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Pharm Exam II > Coagulation and Hyperlipidemia > Flashcards

Coagulation and Hyperlipidemia Flashcards

1
Q

What is hemostasis?

A

Blood coagulation

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2
Q

What is thrombogenesis?

A

Overactive clotting which can lead to thrombus formation and thus vessel occlusion

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3
Q

Why is blood coagulation important?

A

It is needed to prevent excessive hemorrhage from a damaged blood vessel- inadequate blood clotting leads to excessive blood loss

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4
Q

What influences hemostasis?

A

Hyperlipidemia- excessive plasma lipids

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5
Q

Why is lowering plasma lipid levels important?

A

to prevent atherosclerosis- done through medications in conjunction with lifestyle modifications

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6
Q

How is a blood clot broken down?

A

through t-PA (tissue plasminogen activator)- which converts plasminogen to plasmin
-plasmin is an enzyme that directly breaks down the fibrin mesh and destroys the clot
-a fibrinolytic that is given through IV
-successfully treats MIs

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7
Q

What is the framework of a blood clot?

A

strands of fibrin bound together to form a meshlike structure

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8
Q

What are the drugs to treat blood clots?

A
  1. Anticoagulants: To control the synthesis and function of clotting factors
  2. Antiplatelets
  3. Fibrinolytics
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9
Q

What are anticoagulants used for?

A

Used to prevent and treat clots in the venous system: treats venous thrombosis, thromboembolisms and prophylactically for those at risk for DVTs

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10
Q

What is the primary anticoagulant for initial treatment?

A

Heparin- the initial treatment of venous thrombosis b/c effects are seen almost immediately
-given parenterally: IV
-administered 2+ times/day

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11
Q

What has replaced the use of traditional heparin?

A

Low Molecular Weight Heparin- Lovenox
-administered as a subcutaneous injection into fat tissue
-1x/day at home

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12
Q

When is low molecular weight heparin typically used?

A

For those having surgery, those at risk for DVTs and used for several weeks following discharge from hospital

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13
Q

What is the primary anticoagulant for long-term prevention?

A

Coumadin (Wardarin)- interferes with vitamin K metabolism in the liver which impairs the hepatic synthesis of several clotting factors
-administered orally
-takes several days to be effective

**patients must be monitored to ensure is it at a therapeutic dose

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14
Q

What is the acceptable clotting INR range?

A

2-3

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15
Q

Side effects of anticoagulants

A

-Hemorrhage: increased bleeding, blood in stool or urine, bleeding gums, heavy menstrual flow
-Thrombocytopenia: decreases platelets
-GI distress
-Skin reactions

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16
Q

What do anti-platelet drugs do?

A

Prevent excessive clotting caused by increased platelet activity
-primarily prevents arterial clots

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17
Q

Which antiplatelet drugs suppresses natural platelet aggregation?

A

Aspirin- prevents platelet induced thrombosis
-reaches a platelet and inhibits it for the remainder of its life (7-8 days) (irreversible)

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18
Q

What does aspirin help with?

A

-prevents ischemic stroke
-used to prevent DVT (used an in adjunct to heparin or warfain to treat DVTs)

19
Q

Risk of aspirin

A

May increase risk for hemorrhagic stroke

20
Q

What is ADP?

A

Adenosine diphosphate- a chemical that increases platelet activity and platelet induced clotting

21
Q

How do ADP receptor blockers work?

A

Block the ADP receptor which reduces clotting

22
Q

What are ADP receptor blockers used for?

A

used primarily to prevent thrombosis in patients who are at risk for an MI or ischemic stroke:
-pts with unstable angina
-pts with a-fib

23
Q

How do glycoprotein IIB-IIIa receptor blockers work?

A

these drugs inhibit the ability of fibrinogen to activate platelets by blocking the receptor site on the platelet membrane which reduces platelet induced clotting

24
Q

Which drugs are the most powerful inhibitors of platelet activity?

A

Glycoprotein IIb-IIIa receptor blockers- used to prevent thrombosis in those undergoing angioplasty and other interventions

25
Q

Side effects of antiplatelet drugs

A

-increased risk of bleeding
-hypotension
-GI distress

Aspirin:
-gastric irritation
-toxicity to liver and kidneys at high doses

26
Q

What do fibrinolytics do?

A

facilitate the breakdown and helps to dissolve clots that have already formed- used to reopen blood vessels

27
Q

What are fibrinolytics mostly used for?

A

Essential in treating those with MI
-re-establishes blood flow when used at onset of MI
-decreases morbidity and mortality following an MI
-administered one hour within onset of MI reduces mortality by 50%
-via IV into systemic circulation

28
Q

Other uses for fibrinolytics

A

-used to dissolve clots in peripheral arteries: femoral, popliteal)
-used to dissolve DVTs
-used for PEs
-used to treat shunts and bypass grafts

29
Q

Risk factors for fibrinolytics

A

intracranial hemorrhage or other bleeding problems

30
Q

Contraindications for Fibrinolytics

A

-history of hemorrhagic stroke
-active internal bleeding
-other factors that would create an increased risk for hemorrhage

31
Q

Adverse effects of fibrinolytics

A

-hemorrhage
-excessive bleeding during wound care dressing changes
-itching
-nausea
-HA
-allergic reaction

32
Q

What is hemophilia?

A

unable to synthesize adequate amounts of specific clotting factors
-pts develop joint problems due to intra-articular bleeding

33
Q

treatment of hemophilia

A

Missing clotting factors need to be replaced- done prophylactically or acutely

34
Q

Treatment of insufficient vitamin K

A

The liver needs adequate vitamin K to produce clotting factors- admnistration of exogenous vitamin K can resolve this

35
Q

What is hyperlipidemia?

A

Abnormally high concentrations of lipids in the blood- this causes atherosclerosis

36
Q

What is the primary cause of cardiovascular disease?

A

hyperlipidemia

37
Q

The different types of lipids in the blood

A
  1. high density lipoproteins (HDL): good cholesterol
  2. low density lipoproteins (LDL): bad cholesterol
  3. Triglycerides: type of lipid (fat)
38
Q

Treatment of hyperlipidemia

A

Focuses on increasing HDLs and lowering LDLs
-meds used when this cannot be achieved through lifestyle modifications
-examples: satin drugs and fibric acids

39
Q

What do satin drugs do?

A

They reduce cholesterol production especially in liver cells which causes a breakdown in LDL and a decrease in triglycerides and an increase in HDL levels
-decrease mortality and morbidity in those with high cholesterol

40
Q

Which drugs are the mainstay in treating cardiovascular disease and may have anti-cancer effects?

A

statin drugs

41
Q

What do fibric acids do?

A

They decrease triglyceride levels
-may produce an increase in HDL levels and help lower LDL levels

42
Q

adverse effects of lipid lowering drugs

A

-GI distress
-liver dysfunction, gallstones, pancreatitis
-cardiovascular problems: arrhythmias
-neuromuscular problems (statin drugs): myopathy that can progress to rhabdomyolosis if not caught early

43
Q

Rehab implications for anticoagulants

A

-primary problem is increased risk of bleeding (careful with wound care and aggressive manual techniques)
-be aware of signs of intra-joint bleeding (hemophilia)

44
Q

rehab implications for hyperlipidemia

A

Pts need to be educated on nonpharmacological methods at managing their cholesterol (diet, exercise)

Pharm Exam II (9 decks)

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