PBL ILO’s

Question 1

Structure of erythrocytes

Answer 1

Diameter of 7-8 µm possessing an atypical structure in comparison to most other body cells
The RBC structure resembles a donut, they are biconcave wherein their periphery is thicker than their central portion. Courtesy to this feature, the total surface of the cell membrane is maximised enabling exchange of gases and their transport.
These cells are anuclear and do not have any other intracellular organelles as they are lost in erythropoiesis. There are two main structures – cytoplasm engirdled by a cell membrane.
Cytoplasm – filled with haemoglobin
Cell membrane – a lipid layer containing two types of membrane proteins – peripheral and integral.

Question 2

Function of erythrocytes

Answer 2

• Delivers oxygen from the lungs to the tissues all through the body
• Facilitates carbon dioxide transport
• Acts as a buffer and regulates hydrogen ion concentration
• Contributes to blood viscosity
• Carries blood group antigens and Rh factor

Question 3

Types of haemoglobin in adults and babies and what could abnormal haemoglobin cause?

Answer 3

Normal Results
In adults, these are normal percentages of different hemoglobin molecules:
• HbA: 95% to 98% (0.95 to 0.98)
• HbA2: 2% to 3% (0.02 to 0.03)
• HbE: Absent
• HbF: 0.8% to 2% (0.008 to 0.02)
• HbS: Absent
• HbC: Absent

In infants and children, these are normal percentage of HbF molecules:
○ HbF (newborn): 50% to 80% (0.5 to 0.8)
○ HbF (6 months): 8%
○ HbF (over 6 months): 1% to 2%

What Abnormal Results Mean
Significant levels of abnormal hemoglobins may indicate:
• Haemoglobin C disease
• Rare haemoglobinopathy
• Sickle cell anaemia
• Inherited blood disorder in which the body makes an abnormal form of haemoglobin (thalassemia)
You may have false normal or abnormal results if you have had a blood transfusion within 12 weeks of this test.

Question 4

What is erythropoiesis?

Answer 4

Erythropoiesis is the process which produces red blood cells, which is the development from erythropoietic stem cell to mature red blood cell. It is stimulated by decreased O₂ in circulation, which is detected by the kidneys, which then secrete the hormone erythropoietin.

Question 5

Erythropoiesis stages

Answer 5

Proerythroblast: large cell with cytoplasm that stains dark blue

Give rise to erythroblasts (early & late)

Normoblasts: smaller cells
Cytoplasm starts to stain lighter blue
Late normoblasts have extruded nucleus (becoming more mature)

Reticulocyte: contain some ribosomal RNA
Circulates in peripheral blood (1-2 days)

Endpoint: Mature erythrocyte
RNA lost
Duration: approx 7 days
Lifespan: 120 days
175 billion new red blood cells per day

Question 6

Destruction of erythrocytes

Answer 6

90% in liver, spleen and lymph nodes:

The macrophage breaks down globin into amino acids and iron which moves to bone marrow
The Haem group is transformed into bilirubin which enters the blood plasma and travels to the liver and then to the kidney or combines with bile in the intestines

10% in blood circulation:
Haemolysis
Ends up in blood plasma and eventually picked up by macrophage

Question 7

What is the role of a platelet?

Answer 7

Platelets are made by megakaryocytes. Their lifespan is 10 days. The normal count is 150000 – 450000 /mm3. Their role is to clump together (platelet aggregation) and plug gaps where blood clots need to form.

Question 8

How is a platelet formed?

Answer 8

Myeloid stem cell -> megakaryoblast -> promegakaryocyte -> megakaryocytes -> platelets

Question 9

Structure of a platelet

Answer 9

• Membrane network = dense tubular network within cell
• have no nucleus
• they are fragments of cytoplasm from the megakaryocytes
• contain dense bodies and alpha granules
○ Alpha (contains proteins) = factor XIII, platelet activating factor, PDGF, vWF, fibrinogen + platelet factor 4
○ Dense (contains non proteins) = ADP + Ca2+ (needed for contraction and bind to vitamin K dependent factors)
• Biconvex shape
• Plasma membrane has:
○ Glycoprotein coat - needs proteins for receptors
○ Lipid bilayer
• Cytoskeleton = actin, tubulin and spectrin (important for maintenance of cell shape + activation)

Question 10

• Thrombocytopenia
• Thrombocytosis

Answer 10

Not enough platelets
Too many platelets

Question 11

Where are platelets found?

