Fa Pharm: Blood Asthma Gi Rxs

Front 1

Lipid-lowering agents: What is the effect of cholestyramine on the serum triglyceride level?

Back 1

Slight increase (cholestyramine is a bile acid resin)

Front 2

Lipid-lowering agents: What is the effect of colestipol on HDL?

Back 2

No effect! (colestipol is a bile acid resin)

Front 3

Lipid-lowering agents: What is the effect of lovastatin on HDL?

Back 3

Increase (lovastatin is an HMG-CoA reductase inhibitor)

Front 4

Lipid-lowering agents: Name 2 side effects of pravastatin.

Back 4

Increase LFTs and cause myositis (prevastatin is an HMG-CoA reductase inhibitor)

Front 5

Lipid-lowering agents: What is the effect of Niacin on HDL?

Back 5

Increase

Front 6

Lipid-lowering agents: What are the side effects of clofibrate?

Back 6

Incease LFTs and cause myositis (Clofibrate is a "Fibrate")

Front 7

Lipid-lowering agents: Which increases HDL most: simvastatin, niacin, or gemfibrozil?

Back 7

Niacin

Front 8

Lipid-lowering agents: Which decreases triglyceride level most: colestipol, Atorvastatin, niacin, or bezafibrate?

Back 8

Bezafibrate

Front 9

Lipid-lowering agents: What is the main effect of ezetimibe?

Back 9

decrease serum LDL (a cholesterol absorption inhibitor)

Front 10

Lipid-lowering agents: Gemfibrozil increases the activity of which enzyme?

Back 10

Lipoprotein lipase (which converts VLDL to IDL)

Front 11

Lipid-lowering agents: AUTHOR

Back 11

Rafael Vazquez

Front 12

Arachidonic acid products: What enzyme breaks down membrane lipid into arachidonic acid?

Back 12

Phospholipase A2

Front 13

Arachidonic acid products: What two enzymes are responsible for the production of Hydroperoxides (HPETEs) and Endoperoxidases, respectively from arachidonate?

Back 13

Lipoxygenase= HPETE, Cyclooxygenases=endoperoxidases

Front 14

Arachidonic acid products: What major class of products do HPETEs give rise to?

Back 14

Leukotrienes

Front 15

Arachidonic acid products: What are the 3 major products of Endoperoxidases?

Back 15

Prostacyclin (PGI), Prostaglandins (PGE, PGF), Thromboxane (TXA)

Front 16

Arachidonic acid products: In general what effect do leukotrienes have on bronchial tone?

Back 16

Leukotrienes in general increase bronchial tone

Front 17

Arachidonic acid products: In the arachodonic acid pathway, what two enzymes do corticosteroids block?

Back 17

Phospholipase A2, COX-2

Front 18

Arachidonic acid products: NSAIDs, Acetaminophen and COX-2 inhibitors block which arachadonic acid pathway enzymes

Back 18

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

Front 19

Arachidonic acid products: What are the 4 major effects of Prostacyclin

Back 19

decrease platelet aggregation, decrease vascular tone, decrease bronchial tone, decrease uterine tone

Front 20

Arachidonic acid products: What are the 3 major effects of Prostaglandins

Back 20

increased uterine tone, decrease vascular tone, decrease bronchial tone

Front 21

Arachidonic acid products: What are the 3 major effects of Thromboxane

Back 21

increase platelet aggregation, increase vascular tone, increase bronchial tone

Front 22

Arachidonic acid products: Zileuton is a ________ pathway inhibitor?

Back 22

Lipoxygenase

Front 23

Arachidonic acid products: Zariflukast is associated with what enzymes?

Back 23

Lekukotrienes

Front 24

Asthma drugs: Bronchodilation is mediated by what molecule

Back 24

cAMP

Front 25

Asthma drugs: Bronchoconstriction is mediated by _________ and ___________

Back 25

Ach and adenosine

Front 26

Asthma drugs: How many asthma drug categories are there?

Back 26

7- (1) nonspecific B-agonists, (2) B2 agonists, (3) Methylxanthines, (4) muscarinic antagonist, (5) cromolyn, (6) corticosteroids, (7) Antileukotrienes

Front 27

Asthma drugs: What is the only nonspecific B-agonist drug and what are its effects?

