Platelets Flashcards
hemostasis w/out obstruction of blood flow is carried out by the interaction of?
Blood vessels , platelets, coagulation factors
o (injury to a vessel! constriction-> platelet adhesion (primary
hem) activation of coagulation (2ndary hem- fibrin plug)
hemostasis w/out obstruction of blood flow is carried out by the interaction of?
Blood vessels , platelets, coagulation factors
o (injury to a vessel! constriction-> platelet adhesion (primary
hem) activation of coagulation (2ndary hem- fibrin plug)
balanced hemostasis?
Thrombus- increase procoagulation activity, decrease. fibrinolysis. Excessive thrombus—obstruction- hypoxia (pulmonary thromoboembolism)
• Hemorrhage- decrease procoag activity, decrease. PLT #, or function, excessive fibrinolysis! cant form thrombus! hemorrhage! ITP.
what is the average lifespan of a platelet?
3-5 days. 1/3 of platelet mass will reside in the spleen.
What do large giant platelets represent?
Increased platelet production- (macroplatelets- about same size of
RBC)
Life cycle?
Stem cell! megakaryoblast! megakaryocyte. (polyploidy nucleus) w/ abundant cytoplasm)
• Thrombopoeisis! megakaryocyte at the sinus! long proplatelet process extension the sinus lumen and breaks into individual platelets. Maturation time of megkaryoblast to PLT release! 4-5 days
What regulates thrombopoeisis?
Thrombopoeitin (TPO)! increase megakaryocyte production and
differentiation. Binds to PLTS normally. When there is a dec. # of PLT means increase in free plasma TPO which reacts with bone marrow. To increase #, size and ploidy of megakaryocyte and decrease maturation time. EPO- can cross stimulate megakarycotes
Function of PLT?
Increase metabolic activity, primary hemostasis, support 2ndary
hemostasis.
Steps in primary hemostasis?
3-5 mins. Forms hemostatic plug. PLT adhere to subendothelium, are activated (shape change) secrete granules and aggregate to form a PLT plug); adhere, activate, aggregate.
o adhesions! need vWF (binds to GP1b on PLT and bridges PLT and collagen. ADP, CA2+ and serotonin as well
o activation- shape change- allow for filopodia to increase surface area for 2ndary hemostasis (responds to thrombin). Secrete granules factor V and VIII, thromboxane A2, calcium to recruit more PLT, further activate PLT, facilitate coagulation, mediate vessel and repair PLT have neg charge on outer membrane surface- reverses when calcium is bound- allows for factors (that are negative) to then come and bind.
“ recruits more PLT, further PLT activation, facilitate coagulation, mediate vessel repair
o AggregatioN:What do the granule contents do (calcium, serotonin, ADP, vWF)?–> stimulate aggregation, irreversible, fibrinogen binds to activated PLTS and binds adjacent PLT. Final step in platelet plug formation CALCIUM REQURIED
o After- clot retraction! contract actinomysin filaments and allows for wound closure, vessel patency
How do you test PLT concentration in blood?
Collect in an EDTA tube (purple tube)- doesn’t disrupt morphology
and prevents clotting. And they are calcium absorbers-s o they wont activate the platelets make sure the stick in vein is even and not jagged and poking around. Put on blood smear or hematology analyzer- should show 7-10 PLT on 100x lens. Horses- 4-7 minimumPLT concentration morphology and size- look at blood smear or hem. analzyers
Bleeding time tests test platelet function
Bone marrow aspirate- tests production of bone marrow.
• HORSES PLT STAIN PALE
At what platelet count can you see spontaneous hemorrhage?
what can a hematology analyzer demonstrate?
Platelet morphology- MPV (mean platelet volume. – increase in MPV demonstrates thombopoeisis
What does a PLT bleeding test demonstrate?
• Ability of PLT to form a PLT plug. (does not test fibrin plug
formation)!
• Perform a buccal mucosal bleeding time (BMBT- dog1-5 min, cat 1- 3.5 min, horse/cattle- 8-10 mins) PERFORM ON LIP NOT GUM
• Can perform a cuticle bleeding time (toenail)! dog 2-8 min)
• Can also perform platelet function- test for adhesion, aggregation
or secretion- needs special equipment.
If you have a decrease in PLT and look at the bone marrow w/ no mature megkaryoblasts- what does that tell you?
Dz process in bone marrow- targeting platelets or neoplastic.
• If low in PLT- expect PLT secretion to increase and increase
megakaryocyte production
What are clinical features of thrombocytopenia?
Mucosal bleeding, petechial, ecchymosis, spontaneous hemorrhage, +/- hemorrhagic anemia. Clinical signs associated with primary dz. Dx the problem not the specific dz. Remember that thrombocytopenia is not a specific dz but a problem that contributes to it.
