Drugs Flashcards
(59 cards)
Atracurium Mechanism
Isoquinoline Derivative
Atracurium Pharm
Intermediate-acting
-hepatic met. + hofmann elimination
main product (laudanosine) causally related to seizures
-cisatracurium<histamine
Succinylcholine Pharm
- short duration (5-10min)
- rapid hydrolysis by butyrlcholinesterase (liver) and high capacity pseudocholinesterase (plasma)
- neuromuscular junction -sees only small percentage of IV dose, action terminated by diffusion from cleft, plasma cholinesterase strongly influences durability
- genetically variants of plasma cholinesterase
- increased risk for abnormally long effect
- dibucaine test used for identification (inhibits normal enzyme by 80% and abnormal enzyme by only 20%)
Succinylcholine Toxicity
- Hemodynamic changes:brady/tachycardia, ventricular arrythmias, HTN
- hyperkalemia in: large burn injuries, trauma/crush, upper/lower motor neuron injuries, muscular dystrophies, prolonged immobilization
- Prolonged neuromuscular blockade: phase II blockade, atypical pseudocholinesterase
- Increased intraocular or intercrainial pressure
- Muscle Pain
- Myoglobinuria
- Malignant HTN
- Anaphylaxis
Malignant Hyperthermia
treat with dantrolene to correct hyperkalemia/acidosis/cool core temp
-avoid Ca2+ channel blockers
Neostigmine Mechanism
AchE inhibitor
Neostigmine Pharm/Toxicity
Doesn’t cross BBB
- lasts 1.5 hr
- anticholinergic: glycopyrrolate
Pyridostigmine Mechanims
AchE inhibitor
Pyridostigmine Pharm/Toxicity
Doesn’t cross BBB
- lasts 1-2hr
- anticholinergic: glycopyrrolate
Methotrexate Mechanism
-inhibition of AICAR transformylase (which catalyzes the last step in the de novo biosynthesis of inosine monophosphate)
-leads to AICAR riboside accumulation, which inhibits adenosine deaminase, increasing circulation adenosine conc.
-adenosine inhibits lymphocyte proliferation & suppresses secretion of IL-1, INF gamma, TNF, increases IL-4, impairs histamine release, decreases chemotaxis of neutrophils
IMMUNOSUPPRESSION
Methotrexate Pharm
- undergoes polyglutamation-drug stays intercellular
- Elimination: kidney
- Metabolism: hepatic
Methotrexate Toxicity
-Bone marrow suppression/anemia
-Pulmonary toxicity-acute/chronic interstitial pneumonitis, pulmonary fibrosis
Contrindication: HIV, Pregnancy (CAT X), no breastfeeding
-avoid vaccine
-malignant lymphomas, fatal dermatologic rxns, GI toxicity with PUD/ulcerative colitis
Sulfasalazine Mechanism
- metabolized to active - sulfapyridine and mesalamine by bacteria in the colon
- absorbed sulfapyridine is acetylated an dhydroxylated in the liver
- anti-inflammatory properties of mesalamine (inhibitor of PF and LT production)
Sulfasalazine Pharm
Elimination: Renal
Oral
Sulfasalazine Toxicity
Hematotoxicity-fatal blood dyscrasias infrequent
Contraindications: known hypersensitivity to 5-aminosalicylate, salicylate, or sulfonamide drugs
Leflunomide Mechanism
active primary metabolite A77 1726 that inhibits dihydroorotate dehydrogenase (enzyme located in cell mitochondria that catalyzes a key step in de novo pyrimidine synthesis.
- in T&B cell cycle progression is arrested & their collaborative interaction interrupted
- Immunoglobulin production is suppressed
- cytostatic at normal doses
Leflunomide Pharm
Elimination: feces, other metabolites, flucuronide
uricosuric effect
Oral drug
Leflunomide Toxicity
-Hepatic (no alcoholics)
Contraindicated: immunodeficiency, bone marrow dysplasia, uncontrolled infection
CAT X
Hydroxychloroquine Mechanism
- increases intracellular vacuole pH and alters processes (protein deg by acidic hydrolases in lysosome, assembly of macromoleules in endosomes, post-translation modification of proteins in the Golgi apparatus)
- decreases immune response against autoantigenic peptides
Hydroxychloroquine Pharm
Elimination: extensive and slow renal elimination, following partial hepatic metabolism
Oral
Hydroxychloroquine Toxicity
Hepatic disease (alcoholism)
Blood dyscrasias
CNS toxicity: polyneuritis, ototoxicity, seizures, neuromyopathy
Contraindications: ocular disease b/c drug can cause corneal opacities, keratopathy, retinopathy
Abatacept Mechanism
Binds CD80 and CD86 prevents T-cell co-stimulatory signal engaging with CD28
(fusion protein: human CTLA4/IgG1 Fc fragment)
Adalimumab Mechanism
Binds TNF-alpha, blocks its interaction with the p55 and p75 cell surface receptors
(TNF-alpha monoclonal ab)
Anakinra Mechanism
Competitively inhibits IL-1 alpha & IL-1 beta binding to interleukin-1 type 1 receptor (IL-1R1)
