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
2
Q
Causes of anaemia
A
Blood loss
Increased destruction
Lack of production
Defective production
3
Q
If the bone marrow is stressed, what will it do?
A
Tip out more reticulocytes
4
Q
What is the cell before the cell turns into a erythrocyte?
A
Reticulocyte
5
Q
Developmental pathway of a RBC
A
- Ribosome synthesis
- early erythroblast - haemoglobin accumulation
- late erythroblast to normoblast - ejection of nucelus
- reticulocyte
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
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
8
Q
where are macrophages found that remove RBCs?
A
Spleen
Lymph nodes
Lungs
9
Q
Where are the majority of RBCs removed?
A
Spleen
10
Q
How is bilirubin transferred?
A
By haem - bound to the albumin in the plasma
11
Q
Another name for a mature RBC
A
Erythrocyte
12
Q
How long do RBCs last for?
A
120 days
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
14
Q
Congenital anaemias are caused by 1 of 3 causative features
A
- in red cell membrane
- in red cell metabolic pathways (enzymes)
- In haemoglobin synthesis
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
16
Q
What skeletal proteins can have defects?
A
Ankyrin
Spectrum
Band 3
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
18
Q
Presentation of hereditary spherocytosis
A
Variable anaemia jaundice (neonatal) Splenomegaly - due to the spleen working overtime Pigment gallstones (deposits of excess bilirubin)
19
Q
Why does hereditary spherocytosis result in jaundice?
A
Break down a red cell faster than normal -> bilirubin will rise -> jaundice (prolonged)
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)
21
Q
Two pathways of red cell enzymes
A
Glycolysis - provides energy
Pentose phosphate shunt - protects from oxidative damage
22
Q
Two key enzymes that you can get congenital deficiencies of
A
2,3-DPG
Pyruvate kinase
23
Q
What does Glucose 6 phosphate dehydrogenase (G6PD) do?
A
Neutralises free radicals which are highly reactive.
24
Q
Pathology of G6PD deficiency
A
Red cells become very prone to free radical injury resulting in intravascular haemolysis
25
What does G6PD deficiency confer a protection against?
Malaria
26
Genetics of G6PD deficiency
X linked
- Affects males
- Female carriers
27
Features of cells in G6PD deficiency
Blister cells
Bite cells
Heinz bodies
28
Presentation of G6PD Deficiency
```
neonatal jaundice
Drug, broad bean or infection precipitated jaundice and anaemia
- intravascular haemolysis
- haemoglobinuria
Splenomegaly
Pigment gallstones
```
29
Triggers for haemolysis in G6PD Deficiency
```
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
```
30
Pathology of pyruvate kinase deficiency
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
31
Presentation of pyruvate kinase deficiency
Anaemia
Jaundice
Gallstones
32
How common is pyruvate kinase deficiency?
Rare
33
Function of haemoglobin
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
34
Features of the "Bohr effect"
Acidosis
Hyperthermia
Hypercapnia
35
Fetal haemoglobin vs adult haemoglobin
Foetal haemoglobin has a higher affinity than adult haemoglobin for O2
36
What is haemoglobin made up of?
```
A haem molecule
2 alpha chains
4 alpha genes (Chr16)
2 beta (B) chains
2 beta genes (Chr 11)
```
37
Two types of adult haemoglobin
```
Hb A (aaBB) - 97%
Hb A2 (aadd) - 2%
```
38
Genes of foetal haemoglobin
aagg - 1%
39
What happens if all alpha genes are lost in terms of haemoglobin?
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
40
What are haemoglobinopathies?
Inherited abnormalities of haemoglobin synthesis
41
Pathologies of haemoglobinopathies, either...
Reduced or absent globin chain production - thalassaemia
or
mutations leading to structurally abnormal globin chain - HbS, HbC, HbD etc
42
What does HbSS mean/present with?
Sickle cell disease
43
What is sickle cell disease haemoglobin composed of?
