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FA Pharm: Blood Asthma GI Rxs


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Lipid-lowering agents: What is the effect of cholestyramine on the serum triglyceride level?
Slight increase (cholestyramine is a bile acid resin)
Lipid-lowering agents: What is the effect of colestipol on HDL?
No effect! (colestipol is a bile acid resin)
Lipid-lowering agents: What is the effect of lovastatin on HDL?
Increase (lovastatin is an HMG-CoA reductase inhibitor)
Lipid-lowering agents: Name 2 side effects of pravastatin.
Increase LFTs and cause myositis (prevastatin is an HMG-CoA reductase inhibitor)
Lipid-lowering agents: What is the effect of Niacin on HDL?
Lipid-lowering agents: What are the side effects of clofibrate?
Incease LFTs and cause myositis (Clofibrate is a "Fibrate")
Lipid-lowering agents: Which increases HDL most: simvastatin, niacin, or gemfibrozil?
Lipid-lowering agents: Which decreases triglyceride level most: colestipol, Atorvastatin, niacin, or bezafibrate?
Lipid-lowering agents: What is the main effect of ezetimibe?
decrease serum LDL (a cholesterol absorption inhibitor)
Lipid-lowering agents: Gemfibrozil increases the activity of which enzyme?
Lipoprotein lipase (which converts VLDL to IDL)
Lipid-lowering agents: AUTHOR
Rafael Vazquez
Arachidonic acid products: What enzyme breaks down membrane lipid into arachidonic acid?
Phospholipase A2
Arachidonic acid products: What two enzymes are responsible for the production of Hydroperoxides (HPETEs) and Endoperoxidases, respectively from arachidonate?
Lipoxygenase= HPETE, Cyclooxygenases=endoperoxidases
Arachidonic acid products: What major class of products do HPETEs give rise to?
Arachidonic acid products: What are the 3 major products of Endoperoxidases?
Prostacyclin (PGI), Prostaglandins (PGE, PGF), Thromboxane (TXA)
Arachidonic acid products: In general what effect do leukotrienes have on bronchial tone?
Leukotrienes in general increase bronchial tone
Arachidonic acid products: In the arachodonic acid pathway, what two enzymes do corticosteroids block?
Phospholipase A2, COX-2
Arachidonic acid products: NSAIDs, Acetaminophen and COX-2 inhibitors block which arachadonic acid pathway enzymes
NSAIDs-non-selectively block COX-1 and COX-2, acetaminophen doesn't block COX-1 or COX-2, but instead it may block COX-3 in found in the brain, COX-2 inhibitors block COX-2
Arachidonic acid products: What are the 4 major effects of Prostacyclin
decrease platelet aggregation, decrease vascular tone, decrease bronchial tone, decrease uterine tone
Arachidonic acid products: What are the 3 major effects of Prostaglandins
increased uterine tone, decrease vascular tone, decrease bronchial tone
Arachidonic acid products: What are the 3 major effects of Thromboxane
increase platelet aggregation, increase vascular tone, increase bronchial tone
Arachidonic acid products: Zileuton is a ________ pathway inhibitor?
Arachidonic acid products: Zariflukast is associated with what enzymes?
Asthma drugs: Bronchodilation is mediated by what molecule
Asthma drugs: Bronchoconstriction is mediated by _________ and ___________
Ach and adenosine
Asthma drugs: How many asthma drug categories are there?
7- (1) nonspecific B-agonists, (2) B2 agonists, (3) Methylxanthines, (4) muscarinic antagonist, (5) cromolyn, (6) corticosteroids, (7) Antileukotrienes
Asthma drugs: What is the only nonspecific B-agonist drug and what are its effects?
Isoprotenerol-relaxes bronchial smooth muscle (B2) and tachycardia (B1) (adverse effect).
Asthma drugs: What are the two B2 selective agonist asthma drugs?
Albuterol- relaxes bronchial smooth muscle (B2), Salmetrol
Asthma drugs: What are the indications for Albuterol and Salmetrol, respectively?
