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[MBD] NoNa > Haemolytic Anaemias > Flashcards

Haemolytic Anaemias Flashcards

1
Q

What is anaemia ?

A

Anaemia: ↓ Hb = ↓ RBCs = ↓ oxygen-carrying capacity = cannot meet physiological needs

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2
Q

What is haemolytic anaemia ?

A

Anaemia which is due to ⬆ breakdown of RBCs

(↓ RBC survival)

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3
Q

Describe the variation in blood Hb concentration

A

↑ Hb level in neonates

↓ Hb in infants

↑ 1 years old-adulthood (20 years old aprox)

↑ Hb in males

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4
Q

Describe the normal RBC life cycle .

A
  • RBC produced in bone marrow.
  • 7.8 microns diameter - flexible=squeeze through 3.5micron capillaries ( = they deform their shape, cytoplasmic enzymes)
  • Circulate for 120 days (no nuclei/cytoplasmic organelles(mitochondria)).
  • RBC enzymes produce energy to maintain RBC shape.
  • RES removes RBCs after 120 days (reticuloendothelial system=liver/spleen)
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5
Q

What is Haemolysis ?

A
  • Shortened RBC lifespan from 120 days -> 30-80 days
  • BM compensates by ⬆ RBC production

=⬆ immature RBCs (⬆ reticulocytes & nucleated RBCs)

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6
Q

What is compensated haemolysis?

A

⬆ RBC production(BM) compensates for ↓ RBC life span (⬆ RBC destruction) = normal Hb levels

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7
Q

What is incompletely compensated haemolysis?

A

insufficient RBC production to balance out ⬇ RBC life span (↑ haemolysis) = ↓ Hb

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8
Q

What are some clinical findings with haemolysis?

A

Jaundice

Pallor + Fatigue

Splenomegaly

Normal urine

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9
Q

Why does haemolyisis cause jaundice ?

A
  • RBC Hb broken down -> haem + globin.
  • Haem broken down -> protoporphyrin (contains iron).
  • Protoporphyrin broken down -> bilirubin (unconjugated in plasma) = yellow skin + eyes
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10
Q

What is Pallor and why does haemolysis cause this ?

A

Pale appearance linked with fatigue.

-Caused by ↓ Hb = insufficient oxygen to the tissues.

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11
Q

What is splenomegaly and how is it caused ?

A

Spleen = Organ that removes old/damaged RBCs cells

Splenomegaly = Spleen enlarges in haemolysis

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12
Q

What happens to the urine in haemolysis?

A

Haemolysis = ↑ urobilinogen = normal/dark urine

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13
Q

What is haemolytic crisis ?

A

Haemolytic crisis = ↑ anaemia + jaundice with infections/precipitants.

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14
Q

What is aplastic crisis?

A

Aplastic crises = Anaemia involving other cells as well as RBCs

Reticulocytopenia (↓ reticulocytes) and parvovirus infection.

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15
Q

More chronic clinical findings of haemolysis

A
  • Gallstones - pigment stones (due to ⬆ breakdown of RBC -> BILIRUBIN)
  • Leg ulcers - due to vascular stasis/local ischaemia
  • Folate deficiency - due to ⬆ demand due to RBC being broken down and more required
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16
Q

Lab investigation for Haemolytic Anaemia - Bone marrow findings

A

-As a compensatory mechanism to haemolysis, erythroid hyperplasia occurs in BM - normoblasts formed, Myeloid:Erythroid ratio reversal (normal M:E = 2:1-5:1).
Haemolytic anaemia = erythroid hyperplasia = M:E = 1:2-1:5

-Reticulocytosis - variable.
Mild reticulocytosis = 2-10% of reticulocytes ⬆ in BM = haemoglobinopathy.
Moderate-Marked reticulocytosis = 10-60% reticulocytes ⬆ in BM = Immune Haemolytic Anaemia, Hereditary Spherocytosis, G6P Dehydrogenase deficiency

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17
Q

Typical Lab Findings for Haemolytic Anaemia

A
  • ⬆ reticulocyte count (reticulocytosis)
  • ⬆ unconjugated bilirubin in plasma - ⬆ RBC breakdown
  • ⬆ LDH (lactate dehydrogenase) -released from lysed RBC
  • ⬇ serum haptoglobin = protein that binds free haemoglobin. More Hb is being released into plasma, haptoglobin binds to Hb = ⬇ haptoglobin in serum
  • ⬆ urobilinogen. bilirubin is released + metabolised
  • ⬆ urinary hemosiderin

Abnormal blood film

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18
Q

What can we see on the blood film for HA?