• Hemorrhage alone does not cause sig. thormbocytpenia unless acute sever hemorrhage (mild thrombocytopenia)
o Causes- loss, consumption (use of platelets in cascade, DIC, vasculitis, viral infection), destruction (ITP, modified live virus vaccine- 3-10 days post vx.-> will see platelet bleeding pattern- bleeding from mucous membranes and peteciation to ecchymosis ), decreased production (bone marrow hypoplasia, neopalisa, myelonecrosis or meylofibrosis – degree of thrombocytopenia depends on extent of bone marrow dz);, abnormal distribution (sequestration of PLT in large vascular beds- mild to moderate thrombocytopenia, splenomegaly, splenic torsioin, neoplasm. Can show mild/ moderate thormobcytopenia); pseudothrombocytopenia
abnormal (prolonged) when decreased platelet
function and or decreased platelet numbers.
(false decreased in thrombocytes- PLT clumps, or too large
PLT
• REMEMBER w/ ITP! SEVERE THROMBOCYTOPENIA W/ NORMAL COAG PANEL (IT’S A PLATLET ISSUE- NOT COAG ISSUE)
o * when PLT go down, may only see a drop in PLT number, and the function can be fine. If you get a panel w/ low PLT and a MPV in middle high range and normal BMBT and PLT count is 15,000- think ITP, not a function problem.
What are 2 major causes of thrombocytosis?
• Increased production, increased distribution in plasma. Usually
asymptomatic w/ regard to increased platelet count
o Primary neoplastic production or 2ndary/reactive
thrombocytosis.
“ Associated w/ chronic inflam. Dz, Fe def. anemia,
chronic hemorrhage, IMHA, neoplasms (Rare)
“ Often in situations- rebound from thrombocytopenia,
post splenectomy response to some drugs,
excitement/exercise- splenic contraction
Acquired qualitative disorders:
Uremia, drugs, fibrin degradation products (inhibit PLT function), paraproteins)
Inherited causes ?
absence of glycoprotein receptors, absence/reduction in platelet
granules, signal transduction defects, von willebrand dz.
What is von willebrand dz?
No defect in platelets- defect in adhesion that binds PLT and cause platelet plug. – decrease platelet adhesion
• Platelet will float away and no plug will form w/ out vWF (need factor 8 to come along to allow plug as well)
What are the 2 forms of VWD?
• Quantitative deficiency (type 1 and 3)
o Type 1- mild dogs are sublicnial o Type 3- severe
• Qualitative abnormality type 2
• Vwf is carrier for factor VII! w/ type 3 may have factor VIII def.
o Mild- severe bleeding (exacerbated by Sx or trauma) ! signs decrease w/ age and successive pregnancies (doesn’t make much sense but it does)
• Platelet / coagulation panel w/ vWD. dx based on signalment, history , meds, other disorders:
o Normal platelet count, prolonged BMBT, PTT/ACT can be normal but can be prolonged if factor VIII is deficient ; can analyze for vWF concentration in plasma
balanced hemostasis?
Thrombus- increase procoagulation activity, decrease. fibrinolysis. Excessive thrombus—obstruction- hypoxia (pulmonary thromoboembolism)
• Hemorrhage- decrease procoag activity, decrease. PLT #, or function, excessive fibrinolysis! cant form thrombus! hemorrhage! ITP.
what is the average lifespan of a platelet?
3-5 days. 1/3 of platelet mass will reside in the spleen.
What do large giant platelets represent?
Increased platelet production- (macroplatelets- about same size of
RBC)
Life cycle?
Stem cell! megakaryoblast! megakaryocyte. (polyploidy nucleus) w/ abundant cytoplasm)
• Thrombopoeisis! megakaryocyte at the sinus! long proplatelet process extension the sinus lumen and breaks into individual platelets. Maturation time of megkaryoblast to PLT release! 4-5 days
What regulates thrombopoeisis?
Thrombopoeitin (TPO)! increase megakaryocyte production and
differentiation. Binds to PLTS normally. When there is a dec. # of PLT means increase in free plasma TPO which reacts with bone marrow. To increase #, size and ploidy of megakaryocyte and decrease maturation time. EPO- can cross stimulate megakarycotes
Function of PLT?
Increase metabolic activity, primary hemostasis, support 2ndary
hemostasis.
Steps in primary hemostasis?
3-5 mins. Forms hemostatic plug. PLT adhere to subendothelium, are activated (shape change) secrete granules and aggregate to form a PLT plug); adhere, activate, aggregate.
o adhesions! need vWF (binds to GP1b on PLT and bridges PLT and collagen. ADP, CA2+ and serotonin as well
o activation- shape change- allow for filopodia to increase surface area for 2ndary hemostasis (responds to thrombin). Secrete granules factor V and VIII, thromboxane A2, calcium to recruit more PLT, further activate PLT, facilitate coagulation, mediate vessel and repair PLT have neg charge on outer membrane surface- reverses when calcium is bound- allows for factors (that are negative) to then come and bind.
