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Haematology and Immunology > Red Cells > Flashcards

Red Cells Flashcards

1
Q

Definition of anaemia

A

The reduction in red cells or their haemoglobin content

Hb below normal for age and sex

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2
Q

Causes of anaemia

A

Blood loss
Increased destruction
Lack of production
Defective production

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3
Q

If the bone marrow is stressed, what will it do?

A

Tip out more reticulocytes

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4
Q

What is the cell before the cell turns into a erythrocyte?

A

Reticulocyte

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5
Q

Developmental pathway of a RBC

A
  1. Ribosome synthesis
    - early erythroblast
  2. haemoglobin accumulation
    - late erythroblast to normoblast
  3. ejection of nucelus
    - reticulocyte
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6
Q

Substances required for RBC production

A 
Metals
- iron
- copper
- cobalt 
- manganese 
Vitamins
- B12
- Folic acid
- thiamine
- Vit B6
- Vit C
- Vit E 
Amino acids 
Hormones 
- erythropoietin (produced by the liver)
- GM-CSF
- Androgens
- thyroxine
- SCF
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7
Q

Where does RBC breakdown occur and how?

A

reticuloendothelial system by macrophages
Globin - amino acids reutilised
Haem - iron reutilised and haem broken down to biliverdin and eventually to bilirubin

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8
Q

where are macrophages found that remove RBCs?

A

Spleen
Lymph nodes
Lungs

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9
Q

Where are the majority of RBCs removed?

A

Spleen

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10
Q

How is bilirubin transferred?

A

By haem - bound to the albumin in the plasma

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11
Q

Another name for a mature RBC

A

Erythrocyte

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12
Q

How long do RBCs last for?

A

120 days

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13
Q

Features of a RBC

A 
Biconcave disc shape
Membranes
enzymes
haemoglobin 
deformable - can squeeze through the vasculature and allows them to last longer in the circulation
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14
Q

Congenital anaemias are caused by 1 of 3 causative features

A
  1. in red cell membrane
  2. in red cell metabolic pathways (enzymes)
  3. In haemoglobin synthesis
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15
Q

Possible defect in the red cell membrane causing anaemia

A

Defects in skeletal proteins in the lipid bilayer can lead to increased abnormal cells leading to increased haemolysis and increased destruction

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16
Q

What skeletal proteins can have defects?

A

Ankyrin
Spectrum
Band 3

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17
Q

Pathology of hereditary spherocytosis

A 
defects in 5 different structural proteins
- ankyrin 
- alpha spectrin 
- beta spectrin 
- band 3
- protein 4.2 
Red cells are spherical 
Removed by the RE system (extravascular) as the spleen recognises them as the wrong shape
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18
Q

Presentation of hereditary spherocytosis

A 
Variable
anaemia
jaundice (neonatal)
Splenomegaly 
- due to the spleen working overtime 
Pigment gallstones (deposits of excess bilirubin)
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19
Q

Why does hereditary spherocytosis result in jaundice?

A

Break down a red cell faster than normal -> bilirubin will rise -> jaundice (prolonged)

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20
Q

Treatment of hereditary spherocytosis

A 
Folic acid (increased requirements) 
Transfusion (if intermittent illness e.g. virus/drugs/unwell as this causes increased haemolysis)
Splenectomy (due to chronic haemolysis as the spleen is destroying all the RBCs)
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21
Q

Two pathways of red cell enzymes

A

Glycolysis - provides energy

Pentose phosphate shunt - protects from oxidative damage

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22
Q

Two key enzymes that you can get congenital deficiencies of

A

2,3-DPG

Pyruvate kinase

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23
Q

What does Glucose 6 phosphate dehydrogenase (G6PD) do?

A

Neutralises free radicals which are highly reactive.

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24
Q

Pathology of G6PD deficiency

A

Red cells become very prone to free radical injury resulting in intravascular haemolysis

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25
Q

What does G6PD deficiency confer a protection against?

