Coagulation Disorders Flashcards

(47 cards)

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

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2
Q

Role of platlets

A

Platelets adhere to and aggregate at site of injury in vessel

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3
Q

Role of Platelets

A

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

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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

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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

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6
Q

Fibrinolysis

A

Plasmin breaks down fibrin network

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7
Q

Clots migrating from left atrium can cause

A

strokes

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8
Q

Clots migrating from the right atria can cause a

A

pulmonary embolism

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9
Q

Coronary artery clots cause

A

MIs

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10
Q

Heparin (Know this)

A

Enhances antithrombin activity
Decreases thrombin activity
Decreases prothrombinase activity

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11
Q

Low molecular wt Heparin

A

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

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12
Q

When do we use heparin

A

DVT, post stroke, post MI, prevent PE

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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

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14
Q

Antidote for heparin

A

Protamine Sulfate

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15
Q

Adverse effects of heparin

A

Osteoperosis
Bleeding
Skin lesions

Heparin Induced thrombocytopenia

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16
Q

Warfarin used for

A

Prophlaxis of eventls like DVT and PE

prevention of CVA /MI

Does not treat

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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 .

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17
Q

Heparin half life

A

Very brief

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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
What to monitor for pts on Heparin
CBC, INR, PT
25
What pts should be more closely moniored if opn anticoag therapy
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
PT Test
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
INR Test
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
Higher INR means
Longer time for blood clotting
29
Lower INR means increased risk for
Clotting
30
Typical APTT
25-30 seconds
31
Direct Thrombin and Factor Xa inhibitors
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
Why would someone get an apixiban over warfarin
Apixiban requires NO monitoring
33
Direct Thrombin and Factor Xa inhibitors use
Shorter half life, work faster
34
Antiplatlet drugs include
Aspirin Reduces formation of thromboxanes (promotes activation of platelets) ADP receptor antagonists Prevent aggregation by blocking receptor Prevent activation of platelets
35
Mech of action of antiplatlet drugs
Blocks ADP receptors on platelets, inhibiting platelet activation and aggregation, thereby extending clotting times
35
Adverse effects of antiplatlet drugs
Headache, dizziness Flu-like syndrome Diarrhea Bruising Upper respiratory tract infections Rash, pruritis Serious bleeding
36
Direct Xa inhibitors
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
Thrombolysis
Anticoagulants prevent new clot formation Thrombolytics break down existing clots Fibrinolysis breakdown of fibrin fibers leading to disruption of clot
38
Antiplatlet meds are NOT clot buster > T or F
True
39
Therapeutic effects and uses
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
Adverse effects of alteplase
Bleeding Angioedema (Also ace inhibs) Intercranial bleeding
41
What to monitor when administering a thrombolytic?
BP, Pulse Q15 min for and H, then Q30 min INR, CBC, Monitor for internal bleeding
42
Antifibrinolytics
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
Acute uses of fibrinolytics
Acute hemorrhages Prevention of post-operative bleeding
44
aptt used to monitor effectiveness of
Used to monitor the effectiveness of heparin
45
PT used to monitor effectivness of
Warfarin