Albuterol- use during acute exarcebation, Salmetrol- long-acting agent for prophylaxis
Asthma drugs: what are the notable adverse effects of B2 agonist?
arythmias and tremor
Asthma drugs: B2-agonists activate this enzyme in bronchial smooth muscle that leads to an increase in ________ = bronchodilation
B2 agonists activate adenylate cyclase and increase conversion of ATP to cAMP
Asthma drugs: What are the likely mechanism of action theophylline?
bronchodialation by inhibition phosphodiesterase (PDE), decreasing cAMP hydrolysis and antagnonizing adenosine action
Asthma drugs: Why is usage of theophylline limited?
limited b/c narrow therapeutic index (cardiotoxicity, neurotxicity)
Asthma drugs: What kind of drug is Ipratropium?
muscarinic antagonist
Asthma drugs: How does mechanism of action of Ipratropium?
competitive block of muscarinic receptors= prevention of bronchoconstriction
Asthma drugs: cromolyn works by inhibiting the release of _______ from ______ cell?
prevents release of medicators from mast cells
Asthma drugs: Cromolyn is mainly used for the ______ of athsma and it is not indicated for _______ treatment of athsma?
Used only for prophylaxis, not effective during acute episode. Also, toxicity rare
Asthma drugs: __________and ________ are two major corticosteroids used for treatment of what kind of asthma?
Beclomethasone and prednisone are 1st line therapy for chronic asthma
Asthma drugs: What is the mechanism of action of corticosteroids?
inhibits the synthesis of virtually of cytokines-->inactivates NF-KB, the transcription factor that induces the production of TNF-a, amonth other inflammatory agents.
Asthma drugs: Zileuton blocks the conversion of _______ to ________.
zileuton is a 5-lipoxygenase pathway inhibitior. Blocks the conversion of arachidonic acti to leukotrienes
Asthma drugs: Zafirlukast works by_______ ________ ________
bloking leukotriene receptors
Asthma drugs: What the most basic asthma treatment strategy?
avoidance of exposure to antingen (dust, pollen, etc)
Asthma drugs: After exposure to antigen crosslinks IgE on mast cells. This is prevented by the following drugs: _________ and ________
cromolyn and steroids
Asthma drugs: Following allergen exposure mediators are released (ex. _______ and _________). This triggers an ______ asthmatic response characterized by ________ and may be treated with the following 3 asthmatic drug categories to treat the symptoms.
examples of mediators are leukotrienes and histamine. Following allergen exposure an early asthmatic response characterized by bronchoconstriction that can be treated with B-agonsists, methylxanthines, and muscarinic antagonists.
Asthma drugs: Also, mediators elicit a ________ response is which leads to bronchial __________ and is treated with __________.
mediators elicit a late response and this leads to bronchial hyperactivity. This is best treated with steroids.
GI therapy: the following questions are from the diagram at the top of the page
GI therapy: _____ cells are predominatly found in the antrum and _________ cells are predominatly found in the fundus.
Gastrin cells are predominant in the antrum and parietal cells are predominant in the fundus.
GI therapy: What are the 3 main stimuli of acid secretion?
Ach, histamine, gastrin
GI therapy: Gastrin stimulates the ECL cells to secrete histamine that stimulates ______ cells. Gastrin also activate the ______ cells to increase expression of _______ that increases ______secretion.
Gastrin stimulates the ECL cells to secrese histamine that stimulates parietal cells. Parietal cells are also activated by gastrin to increase the expression of the H,K ATPase that increases acid secretion.
GI therapy: This type of drug acts by inhibiting M1 and M3 receptors on ECL cells and Parietal cells, respectively.
muscarinic antagonists block M1 receptors in ECL cells and M3 receptors in parietal cells.
GI therapy: This type of drug inhibits the ability of the ECL cell to stimulate acid secretion by interfering with the _____ receptor.
H2 blocker inhibits the ability of the ECL cell to stimulate acid secretion by interfering with the parietal H2 receptor.
GI therapy: The most direct way of inhibiting acid secretion is by using this type of drug which acts on this enzyme.
the most direct way of inhibiting acid secretion is by using proton pump blockers which inhibit the H,K ATPase on parietal cells.