A haem molecule
2 a chains
2 b (sickle) chains
44
Pathology of sickle cell disease
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
45
Diagnosis of sickle cell disease
Blood film
46
Presentation of sickle cell disease
```
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)
```
47
Treatment of chest crisis of sickle cell disease
```
Resp support
Antibiotics
IV fluids
TRANSFUSION to give HbA
- to keep HbS < 30% so more like a carrier state
```
48
Prognosis of sickle cell disease
life expectancies
- men 42 y/o
- women 48 y/o
perinatal and childhood morality associated with this
49
treatment of sickle cell disease
```
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
```
50
Definition of thalassaemia's
Reduced or absent globin chain production
51
Pathology of thalassaemias
Mutations or deletions in
- alpha genes (alpha thalassaemia)
- beta genes (beta thalassaemia)
Chain imbalance due to deleted genes leading to chronic haemolysis and anaemia
52
Types of thalassaemia's
Homozygous alpha zero thalassaemia
Beta thalassaemia major (homozygous beta thalassaemia)
Non-transfusion dependent thalassaemia (intermedia)
Thalassemia minor
53
Features of homozygous alpha zero thalassaemia
No alpha chains - 4 genes affected
Hydrops fetalis - incompatible with life
Death occurs in utero
54
Features of beta thalassaemia major (homozygous beta thalassaemia)
No beta chains
Hugely metabolic active condition
Transfusion dependent anaemia but will survive
55
Presentation of beta thalassaemia major
```
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
```
56
Treatment of beta thalassaemia major
```
Chronic transfusion support - 4-6 weekly
Iron chelation
- S/C deferoxamine infusions
- oral deferasirox
Bone marrow transplantation (curative)
```
57
What does iron chelation do?
Takes away the excess iron
58
Why does beta thalassaemia major not show any symptoms until 3-6 months of life?
After the foetal haemoglobin goes down and the adult haemoglobin fails to rise do you get symptoms and therefore need a transfusion
59
Life expectancy of beta thalassaemia major
untreated or with irregular transfusions < 10 y/o
| normal life expectancy (>40 y/o) following blood transfusion and iron removal
60
Features of thalassaemia minor
"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
61
Presentation of thalassaemia minor
Very mild anaemia sometimes but usually absaloutly fine
| mostly asymptomatic
62
Most common thalassaemia
Thalassaemia minor
63
Pathology of Haem synthesis defects
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
64
Normal range of Hb for male 12-70 y/o
140-180
65
Normal range of Hb for male > 70 y/o
116-156
66
Normal range of Hb for females 12-70 y/o
120-160
67
Normal range of Hb for females > 70 y/o
108-143
68
Factors influencing normal range of haemoglobin
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
69
Presentation of acquired anaemias
```
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)
```
70
Pathology of acquired anaemia - due to either....
```
Bone marrow
- cellularity
- stroma
- nutrients
Red cell
- membrane
- haemoglobin
- enzymes
Destruction loss
- blood loss
- haemolysis
- hypersplenism
```
71
What do red cell indices do?
Automated measurement of red cell size and haemoglobin content
72
Red cell indices include
MCV
| MCH
73
What does MCV mean?
Mean cell volume
74
What does MCH mean?
Mean cell haemoglobin
| - how much haemoglobin is in each cell
75
Morphological types of anaemia
Hypochromic microcytic
Normochromic normocytic
Macrocytic
76
What morphological type of anaemia is the commonest worldwide?
Hypochromic microcytic
77
Features of hypochromic microcytic anaemia
Small and pale
| Area of central palor with haemoglobin around the edges
78
Causes of hypochromic microcytic anaemia
Iron deficiency
Chronic bleeding
Thalassaemias
Chronic disease
79
Investigations of hypochromic microcytic anaemia
Serum ferritin
80
Interpretations of serum ferritin
```
if low = iron deficiency
if normal or increased
- thalassaemia
- secondary anaemia
- sideroblastic anaemia
```
81
What is secondary anaemia also known as?
Anaemia of chronic disease
82
Features of normochromic normocytic anaemia
looks like normal cells but there is less of them
| big cohort of people will be in this
83
Investigations of normochromic normocytic anaemia
Reticulocyte count
84
Interpretation of reticulocyte count
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
85
Causes of macrocytic anaemia
```
B12 deficiency
folate deficiency
underlying bone marrow problem
alcohol
drugs (methotrexate, ARVs, hydroycarbamide)
Disordered liver function
hypothyroidism
myelodysplasia
```
86
Types of macrocytic anaemia
Megaloblastic
| Non-megaloblastic
87
Causes of megaloblastic macrocytic anaemia
B12 deficiency
- pernicious anaemia
- gastric / ileal disease
Folate deficiency
- dietary
- increased requirements (haemolysis)
- GI pathology
88
Presentation of megaloblastic macrocytic anaemia
```
B12/folate deficiency
- anaemia
- neurological symptoms (rare)
Lemon yellow tinge
- bilirubin, LDH
- red cell friable
```
89
Treatment of megaloblastic macrocytic anaemia
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
Causes of non-megaloblastic macrocytic anaemia
Myelodysplasia
Marrow infiltration
Drugs
91
Investigations for Macrocytic anaemia
B12
Folate
Bone marrow
92
Where is iron stored in the body?
