Glossary of USMLE 1 Pharm
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- amount of drug in body/_______ = Vd
- plasma drug concentration
(Vd is Volume of Distribution)
- rate of elimination of drug/[plasma drug] = ?
- CL (Clearance)
- (.7)(Vd)/CL = ?
- T 1/2
- A drug infused at a constant rate reaches about 94% of steady state after _______ t 1/2s.
- A loading dose is calculated using this formula.
- (Cp)(Vd)/F (note: Cp = target plasma concentration, and F = bioavailability)
- A maintenance dose is calculated using this formula.
- Rate of elimination is proportional to _______ ______ in 1st order elimination.
- drug concentration
- In the case of EtOH, which is elimated by _____ order elimination, a constant amount of drug is eliminated per unit time.
- Phase ____ (I or II) reactions yield slightly polar metabolites that are often _____ (active or inactive)
- I, active
- Phase ____ (I or II) reactions yield very polar metabolites that are often _____ (active or inactive) and are excreted by the _______.
- II, inactive, kidney
- Phase II reactions are often of this type.
- Cytochrome P-450 is involved in _____ phase (I or II) reactions.
- A drug patent lasts for _____ years after filing for application.
- How many phases are there in drug development?
- Drugs are first tested in patients in phase _____ of clinical testing, pharmacokinetic safety is determined in phase ______ of clinical testing, double blind tests are done in phase ____ and post-market surveillance is done in phase _____.
- In a dose response curve, a competitive antagonist shifts the curve _____, while a non-competitive antagonist shifts the curve ______.
- right, down
- What pharmacologic relationship would determine the existence of spare receptors?
- EC50 is lower then Kd
(EC50 is more to the left)
- What does it mean if EC50 and Kd are equal?
- The system does not have spare receptors
- A partial agonist acts on the same receptor system as a full agonist? T/F
- What's the main difference between a partial agonist and a full agonist?
- A partial agonist has a lower maximal efficacy.
- Is a partial agonist less potent than a full agonist?
- Not necessarily. It can be less, more or equally potent as a full agonist.
- The penicillin type drugs work by blocking ------ synthesis, specifically by inhibiting this molecule from cross-linking?
- blocks bacterial cell wall synthesis by inhibition of peptidoglycan synthesis.
- Which other drugs have the same mechanism of action as penicillin?
- - Cephalosporins
- Bacitracin, vancomycin and cycloserine block the synthesis of this molecule, preventing cell wall synthesis
- These drugs block the 50s ribosomal subunit
"buy at 30 CELL @ 50"
- These drugs block the 30s ribosomal subunit
- "buy AT 30, cell @ 50"
- These drugs block nucleotide synthesis by interfering with the folate pathway
- Sulfonamides (e.g. Bactrim), trimethoprim
- These drugs block DNA topoisomerases
- Quinolones (e.g. Cipro)
- Which drug blocks mRNA synthesis
- Which are the bacteriacidal Abx
- Penicillin, cephalosporin, vancomycin, aminoglycosides, fluoroquinolones, metronidazole
- These drugs disrupt the bacterial/fungal cell membranes
- These specific disrupt fungal cell membranes
- FAN the fungal cell:
- Amphotericin B
- What is the mechanism of action of Pentamidine
- Which is the IV form and which is the oral form of Penicillin?
- G = IV
V = oral
- Which of these is not a mechanism of penicillin action:
(1) binds penicillin-binding protein,
(2) blocks peptidoglycan synthesis,
(3) blocks transpeptidase catalyzed cross-linking of cell wall and
(4) activates autolytic enzymes
- Penicillin does not block peptioglycan synthesis, bacitracin, vancomycin and cycloserine do that
- T or F: penicillin is effective against gram pos and gram neg rods
- False: penicillin is used to treat common streptococci (but not staph), meningococci, gram pos bacilli and spirochetes (i.e. syphilis, treponema). Not used to treat gram neg rods.
- What should you watch out for when giving penicillin?
