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Hematology > Bleeding, Thrombic and Fibrinolytic Disorders > Flashcards

Bleeding, Thrombic and Fibrinolytic Disorders Flashcards

1
Q

Immune Thrombocytopenia Purpura (ITP)

A

Antibodies bind to platelets resulting in their premature destruction.
Megakaryocytes may be injured as well - decreased production
Reduced TPO levels

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2
Q

ITP Causes

A

Commonly occurs in childhood
Abrupt onset after viral infxn
Medications
Autoimmune

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3
Q

ITP S/S

A 
Blood blisters in mouth
Petichiae, purpura
spontaneous bruising
nosebleeds
gingival bleeding
retinal hemorrhage
menaggerhea
Menela, hematuria
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4
Q

ITP Lab Findings

A 
Thrombocytopenia
Normal RBC morphology
Prolonged bleeding time
\+/- anemia
PT/PTT normal
Normal or increased megakaryocytes
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5
Q

ITP Tx

A

Prednisolone
IVIG
Platelet transfusion (temporary)
Dexamethasone

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6
Q

Thrombotic Thrombocytopenia Purpura (TTP)

A

90% untreated mortality
Antibodies against ADAMTS-13 which cleaves clots
Extensive platelet aggregation and fibrin bridging
RBC sheering leads to destruction

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7
Q

TTP lab findings

A

Thrombocytopenia

Hemolytic anemia

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8
Q

TTP Causes

A

Generally occurs in adults
Primary: autoimmune
Secondary: Cancer, BMT, Pregnancy, Meds, HIV

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9
Q

Which organs are damage from TTP?

A

Kidneys and Brain

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10
Q

5 Main characterictics of TTP?

A 
Thrombocytopenia
MIcroangiopathic hemolytic anemia
Neurologic symptoms
Kidney failure
Fever (75%)
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11
Q

TTP SYmptoms

A

Malaise
Diarrhea
Thrombocytopenia, bruising, bleeding
Organ damage

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12
Q

TTP Lab Findings

A

Microangiopathic hemolytic anemia
Elevated D.Bili
Decreased serum haptoglobin
Elevated LDH

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13
Q

TTP Tx

A

Plasma exchange
Early dx and tx
90% untreated mortality

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14
Q

Hemolytic Uremic Syndrome

A

Most commonly secondary to E. Coli but may be caused by others
Caused by endothelial damage secondary to bacterial toxins
Inflammation, leukocyte activation, platelet activation, thromboses, RBC’s destroyed

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15
Q

Uremia = ?

A

Kidney failure

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16
Q

HUS S/S

A 
Bloody diarrhea
Abdominal pain
Decreased urine output
Hematuria
Renal Faiure
HTN
Neurologic changes
Edema
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17
Q

HUS Tx

A

Transfuse RBC’s and platelets

Dialysis if uremia

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18
Q

3 signs of HUS?

A

Microangiopathic hemolytic anemia
Acute kidney injury/renal failure
Thrombocytopenia

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19
Q

Who is HUS more common in?

A

Children.

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20
Q

Henoch-Schonelin Purpura

A 
AKA IgA Vasculitis
characterized by::
Palpable purpura
Arthritis, arthralgias
Abd pain
Renal disease
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21
Q

Henoch-Schonelin Purpura Facts

A

90% of cases occur in children 3 - 15 years old
Can be triggered by streptococcal URI
Should not have thrombocytopenia or coagulopathy

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22
Q

Henoch-Schonelin Purpura Tx

A

NSAIDS and Glucocorticoids
Late-onset renal failure. Follow up needed
Biopsy of skin lesions, CBC, CMP, urinalysis

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23
Q

Hemophilia

A

X-linked recessive trait
1:5,000 males
Females are carriers

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24
Q

Hemophilia A

A

Factor VIII Deficiency
80% of patients
2/3 have severe disease

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25
Q

Hemophilia B

A

Factor IX Deficiency

Also known as christmas disease

26
Q

Hemophilia C

A

Factor XI Deficiency
Rare
1:1,000,000

27
Q

Bleeding sites in hemophilia

A

Spontaneous hemarthrosis
Risk of intracerebral hemorrhage
Joints, skin, muscle, GU, GI

28
Q

Hemophillic Arthropathy

A

Arthritis causes by bleeding into the joints

29
Q

Hemophilia Tx

A 
Lifelong replacement of deficient clotting factor
Usually 3 times per week
Avoid Aspirin
Cryoprecipitate works
DDAVP
30
Q

Hemophilia Dx

A

Prolonged PTT
PT, bleeding time, platelets are normal
Dx is confirmed by decrease in factor VIII IX or Xi

