonged QT interval) 5) Gi issues

Answer 202

Bedaquiline

Answer 203

Treatment: XDR-TB or MDR-TB who are treatment-intolerant or non-responsive (collectively “highly drug-resistant TB”)

Answer 204

Classification: alkylating agents MOA: They cross-link DNA at guanine (N7) & they need require bioactivation by liver to be activated Clinical Indications: 1 1) solid tumors 2) leukemia 3) lymphomas 4) rheumatic disease (SLE, granulomatosis with polyangiitis [Wegner’s]) Adverse Effects: 1) alopecia 2) myelosuppression 3) SIADH 4) Fanconi syndrome (ifosfamide) 5) hemorrhagic cystitis and bladder cancer

Answer 205

Ifosfamide & Cyclophosphamide

Answer 206

An [M-phase specific] microtubule inhibitor MOA: It is a vinca alkaloid that binds 𝛃-tubulin and inhibits its polymerization into microtubules which prevents the mitotic spindle formation (M-phase arrest) Overall it decreases microtubule polymerization Clinical Indications: 1) solid tumors 2) leukemias 3) Hodgkin and non-Hodgkin lymphomas 4) Wilms Adverse Effects: 1) alopecia 2) SIADH 3) neurotoxicity (areflexia, peripheral neuritis) 4) constipation (paralytic ileus) no myelosuppression

Answer 207

Vincristine

Answer 208

Classification: anthracyclines MOA: They generate free radicals which intercalates in the DNA leading to breaks in DNA resulting in decreased replication. It interferes with topoisomerase II enzyme Clinical Indications: 1) solid tumors 2) leukemias 3) lymphomas Adverse Effects: 1) cardiotoxicity (dilated cardiomyopathy) 2) myelosuppression, alopecia

Answer 209

Doxorubicin

Answer 210

Use dexrazoxane (iron chelating agent) used to prevent cardiotoxicity

Answer 211

Classification: calcineurin inhibitor MOA: It binds cyclophilin that blocks T-cell activation by preventing IL-2 transcription Clinical Indications: 1) psoriasis 2) rheumatoid arthritis Adverse Effects: 1) nephrotoxic 2) hypertension 3) hyperlipidemia 4) neurotoxicity 5) gingival hyperplasia 6) hirsutism

Answer 212

Classification: alkylating agent (nitrogen mustards) MOA: They cross-link DNA at guanine (N7) & they need bioactivation by liver Clinical Indications: 1) solid tumors 2) leukemia 3) lymphomas 4) rheumatic disease (SLE, granulomatosis with polyangiitis [Wegner’s]) Adverse Effects: 1) alopecia 2) myelosuppression 3) SIADH, Fanconi syndrome (ifosfamide) 4) hemorrhagic cystitis and bladder cancer (prevented with mesna [sulfhydryl group of mesna binds toxic metabolites] and adequate hydration [cyclophosphamide])

Answer 213

cyclophosphamide & ifosfamide

Answer 214

Ifosfamide & Cyclophosphamide

Answer 215

Classification: anthracyclines MOA: It generates free radicals through intercalate in DNA causing breaks in DNA resulting in decreased replication which interferes with topoisomerase II enzyme Clinical Indications: 1) solid tumors 2) leukemias 3) lymphomas Adverse Effects: 1) cardiotoxicity (dilated cardiomyopathy) (use dexrazoxane (iron chelating agent) used to prevent cardiotoxicity 2) myelosuppression 3) alopecia

Answer 216

Doxorubicin

Answer 217

Classification: antimetabolite MOA: It is a folic acid analog that competitively inhibits DHF reductase leading to decrease in dTMP resulting in decreased DNA synthesis Clinical Indications: 1) cancers (leukemia [ALL], lymphoma, & choriocarcinoma sarcoma) 2) non-neoplastic (ectopic pregnancy & medical abortion) 3) rheumatoid arthritis 4) psoriasis 5) IBD 6) vasculitis Adverse Effects: 1) myelosuppression (reversible with leucovorin [folinic acid] rescue) 2) hepatotoxicity 3) mucositis (mouth ulcers) 4) pulmonary fibrosis 5) folate deficiency 6) nephrotoxicity

Answer 218

methotrexate

Answer 219

MOA: They are tyrosine kinase inhibitors of BCR-ABL (encoded by Philadelphia chromosome [t(9;22)] fusion gene in CML) and c-kit (common in GIST) Clinical uses: 1) CML 2) GIST  Adverse E8ffects: fluid retention

Answer 220

What are the adverse effects of Tyrosine Kinase inhibitors? (-tinib) Imatinib Gefitinib Erlotinib Dasatinib Sunitinib Adavosertib