- Hypersensitivity rxn (urticaria,severe pruritus) and hemolytic anemia
- Methicillin, nafcillin, and dicloxacillin are used mainly for what type of infection?
- Staphlococcal infection (hence very narrow spectrum)
- T or F: Methicillin, nafcillin, and dicloxacillin have the same mechanism of action as penicillin
- Are Methicillin, nafcillin, and dicloxacillin penicillinase resistant? If so why?
- Bulkier R group makes these drugs resistant to penicillinase
- What should you watch out for when giving Methicillin, nafcillin, or dicloxacillin?
- Hypersensitivity rxn (urticaria,severe pruritus); methicillin can cuase interstitial nephritis
- T or F: Ampicillin/amoxicillin have the same mechanism of action as penicillin
- Which has greater oral bioavailability: Ampicillin or Amoxicillin?
- amOxicillin (O for Oral)
- What do you use Ampicillin/amoxicillin for?
- Ampicillin/amoxicillin HELPS to kill enterococci (H. influenzae, E. coli, Listeria monocytogenes, Proteus mirabilis, Salmonella)
- Can penicillinase effect Ampicillin/amoxicillin efficacy?
- Yes, they are penicillinase sensitive
- since Ampicillin/amoxicillin are penicillinase sensitive, what inhibitor is used w/ them?
- clavulanic acid
- What should you watch out for when giving Ampicillin/amoxicillin?
- Hypersensitivity rxn
- Why are Carbenicillin, piperacillin, and ticarcillin considered to have an extended spectrum?
- Because they are effective against pseudomonas and other gram neg rods (enterobacter and some species of klebsiella)
- What should you watch out for when giving Carbenicillin, piperacillin, and ticarcillin?
- Hypersensitivity rxn
- Why does concomitant administration with clavulanic acid increase the efficacy of piperacillin and ticarcillin?
- Because they are penicillinase sensitive
- What is the mechanism of action of Cephalosporins?
- inhibit cell wall synthesis
- How are Cephalosporins similar/different from penicillin?
- both have a beta-lactam ring structure but cephalosporins are less susceptible to penicillinases
- What are the main similarities/difference between 1st and 2nd generation cephalosporins?
- 2nd gen has extensive gram neg coverage but weaker gram pos coverage
- 1st gen covers what bugs?
- gram positives (staph and strep),
- 2nd gen Cephalosporins cover what bugs?
- gram positives (staph and strep) though less,
Enterobacter aerogenes, Neisseria,
- What can 3rd generation Cephalosporin drugs do that 1st and 2nd generation can't?
- Cross the blood brain barrier
- What are some other benefits of 3rd gen Cephalosporins?
- better activity against gram neg bugs;
resistant to beta-lactam drugs;
Ceftazidime for Pseudomonas;
Ceftriaxone for N. gonorrhea
- What are the benefits of 4th gen Cephalosporins (e.g. Cefipime)?
- increased activity against Pseudomonas, gram pos organisms and more beta-lactamase resistant (i.e. 4th gen combines 1st gen and 3rd gen characteristics into super drug)
- What drugs should you avoid taking with cephalosporins?
- Aminoglycosides (increases nephrotoxicity) and ethanol (causes a disulfiram-like rxn -- headache, nausea, flushing, hypotension)
- When would you use aztreonam?
- Only to treat:
- Is Aztreonam beta-lactamase resistant?
- Yes, this is one of the huge benefits of the drug, and it is not cross-reactive with PCN!
- Which population of pt. is Aztreonam good for?
- The PCN-allergic patient that can't take aminoglycosides b/c of renal insufficiency
- Are there any toxicity issues with Aztreonam?
- Not really. Generally well tolerated with occasional GI upset. Vertigo, Headache and rare hepatotoxicity have been reported.
- What is imipenem?
- broad spectrum beta-lactamase-resistant abx
- What do you always administer Imipenem with and why?
- cilastatin -- it decreases inactivation of imipenem in renal tubules
- What do you use Imipenem for?
- Gram pos cocci, gram neg rods and anaerobes (broad spectrum)
- What bug is Imipenem the drug of choice for?