31
Q

von Willebrand DIsease factor

A

Binds platelets to form initial platelet plug

Binds Factor VIII to prolong its half life

32
Q

von WIllebrand Disease (vWD)

A

Autosomal dominant affecting both sexes
Most common inherited bleeding disorder
Type 1: 75 - 80% of patients
They don’t have enough

33
Q

vWD Symptoms

A

Easy bruising, skin bleeding, prolonged bleeding, bleeding from mucosal surfaces
Nosebleeds > 10 mins in childhood
Lifelong easy bruising
Heavy menstruation

34
Q

vWD lab fndings

A

Plasma vDW antigen
Factor VIII activity
PT normal
PTT normal or prolonged

35
Q

vWD Tx

A

Treat symptomatically
DDAVP
Avoid aspirin

36
Q

Disseminated Intravascular Coagulation (DIC)

A

Simultaneous thrombosis and hemorrhage
Massive release of tissue factor
Tissue factor sets coag system in place
Coag occurs
Clotting factors and inhibitors are consumed
clots trap circulation leading to ischemia

37
Q

DIC activates?

A

The complement and kinin systems which leads to shock.

38
Q

Causes of DIC

A

MANY

Cancer, Obstetric complications, Sepsis, Infxn, Massive tissue injury (trauma, burns), Snake bites

39
Q

DIC summary

A

Massive tissue release causes a massive release of clotting factors and inhibitors, these are all used up so clots roam freely and bleeding does not stop. This causes simultaneous thrombosis and hemorrhage and multi-system, failure.

40
Q

DIC S/S

A 
Thrombosis and hemorrhage
Petechiae, purpura, gangrene
Renal, liver failure
Acute illness
Slow onset in cancer patients
41
Q

DIC lab findings

A

Thrombocytopenia
Prolonged PT and PTT
Low Fibrinogen
Schistocytes

42
Q

DIC Tx

A

Underlying cause
Anticoagulants to prevent imminent death
Platelets < 50k = platelets or coag factor
FFP or cryo to keep fibro > 100 if significantly elevated PT/INR

43
Q

Things that lead to hypercoagulable states?

A 
Atherosclerosis
DM
Tobacco use
Cancers
Elevated platelets
44
Q

Conditions that accelerate clotting

A 
Pregnancy
OCP
Postsurgical state
Malignancy
Hereditary clotting disorders
45
Q

Other abnormal clotting risk factors

A

Stasis/immobility
Low cardiac output
Obesity
Sleep apnea

46
Q

Protein C deficiency

A

Protein C inactivates factors V and VIII thereby inhibiting coagulation.
A deficiency leads to prolonged action of factors V and VIII.

47
Q

Protein C S/S

A 
Nothing recognized until clots form
Thrombosis
DVT
Pulmonary embolism
Thromboplebitis
48
Q

Protein C work up

A 
Protein C
PTT, PT
Thrombin time
Bleeding time
Hereditary history
49
Q

Protein C Tx

A

Anticoagulants if high risk (surgery, hospitalization)

Chronic anticoagulation of hx of thrombosis

50
Q

Protein S deficiency

A

Protein S is needed for proper fxn of protein C.
S/S and Tx are the SAME
BOOOOOOM!!!!!!!!!!!!!

51
Q

Antithrombin III Deficiency (A3D)

A 
Hereditary disorder that is very serious
Usually autosomal dominant
Recurrent venous thrombosis, PE, repetitive miscarriage
60% have thrombotic episodes.
Peak age of onset is 15 - 35 years old.
52
Q

Antithrombin is a major inhibitor of factors ____ and ___.

A

X and IX
Without this, you have an increased tendency to form clots.
50% reduction = clots.

53
Q

A3D W/U

A

Antithrombin-heparin cofactor assay**

Standard coag tests should be normal

54
Q

A3D Tx?!?

A

Same as Protein C and S Disorders!!!!

BOOM BABBY!!!!! SHITCHEA

55
Q

Factor V Leiden

A

Most common genetic disorder to cause DVT.
5% of general population
Venous blood is more likely to clot
Lack of factor V leiden, works with protein C
Same symptoms as protein C.

56
Q

Factor V Leiden Tx.

A

Same as all the others. Simply stunning. It must be my birthday.

57
Q

Antiphospholipid antibody

A

Autoimmune hypercoagulable state caused by said antibodies.
Lead to arterial and venous clots
Pregnancy complications
End organ damage

58
Q

Types of antiphospholipid antibodies

A

Lupus anticoagulant
Anti-cardiolipin antibody
Anti-beta2 - glycoprotein-I

59
Q

Antiphospholipid Dx

A

Presence of antibodies mentioned in previous slide PLUS a history of thrombosis

60
Q

Antiphospholipid Tx

A

aspirin, warfarin

Hematology (14 decks)

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