A

Malaria

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26
Q

Genetics of G6PD deficiency

A

X linked

  • Affects males
  • Female carriers
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27
Q

Features of cells in G6PD deficiency

A

Blister cells
Bite cells
Heinz bodies

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28
Q

Presentation of G6PD Deficiency

A 
neonatal jaundice 
Drug, broad bean or infection precipitated jaundice and anaemia
- intravascular haemolysis
- haemoglobinuria 
Splenomegaly 
Pigment gallstones
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29
Q

Triggers for haemolysis in G6PD Deficiency

A 
Infection 
acute/intercurrent illness e.g. DKA
Broad (fava) beans 
drugs 
- antimalarials
- sulphonamides and sulphones
- antibacterials (nitrofunantoin)
- analgesics (big doses of aspirin) 
- antihelminthes 
- vit K analogues 
- methylene blue
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30
Q

Pathology of pyruvate kinase deficiency

A

Reduced ATP - leading to blockage
Increased 2,3-DPG - leading to rigid cells
Cells being rigid means that they are more liable to haemolysis in the circulation

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31
Q

Presentation of pyruvate kinase deficiency

A

Anaemia
Jaundice
Gallstones

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32
Q

How common is pyruvate kinase deficiency?

A

Rare

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33
Q

Function of haemoglobin

A

Oxygen binding and unloading
- gives up O2 more readily when you need it e.g. exercise
- vasodilation in e.g. exercise when warm - give up O2 more easily
Gas exchange
- O2 to tissues
- CO2 to lungs

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34
Q

Features of the “Bohr effect”

A

Acidosis
Hyperthermia
Hypercapnia

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35
Q

Fetal haemoglobin vs adult haemoglobin

A

Foetal haemoglobin has a higher affinity than adult haemoglobin for O2

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36
Q

What is haemoglobin made up of?

A 
A haem molecule 
2 alpha chains 
4 alpha genes (Chr16)
2 beta (B) chains
2 beta genes (Chr 11)
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37
Q

Two types of adult haemoglobin

A 
Hb A (aaBB) - 97% 
Hb A2 (aadd) - 2%
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38
Q

Genes of foetal haemoglobin

A

aagg - 1%

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39
Q

What happens if all alpha genes are lost in terms of haemoglobin?

A

Incompatible with life as any combination made requires alpha genes however if other genes were missing e.g. beta chains then other genes can take over e.g. delta

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40
Q

What are haemoglobinopathies?

A

Inherited abnormalities of haemoglobin synthesis

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41
Q

Pathologies of haemoglobinopathies, either…

A

Reduced or absent globin chain production - thalassaemia
or
mutations leading to structurally abnormal globin chain - HbS, HbC, HbD etc

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42
Q

What does HbSS mean/present with?

A

Sickle cell disease

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43
Q

What is sickle cell disease haemoglobin composed of?

A

A haem molecule
2 a chains
2 b (sickle) chains

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44
Q

Pathology of sickle cell disease

A

HbS under conditions of stress e.g. hypoxia
- the Hb crystallises and forms a rigid structure and so then the red blood cell changes shape - SICKLES (this is irreversible). (NOT A DEFECT OF CELL MEMBRANE)
even when trying to carry oxygen again it stays in this sickle shape
This leading to
Red cell injury, cation loss, dehydration (due to leaking)
- HAEMOLYSIS
- chronic lifelong vasculopathy (major risk factor for stroke)
endothelial activation
promotion of inflammation
Vaso occlusion - impaired passage of the RBC clogs vessels and tissue infarcts

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45
Q

Diagnosis of sickle cell disease

A

Blood film

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46
Q

Presentation of sickle cell disease

A 
Painful vasoocclusive arteries 
- bone 
- very severe 
- often requiring very opiates in hospital 
Chest crisis 
- hypoxia 
- chest pain 
- fever 
- infiltrates on X ray 
Stroke / mental retardation
Increased infection risk (hyposplenism) 
chronic haemolytic anaemia 
sequestrian crisis 
Hepatomegaly 
Auditory impairment 
Retinopathy 
Cardiomegaly -> CHF
Bone marrow hyperplasia
Aseptic bone necrosis - > osteomyelitis 
infarcts of extremities 
vaso occlusion 
ulcer
Delayed puberty
Reduced fertility 
Obstetric complications 
Immunosuppression 
Bony deformity (physical disability) 
Priapism (involuntary erection of penis)
splenomegaly 
pulmonary infarcts -> pneumonia
Renal pathology 
Growth impairment (endocrine dysfunction)
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47
Q