A

-Reticulocytes
-Polychromatophilic cells = RBCs basophilic in colour due to ⬆ RNA content, + bigger than normal RBCs
-Nucleated RBCs - being broken down
-Poikilocytes - Different shapes of RBC
-Spherocytes, Sickle cell, Target cells, Schistocytes (fragmented, triangular rbc)
acanthocytes

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19
Q

Classification of Haemolytic Anaemia - 3 categories

A
  • Inheritance - Inherited/Acquired
  • Site of RBC destruction - Intravascular/Extravascular(outside vessels,within reticuloendothelial system=spleen + liver)
  • Origin of RBC damage - Intrinsic/Extrinsic
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20
Q

Inheritance classification of haemolytic anaemia

A
  • Hereditary - Hereditary spherocytosis
  • Acquired - Immune Haemolytic Anaemia
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21
Q

Site of RBC destruction classification of haemolytic anaemia

A

Intravascular - e.g. Haemolytic transfusion reaction.
Thrombotic thrombocytopenic purpura
(Blood disorder which causes clots forming in blood vessels -low RBC, platelets due to breakdown )

Extravascular = outside vascular system, within reticuloendothelial system (liver + spleen) - e.g. Autoimmune haemolysis (antibodies are directed against a person’s own RBC causing them to burst)

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22
Q

Origin of RBC damage classification of haemolytic anaemia

A

Intrinsic (within RBC) - e.g. G6PD deficiency
(Genetic disorder that affects mostly males, G6PD enzyme not enough - red bloods cells don’t work properly

Extrinsic (outside RBC) - e.g. infection
Delayed haemolytic transfusion reaction (present with RBC haemolysis following transfusion)

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23
Q

Describe Acquired RBC haemolysis

A

Immune:

  • Autoimmune (immune system)
  • Alloimmune (immune response to non self antigens)

Non-immune:
-Paroxysmal Noctural haematuria (rare acquired disease which destroys RBC) - not by immune system

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24
Q

Go through the different types/causes of Hereditary RBC haemolysis:

A

RBC enzymopathies :

  • G6PD deficiency
  • PK deficiency

RBC membrane disorders:

  • Hereditary spherocytosis (sphere shaped RBC instead of biconcave)
  • Hereditary elliptocytosis (elliptical rather than biconcave)

Haemoglobinopathies:
-Sickle cell diseases
-Thalassaemia
(no/little haemoglobin production)

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25
Q

Where is the normal site of RBC destruction?

A

Normal RBC destruction = Extravascular haemolysis

  • Reticuloendothelial Macrophages engulf abnormal RBC and break it down into globin + iron + protoporphyrin.
  • Iron + globin are reused to make Hb
  • Protoporphyrin -> bilirubin. Bilirubin becomes unconjugated bilirubin and is taken to liver where it becomes bilurubin glucoronides (conjugated) and is excreted in faeces as stercobilinogen/urine as urobilinogen
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26
Q

Describe intravascular RBC breakdown

A

Intravascular haemolysis = Abnormal

RBC breakdown within vascular system = Hb is released into circulation (free Hb). Some Hb enters kidney + urine (haemoglobinuria). + Hb breakdown forms haemosiderin (also enters urine=haemosiderinuria)

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27
Q

What is the pathway that protoporphyrin undergoes following extravascular haemolysis?

A

Protoporphyrin → Bilirubin

Bilirubin = unconjugated in blood plasma, transported to liver

Bilirubin is carried to liver + gut

Bilirubin is conjugated to stercobilinogen in faeces

OR

Bilirubin is reabsorbed + travels to kidneys = urobilinogen in urine.

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28
Q

Describe the pathway of iron following extravascular RBC breakdown

A

The iron is transported in blood by transferrin.

(transferrin = iron transport protein)

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29
Q

Describe the pathway followed by globin following RBC being broken down extravascular

A

The globin will be broken down into amino acids

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30
Q

What is haemoglobinuria ?

A

The presence of excess haemoglobin in the urine

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31
Q

What is haemosiderinuria

A

Presence of hemosiderin in the urine.

