Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
34 Cards in this Set
- Front
- Back
What is hemostasis? What is the trigger? What is the purpose?
|
stoppage of blood flow; produced by coagulation and blood clotting
Trigger --> tear in blood vessel, wound Purpose? Prevent blood loss |
|
What are the three stages of hemostasis?
|
1. Vascular Phase
2. Platelet Phase 3. Coagulation Phase |
|
What are the four basic steps of hemostasis?
|
1. Vessel injury
2. Vessel spasm 3. Platelets adhere to injury site and aggregate to form plug 4. Formation of insoluble fibrin strands and coagulation |
|
Draw out the steps for the coagulation cascade.
|
Slide 7 lecture 15
|
|
What are anticoagulants? Do they dissolve clots that are already formed? What are they used to treat? Primarily used for _________ in veins.
|
Medications that prolong bleeding time
Do not dissolve clots already formed, but may prevent clots from becoming larger Used to treat MI, venous thrombosis, pulmonary emboli Primarily used for thrombosis in veins |
|
What are two types of anticoagulants and how are they administered?
|
Heparin sodium (Hep-Lock) - IV infusion
- downside: irritation to the blood vessel, requirement of a nurse practitioner in order to administer the drug Warfarin sodium (Coumadin) - Oral (PO) |
|
Name a naturally-occurring anticoagulant. What is it produced by? How is it administered?
What is its half life? |
Heparin - produced by basophils and mast cells
Parenteral route (injection) *degraded if taken orally approx. 1hr half life (must be given continuously via infusion or given frequently) |
|
What does heparin combine with in order to inhibit thrombin from converting fibrinogen to fibrin?
|
AT III (antithrombin III)
|
|
What action does aspirin affect?
|
Platelet aggregation = aspirin
Platelet adhesion to injury site = clopidrogel Clotting factors and cascade = warfarin, heparin and low molecular weight heparins (more biologically available) |
|
Low Molecular Weight Heparin (LMWH) - what is the benefits of using it over heparin?
What is it more effective in preventing and treating? - Less bleeding and fewer episodes of ____-_____ _________ |
Benefits: Greater bioavailability and longer action than heparin
More effective in preventing and treating venous THROMBOEMBOLISM Less bleeding and fewer episodes of heparin-induced thrombocytopenia (shortage of platelets) |
|
What is an adverse effect related to heparin use?
|
Heparin-induced thrombocytopenia syndrome (HITS)
|
|
What is the most common cause of abnormal bleeding? This is a platelet deficiency.
|
Thrombocytopenia
|
|
What happens when platelets aggregate within the blood vessels? What do they use up when they aggregate
|
platelets aggregate within the blood vessels, thereby using up coagulation factors
formation of platelet clots can lead to thrombosis, while the loss of coagulation factors and platelets may result in bleeding |
|
What does Warfarin interfere with and where is it used?
|
Interferes with hepatic synthesis of vitamin K–dependent clotting factors (II, VII, IX, X)
Used on inpatient and outpatient basis for long-term anticoagulation |
|
What are the 2 major adverse effects of warfarin?
|
Purple Blue toe syndrome
Osteoporosis |
|
Purple/Blue Toe Syndrome: When during the treatment? What is it a result from?
|
Early during warfarin treatment (usually within 3 to 8 weeks);
result from small deposits of cholesterol break free and block blood vessels ‘cholesterol embolism’ ---> blood vessel We have a cholesterol concentration which blocks blood vessel and causes damage. |
|
What is warfarin necrosis?
- when during therapy? - what is the demographic effected? - where on the body? - why does it happen? - how is progression affected? - associated with which protein? |
Day 3-10 of therapy with warfarin
Usually in middle aged, obese women. Massive disseminated necrosis, buttocks, thighs, breasts associated with the use of large loading doses at the start of treatment Progression is not altered by discontinuation of the drug after onset of necrosis associated with protein C deficiency; genetic and/or acquired Initial loading doses of warfarin inhibits protein C protein C deficiency Larger initial warfarin dose, the more disrupted the ratio of reduced protein C to other coagulation factors widespread coagulation/thrombosis Blood clots produce superficial tissue ischemia and necrosis |
|
What is protein C? How does it become activated?
