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61 Cards in this Set
- Front
- Back
____ (particularly) and _____ have cytoprotective effects in the GI mucosa and are produced in the (COX1/COX2) pathway. |
PGE2 and PGI2 (^maintains renal fxn / vasomotor tone) |
|
Pro-inflammatory cytokines and growth factors induce (COX1/COX2). |
COX2 (^inc in inflammatory ds (arthritis) & cancer)
(*angiogenesis requires COX-2) |
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Which PG assists with renal function (perfusion)? |
PGE2 |
|
What COX-1 product is inhibited by aspirin and promotes platelet aggregation? |
TXA2 |
|
Primary functions of LTB4 (produced by lipoxygenase)? |
elicits leukocyte (ie: neutrophils) chemotaxis, adherence, and aggregation |
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What LT(s) cause contraction of bronchial SM in asthma and play a role in bronchospasm?
|
LTC4, along with LTD4 and LTE4 |
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Potential therapeutic agents in asthma?
|
Leukotriene antagonists
(aspirin, COX-1 inhibitor may inc bronchospasm in asthma bc it leaves the LT lipoxygenase pathway unopposed) |
|
Thromboxane (COX product) is involved in the pathophys of... |
thrombotic events, MI, and ischemia
*causes platelet aggregation & vasoconstriction |
|
How do PGs,"cause" pain? |
PGs- sensitize the nociceptor by reducing the pain threshold, cause substance P (causes pain) & histamine release
(do NOT directly cause pain)* |
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What drug inhibits lipoxygenase and formation of LTs? |
Zileuton
(inhibits formation NOT antagonist of LT receptor) |
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What drugs prevent LTs from acting on target tissues?
|
Montelukast and zafirlukast
-lukasts (adjunct therapy in COPD/asthma) |
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What category of anti-inflammatory agents are the MOST potent?
|
corticosteroids |
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What drugs inhibit both phospholipase A2 (prevents formation of AA) and COX2? |
corticosteroids |
|
Corticosteroids (oral, inhaled, topical) are indicated for what? |
RA, gout, asthma, eczema |
|
T/F
Long-term use of corticosteroids is relatively safe and recommended. |
False!
Long-term use has profound adverse effects, such as suppressing the HPA axis, immunosuppression, candidiasis, osteoporosis, etc. |
|
What drugs inhibit both COX1 and COX2? |
NSAIDs |
|
NSAIDs are indicated for what? |
Inflammatory conditions, pyresis, analgesia
|
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What drug binds irreversibly and is used for prophylaxis of MI and prevention of recurrence of MI, embolism and stroke? |
Aspirin (inhibits TXA2 (via COX-1) -> inhibits platelet aggregation) |
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Name the 3 PG analogues.
|
Alprostadil (PGE1)
Misoprostol (cytotec, PGE2) Epoprostenol |
|
Indicated in treatment of Erectile Dysfxn? |
Alprostadil (PGE1) |
|
Indicated for prevention of peptic ulcers with patients on high doses of NSAIDs? |
Misoprostol (cytotec, PGE2) |
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Indicated in severe pulmonary HTN?
|
Epoprostenol |
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PGE1 can maintain the patency of the ductus arteriosus in neonates. Therefore... |
a) Alprostadil |
|
T/F |
False! |
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Histamine is stored in high concentrations in what cell types? |
Mast cells and basophils
(released in response to IgE) |
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Histamine is metabolized by what? |
Monoamine oxidase and diamine oxidase |
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Activation of H1 receptors causes...
|
bronchoconstriction, vasodilation (NO release) and local edema (in permeability via EDRF release) |
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(H1/H2) receptor is a G-coupled receptor.
|
H2
Gs -> inc adenyl cyclase -> inc cAMP |
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The final step of gastric acid secretion from the parietal cells is mediated by what?
|
Proton Pump
|
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What receptor mediates gastric acid secretion by the parietal cells in the stomach?
|
H2
(too much--> GERD, peptic ulcer, Zollinger Ellison Syndrome) |
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The tissues with the most histamine content are where?
|
Lung and skin
|
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What are drugs involved in drug-mediated release of histamine?