Answer 11

Peripheral blood and spleen

Question 12

Platelet activation and aggregation

Answer 12

PLATELET ACTIVATION AND AGGREGATION
1. Platelets get exposed to endothelial damage
○ Exposed to vWF, collagen etc leads to activation
2. Intracellular signalling causes release of granules and generation of thromboxane
3. Secondary mediators reinforce the platelets activation and activate further platelets
4. Thrombin generation causes further activation of platelets
5. Intracellular signalling leads to integrin activation
6. Active integrin binds fibrinogen and causes platelet aggregation
7. This forms the platelet aggregate primary plug
8. Thrombin converts fibrinogen in the platelet aggregate to cross linked fibrin
○ This forms the secondary haemostatic plug = thrombus

Question 13

Types of leukocytes

Answer 13

Neutrophils (infection)
Eosinophils (allergic response and parasite infections)
Basophils
Monocytes (become macrophages and engulf pathogens)
Lymphocytes (release T cells and b cells to fight viruses)

Question 14

Neutrophils

What type of cell is it?

Structure

Function

Lifespan

Abundance

Haematopoiesis Process

Answer 14

Neutrophils

Granulocyte and Phagocyte

They have a characterise multilobed nucleus, with 3-5 lobes joined by slender genetic material.

First cell when body is exposed to infection and mature neutrophils (polymorphonuclear neutrophils) ingest microorganisms, help defence of body as they are actively phagocytic.

Lifespan is 5 days with a further 1-2 days in circulation.

Most abundant – about 50-70%

1. Myeloid stem cell 
2. Myeloblast (varying size, large nucleus, no cytoplasmic granules
3. Promyelocytes (primary cytoplasmic granules) 
4. Myelocytes (smaller cells with specific cytoplasmic granules, no noticeable nucleoli) 
5. Metamyelocytes (indented or horse-shoe nucleus, lots of cytoplasmic granules.

Question 15

Esenophil

What type of cell is it?

Structure

Function

Lifespan

Abundance

Haematopoiesis Process

Answer 15

Granulocyte and Phagocyte

Larger cytoplasmic granules, tend not to have more than 3 lobes.

Provide protection against parasite infections.

Involved in the allergic responses.

Lifespan is 8-12 hours in circulation and a further 8-12 days in tissue.

Compose 1-4% of all circulating leukocytes.

1. Myeloid stem cell 
2. Myeloblast (varying size, large nucleus, no cytoplasmic granules
3. Promyelocytes (primary cytoplasmic granules) 
4. Myelocytes (smaller cells with specific cytoplasmic granules, no noticeable nucleoli) 
5. Metamyelocytes (indented or horse-shoe nucleus, lots of cytoplasmic granules.

Question 16

Basophils

What type of cell is it?

Structure

Function

Lifespan

Abundance

Haematopoiesis Process

Answer 16

Basophils

Granulocyte and Phagocyte

Usually consist of 2 nuclear segments, cytoplasmic granules contain heparin and histamine.

They mature in tissues to form mast cells.

Both play a role in hypersensitivity – release inflammatory molecules such as histamine to defend body from allergens, pathogens and parasites.

Basophils also release enzymes to improve blood flow and prevent blood clots.

Life span – 60 – 70 hours.

Rare in normal peripheral blood (less than 1% of leukocytes)

1. Myeloid stem cell 
2. Myeloblast (varying size, large nucleus, no cytoplasmic granules
3. Promyelocytes (primary cytoplasmic granules) 
4. Myelocytes (smaller cells with specific cytoplasmic granules, no noticeable nucleoli) 
5. Metamyelocytes (indented or horse-shoe nucleus, lots of cytoplasmic granules.

Question 17

Monocytes

What type of cell is it?

Structure

Function

Lifespan

Haematopoiesis Process

Answer 17

Monocytes

Phagocyte

Spherical cell with prominent surface ruffles and blebs

Made in bone marrow and travels through the blood to tissues in the body where it differentiates to becomes a macrophage or a dendritic cell when body is exposed to a foreign body.

Macrophages are innate immune cells which are involved in the detection, phagocytosis and destruction of bacteria and other harmful organism.