Treatment of chest crisis of sickle cell disease

A 
Resp support
Antibiotics 
IV fluids 
TRANSFUSION to give HbA
- to keep HbS < 30% so more like a carrier state
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48
Q

Prognosis of sickle cell disease

A

life expectancies
- men 42 y/o
- women 48 y/o
perinatal and childhood morality associated with this

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49
Q

treatment of sickle cell disease

A 
Avoid precipitants 
life long prophylaxis
- vaccination 
- penicillin (and malarial) prophylaxis 
- folic acid 
acute events
- hydration 
- oxygenation 
- prompt treatment on infection 
- analgesia (NSAIDs, opiates) 
Blood transfusion if severe anaemia 
Exchange transfusions to reduce HbS < 30% 
Disease modifying drugs (hydroxycarbamide) 
Bone marrow transplantation 
Gene therapy
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50
Q

Definition of thalassaemia’s

A

Reduced or absent globin chain production

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51
Q

Pathology of thalassaemias

A

Mutations or deletions in
- alpha genes (alpha thalassaemia)
- beta genes (beta thalassaemia)
Chain imbalance due to deleted genes leading to chronic haemolysis and anaemia

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52
Q

Types of thalassaemia’s

A

Homozygous alpha zero thalassaemia
Beta thalassaemia major (homozygous beta thalassaemia)
Non-transfusion dependent thalassaemia (intermedia)
Thalassemia minor

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53
Q

Features of homozygous alpha zero thalassaemia

A

No alpha chains - 4 genes affected
Hydrops fetalis - incompatible with life
Death occurs in utero

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54
Q

Features of beta thalassaemia major (homozygous beta thalassaemia)

A

No beta chains
Hugely metabolic active condition
Transfusion dependent anaemia but will survive

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55
Q

Presentation of beta thalassaemia major

A 
Severe anaemia
- presenting at 3-6 months of age
- expansion of maxillary sinuses and mandible
- expansion of ineffective bone marrow 
- bony deformities
- splenomegaly 
- growth retardation 
- hair on end appearance of skull on X ray 
Failure to thrive
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56
Q

Treatment of beta thalassaemia major

A 
Chronic transfusion support - 4-6 weekly 
Iron chelation 
- S/C deferoxamine infusions
- oral deferasirox 
Bone marrow transplantation (curative)
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57
Q

What does iron chelation do?

A

Takes away the excess iron

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58
Q

Why does beta thalassaemia major not show any symptoms until 3-6 months of life?

A

After the foetal haemoglobin goes down and the adult haemoglobin fails to rise do you get symptoms and therefore need a transfusion

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59
Q

Life expectancy of beta thalassaemia major

A

untreated or with irregular transfusions < 10 y/o

normal life expectancy (>40 y/o) following blood transfusion and iron removal

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60
Q

Features of thalassaemia minor

A

“trait” or carrier state
Hypochromic microcytic red cell indices - small red cells
only really significant if partner has it as well as it may affect baby

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61
Q

Presentation of thalassaemia minor

A

Very mild anaemia sometimes but usually absaloutly fine

mostly asymptomatic

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62
Q

Most common thalassaemia

A

Thalassaemia minor

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63
Q

Pathology of Haem synthesis defects

A

RARE
defects in mitochondrial step of haem synthesis result in SIDEROBLAST ANAEMIA
- ALA synthase mutations
- hereditary X linked
- acquired - myelodysplasia
Defects in cytoplasmic steps result in prophyrias

