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Pharmacology > Chapter 9.3 > Flashcards

Chapter 9.3 Flashcards

1
Q

Define hemorrhage and thrombogenesis

A

Thrombosis: excessive clotting
Hemorrhage: inadequate clotting

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2
Q
  1. 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.
  2. 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.
  3. State the sequence of events in the breakdown of a clot using the terms: tissue plasminogen activator (tPA), plasminogen, plasmin, and clot.
A

These sequences are better explained through the slides

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3
Q

State the primary use for anticoagulants.

A

used in venous thrombosis

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4
Q

heparin mechanism of action (MOA)

A

Heparin acts by increasing effects of antithrombin III

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5
Q

enoxaparin (MOA)

A

is a low molecular weight heparins and it inhibits factor X

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6
Q

warfarin (MOA)

A

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

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7
Q

dabigatran (MOA)

A

direct thrombin inhibitors

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8
Q

Apixaban (MOA)

A

factor X inhibitors

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9
Q

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

A

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

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10
Q

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

A

Type 1 HIT: asymptomatic and resolves spontaneously

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

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11
Q

List common food sources of vitamin K.

A

cabbage, cauliflower, spinach, milk and other green veggies

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12
Q

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

A

don’t dramatically increase vitamin K intake when taking warfarin

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13
Q

Aspirin (MOA)

A

inhibits PG and thromboxane biosynthesis by blocking cyclooxygenase enzyme

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14
Q

clopidogrel (MOA)

A

block effects of ADP on platelet

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15
Q

Abciximab (MOA)

A

block effects of fibrinogen and other activators on platelet

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16
Q

State the role of thromboxane on platelet function.

A

increase platelet activity/aggregation

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17
Q

State the primary indications for the antithrombotic aspirin.

A

Myocardial infarction and ischemic stroke

18
Q

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

A

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

19
Q

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

A

MI and stroke

20
Q

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

A

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

21
Q

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

A

Must rule out a hemorrhage

22
Q

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

A

when using manual techniques like joint mobs and chest percussions

23
Q

State the primary uses of the drug aminocaproic acid.

A

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

24
Q

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

A

using vitamin K supplement

25
Q

hyperlipidemia

A

an abnormally high concentration of lipids in the bloodstream

26
Q

Atherosclerosis

A

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

27
Q

Lipoprotein

A

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

28
Q

atorvastatin and simvastatin (MOA)

A

inhibit HMG-Co A reductase enzyme

29
Q

gemfibrozil (MOA)

A

activate nuclear receptor that affects genes controlling lipid metabolism

30
Q

cholestyramine (MOA)

A

bind to bile to increase excretion of bile

31
Q

niacin (MOA)

A

decrease LDL synthesis and decrease triglycerides

32
Q

Ezetimibe (MOA)

A

inhibits cholesterol absorption from GI tract

33
Q

atorvastatin and simvastatin primary effect (PE)

A

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

34
Q

Gemfibrozil (PE)

A

have bigger effects on decreasing triglycerides and increase LDL breakdown

35
Q

cholestyramine (PE)

A

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

36
Q

Ezetimibe (PE)

A

decreases LDL and cholesterol in general

37
Q

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

A

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

38
Q
  1. List the proposed mechanisms for statin-induced myopathy.
A

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

39
Q

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

A

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

40
Q

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

A

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

Pharmacology (22 decks)

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