Back 27

Isoprotenerol-relaxes bronchial smooth muscle (B2) and tachycardia (B1) (adverse effect).

Front 28

Asthma drugs: What are the two B2 selective agonist asthma drugs?

Back 28

Albuterol- relaxes bronchial smooth muscle (B2), Salmetrol

Front 29

Asthma drugs: What are the indications for Albuterol and Salmetrol, respectively?

Back 29

Albuterol- use during acute exarcebation, Salmetrol- long-acting agent for prophylaxis

Front 30

Asthma drugs: what are the notable adverse effects of B2 agonist?

Back 30

arythmias and tremor

Front 31

Asthma drugs: B2-agonists activate this enzyme in bronchial smooth muscle that leads to an increase in ________ = bronchodilation

Back 31

B2 agonists activate adenylate cyclase and increase conversion of ATP to cAMP

Front 32

Asthma drugs: What are the likely mechanism of action theophylline?

Back 32

bronchodialation by inhibition phosphodiesterase (PDE), decreasing cAMP hydrolysis and antagnonizing adenosine action

Front 33

Asthma drugs: Why is usage of theophylline limited?

Back 33

limited b/c narrow therapeutic index (cardiotoxicity, neurotxicity)

Front 34

Asthma drugs: What kind of drug is Ipratropium?

Back 34

muscarinic antagonist

Front 35

Asthma drugs: How does mechanism of action of Ipratropium?

Back 35

competitive block of muscarinic receptors= prevention of bronchoconstriction

Front 36

Asthma drugs: cromolyn works by inhibiting the release of _______ from ______ cell?

Back 36

prevents release of medicators from mast cells

Front 37

Asthma drugs: Cromolyn is mainly used for the ______ of athsma and it is not indicated for _______ treatment of athsma?

Back 37

Used only for prophylaxis, not effective during acute episode. Also, toxicity rare

Front 38

Asthma drugs: __________and ________ are two major corticosteroids used for treatment of what kind of asthma?

Back 38

Beclomethasone and prednisone are 1st line therapy for chronic asthma

Front 39

Asthma drugs: What is the mechanism of action of corticosteroids?

Back 39

inhibits the synthesis of virtually of cytokines-->inactivates NF-KB, the transcription factor that induces the production of TNF-a, amonth other inflammatory agents.

Front 40

Asthma drugs: Zileuton blocks the conversion of _______ to ________.

Back 40

zileuton is a 5-lipoxygenase pathway inhibitior. Blocks the conversion of arachidonic acti to leukotrienes

Front 41

Asthma drugs: Zafirlukast works by_______ ________ ________

Back 41

bloking leukotriene receptors

Front 42

Asthma drugs: What the most basic asthma treatment strategy?

Back 42

avoidance of exposure to antingen (dust, pollen, etc)

Front 43

Asthma drugs: After exposure to antigen crosslinks IgE on mast cells. This is prevented by the following drugs: _________ and ________

Back 43

cromolyn and steroids

Front 44

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.

Back 44

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.

Front 45

Asthma drugs: Also, mediators elicit a ________ response is which leads to bronchial __________ and is treated with __________.

Back 45

mediators elicit a late response and this leads to bronchial hyperactivity. This is best treated with steroids.

Front 46

GI therapy: the following questions are from the diagram at the top of the page

Back 46

0

Front 47

GI therapy: _____ cells are predominatly found in the antrum and _________ cells are predominatly found in the fundus.

Back 47

Gastrin cells are predominant in the antrum and parietal cells are predominant in the fundus.

Front 48

GI therapy: What are the 3 main stimuli of acid secretion?

Back 48

Ach, histamine, gastrin

Front 49

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.

Back 49

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.

Front 50

GI therapy: This type of drug acts by inhibiting M1 and M3 receptors on ECL cells and Parietal cells, respectively.

Back 50

muscarinic antagonists block M1 receptors in ECL cells and M3 receptors in parietal cells.

Front 51

GI therapy: This type of drug inhibits the ability of the ECL cell to stimulate acid secretion by interfering with the _____ receptor.

Back 51

H2 blocker inhibits the ability of the ECL cell to stimulate acid secretion by interfering with the parietal H2 receptor.

Front 52

GI therapy: The most direct way of inhibiting acid secretion is by using this type of drug which acts on this enzyme.

