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Haematology > Haemolytic Anaemia > Flashcards

Haemolytic Anaemia Flashcards

1
Q

What does the MCV indicate?

A

It indicates the type of anaemia as it shows the relative size of RBC

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2
Q

What is the definition of haemolytic anaemia?

A

Anaemia die to shortened survival of circulating RBC due to premature destruction (can be extravascular or intravascular)

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3
Q

What compensatory mechanism is associated with haemolytic anaemia?

A

Erythroid hyperplasia= increase bone marrow activity to compensate for high RBC destruction

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4
Q

What is the difference between extravascular or intravascular haemolysis?

A

Extra

  • destruction of RBCs by macrophages in spleen, liver and bone marrow due to antibodies
  • Normal plasma Hb due to no haemoglobin leaking into circulation

Intra

  • RBC lysis in circulation and release products to circulation
  • complement activated
  • haemoglobinaemia + haemoglobinuria + urine haemosiderin
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5
Q

What are the features of haemolytic anaemia?

A 
Due to increased RBC destruction: 
high LDH (inside RBC to be used as energy source) 
Low haptoglobin (due to scavenging Hb degradation productions) 
High bilirubin 
Positive DAT
High MCV
Blood film:
-spherocytes 
-polychromasia 
-RBCs fragments

Due to increase RBC production:

  • high reticulocytes
  • erythroid hyperplasia in BM
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6
Q

What is the difference between the direct and indirect anti globulin test?

What are the tests used for?

A

Direct:
Patient RBC coated in antibody and anti-human globulin

Indirect:
Patient plasma used

Used to test for haemolysis antibodies which could be causing the anaemia

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7
Q

What are the main types of HA?

A

Hereditary:
-abnormalities of RBC interior
I.e. Enzyme defects (add)
-haemoglobinopathies

RBC membrane abnormalities

  • hereditary spherocytosis
  • Hereditary elliptocytosis
Acquired:
Hypersplenism 
Antibodies 
Mechanical trauma 
Infections 
Toxins
Drug induced
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8
Q

What is the most common enzymatic disorders of HA? Why is this disorder associated with HA?

A

G6PD deficiency

Metabolic enzyme involved in pentose phosphate pathway= important for RBC metabolism
Protects RBC from ROS due to being involved in forming GSH which acts to convert free radicals to water under normal circumstances
Only source of NADPH

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9
Q

What precipitates HA in G6PD deficiency?

A

Drugs i.e. primaquine, sulphonamides, aspirin, quinine
Infections
Favs beans

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10
Q

How is G6PD diagnosed?

A 
High LDH 
Retix
Low haptoglobin 
DAT -ve i.e. indicates non-immune haemolysis 
Blood film:
-blister cells 
-bite cells = due to damage by free radicals 
-Heinz bodies 
-non-spherocytic haemolytic anaemia
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11
Q

Why is an enzyme assay not done in an acute crisis?

A

False high of G6PD (look up why)

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12
Q

How is G6PD treated?

A

Prevent precipitating factors
Blood transfusion
Folic acid
Splenectomy

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13
Q

What AR enzyme disorder can cause HA?

A

Pyruvate kinase deficiency

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14
Q

What are the physiological and clinical consequences of pyruvate kinase deficiency?

A

Reduced ATP production in RBCs which causes rigidity

Variable anaemia
Gall stones and jaundice

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15
Q

How is pyruvate kinase deficiency diagnosed and treated?

A

Enzyme assay

Folic acid to treat symptoms

Splenectomy

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16
Q

Which haemoglobinopathies are associated with haemolytic anaemia and why?

A

SCD
- HbS in cells causes sickling of RBC structure which leads to destruction of deformed RBC in vessels and spleen

Thalassaemia
-abnormal beta chain synthesis leads to deformed RBC

17
Q

The 3 types of beta-thalassaemia present with different degrees of anaemia severity. What are these different types and severities?

A

B-Thal Major= haemolytic anaemia early in life in combo with failure to thrive

B-Thal intermedia= severe or mild anaemia

B-Thal trait= mild asymptomatic anaemia

18
Q

What are the 2 types of RBC membrane disorders associated with haemolytic anaemia? What is the difference between these disorders?

A

Hereditary Spherocytosis

  • deficiency of beta spectrin or ankyrin leading to SPHERICAL shape= altered RBC deformability when passing through vasculature
  • destroyed in spleen

Heredity elleptocytosis:
-abnormality in anchor protein in RBC i.e. alpha spectrin or protein 4.1 leading to elliptical RBC shape

19
Q

How can you differentiate between the RBC membrane disorders by their clinical presentations?

