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Haematology and Immunology > Red Blood Cells > Flashcards

Red Blood Cells Flashcards

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1
Q

What is anaemia

A

Reduction in red cells or their haemoglobin. Theres multiple aetiologies.

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2
Q

Red cell production in marrow.

A

Haemocytoblast - committed cell (proerythroblast)

Developmental - early erythroblast - late erythroblast - noroblast - reticulocyte - erythrocyte (no nucelus)

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3
Q

Substances required for red cell production

A

Metals: Iron, copper, cobalt, manganese
Vitamins: B12, folic acid, thiamine, Vit.B6, C,E
Amino acids
Hormones: Erythropoietin (made in the kidneys), GM-CSF, androgens, thyroxine, SCF

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4
Q

Red cell breakdown

A

Normal life span is 120 days. They are normally removed from the circulation and replaced. Magrophages of the reticuloendothelial system (liver and the spleen) breakdown. Globin is re-utlised. The haem is broken down into bilirubin and iron. It is then conjugated in the liver and comes out in the bile and stercobiligin in the stool.

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5
Q

The Red Blood Cell

A

Biconcave disk, larger surface area for gas transfer and is able to squeeze through small spaces. Contains membrane, enzymes, haemglobin.

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6
Q

Genetic defects in congenital anaemias

A

Red cell membane, metabolic pathways, haemoglobin. These reduce red cell survival and result in haemolysis. The carrier states are often silent (autosomal recessive).

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7
Q

Red cell membrane

A

Bilipid layer, intrinsic proteins that help maintain the structure of the cell. Skeletal proteins inside to keep the cell flexible.

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8
Q

Defects in red cell membrane.

A

Defects in skeletal protiens leading to increased cell destruction. Mutations in Ankyrin, band 3 and spectrin.

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9
Q

Hereditary Spherocytosis

A

Defects in structural protein resulting in red cells being spherical. These are then removed from circulation by spleen. Leads to anaemia. The most common are autosomal dominant.

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10
Q

Clinical presentation of Herediatry spherocytosis

A

Anaemia
Jaundice (neonatal)
Splenomegaly
Pigment gallstones (due to increased haemolysis and bilirubin)

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11
Q

Treatment of Hereditary Spherocytosis

A

Folic acid (increased requirement)
Transfusion (if severe)
Splenectomy (remove the site of production)

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12
Q

Other rare membrane disorders (for information, don’t need to know)

A 
Hereditary Elliptocytosis (ellipotcytes, look like rods) 
Hereditary Pyropoikilocytosis (cells look an utter mess) 
South East Asian Ovalocytosis
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13
Q

Red cell enzymes

A

Glycolysis (production of ADP provides energy for the cell)

Pentose Phosphate Shunt (Protects from oxidative damage)

GLUCOSE 6-PHOSPHATE DEHYDROGENASE

PYRUVATE KINASE

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14
Q

Glucose 6 Phosphate dehydrogenase

A

Protects red cell proteins (Haemoglobin) from oxidative damage
Produces NADPH - Vital for reduction of glutathione
Reduced glutathione scavenges and detoxifies reactive oxygen species

More likely to break down as a result

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15
Q

G6PD Deficiency

A

Commonest disease causing enzymopathy in the world
Results in the cells vulnerable to oxidative damage.

X-Linked

Bite cells
Blister cells under the microscope.

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16
Q

Clinical Presentation of G6PD deficiency

A 
Neonatal Jaundice
Splenomegaly
Pigment Gallstones
Intravascular haemolysis 
Haemoglobinuria

Only really when exposed to infection, acute illness, drugs etc do symptoms occur

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17
Q

Drugs precipitating Haemolysis in G6PD deficiency

A

Antimalarials
Antibacterials
Analgesics
Antihelminthics

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18
Q

Pyruvate Kinase Deficiency

A

Reduced ATP, increased 2,3-DPG, cells rigid.

Anaemia, jaundice, gallstones.

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19
Q

Function of haemoglobin

A

To carry oxygen and facilitate oxygen delivery to the tissues.

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20
Q

Bohr Effect

A

Acidosis
Hyperthermia
Hypercapnia

Haemoglobin give up oxygen

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21
Q

Normal Adult Haemoglobin

A

2 Alpha Chains (4 alpha chain genes)
2 Beta Chains (1 beta gene)

HbA (alphaalphabetabeta)

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22
Q

Haemoglobinopathies

A

Inherited abnormalities of haemoglobin syntesis.

