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Pharmacology - Block 2 - Part 3

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davidwurbel7's version from 2016-06-30 13:49

NSAIDs

Question Answer
This causes constriction or dilation in vascular smooth muscle cells. Cause aggregation or disaggregation of platelets. Sensitize spinal neurons to pain. Induction of labor. Act on parietal cells in the stomach wall to inhibit acid secretion. Decrease intraocular pressure. Regulate inflammation. Acts on thermoregulatory center to produce feverProstaglandins
Prostaglandin that promotes platelet aggregationThromboxine A2
Prostaglandin that promotes platelet disaggregationProstocylins
Mechanism of action of this class of drug is to reduce production of PGs by inhibiting cyclooxygenaseNSAID
House keeping COX enzyme responsible for GI cytoprotection and platelet aggregationCOX-1
Induced COX enzyme responsible for inflammation, pain and feverCOX-2
Celecoxib, Roficoxib, Valdecoxib and eterocoxib are these types of drugsHighly Seclective COX-2 Inhibitors
Aspirin, Naproxen, Indomethacin, Ibuprofen, Diclofenac sodium, Ketorolac are these types of drugsNon-selective COX Inhibitors
The only NSAID that inhibits COX enzyme irreversibly is this drugAspirin
Adverse effects include gastric and duodenal ulcers, renal toxicity, hepatic toxicity, iron deficiency anemia, may precipitate bronchial asthmaNSAIDs
NSAIDs may precipitate bronchial asthma due to blocking the COX pathway more arachidonic acid is diverted to the production of thisLeukotrienes
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Question Answer
The mechanism of action by acetylation of enzymes, this NSAID, irreversibly inhibits both COX-1 and COX-2Aspirin
Irreversible inhibition of this enzyme by aspirin is responsible for the anticoagulation effectCOX-1
Irreversible inhibition of this enzyme by aspirin is responsible for the anti-inflammatory effectCOX-2
The dose for aspirin when in use as an antiplateletLow Dose (81 mg - 325 mg)
The dose for aspirin when in use as an anti-inflammatoryVery High Dose (4 - 8 g / day)
The only DOC use of aspirin as an anti-inflammatory is the treatment of thisAcute Rheumatic Fever
Vomiting, dehydration, metabolic acidosis, respiratory alkalosis, hypokalemia, hypoglycemia, delirium, hyperthermia, confusion, convulsions, coma are the symptoms associated with thisAspirin Poisoning
External cooling, IV fluids, Sodium Bicarbonate and/or Acetazolamide, gastric lavage, (activated carbon?????) and forced alkaline diuresis is the treatment for thisAspirin Toxicity
Treatment of a child with fever due to virus with aspirin may cause this conditionReyes Syndrome
Occurs with higher dose (both as acute and chronic ) which is characterized by Vomiting, Tinnitus, Vertigo, loss of hearingSalicylism
DOC rheumatoid arthritis, gout, Patent Ductus Arteriosus (PDA) and Ankylosing spondylitisIndomethacin
The most potent anti-inflammatory action of the NSAIDsIndomethacin
The ductus arteriousus is maintained intra-uterine by production of thisProstaglandins
Has poor anti-inflammatory action but has very good analgesicKetorolac
Best used in post operative pain as opposed to using opiatesKetorolac
NSAID that is not good for fever or inflammatory conditionsKetorolac
These NSAIDs should be avoided in patients that have shown allergic reaction to sulfonamidesCOXibs
COXibs should be avoided in patients with known allergic reaction to thisSulfonamides
This drug is related to NSAIDs but is not an NSAIDAcetaminophen
Inhibits COX better in non inflammatory area and therefore not a good anti-inflammatory drug but it is a very good antipyretic and analgesicAcetaminophen
Overdose of this drug can cause hepatic cell necrosisAcetaminophen
Hepatic cell necrosis is most often seen in this age groupChildren
The hepatic cell necrosis can occur in people that use this along with acetaminophenAlcohol
This metabolite is responsible for the hepatic cell necrosisN-Acetyl Benzoquinone (NBQ)
N-Acetyl Benzoquinone (NBQ) is detoxified by this processGlutathione Conjugation
Treatment for acetaminophen poisoning is the administration of thisN-Acetyl Cysteine
The mechanism of action of N-acetyl cysteine in acetaminophen poisoning is thisReplenishes the Glutathione Stores
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Rheumatoid Arthritis

 

Question Answer
These drugs modify the progression of rheumatoid arthritisDMARDs
The NSAID of choice for rheumatoid arthritisIndomethacin
The corticosteroid of choice for rheumatoid arthritisPrednisone
DMARD used in very low dose in rheumatoid arthritis for disease modification (in cancer high dose is used)Methotrexate
DMARD that is a recombinant IL-1 receptor antagonistAnakinara
DMARD that inhibits the mitochondrial enzyme dihydroorotate dehydrogenase, (an enzyme involved in de novo pyrimidine synthesis)Leflunomide
DMARD that mimics the inhibitory effects of naturally occurring soluble TNF receptors. A fusion protein that has a greatly extended half-life in the bloodstream, and therefore a more profound and long-lasting biologic effect than a naturally occurring soluble TNF receptorEtanarecept
Monoclonal antibody used in RA treatment. Acts as TNF-alpha blocker. Also known as "anti-TNF antibodies. Adverse effects: Infections, reactivation of Tb and heptatitis, DLEInfliximab
Infliximab acts on this which prevents inflammationTNF-alpha
This class of drugs can also be useful in treating the psoriasis, crohn’s disease and ulcerative colitisTNF Antagonists
NSAIDs and Colchicine should be used to treat inflammation & symptoms and not to treat the route cause of the disease or to reduce uric acid levelAcute Gout
Probenecid and Allopurinol should be used to reduce the blood uric acid level by - promoting excretion of uric acid and inhibiting the synthesis of uric acidSecondary Gout
Drug acts as anti-inflammatory drug only In gout. Mechanism of action is to inhibit tubulin production. It arrests cells in M phase. It has neither analgesic nor anti-inflammatory actions in any other diseasesColchicine
Mechanism of action inhibiting the tubular reabsorption of uric acid. Promotes excretion of uric acid. thereby it reduces blood level of uric acid. Reduces the effect of diureticsProbenecid
A pro drug. It produces an active metabolite called Alloxanthine. Mechanism of action is to decrease the production of uric acid by preventing the conversion of Hypoxanthine to uric acid. This is done by inhibiting the enzyme Xanthine oxidase. Contraindicated in acute goutAllopurinol
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