A

Spherocytosis

Anaemia and jaunice in neonate period with varying severity in childhood

Elliptocytosis

Dependent on genotype i.e. can be asymptomatic/mild/severe

20
Q

How can hereditary spherocytosis present in childhood?

A

Asymptomatic= mild

Intermittent jaundice/splenomegaly/anaemia= moderate

Bone expansion/pigmented gall stones= severe i.e. BT dependent

21
Q

What are the 2 major categories of acquired haemolytic anaemias? Give examples of each.

A

Immune

  • AI= warm or cold AIHA
  • Alloimmune
  • drug induced

Non-immune:

  • infection i.e. malaria
  • mechanical i.e. prosthetic heart valve
  • PNH (paroxysmal nocturnal haemaglobinuria)
  • TMA (thrombotic microangiopathies)
  • Hyperplenism
  • Oxidant substances
  • DIC (disseminated intravascular coagulation)
  • severe burns
  • extracorpeal circuits
  • renal failure
22
Q

What is autoimmune haemolytic anaemia? What are the 2 subtypes?

A

Host’s immune system acting against own RBC antigens

Warm AIHA

Cold AIHA

23
Q

What are the differences between warm and cold AIHA?

A 
Warm:
-IgG autoantibodies (warm day is Glorious i.e. IgG) which bind at 37 degrees 
-BF= spherocytes and macrocytes 
-DAT not always positive for C3d
-presentation:
Onset HA 
Jaundice

Cold:
-IgM autoantibodies (cold= wear Mittens) which bind at 4 degrees
-BF= red cell agglutination
-DAT +ve for C3d in 90% of patients
-presentation:
HA
Acrocyanosis i.e. blue, cold fingers/toes/ears/nose

24
Q

What are the causes of AIHA?

A

Primary

Secondary

  • malignancy i.e. CLL/Lymphoma/solid organ
  • Infection I.e. hepC/HIV/CMV/TB
  • Immune i.e. SLE/Sjogrens/Scloerderma/UC/post-transplant
  • Drugs i.e. penicillins/interferon/fludarabine
25
Q

How does the management and treatment of warm AIHA differ from cold AIHA?

A

Warm:

  • treat underlying cause
  • short term prednisolone
  • rituximab
  • immunosuppressive eg Ciclosporin/Danazol/Azathioprine
  • splenectomy
  • transfusion if has life threatening complications

Cold:

  • keep px warm
  • transfuse with blood warmer
  • folic acid
  • treat underlying disease
  • rituximab
26
Q

What type of anaemia is haemolytic disease of the Newborn?

A

Alloimmune haemolytic anaemia

27
Q

What antibodies are associated with HDN? How can this be managed and prevented during pregnancy?

A

D, C and Kell

Need to monitory antibody quantity during pregnancy
Routine anti-natal Anti-D prophylaxis (RAADP)
Anti-D given if sensitisation event occurs

28
Q

How would a neonate with HDN present and how can they be treated?

A

Severe haemolytic anaemia and jaundice

Intra-uterine RCE-guided by foetal cranial Doppler US scan
Phototherapy
Neonatal RCE

29
Q

What type of anaemia is microangiopathic haemolytic anaemia? (MAHA) What is the pathological mechanism behind MAHA and what are possible causes?

A

Non-immune acquired haemolytic anaemia

RBC undergo mechanical injury when passing through fibrin strands deposited in small blood vessels

Causes:

  • haemolytic-uraemic syndrome
  • TTP
  • pre-eclampsia
  • disseminated carcinoma
  • collagen vascular disease
  • malignant hypertension
  • collagen vascular diseases
30
Q

What is thrombotic thrombocytopenia purpura? What is the pentad of clinical presentations?

A

Deficiency of ADAMTS13 which leads to formation of ultra large VWF== platelets aggregation and consumption

Pentad:
MAHA 
Thrombocytopenia 
Fever 
Renal failure 
Neurological symptoms
31
Q

What clinical signs would indicate TTP?

A 
RBC fragments on blood film 
-ve DAT 
High troponin= due to microvascular thrombi in cardiac tissue leading to damage 
Renal failure 
Low ADAMTS13 i.e. <5%
32
Q

How is TTP treated?

A

Immediate plasma exchange (PEX)
Steroids i.e. IV methylprednisolone or oral prednisolone w/ oral proton pump inhibitor (due to increased risk of GERD + stomach ulcers with steroid use)

Folic acid

Caplacizumab (Novel)

Rituximab when cardiac or neurological symptoms present

LMWH and Asparin when platelets reached >50

33
Q

What does LDH give a measure of?

A

Cell turnover

Haematology (17 decks)

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