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64
Q

Normal range of Hb for male 12-70 y/o

A

140-180

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65
Q

Normal range of Hb for male > 70 y/o

A

116-156

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66
Q

Normal range of Hb for females 12-70 y/o

A

120-160

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67
Q

Normal range of Hb for females > 70 y/o

A

108-143

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68
Q

Factors influencing normal range of haemoglobin

A

Age
- babies born, within 48 hours are polycythemic and then at 4-6 weeks become anaemic

Sex (M > F due to testosterone)

ethnic origin

time of day sample taken - fasting sample = higher Hb

Time to analysis
= sitting in a tube will affect size and shape of cells

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69
Q

Presentation of acquired anaemias

A 
Tiredness
Palor 
Breathlessness
Yellowing of eyes 
Swelling of ankles
Dizziness
chest pain 
Palpitations 
Angina 
Changed stool colour 
Muscular weakness 
Sore red tongue 
Kolinichia 
symptoms related to underlying cause
- evidence of bleeding (menorrhagia, dyspepsia, PR bleeding)
- malabsorption (diarrhoea, weight loss)
- jaundice (due to haemolysis) 
- splenomegaly/lymphadenopathy (can show in both congenital and acquired)
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70
Q

Pathology of acquired anaemia - due to either….

A 
Bone marrow
- cellularity
- stroma
- nutrients 
Red cell 
- membrane
- haemoglobin 
- enzymes
Destruction loss
- blood loss
- haemolysis
- hypersplenism
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71
Q

What do red cell indices do?

A

Automated measurement of red cell size and haemoglobin content

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72
Q

Red cell indices include

A

MCV

MCH

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73
Q

What does MCV mean?

A

Mean cell volume

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74
Q

What does MCH mean?

A

Mean cell haemoglobin

- how much haemoglobin is in each cell

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75
Q

Morphological types of anaemia

A

Hypochromic microcytic
Normochromic normocytic
Macrocytic

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76
Q

What morphological type of anaemia is the commonest worldwide?

A

Hypochromic microcytic

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77
Q

Features of hypochromic microcytic anaemia

A

Small and pale

Area of central palor with haemoglobin around the edges

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78
Q

Causes of hypochromic microcytic anaemia

A

Iron deficiency
Chronic bleeding
Thalassaemias
Chronic disease

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79
Q

Investigations of hypochromic microcytic anaemia

A

Serum ferritin

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80
Q

Interpretations of serum ferritin

A 
if low = iron deficiency 
if normal or increased
- thalassaemia 
- secondary anaemia 
- sideroblastic anaemia
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81
Q

What is secondary anaemia also known as?

A

Anaemia of chronic disease

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82
Q

Features of normochromic normocytic anaemia

A

looks like normal cells but there is less of them

big cohort of people will be in this

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83
Q

Investigations of normochromic normocytic anaemia

A

Reticulocyte count

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84
Q

Interpretation of reticulocyte count

A

If increased
- bone marrow working well and throwing out reticulocytes to try and compensate so e.g. Acute blood loss, haemolysis

If decreased
- bone marrow not working so e.g. secondary anaemia, hypoplasia, marrow infiltration

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85
Q

Causes of macrocytic anaemia

A 
B12 deficiency 
folate deficiency 
underlying bone marrow problem 
alcohol 
drugs (methotrexate, ARVs, hydroycarbamide)
Disordered liver function 
hypothyroidism 
myelodysplasia
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86
Q

Types of macrocytic anaemia

A

Megaloblastic

Non-megaloblastic

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87
Q

Causes of megaloblastic macrocytic anaemia

A

B12 deficiency

  • pernicious anaemia
  • gastric / ileal disease

Folate deficiency

  • dietary
  • increased requirements (haemolysis)
  • GI pathology
88
Q

Presentation of megaloblastic macrocytic anaemia

A 
B12/folate deficiency 
- anaemia 
- neurological symptoms (rare)
Lemon yellow tinge 
- bilirubin, LDH
- red cell friable
89
Q

Treatment of megaloblastic macrocytic anaemia

A

Replace vitamin
For B12 deficiency
- B12 IM injection (loading dose then 3 monthly)
For folate deficiency
- oral folate replacement
- ensure B12 normal if neuropathic symptoms as giving folate can make neuropathy worse

90
Q

Causes of non-megaloblastic macrocytic anaemia

A

Myelodysplasia
Marrow infiltration
Drugs

91
Q

Investigations for Macrocytic anaemia

A

B12
Folate
Bone marrow

92
Q

Where is iron stored in the body?