Haemosiderin = the protein compound which stores iron in tissues.

When Hb breaks down, it releases iron.

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32
Q

What is Methaemalbumin ?

A

Methaemalbumin = degraded haemoglobin enters the plasma and binds to albumin.

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33
Q

What is haptoglobin ?

A

Haptoglobin = Protein encoded by HP gene.

In blood plasma, haptoglobin binds to free haemoglobin.

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34
Q

Describe the normal structure of a red cell membrane

A
  • Lipid bilayer
  • Integral proteins - protein band 3, glycophorin A, glycophorin C
  • Membrane skeleton

-Cytoskeletal proteins - spectrin alpha, spectrin beta, ankyrin, protein 4.2, protein 4.1, actin

protein defects = hereditary spherocytosis/hereditary elliptocytosis

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35
Q

What are some defects which may arise in the vertical interaction and what can this cause?

A

Causes hereditary speherocytosis.

Defects can occour in the following proteins :

  • Spectrin
  • Band 3
  • Protein 4.2
  • Ankyrin
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36
Q

What are some proteins in which defects in horizontal interactions may result in and what can this cause ?

A

Causes hereditary elliptocytosis.

Defects can occour in the following proteins :

  • Protein 4.1
  • Glycophorin C
  • Spectrin - HPP
  • Loss of interaction b/w ankyrin + spectrin
37
Q

Describe how hereditary spherocytosis may arise

A

Most common RBC membrane defect

Common hereditary haemolytic anaemia

Autosomal dominant inheritance (75%)

Defects in proteins involved in vertical interactions between the membrane skeleton and the lipid bilayer - spectrin + ankyrin, protein 4.2

Decreased membrane deformability

Bone marrow produces biconcave RBC but as membrane is lost, RBC becomes spherical

38
Q

Hereditary Spherocytosis Blood Film

A

Sphere shape

Deeply stained, no central pallor

Polychromatophilic - ⬆ RNA. membrane protein defects

These RBCs go through reticuloendothelial system, can’t retain biconcave shape = attain spherical shape = ⬇ deformability = haemolysis

39
Q

Hereditary elliptocytosis blood film

A

Elongated RBCs but with no pointed ends (teardrop cells have 1 pointed end)

40
Q

How is Haemolytic spherocytosis managed ?

A

Monitored
Folic Acid
Transfusion
Splenectomy

41
Q

MCV in Hereditary Spherocytosis is ……….

A

Normal

42
Q

Clinical Features of Hereditary Spherocytosis

A

Asymptomatic - severe haemolysis

Neonatal jaundice

Splenomegaly - Spleen constantly removing spherical RBCs=spleen enlarges

Pigment gall stones - Caused by constant RBC breakdown ➔ bilurubin (pigment)

Reduced eosin-5-maleimide (EMA) binding - EMA binds to RBC plasma membrane Band 3 protein= test for Hereditary Spherocytosis

Positive family history (autosomal dominant inheritance)

Negative direct antibody test

43
Q

What are enzymopathies ?

A

These are enzymes which are responsible for producing energy in the glycolytic pathway.
This is used to maintain the RBC size and haemoglobin

44
Q

What are the RBC metabolic pathways?

A
  • Glycolysis
  • HMS
  • Rapoport Leubering shunt
45
Q

What are the roles of HMP shunt ?

A

-Generates reduced glutathione
-Protects the cell from oxidative stress
So RBC that are G6P deficient look fine and live a normal amount of time but only when exposed to oxidizing precipitants e.g. drugs, fava beans etc. you get oxidation of membrane proteins and Hb.

46
Q

How do RBC generate energy ?

A

They do this through Glycolysis (Emden-Meyerhof pathway),Hexose Monophosphate shunt , Rapoport Luebering Shunt.

47
Q

What are the two most common enzyme abnormalities ?

A

Glucose -6-Phosphate deficiency
Pyruvate Kinase deficiency

48
Q

G6PD in RBC HMP Shunt (Pentose Phosphate Pathway)

A

Glucose -> G6P (G6PD) -> 6PG.

G6PD enzyme converts G6P -> 6PG. This reaction produces NADPH. NADPH converts oxidised glutathione (GSSG) to reduced glutathione (GSH).