Back 52

the most direct way of inhibiting acid secretion is by using proton pump blockers which inhibit the H,K ATPase on parietal cells.

Front 53

GI therapy: ____________ acts by binding to the ulcer and increasing its healing. It may interfere with drug absorption in the stomach.

Back 53

sucralfate binds to the ulcer base and provides physical protection. It allows HCO3- secretion to reestablish pH gradient in the mucus layer.

Front 54

GI therapy: What hormone binds ECL cells and decreases acid secretion?

Back 54

somatostatin

Front 55

GI therapy: These type of drugs used to decrease pH in the stomach.

Back 55

antacids….duh….jk. (I was instructed to make a question of every word)

Front 56

GI therapy: questions not from the diagram

Back 56

0

Front 57

GI therapy: ____________, ___________, ___________, and ___________ are examples of H2 blockers and they act by (reversibly/irreversibly)

Back 57

cimetedine, ranitidine, famotidine, nizatidine reversilbly block H2 receptors.

Front 58

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.

Back 58

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.

Front 59

GI therapy: _________ and _________ (reversibly/irreversibly) inhibit the H/K ATPase in the stomach _______cells.

Back 59

Omeprazole and Iansoprazole irreversibly inhibit the H/K ATPase in stomach parietal cells

Front 60

GI therapy: Proton pump inhibitors are indicated for peptic ulcer, ________, _______, and _________ syndrome

Back 60

peptic ulcer, gastritis, esophageal reflux, and Zollinger-Ellison syndrome

Front 61

GI therapy: T/F: Bismuth and sucralfate allow HCO3- secretion.

Back 61

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

Front 62

GI therapy: T/F: misoprostol is a PGE2 analog and increases the production and secretion of gastric mucous barrier.

Back 62

False: misoprostol is a PGE1 analog and it increases the production and secretion of gastric mucous barrier.

Front 63

GI therapy: What are the 3 indications for misoprosol?

Back 63

prevention of NSAID-induced peptic ulcers, maintains a PDA and used to induce labor

Front 64

GI therapy: In what population is misoprostol contraindicated?

Back 64

women of childbearing potential (abortifacient). It also casues diarrhea

Front 65

GI therapy: Infliximab is ___________ against ______.

Back 65

monoclonal antibody to TNFa

Front 66

GI therapy: The clinical indication for Infliximab is:

Back 66

Crohn's, along with fistula healing

Front 67

GI therapy: T/F: Infliximab can cause respiratory infection, fever, hypotension

Back 67

TRUE

Front 68

GI Drugs (cont.): This drug offers both anitbacterial action and anti-inflamatory effects. It is used for 2 inflammatory GI diseases ______ and _______.

Back 68

sulfasalazine: combination of sulfapyridine (antibacterial) and mesalamine (anti-inflammatory effects). It is used for Ulcerative colitis and remission of Crohn's.

Front 69

GI Drugs (cont.): T/F: Side effects of the above include: malaise, sulfonamide toxicity, neutropenia

Back 69

false: side effects: malaise, nausea, sulfonamide toxicity

Front 70

GI Drugs (cont.): ___________ is a powerful central-acting antiemetic. It acts by antagonizing the______ receptor.

Back 70

Ondansetron: is a powerful antiemetic. Think: you will not vomit with ondansetron, so you can go on dancing.

Front 71

GI Drugs (cont.): T/F used to treat vomiting preoperatively and for cancer chemo therapy pts.

Back 71

False: it is used to treat vomiting postoperatively.

Front 72

GI Drugs (cont.): Headache and __________ are side effects

Back 72

constipation (can't vomit or poop)

Front 73

GI Drugs (cont.): Antacid overuse can affect:_________, __________, or ______ excretion of other drugs by altering ______ and ______ pH or by delaying gastric _________.

Back 73

Antacid overuse can affect absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying.

Front 74

GI Drugs (cont.): Constipation and (hypo/hyper) phosphatemia is seen with overuse of ________________

Back 74

aluminum hydroxide - Aluminimum amt. of feces

Front 75

GI Drugs (cont.): Magnesium hydroxide overuse = ___________

Back 75

diarhea; Mg = Must go to the bathroom

Front 76

GI Drugs (cont.): Calicium carbonate= hypercalcemia and (increase/decreased) acid

Back 76

causes hypercalcemia and increased acid.

