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Haematology > Anaemia > Flashcards

Anaemia Flashcards

1
Q

What does low vs high reticulocytes mean?

A

LOW RETICULOCYTES = MARROW PROBLEM = DECREASED PRODUCTION

  • Iron, folate, b12
  • BM disorder: pure red cell aplasia, MDS, infiltration
  • Anaemia of chronic disease
  • Kidney disease

INCREASED RETICULOCYTES = MARROW RESPONDING NORMALLY = INCREASED RETICULOCYTES

  • Haemolysis
  • Thalassemia
  • Blood loss
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2
Q

Causes of microcytic, normocytic, macrocytic anaemia

A 
MICROCYTIC (MCV <80)
TAILS
- thalassemia 
- anaplastic anaemia
- iron deficiency anaemia 
- lead poisoning
- sideroblastic anaemia 
NORMOCYTIC (MCV 80-100)
- Decreased Production: 
BM failure 
Chronic disease 
- Increased Red Cell Loss:
Haemolysis 
Bleeding (acute)

MACROCYTIC (>100)
MEGALOBLASTIC
- B12 deficiency
- Folate deficiency

NON-MEGALOBLASTIC

  • Myelodysplasia
  • Liver disease
  • Alcohol
  • Pregnancy
  • Hypothyroidism
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3
Q

Features of the iron cycle

A
  1. Duodenal enterocytes (absorption)
  2. Erythroid precursors (utilisation)
  3. Reticuloendothelial macrophages (iron storage and recycling)
  4. Hepatocytes (iron storage and endocrine regulation)
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4
Q

Ferroportin vs Transferrin

A
  • Iron is either stored in enterocytes as ferritin
  • FERROPORTIN is located on the BASOLATERAL side of the cell, where iron is transferred to the plasma by ferroportin and reaches its target cells bound to TRANSFERRIN
  • TRANSFERRIN CARRIES IRON IN THE PLASMA
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5
Q

Features of hepcidin

A
  • HEPCIDICIN REGULATES FERROPORTIN
  • HEPCIDIN BINDS TO FERROPORTIN AND INDUCES ITS DEGRADATION
  • SYSTEMIC REGULATION OF IRON ABSORPTION
  • Regulated by hypoxia, EPO, HFE, TFR2, HJV, inflammation
  • Acute phase reactant largely mediated by IL-6
  • Hepcidin correlates with ferritin

IRON DEFICIENCY = HEPCIDIN DECREASE = INCREASED ABSORPTION OF IRON

IRON OVERLOAD = HEPCIDIN INCREASE = DECREASE ABSORPTION OF IRON

NOTE:

  • HIF-1a is important for EPO transcription
  • It lowers hepcidin and ferritin levels to increase absorption of iron

In haemochromatosis there is decreased levels of hepcidin and thus increased absorption of iron

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6
Q

Investigation findings of iron deficiency anaemia

A

Blood Film: microcytic hypochromic red cells, pencil cells, anisopoikilocytosis (RBC of different size/shapes).

Iron Studies: 
Low iron 
Low ferritin 
Low transferrin saturation 
High transferrin 
TIBC (total iron binding capacity) increased
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7
Q

Iron studies of anaemia of chronic disease

A

Iron: low - normal
Transferrin: low - normal
Transferrin sat: low- normal
Ferritin: normal to high

Transferrin is DECREASED in inflammation, infection, malignancy, cirrhosis

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8
Q

Structure of normal Hb

A

(A) Haemoglobin A - 95-98% of adult Hb (2 alpha chains and 2 beta protein chains)

  • Alpha chain: chromosome 16
  • Beta chain: chromosome 11

Mutations in globin genes results in decrease in globin chain production = thalassaemia

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9
Q

What is thalassaemia?