Answer 221

Classification: microtubule inhibitors MOA: They are vinca alkaloids that bind β-tubulin and inhibit its polymerization into microtubules which prevents mitotic spindle formation (M-phase arrest) to decrease microtubular polymerization Clinical Indications: 1) solid tumors 2) leukemias 3) Hodgkin and non-Hodgkin lymphomas 4) Wilms Adverse Effects: 1) alopecia 2) SIADH 3) neurotoxicity (areflexia, peripheral neuritis) 4) constipation (paralytic ileus) no myelosuppression

Answer 222

Vincristine

Answer 223

Classification: antimetabolite MOA: A purine (thiol) analog that results in decreasing de novo purine synthesis that is activated by HGPRT Clinical Indications: 1) preventing organ rejection 2) rheumatoid arthritis 3) IBD 4) SLE Adverse Effects: 1) immunosuppression 2) myelosuppression 3) GI and liver toxicity (metabolized by xanthine oxidase, therefore, increase risk of toxicity with allopurinol or febuxostat)

Answer 224

6-Mercaptopurine

Answer 225

adverse effects of 6-Mercaptopurine

Answer 226

Cisplatin & Carboplatin: Ototoxicity & nephrotoxicity Vincristine: Peripheral neuropathy Bleomycin & Busulfan: Pulmonary fibrosis Doxorubicin: Cardiotoxicity Trastuzumab: Cardiotoxicity Cyclophosphamide: Hemorrhagic cystitis

Answer 227

S phase (DNA synthesis) G2 (Double check repair)

Answer 228

Topoisomerase inhibitors: Etoposide Teniposide Irinotecan Topotecan ## Footnote "Topoisomerase Inhibitors Are Tough Enough"

Answer 229

An anticancer drug that inhibits S phase (DNA synthesis)

Answer 230

Antimetabolites: Azathioprine Cladribine Cytarabine 5-Fluorouracil Hydroxyurea Methotrexate 6-Mercaptopurine

Answer 231

G2 phase (Double check repair)

Answer 232

M phase (Inhibits Mitosis)

Answer 233

Microtubule inhibitors Paclitaxel Vinblastine Vincristine

Answer 234

Classification: anthelmintic MOA: It decreases the glucose uptake and decrease microtubular structure Clinical Indications: most intestinal nematodes  Adverse Effects: 1) leukopenia 2) alopecia 3) elevation of LFTs

Answer 235

Albendazole

Answer 236

MOA: An antitumor antibiotic that binds to DNA in the G2 phase of the cell cycle and induces free radical formation to induce DNA breaks

Answer 237

Dactinomycin and actinomycin D are two interchangeable names for the same intercalating agent. MOA: They intercalate into the DNA their molecules insert between two strands of DNA blocking RNA polymerases from accessing DNA strands preventing RNA synthesis in rapidly dividing cells. Used for childhood tumors: 1) Wilms tumor 2) Ewing sarcoma 3) rhabdomyosarcoma Adverse effects: 1) Myelosuppression (obvious)

Answer 238

Dactinomycin & Actinomycin D

Answer 239

Doxorubicin and daunorubicin are chemotherapeutics MOA: 1) They cause DNA strand breaks by inducing free radical formation 2) They can insert themselves or intercalate into DNA 3) These drugs inhibit topoisomerase II (prevents the enzyme from unwinding or fixing knots in DNA) Adverse effects: 1) myelosuppression 2) alopecia 3) cardiotoxicity

Answer 240

Doxorubicin and daunorubicin

Answer 241

 Classification: anthelmintic MOA: It intensifies GABA-mediated neurotransmission in nematodes and causes immobilization of parasites, facilitating the removal by the reticuloendothelial system (does not cross BBB)  Clinical Indications: 1) onchocerciasis 2) cutaneous larva migrans 3) strongyloidiasis 4) filariasis Adverse Effects: 1) fever/headache/ 2) dizziness 3) rash/pruritus 4) tachycardia 5) hypotension 6) pain in joints, muscles and lymph glands contraindicated in pregnancy

Answer 242

Ivermectin

Answer 243

Classification: nitroimidazoles (bactericidal & antiprotozoal) MOA: It forms toxic free radical metabolites in bacterial cell that damage DNA Clinical Indications: 1) Giardia 2) Entamoebae 3) Trichomonas 4) Gardnerella vaginalis 5) Anaerobes (Bacteroides, C. difficile) –– can be used in place of amoxicillin in H. pylori ‘triple therapy’ in case of penicillin allergy Adverse Effects: 1) disulfiram-like reaction (sever flushing, tachycardia, hypotension) with alcohol 2) headache 3) metallic taste

