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82 Cards in this Set

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Bronchodilation is mediated by what molecule (Theophylline inhibits its breakdown)?
cAMP
What is the effect of Ach and adenosine on Bronchial tone? Name two drugs inhibit bronchoconstriction?
1.Bronchonstriction
2. Theophylline and Muscarinic antagonist
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
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?
1.Isoprotenerol-relaxes bronchial smooth muscle (B2) and tachycardia (B1) (adverse effect).

2. Albuterol (B2-bronchodilation)
Used in Acute exacerbation
What are the two B2 selective agonist asthma drugs?
Albuterol- relaxes bronchial smooth muscle (B2), Salmetrol
What are the indications for Albuterol and Salmetrol, in the treatment of asthma?
1. Albuterol- use during acute exarcebation, Salmetrol- long-acting agent for prophylaxis 2. both are B2 agonist
what are the notable adverse effects of B2 agonist?
arythmias and tremor
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
What are the likely mechanism of action theophylline?
bronchodialation by inhibition phosphodiesterase (PDE), decreasing cAMP hydrolysis and antagnonizing adenosine action
Why is usage of theophylline limited?
limited b/c narrow therapeutic index (cardiotoxicity, neurotxicity)
What kind of drug is Ipratropium? Therapeutic goal in the treatment of asthma?
1.muscarinic antagonist 2. Bronchoconstriction
1.What is the mechanism of Cromolyn- an asthma drug? 2.Is it used for the treatment or Prophylaxis of asthma? 3. Toxicity
1.Prevents release of medicators from mast cells 2. Prophylaxis 3.Rare
What are two major corticosteroids used for treatment of what kind of asthma?
Beclomethasone and prednisone are 1st line therapy for chronic asthma
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, along with other inflammatory agents.
What is a methylxanthine? Tx for what? What is the therapeutic index?
1. Theophylline 2. Asthma 3. Very narrow therapeutic index
What the most basic asthma treatment strategy?
avoidance of exposure to antingen (dust, pollen, etc)
After exposure to antigen crosslinks IgE on mast cells. Mediator release or effect can be prevent with what drugs?
cromolyn and steroids
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.
1.Leukotrienes and histamine. 2. bronchoconstriction 3.B-agonists, methylxanthines, and muscarinic antagonists.
1.LKT and histamine can also elicit a inflammatory based late response - is chararized by? Tx
1.Bronchial hyperactivity. 2. Steroids.
1.What are the constituents of the drug Sulfasalazine and their therapeutic goal effect? 2.Treatment for what clinical conditions?
1.Combination of sulfapyridine (antibacterial) and mesalamine (anti-inflammatory effects). 2. Ulcerative colitis and remission of Crohn's.
T/F: Side effects of the above include: malaise, sulfonamide toxicity, neutropenia
false: side effects: malaise, nausea, sulfonamide toxicity
What is Ondansetron?
Ondansetron: is a powerful antiemetic. Think: you will not vomit with ondansetron, so you can go on dancing.
What is used for treat vomiting postoperatively and for cancer chemo therapy pts.
Ondansetron
What are the side effect of Ondansetron (anti emetic drug)
Headache and constipation (can't vomit or poop)
What is the effect of antacid on drugs? Mechanism of effect?
Antacid overuse can affect absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying.
Constipation and (hypo/hyper) phosphatemia is seen with overuse of what type of antacid?
aluminum hydroxide - Aluminimum amt. of feces
Magnesium hydroxide overuse will cause?
diarhea; Mg = Must go to the bathroom
Calicium carbonate antacid causes what?
causes hypercalcemia and increased acid.
T/F: hyperkalemia can be seen with AlOH, MgOH, CaCO2
False! hypokalemia
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?
1.Phospholipase A2
2. Phosphatidylinositol
What two enzymes are responsible for the production of Hydroperoxides (HPETEs) and Endoperoxidases, respectively from arachidonate?
Lipoxygenase= HPETE, Cyclooxygenases=endoperoxidases
What major class of products do Hydroperoxides give rise to? 2. Major site of production? 3.Function?
1.Leukotrienes 2. Mast cells, WBC, Airway epithelium and Platelets 3. Chemotaxis of PMNs and Eosinophils
1.What are the 3 major products of Endoperoxidases? 2. Function?
Prostacyclin (PGI), Prostaglandins (PGE, PGF), Thromboxane (TXA) 2.Increase blood flow and promote edema (not cause)
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?
1.Leukotrienes in general increase bronchial tone (bad for asthma) 2. Lungs LKT get catabolized 3.Zafirlukast and Zileuton and Corticosteriods!
In the arachodonic acid pathway, what two enzymes do corticosteroids block?
1.Phospholipase A2, 2.COX-2 (protein synthesis of Cox2)
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
What are the 4 major effects of Prostacyclin
decrease platelet aggregation, decrease vascular tone, decrease bronchial tone, decrease uterine tone
What are the 3 major effects of Prostaglandins
increased uterine tone, decrease vascular tone, decrease bronchial tone
What are the 3 major effects of Thromboxane? Major site of production?
1. Potent platelet aggregation inducer, potent vasconstrictor (not like PGE and PGI), increase bronchial tone (BAD for asthma) 2. In platelets
Zileuton is a ________ pathway inhibitor? Tx for what clincal condition?
1. 5-Lipoxygenase pathway inhibitor 2. Asthma
Zariflukast is associated with what enzymes? Mechanism of Zariflukast?
1.Lekukotrienes. 2. Works by blocking the Leukotrienes receptors
1.How does heparin work? 2. T1/2 characteristics? 3. What does heparin alter PTT or PT?
1. Catalyzes the activation of antithrombin III, decreases thrombin and Xa (2.)It has a short t1/2 (3.)PTT (intrinsic pathway)
(1.)Heparins used therapeutically for? ( 2.)What is the electical charge of heparin? (3.)How do you treat acute heparin overdose?
1.Pulmonary embolism, stroke, angina, MI, and DVT 2. Negatively charged (3.) Protamine sulfate (+ve charged molecule binds to heparin).
1. T/F: Is heparin used during pregnancy 2. What are side effects of heparin?
1. True: it is used during pregnancy because it does not cross the placenta. 2. Bleeding, thrombocytopenia and drug-drug interaction
Name a lower molecular heparin? How is it better ? How is this one administered?
(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.
What is the mechanism of Warfarin? Another name for Warfarin? T1/2 - long or short?
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
What pathway is affect by Warfarin on the clotting casacade? Which is prolonged PT or PTT?
WEPT - Warfirin affects the Extrinsic pathway and prolongs PT
1. T/F: is used during pregnacy 2. List side effects of Warfarin?
1. False! (warfarin, unlike heparin, can cross the placenta). 2. Teratogenic, Bleeding and drug-drug interaction.
Describe the size and charge of Heparin and Warfarin?
Heparin is a large negatively charged acidic polymer while Warfarin is a small neutral charged lipid-soluble molecule
T/F: Heparin is given orally while warfarin is given SC/IV
False! Heparin is given IV/SC and warfarin is give oral
Site of action and onset: 1. Heparin 2. Warfarin
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
What is the Tx of Warfarin overdose
Tx of warfarin= IV vit. K and fresh frozen plasma.
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)
questions from diagram at bottom of page

