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93 Cards in this Set

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Penicillin MOA
Bind PBP, block transpeptidase, activate autolytic enzymes
Penicillinase-resistant penicillins names
Methicillin, nafcillin, dicloxacillin
Aminopenicillin names and uses
Ampicillin, amoxicillin
uses: extended spectrum used against Haemophilus, E. coli, Listeria, Proteus, Salmonella, and enterococci (HELPS kill enterococci)
Antipseudomonal penicillins
ticarcillin, carbenicillin, piperacillin
should use with clavulanic acid to guard against penicillinases
Aztreonam uses
penicillin replacement in those who are allergic. Only good against gram (-)
Imipenem/cilastatin uses and S/E
uses: very broad spectrum, first line for enterobacter
S/E: GI distress, seizures
Vancomycin S/E
nephrotoxicity, ototoxicity, thrombophlebitis, diffuse flushing
Aminoglycosides are synergistic w/...
B-lactam antibiotics, because they will pop holes into the cell membrane and aminogycosides can then go in
Daptomycin MOA and S/E
MOA: rapidly depolarizes cell membrane leading to disruption of protein, DNA, RNA synthesis
S/E: myositis, peripheral neuropathy, diarrhea
Tetracyline uses
VACUUM THe BedRoom
Macrolide uses and S/E
Mycoplasma, legionella, Chlamydia, Neisseria, URIs, pneumonias, STDs
S/E: prolonged QT, acute cholestatic hepatitis, P450 inhibitor
Clindamycin MOA
blocks peptide bond formation at 50S ribosome
Metronidazole MOA and S/E
Forms toxic metabolites in the bacterial cell that damage DNA
S/E: disulfiram-like reaction, metallic taste, headache
Polymyxins MOA and S/E
bind cell membranes and disrupt their osmotic properties, like detergents
S/E: neurotoxicity, acute renal tubular necrosis
2nd line treatment for TB
cycloserine
Ethambutol MOA and S/E
MOA: inhibits inhibits polymerization of arabinogylcan in cell wall
S/E: decreased visual acuity and red-green color blindness
Pyrazinamide MOA and S/E
MOA: unknown mechanism, but needs pyrazinamidase to work
S/E: dose dependent hepatotoxicity
Isoniazid MOA and S/E
MOA: decreases synthesis of mycolic acids after it is activated by bacterial catalase-peroxidase
S/E: hepatotoxicity, seizures, B6 deficiency
Rifampin MOA and S/E
MOA: inhibits DNA dependent RNA polymerase
S/E: hepatotoxicity, red urine, induces P450
Amphotericin B SE
Fever/chills, hypotension, nephrotoxicity, arrhythmias, IV phlebitis
Caspofungin uses
invasine aspergillosis, candidiasis
Terbinafine (allylamine) uses
Dermatophytoses, especially onychomycoses
Amantadine MOA and S/E
blocks uncoating via M2 protein, which blocks viral penetration into cell
S/E: ataxia, dizziness, slurred speech
Ribavirin MOA and S/E
MOA: inhibits synthesis of guanine nucleotides, leading to inhibition of IMP dehydrogenase
S/E: hemolytic anemia, teratogen
Foscarnet MOA
pyrophosphate analog that doesn't need a viral kinase and inhibits DNA polymerase
Protease inhibitor S/E
lipodystrophy, hyperglycemia, thrombocytopenia
Reverse transcriptase inhibitor S/E
bone marrow suppression, peripheral neuropathy, lactic acidosis (nucleosides), rash (non-nucleoside), megaloblastic anemia (ZDV)
HIV fusion inhibitor
Enfuvirtide, which binds viral gp41
CCR5 antagonist and S/E
maraviroc
S/E: hepatotoxicity
Interferon S/E
neutropenia
Cyclosporine S/E
nephrotoxicity, gingival hyperplasia, excreted in bile
Tacrolimus S/E
nephrotoxicity, pleural effusion, hyperglycemia, excreted via feces
Azathioprine MOA
derivative of 6-MP, blocks purine synthesis
Sirolimus S/E
hyperlipidemia, NO nephrotoxicity, thrombocytopenia
Mycophenolate mofetil
guanine analog that inhibits de novo guanine synthesis
Daclizumab
blocks IL-2 receptor
Hydralazine MOA and S/E
MOA: increases cGMP, leading to relaxation of smooth muscle, specifically arterioles
S/E: salt and fluid retention, drug induced lupus, tachycardia
Minoxidil MOA and S/E
MOA: K+ channel opener, leads to hyperpolarization of cells and relaxation of smooth muscle
S/E: increased hair growth, pericardial effusion, decreased insulin release
Verapamil S/E
constipation, gingival hyperplasia, AV block
Nifedipine S/E
Peripheral edema, flushing, dizziness, gingival hyperplasia
Fenoldopam
D1 receptor agonist that increases blood flow to kidneys
Diazoxide MOA
K+ channel opener that relaxes smooth muscle and decreases insulin release
Statins MOA and S/E
MOA: inhibit HMG coa reductase, mainly decreasing LDL
S/E: hepatotoxicity, myositis
Niacin MOA and S/E
MOA: decrease release of VLDL, increase LPL activity, mainly decreases LDL and increases HDL
S/E: flushing, hyperglycemia, hypotension, hyperuriciemia
Bile acid resins MOA and S/E
MOA: decrease absorption of bile acids, so liver has to make its own
S/E: increased triglycericdes, gallstones, bad taste
Ezetimibe MOA
prevent cholesterol reabsorption in the small intestines
Fibrates MOA and S/E
MOA: upregulate LPL, major effect on TGs
S/E: gallstones, myositis, hepatotoxicity, SIADH
Class IA names and MOA
disopyramide, quinine, procainamide
MOA: blocks phase 0 and also K+ channels (phase 3), leading to an elongated AP
Class IA S/E
torsades, tinnitus (cinchonism), thrombocytopenia
Class IB names and MOA
names: mexlitine, lidocaine, phenytoin, tocainide
MOA: blocks phase 0, shortens AP duration, preferentially acts on active cells (good post-MI)
Class IC names and MOA
names: encainide, flecainide, propafenone
MOA: blocks phase 0, doesn't change AP duration, not good post MI
Adenosine MOA and S/E
MOA: increase K+ out of cells
S/E: flushing, hypotension, chest pain
GLP-1 mimetics name, MOA, and S/E
exenatide, increases insulin and decreases glucagon
S/E: pancreatitis
Treatment for fatties
orlistat (inhibits pancreatic lipase) and sibutramine (5-HT and NE reuptake inhibitor)
Demeclocycline uses
it's an ADH antagonist, so it's used in SIADH
Misoprostal MOA
PGE1 analog that increases secretion of gastric mucosa and also induces uterine contractions (similar to dinoprostone)
Propantheline, pirenzepine MOA
Block M1 receptors on ECL cells and M3 on parietal cells, leading to decreased H+ secretion
Sulfasalazine MOA and S/E
MOA: combo of sulfapyridine (antibacterial) and salicylic acid (anti-inflammatory) that's activated by colonic bacteria
S/E: toxicity, oligospermia
Metoclopramide interacts with what drugs?
