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CRRAB II > PBL pharmacology > Flashcards

PBL pharmacology Flashcards

1
Q

Fluoroquinolones (Ciprofloxacin, norfloxacin, levofloxacin, ofloxacin, moxifloxacin, gemifloxacin, enoxacin) MOA

A

Inhibit prokaryotic enzymes topo II (DNA gyrase) and topo IV. Bactericidal. Do NOT take with antacids.

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2
Q

Fluoroquinolone clinical use

A

G- rods of urinary and GI tracts and some G+ organisms. Pyelonephritis (1st line treatment).

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3
Q

Fluoroquinolone toxicity

A

GI upset, superinfections, skin rashes, HA, dizziness. Can cause leg cramps and myalgias. Contraindicated in pregnant/nursing mothers and children under 18. Can damage tendons.

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4
Q

Fluoroquinolone mechanism of resistance

A

Chromosome encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps

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5
Q

Trimethoprim MOA

A

Inhibits bacterial dihydrofolotate reductase. Bacteriostatic. Use with sulfonamide.

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6
Q

Trimethoprim clinical use

A

In combo with sulfonamides, causing sequential block of folate synthesis. Combination used for UTIs (pyelonephritis only if susceptible), pneumonia treatment and prophylaxis.

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7
Q

Trimethoprim toxicity

A

Megaloblastic anemia, leukopenia, granulocytopenia.

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8
Q

Sulfonamides (sulfamethoxazole, sulfisoxazole, sulfadiazine) MOA

A

Inhibits folate syntheses. PABA antimetabolites inhibit dihydropteroate synthase. Bacteriostatic. Bacteriocidal when used with trimethoprim.

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9
Q

Sulfonamide clinical use

A

G+ and G-. UTI treatment with trimethoprim or just SMX with simple UTI

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10
Q

Sulfonamide toxicity

A

Hypersensitivity reactions, hemolysis if G6PD deficient, nephrotoxicity, photosensitivity, kernicterus in infants.

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11
Q

Sulfonamide mechanism of resistance

A

Altered enzyme, decreased uptake or increased PABA synthesis.

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12
Q

Ceftriaxone MOA

A

3rd generation cephalosporin. Inhibits bacterial cell wall synthesis by binding to penicillin-binding proteins (PBPs) which inhibits the final transpeptidation step of peptidoglycan synthesis in bacterial cell walls. Inhibiting cell wall biosynthesis.

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13
Q

Ceftriaxone clinical use

A

Can be given to treat pyelonephritis if the fluoroquinolone resistance of E. Coli is greater than 10%.

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14
Q

Aminoglycoside (Gentamicin, neomycin, amikacin, tobramycin, streptomycin) MOA

A

Bactericidal. Irreversible inhibition of complex by binding 30S subunit. Can cause misreading of mRNA. Block translocation. Require O2 for uptake. Ineffective against anaerobes.

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15
Q

Aminoglycoside clinical use

A

Treat pyelonephritis if fluoroquinolone resistance of E coli greater than 10%

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16
Q

First line empiric treatment for uncomplicated cystitis

A

Nitrofurantoin or Trimethoprim/Sulfamethoxazole or fosfomycin

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17
Q

Fosfomycin MOA

A

Phosphoric acid derivative, inhibits bacterial wall synthesis (bactericidal) by inactivating the enzyme, pyruvyl transferase, which is critical in the synthesis of cell walls by bacteria

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18
Q

Fosfomycin clinical use

A

Cystitis

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19
Q

Nitrofurantoin MOA

A

Reduced by bacterial flavoproteins to reactive intermediates that inactivate or alter bacterial ribosomal proteins leading to inhibition of protein synthesis, aerobic energy metabolism, DNA, RNA, and cell wall synthesis. Nitrofurantoin is bactericidal in urine at therapeutic doses.

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20
Q

Nitrofurantoin clinical use

A

UTI treatment (not pyelonephritis) and acute cystitis

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21
Q

First line treatments for pyelonephritis

A

Fluoroquinolones unless resistance greater than 10% (than use ceftriaxone or aminoglycoside). Can use Trimethoprim-Sulfamethoxazole if susceptible

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22
Q

Rapid acting insulin (names, onset, time to peak effect, duration of action)

A
  • -Can be taken immediately before a meal
  • -Onset: 10-30 min
  • -Time to peak effect: 30-60 min
  • -Duration of action: 3-5 hours
  • -Names: Aspart, lispro, glulisine
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23
Q

Regular (short) acting insulin

A
  • -Onset: 30-60 min (U-100), 30 min (U-500)
  • -Time to peak effect: 1.5-2 hrs (U-100), 4-8 hrs (U-500)
  • -Duration of action: 5-12 hrs (U-100), 14-15 hrs (U-500)
  • -Names: Humulin R and Novolin R (U-100), Humulin R (U-500)
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24
Q