- What are its side-effects of Imipenem?
- GI distress,
seizures at high conc.
- Is Vancomycin bactericidal or bacteriastatic and why?
- Bactericidal because it blocks cross linkage and elongation of peptidoglycan by binding D-ala D-ala protion of cell wall.
- How does resistance to Vanco occur?
- D-ala D-ala is replaced with D-ala D-lactate which vanco does not block
- What is Vancomycin used for?
- Used for serious infection that is resistant to other drugs (e.g. gram pos multi-drug resistant organisms like S. aureus and C. difficile, methicillin resistant staph (MRSA))
- What are the important toxicities of vanco?
- generally NOT many problems except, Nephrotoxicity, Ototoxicity and Thrombophlebitis
- What can happen with rapid infusion of Vancomycin?
- Red man's syndrome.
Diffuse flushing which can be controlled by pretreatment with anti-histamines and with slow infusion rate
- Which drugs target bacterial protein synthesis by blocking the 30S unit vs 50S unit?
- Buy AT 30, CELL at 50
- What does AT stand for?
- A = Aminoglycosides
(streptomycin, gentamicin, tobramycin and damikacin)
T = Tetracyclines
- What does CELL stand for?
- C = Chloramphenicol,
- Which of the protein synthesis inhibitors are bactericidal?
- Only the aminoglycosides are, the rest are bacteriostatic
- Name some aminoglycosides?
- Gentamicin, neomycin, amikacin, tobramycin and streptomycin
- How do Aminoglycosides work?
- They inhibit formation of the initiation complex in mRNA translation
- Why are Aminoglycosides ineffective against anaerobes?
- They require oxygen for uptake into bacteria
- When would you use aminoglycosides?
- against severe gram-negative rod infections
- What drugs can you use aminoglycosides with for synergy?
- the drugs that inhibit cell wall synthesis (e.g. penicillin and cephalosporins -- the beta-lactam antibiotics). Presumably this allows the drug to get in with out reliance on oxygen transport
- What drug in the Aminoglycosides class is commonly used for bowel surgery?
- What are the two major Aminoglycoside toxicities?
- Nephrotoxicity (esp. when used with cephalosporins) and Ototoxicity (esp. when used with loop diuretics). amiNOglycosides
- Name some tetracylcines
- Tetracycline, doxycycline, demeclocycline, minocycline
- How do Tetracyclines work?
- Blocks t-RNA attachment to 30S subunit
- Which tetracycline can you use in patients with renal failure and why?
because its elimination is fecal
- What drug class should you not take with a glass of milk?
- What are tetracyclines used for?
- VACUUM your Bed Room -- Vibrio cholerae, Acne, Chlamydia, Ureaplasma, Urealyticum, Mycoplasma pneumoniae, Borrelia burgdorferi, Rickettsia, tularemia
- What are the common toxicities of Tetracyclines?
- Teeth discoloration,
inhibition of bone growth in children;
- Name (3) macrolides?
- How do Macrolides work?
- inhibit protein synthesis
- What are Macrolides used for?
- URIs, pneumonias, STDs -- gram pos cocci in patients that are allergic to PNC --- Mycoplasm, Legionella, Chlamydia, Neisseria.
- Pneumonic for Macrolide use?
- Eryc's Nipple is at his Mid Clavicular Line:
- What are the major toxicities of Macrolides?
- Macros make you GASE:
Acute cholestatic hepatitis,
- What is the most common cause for non-compliance to macrolides?
- GI discomfort
- How does Chloramphenicol work?
- inhibits 50S peptidyltransferase
- Main use of Chloramphenicol?
(H. influenzae, N. meningitides, S. pneumo)
Used conservatively b/c of toxicity
- What are the main toxicities of Chloramphenicol?
- Anemia and aplastic anemia
(both dose dependent),
Gray baby syndrome
(in premes b/c they lack UDP-glucoronyl transferase)
- How does Clindamycin work?
- blocks peptide bond formation at 50S
- When do you use Clindamycin?
