IHO Week 6 (EH) > Bleeding Disorders > Flashcards

Bleeding Disorders Flashcards

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1
Q

Clinical features platelet bleeding

A

Superficial (skin)
Petechiae (bigger areas = purpura)
Spontaneous

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2
Q

Clinical features factor bleeding

A

Deep (joints)
Big bleeds
Trauma

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3
Q

Von Willebrand Disease TYMK

A

Most common hereditary bleeding disorder
Autosomal dominant
vW factor decreased (or abnormal)
Variable severity

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4
Q

most common hereditary bleeding disorder

A

VW disease

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5
Q

most common factor disorder

A

hemophilia (VW is not considered a factor disorder)

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6
Q

inheritance VWD

A

Autosomal dominant

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7
Q

von willebrand factor

A

Huge multimeric protein

Decreased or abnormal in vW disease

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8
Q

von willebrand factor function

A

Glues platelets to subendothelium

Carries factor VIII

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9
Q

von willebrand factor made by

A

Made by megs and endothelial cells

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10
Q

von willebrand disease is a platelet/factor disorder

A

platelet - but if really bad, because carries factor VIII, can look like a factor disorder as well

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11
Q

Types of vW disease

A 
Type 1 (70%): Decreased vWF
Type 2 (25%): abnormal vWF
Type3 (5%): no vWF
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12
Q

symptoms of vW disease

A

Mucosal bleeding in most patients

Deep joint bleeding in severe cases

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13
Q

Lab Tests in Von Willebrand Disease

A 
Bleeding time: prolonged
PTT: prolonged (severe) (“corrects” with mixing study) 
INR: normal
vWF level decreased (normal in type 2)
Platelet aggregation studies abnormal
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14
Q

What binds to vWF

A

GP Ib on membrane of platelet (glycoprotein)

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15
Q

what doesn’t wF disease work with in platelet aggregation test?

A

Ristocetin

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16
Q

treatment of vW disease

A

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

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17
Q

Hemophilia A TYMK

A 
Most common factor deficiency
X-linked recessive in most cases 
    (30% are random mutations)
Factor VIII level decreased
Variable amount of “factor” bleeding
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18
Q

Most common factor deficiency

A

Hem A

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19
Q

Hem A inheritance

A

X-linked recessive

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20
Q

what factor is decreased in Hem a

A

Factor VIII

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21
Q

Symptoms Hem A

A 
Severity depends on amount of VIII
Typical “factor” bleeding
deep joint bleeding
prolonged bleeding after dental work
Rarely, mucosal hemorrhage
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22
Q

Lab Tests in Hem A

A

INR, TT, platelet count, bleeding time: normal (these are platelet issues, hem is a fibrin issue)
PTT: prolonged (“corrects” with mixing study)
Factor VIII assays: abnormal
DNA studies: abnormal

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23
Q

Treatment Hem A

A

DDAVP (release stores of vWF and VIII)

Factor VIII

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24
Q

Hem B TYMK

A

Factor IX level decreased
Much less common than hemophilia A
Same inheritance pattern
Same clinical and laboratory findings

