Week 2: Pharmacology Iv

Front 1

Bronchodilation is mediated by what molecule (Theophylline inhibits its breakdown)?

Back 1

cAMP

Front 2

What is the effect of Ach and adenosine on Bronchial tone? Name two drugs inhibit bronchoconstriction?

Back 2

1.Bronchonstriction
2. Theophylline and Muscarinic antagonist

Front 3

How many asthma drug categories are there?

Back 3

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

Front 4

1.What is the only nonspecific B-agonist drug used for asthma and what are its effects?
2. Name the specific B-agonist used for asthma? In what type of asthmatic presentation do you use this drug?

Back 4

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

2. Albuterol (B2-bronchodilation)
Used in Acute exacerbation

Front 5

What are the two B2 selective agonist asthma drugs?

Back 5

Albuterol- relaxes bronchial smooth muscle (B2), Salmetrol

Front 6

What are the indications for Albuterol and Salmetrol, in the treatment of asthma?

Back 6

1. Albuterol- use during acute exarcebation, Salmetrol- long-acting agent for prophylaxis 2. both are B2 agonist

Front 7

what are the notable adverse effects of B2 agonist?

Back 7

arythmias and tremor

Front 8

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

Back 8

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

Front 9

What are the likely mechanism of action theophylline?

Back 9

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

Front 10

Why is usage of theophylline limited?

Back 10

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

Front 11

What kind of drug is Ipratropium? Therapeutic goal in the treatment of asthma?

Back 11

1.muscarinic antagonist 2. Bronchoconstriction

Front 12

1.What is the mechanism of Cromolyn- an asthma drug? 2.Is it used for the treatment or Prophylaxis of asthma? 3. Toxicity

Back 12

1.Prevents release of medicators from mast cells 2. Prophylaxis 3.Rare

Front 13

What are two major corticosteroids used for treatment of what kind of asthma?

Back 13

Beclomethasone and prednisone are 1st line therapy for chronic asthma

Front 14

What is the mechanism of action of corticosteroids?

Back 14

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

Front 15

What is a methylxanthine? Tx for what? What is the therapeutic index?

Back 15

1. Theophylline 2. Asthma 3. Very narrow therapeutic index

Front 16

What the most basic asthma treatment strategy?

Back 16

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

Front 17

After exposure to antigen crosslinks IgE on mast cells. Mediator release or effect can be prevent with what drugs?

Back 17

cromolyn and steroids

Front 18

1. Give 2 examples of Allergen exposure mediators ?
2.This triggers a late and early asthmatic response.How is the early response characterized? 3.treated with the following 3 asthmatic drug categories to treat the symptoms.

Back 18

1.Leukotrienes and histamine. 2. bronchoconstriction 3.B-agonists, methylxanthines, and muscarinic antagonists.

Front 19

1.LKT and histamine can also elicit a inflammatory based late response - is chararized by? Tx

Back 19

1.Bronchial hyperactivity. 2. Steroids.

Front 20

1.What are the constituents of the drug Sulfasalazine and their therapeutic goal effect? 2.Treatment for what clinical conditions?

Back 20

1.Combination of sulfapyridine (antibacterial) and mesalamine (anti-inflammatory effects). 2. Ulcerative colitis and remission of Crohn's.

Front 21

T/F: Side effects of the above include: malaise, sulfonamide toxicity, neutropenia

Back 21

false: side effects: malaise, nausea, sulfonamide toxicity

Front 22

What is Ondansetron?

Back 22

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

Front 23

What is used for treat vomiting postoperatively and for cancer chemo therapy pts.

Back 23

Ondansetron

Front 24

What are the side effect of Ondansetron (anti emetic drug)

Back 24

Headache and constipation (can't vomit or poop)

Front 25

What is the effect of antacid on drugs? Mechanism of effect?

Back 25

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

Front 26

Constipation and (hypo/hyper) phosphatemia is seen with overuse of what type of antacid?

Back 26

aluminum hydroxide - Aluminimum amt. of feces

Front 27

Magnesium hydroxide overuse will cause?

Back 27

diarhea; Mg = Must go to the bathroom

Front 28

Calicium carbonate antacid causes what?

Back 28

causes hypercalcemia and increased acid.

Front 29

T/F: hyperkalemia can be seen with AlOH, MgOH, CaCO2

Back 29

False! hypokalemia

Front 30

1.What enzyme breaks down membrane lipid into arachidonic acid?
2. What is the name of the membrane lipid that Arachidonic acid is formed from?

Back 30

1.Phospholipase A2
2. Phosphatidylinositol

Front 31

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

Back 31

Lipoxygenase= HPETE, Cyclooxygenases=endoperoxidases

Front 32

What major class of products do Hydroperoxides give rise to? 2. Major site of production? 3.Function?

Back 32

1.Leukotrienes 2. Mast cells, WBC, Airway epithelium and Platelets 3. Chemotaxis of PMNs and Eosinophils

Front 33

1.What are the 3 major products of Endoperoxidases? 2. Function?