- Anaerobic infections
(e.g. Bacteroides fragilis and C. Perfringens)
- Toxicities of Clindamycin?
- Pseudomembranous colitis,
- MC sulfonamide
- Sulfamethoxazole (SMX)
- How do Sulfonamides work?
- Inhibits bacterial folic acid synthesis from PABA
(by blocking dihydropteroate synthase)
- What are its uses?
- Toxicities of Sulfonamides?
- hypersensitivity rxn,
hemolysis if G6PD deficient,
kernicterus in infants,
displaces other drugs from albumin (e.g. warfarin)
- How does Trimethoprim work?
- inhibits folic acid pathway by blocking dihydrofolate reductase
- What are Trimethoprim's uses?
- used in combo with Sulfamethoxazole (TMP-SMX) for recurrent UTIs,
prophylaxis for PCP in AIDS patients
- Toxicities of Trimethoprim?
- Megaloblastic anemia,
(may be alleviated with supplemental folic acid)
- What the most famous floroquinolone?
- Ciprfloxacin (treatment for Anthrax)
- How do Fluoroquinolones work?
- inhibits DNA gyrase (topoisomerase II)
- What are Fluoroquinolones uses?
- Gram neg,
First line for Pseudomonas UTI,
- What population is contraindicated for Fluoroquinolone use?
- pregnancy and children
- What are Fluoroquinolone toxicities?
- FluoroquinoLONES hurt attachment to BONES:
Tendonitis and tendon rupture in adults
- How does Metronidazole work?
- forms toxic metabolites in the bacteria
- What are Metronidazole uses?
- What is the role of Metronidazole in H. pylori infection?
- Used as part of triple therapy:
Bismuth, Amoxicillin and Metronidazole
- Main toxicity of Metronidazole?
- disulfiram-like (antabuse) reaction to alcohol and headache
- Which drug do you use to treat anaerobic infections above the diaphram and below the diaphram?
- Anaerobes above diaphram:
Anaerobes below diaphram:
- How do Polymyxins work?
- disrupts osmotic properties of bacteria, acts like a detergent
- What are Polymyxins used for?
- resistant gram negative infections
- Toxicities of Polymyxins?
- p. 296
- How does it work?
- inhibits DNA-dependent RNA polymerase
- What is it used for?
- MTB, meningococcal prophylaxis
- Minor hepatotoxicity and increases P-450
- What vitamin prevents neurotoxicity
- Vitamin B6 (pyridoxine)
- Why are toxicities particularly important to monitor in patients taking INH?
- INH half-lives are different in fast versus slow acetylators!
- P. 296
- How can it be used for leprosy?
- rifampin delays resistance to dapsone when used for leprosy
- What would happen if you used rifampin alone?
- get rapid resistance
- What does it do to bodily fluids?
- makes them red/orange in color
- What are the 4 R's of Rifampin
- RNA polymerase inhibitor, Revs up microsomal p-450, Red/Orange body fluids, Resistance is rapid
- Anti-TB Drugs
- p. 296
- What are the anti-TB drugs?
- Rifampin, Ethambutol, Streptomycin, Pyrazinamide, Isoniazid (INH) -- RESPIre
- What do you use for TB prophylaxis?
- What toxicity is common to all?
- arachadonic acid products
- pg 150
- name the enzyme that liberates AA from the cell membrane
- phospholipase A2
- what does the lipoxygenase pathway yield
- leukotrienes (L for Lipoxygenase and Leukotrienes)
- LTB4 is a____
- neutrophil chemotactic agent
- which leukotrienes are involved in bronchoconstriction, vasoconstriction, smooth muscle contraction, and increased vascular permeability
- LT C4, D4, E4 (SRS-A)
- what are the 3 products of the cyclooxygenase pathway?
- thromboxane, prostacyclin, prostaglandin
- what are the 2 functions of TxA2
- platelet aggregation, vasoconstricion
- what are the 2 functions of PGI2
- inhibition of platelet aggregation; vasodilation (Platelet Gathering Inhibitor)
- pg 150
- what are the shape and dimensions of a microtubule?
