6.2 Platelets and Platelet Disorders Flashcards
1
Q
Platelets and Clotting Disorders
A
Platelet Count - 150,000 - 450,000 uL
- Smallest blood cells in the body
- Fragments of Megakaryocytes
- Active for 10 days
- Become active when traveling to damaged blood vessels
- Removed by clot formation
- Senescent platelets are consumed by neutrophils and monocytes in circulation or macrophages in liver and spleen
2
Q
Hemostasis
A
- Stoppage of bleeding.
- Relies on platelets and coagulation factors
3
Q
Thrombopoiesis
A
- Development of platelets occurs via endomitosis.
- Megakaryocyte goes through mitosis but fails cytokinesis (end phase) resulting being broken into fragments (platelets)
- Interleukin (inflammatory cytokine) stimulates production of thrombogenic platelets
- Removed from clot formations and consumed by neutrophils/monocytes in circulation and macrophages in liver/spleen
4
Q
Coagulation Cascade
A
- Positive feedback mechanism where coagulation factors are activated one after the other which results in a blood clot.
5
Q
Coagulation Cascade Pathways
A
Intrinsic Pathway - Exposure of subendothelial surface to blood resulting in activation of Factor 7 (Hageman)
Extrinsic Pathway - Primary pathway triggered by tissue injury resulting in release of thromboplastin
Common Pathway - Thrombin catalyzes conversion of fibrinogen to fibrin which stabilizes the clot.
6
Q
Atherosclerosis
A
- Hard fatty mush
- Presence increases risk of thrombus development
- Can affect any organ or tissue and often involves arteries supplying the heart
- Heart can cause myocardial infarction (MI)
- Brain can cause Stroke
- Leg can cause DVT
7
Q
Arterial Thrombosis
A
- Caused by Atherosclerotic plaque and/or hypertension
- Turbulent blood flow causes damage to arterial endothelium and activates platelets for coagulation
- Cause disease such as ischemia or infarction by blood flow obstruction
8
Q
Venous Thrombosis
A
Associated with Venous Stasis (sluggish blood flow)
- Less cohesive than arterial thrombosis
(Emboli more likely to detach and travel)
- Can cause deep vein thrombosis and embolization (stops blood flow)
9
Q
Bleeding Disorders (Platelet Defects)
A
- Platelets reach 10,000 - 20,000 uL before bleeding is evident in a disorder
Manifestations - Bleeding from mucous membranes (nose, throat, GI Tract, Vagina)
- Petechiae - Pinpoint purplish-red spots
- Purpura - Purple, pooled area under the skin
10
Q
Thrombocytopenia
A
- Decrease in number of circulating platelets (<100,000/uL)
Causes - Decrease in platelet production in marrow, increased pooling of platelets in spleen, decreased platelet survival due to immune destruction, drug induced damage to platelets.
11
Q
Thrombocytopathia
A
- Impaired platelet function caused by inherited disorders of adhesion or acquired deficit by drugs.
- Aspirin (ASA) and NSAIDs (Non-steroid anti-inflammatory drugs) are the most common cause
- Drugs inhibit prostaglandin a2 (TXA2) which is required for platelet aggregation.
- Aspirin effect lasts the life of the platelet
- NSAIDS lasts duration of drug effet
12
Q
Anticoagulants
A
- Prevents new blood clots and extension of blood clots
- Does not dissolve formed clots
- Improves blood flow in tissues around clots or prevent ischemic damage beyond clots.
Indication - Prevention and management of thromboembolic disorders like thrombophlebitis, DVT, pulmonary embolism.
Adverse Effects - Bleeding
13
Q
Heparin
A
- Prevents conversion of prothrombin to thrombin
- Preferred anticoagulant during pregnancy and in situations that require rapid onset of anticoagulation
- Administered via IV or SQ
Contraindications - Hypersensitivity to beef or pork, thrombocytopenia, bleeding disorders
- aPPT assessed every 4 hours. Monitor for bleeding, ecchymosis (bruising), hematoma, avoid IM
14
Q
Low Molecular Weight (LMW) Heparin
A
- Activates factor Xa (less able to inactivate thrombin than unfractionated heparin)
- Prevents DVT after abdominal, hip and knee surgery, treatment of DVT, prevention of ischemic complications in patients with unstable angina or non-Q-wave MI
- Longer half life than unfractionated heparin. Given twice a day. Greater bioavailability leads to predictable plasma levels. No need to monitor aPTT. Commonly given SQ but can be given IV
- Adverse effects include bleeding, thrombocytopenia, severe neurological injuries.
15
Q
Warfarin (Coumadin)
A
- Blocks vitamin K and prevents activation of prothrombin and other factors
- Administered orally (maximum effect after 3-4 days)
- Monitored by INR (International Normalized Ratio)
- INR should be 2-3 for use. 3 - 4.5 for patients with mechanical heart valves or recurrent systemic emboli
- Antidote is Vitamin K
- Adverse effects are bleeding, avoid during pregnancy (fetal warfarin syndrome)
- Avoid aspirin, increased vitamin K intake (dark leafy greens), NSAIDs. Effect remains for 2-5 days after use