GI therapy: ____________ acts by binding to the ulcer and increasing its healing. It may interfere with drug absorption in the stomach.
sucralfate binds to the ulcer base and provides physical protection. It allows HCO3- secretion to reestablish pH gradient in the mucus layer.
GI therapy: What hormone binds ECL cells and decreases acid secretion?
GI therapy: These type of drugs used to decrease pH in the stomach.
antacids⬦.duh⬦.jk. (I was instructed to make a question of every word)
GI therapy: questions not from the diagram
GI therapy: ____________, ___________, ___________, and ___________ are examples of H2 blockers and they act by (reversibly/irreversibly)
cimetedine, ranitidine, famotidine, nizatidine reversilbly block H2 receptors.
GI therapy: This H2 blocker is the only one that has many side effects which include potent inhibition of ______, _____ effects, and _____ renal excretion of creatinine.
cimetedine is a potent inhibitor of P450, it has antiandrogenic effect and decrease renal excretion of creatinine. Other H2 blockers are relatively free of these effects.
GI therapy: _________ and _________ (reversibly/irreversibly) inhibit the H/K ATPase in the stomach _______cells.
Omeprazole and Iansoprazole irreversibly inhibit the H/K ATPase in stomach parietal cells
GI therapy: Proton pump inhibitors are indicated for peptic ulcer, ________, _______, and _________ syndrome
peptic ulcer, gastritis, esophageal reflux, and Zollinger-Ellison syndrome
GI therapy: T/F: Bismuth and sucralfate allow HCO3- secretion.
True: bismuth and sucralfate bind to ulcer base and provide physical protection, and allow HCO3- secretion to reestablish pH gradient in the mucus layer=increased ulcer healing
GI therapy: T/F: misoprostol is a PGE2 analog and increases the production and secretion of gastric mucous barrier.
False: misoprostol is a PGE1 analog and it increases the production and secretion of gastric mucous barrier.
GI therapy: What are the 3 indications for misoprosol?
prevention of NSAID-induced peptic ulcers, maintains a PDA and used to induce labor
GI therapy: In what population is misoprostol contraindicated?
women of childbearing potential (abortifacient). It also casues diarrhea
GI therapy: Infliximab is ___________ against ______.
monoclonal antibody to TNFa
GI therapy: The clinical indication for Infliximab is:
Crohn's, along with fistula healing
GI therapy: T/F: Infliximab can cause respiratory infection, fever, hypotension
GI Drugs (cont.): This drug offers both anitbacterial action and anti-inflamatory effects. It is used for 2 inflammatory GI diseases ______ and _______.
sulfasalazine: combination of sulfapyridine (antibacterial) and mesalamine (anti-inflammatory effects). It is used for Ulcerative colitis and remission of Crohn's.
GI Drugs (cont.): T/F: Side effects of the above include: malaise, sulfonamide toxicity, neutropenia
false: side effects: malaise, nausea, sulfonamide toxicity
GI Drugs (cont.): ___________ is a powerful central-acting antiemetic. It acts by antagonizing the______ receptor.
Ondansetron: is a powerful antiemetic. Think: you will not vomit with ondansetron, so you can go on dancing.
GI Drugs (cont.): T/F used to treat vomiting preoperatively and for cancer chemo therapy pts.
False: it is used to treat vomiting postoperatively.
GI Drugs (cont.): Headache and __________ are side effects
constipation (can't vomit or poop)
GI Drugs (cont.): Antacid overuse can affect:_________, __________, or ______ excretion of other drugs by altering ______ and ______ pH or by delaying gastric _________.
Antacid overuse can affect absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying.
GI Drugs (cont.): Constipation and (hypo/hyper) phosphatemia is seen with overuse of ________________
aluminum hydroxide - Aluminimum amt. of feces
GI Drugs (cont.): Magnesium hydroxide overuse = ___________
diarhea; Mg = Must go to the bathroom
GI Drugs (cont.): Calicium carbonate= hypercalcemia and (increase/decreased) acid
causes hypercalcemia and increased acid.