Front 77

GI Drugs (cont.): T/F: hyperkalemia can be seen with AlOH, MgOH, CaCO2

Back 77

False! hypokalemia

Front 78

heparin: Catalyzes activation of ____________, decreases ________ and __________. It has a ____t1/2. check PTT

Back 78

catalyzes the activation of antithrombin III, decreases thrombin and Xa. It has a short t1/2

Front 79

heparin: It is used for immediated anticoagulation for pulmonary embolism,_______, _______, MI, and ________. Follow PTT

Back 79

used for pulmonary embolism, stroke, angina, MI, and DVT.

Front 80

heparin: T/F: Is used during pregnancy

Back 80

true: it is used during pregnancy because it does not cross the placenta.

Front 81

heparin: It can cause bleeding,___________, and drug-drug interactions.

Back 81

thrombocytopenia

Front 82

heparin: ___________ is used for rapid reversal of heparization (it is a _______ charged molecule that binds the ________ charged heparin)

Back 82

protamine sulfate is used for rapid reversal of heparinization (it is a positively charged molecule that binds the negatively charged heparin).

Front 83

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.

Back 83

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.

Front 84

warfirin (coumandin): Interferes with normal synthesis and gamma-carboxylation of vitamin K-dependent factors ___, ___, ___, and ___, also, ___ and ___ via ______ antagonism.

Back 84

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.

Front 85

warfirin (coumandin): t1/2 (short/long)

Back 85

long

Front 86

warfirin (coumandin): Used for _______ anticoagulation. Follow PT

Back 86

WEPT - Warfirin affects the Extrinsic pathway and prolongs PT

Front 87

warfirin (coumandin): T/F: is used during pregnacy

Back 87

False! (warfarin, unlike heparin, can cross the placenta).

Front 88

warfirin (coumandin): Toxicity: bleeding, _________, drug-drug interactions

Back 88

teratogenic

Front 89

heparin vs. warfarin: Heparin is a (large/small) _____charged acicid polymer while Warfarin is (large/small) (charged/neutral) molecule

Back 89

Heparin is a large negatively charged acidic polymer while Warfarin is a small neutral charged lipid-soluble molecule

Front 90

heparin vs. warfarin: T/F: Heparin is given orally while warfarin is given SC/IV

Back 90

False! Heparin is given IV/SC and warfarin is give oral

Front 91

heparin vs. warfarin: Site of action: heparin _________, warfarin ______

Back 91

heparin's site of action is the blood; warfarin's site of action is the liver (synthesises clotting factors)

Front 92

heparin vs. warfarin: Onset of action of _________ is slow; the onset of action of ______ is rapid

Back 92

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.

Front 93

heparin vs. warfarin: Warfarin works by imparing the synthesis of _______ dependent factors __, ___, ___, and ___ also _____, and ____; heparin activates _____, ____ and ___

Back 93

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.

Front 94

heparin vs. warfarin: Heparin 's duration of action is (acute/chronic); warfarin's duration of action is (actue/chronic)

Back 94

Heparin's duration of action is actute and warfarin's duration of action is chronic.

Front 95

heparin vs. warfarin: Tx of acute OD: Heparin = _________; warfarin=______

Back 95

Tx of heparin OD is protamine sulfate; Tx of warfarin= IV vit. K and fresh frozen plasma.

Front 96

heparin vs. warfarin: Warfarin is monitored by _________ while Heparin is monitored by ___________.

Back 96

Warfrin is monitored by PT (extrinsic pathway) (WEPT) and heparin is monitored by PTT (intrinsic pathway)

Front 97

Thrombolytics: questions from diagram at bottom of page

Back 97

0

Front 98

Thrombolytics: plasmin is the major ___________ enzyme. It breaks down both _______ and _______

Back 98

fibrinolytic enzyme. It accelerates breaks down of both fribin and fibrinogen yielding fibrin splip products and degradation products, respectively.

Front 99

Thrombolytics: Fibrinogen is converted to fibrin by _________

Back 99

thrombin

Front 100

Thrombolytics: tPA and urokinase promote the converson of ______ to ________ thereby increasing fibrinolysis.