NPH (intermediate) insulin

A
  • -Onset: 1-2 hours
  • -Time to peak effect: 4-8 hours
  • -Duration of action: 10-20 hours
  • -Names: Humulin N, Novolin N (insulin isophane suspension)
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25
Q

Glargine insulin

A
  • -Onset: 1-2 hrs
  • -Time to peak effect: No peak, max 4-6 hours though
  • -Duration of action: 24 hrs
  • -Names: lantus
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26
Q

Azathioprine MOA (and use)

A
  • -Imidazolyl derivative of mercaptopurine.
  • -Metabolites incorporated into replicating DNA and halt replication–> block pathway for purine synthesis.
  • -Immunosuppressive and toxic effects.
  • -6-thioguanine nucleotides mediate.
  • -Sometimes used to treat HSP
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27
Q

Cyclophosphamide MOA (and use)

A
  • -Alkylating agent
  • -Prevents cell division by cross-linking DNA strands and decreases DNA synthesis.
  • -CCNS agent
  • -Immunosuppressant.
  • -Prodrug metabolized in liver
  • -HSP treatment when crescents present
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28
Q

Mycophenolate mofetil MOA (and use)

A
  • -Cytostatic effect on T and B lymphocytes
  • -Inhibits inosine monophosphate dehydrogenase (enzyme that controls rate of synthesis of GMP in de novo purine pathway).
  • -Inhibits de novo guanine synthesis
  • -Sometimes used for severe HSP
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29
Q

Corticosteroid (Prednisone) MOA

A
  • -Metabolic, catabolic, anti-inflammatory, immunosuppressive effects
  • -Mediated by interactions w/glucocorticoid response elements (GRE), inhibition of phospholipase A2, inhibition of transcription factors such as NF-kB.
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30
Q

Opioid (Morphine, fentanyl, codeine, loperamide, methadone, meperidine, dextromethorphan, diphenoxylate, pentazocine) MOA

A
  • -Acts as agonists at opioid receptors (u=morphine, delta= enkephalin, k=dynorphin) to modulate synaptic transmission
  • –Opens K+ channels, close Ca++ channels–>DECREASE synaptic transmission.
  • -Inhibit release of ACh, NE, 5-HT, glutamate, substance P
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31
Q

Rifamycins (Rifampin, Rifabutin) MOA

A

Inhibits DNA-dependent RNA polymerase. Bactericidal animycobacterial agents, IC and EC activity

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32
Q

4 R’s of rifampin

A

RNA polymerase inhibitor
Ramps up microsomal cytochrome P-450
Red/orange body fluids
Rapid resistance if used alone

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33
Q

What is different about rifampin vs rifabutin

A

Rifampin ramps up P-450 but rifabutin doesn’t

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34
Q

Rifamycins toxicity

A

–Minor hepatotoxicty, drug interactions, red/orange body fluids (non-hazardous side effects)

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35
Q

Which Rifamycin drug is preferred when pt is HIV+

A

Rifabutin because it doesn’t have as much cytochrome P-450 activity.

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36
Q

Mechanism of resistance of Rifamycins

A

Mutations reduce drug binding to RNA polymerase.

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37
Q

Isoniazid MOA

A

Decreases synthesis of myocolic acids. Bacterial catalase-perioxidase needed to convert Inh to active metabolite. I

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38
Q

Isoniazid use

A

Mycobacterium TB. Only agent used as solo prophylaxis against TB.

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39
Q

Isoniazid toxicity

A

Neurotoxicity, hepatoxicity. Pyridoxine (Vit B6) can prevent neurotoxicity.

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40
Q

Isoniazid mechanism of resistance

A

Mutations leading to underexpression of KatG (needed to convert prodrug to active drug)

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41
Q

Pyrazinamide

A

Mechanism uncertain. Prodrug converted to active compound pyrazinoic acid. Acts intracellularly. Toxicity includes hyperuricemia and hepatotoxicity.

42
Q

Ethambutol Mechanism

A

Decreases carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase.

43
Q

Ethambutol use

A

Mycobacterium tubuerculosis

44
Q

Rifamycin use

A

Mycobacterium tuberculosis. Delay resistance to dapsone when used for leprosy. Meningococcal prophylaxis in kids w/HIB.

45
Q

Ethambutol toxicity

A

Optic neuropathy (leading to red-green color blindness)

46
Q

Pyridoxine (Vitamin B6) MOA

A

Precursor to pyridoxal. Functions in metabolism of proteins, carbs, fats. Also aids in release of liver and muscle stored glycogen and synthesis of GABA and heme.