GI Drugs (cont.): T/F: hyperkalemia can be seen with AlOH, MgOH, CaCO2
False! hypokalemia
heparin: Catalyzes activation of ____________, decreases ________ and __________. It has a ____t1/2. check PTT
catalyzes the activation of antithrombin III, decreases thrombin and Xa. It has a short t1/2
heparin: It is used for immediated anticoagulation for pulmonary embolism,_______, _______, MI, and ________. Follow PTT
used for pulmonary embolism, stroke, angina, MI, and DVT.
heparin: T/F: Is used during pregnancy
true: it is used during pregnancy because it does not cross the placenta.
heparin: It can cause bleeding,___________, and drug-drug interactions.
heparin: ___________ is used for rapid reversal of heparization (it is a _______ charged molecule that binds the ________ charged heparin)
protamine sulfate is used for rapid reversal of heparinization (it is a positively charged molecule that binds the negatively charged heparin).
heparin: Newer________________ (enoxaparin) act more on _____, have better bioavailability and 2-4 times longer t1/2. Can be administered subcut and (with/without) lab monitoring.
lower-molecular-weight heparins (enoxaparin) act more on Xa, have better bioavailabitlity and 2-4 times longer half-life. Can be adm. Subcut and without lab monitoring.
warfirin (coumandin): Interferes with normal synthesis and gamma-carboxylation of vitamin K-dependent factors ___, ___, ___, and ___, also, ___ and ___ via ______ antagonism.
Interferes with normal synthesis and gamma-carboxylation of vitamin K-dependent clotting factors II, VII, IX, and X, protein C and S via vitamin K antagonism.
warfirin (coumandin): t1/2 (short/long)
warfirin (coumandin): Used for _______ anticoagulation. Follow PT
WEPT - Warfirin affects the Extrinsic pathway and prolongs PT
warfirin (coumandin): T/F: is used during pregnacy
False! (warfarin, unlike heparin, can cross the placenta).
warfirin (coumandin): Toxicity: bleeding, _________, drug-drug interactions
heparin vs. warfarin: Heparin is a (large/small) _____charged acicid polymer while Warfarin is (large/small) (charged/neutral) molecule
Heparin is a large negatively charged acidic polymer while Warfarin is a small neutral charged lipid-soluble molecule
heparin vs. warfarin: T/F: Heparin is given orally while warfarin is given SC/IV
False! Heparin is given IV/SC and warfarin is give oral
heparin vs. warfarin: Site of action: heparin _________, warfarin ______
heparin's site of action is the blood; warfarin's site of action is the liver (synthesises clotting factors)
heparin vs. warfarin: Onset of action of _________ is slow; the onset of action of ______ is rapid
onset of action of heparin is rapid (secs) and the onset of action of warfarin is slow, limitd by t1/2 of normal clotting factors.
heparin vs. warfarin: Warfarin works by imparing the synthesis of _______ dependent factors __, ___, ___, and ___ also _____, and ____; heparin activates _____, ____ and ___
Warfarin works by imparing the synthesis of vitamin K dependent factors II, VII, IX, and X also protein S and protein C; heparin activates ATIII, Iia (thrombin) and Xa.
heparin vs. warfarin: Heparin 's duration of action is (acute/chronic); warfarin's duration of action is (actue/chronic)
Heparin's duration of action is actute and warfarin's duration of action is chronic.
heparin vs. warfarin: Tx of acute OD: Heparin = _________; warfarin=______
Tx of heparin OD is protamine sulfate; Tx of warfarin= IV vit. K and fresh frozen plasma.
heparin vs. warfarin: Warfarin is monitored by _________ while Heparin is monitored by ___________.
Warfrin is monitored by PT (extrinsic pathway) (WEPT) and heparin is monitored by PTT (intrinsic pathway)
Thrombolytics: questions from diagram at bottom of page
Thrombolytics: plasmin is the major ___________ enzyme. It breaks down both _______ and _______
fibrinolytic enzyme. It accelerates breaks down of both fribin and fibrinogen yielding fibrin splip products and degradation products, respectively.
