Pharmacology - Hodge Podge (Blood, Gut, Teratogens)

Front 1

What are the advantages of using streptokinase over other plasminogen activators? (2)

Back 1

1) Systemic activation

2) relatively inexpensive

Front 2

Why might a person use a recombinant human tissue plasminogen activator over streptokinase, which is cheaper? (2 reasons)

Back 2

1) The human versions seem to be more specific for fibrin in clots.

2) The bacterial forms, being foreign protein elicit antibody responses.

Front 3

What is modified streptokinase called? How is it modified?

Back 3

Anistreplase -> has an anisoyl moiety

Front 4

What are the advantages of anistreplase over streptokinin? (3)

Back 4

1) More specific for fibrin in clots.

2) Slower activation.

3) Longer half-life

Front 5

What is the -suffix of recombinant human tissue-type plasminogen activator?

Back 5

-teplase

Front 6

What are the two names of recombinant human tissue-type plasminogen activator? (2)

Back 6

1) Tenecteplase

2) Alteplase

Muslim and Hebrew: ALlah and TNK

Front 7

Which human tissue plasminogen activator has a longer half-life?

Back 7

Tenecteplase.

(The Hebrew religion has been around much longer than Islam.)

Front 8

Which human tissue plasminogen activator is more expensive?

Back 8

Al-teplase

(Um, I once heard a rumor of a stereotype that Hebrews were , um, cheap. I may have made that up though. Thus, TNK-teplase is cheaper.)

(PS, I love Hebrews. I am not anti-Semitic. I just remembered which one was cheaper this way. It works. Just go with it.)

Front 9

What is the antidote for plasminogen poisoning?

Back 9

Aminocaproic acid

Front 10

How does the antidote for plasminogen poisoning work?

Back 10

Competitively inhibits binding of plasminogen and plasmin and fibrin.

Front 11

How does aminocaproic acid work?

Back 11

Competitively inhibits binding of plasminogen and plasmin and fibrin.

Front 12

How does heparin work?

Back 12

Activation of endogenous ATIII?

Front 13

Heparin-ATIII inhibits which molecules in the clotting cascade?

Back 13

10a and 2a

Front 14

Lovenox-ATIII inhibits which molecules in the clotting cascade?

Back 14

10a >>>>> 2a

Front 15

Fondaparinux inhibits which molecules in the clotting cascade?

Back 15

10a

Front 16

Why is fondaparinux preferable to enoxaparin?

Back 16

1) more effective in preventing post-operative DVTs

2) does not bind platelet factor 4 -> lower risk of HIT

Front 17

What is the generic name of Lovenox?

Back 17

Enoxaparin

Front 18

What is the suffix of the low molecular weight heparins?

Back 18

-parin

Front 19

Name the three LMWH's.

Back 19

Enoxa-parin
Dalte-parin
Arde-parin

Front 20

What are the major advantages of using LMWH instead of heparin?

Back 20

1) Better bioavailability
2) Longer duration of action
3) more predictable -> less risk of major bleeding -> NO ROUTINE LAB MONITORING

Front 21

What is the name of synthetic heparin?

Back 21

fondaparinux

Front 22

What is fondaparinux?

Back 22

synthetic heparin.

Front 23

What is enoxaparin?

Back 23

a LMWH

Front 24

What is dalteparin?

Back 24

a LMWH

Front 25

What is ardeparin?

Back 25

a LMWH

Front 26

What is bivalirudin?

Back 26

A direct thrombin (IIa) inhibitor, derived from hirudin of leeches).

Front 27

What is argatroban?

Back 27

Argatroban is a small molecule inhibitor of thrombin (IIa). It is less immunogenic than bivalirudin.

Front 28

What are the classes of antiplatelet drugs?

Back 28

1) Block synthesis of intermediary factors

2) Block effects of those mediators

3) Block fibrinogen from interacting with platelets, thus preventing aggregation

Front 29

Name an example of a class 1 anti-platelet drug.

Back 29

Aspirin

Front 30

Name an example of a class 2 anti-platelet drug.

Back 30

Plavix (Clopidogrel)

Front 31

Name an example of a class 3 anti-platelet drug.

Back 31

Reo Pro (Abciximab)

Front 32

What is the generic name of plavix?

Back 32

clopidogrel

Front 33

What is the generic name of Reo Pro?

Back 33

Abciximab

Front 34

What does abciximab do?

Back 34

Inhibits platelet interactions with fibrin via GIIb/IIIa inhibition.

Front 35

What does clopidogrel do?

Back 35

Inhibits ADP actions on platelets by blocking GpIIb/IIIa receptors.

Front 36

There are 2 thrombin (IIa) inhibitors. Which is metabolized by the kidney and which is metabolized by the liver?

Back 36

Bivalirudin -> kidney metabolism.

Argatroban -> liver metabolism

Front 37

What are the major potential adverse events when taking a statin?

Back 37

1) rhabdomyolysis
2) liver dysfunction

Front 38

A patient with familial hypercholesterolemia seeks treatment. What drugs are best?

Back 38

1) Cholestyramine
2) Ezetimibe (Zetia)

Front 39

Why isn't ezetimibe used more often?

Back 39

Only half of patients can tolerate its side effects: HA and diarrhea.

Front 40

How does cholestyramine work?