“ recruits more PLT, further PLT activation, facilitate coagulation, mediate vessel repair
o AggregatioN:What do the granule contents do (calcium, serotonin, ADP, vWF)?–> stimulate aggregation, irreversible, fibrinogen binds to activated PLTS and binds adjacent PLT. Final step in platelet plug formation CALCIUM REQURIED
o After- clot retraction! contract actinomysin filaments and allows for wound closure, vessel patency
How do you test PLT concentration in blood?
Collect in an EDTA tube (purple tube)- doesn’t disrupt morphology
and prevents clotting. And they are calcium absorbers-s o they wont activate the platelets make sure the stick in vein is even and not jagged and poking around. Put on blood smear or hematology analyzer- should show 7-10 PLT on 100x lens. Horses- 4-7 minimumPLT concentration morphology and size- look at blood smear or hem. analzyers
Bleeding time tests test platelet function
Bone marrow aspirate- tests production of bone marrow.
• HORSES PLT STAIN PALE
At what platelet count can you see spontaneous hemorrhage?
what can a hematology analyzer demonstrate?
Platelet morphology- MPV (mean platelet volume. – increase in MPV demonstrates thombopoeisis
What does a PLT bleeding test demonstrate?
• Ability of PLT to form a PLT plug. (does not test fibrin plug
formation)!
• Perform a buccal mucosal bleeding time (BMBT- dog1-5 min, cat 1- 3.5 min, horse/cattle- 8-10 mins) PERFORM ON LIP NOT GUM
• Can perform a cuticle bleeding time (toenail)! dog 2-8 min)
• Can also perform platelet function- test for adhesion, aggregation
or secretion- needs special equipment.
If you have a decrease in PLT and look at the bone marrow w/ no mature megkaryoblasts- what does that tell you?
Dz process in bone marrow- targeting platelets or neoplastic.
• If low in PLT- expect PLT secretion to increase and increase
megakaryocyte production
What are clinical features of thrombocytopenia?
Mucosal bleeding, petechial, ecchymosis, spontaneous hemorrhage, +/- hemorrhagic anemia. Clinical signs associated with primary dz. Dx the problem not the specific dz. Remember that thrombocytopenia is not a specific dz but a problem that contributes to it.
• Hemorrhage alone does not cause sig. thormbocytpenia unless acute sever hemorrhage (mild thrombocytopenia)
o Causes- loss, consumption (use of platelets in cascade, DIC, vasculitis, viral infection), destruction (ITP, modified live virus vaccine- 3-10 days post vx.-> will see platelet bleeding pattern- bleeding from mucous membranes and peteciation to ecchymosis ), decreased production (bone marrow hypoplasia, neopalisa, myelonecrosis or meylofibrosis – degree of thrombocytopenia depends on extent of bone marrow dz);, abnormal distribution (sequestration of PLT in large vascular beds- mild to moderate thrombocytopenia, splenomegaly, splenic torsioin, neoplasm. Can show mild/ moderate thormobcytopenia); pseudothrombocytopenia
abnormal (prolonged) when decreased platelet
function and or decreased platelet numbers.
(false decreased in thrombocytes- PLT clumps, or too large
PLT
• REMEMBER w/ ITP! SEVERE THROMBOCYTOPENIA W/ NORMAL COAG PANEL (IT’S A PLATLET ISSUE- NOT COAG ISSUE)
o * when PLT go down, may only see a drop in PLT number, and the function can be fine. If you get a panel w/ low PLT and a MPV in middle high range and normal BMBT and PLT count is 15,000- think ITP, not a function problem.
What are 2 major causes of thrombocytosis?
• Increased production, increased distribution in plasma. Usually
asymptomatic w/ regard to increased platelet count
o Primary neoplastic production or 2ndary/reactive
thrombocytosis.
“ Associated w/ chronic inflam. Dz, Fe def. anemia,
chronic hemorrhage, IMHA, neoplasms (Rare)
“ Often in situations- rebound from thrombocytopenia,
post splenectomy response to some drugs,
excitement/exercise- splenic contraction
Acquired qualitative disorders:
Uremia, drugs, fibrin degradation products (inhibit PLT function), paraproteins)
Inherited causes ?
absence of glycoprotein receptors, absence/reduction in platelet
granules, signal transduction defects, von willebrand dz.
What is von willebrand dz?
No defect in platelets- defect in adhesion that binds PLT and cause platelet plug. – decrease platelet adhesion
• Platelet will float away and no plug will form w/ out vWF (need factor 8 to come along to allow plug as well)
What are the 2 forms of VWD?
• Quantitative deficiency (type 1 and 3)
o Type 1- mild dogs are sublicnial o Type 3- severe
• Qualitative abnormality type 2
• Vwf is carrier for factor VII! w/ type 3 may have factor VIII def.
o Mild- severe bleeding (exacerbated by Sx or trauma) ! signs decrease w/ age and successive pregnancies (doesn’t make much sense but it does)
• Platelet / coagulation panel w/ vWD. dx based on signalment, history , meds, other disorders:
o Normal platelet count, prolonged BMBT, PTT/ACT can be normal but can be prolonged if factor VIII is deficient ; can analyze for vWF concentration in plasma