A

Autosomal Recessive

  • Thalassaemia is the disruption of normal ratio of alpha globin to beta globin chains = REDUCED GLOBIN CHAIN SYNTHESIS
  • Unpaired chains precipitate causing destruction to erythroid precursors in bone marrow (ineffective erythopoeisis) and shortened survival in circulation
  • Inadequate Hb production
  • Distorted a:B ratios
  • Ineffective erythropoiesis and haemolysis
Quantitative disorder 
- Beta thalassemia 
- Alpha thalassemia 
Qualitative diorder 
HbS: sickle cell disease
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10
Q

Alpha Thalassaemia Syndromes

A
  • 2 alpha genes on each chromosome 16 = 4 genes in total
    (a) Silent Carrier: aa/a- = normal Hb, normal MCV

(b) Minor: aa/– or a-/a-: mild microcytic anaemia
Alpha thalassemia trait = A loss of two of the four alpha-globin alleles

(c) HbH disease: a-/– = moderate microcytic anaemia
Splenomegaly + iron overload
Elevated HbH inclusion bodies

(d) Hydrops fetalis, severe in utero anaemia: –/–

HbA2 NORMAL
Note: B thalassemia - HbA2 ELEVATED

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11
Q

Beta thalassaemia Syndromes

A
  • Beta globin gene mutations lead to impaired production of beta globin chains
  • Classified according to degree of reduction
    B+ = some protein produced
    B0 = no protein produced
  • Severity of thalassaemia syndrome depends on nature of beta globin gene mutation

HbA2 (2 alpha, 2 delta) ELEVATED
Elevated HbF
TARGET CELLS

(a) MAJOR (transfusion dependent) = B0/B0 or B0/B+ =
Severe microcytic anaemia

(b) INTERMEDIATE (non-transfusion dependent) = B+/B+ = Moderate microcytic anaemia
(c) MINOR (trait/carrier) = B/B0, B/B+ = mild microcytic anaemia

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12
Q

Investigations and Management of thalassemia

A

INVESTIGATIONS

  • Peripheral blood smear: HbH inclusion bodies, target cells, teardrop cells, anisopoikilocytosis
  • Confirmatory: Hb electrophoresis

Hbh disease alpha thalassemia: low MCV, normal HbA2, normal HbF, HbH present

beta thalassemia: low MCV, high HbA2, high HbF, absent HbH

  • Transfusion therapy in thalassaemia major and some thalassaemia intermedia (stressful periods) to minimise complications of anaemia and suppress extra-medullary haematopoiesis
  • Management excess iron and complications (cardiopulmonary, liver, endocrine, bone health)
  • Folic acid
  • LUSPATERCEPT - IMPROVES RBC MATURATION
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13
Q

Structural variants of haemoglobin

A

Haemoglobin S/C/E are the most common

Hb S = sickle cell disease

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14
Q

Features and management of haemoglobin S disease

A

Haemoglobin S (sickle cell disease)

  • An abnormal haemoglobin from POINT MUTATION IN THE BETA GENE = substitution of a VALINE FOR GLUTAMIC ACID IN 6TH AMINO ACID OF BETA GLOBIN GENE)
  • Resulting Hb TETRAMER (alpha2/betaS2) becomes poorly soluble when deoxygenated
  • Potential life threatening complications from VASO-OCCLUSION in multiple organs - can cause INFARCTION in spleen/marrow/brain/kidney

HbS ELEVATED

BLOOD FILM

  • Sickle cells
  • Howell jolly bodies
  • Target cells
  • Achanthocytes

MANAGEMENT

  • Avoid triggers and complications, eg: pain, infection
  • Hydroxyurea - increases HbF percentage, protective against sickling
  • Sickle Crisis: hydration, analgesia, O2, thrombo-prophylaxis, red cell exchange
  • Immunisations
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15
Q

Drug induced macrocytic anaemia (megaloblastic)

A

Anti-Folate Drugs: methotrexate, trimethoprim

DNA Synthesis: azathioprine, hydroxyurea, gemcitabine

Reduced Absorption: metformin, PPI, alcohol, phenytoin, isoniazid

NOTE: alcohol only affects folate, NOT B12

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16
Q

Causes of macrocytic anaemia

A

Megaloblastic: folate deficiency, B12 deficiency

Non-Megaloblastic: hypothyroidism, alcohol, myelodysplasia, liver disease, pregnancy