- cylindrical, 24 nm in diameter, variable length.
- what are the components of a microtubule
- polymerized dimers of alpha and beta tubulin (+2 GTPs per dimer)
- where are microtubules found
- cilia, flagella, mitotic spindles, neuronal axons (slow axoplasmic transport)
- antihelminthic drug that acts on microtubules
- anti breast cancer drug that acts on microtubules (prevent disassembly)
- antifungal drug that acts on microtubules
- anti cancer drug that acts on microtubules (prevent assembly)
- anti gout drug that acts on microtubules
- Resistance mechanisms for various antibiotics
- Most common resistance mechanism for penicillins / cephalosporins.
- Beta-lactamase cleavage of beta-lactam ring.
- Most common resistance mechanism for aminoglycosides.
- Modification via acetylation, adenylation, or phosphorylation.
- Most common resistance mechanism for vancomycin.
- Terminal D-ala of cell wall component replaced with D-lac; decrease affinity.
- Most common resistance mechanism for Chlorampenicol.
- Modification via acetylation.
- Most common resistance mechanism for macrolides.
- Methylation of rRNA near erythromycin's ribosome-binding site.
- Most common resistance mechanism for tetracycline.
- Decrease uptake or increase transport out of cell.
- Most common resistance mechanism for sulfonamides.
- Altered enzyme (bacterial dihydropteroate synthetase), decrease uptake, or increase PABA synthesis.
- Nonsurgical antimicrobial prophylaxis
- Drug of choice for meningococcal infection.
- Rifampin (drug of choice), minocycline.
- Drug of choice for gonorrhea.
- Drug of choice for syphilis.
- Benzathine penicillin G.
- Drug of choice for history of recurrent UTIs.
- Drug of choice for Pneumocystis carinii pneumonia.
- TMP-SMX (drug of choice), aerosolized pentamindine.
- Anti-fungal therapy
- Mechanism of action of the anti-fungal therapy polyenes.
- Form artificial pores in the cytoplasmic membrane.
- Mechanism of action of the anti-fungal therapies terbinafine and azoles.
- Terbinafine blocks the conversion of squalene to lanosterol. Azoles block the conversion of lanosterol to ergosterol.
- Mechanism of action of the anti-fungal therapy flucytosine.
- Blocks the production of purines from the precurors.
- Mechanism of action of the anti-fungal therapy griseofulvin.
- Disrupts microtubles.
- Amphotericin B
- Mechanism of action of Amphotericin B.
- Binds ergosterol (unique to fungi); forms membrane pores that allow leakage of electrolytes and disrupt homeostasis. "Amphotericin 'tears' holes in the fungal membrane by forming pores."
- Clinical uses of Amphotericin B.
- Used for a wide spectrum of sytemic mycoses. Cryptococcus, Blastomyces, Coccidioides, Aspergillus, Histoplasma, Candida, Mucor (systemic mycoses). Intrathecally for fungal meningitis; does not cross blood-brain barrier.
- Symptoms of Amphotericin B toxicity.
- Fever/chills ("shake and bake"), hypotension, nephrotoxicity, arrhythmias ("amphoterrible").
- Mechanism of action of Nystatin.
- Binds to ergosterol, disrupting fungal membranes.
- Clinical use of Nystatin.
- "Swish and swallow" for oral candidiasis (thrush).
- Fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole.
- Mechanism of action for fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole.
- Inhibits fungal steroid (ergosterol) synthesis.
- Clinical uses of fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole.
- Systemic mycoses. Fluconazole for cryptococcal meningitis in AIDS patients and candidal infections of all types (i.e., yeast infections). Ketoconazole for Blastomyces, coccidioides, Histoplasma, Candida albicans; hypercortisolism.
- Symptoms of fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole toxicity.
- Hormone synthesis inhibition (gynecomastia), liver dysfunction (inhibits cytochrome P-450), fever, chills.
- Mechanism of action of Flucytosine.
- Inhibits DNA synthesis byconversion to fluorouracil, which competes with uracil.
- Clinical uses of Flucytosine.