Back 40

Binds bile acids -> bile acid secretion rather than absorption -> hepatocytes make more bile acids -> hepatocytes upregulate LDL to receive more cholesterol from the blood stream

Front 41

What are the major side effects of cholestyramine? (2)

Back 41

1) Decreased absorption of fat-soluble vitamins

2) GI side effects: diarrhea/constipation, bloating

Front 42

What SYSTEMIC side effects does cholestyramine have?

Back 42

None, all its side effects pertain to the gut

Front 43

How effective is atorvastatin in lowering LDL?

Back 43

Lowers LDL by 25-55% (~1/4 to 1/2)

Front 44

How effective is cholestyramine in lowering LDL?

Back 44

Lowers LDL by 10-33% (~1/10 to 1/3)

Front 45

How effective is ezetimibe in lowering LDL?

Back 45

Lowers LDL by 17%

Front 46

Which cholesterol-lowering drug is notorious for taking a very long time to work?

Back 46

cholestyramine

Front 47

Which cholesterol-lowering drug is notorious for being poorly adhered to because of its side effects?

Back 47

ezetimibe (Zetia) -> 50% quit due to HA or diarrhea

Front 48

How does niacin reduce triglyceride levels (4)?

Back 48

Lowers VLDL by 4 mechanisms

1) Decreases triglyceride synthesis

2) Decreases VLDL production

3) Increases lipoprotein lipase -> increases VLDL destruction

4) Increases HDL

Front 49

What two drugs bind to PPAR-alpha?

Back 49

1) Gemfibrozil

2) Omacor (Omega-3-FA's)

Front 50

What is the trade name of omega-3-fatty acids, when used to lower triglycerides?

Back 50

Omacor

Front 51

Binding of PPAR-alpha has what effects on VLDL and triglycerides? (3)

Back 51

PPAR-alpha activation ->

1) Decreased expression of apoC-III

2) Decreases VLDL production

3) Increases lipoprotein lipase -> increases VLDL destruction

Front 52

What effects does gemfibrozil have on VLDL and triglycerides? (3)

Back 52

PPAR-alpha activation ->

1) Decreased expression of apoC-III

2) Decreases VLDL production

3) Increases lipoprotein lipase -> increases VLDL destruction

Front 53

What effects does Omacor have on VLDL and triglycerides? (3)

Back 53

1) Decreased expression of apoC-III

2) Decreases VLDL production

3) Increases lipoprotein lipase -> increases VLDL destruction

Front 54

What drug lowers ApoC-III?

Back 54

Gemfibrozil

Front 55

What does ApoC-III do?

Back 55

ApoC-III inhibits lipoprotein lipase -> increases VLDL levels

Front 56

What are the side effects of gemfibrozil? (4)

Back 56

1) myositis, especially when combined with statins

2) gallstones

3) rashes (dermatomyositis?)

4) GI upset

Front 57

What drug is the most effective at lowering triglyceride levels?

Back 57

Gemfibrozil (lopid)

Front 58

What are the side effects of niacin? (2)

Back 58

1) Intense flushing

2) GI upset

Front 59

What are the 3 main side effects of cimetidine?

Back 59

1) Antiandrogenic effect -> gynecomastia
2) Reduces hepatic blood flow
3) Inhibits CYP50

* - It also has a special proclivity for inducing rebound acid secretion.

Front 60

What GI drugs can't be combined with antacids? Why?

Back 60

Acid blockers -> Prodrugs require highly acidic env't to be converted to active form

Front 61

Do the H2-blockers differ in potency?

Back 61

yes, but not in efficacy.

Front 62

Do the H2-blockers differ in efficacy?

Back 62

no, only in potency

Front 63

Aluminum-containing antacids can cause what serious side effect?

Back 63

Phosphate depletion -> bone/teeth abnormalities

Front 64

What is the biochemical nature of sucralfate?

Back 64

Sucralfate is an aluminum salt of sucrose sulfate.

Front 65

Which drug is an aluminum salt of sucrose sulfate?

Back 65

sucralfate

Front 66

How does sucralfate work? (2)

Back 66

1) Binds damaged tissue -> protects it from PEPSIN and BILE SALTS

2) Inhibits growth of H. pylori

Front 67

Which non-antibiotic drug inhibits the growth of H. pylori?

Back 67

Sucralfate

Front 68

Which anti-diarrheal opioid crosses the BBB, so it must be combined with atropine to minimize abuse?

Back 68

Diphenoxylate

Lomotil=diphenoxylate+atropine

Front 69

What is diphenoxylate?

Back 69

An anti-diarrheal opioid that crosses the BBB, so it must be combined with atropine to minimize abuse.

Front 70

Name the three gel-forming absorbants.

Back 70

Aluminum silicate

Pectin

Kaolin

Front 71

What do the gel-forming absorbants do?

Back 71

Increase the viscosity of stool -> Blocks both diarrhea and constipation.

Front 72

What does aluminum silicate do?

Back 72

Increases the viscosity of stool -> Blocks both diarrhea and constipation.

Front 73

What does kaolin do?

Back 73

Increases the viscosity of stool -> Blocks both diarrhea and constipation.

Front 74

What does pectate do?

Back 74

Increases the viscosity of stool -> Blocks both diarrhea and constipation.