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17
Q

Relationship between homocysteine and folate/b12

A

Folic acid (folate) is one of the ‘B’ vitamins that is needed to metabolise homocysteine. Vitamin B12, another B vitamin, helps keep folate in its active form, allowing it to keep homocysteine levels low. Therefore, people who are deficient in these vitamins may have increased levels of homocysteine

High homocysteine = vitamin b12 /folate deficiency

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18
Q

Absorption of B12

A
  • Gastric parietal cells produce intrinsic factor

- IF-B12 complex is absorbed in the terminal ileum

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19
Q

Causes of B12 deficiency

A

(A) Pernicious Anaemia

  • Autoimmune destruction of gastric mucosa/parietal cells leading to reduced production of IF
  • Therefore B12 cannot be absorbed in terminal ileum
  • IF Ab (very specific but only 50% sensitive)
  • Parietal cell Ab: sensitive but not specific

(B) Ileal Pathology

  • Crohn’s disease
  • Ileal resection
  • Mutation/deficiency of receptor for IF

(C) Gastrectomy

(D) Nutrition

(E) Nitrous oxide poisoning - neuropathy

20
Q

Clinical features of B12 deficiency

A
  • Glossitis, angular stomatitis, increased melanin
  • Neural tube defects
  • Subacute combined degeneration of the cord: reduced proprioception, weakness, sensory changes, Romberg sign, Lhermitte sign

Subacute combined degeneration of the cord: loss of propriopception, loss of reflexes, mild-moderate weakness, increased tone, extensor plantars, ataxia

21
Q

Blood film findings for b12 deficiency

A

Blood Film

  • Macrocytic anaemia
  • Hypersegmented neutrophils
  • Low reticulocyte count
22
Q

Folate deficiency

  • Site of absorption
  • Causes
A
  • ABSORPTION: SMALL INTESTINE - jejunum

Causes:

  • Reduced dietary intake
  • Increased requirements: haemolysis, pregnancy, chronic inflammation
  • Malabsorption: small bowel pathology, drugs (phenytoin, isoniazid, alcohol)
  • Impaired utilisation - methotrexate
23
Q

Causes of normocytic anaemia

A

Reduced Production

  • Bone marrow failure
  • Chronic disease

Increased Red Cell Loss

  • Haemolysis
  • Bleeding (acute)
24
Q

What is haemolysis and laboratory findings

A
  • Shortened survival of circulating red blood cells (<100-120 days)
  • Elevated reticulocytes
  • Elevated LDH
  • Elevated unconjugated bilirubin
  • Decreased haptoglobin (glycoprotein from liver, binds free Hb)
  • Elevated faecal urinary urobilinogen

INTRAVASCULAR HAEMOLYSIS

  • Haemglobinuria
  • Urinary haemosiderin
  • Methemalbbuminaemia

SUMMARY

  • Increased reticuloyctes, LDH, unconjugated Bili
  • Decreased haptoglobin
  • Urine haemosiderin if suspecting INTRAVASCULAR haemolysis
  • Difficult if liver disease
  • DAT to confirm autoimmune
  • Blood film
  • If thrombocytopenia - look out for TTP
25
Q

Cause of haemolysis

A

Intracorpuscular (Intrinsic) Defects

  • Enzyme Deficiency: pyruvate kinase deficiency, G6PD
  • Membrane or cytoskeletal defect: hereditary spherocytosis, hereditary elliptocytosis, PNH
  • Hb Synthesis: sickle cell disease, haemoglobin C disease, thalassemia
  • Acquired: Paroxysmal Nocturnal Haemoglobinuria

Extracorpuscular (Extrinsic) Defects

  • Immune: Autoimmune haemolytic anaemia
  • Microangiopathic: DIC, HUS, TTP, HELLP, prosthetic valve (non immune)
  • Infections: Malaria, clostridium
  • Hypersplenism
26
Q

Compare laboratory findings for intravascular vs extravascular haemolysis

A

Elevated LDH
Elevated unconjugated bilirubin
Elevated reticulocytes
Decreased haptoglobin