Reduced glutathione = antioxidant, protects RBC membrane + RBC Hb against oxidative stress

Absent reduced glutathione = RBC exposed to oxidative stress = haemolysis

Absent reduced glutathione = Hb oxidation = Hb denatures + aggregates + forms Heinz bodies within RBC

Absent reduced glutathione = membrane proteins oxidise = ⬇ RBC deformability

49
Q

Describe G6PD deficiency

A
  • Hereditary, X-linked disorder (if its in the X chromosome, men have it and it can also occur in women-In cells they randomly switch off 1 of the genes and so 50% of cells will be G6P Deficient)
  • Common in African, Asian, Mediterranean and Middle Eastern populations
  • Mild in African (type A), more severe in Mediterraneans (type B)
  • Clinical features range from asymptomatic (except for neonatal jaundice)until they get exposed to things to acute episodes to chronic haemolysis (which is less common)
50
Q

What are the effects of oxidative stress?

A

Oxidation of Hb by oxidant radicals

  • Resulting in denatured Hb aggregates and forms Heinz bodies (bind to membrane)
  • Oxidised membrane proteins-Reduced RBC deformability
51
Q

What are some oxidative precipitants ?

A

-Infections
-Fava/broad beans
-Drugs :
Anti-biotics/Anti-Malarial
Dapsone
Nitroflurantoin
Ciprofloxacin
Primaquine - antimalarial drug = causes oxidative stress + Heinz bodies + impact RBC membrane

52
Q

Patients with G6PD deficiency have protection against………

A

Severe malaria

53
Q

What exactly does the HMP shunt do ?

A

The HMP shunt extends the life span of RBC by maintaining membrane proteins and lipids.
It diverts Glucose-6-phosphate to 6-phosphogluconate through Gluycose-6-phosphate dehydrogenase

54
Q

What are the features of G6PD deficiency ?

A
  • Haemolysis
  • Blood Film - target cells, bite cells, blister cells, ghost cells, Heinz bodies with methylene blue)
55
Q

How can you make a diagnosis of G6PD deficiency?

A

This can be done using an enzyme assay.

  • May be falsely normal if reticlocytosis is occurring after a recent episode as reticulocytes usually have high enzyme levels .
  • Wait for the reticlocytes to decrease or check ratios between enzyme levels .
56
Q

What happens to patients who are having a acute Haemolytic episode ?

A
  • They will be come acutely jaundiced.
  • May have intravascular Haemolysis, dark urine from Hb in the urine.
  • Anaemic
57
Q

What is the morphology of oxidative haemolysis ?

A

The presence of Heinz bodies and bite cells

58
Q

What are bite cells?

A

These are abnormally shaped mature RBC with one or more semicircular portions removed from the cell margin.

59
Q

What are Heinz bodies?

A

These are inclusions within RBC composed of denatured Hb

60
Q

Describe Pyruvate Kinase deficiency

A

-Pyruvate kinase is required to generate ATP.
-This is essential for membrane cation pumps (deformability)
-Autosomal recessive and much rarer.
-Can cause chronic haemolytic anaemia
Mild to transfusion dependent
(Depends on genetics do you make a tiny bit less or do you make no PK)
Improves with splenectomy (HS goes to normal Hb remember)
what you see characteristically on a blood film are prickle cells (small and spikey), polychromasia.

PK deficiency = ⬇ intracellular ATP

ATP maintains RBC shape + deformability

Na+/K+ ATPase pump = cell dehydrates + lyses

Blood film - prickle cells, large central pallor = ⬇ Hb

non-spherocytic haemolytic anaemia

61
Q

What are Haemoglobinopathies ?

A

This is a group of disorders which are inherited. They cause a abnormal production or structure of Hb.
Example is SCD

62
Q

What is the normal structure of Haemoglobin ?

A

Ferrous iron + Protoporphoryin IX =Haem

Globin protein

Haem + Globin = Haemoglobin

63
Q

Describe normal Haemoglobin

A

HbA -Adult which consists of α2β2 (97%)with some α2 delta2 e (2-3.5%)
and alpha2 gamma 2 (foetal Hb)

64
Q

Describe the globin gene expression during foetal development

A

Alpha chains are expressed from the beginning and if problems occur in utero , alpha chains are required.
For e.g. Alpha thalassemia zero
Beta chains are not expressed until a few weeks old during the neonatal period.
The most common haemoglobinopathies are Beta chains.

65
Q

What are the 2 groups of globin disorders?

