Haem Flashcards
Causes of a microcytic anaemia (low MCV) vs Normocytic (normal MVC) 80-100 vs Microcytic
Microcytic anaemia (FAT)
1) Fe deficiency (low ferritin)
2) Anaemia of chronic disease e.g. RA. (normal/high ferritin)
3) Thalassaemia (alpha or beta)
Normocytic anaemia
Infection, inflammation, malignancy duh
- also anaemia of chronic disease
1) Anaemia of chronic disease, acute blood loss
2) Haemolysis, hypothyroid
3) Failure - BM (aplastic anaemia), Renal
4) Pregnancy
Macrocytic anaemia
1) Megaloblastic - folate/B12 deficiency
2) Non megaloblastic - Alcohol, Haemolysis
Blood findings in Fe deficiency anaemia
Symptoms/signs
Treatment
including dose, duration and side effects
Low ferritin (iron storage) High transferrin
Blood film: Microcytic, hypo chromic
- Variation in size (anisocytosis)
- Variation in shape (poikilocytosis)
- Pencil cells
Signs
- Pallor, lethargy, SOB
- Atrophic glossitis; Angular stomatitis (cheilitis)
- Koilonychia (spoon shaped nails)
- Post cricoid webs (Plummer vinson syndrome)
Treatment
65 mg elemental iron (ferrous sulphate 200 mg) 3x daily
- Recheck Hb in 4 weeks (should go up by
- Continue at least 3 months after Hb normalises
Side effects of ferrous sulphate: Nausea, abdominal discomfort, diarrhoea or constipation, black stool
Petechiae cause
Differential diagnosis
Thrombocytopenia (low platelets)
Leukaemia Meningococcal septicaemia Vasculitis Henoch-Schonlein Purpura (HSP) Idiopathic Thrombocytopenia Purpura (ITP) Non-accidental injury
B12 deficiency
Causes
Clinical features
Investigations
Causes:
Low intake - vegan (found in meat, fish and dairy)
Low absorption - Pernicious anaemia (antibodies against IF/Parietal cells), Ilieal resection, Chron’s, bacterial overgrowth, tape worms
Importance of B12
B12 helps synthesize thymidine, and hence dna, so in deficiency RBC production is slow. Untreated, it can lead to megaloblastic anaemia and irreversible CNS complications
Clinical features
- General: Jaundice (due to haemolysis), glossitis, angular stomatitis
- Neuro: Irritability, depression, psychosis
- Spinal cord degeneration: Paraesthesiae, peripheral neuropathy. Also subacute combined degeneration of the spinal cord, a combination of peripheral sensory neuropathy with both upper and lower motor neuron signs due to ↓b12. The patient may display the classical triad of:
(1) Extensor plantars (UMN)
(2) Loss of knee jerk (LMN)
(3) Loss of ankle jerk (LMN)
Pernicious anaemia - what is it
Blood results
Management
Autoimmune condition in which atrophic glossitis –> lack of IF secretion from parietal cells of the stomach. Dietary B12 remains unbound and so can’t be absorbed in terminal ileum
Blood results
- Microcytic anaemia
- Low serum B12
- Hypersegmented neutrophils (>5 losses) = megaloblastic anaemia
- Parietal cell antibodies found in 90%
- IF antibodies, specific for PA but lower sensitivity
Management (of B12 deficiency)
- Treat the cause if possible
- If due to malabsorption - IM Hydroxocobalamin (B12) 1mg IM alternate days for 2 weeks, then every 3 months for live
- If due to poor oral intake: Oral B12 after the initial IM course (50-150mcg daily between meals)
What is thalassaemia?