INTRAVASCULAR (IHSc)
- Increased destruction of RBC within the blood vessels

CAUSES

  • Toxins, eg: snake bites
  • G6PD deficiency
  • ABO incompatibility
  • Complement mediated haemolysis: PNH
  • Macroangiopathic anemia - mechanical destruction by prosthetic valve
  • Microangiopathic anaemia - TTP, HUS, DIC, HELLP, SLE
  • Blood Smear: SCHISTOCYTES
  • Urine haemoglobin/hemosiderin: POSITIVE
  • DAT NEGATIVE

EXTRAVASCULAR (EUSp)
- Increased destruction of RBCs by the reticuloendothelial system (primarily the spleen)

CAUSES

  • RBC defects - sickle cell disease, spherocytosis, pyruvate kinase deficiency
  • Autoimmune haemolytic anaemia
  • PNH
  • Blood smear: SPHEROCYTES
  • Urine haemoglobin/hemsiderin: NEGATIVE
  • Urobilinogen: POSITIVE
  • DAT POSITIVE
27
Q

Features of hereditary spherocytosis

A
  • Autosomal dominant
  • MCHC (mean cell haemoglobin concentration) increased (>360g/L)
  • Primary defect in cytoskeleton of RBC membrane - defective spectrin and protein 4:1 interaction
  • Results in spherocytes and increased osmotic fragility
  • DAT negative
  • Flow cytometry: eosin 5 malemide (EMA) binding

Management

  • Folate supplementation
  • Splenectomy

Red Cell Cytoskeleton: hereditary spherocytosis and hereditary elliptocytosis

28
Q

G6PD Deficiency

A
  • Glucose 6 phosphate dehydrogenase normally produces NADPH which is essential for converting oxidized glutathione back to its reduced form which protects RBCs from oxidative damage –> deficiency results in haemolysis of RBC (occurs in spleen, spherocytes occur)
  • In the absence of reduced glutathione (e.g., due to G6PD deficiency), RBCs become susceptible to oxidative stress that can damage erythrocyte membranes, resulting in intravascular and extravascular hemolysis
  • X linked inheritance
  • Affects primarily males of African, Mediterranean, and Asian descent

Causes:
Acute haemolytic anaemia - in the setting of oxidant injury from:
- medications: antimalarial drugs (eg: chloroquine, primaquine), sulfa drugs (bactrim)
- illness - baxterial and viral infections
- food (eg: fava beans, legumes)

Clinical Features

  • Sudden onset of back/abdominal pain, jaundice, dark urine, transient splenomegaly
  • Acute haemolytic anaemia - in the setting of oxidant injury from medications, illness, food (eg: fava beans, legumes)
  • Chronic haemolysis in severe disease

BLOOD SMEAR
- bite cells, blister cells, heinz bodies
Intravascular haemolysis
G6PD enzyme analysis

DAT negative

Note: Selective advantage in areas of endemic malaria: : As with sickle cell anemia, carriers of the G6PD deficiency may be less severely affected by malaria, especially if the disease is caused by Plasmodium falciparum

29
Q

Liver disease and haemolysis

A
  • In liver disease, already have raised LDH and bilirubin and low production of haptoglobin
  • SPUR CELLS are seen in haemolysis in severe liver disease
30
Q

Paroxysmal Nocturnal Haemoglobinuria

  • Description
  • Clinical Features
A

Physiologically, a membrane-bound glycosylphosphatidylinositol (GPI) anchor protects RBCs against complement-mediated haemolysis.

  • Acquired clonal disorder of stem cells defective in PIG-A gene –> loss of enzymes (glycosyl-phosphatidyl-inositol GPI) that attaches surface proteins (CD55, CD59) to cell membranes (eg: erythrocytes, leukocytes, platelets) via the GPI anchor –> PNH cells more susceptible to complement mediated lysis (typically nocte due to lower pH)

CLINICAL FEATURES

  • Cytopenia, aplastic anaemia
  • Thrombosis in atypical locations - venous and arterial
  • Smooth muscle dystonia
  • Venous thrombosis, Budd chiari (hepatic vein thrombosis)
  • Chronic intravascular haemolysis, dark urine
  • Risk of developing MDS, aplastic anaemia
  • Intermittent jaundice
  • Vasoconstriction: headache, pulmonary HTN
  • Abdominal pain, dysphagia
31
Q