Answer 244

Metronidazole

Answer 245

Classification: antituberculosis MOA: It decreases the synthesis of mycolic acid. It needs bacterial catalase peroxidase (encoded by KatG) in order to convert INH to active metabolite Clinical Indications: 1) mycobacterium tuberculosis (only agent used as solo prophylaxis against TB and monotherapy for latent TB) Adverse Effects: 1) hepatoxicity 2) hemolysis in G6PD deficiency 3) cytochrome P-450 inhibition 4) drug-induced SLE 5) anion gap metabolic acidosis 6) vitamin B6 deficiency (peripheral neuropathy, sideroblastic anemia) 7) seizures (high doses –– refractory to benzodiazepines) –– administer with pyridoxine

Answer 246

Mechanism of Resistance: mutations leading to under expression of KatG

Answer 247

Classification: folic acid synthesis inhibitor MOA: They inhibit dihydropteroate synthase, thus inhibiting folate synthesis it is a bacteriostatic (bactericidal when combined with trimethoprim)  Clinical Indications: 1) Gram-positive organisms (e.g. Nocardia) 2) gram negative Adverse Effects: 1) hypersensitivity reactions 2) hemolysis if G6PD deficient 3) nephrotoxicity (tubulointerstitial nephritis) 4) photosensitivity 5) SJS 6) kernicterus in infants 7) displace other drugs from albumin

Answer 248

Sulfonamides Sulfamethoxazole (SMX) Sulfisoxazole Sulfadiazine

Answer 249

Through altered enzyme (bacterial dihydropteroate synthase), decrease uptake or increase PABA synthesis

Answer 250

Classification: sulfones MOA: inhibit dihydropteroate synthase, to inhibit folate synthesis it is a bacteriostatic (bactericidal when combined with trimethoprim) Clinical Indications: 1) leprosy 2) PJP prophylaxis or treatment when combined with TMP Adverse Effects: 1) hemolysis if G6PD deficient 2) methemoglobinemia 3) agranulocytosis

Answer 251

Classification: antimetabolite MOA: A purine (thiol) analog leading to decrease de novo purine synthesis that is activated by HGPRT Clinical Indications: 1) preventing organ rejection 2) rheumatoid arthritis 3) IBD 4) SLE –– used to wean patients off steroids in chronic disease and to treat steroid-refractory chronic disease Adverse Effects: 1) immunosuppression 2) myelosuppression 3) GI and liver toxicity (metabolized by xanthine oxidase, therefore, increase risk of toxicity with allopurinol or febuxostat)

Answer 252

6-Mercaptopurine

Answer 253

Classification: antiprotozoal Mechanism of Action: unknown?  Clinical Indications: 1) P. vivax 2) P. ovale 3) PJP Adverse Effects: 1) GI distress 2) pruritus 3) headache 4) methemoglobinemia 5) blood cytopenia's 6) hemolysis in G6PD deficiency Contraindicated in pregnancy

Answer 254

Primaquine

Answer 255

MOA: They are tyrosine kinase inhibitors of BCR-ABL (encoded by Philadelphia chromosome [t(9;22)] fusion gene in CML) and c-kit (common in GIST) Clinical Indications: 1) CML 2) GIST Adverse Effects: fluid retention

Answer 256

Tyrosine Kinase Inhibitors (-tinib)

Answer 257

Classification: NSAID MOA: An NSAID that irreversibly inhibits cyclooxygenase (both COX-1 and COX-2) by covalent acetylation leading to decrease synthesis of TXA2 and prostaglandins. It increases bleeding time but doesn't effect PT & PTT  Clinical Indications: 1) decrease platelet aggregation (low dose) 2) antipyretic and analgesic (intermediate dose) 3) anti-inflammatory (high dose) Adverse Effects: 1) gastric ulceration 2) tinnitus (CN VIII) 3) allergic reactions (patients with asthma or nasal polyps) 4) acute kidney injury (chronic) 5) interstitial nephritis 6) GI bleeding 7) Risk of Reye syndrome in children treated with aspirin for viral infection

Answer 258

treatment of overdose: NaHCO3-.

Answer 259

Classification: NSAID MOA: It reversibly inhibit cyclooxygenase (1 & 2) to block prostaglandin synthesis Clinical Indications: 1) antipyretic 2) analgesic 3) anti-inflammatory Adverse Effects: 1) interstitial nephritis 2) gastric ulcer (prostaglandins protect gastric mucosa) 3) renal ischemia (prostaglandins vasodilate afferent arteriole) 4) aplastic anemia

Answer 260

Classification: anthelmintic MOA: Bactericidal and bacteriostatic  Clinical Indications: 1) UTI (not Proteus or Pseudomonas)  Adverse Effects: 1) GI distress 2) rash 3) pulmonary infiltrates 4) phototoxicity 5) neuropathies 6) hemolysis in G6PD deficiency

Answer 261

Nitrofurantoin

Answer 262

Acute sinusitis Animal bites Aspiration pneumonia

Block 3 ALL Flashcards

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