A

Quantitative =thalassaemias
(The production of increased/decreased amount of globin chain) - Reduced/absent alpha/beta globin chain synthesis, structurally normal
Qualitative =variant haemoglobins - Production of a structurally abnormal globin chain.

66
Q

Describe the different Haemoglobin disorders

A

HbS =This decrease solubility and causes polymerisation
Hb Koln=Decreases stability and increases Heinz body formation
HbC=Decreases solubility and increases crystallisation

67
Q

What are Thalassaemias?

A

This is an imbalanced alpha and beta chain production
Excess unpaired globin chains are unstable
-Precipitate and damage RBC and precursors
-Ineffective erythropoiesis in bone marrow
-Haemolytic anaemia

68
Q

What are the 2 types of Beta thalassaemia that can be inherited?

A

Beta thalassaemia trait
Beta Thalassaemia major

69
Q

How do we diagnose the thalassaemia trait ?

A

-Asymptomatic
-Microcytic hypochromic anaemia
-Low Hb, MCV, MCH
-Increased RBC
-Often confused with Fe deficiency
Because your making less β chains, HbA2 is increased in b-thal trait –(diagnostic test)
a-thal trait often by exclusion
-globin chain synthesis (rarely done now)
-DNA studies (expensive)

70
Q

Beta thalassaemia major

A

Absence of both beta globin chains

Severe anaemia, 3-6 months after birth

Pallor

Progressive hepatosplenomegaly - erythroid hyperplasia

Bone marrow expansion – facial bone abnormalities

Mild jaundice

Transfusion = Iron overload, affects endocrine organs

Splenectomy = Intermittent infections

Microcytic hypochromic RBCs with ⬇ MCV, ⬇ MCH, ⬇ MCHC

Anisopoikilocytosis: target cells, nucleated RBC, tear drop cells

Reticulocytes ⬆ >2%

71
Q

Describe Beta Thalassaemia major

A
  • Transfusion dependent in 1st year of life
  • When they stop making Foetal Hb they become progressively anaemic

-If not transfused:
Failure to thrive
Progressive hepatosplenomegaly (big liver and spleen and so have big tummies)
Bone marrow expansion – skeletal abnormalities (facial shape changes aswell)
Death in 1st 5 years of life from anaemia

Side effects of transfusion:
Iron overload from the excess iron in the transfused blood - usually treated through medication (iron chelators help iron be excreted in urine) if not can cause:

Endocrinopathies
Heart failure
Liver cirrhosis

And so Treated with transfusions and iron chelators

72
Q

β-thalassaemia trait (minor)

A

Asymptomatic
Often confused with Fe deficiency
α-thal trait often by exclusion
HbA2 increased in b-thal trait – (diagnostic - electrophoresis) - both beta thalassaemia trait + beta thalassaemia major A2 bands are increased

73
Q

What are the chronic complications of SCD?

A

Silent infarcts
Pulmonary hypertension
Chronic lung disease, bronchiectasis
Erectile dysfunction
Azoospermia
Chronic pain syndromes
Delayed puberty
Avascular necrosis
Moya-moya
Retinopathy, visual loss

74
Q

Describe Sickle cell disease

A

Tested for in newborn babies in the UK
Clinically significant sickling syndromes:
HbSS
HbSC
HbS-D Punjab (started in india)
HbS- O Arab (started in arab peninsula)
HbS- β thalassaemia – ( the other gene can’t make beta chains and so you get SC)
And so as you can see you can get a sickle cell disease by having one S mutation on a beta gene matched up with other mutations on the other gene.
Point mutation in the β globin gene: glutamic acid → valine

Insoluble haemoglobin tetramer when deoxygenated → polymerisation

“Sickle” shaped cells
SC cause a huge spectrum of problems; intravascular haemolysis and so changes in NO, Abnormal shaped RBC have abnormal membranes which effect vasculature.

75
Q

What are the acute complications of SCD?

A

Stroke-Ischaemia and Haemorrhagic
Cholecystitis
Hepatic sequestration
Dactylitis
Bone pain & infarcts
Osteomyelitis
Retinal detachment
Vitreous haemorrhage
Chest syndrome
Splenic sequestration
Haematuria: papillary necrosis
Priapism
Aplastic crisis
Leg ulcers

76
Q

What are the clinical features of SCD

A

Painful crises
Aplastic crises
Infections

Acute sickling:
Chest syndrome
Splenic sequestration
Stroke

Chronic sickling effects:

  • Renal failure
  • Avascular necrosis bone
77
Q

What are the laboratory features of SCD?