Thrombolytics: Fibrinogen is converted to fibrin by _________
Thrombolytics: tPA and urokinase promote the converson of ______ to ________ thereby increasing fibrinolysis.
plasminogen to plasmin
Thrombolytics: Various stimuli activate a blood proactivator to a blood activator that promotes conversion of _________ to blank thereby increasing fibrinolysis
plasminogen to plasmin
Thrombolytics: Streptokinase and anistreplase both activate and Activator that increases convesion of plasminogen to plasmin.
Thrombolytics: Aminocaproic acid:____________ fibrinolysis.
inhibits fibrinolysis by inhibition of plasminogen conversion to plasmin.
Thrombolytics: 4 examples of thrombolytics include: ________, _________, _____________, and ___________
Streptokinase, urokinase, tPA(altepalse), APSAC (anistreplase)
Thrombolytics: work by directly or indirectly aiding the conversion of ___________ to __________, which cleaves ______ and ________ clots. tPA specifically coverts _______________ to plasmin
Directly or indirectly aid conversion of plaminogen to plasmin, which cleaves thrombin and fribrin clots. It is claimed that tPA specifically coverts fribrin-bound plasminogen to plasmin.
Thrombolytics: T/F: clinical use is for DVTs
False: used for early MI
Thrombolytics: pts. receiving this medication are at most risk for: ______
Hematologic Drugs: mechanism of antiplatelet interaction
Hematologic Drugs: questions from diagram at top of page
Hematologic Drugs: When a break in the endothelium occurs _________ and _________ are exposed.
collagen and vWF
Hematologic Drugs: Platelets are activated by binding to the above macromolecules. The two structures expressed by the platelets involved in this process are __________ and _________ and they bind to _________ and __________, repectively
Platelets bind to collagen and vWF. The two structures expressed by platelets that are involved in this process are GP 1a and GP 1b. GP 1a and GP 1b bind to collagen and vWF, respectively.
Hematologic Drugs: After platelet activation _________ is expressed on their surface. What is the role of this structure?
after platelets are activated they express GP IIb/IIIa. This molecule is important in platlelet-platelet aggregation.
Hematologic Drugs: _________ and _________ interaction is needed in order for platelet aggregation to occur.
GP IIb/IIIa and fribinogen
Hematologic Drugs: 5-HT, _______, and ________ are molecules that play a role in the glycoprotein expression of activated platelets.
5-HT, ADP, and TxA2 are molecules that play a role in the glycoprotein expression of activated platelets.
Hematologic Drugs: Aspirin acts by inhibiting production of ________ that in turn inhibits glycoprotein expression in activated platelets.
Hematologic Drugs: ADP production is inhibited by the drug _________.
Hematologic Drugs: This antibody drug targets the _______ on platelets.
Copidogrel, ticlopidine: T/F: inhibits platele aggregation by irreversibly inhibiting the ADP pathway involved in the binding of fibrinogen
Copidogrel, ticlopidine: It is used for ______ ________ syndrome, coronary _______, and it has been shown to decrease the incidence or recurrence of___ ____.
it is used for acute coronary syndrome, coronary stenting. Decreases incidence or recurrence of thrombotic stroke
Copidogrel, ticlopidine: Ticlopidine is associated with_________ as a side effect.
Ticlopidine causes neutropenia and it is reserved for those who cannot tolerate aspirin.
Abciximab: This drug binds to __________ on activated platelets.
gp IIb/Iia
Abciximab: It is used for ___________ and ________ _________ ___________ ___________
acute coronary syndromes and percutanous transluminal coronary angioplasty
Abciximab: toxiciites are _______ and ________
bleeding and thrombocytopenia
Aspirin: It ________ and (reversibly/irreversibly) inhibits COX1 and COX2 to prevent the conversion of _______ to prostaglandins.
acetilates and irreversably inhibits COX-1 and COX-2
Aspirin: T/F: aspirin has an effect of PT, PTT
false it has no effect
Aspirin: What are the 4 A's of aspirin and NSAIDS in general
Antipyretic, Analgesic, Anti-inflam, antiplatelet
Aspirin: Important toxicities include _________, bleeding, hyperventilation, __________- in children, and CN ____ toxicity
gastric ulceration, bleeding, hyperventilation, Reyes syndrome and tinnitus (CNVIII).

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