Coagulation Disorders Flashcards

1
Q

Three major steps in the process of hemostasis

A

Prothrombinase converts prothrombin to thrombin
Thrombin converts fibrinogen to fibrin
Fibrin strands trap RBCs forming clot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Role of platlets

A

Platelets adhere to and aggregate at site of injury in vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Role of Platelets

A

Platelet activation leads to formation of fibrin network that trap RBCs forming clot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Role of Cofactors in Hemostasis

A

Ca+2 and Vitamin K are critical for synthesis of clotting factors which stop wounds from bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Deep venous thrombosis (DVT)

A

Venous clots often develop in the legs as a DVT, but can migrate to lungs creating a pulmonary embolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Fibrinolysis

A

Plasmin breaks down fibrin network

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Clots migrating from left atrium can cause

A

strokes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Clots migrating from the right atria can cause a

A

pulmonary embolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Coronary artery clots cause

A

MIs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Heparin (Know this)

A

Enhances antithrombin activity
Decreases thrombin activity
Decreases prothrombinase activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Low molecular wt Heparin

A

Similar activity
Fewer adverse effects than heparin
Less risk of thrombocytopenia compared to heparin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

When do we use heparin

A

DVT, post stroke, post MI, prevent PE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Mech of action for Heparin

A

Activates antithrombin III, which inhibits thrombin and factor Xa (prothrombinase).

Remember prothrombin istransformed into thrombin by a clotting factor known as factor X or prothrombinase and then thrombin acts to transform fibrinogen, also present in plasma, into fibrin, which, in combination with platelets from the blood, forms a clot
-DONT NEED TO KNOW

Prevents clot formation; does not break down existing clots

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Antidote for heparin

A

Protamine Sulfate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Adverse effects of heparin

A

Osteoperosis
Bleeding
Skin lesions

Heparin Induced thrombocytopenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Warfarin used for

A

Prophlaxis of eventls like DVT and PE

prevention of CVA /MI

Does not treat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Low molecular wt heparin advantages

A

Possess the same degree of anticoagulant activity as heparin but have several advantages which are;
Less likely to cause thrombocytopenia
Duration of action is 2 to 4 times longer.
Produce a more stable response.
Fewer follow up labs are needed.
Client can be trained to give S/C injections at home.
Often the drug of choice now .

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Heparin half life

A

Very brief

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Mech of action - Warfarin

A

Warfarin inhibits/blocks two enzymes that use Vitamin K to produce clotting factors

-

19
Q

Adverse effects of Warfarin

A

Purple toe syndrom
Microembolism, osteperosis
Bone fractures
Abnormal bleeding

20
Q

Antidote for warfarin

21
Q

Dietary reccomendations for Warfarin

A

Avoid Vit K high foods

22
Q

Nursing considerations for pts recieving anticoagulant therapy

A

Obtain a complete health history including allergies and drug history

Obtain baseline vital signs, especially heart rate and blood pressure, and clotting times

23
Q

What to be careful of for someone on anticoag therapy

A

Any accidental bumps
Aggressive teeth brushing

24
Q

What to monitor for pts on Heparin

A

CBC, INR, PT

25
Q

What pts should be more closely moniored if opn anticoag therapy

A

Also monitor patients with kidney or liver disease, GI, diabetes with extra care.

At increased risk for bleeding/low platelets (liver)

DM increases risk of blood clotting

26
Q

PT Test

A

PT stands for prothrombin time. It is a measure of how quickly blood clots. The traditional method for performing a PT test is to blood drawn and sent to a lab. At the lab, a substance called a reagent is added to the blood. The reagent causes the blood to begin clotting. The PT result is the time in seconds that is required for the blood to clot.

27
Q

INR Test

A

INR stands for International Normalized Ratio. As its name suggests, one INR result can be compared to another INR result regardless of how or where the result was obtained. So, the INR is just the standard unit used to report the result of a PT test.

Range: Varies for person to person

Most common is bw 2 and 4

Normal pt would have 1

28
Q

Higher INR means

A

Longer time for blood clotting

29
Q

Lower INR means increased risk for

30
Q

Typical APTT

A

25-30 seconds

31
Q

Direct Thrombin and Factor Xa inhibitors

A

Newer drugs in the prevention and TX of venous thromboembolism and pulmonary emboli.

Originally derived from chemicals found in leeches.

Directly inhibit thrombin preventing the formation of fibrin used for the same types of indications as heparin or LMWH>

32
Q

Why would someone get an apixiban over warfarin

A

Apixiban requires NO monitoring

33
Q

Direct Thrombin and Factor Xa inhibitors use

A

Shorter half life, work faster

34
Q

Antiplatlet drugs include

A

Aspirin
Reduces formation of thromboxanes (promotes activation of platelets)
ADP receptor antagonists
Prevent aggregation by blocking receptor
Prevent activation of platelets

35
Q

Mech of action of antiplatlet drugs

A

Blocks ADP receptors on platelets, inhibiting platelet activation and aggregation, thereby extending clotting times

35
Q

Adverse effects of antiplatlet drugs

A

Headache, dizziness
Flu-like syndrome
Diarrhea
Bruising
Upper respiratory tract infections
Rash, pruritis

Serious bleeding

36
Q

Direct Xa inhibitors

A

Direct Oral Anticoagulants DOAC
Only given PO
Result in prolonged clotting time
Reduce risk of stroke and systemic embolism in clients with nonvalvular a fib.
TX of DVT and Pulmonary embolism
Prophylaxis of DVT in client who have undergone knee or hip surgery. Apixaban and rivaroxaban.
Adverse effect bleeding and there is no antidote.
Abrupt discontinuation increases risk for thromboembolism.
Increased risk of spinal and epidural hematomas in uncoagulated patients

37
Q

Thrombolysis

A

Anticoagulants prevent new clot formation
Thrombolytics break down existing clots
Fibrinolysis
breakdown of fibrin fibers leading to disruption of clot

38
Q

Antiplatlet meds are NOT clot buster > T or F

39
Q

Therapeutic effects and uses

A

Thrombotic CVA
Off-label use to restore IV catheter patency
Mechanism of action
Converts plasminogen to plasmin which breaks down fibrin in clot
Lowers circulating fibrinogen and plasminogen

40
Q

Adverse effects of alteplase

A

Bleeding
Angioedema (Also ace inhibs)
Intercranial bleeding

41
Q

What to monitor when administering a thrombolytic?

A

BP, Pulse
Q15 min for and H, then Q30 min

INR, CBC, Monitor for internal bleeding

42
Q

Antifibrinolytics

A

Used to prevent and treat excessive bleeding post-surgery

Formation of abnormal clots, possibly pulmonary clots

Inactivates plasminogen precursor for plasmin that digests the fibrin clot.

Very rare

43
Q

Acute uses of fibrinolytics

A

Acute hemorrhages
Prevention of post-operative bleeding

44
Q

aptt used to monitor effectiveness of

A

Used to monitor the effectiveness of heparin

45
Q

PT used to monitor effectivness of