What is beta thalassaemia
Types of beta thalassaemia
- for the worst give signs, blood film, electrophoresis, treatment
Genetic diseases of unbalanced Hb synthesis, with underproduction (or no production) of one globin chain. Unmatched globing precipitate, damaging RBC membranes, causing their haemolysis while still in the marrow
Beta thalassaemia: Point mutations in beta globin genes on chromosome 11
1) Beta thalassaemia minor/trait (heterozygous trait)
- Usually asymptomatic
- Mild, well tolerated anaemia (Hb >90) - may worsen in pregnancy
- MCV <75, HbA2 >3.5%, slight increase in HbF
2) Beta thalassaemia intermedia
- Moderate anaemia but not requiring transfusion
- May be splenomegaly
- Causes: Mild homozygous mutations, co inheritance with another trait e.g. HbC thalassaemia
3) Beta thalassaemia major
- Significant abnormalities in both beta-globin genes
- Presents in 1st year: Severe anaemia + FTT
- Extra-medullar Haematopoesis: RBCs made outside marrow: Skull bossing + hepatosplenomegaly (due to haemolysis)
- Osteopenia
- Life long blood transfusions needed - iron overload seen in 10yrs as endocrine failure (pituitary, thyroid, pancreas –> DM), liver disease and cardiac toxicity
- Blood film: Hypochromic anaemia, Target cells, Increased reticulocyte count
- Hb electrophoresis: ⇈HbF, HbA2 variable, HbA absent
CLL
Staging system
Symptoms
Signs
Blood results
Disease progression
Rai staging
0Lymphocytosis alone
Median survival >13yrs
I Lymphocytosis + lymphadenopathy
Median survival 8yrs
IILymphocytosis + spleno- or hepatomegaly
Median survival 5yrs
III Lymphocytosis + anaemia (Hb <110g/L)
2yrs Median survival
IV Lymphocytosis + platelets <100 × 109/L
1yr Median survival
Symptoms - Often non - surprise on routine FBC - May have anaemia, infection prone, or weight loss/anorexia/night sweats if severe Signs - Enlarged rubbery lymph nodes - Splenomegaly, hepatomegaly
Bloods
↑Lymphocytes—may be marked
Later: autoimmune haemolysis, marrow infiltration: ↓Hb, ↓neutrophils, ↓platelets.
Smear cells
Natural history - commonest leukaemia
⅓ never progress (or even regress), ⅓ progress slowly, and ⅓ progress actively. cd23 and β2 microglobulin correlate with bulk of disease and rates of progression. Death is often due to infection or transformation to aggressive lymphoma (Richter’s syndrome).
differential for enlarged spleen
- enlarged left kidney; unless enormous, there is resonance over the swelling anteriorly as it is covered by the gas containing colon
- carcinoma of the cardio or upper part of the body of the stomach; by the time it’s this big they were usually symptoms of gastric obstruction
- enlarged left lobe of the liver
Classification for enlargement of the spleen
massive splenomegaly causes
1.infections Dash viruses: glandular fever Dash bacterial: Typhus, typhoid, septicemia - Protozoa,: malaria, schistosomiasis - Parasitic: Hydatid
- Hematological disease
- leukemia: CML & CLL
- lymphoma: Hodgkins and non-Hodgkin’s
- Milo fibrosis, I TP, polycythemia rubra vera
- Hemolytic anemia is: e.g. spherocytosis, beta thalassemia - Portal hypertension
Increased pressure in the portal system causes progressive enlargement spleen and may lead to hypersplenism [e.g. excess removal of platelets resulting in thrombocytopenia] - Metabolic and collagen disease disease
- Amyloid Secondary to our ARA, collagen disease, chronic sepsis
- storage disease is e.g. Gaucher’s disease - Cysts, abscesses and tumors of the spleen
All uncommon
massive splenomegaly CML Myelofibrosis Lymphoma Polycythemia Portal hypertension
Indications for splenectomy
complications
Indications Rupture Hematological disease Tumors insists Part of another procedure e.g. radical excision of stomach cancer, distal pancreatectomy, splenorenal anastomosis For portal hypertension
complications
- Gastric dilation
- Thrombocytosis: DVT and PE risk. Antiplatelets like aspirin are given a prophylaxis in addition to MMWH
- Post splenectomy sepsis ( in capsulated microorganisms especially) - Immunization with Nakul, meningococcal an H influenza type B vaccines should be given preop. Adult should have penicillin for at least two years after splenectomy (Children get it until they are adults]. Annual flu vaccine also.
Howell-jolly bodies
What do they look like
Cause
Nuclear remnant in circulating erythrocytes
Hyposplenism
Heinz bodies cause
Other things seen on blood film
G6PD deficiency
Irregularly contracted cells
Schistocytes causes
MAHA
Prosthetic valve
Target cells
What do they look like
Causes
Targets?
Hyposplenism
Thalassaemia
Liver disease
Pencil cells cause
Iron deficiency anaemia