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25
what factor decreased in Hem B
Factor IX
26
Inheritance pattern Hem B
x-linked recessive (30% lab findings)
27
clinical findings Hem B
``` Severity depends on amount of VIII Typical “factor” bleeding deep joint bleeding prolonged bleeding after dental work Rarely, mucosal hemorrhage ```
28
lab tests Hem B
INR, TT, platelet count, bleeding time: normal (these are platelet issues, hem is a fibrin issue) PTT: prolonged (“corrects” with mixing study) Factor VIII assays: abnormal DNA studies: abnormal
29
XI deficiency
bleeding only after trauma
30
XIII deficiency
severe neonatal bleeding
31
Bernard-Soulier Syndrome
Abnormal Ib (binds vWF) Abnormal adhesion Big platelets Severe bleeding
32
Glanzmann Thrombasthenia
No IIb-IIIa (what binds fibrinogen) No aggregation Severe bleeding
33
Gray Platelet Syndrome
No alpha granules Big, empty platelets Mild bleeding
34
Delta granule deficiency
No delta granules | Can be part of syndrome (e.g., Chediak-Higashi)
35
alpha granules
fibrinogen, vWF
36
delta granules
serotonin, ADP, ca2+
37
DIC TYMK
Lots of underlying disorders Something triggers coagulation, causing thrombosis Platelets and factors get used up, causing bleeding Microangiopathic hemolytic anemia
38
Causes of DIC can be separated into
dumpers (into vascular system to set off cascade) | rippers (rip up endothelium)
39
DIC causes: Dumpers
Obstetric complications Adenocarcinoma Acute promyelocytic leukemia
40
DIC causes: Rippers
Bacterial sepsis Trauma Burns Vasculitis
41
Causes of DIC to remember
``` Malignancy OB complications Sepsis Trauma (MOST) ```
42
Symptoms of DIC
Insidious or fulminant Multi-system disease Thrombosis and/or bleeding
43
Lab Tests in DIC
INR, PTT, TT prolonged FDPs: increased Fibrinogen: decreased
44
Treatment of DIC
Treat underlying disorder | Support with blood products
45
Idiopathic thrombocytopenia Purpura TYMK
``` Antiplatelet antibodies Acute vs. chronic Diagnosis of exclusion Steroids or splenectomy Remember how different this is from DIC ```
46
Pathogenesis of ITP
Autoantibodies to platelets = GP IIb-IIIa or Ib Bind to platelets (yummy!) Splenic macrophages eat platelets
47
two kinds of itp
chronic | acute
48
chronic ITP
Adult women Primary or secondary Insidious: nosebleeds, easy bruising Danger: bleeding into brain
49
acute ITP
Children Abrupt; follows viral illness Usually self-limiting May become chronic
50
Lab tests ITP
``` Signs of platelet destruction: - thrombocytopenia - normal/increased megakaryocytes - big platelets INR/PTT normal No specific (ab) diagnostic test for ITP ```
51
Other causes of thrombocytopenia
``` Aplastic anemia Bone marrow replacement Big spleen Consumptive processes (DIC, TTP, HUS) Drugs ```
52
tx of ITP
Glucocorticoids Splenectomy Intravenous immunoglobulin
53
Thrombotic microangiopathies all have
thrombi, thrombocytopenia, and MAH
54
Thrombotic microangiopathies include
TTP and HUS (can be hard to distinguish) | Different from DIC
55
thrombotic microangiopathies = something triggers _______
platelet activation
56
Thrombotic thrombocytopenic purpura TYMK
Pentad: MAHA, thrombocytopenia, fever, neurologic defects, renal failure Deficiency of ADAMTS13 Big vWF multimers trap platelets Plasmapheresis or plasma infusions
57
pentad TTP
MAHA, thrombocytopenia, fever, neurologic defects, renal failure
58
TTP deficiency in
ADAMTS13
59
Pathogenesis TTP
Just-released vWF is unusually large (UL) UL vWF causes platelet aggregation ADAMTS13 cleaves UL vWF into less active bits! TTP is due to ADAMTS13 deficiency
60
Clinical findings in TTP
``` Hematuria, jaundice (MAHA) Bleeding, bruising (thrombocytopenia) Fever Bizarre behavior (neurologic deficits) Decreased urine output (renal failure) ```
61
Treatment of TTP
Acquired TTP: plasmapheresis | Hereditary TTP: plasma infusions
62
Hemolytic Uremic Syndrome TYMK
MAHA and thrombocytopenia Epidemic (E. coli) vs. non-epidemic Toxin (or ?) damages endothelium Treat supportively
63
Pathogenesis of HUS has 2 main causes
Epidemic | Non-epidemic
64
HUS epidemic pathogenesis
E. coli O157:H7 (raw hamburger) Makes nasty toxin (shiga or shiga-like) Injures endothelial cells
65
HUS non-epidemic pathogenesis
Defect in complement factor H (protective) Inherited or acquired How does this activate platelets?
66
HUS epidemic associated with usually
E. coli O157:H7
67
Clinical findings in HUS epidemic
Children, elderly Bloody diarrhea, then renal failure Dont give Abx (expose toxin) Fatal in 5% of cases
68
Clinical findings in HUS non-epidemic
Renal failure Relapsing-remitting course Fatal in 50% of cases
69
Treatment HUS
Supportive care Dialysis NOT antibiotics (may increase toxin release!)
IHO Week 6 (EH)
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