Pharmacology Test 2

Front 1

heparin

Back 1

an indirect anticoagulant that binds to antithrombin III (ATIII) and produces a conformational change. This complex then binds and inhibits clotting factors (thrombin and FXa) which prevents the conversion of fibrinogen to fibrin.

Front 2

protamine sulfate

Back 2

rapidly neutralizes heparin because it is positively charged (heparin is negative)

Front 3

LMWH (low molecular weight heparin)

Back 3

only 4000-5000 daltons, and the chain must be at least 18 saccharide units long to bind to FIIa. Must be 5 saccharides long for FXa. More effective for FXa. 90% bioavailability and has reduced binding to proteins and cells (more predictable)

Front 4

direct thrombin inhibitors

Back 4

block circulating and clot-bound thrombin by directly binding to the active site. An alternative to UFH in patients with heparin-induced thrombocytopenia

Front 5

dabigatran etexilate

Back 5

first in the class of oral direct thrombin inhibitors. It is a prodrug that directly inhibits the production of thrombin

Benefits:

1. Predictable

2. Rapid onset

3. Low food or drug interactions

Adverse:

1. Dyspepsia, abdominal pain, esophagitis

2. Bleeding (trouble because treatment is not monitored)

Front 6

Factor Xa inhibitors

Back 6

inhibit platelet activation and fibrin clot formation via. direct, selective, and reversible inhibition of FXa

Front 7

fondaparinux

Back 7

binds to ATIII and potentiates the neutralization of FXa. It has similar pharmacokinetics to LMWH, but has no reversal

Front 8

warfarin

Back 8

a vitamin K antagonist that inhibits the synthesis of vitamin K dependent clotting factors in the liver by inhibiting vitamin K epoxide reductase (VKOR). This prevents the recycling of vitamin K. Peak anticoagulation is not achieved for 72-96 hours, and has a narrow therapeutic index.

Front 9

warfarin interactions

Back 9

1. impairment of absorption

2. induction/inhibition of metabolism (CYP2C9, CYP2C19, CYP3A4)

3. Competition for binding sites

4. Platelet inhibition

5. Drugs that increase bleeding risks and lessen warfarin efficency

6. Vitamin K rich foods

Front 10

bridge therapy

Back 10

initiate warfarin 2-5 days into therapy with UFH or LMWH. Discontinue the UFH/LMWH once the INR is >2 for 2 days.

Front 11

vitamin K, FFP (fresh frozen plasma), and factor replacement

Back 11

used to reverse warfarin

Front 12

alteplase

Back 12

modified form of tissue plasminogen activator produced by recombinant DNA technology. It binds to fibrin and converts plasminogen to plasmin, leading to local fibrinolysis.

Front 13

prostacyclin (PGI2)

Back 13

released by endothelial cells lining the blood vessels, and it works with NO to keep platelets in their inactive form

Front 14

platelet aggregation

Back 14

the platelets are normally held inactive, but when the cell wall is damaged, receptors are revealed that they can bind to (decreased levels of PGI2 help) and they activate inactive platelets to clump together by secreting thromboxane A2.

Front 15

thromboxane A2

Back 15

platelet agonists that activates inactive platelets and recruit them to the site of vascular injury

Front 16

aspirin

Back 16

the irreversible inhibitor of COX-1. This decreases the rate of thromboxane A2 synthesis. It is rapidly absorbed (30-40 minutes). Initially a prodrug that is hydrolyzed to active state. Gastrointestinal adverse effects are most common (eg. bleeding)

Front 17

COX-1 (cyclooxygenase)

Back 17

a rate limiting enzyme in the production of prostagladins.

Front 18

glycoprotein IIb/IIIa complex

Back 18

a major platelet surface receptor for fibrinogen

Front 19

ADP receptor inhibitors

Back 19

prevents ADP-dependent activation of GPIIb/IIIa complex (it is one of the ways to inhibit platelet adhesion/aggregation)

Front 20

clopidogrel

Back 20

an ADP receptor inhibitor that selectively and irreversibly blocks the bondings of ADP to the platelet. It is a prodrug that is metabolized by the liver (big surprise) to its active form (substrate of CYP2C19)

Front 21

albuterol

Back 21

a short-acting B2 adrenergic agnoist that is a 50:50 mixture of R- and S- albuterol

Front 22

Levalbuterol

Back 22

a short-acting B2 adrenergic agonist that is only the R-enatiomer of albuterol. Hypothesized that it may be more effective and cause fewer side effects

Front 23

anticholinergics

Back 23

drugs that are competitive inhibitors of acetylcholine at the parasympathetic sites of smooth muscle. They have a minimal systemic absorption, and can be used as an alternative to people who cannot tolerate SABA. Adverse effects include headache, cough, dry mouth, worsening glaucoma, enlarged prostate and bladder, and neck issues

Front 24

ipratropium

Back 24

an anticholinergic with a half-life of 2 hours

Front 25

tiotropium

Back 25

an anticholinergic that has a half life of 5-6 days

Front 26

corticosteroids

Back 26

effects are mediated through glucocorticoid receptors widely distributed throughout the body. It directly targets the underlying inflammation.