Predominately liver
| Some in muscle
93
Is there an active pathway/mechanism for the excretion of iron?
No
94
Role of hepcidin
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
Where is hepcidin made and in response to what?
```
Liver (hepatocytes)
In response to
- inflammation
- renal failure
- increased iron levels
```
96
What is the most common cause of anaemia worldwide?
Iron deficiency anaemia
97
What kind of anaemia is iron deficiency anaemia?
Hypochromic microcytic
98
Things to ask in the history about of iron deficiency anaemia
```
Dyspepsia
GI bleeding
other bleeding e.g. menorrhagia
Diet (note children and elderly)
Increased requirements in pregnancy
Signs of iron deficiency
```
99
What are the signs of iron deficiency?
Sore atrophic tongue
Angular cheilitis
Koilonychia (spoon shaped nails)
100
Causes of iron deficiency anaemia
GI blood loss
Menorrhagia
Malabsorption
- gastrectomy
- absorption problems e.g. coeliac disease
- increased GI transit time e.g. diarrhoea
101
Management of iron deficiency anaemia
```
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
What kind of anaemia is haemolytic anaemia?
Normochromic normocytic
103
Pathology of haemolytic anaemia
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
Types of haemolytic anaemia
Congenital
| Acquired
105
Congenital Haemolytic anaemias
```
Hereditary spherocytosis (HS)
Enzyme deficiency (G6PD deficiency)
Haemoglobinopathy (HbSS)
```
106
Acquired haemolytic anaemias
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
Diagnosis of haemolytic anaemias
```
History and exam
Direct antiglobulin test (DAT)
urine for hemosiderin/urobilinogen
FBC
reticulocyte count
Blood filml
Serum bilirubin (direct/indirect)
LDH
Serum haptoglobin
```
108
Bilirubin levels in haemolysis
Bilirubin will be high (unconjugated)
109
Serum haptoglobin levels in haemolysis
mops up free haemoglobin and so in haemolysis these levels are low
110
What does DAGT show in haemolysis?
If positive = immune mediated
| If negative = non immune mediated
111
Three types of immune haemolysis
Warm auto antibody
Cold auto antibody
Alloantibody
112
Features of warm auto antibody immune haemolysis
Antibodies that only bind at warm temperatures - 37C so can cause haemolysis in the body
Usually IgG antibodies
The more troublesome autoimmune anaemia
113
Causes of warm auto antibody immune haemolysis
Autoimmune
drugs
CLL
114
Features of cold auto antibody haemolysis
Antibodies that bind in the cold
Haemolysis less severe
Less clinical haemolysis and sometimes an incidental finding
115
Causes of cold auto antibody haemolysis
CHAD
infections
lymphoma
116
When does alloantibody occur?
Transfusion reaction
117
Management of haemolytic anaemia
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
What does the Direct antiglobulin test (DAT) detect?
Antibody or complement on red cell membrane
119
In DAT, the reagent either contains what and what does it do?
Anti-human IgG
Anti-complement
Reagent binds to Ab (or complement) on red cell surface and causes agglutination in vitro
120
What does DAT imply?
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
What is secondary anaemia?
Anaemia of chronic disease
122
What type of anaemia is secondary anaemia?
70% normochromic normocytic
| 30% hypochromic microcytic
123
Pathology of secondary anaemia
Defective iron utilisation
- increased hepcidin in inflammation
- ferritin often elevated
124
Possible causes of secondary anaemia
infection
inflammation
malignancy
125
How does vitamin B12 get absorbed?
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
Who gets pernicious anaemia?
Older people
| Runs in families
127
Pernicious anaemia has antibodies against….
```
Intrinsic factor (diagnostic)
Gastric parietal cells (less specific)
```
128
Presentation of pernicious anaemia
Malabsorption of dietary B12
| Symptoms / signs take 1-2 years to develop
129
Diagnosis of pernicious anaemia
Schilling test
130
Treatment of pernicious anaemia
IM vitamin B12
131
Very low haemoglobin result - what to think about first?