47
Q

Amphotericin B and nystatin MOA

A

Binds ergosterol and forms membrane pores that allows leakage of electrolytes. Fungicidal.

48
Q

Amphotericin B use

A

Serious, systemic mycoses. Cryptococcus, blastomyces, coccidioides, histoplasma, candida, mucor. Intrathecally for fungal meningitis. Supplement K+ and Mg++ because of altered renal tubule permeability.

49
Q

Amphotericin B toxicity

A

Fever/chills, hypotension, nephrotoxicity, arrhythmias, anemia, IV plebitis. Hydration will decrease nephrotoxicity. Liposomal amphotericin decreases toxicity

50
Q

Nystatin use

A

Only topical. Too toxic for systemic use. “Swish and swallow for thrush, topical for diaper rash or vaginal candidiasis

51
Q

Flucytosine MOA

A

Inhibits DNA and RNA biosynthesis by conversion of 5-FU by cytosine deaminase

52
Q

Clinical use of flucytosine

A

Systemic fungal infections (esp. meningitis caused by cryptococcus). Used in combo w/amphotericin B

53
Q

Flucytosine toxicity

A

Bone marrow suppression

54
Q

Azoles (6 names)

A

Clotrimazole, fluconazole, itraconazole, ketoconazole, miconazole, voriconazole

55
Q

-Azoles MOA

A

Inhibit fungal sterol (erggosterol) synthesis by inhibiting cytochrome P-450 enzyme that converts lanosterol to ergosterol

56
Q

-Azoles clinical use

A

Local and less serious systemic mycoses. Fluconazole for chronic suppression of cryptococcal meningitis in AIDS patients and all types of candidal infections. Itraonazole for blastomycoses, coccidioides, histoplasma. Clotrimazole and miconazole for topical infections

57
Q

-Azoles toxicity

A

–Testosterone synthesis inhibition (gynecomastia), liver disfunction (altered cytochrome P-450.

58
Q

Protease inhibitors MOA

A
  • -Prevent maturation of new viruses by inhibiting protease, which is needed to cleave polypeptide products of HIV mRNA into functional parts
  • -Does nothing for cells that are already infected because it doesn’t inhibit provirus
59
Q

Protease inhibitor names

A
  • -END IN -NAVIR

- -Atazanavir, darunavir, fosamprenavir, indinavir, lopinavir, ritonavir, saquinavir

60
Q

Protease inhibitor toxicty

A

Hyperglycemia, GI intolerance, lipodystrophy, nephropathy, hematuria (indinavir). Rifampin is contraindicated with protease inhibitors because it can decrease drug concentration.

61
Q

Integrase inhibitors (drug name)

A

Raltegravir

62
Q

Raltegravir MOA

A

Inhibits HIV genome integration into host cell chromosome

–Reversibly inhibits HIV integrase

63
Q

Raltegravir toxicity

A

Increases creatine kinase

64
Q

Ritonavir boosting

A

Can be used at low doses to “boost” other drug concentrations by inhibiting P-450 and CPYP3A4

65
Q

Fusion inhibitors (2 drugs)

A

Enfuvirtide and maraviroc

66
Q

Enfuvirtide MOA

A

Binds gp41 and inhibits viral entry

67
Q

Enfuvirtide toxicity

A

Skin reactions at injection sites (this makes it not a first line drug choice)

68
Q

Maraviroc MOA

A

Binds CCR-5 on surface of T cells/monocytes. Inhibits interactions w/gp120.
–Only useful is strains that have single CCR-5 tropism

69
Q

Maraviroc toxicity

A

Pyrexia, rash, postural dizziness

70
Q

NRTIs (Nucleoside reverse transcriptase inhibitors) (Drug names)

A
  • -Abacavir
  • -Didanosine
  • -Emtricitabine
  • -Lamivudine
  • -Stavudine
  • -Tenofovir
  • Zidovudine
71
Q

NRTI MOA

A

Competitively inhibit nucleotide binding to reverse transcriptase and terminate DNA change. Tenofovir nucleotide and the rest are nucleosides (need to be phosphorylated to be active).

72
Q

What drug is used as general prophylaxis and during pregnancy to decrease risk of fetal transmission?

A

Zidovidine (AZT or ZDV)

73
Q

NRTI toxicity

A
  • -Bone marrow suppression (can reverse w/G-CSF)
  • -Peripheral neuropathy
  • -Lactic acidosis (nucleosides)
  • -Granulocytopenia and anemia (AZT)
  • -Pancreatitis (Didanosine)
74
Q

NNRTI drug names

A
  • -Delavirdine
  • -Efavirenz
  • -Nevirapine
75
Q

NNRTI MOA

A

Bind to reverse transcriptase at different site from NRTIs. Don’t require phosphorylation to be active or compete with nucleosides. Allosteric inhibitors.