- Used in sytemic fungal infections (e.g. Candida, Cryptococcus).
- Symptoms of Flucytosine toxicity.
- Nausea, vomitting, diarrhea, bone marrow suppression.
- Mechanism of action for Caspofungin.
- Inhibits cell wall synthesis.
- Clinical use of Caspofungin.
- Invasive aepergillosis.
- Symptoms of Caspofungin toxicity.
- GI upset, flushing.
- Mechanism of action of Terbinafine.
- Inhibits the fungal enzyme squalene epoxidase.
- Clinical use of Terbinafinel.
- Used to treat dermatophytoses (especially onychomycosis).
- Mechanism of action of Griseofulvin.
- Interfers with microtubule function; disrupts mitosis. Deposits in keratin-contianing tissues (e.g. nails).
- Clinical use of Griseofulvin.
- Oral treatment of superficial infections; inhibits growth of dermatophytes (tinea, ringworm).
- Symptoms of Griseofulvin toxicity.
- Teratogenic, carcinogenic, confusion, headaches, increase warfarin metabolism.
- Antiviral chemotherapy
- Viral adsorption and penetration into the cell is blocked by ---------.
- Gama-globulins (non-specific).
- Uncoating of the virus after its penetration into the cell is blocked by --------.
- Amantadine (influenza A).
- Early viral protein synthesis is blocked by --------.
- Fomivirsen (CMV).
- Viral nuclei acid synthesis is blocked by --------.
- Purine, pyrimidine analogs; reverse transcriptase inhibitors.
- Late viral protein synthesis and processing is blocked by --------.
- Methimazole (variola); protease inhibitors.
- Packaging and assembly of new viron is blocked by --------.
- Rifampin (vaccinia).
- Mechanism of action of Amantadine.
- Blocks viral penetration/uncoating; may buffer pH of endosome. Also causes the release of dopamine from intact nerve terminals. "Amantadine blocks influenza A and rubellA and causes problems with the cerebellA."
- Clinical uses of Amantadine.
- Prophylaxis for influenza A; Parkinson's disease.
- Symptoms of Amantadine toxicity.
- Ataxia, dizziness, slurred speech. (Rimantidine is a derivative with fewer CNS side effects.)
- Mechanism of action of Zanamivir.
- Inhibits influenza neuraminidase.
- Clinical use of Zanamivir.
- Both influenza A and B.
- Mechanism of action of Ribavirin.
- Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase.
- Clinical use of Ribavirin.
- RSV (respiratory syncytial virus).
- Symptoms of Ribavirin toxicity.
- Hemolytic anemia. Severe teratogen.
- Mechanism of aciton of Acyclovir.
- Perferentially inhibits viral DNA polymerase when phosphorylated by viral thymidine kinase.
- Clinical use of Acyclovir.
- HSV, VZV, EBV. Mucocutaneous and genital herpes lesions. Prophylaxis in immunocompromised patients.
- Symptoms of Acyclovir toxicity.
- Delirium, tremor, nephrotoxicity.
- Ganciclovir (DHPG dihydroxy-2-propoxymethyl guanine)
- Mechanism of action of Ganciclovir.
- Phosphorlation by viral kinase; perferentially inhibits CMV DNA polymerase.
- Clinical use of Ganciclovir.
- CMV, especially in immunocompromised patients.
- Symptoms of Ganciclovir toxicity.
- Leukopenia, neutropenia, thrombocytopenia, renal toxicity. More toxic to host enzymes than acyclovir.
- Mechanism of action of Foscarnet.
- Viral DNA polymerase inhibitor that binds to the pyrophophate binding site of the enzyme. Does not require activation by viral kinase. "FOScarnet = pyroFOSphate analog."
- Clinical use of Foscarnet.
- CMV retinitis in immunocompromised patients when ganciclovir fails.
- Symptoms of Foscarnet toxicity.
- HIV therapy
- Saquinavir, ritonavir, indinavir, nelfinavir, amprenavir are example of this type of anti-HIV drug.
- Protease inhibitor.
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