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Coag > Platelets > Flashcards

Platelets Flashcards

1
Q

Quantitative platelet disorders

A

Thrombocytopenia and thrombocytosis

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2
Q

Qualitative platelet disorders

A

Abnormal platelet function

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3
Q

Thrombocytopenia

A

A disorder in which there is a relative decrease of platelets present in blood, normal count is 150,000 to 450,000 platelets per microliter

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4
Q

Clinical features of thrombocytopenia

A

Easy bruising, petechiae, prolonged bleeding, bleeding from gums or nose, blood in urine and stools, heavy menstrual flows, fatigue, enlarged spleen, jaundice

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5
Q

Lab tests for abnormal bleeding

A

Platelet count, PT, APPT, bleeding test

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6
Q

Thrombocytopenia causes

A

Decreased production, increased destruction, sequestration, pseudothrombocytopenia, dilutional thrombocytopenia

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7
Q

Pseudothrombocytopenia

A

Artifactually low platelet count due to in vitro clumping of platelets, usually caused by antibodies that bind platelets only in presence of EDTA, seen in healthy individuals and in many disease states

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8
Q

Diagnosis of pseduothrombocytopenia

A

Marked fluctuations in platelet count, thrombocytopenia disproportionate to symptoms, clumped platelets on smear, Platelet satellites, abnormal platelet/leukocyte histograms, platelet count varies with different anticoagulants

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9
Q

Platelet satellitism

A

IgG antibody coats platelets, platelets rosette around segs, bands, and sometimes monocytes, if huddled around WBCs, not counted by automation, causing false decrease

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10
Q

Dilutional thrombocytopenia

A

Large quantities of PRBC transfusion to treat massive hemorrhage can lead to dilution TP, due to absence of viable platelets in packed RBCs, usually platelet counts in patients receiving 15 to 20 units of PRBCs in 24 hours in 50k to 100k, can be prevented by giving platelets

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11
Q

Decreased platelet production

A

Marrow failure, B-12, folate or iron deficiency, viral infection, drugs, amegakaryocytic thrombocytopenia, cyclic thrombocytopenia, inherited thrombocytopenia

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12
Q

Thrombocytopenia and ppregnancy

A

Benign thrombocytopenia of pregnancy, occurs in 5% of term pregnancies, accounts for ~ 75% of cases of thrombocytopenia, asymptomatic, mild, occurs late in gestation, microangiopathy, ITP

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13
Q

Increased platelet consumption

A

Immune destruction, non-immune destruction

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14
Q

Non-immune mechanisms of destruction

A

Disseminated intravascular coagulation, thrombotic thrombocytopenic purpura, hemolytic uremic syndrome, mechanical destruction by artificial heart valves

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15
Q

Immune platelet destruction

A

Autoimmune (ITP), drug-induced (heparin, Quinine), Immune complex (infection), Alloimmune (post-transfusion purpura, neonatal purpura)

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16
Q

Post-transfusion purpura

A

caused by re-exposure to foreign platelet antigen via blood transfusion, almost all cases in multiparous women, antibodies cause destruction of patient’s own platelets by uncertain mechanism, typically presents as sudden onset of severe thrombocytopenia 5-7 days after transfusion

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17
Q

Neonatal alloimmune thrombocytopenia

A

Maternal alloantibodies against a platelet antigen (HPA 1a and 1b), symptoms appear at or shortly after birth and are self limited, rarely high mortality due to CNS bleeding

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18
Q

Thrombocytopenia and infection

A

Immune complex-mediated platelet destruction, activation of coag cascade, vascular/endothelial cell damage, damage to platelet membrane components by bacterial enzymes, decreased platelet production, mixed production defect/immune consumption

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19
Q

ITP childhood form

A

most < 10 years old), may follow viral infection or vaccination, peak incidence in fall and winter, ~50% receive some treatment, >75% in remission within 6 months

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20
Q

ITP adult form

A

No prodrome, chronic, recurrences common, spontaneous remission rate ~5%

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21
Q

ITP adult apidemiology

A

1-10/100,000, slightly more common in women, about 40% have an associated disorder

22
Q

ITP peak age

A

Children: 2-4 years
Adults: 20-40 years

23
Q

ITP platelet count

A

Acute: <20 x 10^9/L
Chronic: 30-80 x 10^9/L

24
Q

ITP Onset

A

Acute: Abrupt
Chronic: Insidious

25
Q

ITP antecedent infection

A

Acute: Common - 1-3 weeks
Chronic: Unusual

26
Q

ITP spontaneous remission

A

Acute: ~93%
Chronic: Rare, course of disease fluctuates

27
Q

ITP therapy

A

Acute: corticosteroids, Anti-D, IVIg
Chronic: Corticosteroids, splenectomy

28
Q

ITP management in children

A

Platelets > 20-30K, no bleeding = no Rx
Platelets <10K or <20K with significant bleeding = IVIg or corticosteroids
Splenectomy reserved from chronic ITP or refractory disease with life-threatening bleeding

