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Clin Med III - Heme/Onc > Thrombocytopenia > Flashcards

Thrombocytopenia Flashcards

1
Q

What are thrombocytes and where are they produced?

A
  • Platelets
  • Small cell fragments w/o nucleus
  • Produced in BM
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2
Q

Avg lifespan of a platelet?

A

5-9 days

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3
Q

Where are reserve platelets stored?

A

Spleen

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4
Q

Where are old platelets destroyed?

A

Spleen

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5
Q

Normal platelet range

A

150-450,000

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6
Q

30,000 - 50,000 platelets may manifest as:

A

Purpura

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7
Q

10,000 - 30,000 platelets may cause:

A

Bleeding (w/minimal trauma)

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8
Q

Platelets less than 5,000 may cause:

A

Spontaneous bleeding

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9
Q

Define primary hemostasis

A
  • Occurs instantly after a blood vessel endothelium injury

- Platelet plug is formed

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10
Q

Define secondary hemostasis

A
  • Occurs simultaneously w/primary hemostasis
  • Exposure to TF to Factor 7 and other clotting factors
  • Fibrin strands to strengthen platelet plug
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11
Q

Define prothrombin time (PT) and what it tests

A
  • Time to clot in presence of tissue thromboplastin

- Tests EXTRINSIC and common pathways (factors 5, 7, 10, prothrombin, fibrinogen)

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12
Q

Define partial thromboplastin time (PTT) and what it tests

A
  • Time to clot in presence of kaolin (activates factor 12) and cephalin (substitute platelet phospholipid)
  • Tests INTRINSIC and common pathways (factors 5, 8, 9, 10, 11, 12, prothrombin, fibrinogen)
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13
Q

Define bleeding time and what it tests

A
  • Time required to stop bleeding from a standardized skin puncture
  • Tests primary hemostasis (platelet number and function)
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14
Q

General causes of thrombocytopenia

A
  • Decreased production (not enough platelets made in BM)
  • Increased destruction (breakdown of platelets in bloodstream, spleen or liver)
  • Med induced
  • Other
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15
Q

What conditions cause decreased production of platelets?

A
  • Aplastic anemia
  • Leukemia
  • Cirrhosis
  • Folate/B12 deficiency
  • Infections of BM
  • MDS
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16
Q

What conditions cause increased destruction of platelets?

A
  • ITP
  • TTP
  • DIC
  • HIT
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17
Q

Define idiopathic thrombocytopenic purpura (ITP)

A
  • Autoimmune
  • Antibodies against several platelet surface antigens (present in 60% of cases)
  • Results in destruction of platelets (thrombocytopenia)
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18
Q

Who is MC affected by ITP?

A
  • Children (50% of cases)
  • Adults are diagnosed 56-60 yo
  • In adults, females MC
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19
Q

How do adults with ITP typically present?

A

With a chronic condition (idiopathic, lasts longer than 6 months)

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20
Q

How do children with ITP typically present?

A

With an acute condition (usually follows an infection, spontaneous resolution within 6 months)

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21
Q

Pathophys of ITP

A

IgG autoantibodies attack platelet membrane glycoproteins and megakaryocytes (precursor platelets)

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22
Q

Clinical s/s of ITP

A
  • Petechiae, purpura, gingival bleeding
  • Isolated thrombocytopenia
  • NORMAL blood smear
23
Q

When is BM testing indicated in ITP workup?

A
  • Pts w/unexplained cytopenias
  • Pts over 60 yo
  • Pts who do not respond to therapy
24
Q

What is Evans syndrome?

A

ITP with co-existent autoimmune hemolytic anemia

25
Q

Treatment of ITP

A
  • Only if plt count is under 20-30,000 OR significant bleeding
  • Steroids, IVIG
  • Platelet transfusion is CONTRAINDICATED
26
Q

Describe thrombotic thrombocytopenic purpura (TTP)

A
  • Rare disorder of blood coagulation system

- Causes extensive microscopic clots to form in small blood vessels throughout the body

27
Q

Who is MC affected by TTP?

A

Females 3:2

AAs

28
Q

Etiology of TTP

A
  • Autoimmune (antibody that inhibits ADAMTS13 enzyme activity)
  • Secondary
  • Inherited (Upshaw-Schulman Syndrome)
29
Q

What is Upshaw-Schulman Syndrome?