A

Predominately liver

Some in muscle

93
Q

Is there an active pathway/mechanism for the excretion of iron?

94
Q

Role of hepcidin

A

Iron is absorbed in the duodenum - Fe2+ -> Fe3+
- transported from enterocytes and macrophages by ferroportin
- transported in plasma bound to transferrin
- stored in cells as ferritin
Hepcidin binds to ferroportin and blocks its function and so stops transporting iron from duodenal enterocytes into the circulation
- so reduces intestinal iron absorption and mobilisation from reticuloendothelial cells
Iron is there but it is stick - in duodenal enterocytes, macrophages etc

95
Q

Where is hepcidin made and in response to what?

A 
Liver (hepatocytes)
In response to 
- inflammation 
- renal failure
- increased iron levels
96
Q

What is the most common cause of anaemia worldwide?

A

Iron deficiency anaemia

97
Q

What kind of anaemia is iron deficiency anaemia?

A

Hypochromic microcytic

98
Q

Things to ask in the history about of iron deficiency anaemia

A 
Dyspepsia
GI bleeding
other bleeding e.g. menorrhagia 
Diet (note children and elderly) 
Increased requirements in pregnancy 
Signs of iron deficiency
99
Q

What are the signs of iron deficiency?

A

Sore atrophic tongue
Angular cheilitis
Koilonychia (spoon shaped nails)

100
Q

Causes of iron deficiency anaemia

A

GI blood loss
Menorrhagia
Malabsorption
- gastrectomy
- absorption problems e.g. coeliac disease
- increased GI transit time e.g. diarrhoea

101
Q

Management of iron deficiency anaemia

A 
Correct the deficiency 
- oral iron 
- IV iron if intolerant to oral 
- blood transfusion rarely indicated
Correct the cause
- diet
- ulcer therapy
- gynae interventions 
- surgery
102
Q

What kind of anaemia is haemolytic anaemia?

A

Normochromic normocytic

103
Q

Pathology of haemolytic anaemia

A

Accelerated red cell destruction (lead to decreased Hb)
Compensation by bone marrow (increased retics)
Levels of Hb - balance between red cell production and destruction

104
Q

Types of haemolytic anaemia

A

Congenital

Acquired

105
Q

Congenital Haemolytic anaemias

A 
Hereditary spherocytosis (HS)
Enzyme deficiency (G6PD deficiency) 
Haemoglobinopathy (HbSS)
106
Q

Acquired haemolytic anaemias

A

Immune (mostly extravascular)
- auto immune haemolytic anaemia
Non-immune (intravascular)
- mechanical e.g. artificial valve can shear the red cells
- severe infection / DIC - can get haemolysis due to the toxins of the infection
- PET/HUS/TTP (Thrombotic thrombocytopenic purpura) = microangiopathic haemolytic anaemias `

107
Q

Diagnosis of haemolytic anaemias

A 
History and exam
Direct antiglobulin test (DAT)
urine for hemosiderin/urobilinogen 
FBC
reticulocyte count
Blood filml 
Serum bilirubin (direct/indirect)
LDH
Serum haptoglobin
108
Q

Bilirubin levels in haemolysis

A

Bilirubin will be high (unconjugated)

109
Q

Serum haptoglobin levels in haemolysis

A

mops up free haemoglobin and so in haemolysis these levels are low

110
Q

What does DAGT show in haemolysis?