20-40 hours

2. Myeloid stem cell 
3. Monoblast (first committed cell)
4. Promonocyte (large cell with indented nucleus only found in bone marrow
5. Monocyte (stay for 20-40 hours in peripheral blood circulation, the nucleus is kidney shaped) 
6. Macrophages (migrate to tissues and mature)

Question 18

Lymphocytes

Structure

Function

Lifespan

Abundance

Haematopoiesis Process

Answer 18

Lymphocytes

3 types of lymphocytes:
T cells
B cells
Natural killer cells

Blood T and B cells are indistinguishable on light and electron microscopy

NK cells tend to be larger cells with relatively large granules scattered in their cytoplasm.

T cells:
responsible for cell-mediated cytotoxic reactions and for delayed hypersensitivity responses. T lymphocytes also produce the cytokines that regulate immune responses and provide helper activity for B cells

B cells:
B lymphocytes can capture, internalize, and present antigens to T cells and are the precursors of immunoglobulin-secreting plasma cells

Natural killer cell:
NK cells account for innate immunity against infectious agents and transformed cells that have altered expression of transplantation antigens

T cells:
30–160 days

B cells:
5-6 weeks

Natural killer cells:
varies from weeks to years

T cells – 80-90%

B cells – 10-20%

Natural killer cells – 5- 15%

1. Lymphoid Stem cell
2. Differentiate into B lymphocyte, T lymphocyte or natural killer cells.
3. B lymphocytes further mature into plasma cells in lymph nodes
   • T lymphocytes tend to mature in thymus
   • B lymphocytes differentiation in foetus occurs in liver but in adults in the bone marrow.

Question 19

Emergency measures of a haemorrhage

Answer 19

Haemorrhage - Dial 2222
Major Haemorrhage is defined as:
• Blood loss of more than one blood volume within 24 hours
• 50% of total blood volume lost in less than 3 hours
• Bleeding in excess of 150 mL/minute

In acute scenario where the above cannot be measured major haemorrhage can be presumed when bleeding is visible or indicate, and results in:
• BP <90mmHg Systolic
• HR >110bpm

To locate haemorrhage: Mnemonic device On the floor, and four more
“On the floor” refers to visible blood loss from an external wound

“Four more” refers to four more potential spaces within the body, where a large volume of blood can be lost and reside. These are:
• Chest cavity - i.e. Haemothorax
• Abdominal Cavity - Damage to solid organ like the spleen, or damage to a major blood vessel
• Pelvis - classically from a pelvic fracture
• Long Bones - long bone fractures can account for significant blood loss

Investigations to locate bleeding
• CT
• Ultrasound

Stopping the bleeding
• Direct pressure, dressings and or tourniquet for external bleeding
• Pelvic fracture blood loss can be controlled with a pelvic binder
• Pharmacological management with Tranexamic acid and anticoagulation reversal
• Surgery for internal or uncontrollable haemorrhage

Replace lost Blood Volume
• Replace blood with blood, a 1:1 ratio of units of plasma and red blood cells.
• Avoid use of crystalloids for volume replacement in hospital setting

Cannulation
• Establish venous access - use wide bore cannula 14G or 16G and take blood tests for crossmatch or group and save

Blood tests
• FBC
• U&Es
• LFTs
• Coagulation screen
• Group & save (+/- crossmatch)
• Toxicology screen (if you suspect drug overdose)
• Lactate (to assess for evidence of inadequate end-organ perfusion)

Do an ECG to check for heart strain and cardiac tamponade

Coagulation Tests
• Prothrombin Time (PT) -
• Activated Partial Prothrombin Time (APTT)
• Bleeding Time
• Thrombin Time
• FBC
• LFT
• Albumin
• D-Dimer

Question 20

Anatomical sites of haematopoeisis changes during the development of embryo and foetus

Answer 20

• RBC formation first occurs within the yolk sac at 2 weeks’ gestation (period between conception and birth)
○ In this primitive phase of haematopoiesis, clusters of cells called blood islands form in the yolk sac
○ The peripheral cells differentiate to become walls of blood vessels
○ The central cells become primitive red cells or haemocytoblasts
• These primitive erythroblasts begin to enter the embryo proper at 21 to 22 days’ gestation and circulate for approx 12 weeks of gestation
• A second wave of yolk-sac derived definitive erythroid progenitors go to the liver a 5 weeks’ gestation
• Haematopoietic progenitors are not seen in the yolk sac after 7 weeks’ gestation
• Haematopoiesis continues mostly in the liver and to a lesser extent in the spleen between 7-15 weeks’ gestation
• Liver continues as the main site of haematopoiesis through the fifth month of gestation and continues to produce blood cells through the first week of life
• Bone marrow haemotopoiesis begins during the third and fourth months of gestation and it becomes the predominant site after birth

Question 21

Pre transfusion test: group and save

Answer 21

Pre-transfusion testing establishes the ABO and D blood group of the patient and determines if there are red cell antibodies that could result in an incompatible blood transfusion.