Reduced or absent globin chain production (Thalassaemia)

Point Mutations leading to structurally abnormal globin chain (HbS Sickle Cell anaemia)

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23
Q

Inheritance of Haemoglobinopathies

A

Autosomal Recessive Inheritance.

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24
Q

Sickle Haemoglobin

A

2 alpha chains
2 abnormal sickle beta chains.

When it is deoxygenated it crystallises and changes the shape to become a rigid abnormally shaped cell.

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25
Consequences of HbS Polymerisation in Sickle Cell dDisease
Red cell injury, cation loss, dehydration resulting in haemolysis of the red cells. Endothelial activation Promotion of inflammation Coagulation activation Dysregulation of vasomotor tone by vasodilator mediators (NO) ALL RESULTING in VASO-OCCLUSION
26
Sickle Cell Disease Clinical Presentation
Painful Vaso-Occlusive Crises (bone pain) Chest crises Stroke Increased infection risk (hyposplenism due to autoinfarction) Chronic haemolytic anaemia (gallstones, aplastic crisis) Sequestration Crises (when blood pools in the liver or spleen resulting in redution in blood volume)
27
Sickle Cell Painful Crises
Severe pain which often requires Opiates (30 minutes of presentation), hydration, oxygen, consider antibiotics (crises triggered by infection)
28
Sickle Cell Chest Crises Presentation
Chest Pain Fever Worsening hypoxia Infiltrates on CXRay
29
Chest Crises Treatment
``` Respiratory support Antibiotics IV fluids Analgesia Transfusion - top up or exchange target HbS <30%. ```
30
Life long prophylaxis of Sickle Cell Disease
Vaccination Penicillin prophylaxis Folic Acid
31
Other management of Sickle Cell Disease
Blood transfusion Hydroxycarbamide Bone marrow transplantation Gene Therapy
32
Thalassaemias
Reduced or absent globin chain production. Mutations or deletions in genes. Chain imbalance results in chronic haemolysis and anaemia.
33
Homoygous alpha zero thalassaemia (alpha0/alpha0)
``` No alpha chains Hydrops Fetalis (incompatible with life) ```
34
Thalassaemia Major
No beta chains | Transfusion dependent anaemia
35
Thalassaemia Minor
"trait" or carrier state | Hypochromic microcytic red cell indices
36
Presentation of Beta Thalassaemia Major
Severe anaemia presenting at 3-6 months. There is an expansion of ineffective bone marrow, bony deformities (marrow expansion) splenomegaly, growth retardation
37
Life expectancy of untreated Beta Thalassaemia Major
<10 years
38
Treatment of Beta Thalassaemia Major
Chronic transfusion support - 4-6 weekly. | Normal growth and development but Iron Overloading, Iron collaters which remove the iron.
39
Iron Chelation Therapy
``` s/c desferrioxamine infusions (desferal) Oral deferasirox (exjade) ```
40
Rare Defects in Haem Synthesis
Defects in mitochondrial steps of Haem Synthesis resulting in sideroblastic anaemia. ALA Synthase mutations, X-linked.
41
Factors influencing normal haemoglobin
``` Age Sex Ethic Origin Time of day sample taken Time to analysis ```
42
Haemoglobin Male 12-70
(140-180)
43
Haemoglobin Male >70
116-156
44
Haemoglobin Female 12-70
120-160
45
Haemoglobin Female >70
108-143
46
General features of anaemia
``` Tiredness/Breathlessness Breathlessness Swelling of Ankles (due to heart failure) Dizziness (hyperdynamic blood flow) Chest Pain (reduce cardiac blood flow) ```
47
Red Cell Indices
Automated measurement of red cell size and haemoglobin content. MCV = mean cell volume (cell size) MCH = mean cell haemoglobin
48
Descriptions of anaemia Hypochromic Microcytic
Small pale cells. Do serum ferritin (measure of the bodies iron stores). Commonest cause is iron deficiency.
49
Descriptions of anaemia Normochromic Normocytic
Normal colour (haemoglobin normal) and normal size. Do reticulocyte count (tests bone marrow function)
50
Descriptions of anaemia Macrocytic
Large cells. Do B12/folate and bone marrow tests (bone marrow infiltration). Deficiency in B12 or folate results in macrocytic anaemia.
51
Serum Ferritin (Low)
Iron deficiency anaemia
52
Serum Ferritin (normal or increased)
Thalassaemia (without iron deficiency but looks like iron deficiency anaemia under the microscope due to microcytic hypochromic cells) Sideroblastic anaemia