Back 33

Prostacyclin (PGI), Prostaglandins (PGE, PGF), Thromboxane (TXA) 2.Increase blood flow and promote edema (not cause)

Front 34

In general what effect do leukotrienes have on bronchial tone? 2.Where do they get metabolized? 3. What can be used to inhibit the production of Leukotrienes?

Back 34

1.Leukotrienes in general increase bronchial tone (bad for asthma) 2. Lungs LKT get catabolized 3.Zafirlukast and Zileuton and Corticosteriods!

Front 35

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

Back 35

1.Phospholipase A2, 2.COX-2 (protein synthesis of Cox2)

Front 36

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

Back 36

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 37

What are the 4 major effects of Prostacyclin

Back 37

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

Front 38

What are the 3 major effects of Prostaglandins

Back 38

increased uterine tone, decrease vascular tone, decrease bronchial tone

Front 39

What are the 3 major effects of Thromboxane? Major site of production?

Back 39

1. Potent platelet aggregation inducer, potent vasconstrictor (not like PGE and PGI), increase bronchial tone (BAD for asthma) 2. In platelets

Front 40

Zileuton is a ________ pathway inhibitor? Tx for what clincal condition?

Back 40

1. 5-Lipoxygenase pathway inhibitor 2. Asthma

Front 41

Zariflukast is associated with what enzymes? Mechanism of Zariflukast?

Back 41

1.Lekukotrienes. 2. Works by blocking the Leukotrienes receptors

Front 42

1.How does heparin work? 2. T1/2 characteristics? 3. What does heparin alter PTT or PT?

Back 42

1. Catalyzes the activation of antithrombin III, decreases thrombin and Xa (2.)It has a short t1/2 (3.)PTT (intrinsic pathway)

Front 43

(1.)Heparins used therapeutically for? ( 2.)What is the electical charge of heparin? (3.)How do you treat acute heparin overdose?

Back 43

1.Pulmonary embolism, stroke, angina, MI, and DVT 2. Negatively charged (3.) Protamine sulfate (+ve charged molecule binds to heparin).

Front 44

1. T/F: Is heparin used during pregnancy 2. What are side effects of heparin?

Back 44

1. True: it is used during pregnancy because it does not cross the placenta. 2. Bleeding, thrombocytopenia and drug-drug interaction

Front 45

Name a lower molecular heparin? How is it better ? How is this one administered?

Back 45

(1.)Enoxaparin ( 2.) act more on Xa, have better bioavailabitlity and 2-4 times longer half-life. 3.) Can be adm. SubQ and without lab monitoring.

Front 46

What is the mechanism of Warfarin? Another name for Warfarin? T1/2 - long or short?

Back 46

1.)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. 2.) Coumadin 3.) Long T1/2

Front 47

What pathway is affect by Warfarin on the clotting casacade? Which is prolonged PT or PTT?

Back 47

WEPT - Warfirin affects the Extrinsic pathway and prolongs PT

Front 48

1. T/F: is used during pregnacy 2. List side effects of Warfarin?

Back 48

1. False! (warfarin, unlike heparin, can cross the placenta). 2. Teratogenic, Bleeding and drug-drug interaction.

Front 49

Describe the size and charge of Heparin and Warfarin?

Back 49

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

Front 50

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

Back 50

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

Front 51

Site of action and onset: 1. Heparin 2. Warfarin

Back 51

1. Heparin's site of action is the blood and rapid onset (secs); 2.) Warfarin's site of action is the liver (synthesises clotting factors) and slow onset

Front 52

What is the Tx of Warfarin overdose

Back 52

Tx of warfarin= IV vit. K and fresh frozen plasma.

Front 53

Warfarin is monitored by _________ while Heparin is monitored by ___________.

Back 53

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

Front 54

questions from diagram at bottom of page

Front 55

What type of enzyme is plasmin? Function?

Back 55

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

Front 56

tPA and urokinase are prothrombic or profibrolytic? Function? Name 2 other similar compounds to tPA and Urokinase?

Back 56

1. Profibrolytic 2. Activate plasminogen to plasmin 3. Streptokinase and Anistreplase

Front 57

Aminocaproic acid inhibits fibrinolysis by?

Back 57

inhibition of plasminogen conversion to plasmin.

Front 58

Name four thrombolytics? What is the clinical use of these thrombolytic - is it DVT's? Risks?

Back 58

1.Streptokinase, urokinase, tPA(altepalse), APSAC (anistreplase) 2. Not DVTs! Used for early MI (3) Bleeding

Front 59

When a break in the endothelium what molecules that that bind platelets are exposed? Name the receptors on the platelets that bind to them?

Back 59

collagen (GP 1a) and vWF (GP 1b)

Front 60

What receptor is expressed in activated platelets that promotes platelet-platelet aggregation via fribinogen binding? What drug prevents this binding?

Back 60

1. GP IIb/IIIa. 2. Abciximab

Front 61

Name the molecules that play a role in the glycoprotein expression of activated platelets? What drugs inhibit the glycoprotein expression?

Back 61

(1.)5-HT, ADP, and TxA2 are molecules that play a role in the glycoprotein expression of activated platelets. (2.) Aspirin and Ticlopidine

Front 62

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

Back 62

TxA2

Front 63

How do Clopidogrel work in antiplatelet interaction? 2.) Name another drug with the same effect. 3. List any special side effect of both drugs?