What is its main action? What is genetic protein C deficiency associated with? What kind of protease is it? |
Protein C (autoprothrombin IIA/ blood coagulation factor XIV)
Circulates inactive form, becomes activated by thrombin/thrombomodulin to become activated protein C (APC) serine protease Anticoagulant action proteolytically inactivates proteins Factor Va and Factor VIIIa Genetic protein C deficiency associated with risk venous thrombosis, other clotting abnormalities *NEGATIVE REGULATION IS PRESENT! |
|
Describe warfarin necrosis. What happens to affected tissue?
|
Initial loading doses of warfarin inhibits
protein C protein C deficiency Larger initial warfarin dose, the more disrupted the ratio of reduced protein C to other coagulation factors widespread coagulation/thrombosis Blood clots produce superficial tissue ischemia and necrosis |
|
Which oral anticoagulant is a direct factor Xa inhibitor? Does it inhibit only free factor Xa?
What pathway does it interrupt for the blood coagulation cascade? |
Rivaroxaban
Intrinsic and extrinsic pathways inhibits both thrombin formation and development of thrombi inhibits both free Factor Xa and Factor Xa bound in the prothrombinase complex |
|
What is the ultimate goal of rivaroxaban?
|
to reduce blood clotting through the inhibition of factor Xa
|
|
Which drug acts as a direct thrombin (factor IIa) inhibitor? Is it a competitive or reversible direct thrombin inhibitor? Which type of fibrin does it inactivate?
|
Dabigatran (Pradaxa)
BOTH COMPETITIVE AND REVERSIBLE inactivates both fibrin-bound and free thrombin through binding to the active site *Ultimately prevents the formation of fibrin --> reduced blood clotting |
|
What are anti-platelets used for? Provide an example.
|
Prevent platelets from binding together
Used to prevent clot formation in arteries, in MI and stroke Asprin |
|
What does Clopidogrem (Plavix) do?
|
irreversibly inhibits platelet activation
|
|
How does Clopidogrel (Plavix) work?
|
- irreversible blockade of P2Y12 receptor
- platelet aggregation - cross-linking of platelets by fibrin **potent oral antiplatelet agent |
|
What do Thrombolytics do? What is the process called? When are they used and provide two examples.
|
dissolve blood clots in a process called thrombolysis
limit the damage caused by the blockage of the blood vessel used in for myocardial infarction, ischemic strokes, deep vein thrombosis and pulmonary embolism Examples: t-PA, streptokinase |
|
Tissue plasminogen activator (abbreviated PLAT or tPA)
- where is it found? - what does it do? - What is the name of the recombinant form? |
serine protease normally found on the surface of endothelial cells of veins, capillaries, the pulmonary artery
t-PA converts proenzyme plasminogen --> plasmin, a fibrinolytic enzyme Recombinant form- alteplase (rtPA). *synthesized in the lab also |
|
When is t-PA administered? what percentage of patients qualify for this treatment?
|
- within the first 3h of the event (via IV)
- Or// within 6h if administered through an arterial catheter directly to the site of blockage Guideline in Ontario, Canada hospitals for Ischemic strokes is that tPA must be given within 3 h of the onset of symptoms **only about 3% of patients qualify for this treatment. |
|
What is streptokinase and how does it work? When is it used?
|
extracellular metallo-enzyme produced by β-haemolytic streptococcus
used as an effective and cheap clot-dissolving medication in some cases of MI and pulmonary embolism. Fibrinolytic medication works by converting plasminogen plasmin |
|
What are the colour coded caps for, for the bottles of anticoagulants?
|
Colour coded (caps) denote different additives in tube prior to blood collection
|
|
How do additives in the tubes for storing blood work?
|
Apart from heparin, most of additives in tubes work by binding Ca2+ (CHELATION), preventing the coagulation process
|
|
What are Vacutainer Tubes? What is the purple cap for? what is the blue cap for?
|
Laboratory blood collection tubes
EDTA is denoted by mauve or purple caps on Vacutainer brand test tubes. EDTA chemical strongly and irreversibly binds Ca2+. Citrate is usually in blue Vacutainer tube. Eliminates the Ca2+, but not as strongly as EDTA. |
|
What is required to be injected for an angiogram?
|
Angiogram- contrast agent injected via catheter/guide wire in femoral artery, requires heparin
|
|
What do you need to take for a medicated stent?
|
plavix - may need to take anti-platelet medication
|