What type of enzyme is plasmin? Function?
fibrinolytic enzyme. It accelerates breaks down of both fribin and fibrinogen yielding fibrin splip products and degradation products, respectively.
tPA and urokinase are prothrombic or profibrolytic? Function? Name 2 other similar compounds to tPA and Urokinase?
1. Profibrolytic 2. Activate plasminogen to plasmin 3. Streptokinase and Anistreplase
Aminocaproic acid inhibits fibrinolysis by?
inhibition of plasminogen conversion to plasmin.
Name four thrombolytics? What is the clinical use of these thrombolytic - is it DVT's? Risks?
1.Streptokinase, urokinase, tPA(altepalse), APSAC (anistreplase) 2. Not DVTs! Used for early MI (3) Bleeding
When a break in the endothelium what molecules that that bind platelets are exposed? Name the receptors on the platelets that bind to them?
collagen (GP 1a) and vWF (GP 1b)
What receptor is expressed in activated platelets that promotes platelet-platelet aggregation via fribinogen binding? What drug prevents this binding?
1. GP IIb/IIIa. 2. Abciximab
Name the molecules that play a role in the glycoprotein expression of activated platelets? What drugs inhibit the glycoprotein expression?
(1.)5-HT, ADP, and TxA2 are molecules that play a role in the glycoprotein expression of activated platelets. (2.) Aspirin and Ticlopidine
Aspirin acts by inhibiting production of ________ that in turn inhibits glycoprotein expression in activated platelets.
TxA2
How do Clopidogrel work in antiplatelet interaction? 2.) Name another drug with the same effect. 3. List any special side effect of both drugs?
1. Irreversibly inhibits ADP in platelets - ADP is important in the binding of platelets via fibrinogen (2.) Ticlopidine (3.)Neutropenia (ticlopidine)
What drug is reserved for people who cannot tolerate aspirin?
Ticlopidine and Clopidogrel
Ticlopidine and Clopidogrel are used for the treatment of heart and cardiovascular conditions?
it is used for acute coronary syndrome, coronary stenting. Decreases incidence or recurrence of thrombotic stroke
Abciximab is used for what syndrome and what procedures? What are the toxicities of the drug?
1. Acute coronary syndromes and percutanous transluminal coronary angioplasty 2. Bleeding and thrombocytopenia
1.How does Aspirin work? Effect on 2.PT, PTT?
3.Major side effect?
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)
T/F: aspirin has an effect of PT, PTT
false it has no effect
What are the 4 A's of aspirin and NSAIDS in general
Antipyretic, Analgesic, Anti-inflam, antiplatelet
Important toxicities include _________, bleeding, hyperventilation, __________- in children, and CN ____ toxicity
gastric ulceration, bleeding, hyperventilation, Reyes syndrome and tinnitus (CNVIII).
1. What kind of receptor is the insulin receptor?
2. Mechanism of insulin in liver and muscles and Adipose cells?
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.
1.Effect of Insulin on K+?
2. Therapeutic benefits of insulin (3)?
3. Toxcities of Insulin?
1. Increases K+ intake (by muscle cells)
2. Diabetes, Life-threatning Hyper-K+, Stress induced hyperglycemia