Group and screen

• "Group and Save" request samples are ABO and Rh (D) grouped and screened for atypical antibodies in the patients plasma.

	○ If atypical antibodies are detected as a result of a previous transfusion or pregnancy, further testing is required to determine the specific types.

• Samples are kept for up to seven days depending on the patient's transfusion history.

	○ If a patient has not received a transfusion, is not pregnant or has not been pregnant in the last three months; the sample is valid for seven days.

• Store plasma at -30°C, store red blood cells at 4°C.

Question 22

Pre transfusion test: cross match

Answer 22

Crossmatch

Must have a valid Group & Screen.

ABO and Rh (D) compatible donor units are selected and crossmatched for named patients and held for that patient until 9am, 48 hours after the date the request was made.

If your patient has been transfused, a fresh sample for further crossmatching will be required after 72 hours (3 days). You should allow as much time as possible to complete grouping, both antibody screening and cross-matching, in case atypical antibodies are found.

• If your patient has atypical antibodies, antigen negative blood must be crossmatched serologically. 

Without a valid Group & Screen

• 2 units of O Neg can be given if blood is required immediately
• ABO and RhD compatibility must be achieved if blood is required within 10 minutes
• A full crossmatch must be achieved if the blood is required within 20 minutes

Question 23

Haemolytic transfusion reactions (HTR)

Answer 23

A Haemolytic Transfusion Reaction (HTR) occurs when antibodies in the patient’s plasma react with antigens on transfused allogeneic red blood cells, causing haemolysis (rupture of red blood cells).

HTR occurring during or within 24 hours of transfusion is classed as acute; a delayed HTR can occur days to weeks after the transfusion.

Symptoms include fever, rigors, chills, hypotension, pain, dyspnoea, tachycardia, nausea, restlessness or DIC; acute HTR can be life-threatening.

• Infusion of ABO incompatible blood almost always arises from errors in labelling sample tubes/request forms or from inadequate checks at the time of transfusion. 
• Where red cells are mistakenly administered, there is about a 1 in 3 risk of ABO incompatibility and 10% mortality with the severest reaction seen in a group O individual receiving group A red cells.

Question 24

Severe allergic reaction or anaphylaxis during blood transfusion

Answer 24

Severe allergic reaction or anaphylaxis

Allergic reactions occur when patients have immunoglobulin E (IgE) or IgG antibodies that react with proteins in transfused blood components.

Patients with anaphylaxis become acutely dyspnoeic due to bronchospasm and laryngeal oedema and may complain of chest pain, abdominal pain and nausea.

• Symptoms are usually controlled by slowing the transfusion and giving antihistamine, and the transfusion may be continued if there is no progression at 30 minutes.

• Pre-treatment with chlorphenamine should be given when a patient has experienced repeated allergic reactions to transfusion.

Question 25

Iron overload during blood transfusion

Answer 25

Iron overload

Each unit of blood contains 200-250 mg of iron and those receiving red cells over a long period may develop iron accumulation in cardiac and liver tissues.

Chelation therapy (with desferrioxamine) is used to minimise iron accumulation in those most at risk.

Question 26

Describe anaemia

Answer 26

Anaemia: low level of haemoglobin in the blood. Is a result of an underlying disease and is not a disease itself.

Question 27

Signs and symptoms of anaemia

Answer 27

Symptoms of anaemia
• Tiredness
• Shortness of breath
• Headaches
• Dizziness
• Palpitations
• Worsening of other conditions e.g. angina, heart failure, or peripheral vascular disease

Signs of anaemia
• Pale skin
• Conjunctival pallor
• Tachycardia
• Raised respiratory rate

Question 28

Signs of specific causes of anaemia

Answer 28

Signs of specific causes of anaemia
• Koilonychia is spoon shaped nails and can indicate iron deficiency
• Angular chelitis can indicate iron deficiency
• Atrophic glossitis is a smooth tongue due to atrophy of the papillae and can indicate iron deficiency
• Brittle hair and nails can indicate iron deficiency
• Jaundice occurs in haemolytic anaemia
• Bone deformities occur in thalassaemia
• Oedema, hypertension and excoriations on the skin can indicate chronic kidney disease

Microcytic anaemia
• Low MCV (<80) indicating small RBCs

Question 29

What is microcytic anaemia and what are some of the common causes?