29
Q

ITP in pregnancy

A

Mild cases are indistinguishable from gestational thrombocytopenia, rule out eclampsia, treatment if IVIg, splenectomy for severe, refractory disease, potential for neonatal thrombocytopenia

30
Q

Thrombotic microangiopathies

A

Presence of hemolytic anemia, low platelets, and organ damage due to formation of microscopic blood clots in capillaries and small arteries

31
Q

Thrombotic microangiopathies causes

A

infection, medications, connective tissue diseases, cancer, vasculitis, pregnancy, malignant hypertension, organ transplant, and metabolic disorders

32
Q

Thrombotic thrombocytopenic purpura presentation

A

abdominal pain, nausea, vomiting, weakness, 1/2 will have neurologic abnormalities

33
Q

The pentad for TTP

A

Microangiopathic hemolytic anemia, thrombocytopenia often with purpura, acute renal insufficiency, neurologic abnormalities, fever

34
Q

Causes of TTP

A

Idiopathic, drug-associated, autoimmune disease, infection, pregnancy/postpartum, bloody diarrhea prodrome, hematopoietic cell transplantation

35
Q

ADAMTS13 deficiency

A

VWF-cleaving protease, normally cleaves long VWF multimers secreted by endothelial cells, without ADAMTS13, long stick VWF multimers accumulate, react with platelets and cause formation of disseminated platelet thrombi

36
Q

Testing for ADAMTS13 deficiency

A

Assay techniques, severe deficiency predicts an increased rick of relapse

37
Q

Testing for ADAMTS13 deficiency

A

Assay techniques, severe deficiency predicts an increased risk of relapse

38
Q

HUS symptoms

A

Diarrhea, vomiting, urine output reduction, neurologic symptoms, typically follows GI infection

39
Q

Disseminated intravascular coagulation (DIC) causes

A

Excess tissue factor and endothelial damage, activation of fibrinolysis, other procoagulant or profibrinolytic substances

40
Q

Complications of DIC

A

bleeding, thrombosis, tissue necrosis

41
Q

Causes of bleeding in DIC

A

Clotting factor consumption, high levels of FDP, endothelial damage, increased fibrinolytic activity

42
Q

Thrombosis in DIC

A

Large vessel thrombosis is uncommon, more common in chronic DIC, clots may form around intravascular catheters

43
Q

Contributing factors of tissue necrosis and DIC

A

intravascular fibrin, endothelial damage, downregulated fibrinolysis, hypotension, pressor administration, acquired protein C deficiency

44
Q

Protein C

A

Physiological anticoagulant, Vitamin K dependent, destroys factors Va and VIIIa, activated by thrombin bound to endothelium, protective effect on endothelium, severe deficiency of protein C can cause tissue necrosis

45
Q

Protein C

A

Physiological anticoagulant, Vitamin K dependent, destroys factors Va and VIIIa, activated by thrombin bound to endothelium, protective effect on endothelium, severe deficiency of protein C can cause tissue necrosis

46
Q

DIC summary

A

Excess tissue factor + flowing blood = DIC, inflammatory cytokines set the stage for DIC and contribute to tissue damage, excessive fibrinolysis associated with higher bleeding risk, acquired protein C deficiency associated with high risk of tissue necrosis/purpura

46
Q

DIC summary

A

Excess tissue factor + flowing blood = DIC, inflammatory cytokines set the stage for DIC and contribute to tissue damage, excessive fibrinolysis associated with higher bleeding risk, acquired protein C deficiency associated with high risk of tissue necrosis.purpura

47
Q

Diagnosis of DIC

A

Platelet count, increased fibrinogen degradation products

48
Q

Thrombocytosis cause essential

A

primary, other myeloproliferative disorders

49
Q

Thrombocytosis cause reactive

A

Secondary, inflammation, surgery, hyposplenism, asplenia, hemorrhage and/or iron deficiency

50
Q

Criteria for essential thrombocytosis

A

Platelet > 450K, megakaryocytic proliferation with large, mature morphology and with little granulocytic or erythroid expansion, not meeting other myeloid criteria, demonstration of JAK2V617F or other clonal marker or lack of evidence of a secondary

Coag (3 decks)

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