3. Hypoglycemia and Rare Hypersensitivity rxn
Name the Diabetic family drugs and give some examples?
1. Insulin -
2. Sulfonylureas - Tolbutamide, glyburide, Chlorpropamide, glipizide
3. Metformin
4. Glitazones
5. a-glucosidase inhibitors
What is the family of drugs stimulate the release of endogenous insulin?
What is their mechanism?
1. Sulfonylureas
2. Block K+ channel and causes the Beta pancreatic cells to fire causing an influx of Calcium ---> leading Insulin release.
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?
1. Glyburide and Glipizide - Hypoglycemia is very common

2. Cholpropamide and Tolbutamide - Disulfiram-like effects (not seen in 2nd gen)
What is Metformin?
What is its mechanism?
What are the grave adverse effect?
Islet function required? (so type I or type II)?
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)
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
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
Side effect of Troglitazone?
Weight gain and Hepatoxicity(this side effect sets it apart from the other members of the glitazone family)
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?
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)
1.Name a GnRH analog?
2. Acts what when used in
a. Pulsatile fashion
b.Continuous fashion
Clinical use?
1. Leuprolide
2.
a. Pulsatile" Agonist properties
used for infertility
b. Continuous: antagonist properties
used for Prostate cancer with Flutamide.
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?
1. Flutamide

2. Transient initial bust of LH and FSH

3. Antiandrogen(prostate cancer), nausea, vomiting
1.Name the popular drug used for Hyperthyroidism? (PTU)
2. Mechanism?
3. Side effects?
1.Propylthiouracil (PTU)
2. inhibits synthesis of thyroid hormone (organification and coupling)
3. Skin rash, aplastic anemia and agranulocytosis (rare)