Answer 29

Microcytic anaemia
• Low MCV (<80) indicating small RBCs

Causes (TAILS):
• Thalassaemia
• Anaemia of chronic disease
• Iron deficiency anaemia
• Lead poisoning
• Sideroblastic anaemia
• Most common cause is Iron deficiency anaemia

Question 30

What would the serum iron, % saturation, ferritin and TIBC levels be in someone with iron deficient anaemia?

Answer 30

Iron deficiency anaemia

Serum iron- Low

% saturation- Low

Ferritin- Low (all of the stored iron is used up because serum iron is depleted)

TIBC- High

Question 31

What would the serum iron, % saturation, ferritin and TIBC levels be in someone with anaemia of chronic disease?

Answer 31

Anaemia of chronic disease

Serum iron- Low

% saturation- Low

Ferritin- High (due to built up stores from hepcidin)

TIBC- Low

Question 32

What would the serum iron, % saturation, ferritin and TIBC levels be in someone with sideroblastic anaemia?

Answer 32

Sideroblastic anaemia

Serum iron- High (iron builds up in cells and released into serum once the cell bursts)

% oxygen saturation- High

Ferritin- High (iron overloaded state)

TIBC- Low

Question 33

What would a peripheral blood film show in iron deficiency anaemia?

Answer 33

• Cells are hypochromic (pale)
• Microcytic (small)
• Varying sizes (anisocytosis)
• Abnormal shapes (poikilocytosis)

Question 34

Microcytic anaemia treatment

Answer 34

Treatment
• Treat underlying cause - usually involves taking iron tablets (treat the anaemia - ferrous sulphate) as well as vitamin C supplements (increase ability to absorb iron)
• Eat iron-rich food

Question 35

Normocytic anaemia

Answer 35

Normocytic anaemia
• MCV 80-100, size of RBCs isn’t altered (usually normochromic) so cause is either haemolysis (intravascular/extravascular) or underproduction of normal-sized RBCs
• Reticulocyte count enables differentiation between the 2 causes
- High: bone marrow functioning normally, anaemia not likely due to underproduction

Question 36

Peripheral blood film in sickle cell anaemia

Answer 36

RBC sickle cell shaped

Question 37

Treatment of normocytic anaemia

Answer 37

Treatment
• Controlling blood loss
• Treatment of underlying disease
• Blood transfusion
• Medication to promote red cell production

Question 38

Haemolytic anaemia

Answer 38

Haemolytic anaemia
Haemolytic anaemia is an umbrella term for a range of conditions which result in a premature destruction of RBCs.
• Most common defect in RBC metabolism after G6PD deficiency
• Defect leads to reduced production of ATPàrigid red cells.
The main forms of haemolytic anaemia:

Intravascular
· red cell destruction within the vasculature due to complement mediated lysis or direct cell trauma.
· Examples include: prosthetic heart valves, , Glucose-6-phosphate dehydrogenase (G6PD) deficiency, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation and paroxysmal nocturnal haemoglobinuria, sickle cell disease and Thalassaemia.

Extravascular
· Most common form of Haemolytic Anaemia
· Accelerated Red blood cell destruction by immune targeting antibodies
· Warm Haemolytic anaemia – SLE, lymphoma and CCL
· Cold Haemolytic anaemia – Idiopathic, infection or malignancy
· Drug induced – penicillin, cephalosporins, NSAID, Trimethoprim

Question 39

What would a FBC show in haemolytic anaemia?

Answer 39

FBC
· Low Hb
· platelets normal in most cases but can vary
· thrombocytopenia in SLE, CLL, thrombotic thrombocytopenic purpura, DIC etc
· normal MCV and MCH

Question 40

Signs and symptoms of haemolytic anaemia?

Answer 40

Signs&symptoms

• May be asymptomatic
• Recent medication hx
• May complain of SOB, palpitations and or chest pain
• Weakness/lethargy
• Dark urine (intravascular Haemolysis)

Question 41

Macrocytic anaemia

Answer 41

Macrocytic anaemia

· (large MCV indicating large RBCs)
· Macrocytic anaemia can be megaloblastic or normoblastic. Megaloblastic anaemia is the result of impaired DNA synthesis preventing the cell from dividing normally.
· Rather than dividing it keeps growing into a larger, abnormal cell. This is caused by a vitamin deficiency.