53
Iron Metabolism
Amount you absorb from the duodenum of the gut (bound to plasma protein transferrin) is secreted in urine, faeces, nails, hair and skin Iron is recycled from bone marrow to haemoglobin to macrophages to plasma, in a cycle
54
Iron is stored
In ferritin in the liver
55
Ferroportin
Protein that allows Iron to be transferred from the duodenum to transferrin. Also need this to put into the hepatocytes and the bone marrow.
56
Hepcidin
Control ferroportins action, preventing it working, prevention of absorption of iron when it is not needed. Synthesised in the hepatocytes in response to inflammation.
57
Commonest cause of Anaemia
Iron Deficient Anaemia
58
Common history of iron deficient anaemia
Dyspepsia - GI bleeding, carcinoma of the colon, gastritis Menorrhagia Diet Increased requirement (pregnancy) Malabsorption - gastrectomy, coeliac disease
59
Clinical Features of Iron Deficiency
Koilonychia Atrophic tongue Angular Chelitis
60
Investigations of Iron Deficinecy Anaemia
endoscopy | Barium Studies
61
Management of Iron Deficient Anaemia
Correct the cause with diet, ulcer therapy, surgery if bleeding Iron (oral adequate) Transfusion if severe.
62
Increased Reticulocyte Count
``` Blood Loss (acutely) Haemolysis ```
63
Normal Reticulocyte Count
Secondary Anaemia
64
Haemolytic Anaemia
This is accelerated red cell destruction, compensation by the bone marrow by producing reticulocytes.
65
Intravascular Haemolysis
Red cells are destroyed in the circulation due to toxins or drugs, valve related.
66
Congential Haemolytic Anaemia
``` Hereditary spherocytosis (HS) Enzyme deficiency (G6PD deficiency) Haemoglobinopathy (HbSS) ```
67
Acquired Haemolytic Anaemia
Autoimmune Haemolytic Anaemia (extravascular) Mechanical (valve) Severe infection Drugs
68
Direct Antiglobulin Test
Detects antibody or complement on the red cell membrane. Reagent contains either anti-human IgG anti-complement Reagent binds to antibodies on red cell surface and causes agglutination in vitro. Implies immune basis for haemolysis.
69
Postive Direct Antiglobulin Test
Immune mediated haemolysis
70
Warm Autoantibody
Autoimmune Drugs CLL
71
Cold Autoantibody
CHAD Infections (mycoplasma infections) Lymphoma
72
Alloantibody
Transfusion reaction, antibodies made after transfusions
73
Immune Haemolysis Film
Spherocytes on the film Agglutination in cold AIHA
74
Antibody in autoimmune haemolytic anaemia (extravascular)
IgM
75
Intravascular haemolysis blood film
Red cell fragments (schistocytes) Results in free haemologin which is very toxic to the kidneys
76
Evidence that the patient is haemolysing
FBC, reticulocyte count, blood film Serum bilirubin (direct/indirect), LDH (due to increased haemolysis results in increased unconjugated haemoglobin) Serum haptoglobin
77
Deciding the mechanism of Haemolytic Anaemia
History and examination Blood film Direct Antiglobulin Test (Coombs’ test) Urine for haemosiderin/urobilinogen
78
Management of Haemolytic Anaemia
Folic acid (supports bone marrow function) Correct the cause Immunosuppression if autoimmune Remove the site of red cell destruction Consider transfusion
79
Secondary Anaemia
Anaemia of chronic disease. Mostly normochromic normocytic with increased ferrtin and hepcidin. Treat underlying cause
80
Megaloblastic Anaemia (B12/Folate Deficinecy)
Anaemia and neurological symptoms (unexplained neuropathy)
81
Causes of B12 deficiency
Pernicious anaemia | Gastric/ileal disease
82
Folate deficiency causes
Dietary Increased requirements (haemolysis) GI pathology
83
Signs of megaloblastic anaemia
Lemon yellow tinge to the skin. Elevated Bilirubin and LDH. Oval macrocytes of blood film
84
Vitamin B12 Absorption
``` 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 ```
85
Pernicious Anaemia
Autoimmune disease against intrinsic factors, resulting in malabsorption of vitamin B12.
86
Treatment of Megaloblastic Anaemia
B12 deficiency by B12 IM loading dose then 3 monthly maintenance Folate Deficiency oral folate replacement
87
Other causes of Macrocytosis
``` Alcohol Drugs Methotrexate, Antiretrovirals, hydroxycarbamide Disordered liver function Hypothyroidism Myelodysplasia ```

Haematology and Immunology (20 decks)

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