|
Tubocurarine |
|
How does a large dose of histamine (anaphylaxis) cause a progressive loss in blood pressure? |
Histamine activates the H1 receptors, which causes the cell to produce and release NO. NO causes SM relaxation, leading to vasodilation |
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Drug of choice for anaphylaxis?
|
Epinephrine (epi-pen)
|
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What is the triple response of histamine? |
Wheal (edema d/t inc capillary permeability) |
|
H1 activation has what effects; |
inc capillary dilation--> dec BP inc capillary permeability--> inc edema inc bronchiolar sm muscle contraction inc peripheral nociceptive receptors (pain) dec AV nodal conduction |
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H2 activation has what effects, besides incr. gastric acid secretion? |
increased SA nodal rate, positive cardiac inotrope, increased cardiac automaticity |
|
Sedative nonspecific effects are predominant in (1st/2nd) generation H1 antagonists. |
1st generation |
|
1st generation H1 antagonists (anti-histamines) are indicated in the treatment for what? |
allergies, rhinitis, inflammation and nausea a/w motion sickness
*prophylactic tx of hives (prevents formation) |
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1st generation H1 antagonists interact with what other receptors (besides H1)? |
Muscarinic, cholinergic, and adrenergic (low specificity) |
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Name the 1st generation H1 antagonists. |
Azelastine Hydroxyzine |
|
Which drugs are indicated for motion sickness (& nausea & vomiting in pregnancy) and also antagonize M1 receptors? |
Meclizine
|
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Name the long-acting drug that is widely used for skin allergies and is also used as a mild anxiolytic. |
Hydroxyzine |
|
What drug is used for allergies, sedation, nasal decongestant, and as an adjunct in Parkinson's disease? |
Diphenhydramine (benadryl) |
|
What drug is indicated for allergic reactions and prophylaxis and treatment of motion sickness and post-op pain (adjunct to analgesics)?
This drug causes the MOST sedation!! |
Promethazine |
|
What is azelastine used for? |
nasal spray and ophthalmic agent, intranasally it reduces hyper-reactivity of airways and increases motility of bronchial cilia |
|
What is the active metabolite of Azelastine?
|
desmethylazelastine
|
|
Adverse effects (overdose) of 1st generation H1 antagonists? |
sedation, GI distress, N/V (in high doses), extrapyramidal reactions
|
|
H1 (1st generation) antagonists potentiate the effects of what drugs?
|
CNS depressants and alcohol (overall too much sedation) Monoamine oxidase inhibitors (anti-depressants) (very high inc in dopa) |
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(1st/2nd) generation H1 antagonists are less lipid soluble.
|
2nd, by far
(don't go into CNS) |
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Most 2nd generation H1 antagonists are extensively metabolized in the ______ and have a half-life of 12-24 hours.
|
Liver
|
|
(1st/2nd) generation H1 antagonists are better for chronic treatment of rhinitis & allergies. |
2nd, much less sedative/autonomic effects
(generally preferred tx**)
(worse for motion sickness)* |
|
Name the 2nd generation H1 antagonists. |
Fexofenadine (Allegra) |
|
What are the H2 antagonists? |
Cimetidine |
|
The typical half-life of H2 antagonists is how long?
|
1-3 hours (H1 was 12-24) |
|
T/F
H2 antagonists also have effects on H1 receptors and autonomic receptors. |
False!
They are relatively selective and have no actions on H1 receptors or autonomic receptors. They produce a surmountable pharm blockade of H2 receptors! |
|
What are H2 antagonists used for? |
Duodenal (specifically) and gastric ulcers, Zollinger Ellison Syndrome, GERD, reflux esophagitis |
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How are acute ulcers treated with H2 antagonists vs recurring ulcers? (specifically duodenal)
|
acute - 2 or more doses per day |
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What disease is characterized by acid hypersecretion, severe recurrent peptic ulceration, GI bleeding, and diarrhea? |
Zollinger-Ellison Syndrome |
|
What drugs are more effective than H2 antagonists in treating Zollinger-Ellison Syndrome? |
PPIs (proton pump inhibitors)
(bc H2 antagonists are competitive blockers, they require constant and high doses to help w/ over-secretion) |
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Which H2 antagonist inhibits cyt P450, causing lots of drug interactions (esp w/ Warfarin)? |
Cimetidine |