Is the patient stable or unstable?
| Are they bleeding?
132
What type of cancer comes from mesenchymal cells?
Sarcoma
133
What type of cancer comes from epithelial cells?
Carcinoma
- squamous
- glandular
134
Acute causes of bleeding
```
Bronchiectasis
TB
Lung carcinoma
GI bleeding
- varices
- carcinoma
Spleen rupture
```
135
Causes of normochromic normocytic anaemia
```
Acute bleeding
Haemolytic anaemia
Leukaemia (no space for them)
Anaemia of chronic disease
Chronic kidney disease
Aplastic anaemia
```
136
Is iron deficiency common? - males vs females
Males - not common
| Females - tiny amount of blood loss over time so not concerning in women of reproductive age
137
What would iron deficiency in a male indicate?
Bowel cancer
138
Pathology of anaemia of chronic disease
Due to inflammatory environment
| Cytokines interfere so iron accumulates in macrophages so the iron is there, but we cannot use it
139
If a patient has a chronic disease, what do you need to consider?
If there is an inflammatory background in the chronic disease as this may be interfering with ferritin
140
What is TSAT?
Transferrin saturation
141
What commonly taken drug can cause small amounts of GI bleeding?
NSAIDs
142
Why in chronic kidney disease can you become anaemic?
Because erythropoietin is produced in the kidneys
143
Function of erythropoietin
Released into bloodstream during hypoxia
| It is carried to the bone marrow where it works to stimulate stem cells to become RBCs
144
Cause of anaemia in the young
Genetic cause
145
In hereditary spherocytosis, what happens due to the shape of the red cells?
They cant go through the vasculature and so they break
146
What does G6PD stand for?
Glucose-6-phosphate dehydrogenase
147
Where is globin synthesised?
In the RER in the ribosomes
148
What chains of haemoglobin are present in both the adult and the foetus?
Alpha chains
149
The genes and their relation to the two types of Beta Thalassaemia
1 defective gene - minor
| 2 defective genes - major
150
What happens to the bone marrow in Beta thalassaemia major?
It expands
| As trying to compensate for the anaemia
151
What is the iron chelating agent used?
Desferioxamine
152
What type of mutation is sickle cell disease?
Missense mutation
| Glutamic acid becomes valene
153
What can cause sickle cell crisis and therefore sickling?
Tipping the balance e.g.
- fever
- lowering pH
154
What do reticulocytes look like on blood film?
Blue and bigger
| some still have RNA
155
What does Sickle cell haemoglobin look like on electrophoresis if you were a carrier?
Would have the sickle ad but also have the adult haemoglobin band
156
Acquired causes of anaemia
Drugs
Mechanical value; shear stress
Autoimmune haemolytic anaemia
157
Pathology of autoimmune haemolytic anaemia
RBCs are coated with antibodies which are recognised by splenic macrophages to eat
Extravascular
158
What does autoimmune haemolytic anaemia look like on blood film?
Shows fragmented/bite cells - these will be eventually eaten
159
What is the most common form of autoimmune haemolytic anaemia?
Warm antibody haemolytic anaemia
160
Who is warm antibody haemolytic anaemia common in?
Women
161
What temperature do autoantibodies generally react at in warm antibody haemolytic anaemia?
> 37 C
162
Pathology of haemolysis in warm antibody haemolytic anaemia
Occurs primarily in the spleen
| Not due to direct lysis of RBCs
163
What temperature do autoantibodies react at in cold antibody haemolytic anaemia?
< 37C
164
Pathology of haemolysis in cold antibody haemolytic anaemia
Occurs largely in extravascular mononuclear phagocyte system of the liver and spleen
165
Prognosis of cold antibody haemolytic anaemia
Anaemia usually mild
166
Type of antibodies in warm antibody haemolytic anaemia
IgG
167
Type of antibodies in cold antibody haemolytic anaemia
IgM
168
Prognosis of warm antibody haemolytic anaemia
Usually severe
| Can be fatal
169
Levels of ferritin in anaemia of chronic disease
Normal to high
170
What type of anaemia is seen in beta thalassaemia major?
Microcytic hypochromic
171
What happens to the reticulocyte count in autoimmune haemolytic anaemia?
It increases
172
When are hypersegmented neutrophils seen?