digoxin and diabetic agents
Methotrexate S/E
macrovesicular fatty change, mucositis, teratogenic
Difference between 6-MP and 6-TG
6-TG can be given w/ allopurinol because it's not metabolized by xanthine oxidase
Cytarabine MOA and S/E
MOA: pyrimidine analog that inhibits pyrimidine synthesis
S/E: leukopenia, thrombocytopenia, megaloblastic anemia
Dactinomycin MOA and S/E
MOA: intercalates DNA
S/E: myelosuppresion
Doxorubicin MOA and S/E
MOA: noncovalently intercalates DNA, produces free radicals, disrupts membrane ion transport
S/E: cardiotoxicity, alopecia, GI toxicity
Bleomycin MOA and S/E
MOA: produces free radicals that damage DNA, G2 phase specific
S/E: pulmonary fibrosis, skin pigmentation, minimal myelosuppression
Etoposide, teniposide MOA and S/E
MOA: blocks topoisomerase II, increases DNA degredation, G2 and S phase specific
S/E: myelosuppression, alopecia
Cyclophosphamide MOA and S/E
MOA: binds guanine N-7 and covalently cross-links DNA, requires bioactivation by liver
S/E: hemorrhagic cystitis
Two cancer drugs that require bioactivation
cyclophosphamide and nitrosureas
Nitrosureas MOA and S/E
MOA: cross BBB and cross-link DNA strands
S/E: neurotoxicity
Busulfan MOA and S/E
MOA: alkylates DNA
S/E: pulmonary fibrosis, skin pigmentation
Vinca alkyloids MOA and S/E
MOA: inhibit microtubule polymerization
S/E: blast -> bone marrow suppression. Crist -> peripheral neuropathy, paralytic ileus
Paclitaxel MOA and S/E
MOA: inhibits microtubule depolymerization
S/E: myelosuppresion and hypersensitivity
Cisplatin MOA and S/E
MOA: cross-links DNA
S/E: nephrotoxicity, acoustic nerve damage
Hydroxyurea MOA and S/E
MOA: inhibits ribonucleotide reductase
S/E: myelosuppression
Trastuzumab MOA and S/E
MOA: monoclonal antibody against HER-2
S/E: cardiotoxicity
Imatinib MOA and S/E
MOA: inhibits tyrosine kinase
S/E: fluid retention
How do cholinomimetics and prostglandins work on glaucoma
they increase the outflow of aqueous humor, unlike the other drugs that decrease secretion/synthesis of aqueous humor
Treatment for myoclonic seizures
valproate
Thiopental pharmacokinetics
high potency, high lipid solubiity, rapid entry into brain
effect terminated by rapid redistribution into tissues and fat
Local anesthetics S/E
CNS excitation, severe CV toxicity (bupivicaine), arrhythmias (cocaine)
Memantine MOA
NMDA receptor antagonist
Donepezil, galantamine, rivastigmine MOA
acetylcholinesterase inhibitors used in AD
Sumatriptan MOA
5-HT1B/1D agonist that causes vasoconstriction
Leuprolide S/E
antiadnrogen, nausea and vomiting like a loopy rollercoaster
Clomiphene MOA
Partial agonist at ER in hypothalamus, leads to decrease feedback inhibition and an increase in LH and FSH release from the pituitary
Aromatase inhibitor names
anastrozole, exemestane
Dinoprostone MOA
PGE2 analog that causes cervical dilation and induces labor
Ritodrine, terbutaline MOA and S/E
MOA: B2-agonists that relax uterus, prevent labor
S/E: terbutaline crosses the placenta and should only be used when risks outweigh benefits
Sildenafil S/E
headache, flushing, impaired blue-green color vision
1st generation antihistamine names and S/E
names: diphenhydramine, chlorpheniramine, dimenhydrinate, hydroxyzine
S/E: sedation, antimuscarinic, anti-alpha adrenergic
2nd generation antihistamine names and S/E
names: loratidine, desloratidine, fexofenadine, cetirizine
S/E: far less sedation because it's lipophobic and doesn't cross the BBB
Corticosteroid MOA w/ respect to asthma
decreases NF-kB, a transcription factor that induces production of cytokines
Gauifenesin MOA
Removes excess sputum, but doesn't suppress cough reflex