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IHO Week 6 > Bleeding Disorders > Flashcards

Bleeding Disorders Flashcards

(57 cards)

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1
Q

Platelet bleeding

A

Superificial
Petechiae
Spontaneous

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2
Q

Factor bleeding

A

Deep (joints)
Trauma
Big Bleeds

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3
Q

Von Willebrand Disease - must knows

A

Most common hereditary bleeding disorder (NOT factor)
Autosomal dominant
vW factor decreased or abnormal
Variable severity

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4
Q

What is vWF

A

Huge multimeric protein made by megakaryocytes and endothelial cells
Glues platelets to subendothelium
Carries factor VIII

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5
Q

Type 1 vWF

A

Decreased vWF (70% of cases)

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6
Q

Type 2 vWF

A

Abnormal vWF (25% of cases)

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7
Q

Type 3 vWF

A

No vWF (5%)

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8
Q

Symptoms of vWF disease

A

Mucosal bleeding

Deep joint bleeding (severe cases)

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9
Q

Lab tests in vWF disease

A 
Bleeding time: prolonged
PTT: prolonged (corrects with mixing study)
INR: normal
vWF: level decreased (normal in type 2)
Platelet aggregation studies abnormal
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10
Q

What binds vWF?

A

GP Ib (membrane)

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11
Q

Treatment of vWF disease

A

DDAVP (raise VIII and vWF levels)
Cryoprecipitate (contains vWF and VIII)
Factor VIII

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12
Q

Hemophilia A is a ______ genetic disorder

A

X linked

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13
Q

Dads affected with hemophilia A

A

will have carrier daughters

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14
Q

Moms who are carriers of hemophilia A

A

Son may have disease, daugher may carry

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15
Q

Hemophilia A

A

Most common FACTOR deficiency

Factor VIII decreased

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16
Q

Symptoms of Hemophilia A

A

Severity depends on amount of VIII
Typical ‘factor’ bleeding (deep joint bleeding, prolonged bleeding after dental work)
Rarely - mucosal hemhorrhage

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17
Q

Lab tests in hemophilia A

A

INR, TT, Platelet count, bleeding time: NORMAL
PTT: prolonged (corrects with mixing)
Factor VIII assays: abnormal
DNA studies: abnormal

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18
Q

Treatment of Hemophilia A

A

DDAVP

Factor VIII

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19
Q

Hemophilia B

A

Factor IX deficiency
Less common than Hemophilia A
Same inheritance pattern (x linked)
Same clinical and laboratory findings

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20
Q

Factor XI deficiency

A

Bleeding only after trauma (rare)

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21
Q

Factor XIII deficiency

A

severe neonatal bleeding (no cross links, can kill you)

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22
Q

Hereditary platelet disorders (4)

A
  1. Bernard Soulier Syndrome
  2. Glanzmann Thrombasthenia
  3. Gray Platelet Syndrome
  4. Delta Granule Deficiency
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23
Q

Bernard Soulier Syndrome

Study These Flashcards
A

Abnormal Ib (binds vWF)
Abnormal adhesion
Big platelets
Severe Bleeding

24
Q

Glanzmann Thrombasthenia

Study These Flashcards
A

No IIb-IIIa (binds fibrinogen)
No aggregation
Severe bleeding

25
Gray Platelet syndrome
No a-granules - why gray Big, empty platelets Mild bleeding
26
Delta granule deficiency
No d-granules | Can be part of syndrome (Chediak-Higashi)
27
Acquired Bleeding disorders (2)
1. DIC | 2. Idiopathic Thrombocyopenic Purpura
28
Disseminated Intravascular Coagulation (DIC)
Lots of underlying disorders Something triggers coagulation, causing thrombosis Platelets and factors get used up, cause bleeding Microangiopathic hemolytic anemia
29
Causes of DIC
Dumpers and Rippers
30
Dumpers
OB complications Adenocarcinoma AML-3 (granules are pro coag)
31
Rippers
Bacterial sepsis Trauma Burns Vasculitis
32
What are the big 4 for DIC (hint.. MOST)
Malignancy Obstetric Complications Sepsis Trauma
33
Symptoms of DIC
Can be nsidious or fulminant Multisystem disease Thrombosis and or bleeding
34
Lab tests in DIC
INR, PTT, TT prolonged FDPs increased Fibrinogen decreased
35
Treatment of DIC
Treat underlying disorder | Support with blood products
36
Idiopathic Thrombocytopenic Purpura
Antiplatelet antibodies Acute vs chronic Diagnosis of exclusion Steroids or splenectomy
37
Pathogenesis of ITP
Autoantibodies to GP IIb-IIa or Ib Bind to platelets Macrophages eat platelets
38
Two kinds of ITP
Chronic or Acute
39
Chronic ITP
Adult women Primary or secondary Insidious - nosebleeds, easy bruising Danger - bleeding into brain
40
Acute ITP
Children Abrupt following illness Usually self limiting May become chronic
41
Lab tests in ITP
- Signs of platelet destruction : thrombocytopenia, normal/increased megakaryocytes, big platelets - INR/PTT normal - No specific diagnostic test
42
Thrombocytopenia
Caused by many things - aplastic anemia, bone marrow replacement, big speen, consumptive processes (DIC, TTP, HUS), drugs
43
Treatment of ITP
glucocorticoids splenectomy IV immunoglobulin
44
Thrombotic microangiopathies
All have thrombi, thrombocytopenia and MAHA Include TTP and HUS Hard to distinguish from TTP from HUS
45
in thrombotic microangiopathies something triggers ______
platelet aactivation
46
Thrombotic Thrombocytopenic Purpora
Pentad: MAHA, thrombocytopenia, renal failure, fever, neurologic defects
47
TTP deficiency
ADAMTS13 | Big vWF aren't cleaved, trap platelets
48
How do deal with TTP
plasmapheresis or plasma infusions
49
Brief pathogenesis of TTP
Just released vWF is unusually large (UL), causes vWF to aggregate. Usually ADAMTS13 cleaves into less active bits. TTP is deficient in ADAMTS13
50
Clinical findings of TTP
``` Hematuria, jaundice (MAHA) Bleeding, brusing (thrombocytopenia) Fever Decreased urine output (Renal Failure) Bizarre behavior (Neurological defects) ```
51
Treatment of TTP
Acquired: plasmapheresis Hereditary: Plasma infusions
52
Hemolytic Uremic Syndrome
MAHA and thrombocytopenia Epidemic (e coli) vs. non epidemic Toxin? damages epithelium Treat supportively
53
Pathogenesis of HUS - epidemic
E coli O157:H7 (raw hamburger) Makes nasty toxin Injures endothelial cells
54
Pathogenesis of HUS - non epiodemic
Defect in complement factor H | Inherited or acquired
55
Clinical findings in HUS - epidemic
Children and elderly Bloodly diarrhea, renal failure Fatal in 5% of cases
56
Clinical findings in HUS - non epidemic
Renal failure Relapsing remitting course Fatal in 50% of cases
57
Treatment of HUS
Supportive Care Dialysis Not antibiotics (increase toxin release)

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