Back 100

plasminogen to plasmin

Front 101

Thrombolytics: Various stimuli activate a blood proactivator to a blood activator that promotes conversion of _________ to blank thereby increasing fibrinolysis

Back 101

plasminogen to plasmin

Front 102

Thrombolytics: Streptokinase and anistreplase both activate and Activator that increases convesion of plasminogen to plasmin.

Back 102

0

Front 103

Thrombolytics: Aminocaproic acid:____________ fibrinolysis.

Back 103

inhibits fibrinolysis by inhibition of plasminogen conversion to plasmin.

Front 104

Thrombolytics: 4 examples of thrombolytics include: ________, _________, _____________, and ___________

Back 104

Streptokinase, urokinase, tPA(altepalse), APSAC (anistreplase)

Front 105

Thrombolytics: work by directly or indirectly aiding the conversion of ___________ to __________, which cleaves ______ and ________ clots. tPA specifically coverts _______________ to plasmin

Back 105

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.

Front 106

Thrombolytics: T/F: clinical use is for DVTs

Back 106

False: used for early MI

Front 107

Thrombolytics: pts. receiving this medication are at most risk for: ______

Back 107

bleeding

Front 108

Hematologic Drugs: mechanism of antiplatelet interaction

Back 108

0

Front 109

Hematologic Drugs: questions from diagram at top of page

Back 109

0

Front 110

Hematologic Drugs: When a break in the endothelium occurs _________ and _________ are exposed.

Back 110

collagen and vWF

Front 111

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

Back 111

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.

Front 112

Hematologic Drugs: After platelet activation _________ is expressed on their surface. What is the role of this structure?

Back 112

after platelets are activated they express GP IIb/IIIa. This molecule is important in platlelet-platelet aggregation.

Front 113

Hematologic Drugs: _________ and _________ interaction is needed in order for platelet aggregation to occur.

Back 113

GP IIb/IIIa and fribinogen

Front 114

Hematologic Drugs: 5-HT, _______, and ________ are molecules that play a role in the glycoprotein expression of activated platelets.

Back 114

5-HT, ADP, and TxA2 are molecules that play a role in the glycoprotein expression of activated platelets.

Front 115

Hematologic Drugs: Aspirin acts by inhibiting production of ________ that in turn inhibits glycoprotein expression in activated platelets.

Back 115

TxA2

Front 116

Hematologic Drugs: ADP production is inhibited by the drug _________.

Back 116

ticlopidine

Front 117

Hematologic Drugs: This antibody drug targets the _______ on platelets.

Back 117

Abciximab

Front 118

Copidogrel, ticlopidine: T/F: inhibits platele aggregation by irreversibly inhibiting the ADP pathway involved in the binding of fibrinogen

Back 118

TRUE

Front 119

Copidogrel, ticlopidine: It is used for ______ ________ syndrome, coronary _______, and it has been shown to decrease the incidence or recurrence of___ ____.

Back 119

it is used for acute coronary syndrome, coronary stenting. Decreases incidence or recurrence of thrombotic stroke

Front 120

Copidogrel, ticlopidine: Ticlopidine is associated with_________ as a side effect.

Back 120

Ticlopidine causes neutropenia and it is reserved for those who cannot tolerate aspirin.

Front 121

Abciximab: This drug binds to __________ on activated platelets.

Back 121

gp IIb/Iia

Front 122

Abciximab: It is used for ___________ and ________ _________ ___________ ___________

Back 122

acute coronary syndromes and percutanous transluminal coronary angioplasty

Front 123

Abciximab: toxiciites are _______ and ________

Back 123

bleeding and thrombocytopenia

Front 124

Aspirin: It ________ and (reversibly/irreversibly) inhibits COX1 and COX2 to prevent the conversion of _______ to prostaglandins.

Back 124

acetilates and irreversably inhibits COX-1 and COX-2

Front 125

Aspirin: T/F: aspirin has an effect of PT, PTT

Back 125

false it has no effect

Front 126

Aspirin: What are the 4 A's of aspirin and NSAIDS in general

Back 126

Antipyretic, Analgesic, Anti-inflam, antiplatelet

Front 127

Aspirin: Important toxicities include _________, bleeding, hyperventilation, __________- in children, and CN ____ toxicity

Back 127

gastric ulceration, bleeding, hyperventilation, Reyes syndrome and tinnitus (CNVIII).