Question 42

Causes of megaloblastic anaemia

Answer 42

B12 deficiency
Folate deficiency

Question 43

Causes of normoblastic macrocytic anaemia

Answer 43

· Alcohol
· Reticulocytosis (usually from haemolytic anaemia or blood loss)
· Hypothyroidism
· Liver disease
· Drugs such as azathioprine

Question 44

Treatment of B12 deficiency

Answer 44

Treating vitamin b12 deficiency (NICE)
· Initially administer hydroxocobalamin 1 mg intramuscularly three times a week for 2 weeks.
· The maintenance dose depends on whether the deficiency is diet related or not. For people with B12 deficiency that is:
- Not thought to be diet related — administer hydroxocobalamin 1 mg intramuscularly every 2–3 months for life.
- Thought to be diet related — advise people either to take oral cyanocobalamin tablets 50–150 micrograms daily between meals, or have a twice-yearly hydroxocobalamin 1 mg injection.
· Give dietary advice about foods that are a good source of vitamin B12 — good sources of vitamin B12 include:
- Eggs.
- Foods which have been fortified with vitamin B12 (for example some soy products, and some breakfast cereals and breads) are good alternative sources to meat, eggs, and dairy products.
- Meat.
- Milk and other dairy products.
- Salmon and cod.
· After 8 weeks of treatment, and also measure iron and folate levels.
- The mean cell volume (MCV) should have normalised.

Question 45

ABO antigens

Answer 45

In the ABO system, there are two erythrocyte antigens of note, with four possible combinations and thus four different ABO blood groups.
A person’s ABO blood type describes the antigens present on their erythrocytes:1,2
• Group A erythrocytes only have the A antigen
• Group B erythrocytes only have the B antigen
• Group AB erythrocytes have both the A and B antigens
• Group O erythrocytes do not have any ABO antigens

Question 46

Rh system

Answer 46

The Rh blood group system is comprised of over 50 different antigens, but the most significant is the D antigen, as it is the most immunogenic.2 Its presence or absence gives a patient the ‘positive’ or ‘negative’ status in typical transfusion nomenclature.
Like most blood group antibodies, anti-D antibodies are only generated through exposure to the foreign antigen. Thus, people with a Rh-negative blood group will not typically have anti-D antibodies unless previously exposed.

Question 47

Rhesus compatibility/ incompatibility in pregnancy

Answer 47

Women that are rhesus-D positive do not need any additional treatment during pregnancy

When a woman that is rhesus-D negative becomes pregnant, we have to consider the possibility that her child will be rhesus positive. It is likely at some point in the pregnancy (i.e. childbirth) that the blood from the baby will find a way into the mother’s bloodstream. When this happens, the baby’s red blood cells display the rhesus-D antigen. The mother’s immune system will recognise this rhesus-D antigen as foreign, and produce antibodies to the rhesus-D antigen. The mother has then become sensitised to rhesus-D antigens.

Management
Prevention of sensitisation is the mainstay of management. This involves giving intramuscular anti-D injections to rhesus-D negative women. There is no way to reverse the sensitisation process once it has occurred, which is why prophylaxis is so essential.

Anti-D injections are given routinely on two occasions:
• 28 weeks gestation
• Birth (if the baby’s blood group is found to be rhesus-positive)

Anti-D injections should also be given at any time where sensitisation may occur, such as:
• Antepartum haemorrhage
• Amniocentesis procedures
• Abdominal trauma

Anti-D is given within 72 hours of a sensitisation event. After 20 weeks gestation, the Kleinhauer test is performed to see how much fetal blood has passed into the mother’s blood, to determine whether further doses of anti-D are required.

Question 48

Kleihauer test

Answer 48

Kleihauer Test
The Kleihauer test checks how much fetal blood has passed into the mother’s blood during a sensitisation event. This test is used after any sensitising event past 20 weeks gestation, to assess whether further doses of anti-D is required.
The Kleihauer test involves adding acid to a sample of the mother’s blood. Fetal haemoglobin is naturally more resistant to acid, so that they are protected against the acidosis that occurs around childbirth. Therefore, fetal haemoglobin persists in response to the added acid, while the mothers haemoglobin is destroyed. The number of cells still containing haemoglobin (the remaining fetal cells) can then be calculated.