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70 Cards in this Set

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