A

Anaemia (Hb often 65-85)
Reticulocytosis
Increased NRBC (nucleated RBC)
Raised Bilurubin - increased RBC breakdown
Low creatinine

78
Q

How can we confirm the diagnosis of SCD ?

A

-Through a solubility test
Expose blood to reducing agent
HbS precipitated
Positive in trait and disease

-Using electrophoresis structure
A-C =SCT
D-E = HbC trait
F= SCD

-HPLC
The extra portion at the end of the trait machine result when compared to normal.
SS patient= no HbA.

To diagnose SCD, use HPLC/Hb electrophoresis

79
Q

What are the two types of acquired Haemolytic anaemia ?

A

Autoimmune
Alloimmune

80
Q

Describe Autoimmune Haemolytic Anaemia

A

Idiopathic
(Usually warm)
(IgG, IgM)
Drug mediated
Cancer associated
(LPDs)

81
Q

Describe Alloimmune Haemolytic Anaemia

A

Transplacental transfer:
Haemolytic disease of the newborn:D, c, L
ABO incompatability
Transfusion related:
Acute haemolytic transfusion reaction
ABO
Delayed haemolytic transfusion reaction:
E.g Rh groups, Duffy

82
Q

Describe Non-Immune acquired haemolysis

A

Paroxysmal nocturnal haemoglobinuria
RBC become vulnerable through a mutation in proteins which protects the cell normally from the complement mediated lysis. And so there is intravascular Haemolysis through the lysis of the RBC.

Fragmentation haemolysis:
Mechanical
Microangiopathic haemolysis
Disseminated intravascular coagulation – fibrin strands from clotting factors because of sepsis in the capillaries, damage the red cells
Thrombotic thrombocytopenic purpura

Other:
Severe burns
Some infections: e.g. malaria

83
Q

Breakdown of RBCs in Haemolytic anaemia is often accompanied by……….
This may maintain……

A

⬆ RBC production
Normal Hb level (if it compensates for shortened RBC lifespan)

84
Q

Anaemia can be classified based on:

A

Cause of anaemia:

  • RBC loss
  • Insufficient normal RBC production
  • Excessive destruction of RBCs (haemolytic anaemia)

RBC morphology:

  • Microcytic
  • Macrocytic
  • Normocytic
85
Q

Haemolytic Anaemia - Intrinsic Classification

A

Membrane defects:

  • Hereditary Spherocytosis
  • Hereditary Elliptocytosis
  • Hereditary Pyropoikilocytosis

Enzyme Defects:

  • G6PD deficiency
  • PK deficiency

Haemoglobin Defects:

  • Sickle Cell Disease
  • Thalassaemias
86
Q

Haemolytic Anaemia - Extrinsic Classification

A

Immune-Mediated:

-Autoimmune:

  • Warm - high temp. 37oC
  • Cold - low temp. 4oC-37oC
  • Drug-induced

-Alloimmune:

  • Haemolytic Disease of Newborn
  • Haemolytic Transfusion Reaction

Non-Immune-Mediated:

-RBC Fragmentation Syndrome:

-Mechanical damage - e.g. artificial valve destroys RBCs

-Microangiopathic Haemolytic Anaemia = destroy RBCs within vascular system, caused by fibrin deposited in vascular endothelium - e.g. Haemolytic Urinic Syndrome, Thrombotic thrombocytopenic purpura
(Blood disorder which causes clots forming in blood vessels -low RBC, platelets due to breakdown), Disseminated Intravascular Coagulation

  • Drugs + Chemicals
  • Infection - e.g. Malaria, Clostridium
  • March Haemoglobinuria
  • Hypersplenism
87
Q

Intravascular Haemolytic Anaemia

A
  • G6PD deficiency
  • PK deficiency
  • Drug-induced
  • Haemolytic transfusion reaction
  • RBC fragmentation syndrome
  • Infection
  • March haemoglobinuria
88
Q

Poikilocytosis =

Anisocytosis =

Hypochromic =

A

Poikilocytosis = RBCs of diff. shapes

Anisocytosis = RBCs of diff. sizes

Hypochromic = RBCs with larger central pallor

[MBD] NoNa (28 decks)

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