Pathognomonic findings Flashcards
Schistocytes (fragmented RBCs)
AKA helmet cells
Fragmented RBCs due to shear stresses in the small vessels
Microangiopathic haemolytic anaemia (MAHA):
- thrombotic thrombocytopenic purpura
- haemolytic uremic syndrome
- disseminated intravascular coagulation
- HELLP syndrome
- defective valvular prosthesis
Target cells
Thin RBCs with Hb precipitated inside (look like a target)
IDA (will also have microcytosis, hypochromic pencil cells)
Sickle cell, thalassaemia
Liver disease (will have high MCV)
Post-splenectomy (will also get Howell Jolly bodies)
Giant platelets
ITP
Rouleaux formation
Stacked RBCs, indicating hyperviscosity
- Multiple myeloma
- Waldenstrom’s
- Other cause of HVS
Howell-Jolly bodies
Nuclear remnants within red cells, normally removed by the spleen. Look like a little purple blot in the erythrocyte
Caused by hyposplenism/asplenism (e.g. SCD, splenectomy, coeliac dx)
Dark brown urine (dipstick positive for blood) but no red cells seen on microscopy
a) Diagnosis
b) What is it, and how does this usually present?
c) Conditions that may cause PNH
d) Treatment
e) Complications
a) Paroxysmal nocturnal haemoglobinuria
- Intravascular haemolysis causes free Hb found in the urine but no red cells
- Confirm diagnosis with flow cytometry looking for absence of red cell membrane proteins - CD55 and CD59
- Positive Ham test - fragile RBCs (not often used now)
- Other features of intravascular haemolysis - raised bilirubin, raised LDH, low Hb, low haptoglobins
b) A membranopathy:
- Most cases due to mutation in PIG-A gene causing defective PIGA enzyme causing defective glyclolipids on red cell membrane
- Leads to haemolysis
- In normal circumstances, this would be mopped up by haptoglobins, but the system is overloaded in PNH, causing free Hb to enter the glomeruli and cause haemoglobinuria
Dark red/tea coloured urine worse in the morning (concentrated overnight), eases throughout the day
- Haemolytic anaemia, thrombosis (e.g. portal vein, mesenteric, hepatic vein), bone marrow failure
c) Aplastic anaemia, MDS
d) Eculizumab
- alternative: steroids
e) Venous thrombosis
Pappenheimer bodies
Iron accumulation around the nuclei of developing erythrocytes
Sideroblastic anaemia
- Primary
- Secondary - alcohol excess, lead poisoning, MDS
Showers of petechiae over upper half of body/axillae
Fat embolism
Erythrocytes with high osmotic fragility
Spherocytosis
- treat with splenectomy if recurrent episodes of anaemia/gallstones/jaundice
Anti-PF4 antibodies
Type 2* heparin induced thrombocytopenia (90%)
- falling PLT count usually 5-10 days after heparin administration (may be up to 100 days after exposure)
- associated with increased risk of arterial and venous thrombosis
*Type 2 = immune mediated thrombocytopenia
This is in contrast to type 1 HIT, which is a non-immune reaction that occurs within the first 5 days (usually day 1 or 2), causes a transient drop in platelets but no other complications.
Platelet count will recover even if heparin continued
Hypersegmented neutrophils
Megaloblastic anaemia
Hypocellular marrow with no abnormal cells
Aplastic anaemia
Leukoerythroblastic picture
a) Features
b) Causes
c) with teardrop cells on blood film
a) - Left shift of granulocytes - increased band forms, metamyelocytes, myelocytes, promyelocytes
- Nucleated red blood cells - immature red cells which have not yet extruded their nuclei
b) Bone marrow infiltration
- Haematological malignancy, bone marrow metastases, myelofibrosis, MDS
Acute stress- haemorrhage, shock
c) Myelofibrosis
- Sad that my bone marrow is scarred
Rheumatoid, neutropenia, splenomegaly
Felty syndrome
Heinz bodies, bite cells and blister cells
G6PD
If they bite on some Heinz (fava) beans they get blistering haemolysis
