1. Thrombocytopenia History:
PMHx: Drug, EtOH, cancer, hypothyroidism and autoimmune disease
Causes:
Marrow Hypoplasia Idiopathic Investigations:
disorders Drug-induced: cytotoxics, FBC
antimetabolites, thiazides PBF
CT disease – a/w HypoT4 – do TFT LFT
Infiltration Leukaemia U/S HBS – for splenomegaly & liver cirrhosis
Myeloma Bone marrow biopsy - ↑ or normal megakaryocytes in ITP
Carcinoma Hepatitis B serology
Myelofibrosis ANA, dsDNA
Osteopetrosis
B12 / Folate deficiency – a/w alcoholism Rx:
↑ pltlet DIVC – usually secondary to an infection Treat underlying condition
consumption ITP Pltlet transfusion if <10 X 109/L, persistent bleeding or life threatening
TTP bleeds (eg GI hemorrhage)
Viral infections eg EBV, HIV ± splenectomy for hyperspenism—vaccinate pt first
Bacterial infections: eg Gram – septicaemia
Hypersplenism Lymphomas
Liver disease – commonly caused by alcohol or Hep
B. Causes portal hypertension resulting in
hypersplenism, and ↓ production of thrombopoeitin
which ↓ pltlet production in turn
* exclude medications as a cause of bruising – aspirin, antipltlets, warfarin,
NSAIDs, sulphur drugs, anti-malaria
Features:
Spontaneous bleeding – when platelet < 30 X 109/L
Purpura / bruising / petechiae
Oral (gums) / nasal (epistaxis) / GI / GU bleeding (menorrhagia)
Optic fundal hemorrhage – in severe thrombocytopenia; may lead to
fatal intracranial bleed
**need to ddx from clotting factor d/o: haemarthrosis, previous h/o
bleeding tendencies and probs during op (is it new acquired prob or
congenital?)
Digitally signed by DR WANA HLA SHWE
DN: cn=DR WANA HLA SHWE, c=MY, o=UCSI University,
School of Medicine, KT-Campus, Terengganu, ou=Internal
Medicine Group, email=wunna.hlashwe@gmail.com
Reason: This document is for UCSI University, School of
Medicine students.
Date: 2009.03.08 09:33:27 +08'00'

2. Idiopathic Thrombocytopenic Purpura (ITP) Thrombotic Thrombocytopenic Purpura (TTP)
Pathophysiology: Pathophysiology:
AutoAb vs pltlet membrane glycoprotein IIb-IIIa causing premature Defective metopoproteinen resulting in difficulties breaking down fibrin,
removal of pltlets by monocytes/macrophages which causes thrombosis and thrombocytopenia.
Presents in 2 settings: in children, and in adults
Dx by exclusion Clinical features: similar to HUS except HUS afx K more (commonest
cause of ARF in children) and brain less cf TTP brain more, K less
Clinical features: Pentad of -
1. In Children Onset 2-3 wks post viral illness 1. Fever
Sudden onset purpura, oral and nasal bleeding 2. Thrombocytopenia
No palpable splenomegaly 3. Microangiopathic haemolytic anaemia (MAHA)
Normal PBF other than thrombocytopenia 4. Renal dysfunction / impairment
Bone marrow: increased megakaryocytes 5. Neurological symptoms – fits, weakness, confusion, loss of vision
Check that there is no DIVC or other systemic Purpura
illnesses GI & intracerebral bleeds
Haematuria
2. In Adults More common in females Proteinuria
Insidious onset Raised bilirubin and LDH; decreased haptoglobulin
Chronic with remissions and relapses a/w CA stomach – check for this
* Thrombosis leads to renal dysfunction, anaemia and neurological
Management: symptoms
1. Children Usually self-limiting within a few wks - Withhold treatment
if only mild symptoms Causes : similar causes to HUS
Prednisolone 2mg/kg/day – for moderate or severe • Infection—E. coli O157, Shigella, pneumococcus, Coxsackievirus
purpura, bruising or epistaxis, or pltlet <10 X 109/L • Drugs—OCP, cyclosporine, 5FU, ticlopidine
Pltlet transfusion – for persistent epistaxis, GI bleed, • Tumours
retinal hemorrhages suggestive of intracranial bleed • Pregnancy
IVIg – for persistent bleed while on steroids • HIV
2. Adults Less responsive to treatment. Relapses common • SLE
Prednisolone 1mg/kg/day Inx:
Pltlet transfusion for persistent / potentially life- • FBC—low Hb and platelets, raised neutrophils
threatening bleeds • PBF—fragmented RBC
IVIg (1g/kg) for severe hemorrhage or life-threatening
• U/E/Cr—low Na, high urea/Cr/uric acid
bleeds to raise pltlets temporarily.
• Decreased haptoglobulin, Increased bili, LDH (haemolysis)
Splenectomy + vaccination (pneumococcus,
Management:
meningococcus & H. influenzae) – if 2 relapses occur.
Replaces metopoproteinen by plasmaphoresis or FFP
2/3 response rate.
Platelet infusion for severe bleeding
Life-long steroids if relapses are frequent
Steroids
Immunosuppressants (eg vincristine,
Vincristine and splenectomy for relapses
cyclophosphamide) – if unresponsive to splenectomy