Megaloblastic anaemia
173
Features of B12 deficiency
Cytopenia
Leucocytopenia
Hypersegmented neutrophils
174
What can cause fragmented red cells caused by intravascular haemolysis?
DIC
Mechanical heart valves
Malignant HTN
175
What is aplastic anaemia?
Primary bone marrow failure so bone marrow just becomes fat
176
Features of aplastic anaemia
Pancytopenia
| Normochromic normocytic anaemia
177
Shape of RBCs
Biconcave
Anucleated
Haemoglobin
178
What is haematocrit?
% volume of RBC/volume of whole blood
179
Normal Ht values for males
40-50%
180
Normal Ht vales for females
35-48%
181
What can cause increased Ht?
Dehydration
| Increased RBC mass
182
What can cause reduced Ht?
Acute haemorrhage
| Haemodiluation
183
What is MCH increased in?
Macrocytic anaemias
184
What is MCH decreased in?
Hyperchromic anaemias
185
What does MCHC stand for?
Mean corpuscular haemoglobin concentration
186
What is MCHC increased in?
Hyperchromic conditions e.g. sickle cell disease
187
What is MCHC decreased in?
Microcytic conditions
188
What is RDW?
Red blood cell distribution width (average volume)
189
What can increase ferritin?
Infection
Any inflammatory disorder
Malignancy
Pregnancy proteins
190
Ferritin levels in iron deficiency anaemia
Low
| But loads of things increase ferritin so can still be iron deficient with a normal ferritin level
191
Another name for transferrin
Total iron binding capacity (TIBC)
192
How to take iron supplements
With food
| Not too close together as can close down the iron transporter
193
How many genes are affected in alpha thalassaemia and theyre effects
1 gene - rarely any significant anaemia
2 genes - clinically equivalent to beta thalassaemia minor
3 - similar to beta thalassaemia major
194
If have the genes HbAS, what is this known as?
Sickle cell trait
195
What is vit B12 needed for?
Helps make DNA in every cell
196
Causes of vit B12 deficiency
```
Gastrectomy
PPIs
Metformin
Antibodies to gastric parietal cells or intrinsic factor
Chrons
Coeliac disease
UC
Resection
Fish tape worm - diphillobothrium latum
```
197
What foods is folate found in?
Brown rice
Broccoli
Brussel sprouts
Fortified cereals
198
Causes of folate deficiency
```
Diet
Increased cell turnover
- psoriasis
- haemolytic anaemia
- cancers
```
199
What would cold autoantibody autoimmune haemolytic anaemia be following?
Viral infection - CMV, EBV, chickenpox, measles, mumps, mycoplasma pneumonia
Idiopathic
Lymphoma
200
What would warm antibody autoimmune haemolytic anaemia be seen in?
RA
SLE
CLL
Idiopathic
201
What anaemia would hypothyroidism result in?
Macrocytic - non megaloblastic / normoblastic
202
What anaemia does myelodysplasia result in?
Normoblastic macrocytic anaemia
203
Causes of normocytic megaloblastic anaemia
```
Alcohol
Liver disease
Hypothyroidism
Pregnancy
Reticulocytosis
MDS
Cytotoxic drugs
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204
What anaemia does chronic kidney disease result in?
Normocytic
205
What does congenital sideroblastic anaemia result in? (type of anaemia)
Microcytic
206
What shows target cells on blood film?
Sickle cell
Thalassaemias
Hyposplenism
Liver disease
207
What shows tear drop poikilocytes on blood film?
Myelofibrosis
208
What shows Spherocytes on blood film?
Hereditary spherocytosis
| Autoimmune haemolytic anaemia
209
What shows basophilic stippling on blood film?
Lead poisoning
Thalassaemia
Sideroblastic anaemia
Myelodysplasia
210
What shows Howell-Jolly bodies on blood film?
Hyposplenism
211
What shows Heinz bodies on blood film?
G6PD deficiency
| A-thalassaemia
212
What shows shistocytes (helmet cells) on blood film?
Intravascular haemolysis
Mechanical heart valve
DIC
213
What does DIC stand for?
Disseminated intravascular coagulation
214
What shows pencil poikilocytes on blood film?
Iron deficiency
215
What shows burr cells on blood film?
Uraemia
| Pyruvate kinase deficiency
216
What shows hypersegmented neutrophils on blood film?
Megaloblastic anaemia