76
Q

NNRTI toxicity

A
  • -Rash
  • -Hepatotoxicity
  • -Vivid dreams and CNS symptoms (common with efavirenz)
  • -Delavirdine and efavirenz contraindicated in pregnancy.
77
Q

Albuterol and pirbuterol class and use

A
  • -Short-acting B2 agonist

- -Acute exacerbations of asthma and COPD (obstructive airway disease)

78
Q

Albuterol and pirbuterol MOA

A

Stimulates B2 receptors —>
Relaxes bronchial smooth muscle
–Acts on AC (ATP–> cAMP)

79
Q

Pharmacokinetics of Albuterol and pirbuterol

A
  • -Max. effect in 15 min
  • -Lasts 3-4 hours
  • -Liver metabolism
  • -Urine excretion (30% unchanged)
80
Q

B2 agonist side effects

A

Tachycardia, skeletal muscle tremors and cramping, HA, palpitations, prolongation of QT interval, insomnia, hypokalemia, increases in serum glucose, tolerance with long-term use

81
Q

Albuterol and pirbuterol delivery device

A
  • -Metered dose inhalers

- -Nebulizer

82
Q

Salmeterol, formoterol, aformoterol class and use

A
  • -Long-acting B2 agonists
  • -Prevention of bronchospasm in COPD and asthma
  • -Not usually monotherapy
83
Q

Salmeterol, formoterol, aformoterol MOA

A

Stimulates B2 receptors–> relaxes bronchial smooth muscle. Long-acting agents

84
Q

Salmeterol, formoterol, aformoterol pharmacokinetics

A
  • -12+ hr duration of action
  • -High lipid solubility.
  • -Enter smooth muscle cell in high concentration
  • -Interact w/inhaled corticosteroids
85
Q

Salmeterol delivery device

A

Dry-powder inhaler

86
Q

Formoterol delivery device

A
  • -Dry-powder inhaler

- -Nebulizer

87
Q

Aformoterol delivery device

A

Nebulizer

88
Q

Ipratropium delivery device

A
  • -Nebulizer

- -Metered dose inhaler

89
Q

Ipratropium MOA

A

Competitively blocks muscarinic acetylcoline receptors–> prevents bronchoconstriction

90
Q

Ipratropium use

A

Asthma and COPD

91
Q

Ipratropium and Tiotropium side effects

A
  • -Dry mouth
  • -Pharyngeal irritation
  • -Urinary retention
  • -Increases in intraocular pressure
92
Q

Tiotropium MOA

A

Blocks muscarinic receptors–> reduces smooth muscle contraction and mucus secretion

93
Q

Tiotropium class

A

Long-acting muscarinic antagonists

94
Q

Tiotropium delivery device

A

Dry-powder inhaler

95
Q

Inhaled corticosteroids (Fluticasone, Budesonide, Triamcinolone, Beclomethasone, Flunisolide) MOA

A
  • -Inhibit PLA2–> decreases amino acid synthesis and its inflammatory metabolites.
  • -Inhibits NF-kB–> suppresses TNF-a and other inflammatory agents. Inhibits synthesis of virtually all cytokines–> reduces bronchial hyper-reactivity
96
Q

Fluticasone and budesonide delivery device

A

Dry-powder inhaler

Nebulizer

97
Q

Inhaled corticosteroids uses

A

1st line therapy for chronic asthma w/long acting B2 agonists. Also used for other obstructive lung diseases

98
Q

Inhaled corticosteroid side effects

A
  • -Oral candidiasis (most common)
  • -Cushingoid changes
  • -Dysphonia
  • -Osteoporosis
  • -Pneumonia
  • -Side effects are all less common than in systemic forms
99
Q

Systemic corticosteroids (Methylprednisolone, prednisone, dexamethasone, betamethasone) MOA

A
  • -Transcriptionally regulate/inactivate synthesis of PLA2–> inhibit synthesis of inflammatory agents
  • -Inhibit NF-kB. Suppress both B and T cell function by decreasing transcription of many cytokines
100
Q

Systemic corticosteroid delivery system

A
  • -IV

- -Orally

101
Q

Systemic corticosteroid side effects

A
  • Iatrogenic Cushing Syndrome (HTN, weight gain, moon facies, osteoporosis, hyperglycemia, amenorrhea, Buffalo hump, immunosuppression),
  • -Adrenocortical atrophy
  • -Peptic ulcers
  • -Steroid diabetes
  • -Steroid psychosis.
  • -Adrenal insufficiency when stopped abruptly after chronic use.

CRRAB II (13 decks)

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