Bleeding

Hemorrhagic Diathesis

Causes:

Increased fragility of

vessels

Platelet deficiency or

dysfunction

Derangement of

coagulation

Vessel Wall Abnormalities

Common but bleeding is LESS

Serious

Normal Coagulation test

1. Microbial damage to

Microvasculature or DIC

2. Scurvy – Impaired formation of

collagen needed for vessel wall

support

3. Drugs – immune complex deposits in vessel wall

4. Hemoch-Scheonlein purpura –unknown systemic

hypersensitivity diseaseinvolve vessels throughout the body & glomerular mesangium

5. Amyloid Infiltration of blood vessels – weakens the wall

Vessel Wall Abnormalities

R/T THROMBOCYTOPENIA

Decrease production

Aplastic anemia

Leukemias

Megalobalstic anemia

Decrease platelet survival

Immune – mediated

Non-immune – mechanical

Sequestration – seen in marked

splenomegaly

Dilutional – blood stored > 24hours has

less viable platelets

R/T THROMBOCYTOPENIA

Idiopathic Immune

Thrombocytopenic

Purpura ( Autoimmune )

1. Acute

Self-limited Hgic diseaseResolve w/in 6mos.

Children after Viral infxn 2 week

later Sudden petechiae,

purpura

Risk for cerebral bleed

Severe cases Tx w/

corticosteroids

2. Chronic

Adults women < 40y/o

Associated withCollagen Vascular Disease

CLL

HIV

Repeated episodes of Bleeding

Tx Steroids. IgG, Splenectomy in

severe cases

Idiopathic Immune

Thrombocytopenic

Purpura ( Autoimmune )

Deposition of Ig

fragments in

Amyloidosis

Thrombotic Microangipathies

I. Thrombotic Thrombocytopenic

Purpura1. Fever

2. Thrombocytopenia

3. Microangioapthic hemolytic anemia

4. Transient Neurological damage

5. Renal Failure

Deficiency of ADAMTS 13 enzyme

Results to accumulation of VHMW vWF

promote widesopread platelet

Microaggregation

II. Hemolytic –Uremic Syndrome1. Microangiopathic Hemolytic anemia

2. Thrombocytopenia

3. Prominence of renal failure

4. No Neurological damage

Hx of Enteric infection E. coli

Release of Shiga –like toxin Absorbed in

GIT Binds and Damage endothelial cells in

Glomerulus & other sites Platelet Activation

& Aggregation

Thrombotic Microangipathies

Widespread formation of hyaline

thrombi in microcircualtion

Platelet consumption & Intravascular

thrombi

Microangiopathic hemolytic anemia

Multiple Organ failure

Activation of coagualtion cascades is

NOT OF PRIMARY IMPORTANCE

PT/PTT – usually Normal

Thrombotic Microangipathies

Plasmin Act.

Proteolysis of

clotting facotrs