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70 Cards in this Set
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Arachidonic pathway: what is the first and common step
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Membrane lipid (phosphatidylinositol) is converted to arachidonic acid via phospholipase A2
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Arachidonic pathway: what drug inhibts phospholipase A2
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Corticosteroids
They also inhibit the protein synthesis which contributes to cyclooxygenase (COX) pathways |
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Arachidonic pathway: what are the 2 pathways after arachidonic acid is made
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1. Hyproperoxides are made into leukotrienes
2. Endoperoxides are made into prostaglandins/cyclins and thromboxane |
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Arachidonic pathway: what is the pathway for leukotrienes
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1. Arachidonic acid is made into hydroperoxides via lipooxygenase
2. Hydroperoxides are then converted into leukotrienes |
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Arachidonic pathway: what are the leukotrienes and what do they do
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1. LTB4 -- attracts neutrophils
2. LTC4, LTD4, LTE4 -- promote bronchoconstriction |
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Arachidonic pathway: what drug inhibits leukotriene formation by inhibiting hydroperoxide formation
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Zileuton inhibibts lipooxygenase therby stopping luekotriene formation by preventing hydroperoxide synthesis
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Arachidonic pathway: what drugs inhibit leukotriene binding and what are they used for
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The "-kast" drugs inhibit binding of LTC4, LTD4, LTE4 from binding to leukotriene receptors.
They prevent bronchoconstriction and are used for asthma |
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Arachidonic pathway: what is the pathway for prostaglandins/cyclins and thromboxane
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1. Arachidonic acid is made into endoperoxidase (PGG2 and PGH2) via cyclooxygenases (COX-1,2)
2. Endoperoxides are then made into prostacyclin (PGI2), prostaglandin (PGE2) and thromboxane (TXA2). |
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Arachidonic pathway: what is PGG2
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Endoperoxidase
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Arachidonic pathway: what is PGH2
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Endoperoxidase
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Arachidonic pathway: what is PGI2
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Prostacyclin
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Arachidonic pathway: what is PGE2
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Prostaglandin
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Arachidonic pathway: what is TXA2
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Thromboxane
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Arachidonic pathway: what are the cyclooxygenases
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COX 1 and 2
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Arachidonic pathway: what does PGI2 do
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PGI2 = prostacyclin
1. Decreases platelet aggregation 2. Increases vasodilation 3. Decreases uterine tone |
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Arachidonic pathway: what does PGE2 do
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PGE2 = prostaglandin
1. Increases vascular tone 2. Increases pain 3. Increases uterine tone 4. Decreases temperature |
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Arachidonic pathway: what does TXA2 do
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TXA2 = thromboxane
1. Increases platelet aggregation 2. Increases vasoconstriction |
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Arachidonic pathway: what drugs inhibit cyclooxygenase
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1. NSAIDs
2. Acetaminophen 3. COX2 inhibitors 4. Aspirin |
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Aspirin: what enzyme does it inhibit
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Aspirin irreversibly inhibits cyclooxygenase
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Aspirin: which down stream substances are affected
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1. Decreased thromboxane (TXA2)
2. Decreased prostoglandin (PGE2) |
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Aspirin: which down stream substances are not affected
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Prostocyclin (PGI2) is not affected
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Aspirin: what is a low dose and what is the effect
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< 300 mg/day = decreased platelet aggregation
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Aspirin: what is a medium dose and what is the effect
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300-2400 mg/day = antipyretic and analgesic
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Aspirin: what is a high dose and what is the effect
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2400-4000 mg/day = anti-inflammatory
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Aspirin: toxicities
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1. GI upset
2. Chronic use = acute renal failure, interstitial mephritis and upper GI bleeds 3. Reye's syndrome in kiddies who have a viral infection |
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NSAIDs: name some
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1. Ibuprofen
2. Naproxen 3. Indomethacin 4. Ketorlac |
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NSAIDs: mechanism
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Reversibly inhbits cyclooxygenase (COX 1 and 2)
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NSAIDs: what down stream substances are altered
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Decreased prostaglandin synthesis
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NSAIDs: usage
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1. Antipyretic
2. Analgesic 3. Anti-inflammatory |
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NSAIDs: what is indomethacin used for in infants
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To close a PDA
PGE2 keeps PDA open, indomethacin closes it |
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NSAIDs: toxicity
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1. Renal damage
2. Fluid retention 3. Aplastic anemia 4. GI distress 5. Ulcers |
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COX2 inhibitors: name one
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Celecoxib
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COX2 inhibitors: mechanism
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Reversibly inhibits COX 2
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COX2 inhibitors: where is COX2 found
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1. Inflammatory cells
2. Vascular endothelium |
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COX2 inhibitors: which COX is spared and what is the effect
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COX1 is not affected --
Action of COX1 helps maintain the gastric mucosa |
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COX2 inhibitors: usage