A

If positive = immune mediated

If negative = non immune mediated

111
Q

Three types of immune haemolysis

A

Warm auto antibody
Cold auto antibody
Alloantibody

112
Q

Features of warm auto antibody immune haemolysis

A

Antibodies that only bind at warm temperatures - 37C so can cause haemolysis in the body
Usually IgG antibodies
The more troublesome autoimmune anaemia

113
Q

Causes of warm auto antibody immune haemolysis

A

Autoimmune
drugs
CLL

114
Q

Features of cold auto antibody haemolysis

A

Antibodies that bind in the cold
Haemolysis less severe
Less clinical haemolysis and sometimes an incidental finding

115
Q

Causes of cold auto antibody haemolysis

A

CHAD
infections
lymphoma

116
Q

When does alloantibody occur?

A

Transfusion reaction

117
Q

Management of haemolytic anaemia

A

Support marrow function - haemolysis
correct cause
- immunosuppression if autoimmune (steroids, treat trigger e.g. CLL, lymphoma)
- remove site of cell destruction (splenectomy)
- Treat sepsis, leaky prostatic valve, malignancy etc if intravascular
Consider transfusion

118
Q

What does the Direct antiglobulin test (DAT) detect?

A

Antibody or complement on red cell membrane

119
Q

In DAT, the reagent either contains what and what does it do?

A

Anti-human IgG
Anti-complement
Reagent binds to Ab (or complement) on red cell surface and causes agglutination in vitro

120
Q

What does DAT imply?

A

Immune basis for haemolysis

  • detects antibodies on the surface of red cells (autoimmune antibodies)
  • if had red cell transfusion and if you take it out there may be alloantibodies made by transfused cells
121
Q

What is secondary anaemia?

A

Anaemia of chronic disease

122
Q

What type of anaemia is secondary anaemia?

A

70% normochromic normocytic

30% hypochromic microcytic

123
Q

Pathology of secondary anaemia

A

Defective iron utilisation

  • increased hepcidin in inflammation
  • ferritin often elevated
124
Q

Possible causes of secondary anaemia

A

infection
inflammation
malignancy

125
Q

How does vitamin B12 get absorbed?

A

Dietary B12 binds to intrinsic factor secreted by gastric parietal cells
B12-IF complex attaches to specific IF receptors in distal ileum
Vitamin B12 bound by transcobalamin II in portal circulation for transport to marrow and other tissues

126
Q

Who gets pernicious anaemia?

A

Older people

Runs in families

127
Q

Pernicious anaemia has antibodies against….

A 
Intrinsic factor (diagnostic)
Gastric parietal cells (less specific)
128
Q

Presentation of pernicious anaemia

A

Malabsorption of dietary B12

Symptoms / signs take 1-2 years to develop

129
Q

Diagnosis of pernicious anaemia

A

Schilling test

130
Q

Treatment of pernicious anaemia

A

IM vitamin B12

131
Q

Very low haemoglobin result - what to think about first?

A

Is the patient stable or unstable?

Are they bleeding?

132
Q

What type of cancer comes from mesenchymal cells?

133
Q

What type of cancer comes from epithelial cells?

A

Carcinoma

  • squamous
  • glandular
134
Q

Acute causes of bleeding

A 
Bronchiectasis 
TB
Lung carcinoma 
GI bleeding
- varices
- carcinoma 
Spleen rupture
135
Q

Causes of normochromic normocytic anaemia

A 
Acute bleeding
Haemolytic anaemia 
Leukaemia (no space for them)
Anaemia of chronic disease 
Chronic kidney disease 
Aplastic anaemia
136
Q

Is iron deficiency common? - males vs females

A

Males - not common

Females - tiny amount of blood loss over time so not concerning in women of reproductive age

137
Q

What would iron deficiency in a male indicate?

A

Bowel cancer

138
Q

Pathology of anaemia of chronic disease

A

Due to inflammatory environment

Cytokines interfere so iron accumulates in macrophages so the iron is there, but we cannot use it

139
Q

If a patient has a chronic disease, what do you need to consider?

A

If there is an inflammatory background in the chronic disease as this may be interfering with ferritin

140
Q

What is TSAT?

A

Transferrin saturation

141
Q

What commonly taken drug can cause small amounts of GI bleeding?

142
Q

Why in chronic kidney disease can you become anaemic?