A
  • Inherited type of TTP

- Deficiency of ADAMTS13

30
Q

Pathophys of TTP

A
  • Spontaneous aggregation of platelets, platelets are consumed (decreasing platelet count)
  • Circulating platelet-vWF complexes are unopposed by ADAMTS13 resulting in microthrombi
  • Microthrombi cause obstruction and shearing/fragments of RBCs (schistocytes)
31
Q

What is the main defect of autoimmune TTP?

A

Severely decreased ADAMTS13 activity

32
Q

What is the main defect of secondary TTP?

A
  • Poorly understood
  • Develop TTP in situations w/increased vWF (e.g. infection)
  • ADAMTS13 activity is generally normal
33
Q

Activity of ADAMTS13 in autoimmune TTP vs. secondary TTP?

A
  • Decreased activity in autoimmune

- Normal activity in secondary

34
Q

What is ADAMTS13?

A
  • Metalloproteinase responsible for breakdown of UL-vWF

- Without proper cleavage of vWF by ADAMTS13, coagulation occurs at a higher rate (e.g. TTP)

35
Q

Clinical presentation of TTP?

A

Pentad

  1. Thrombocytopenia
  2. Microangiopathic hemolytic anemia
  3. Neuro symptoms
  4. Renal insufficiency
  5. Fever
36
Q

What is the pentad?

A
  • Clinical presentation of both TTP and Hemolytic Uremic Syndrome (HUS)
  • Thrombocytopenia, microangiopathic hemolytic anemia, neuro symptoms, renal failure, fever
37
Q

When a patient presents with the pentad s/s, how to tell TTP vs. HUS?

A
  • If renal failure dominates, it is usually called HUS

- MC in children

38
Q

What is the MC cause of acquired renal failure in childhood?

A

HUS

39
Q

What are TTP and HUS known as?

A

Systemic thrombotic microangiopathy (TMA) - leads to thrombotic events, organ damage, death

40
Q

Lab findings of TTP

A
  • Microangiopathic hemolytic anemia with thrombocytopenia

- Schistocytes on blood smear

41
Q

Treatment of autoimmune TTP

A

Plasmapheresis and steroids

42
Q

Treatment of refractory/relapsing TTP

A
  • Immunosuppressive and steroids

- Possible splenectomy?

43
Q

Treatment of hereditary TTP (Upshaw-Schluman Syndrome)

A

Prophylactic plasma every 2-3 wks (maintains adequate levels of functioning ADAMTS13)

44
Q

Tranfusion in TTP?

A

Transfusion is CONTRAINDICATED (fuels coagulopathy)

45
Q

Describe disseminated intravascular coagulation (DIC)

A
  • Acquired clinical syndrome
  • Widespread activation of coagulation and fibrinolysis
  • Thrombi formation and bleeding
46
Q

Etiology of DIC

A
  • Severe trauma
  • Sepsis
  • Malignancy
  • Pregnancy complications
  • Liver disease
47
Q

Pathophys of DIC

A
  • Release of TF triggers over clotting within the body

- This disrupts clotting elsewhere in the body causing abnormal bleeding

48
Q

Clinical presentation of DIC

A
  • Bleeding
  • Renal and hepatic dysfunction
  • Respiratory dysfunction
  • Shock
49
Q

Lab findings of DIC

A
  • Thrombocytopenia
  • Reduced fibrinogen
  • Prolonged PT/bleeding time
  • Elevated D-dimer
50
Q

Treatment of DIC

A
  • Treat underlying condition
  • Heparin
  • FFP (temporary/may result in thrombosis)
  • Platelet replacement if under 5-10,000 and hemorrhaging (temporary/may result in thrombosis)
51
Q

Clinical presentation of HIT

A
  • 5-14 days after starting Heparin
  • Thrombocytopenia
  • Thrombosis
52
Q

Pathophys of HIT

A
  • Antibodies against heparin are formed when it is bound to platelet factor 4 (PF4)
  • Results in platelet activation and formation of clots, dropping platelet count
53
Q

Treatment of HIT

A
  • STOP heparin, replace with DTI therapy

- AVOID platelet transfusion

Clin Med III - Heme/Onc (8 decks)

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