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1. Rheumatoid arthrtis
2. Osteoarthritis |
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COX2 inhibitors: toxicity
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1. Increased risk of thrombosis
2. Sulfa allergy 3. Less GI toxicity than NSAIDS due to COX1 sparing |
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Acetominophen: mechanism
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Reversible COX inhibition
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Acetominophen: where in the body is it most active
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It inhibits COX mostly in the CNS
It is inactivated in the periphery |
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Acetominophen: usage
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1. Antipyretic
2. Analgesic |
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Acetominophen: what properties does it NOT have
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It has NO anti-inflammatory properties
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Acetominophen: what is this drug substituted for in children
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Acetominophen is given to kids instead of aspirin because it is not associated with Reye's syndrome
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Acetominophen: what happens in OD and how is it treated
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Produces hepatic necrosis -- acetominophen metabolite depletes glutathione which leads to toxic tissue adducts
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What is an adduct
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The product of a reaction in which the product contains every part of the reactants
N-acetylcuysteine is given to restore glutathione |
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How does acetominophen compare to NSAIDs
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Acetominophen = NSAID minus anti-inflammatory
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How does aspirin compare to NSAIDs
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Aspirin = NSAID + anti-platelet
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Bisposhponates: name some
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They all end with "-dronate"
1. Etidronate 2. Panidronate 3. Alendronate 4. Risendronate |
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Bisposhponates: mechanism and effect
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They inhibit osteoclast activity which reduces both formation and reabsorption of hydroxyapetite
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Bisposhponates: usage
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1. Malignancy associated hypercalcemia
2. Paget's disease of the bone 3. Post-menopausal osteoporosis |
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Bisposhponates: toxicities
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1. Corrosive esophagitis
2. NVD 2. Osteonecrosis of the jaw |
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Gout drugs: what is the cause of gout
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Hyperuricemia
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Gout drugs: what leads to increased purine synthesis
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1. Diet
2. high nucleic acid turnover (e.g. tumor lysis syndrome) |
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Gout drugs: what happens to excess purines in the gout pathway
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1. Purines are converted into hypoxanthine
2. Hypoxanthine is converted into xanthine vis xanthine oxidase 3. Xanthine is converted into uric acid via xanthine oxidase |
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Gout drugs: what happens to serum uric acid in the gout pathway
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1. Excess amounts precipitate to form monosodium urate crystals
2. Some is excreted in the kidneys |
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Gout drugs: what drug inhibits xanthine oxidase
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Allupurinol
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Gout drugs: what drug inhibits tubular reabsorption of uric acid
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These drugs inhibit uric acid from being reabsorbed from the tubules and back into the serum (beneficial for gout)
1. Probenecid 2. High=dose salicylates |
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Gout drugs: what drug inhibits tubular secretion of uric acid
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These drugs inhibit uric acid from being secreted from the serum and into the tubule (bad for gout)
1. Diuretics 2. Low-dose salicylates |
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Colchicine: what is it used for
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Acute gout attacks
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Colchicine: mechanism
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Binds and stabilizes tubulin which impairs leukocytes chemotaxis and degranulation
It is basically and anti-inflammatory drug that has only been approved for gout |
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Colchicine: toxicity
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1. GI upset -- esp if given orally
2. Nephrotoxic -- contraindicated in kidney patients |
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Colchicine: what else is used for acute gout and why
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Indomethacin is used for acute got because it is less toxic
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Probenecid: use
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Chronic gout tx
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Probenecid: mechanism
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Inhibition of uric acid reabsorption in the PCT
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Probenecid: what else does it inhibit
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Also inhibits secretion of penicillin, thus it will decrease penicillin excretion and raise blood levels
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Allopurinol: use
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Chronic gout tx
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Allopurinol: mechanism
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Inhibition of xanthine oxidase --> decreased uric acid formation
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Allopurinol: when else is it used
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Tumor lysis syndrome:
Used during lymphoma and leukemia (chemo?) when there is high cell turnover to prevent urate nephropathy |
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Allopurinol: what drugs levels does it affect and why
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Increases drug levels of azathioprine and 6-MP because these are metabolized by xanthine oxidase
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What drugs should not be given for acute gout
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Allopurinol and probenecid
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What drugs work in theory but shouldn't be used to treat gout and why
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Don't use salicylates to treat gout
Low doses actually increases uric acid levels by decreasing renal secretion Only super high (i.e. toxic) doses inhibit tubular reabsorption of uric acid |