A

Because erythropoietin is produced in the kidneys

143
Q

Function of erythropoietin

A

Released into bloodstream during hypoxia

It is carried to the bone marrow where it works to stimulate stem cells to become RBCs

144
Q

Cause of anaemia in the young

A

Genetic cause

145
Q

In hereditary spherocytosis, what happens due to the shape of the red cells?

A

They cant go through the vasculature and so they break

146
Q

What does G6PD stand for?

A

Glucose-6-phosphate dehydrogenase

147
Q

Where is globin synthesised?

A

In the RER in the ribosomes

148
Q

What chains of haemoglobin are present in both the adult and the foetus?

A

Alpha chains

149
Q

The genes and their relation to the two types of Beta Thalassaemia

A

1 defective gene - minor

2 defective genes - major

150
Q

What happens to the bone marrow in Beta thalassaemia major?

A

It expands

As trying to compensate for the anaemia

151
Q

What is the iron chelating agent used?

A

Desferioxamine

152
Q

What type of mutation is sickle cell disease?

A

Missense mutation

Glutamic acid becomes valene

153
Q

What can cause sickle cell crisis and therefore sickling?

A

Tipping the balance e.g.

  • fever
  • lowering pH
154
Q

What do reticulocytes look like on blood film?

A

Blue and bigger

some still have RNA

155
Q

What does Sickle cell haemoglobin look like on electrophoresis if you were a carrier?

A

Would have the sickle ad but also have the adult haemoglobin band

156
Q

Acquired causes of anaemia

A

Drugs
Mechanical value; shear stress
Autoimmune haemolytic anaemia

157
Q

Pathology of autoimmune haemolytic anaemia

A

RBCs are coated with antibodies which are recognised by splenic macrophages to eat
Extravascular

158
Q

What does autoimmune haemolytic anaemia look like on blood film?

A

Shows fragmented/bite cells - these will be eventually eaten

159
Q

What is the most common form of autoimmune haemolytic anaemia?

A

Warm antibody haemolytic anaemia

160
Q

Who is warm antibody haemolytic anaemia common in?

161
Q

What temperature do autoantibodies generally react at in warm antibody haemolytic anaemia?

162
Q

Pathology of haemolysis in warm antibody haemolytic anaemia

A

Occurs primarily in the spleen

Not due to direct lysis of RBCs

163
Q

What temperature do autoantibodies react at in cold antibody haemolytic anaemia?

164
Q

Pathology of haemolysis in cold antibody haemolytic anaemia

A

Occurs largely in extravascular mononuclear phagocyte system of the liver and spleen

165
Q

Prognosis of cold antibody haemolytic anaemia

A

Anaemia usually mild

166
Q

Type of antibodies in warm antibody haemolytic anaemia

167
Q

Type of antibodies in cold antibody haemolytic anaemia

168
Q

Prognosis of warm antibody haemolytic anaemia

A

Usually severe

Can be fatal

169
Q

Levels of ferritin in anaemia of chronic disease

A

Normal to high

170
Q

What type of anaemia is seen in beta thalassaemia major?

A

Microcytic hypochromic

171
Q

What happens to the reticulocyte count in autoimmune haemolytic anaemia?

A

It increases

172
Q

When are hypersegmented neutrophils seen?

A

Megaloblastic anaemia

173
Q

Features of B12 deficiency

A

Cytopenia
Leucocytopenia
Hypersegmented neutrophils

174
Q

What can cause fragmented red cells caused by intravascular haemolysis?

A

DIC
Mechanical heart valves
Malignant HTN

175
Q

What is aplastic anaemia?

A

Primary bone marrow failure so bone marrow just becomes fat

176
Q

Features of aplastic anaemia

A

Pancytopenia

Normochromic normocytic anaemia

177
Q

Shape of RBCs

A

Biconcave
Anucleated
Haemoglobin

178
Q

What is haematocrit?

A

% volume of RBC/volume of whole blood

179
Q

Normal Ht values for males

180
Q

Normal Ht vales for females

181
Q

What can cause increased Ht?

A

Dehydration

Increased RBC mass

182
Q

What can cause reduced Ht?