Front 27

systemic oral corticosteroids

Back 27

short-term burst therapy for moderate and severe exacerbation as adjuncts to SABAs

Front 28

rhinitis

Back 28

inflammation of mucous membranes

Front 29

mast cells

Back 29

release mediators such as histamine, leukotrienes, and chemotactic factors that promote bronchospasm and mucosal thickening

Front 30

leukotrienes

Back 30

act as a chemoattractant for neutrophils and eosiniphils

Front 31

mast cell stabilizers

Back 31

inhibit antigen-induced bronchospasms. Are only for severe cases! NOT for acute exacerbations!

Front 32

montelukast

Back 32

a LTRA (leukotriene receptor antagonist) that is a selective antagonist of the cysteinyl leukotriene-1 receptor. Genereally well tolerated, but can cause GI upset, headache, and elevation in liver enzymes

Front 33

cromolyn

Back 33

an anti-inflammatory that inhibits mast cell degranulation and the release of histimine. Lacks in bronchodilator activity, and is ineffective against inflammatory mediators that had already been released

Front 34

Omalizumab

Back 34

a monoclonal antibody that inhibits IgE binding to mast cells and basophils. Injected by SC administration every 2-4 weeks

Front 35

Benadryl

Back 35

diphenhydramine

Front 36

claratin

Back 36

loratadine

Front 37

zyrtec

Back 37

cetirizine

Front 38

allegra

Back 38

fexofenadine

Front 39

guaifenesin

Back 39

an expectorant that irritates the gastric mucosa and stimulates respiratory tract secretions. It increases respiratory fluid volumes and decreases mucous viscosity

Front 40

dextromethorphan

Back 40

decreases the sensitivity of cough receptors and interrupts cough impulse transmission. Causes euphoria at high doses.

Front 41

ototoxicity

Back 41

must have caution when administering loop diuretics with other ototoxic drugs

Front 42

eplerenone

Back 42

a potassium sparing diuretic that has a lower affinity compared to spironolactone for the mineralcorticoid receptor. As a result, it has less steroid hormone-like adverse effects (antiandrogen effects)

Front 43

spironolactone

Back 43

can cause antiandrogen effects such as gynecomastia, decreased libido, and impotence in men as well as menstural irregularities and hair growth in women

Front 44

ACE Inhibitors

Back 44

suppress the synthesis of angiotensin II. Increase plasma renin and bradykinin while decreasing aldosterone secretion. Results in a decrease in blood pressure by decreasing Na+ and decreasing water retention

Front 45

ARBs

Back 45

they inhibit the angiotension receptors, but have no action on bradykinin. Have the same side effects as ACEI's, but they don't have the cough.

Front 46

inotropic drugs

Back 46

enhance cardiac contractility, resulting in an increase in cardiac output. Also causes an increase in cytoplasmic Ca2+ concentration (eg. digoxin)

Front 47

digoxin

Back 47

this is an inotropic drug that has a narrow therapeutic index, a long half-life, and gets excreted by the kidney entirely unchanged. It inhibits Na/K ATPase. Causes increased contractile due to the increase calcium in the cytoplasm (reduces ejection of Ca leading to more available). Toxicity results in nausea, vomiting, and loss of appetite

Front 48

hyperkalemia

Back 48

reduces enzyme inhibition

Front 49

hypokalemia

Back 49

may lead to excess inhibition

Front 50

hypercalcemia

Back 50

increases the risk of arrhythmias

Front 51

hypomagnesemia

Back 51

a risk factor for arrhythmias

Front 52

sulfonylureas

Back 52

insulin secretagogues. They stimulate the beta cells in the pancreas to produce more insulin. This requires the beta cells to be functional though. Give 30 minutes before eating, and should not take if not eating. Results in hypoglycemia, weight gain, GI intolerance. Use in caution in patients with sulfa allergies. Do not use with meglitinides

Front 53

meglitinides

Back 53

insulin secretagogues (similar to sulfanylureas). Rapid onset and shorter halflife than sulfanylureas. Less hypoglycemia. Causes weight gain.

Front 54

Thiazolidinediones (TZDs)

Back 54

insulin sensitizers that decrease insulin resistance by enhancing the sensitive of insulin receptors. Causes weight gain, fluid retention, bladder cancer, elevated risks of cardiovascular events, and osteopenia

Front 55

Metformin

Back 55

an insulin sensitizer that is the drug of choice. (biguanade??). It decreases the glucose created by the liver and it improves insulin receptor sensitivity and glucose intake. The adverse effects are dose-related diarrhea and lactic acidosis. Also has some weight loss benefits without increasing risk of hypoglycemia.

Front 56

DPP-4 inhibitors

Back 56

inhibit DPP-4 (an enzyme that rapidly inactivates incretin). It prevents the breakdown of GLP-1. This increases insulin release in response of meals and decreases secretion of glucagon. Adverse effects include cold, headache, acute pancreatitis, an upper respiratory infection! Does not cause weight gain!

Front 57

GLP-1 receptor agonists

Back 57

analogue of the hormone incretin. It mimics GLP-1 and slows gastric emptying (decreases post-meal glucose). Causes a decrease in appetite and is associated with weight loss. Also causes nausea, constipation, and acute pancreatitis

Front 58

SGLT2 inhibitors

Back 58

blocks the reabsorption of glucose by the kidney, increasing glucose excretion, and lowering blood glucose levels. Adverse effects include vaginal yeast infections and UTIs. Also causes orthostatic hypotension.