Chapter 9.3

Question 1

Define hemorrhage and thrombogenesis

Answer 1

Thrombosis: excessive clotting
Hemorrhage: inadequate clotting

Question 2

2. State the sequence of events in the intrinsic system of clotting using the following terms: clotting factor XII, damaged vessel (collagen), clotting factor X, prothrombin, thrombin, fibrinogen, fibrin, and clot.
3. State the sequence of events in the extrinsic system of clotting using the following terms: clotting factor VII, tissue factor (thromboplastin), clotting factor X, prothrombin, thrombin, fibrinogen, fibrin, and clot.
4. State the sequence of events in the breakdown of a clot using the terms: tissue plasminogen activator (tPA), plasminogen, plasmin, and clot.

Answer 2

These sequences are better explained through the slides

Question 3

State the primary use for anticoagulants.

Answer 3

used in venous thrombosis

Question 4

heparin mechanism of action (MOA)

Answer 4

Heparin acts by increasing effects of antithrombin III

Question 5

enoxaparin (MOA)

Answer 5

is a low molecular weight heparins and it inhibits factor X

Question 6

warfarin (MOA)

Answer 6

inhibit vitamin K function in liver and decrease synthesis of certain clotting factors

Question 7

dabigatran (MOA)

Answer 7

direct thrombin inhibitors

Question 8

Apixaban (MOA)

Answer 8

factor X inhibitors

Question 9

List the differences between unfractionated heparin and low molecular weight heparins.

Answer 9

administration is different. Unfractionated heparin needs several injections which can lead to side effects. Whereas LMWH is once a day. LMWH is safer and their mechanisms are different

Question 10

Define and distinguish type I and type II heparin-induced thrombocytopenia (HIT).

Answer 10

Type 1 HIT: asymptomatic and resolves spontaneously

Type 2 HIT: immune reaction and caused thrombosis that is life threatening

Question 11

List common food sources of vitamin K.

Answer 11

cabbage, cauliflower, spinach, milk and other green veggies

Question 12

State the relationship between warfarin anticoagulation effects and the dietary intake of vitamin K.

Answer 12

don’t dramatically increase vitamin K intake when taking warfarin

Question 13

Aspirin (MOA)

Answer 13

inhibits PG and thromboxane biosynthesis by blocking cyclooxygenase enzyme

Question 14

clopidogrel (MOA)

Answer 14

block effects of ADP on platelet

Question 15

Abciximab (MOA)

Answer 15

block effects of fibrinogen and other activators on platelet

Question 16

State the role of thromboxane on platelet function.

Answer 16

increase platelet activity/aggregation

Question 17

State the primary indications for the antithrombotic aspirin.

Answer 17

Myocardial infarction and ischemic stroke

Question 18

State the mechanism of action of the following thrombolytics: tissue plasminogen activator and urokinase.

Answer 18

tissue plasminogen activator MOA: activates plasminogen starting clot breakdown
Urokinase MOA: Has the same effect as Tissue plasminogen

Question 19

State the common indications for the use of a thrombolytic agent.

Answer 19

MI and stroke

Question 20

State the timeline for administering a thrombolytic in the treatment of a myocardial infarction.

Answer 20

1 hour after symptom onset and still helpful after 3-12 hours

Question 21

State the considerations that must be considered when using thrombolytics in the treatment of an ischemic stroke.

Answer 21

Must rule out a hemorrhage

Question 22

List the primary concerns of a physical therapist treating a patient using anticlotting drugs

Answer 22

when using manual techniques like joint mobs and chest percussions

Question 23

State the primary uses of the drug aminocaproic acid.

Answer 23

fibrinolysis inhibitor: clot breakdown. Help treat hemophilia and hyperfibrinolysis syndrome

Question 24

State the primary treatment for a patient receiving an excessive dose of warfarin.

Answer 24

using vitamin K supplement

Question 25

hyperlipidemia

Answer 25

an abnormally high concentration of lipids in the bloodstream

Question 26

Atherosclerosis

Answer 26

deposition of fatty plaque like lesions on the walls of large and medium-sized arteries

Question 27

Lipoprotein

Answer 27

lipids such as cholesterol are transported in the bloodstream as part of a lipoprotein complex known as a lipoprotein

Question 28

atorvastatin and simvastatin (MOA)

Answer 28

inhibit HMG-Co A reductase enzyme

Question 29

gemfibrozil (MOA)

Answer 29

activate nuclear receptor that affects genes controlling lipid metabolism

Question 30

cholestyramine (MOA)

Answer 30

bind to bile to increase excretion of bile

Question 31

niacin (MOA)

Answer 31

decrease LDL synthesis and decrease triglycerides

Question 32

Ezetimibe (MOA)

Answer 32

inhibits cholesterol absorption from GI tract

Question 33

atorvastatin and simvastatin primary effect (PE)

Answer 33

decreased cholesterol biosynthesis in liver and increase hepatic LDL breakdown. May also decrease triglycerides and increase HDL

Question 34

Gemfibrozil (PE)

Answer 34

have bigger effects on decreasing triglycerides and increase LDL breakdown

Question 35

cholestyramine (PE)

Answer 35

liver makes more bile and uses cholesterol bile decreasing plasma cholesterol to make more bile

Question 36

Ezetimibe (PE)

Answer 36

decreases LDL and cholesterol in general

Question 37

List the adverse effects associated with the anti-lipid drugs.

Answer 37

GI problems, liver toxicity, pancreatitis, blood dyscrasias and arrythmias. Main effect for us as PTs is neuromuscular problems

Question 38

25. List the proposed mechanisms for statin-induced myopathy.

Answer 38

Decrease cholesterol in muscle cell membrane. Decrease Coenzyme Q 10. Decrease prenylated proteins. Increase enzymes that regulate protein turnover

Question 39

List the factors predisposing to the development of statin-induced myopathy.

Answer 39

Renal failure, genetics, advanced age and female. Medications, high dose, lipophilic and heavy exercise

Question 40

List the primary concerns of a physical therapist treating a patient using lipid lowering drugs

Answer 40

Delayed onset muscle soreness due to exercise. We have to be careful that it is actually the exercise that is inducing DOMS or is it statin induced myopathy