A

Acute haemorrhage

Haemodiluation

183
Q

What is MCH increased in?

A

Macrocytic anaemias

184
Q

What is MCH decreased in?

A

Hyperchromic anaemias

185
Q

What does MCHC stand for?

A

Mean corpuscular haemoglobin concentration

186
Q

What is MCHC increased in?

A

Hyperchromic conditions e.g. sickle cell disease

187
Q

What is MCHC decreased in?

A

Microcytic conditions

188
Q

What is RDW?

A

Red blood cell distribution width (average volume)

189
Q

What can increase ferritin?

A

Infection
Any inflammatory disorder
Malignancy
Pregnancy proteins

190
Q

Ferritin levels in iron deficiency anaemia

A

Low

But loads of things increase ferritin so can still be iron deficient with a normal ferritin level

191
Q

Another name for transferrin

A

Total iron binding capacity (TIBC)

192
Q

How to take iron supplements

A

With food

Not too close together as can close down the iron transporter

193
Q

How many genes are affected in alpha thalassaemia and theyre effects

A

1 gene - rarely any significant anaemia
2 genes - clinically equivalent to beta thalassaemia minor
3 - similar to beta thalassaemia major

194
Q

If have the genes HbAS, what is this known as?

A

Sickle cell trait

195
Q

What is vit B12 needed for?

A

Helps make DNA in every cell

196
Q

Causes of vit B12 deficiency

A 
Gastrectomy
PPIs
Metformin 
Antibodies to gastric parietal cells or intrinsic factor 
Chrons 
Coeliac disease 
UC 
Resection 
Fish tape worm - diphillobothrium latum
197
Q

What foods is folate found in?

A

Brown rice
Broccoli
Brussel sprouts
Fortified cereals

198
Q

Causes of folate deficiency

A 
Diet 
Increased cell turnover
- psoriasis
- haemolytic anaemia 
- cancers
199
Q

What would cold autoantibody autoimmune haemolytic anaemia be following?

A

Viral infection - CMV, EBV, chickenpox, measles, mumps, mycoplasma pneumonia
Idiopathic
Lymphoma

200
Q

What would warm antibody autoimmune haemolytic anaemia be seen in?

A

RA
SLE
CLL
Idiopathic

201
Q

What anaemia would hypothyroidism result in?

A

Macrocytic - non megaloblastic / normoblastic

202
Q

What anaemia does myelodysplasia result in?

A

Normoblastic macrocytic anaemia

203
Q

Causes of normocytic megaloblastic anaemia

A 
Alcohol 
Liver disease
Hypothyroidism 
Pregnancy 
Reticulocytosis 
MDS
Cytotoxic drugs
204
Q

What anaemia does chronic kidney disease result in?

A

Normocytic

205
Q

What does congenital sideroblastic anaemia result in? (type of anaemia)

A

Microcytic

206
Q

What shows target cells on blood film?

A

Sickle cell
Thalassaemias
Hyposplenism
Liver disease

207
Q

What shows tear drop poikilocytes on blood film?

A

Myelofibrosis

208
Q

What shows Spherocytes on blood film?

A

Hereditary spherocytosis

Autoimmune haemolytic anaemia

209
Q

What shows basophilic stippling on blood film?

A

Lead poisoning
Thalassaemia
Sideroblastic anaemia
Myelodysplasia

210
Q

What shows Howell-Jolly bodies on blood film?

A

Hyposplenism

211
Q

What shows Heinz bodies on blood film?

A

G6PD deficiency

A-thalassaemia

212
Q

What shows shistocytes (helmet cells) on blood film?

A

Intravascular haemolysis
Mechanical heart valve
DIC

213
Q

What does DIC stand for?

A

Disseminated intravascular coagulation

214
Q

What shows pencil poikilocytes on blood film?

A

Iron deficiency

215
Q

What shows burr cells on blood film?

A

Uraemia

Pyruvate kinase deficiency

216
Q

What shows hypersegmented neutrophils on blood film?

A

Megaloblastic anaemia

Haematology and Immunology (18 decks)

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