Paroxysmal Nocturnal Haemoglobinuria

  • Investigations
  • Management
A

INVESTIGATIONS

  • Absence of CD55, CD59 and CD16 on cell surface of RBC/neutrophils
  • Positive urinary haemosiderin - takes 24-48 hours to appear
  • DAT negative
  • Haemolysis
  • Blood Film: SPHEROCYTES

MANAGEMENT

  • Eculizumab - against C5, inhibits activation of terminal component of complement cascade
  • Thrombosis: prophylaxis and if event anticoagulation if VTE
32
Q

Indications/clues that may point to PNH

A
  • Thrombosis with unusual features
  • Unexplained Coombs-negative hemolysis and/or hemoglobinuria
  • Consider performing as part of the workup for unexplained cytopenias, aplastic anemia, and myelodysplastic syndrome (MDS)

CATCH PNH by testing:

  • Cytopenia
  • Aplastic anemia
  • Thrombois
  • Coombs negative
  • Haemoglobinuria
33
Q

What is the mutation i Haemoglobin C disease?

A

B globin mutation - glutamate is replaced by lysine

In haemoglobin C disease, lyCine (lysine) replaces the amino acid glutamic acid

34
Q

Autoimmune haemolytic anaemia

A

DAT POSITIVE

  • Warm Autoimmune Haemolysis: IgG
  • Cold Autoimmune Haemolysis: IgM
35
Q

Warm Autoimmune Haemolytic Anaemia

A

A) WARM AUTOIMMUNE HAEMOLYSIS

  • IgG antibodies react to protein on RBC at body temperature
  • Most are idiopathic
  • Blood film: SPHEROCYTES

CAUSES

  • Malignancy: lymphoma, CLL
  • Autoimmune: SLE
  • Certain drugs: rifampin, phenytoin, penicillins, a-methyldopa

Warm weather is Great - IgG

TREATMENT
- Treat underlying associated disorders

Initial Therapy

  • Steroids +/- Ritux
  • DVT prophylaxis - high risk of DVT
  • Folate supplement
  • IVIG useful as adjunct

2nd line for persistent disease

  • Splenectomy
  • Mycophenolate/cyclophosphamide/azathioprine/PEX
36
Q

Cold Autoimmune Haemolytic Anaemia

A

COLD AUTOIMMUNE HAEMOLYSIS

  • Antibodies that recognise antigens on RBC at below core body temperatures causing agglutination of RBC, extravascular haemolysis
  • Typically IgM ab (C3d only) which recruits components of the classical complementary pathway, C3b coated RBC engulfed by reticuloendothelial system

CAUSES

  • Infectious mononucleosis (EBV)
  • Mycoplasma pnuemonia
  • Malignancy (CLL/non hodgkin), Waldenstrom macroglobulinaemia

CLINICAL FEATURES
- Cold induced symptoms: acrocyanosis (painful cyanosis of extremities), Raynauds, livedo reticularis, urticaria, cutaneous necrosis

Blood Film: RED CELL AGGLUTINATION
Haemolysis is intravascular so no spherocytes

Cold weather is MMMMiserable: Cold (IgM) AIHA is seen Malignancy (CLL), Mycoplasma pneumonia, Mononucleosis

TREATMENT

  • Keep warm, steroids or splenectomy NOT effective
  • For severe or symptomatic anaemia from active haemolysis - transfusion support and IVIG/PEX may be used as temporising measure
  • Treat underlying cause
  • Rituximab - but less efficient compared to when used in war
  • Severe refractory cases - bortezomib, daratumumab, anti-complement

Note: splenectomy is not effective in cold as most extravascular haemolysis occurs in the liver

37
Q

Features and disorders associated with microangiopathic haemolytic anaemia

A

Peripheral red blood cell fragmentation

  • Polychromasia
  • Thrombocytopenia
  • Evidence of haemolysis - schistocytes

Disorders

  • TTP
  • HUS
  • DIC
  • HELLP
  • Prosthetic valves
38
Q

Features of TTP

A

Pentad:

  1. MAHA - Microangiopathic hemolytic anaemia
  2. Thrombocytopenia
  3. Fever
  4. Neurological manifestations: Headache/altered mental state
  5. Renal failure

CAUSE

(a) ADAMTS-13 DEFICIENCY
- Cleaves the high molecular weight multimers of vWF
- Decrease in activity = accumulation of ultra large clumps of vWF multimers which binds to platelets leading to microvascular occlusion and thrombocytopenia
- Schistocytes form as erythrocytes are damaged by tangles of vWF and platelets
(b) Secondary: drugs such as quinine, cyclosporin, gemcitabine

DIAGNOSIS

  • ADAMTS 13 <10%
  • Schistocytes
  • Haemolysis

Tx:

  • Steroids – no evidence
  • PLASMA EXCHANGE!
  • FFP
  • Rituximab – refractory or relapsing cases or even in patients with neurological and cardiac involvement
  • Vincristine – refractory cases
39
Q

Compare the red cell enzyme defects G6PD vs Pyruvate Kinase Deficiency

A

G6PD

  • Hexose monophosphate pathway: pentose phosphate pathway
  • Acute haemolytic crisis
  • Susceptibility to oxidative stress
  • X linked - common

Pyruvate Kinase Deficiency

  • Glycolytic pathway
  • Chronic haemolysis
  • Reduced ATP formation - RBC rigidity
  • Autosomal recessive: rare
40
Q

Haemolysis Summary (DM)

A

INTRAVASCULAR

  • Red cell fragmentation ( TTP - ADAMTS13 <10%)
  • Paroxysmal nocturnal haemoglobinuria (flow cytometry for CD55, CD59)

EXTRAVASCULAR

  • Autoimmune haemolytic anaemia - DAT
  • Red cell membrane defects - blood film + flow cytometry
  • Red cell enzyme defects - G6PD deficiency
41
Q

Immune/Idiopathic Thrombocytopenic Purpura (ITP)

A
  • Immune mediated thrombocytopenia
  • Antibody mediated, platelet destruction by liver and spleen
  • Reduced platelet half life with compensatory increase in marrow production

Ix:

  • Isolated thrombocytopenia
  • May present with mucocutaneous bleeding
  • Diagnosis of exclusion

Associations

  • AIHA
  • CLL
  • Autoimmune disease: RA/SLE
  • H pylori
  • Hep C
42
Q

Treatment for ITP

A
  • Aim of tx is to maintain platelet count high enough to prevent significant bleeding
  • Observation if Plt >30
  • First line: pred
  • IVIG - more rapid response
  • Splenectomy + vaccination - most effective therapy

Newer Drugs
- Romiplostim: TPO receptor agonist

43
Q

Thrombocytopenia in pregnancy

A

(A) Gestational Thrombocytopenia

  • 3rd trimester, spontaneous resolution
  • Mild, platelets >80
  • Pre-pregnancy plt count normal
  • 5% of pregnancies
  • Neonate unaffected

(B) ITP

  • Earlier onset, may be more severe (<80), pre-existing low Plt
  • Diagnosis of exclusion
  • Tx: Pred, IVIG, monitoring and planning for delivery (36/40)

(C) HELLP/AFLP/DIC/pre-eclampsia

43
Q

Thrombocytopenia in pregnancy

A

(A) Gestational Thrombocytopenia

  • 3rd trimester, spontaneous resolution
  • Mild, platelets >80
  • Pre-pregnancy plt count normal
  • 5% of pregnancies
  • Neonate unaffected

(B) ITP

  • Earlier onset, may be more severe (<80), pre-existing low Plt
  • Diagnosis of exclusion
  • Tx: Pred, IVIG, monitoring and planning for delivery (36/40)

(C) HELLP/AFLP/DIC/pre-eclampsia

44
Q

Cause of target cells

A

The finding of target cells is nonspecific and may indicate various hemoglobinopathies, such as thalassemia, liver disease, or asplenia.

45
Q

Causes of teardrop cells

A

Teardrop-shaped erythrocytes, known as dacrocytes, are found in conditions that involve extramedullary hematopoiesis (e.g., myelofibrosis, thalassemia, splenomegaly).

Haematology (7 decks)

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