Back 63

1. Irreversibly inhibits ADP in platelets - ADP is important in the binding of platelets via fibrinogen (2.) Ticlopidine (3.)Neutropenia (ticlopidine)

Front 64

What drug is reserved for people who cannot tolerate aspirin?

Back 64

Ticlopidine and Clopidogrel

Front 65

Ticlopidine and Clopidogrel are used for the treatment of heart and cardiovascular conditions?

Back 65

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

Front 66

Abciximab is used for what syndrome and what procedures? What are the toxicities of the drug?

Back 66

1. Acute coronary syndromes and percutanous transluminal coronary angioplasty 2. Bleeding and thrombocytopenia

Front 67

1.How does Aspirin work? Effect on 2.PT, PTT?
3.Major side effect?

Back 67

1.acetilates and irreversably inhibits COX-1 and COX-2
2. No effect on PT and PTT
3. Gastric ulcers, hyperventilation, Reyes's syndrome, Tinnitus (CNVIII)

Front 68

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

Back 68

false it has no effect

Front 69

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

Back 69

Antipyretic, Analgesic, Anti-inflam, antiplatelet

Front 70

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

Back 70

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

Front 71

1. What kind of receptor is the insulin receptor?
2. Mechanism of insulin in liver and muscles and Adipose cells?

Back 71

1. Tyrosine kinase activity
2. Liver: increase in glucose storage =glycogen synthesis.
Muscle: Stimulates glycogen and protein synthesis, K+ uptake
Adipose cells: Increase in triglyceride storage.

Front 72

1.Effect of Insulin on K+?
2. Therapeutic benefits of insulin (3)?
3. Toxcities of Insulin?

Back 72

1. Increases K+ intake (by muscle cells)
2. Diabetes, Life-threatning Hyper-K+, Stress induced hyperglycemia

3. Hypoglycemia and Rare Hypersensitivity rxn

Front 73

Name the Diabetic family drugs and give some examples?

Back 73

1. Insulin -
2. Sulfonylureas - Tolbutamide, glyburide, Chlorpropamide, glipizide
3. Metformin
4. Glitazones
5. a-glucosidase inhibitors

Front 74

What is the family of drugs stimulate the release of endogenous insulin?
What is their mechanism?

Back 74

1. Sulfonylureas
2. Block K+ channel and causes the Beta pancreatic cells to fire causing an influx of Calcium ---> leading Insulin release.

Front 75

Name the 2nd generation Sulfonylurea drugs?
Name the 1st gen?

Also what are common effects attributed to the each of the generation drug of sulfonylureas?

Back 75

1. Glyburide and Glipizide - Hypoglycemia is very common

2. Cholpropamide and Tolbutamide - Disulfiram-like effects (not seen in 2nd gen)

Front 76

What is Metformin?
What is its mechanism?
What are the grave adverse effect?
Islet function required? (so type I or type II)?

Back 76

1. Oral -hypoglycemic
2. Inhibit gluconeogenesis and increase glycolysis. Reduces glucose levels
3. Lactic acidosis
4. No (so can be used in type I or II)

Front 77

What are Pioglitazone and rosiglitazone, and name a third one?
Mechanism?
Can be used as a monotherapy in what diabetes?
Side Effects? Look at its mechanism

Back 77

1. Glitazone - Troglitazone
2. Increase cell sensitivity of insulin
3. Diabetes II. Or as combo in typeI or II

4. Weight Gain,
Troglitazone= is hepatoxic

Front 78

Side effect of Troglitazone?

Back 78

Weight gain and Hepatoxicity(this side effect sets it apart from the other members of the glitazone family)

Front 79

1.Alpha-glucosidase inhibitors are used for diabetes treatment- how do they work?
2.Effect after meals?
3.How are they used (similiar to glitazones)?
4.Major toxicity?

Back 79

1. Inhibit intestinal brush border alpha glucosidases -they sugars and glucose
2. Decrease in postprandial hyperglycemia
3. monotherapy(typeII) or combo
4. GI disturbances (malabsorbtion)

Front 80

1.Name a GnRH analog?
2. Acts what when used in
a. Pulsatile fashion
b.Continuous fashion
Clinical use?

Back 80

1. Leuprolide
2.
a. Pulsatile" Agonist properties
used for infertility
b. Continuous: antagonist properties
used for Prostate cancer with Flutamide.

Front 81

1.Continuous adminstration of Leuprolide use used to treat prostate cancer in combination with what other drug?
2. Effects on LH and FSH in this fashion of adminstration?
3. Toxicities of Leuprolide?

Back 81

1. Flutamide

2. Transient initial bust of LH and FSH

3. Antiandrogen(prostate cancer), nausea, vomiting

Front 82

1.Name the popular drug used for Hyperthyroidism? (PTU)
2. Mechanism?
3. Side effects?

Back 82

1.Propylthiouracil (PTU)
2. inhibits synthesis of thyroid hormone (organification and coupling)
3. Skin rash, aplastic anemia and agranulocytosis (rare)