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Phase 4 > Haematology > Flashcards

Haematology Flashcards

1
Q

What is serum?

A

Blood minus clotting factors.
Serum contains:
Glucose
Electrolytes such as sodium and potassium
Proteins such as immunoglobulins and hormones

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2
Q

What is plasma?

A

The liquid component of blood. Contains RBCs, WBCs, platelets and clotting factors (eg fibrinogen).

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3
Q

What is the bone marrow and what does it do?

A

Found in pelvis, vertebrae, ribs and sternum. Blood cells develop in the BM.

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4
Q

What can pluripotent haematopoietic stem cells develop into?

A

Myeloid Stem Cells (–> reticulocytes –> RBCs)
Lymphoid Stem Cells
Dendritic Cells

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5
Q

What are reticulocytes?

A

Reticulocytes are immature red blood cells

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6
Q

What are platelets? What is their lifespan?

A

Platelets clump together to cause clots to stop bleeding. They are made by megakaryocytes. Their lifespan is 10 days.

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7
Q

Promyelocytes become:

A 
Monocytes then macrophages
Neutrophils
Eosinophils
Mast Cells
Basophils
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8
Q

Lymphoid stem cells become:

A

B cells or T cells.

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9
Q

B cells mature in the:

A

Bone marrow

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10
Q

T cells mature in the:

A

Thymus gland

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11
Q

B cells become

A

plasma cells and memory B cells

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12
Q

T cells become

A

CD4 (T helper) cells, CD8 (T killer cells), natural killer cells

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13
Q

What does anisocytosis mean and what does it indicate?

A

Variation in size of RBCs on blood film. Seen in myelodysplasic syndrome

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14
Q

What do target cells indicate?

A

Seen on blood film in iron deficiency anaemia and post-splenectomy.

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15
Q

What do Heinz bodies indicate?

A

Denatured globin on blood film, seen in G6PD and alpha-thalassaemia.

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16
Q

What do Howell-Jolly bodies indicate?

A

DNA material seen in RBCs on blood film, post-splenectomy and severe anaemia.

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17
Q

What do reticulocytes on blood film indicate?

A

Immature RBCs, large, contain RNA. High reticulocytes = rapid turnover of RBCs, high BM activity eg haemolytic anaemia.

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18
Q

What do schistocytes on blood film indicate?

A

Fragments of RBCs. Indicate damage (‘schearing) of RBCs, possibly due to small vessel clots –> HUS, DIC, TTP, or in replacement metallic heart valves, haemolytic anaemias.

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19
Q

What do sideroblasts on blood film indicate?

A

Immature RBCs that contain blobs of iron. BM unable to incorporate iron into hb molecules eg myelodysplasic syndrome.

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20
Q

What do smudge cells on blood film indicate?

A

Ruptured WBCs that occur during process of preparing blood film due to aged or fragile WBCs, eg CLL

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21
Q

What do spherocytes on blood film indiate?

A

Spherical RBCs, eg in autoimmune haemolytic anaemia or hereditary spherocytosis.

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22
Q

Give 2 causes of microcytic anaemia.

A 
Thalassaemia
Anaemia of chronic disease
Iron deficiency
Lead poisoning
Sideroblastic
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23
Q

Give 2 causes of normocytic anaemia.

A 
Acute blood loss
Anaemia of chronic disease
Aplastic
Haemolytic
Hypothyroidism
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24
Q

Give 2 causes of megaloblastic macrocytic anaemia.

A

B12 and folate deficiency. Causes impaired DNA synthesis preventing cell from dividing normally, so it keeps growing into a larger, abnormal cell.

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25
Q

Give 3 causes of normoblastic macrocytic anaemia.

A 
Alcohol
Reticulocytosis (haemolytic/blood loss)
Hypothyroidism
Liver disease
Drugs eg azathioprine.
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26
Q

How does anaemia present?

A

Tiredness
Shortness of breath
Headaches
Dizziness
Palpitations
Worsening of other conditions such as angina, heart failure or peripheral vascular disease
Signs: pale, conjuctival pallor, tachycardia, tachypnoea

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27
Q

Give 3 specific features of iron deficiency anaemia.

A

Pica - dietary cravings for abnormal things such as dirt and can signify iron deficiency
Gradual patchy hair loss/brittle hair and nails
Koilonychia (spoon nails)
Angular chelitis
Atrophic glossitis (smooth tongue due to atrophy of papillae)

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28
Q

What type of anaemia is indicated by jaundice?

A

Haemolytic.

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29
Q

What type of anaemia can cause bone deformities?

A

Thalassaemia.

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30
Q

What could cause anaemia with oedema, hypertension and excoriations?

A

Chronic kidney disease

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31
Q

What investigations would you do for anaemia?

A

Bloods - Hb, MCV, B12, folate, ferritin, blood film
OGD - bowel cancer (iron deficiency)
BM biopsy if cause is unclear. These are usually taken from the posterior superior iliac rest.

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32
Q

Give 4 causes of iron deficiency.

A

increased demand eg pregnancy
reduced supply eg malabsorption, diet
loss eg bleed from colon cancer or peptic ulcer, menstruation

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33
Q

How do PPIs interfere with iron absorption?

A

Raise stomach pH. Lower acid means Fe2+ changes to Fe3+ which is insoluble.

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34
Q

What is TIBC? What are levels like in iron deficiency?

A

Total iron binding capacity = Total space on transferrin molecules for iron to bind for. Transferrin saturation = serum iron/TIBC.
Levels increase in iron deficiency.

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35
Q

How is iron stored and transported in the body?

A

Fe3+ bound to transferrin. It is stored as ferritin.

36
Q

What are ferritin levels in iron deficiency?

A

May be low but may also be normal or high as ferritin is raised in inflammation.

37
Q

What are serum iron levels in iron deficiency?

A

Varying with dietary intake - not a useful measure as doesnt show if the iron can be used.

38
Q

What are transferrin saturation levels in iron deficiency?

A

Indication of total body iron. Should be 30% in adults. Less iron –> less saturated transferrin –> reduced transferrin saturation levels. Should be fasted as may increase temporarily after dietary intake.

39
Q

What could give false readings in IDA?

A

Iron supplementation

Acute liver damage - iron stored in liver –> damage could lead to more iron in blood.

40
Q

How is iron deficiency managed?

A 
Investigate for cause eg OGD + colonoscopy to look for GI cancer
Treat underlying cause
PO iron (ferrous sulphate 200mg TDS).
IV iron eg cosmofer - if malabsorption.
Blood transfusion
41
Q

What are the side effects of oral iron?

A

Constipation, diarrhoea, black stools.

Unsuitable where malabsorption is the cause.

42
Q

What are the risks and contra-indications of iron infusion?

A

Anaphylaxis (small risk)

contraindicated in SEPSIS - iron ‘feeds’ bacteria

43
Q

How much would you expect Hb to rise by per week when correcting IDA with iron?

A

10g/L/week

44
Q

What is pernicious anaemia?

A

Autoimmune antibodies against IF or parietal cells causing malabsorption of B12 in the ileum, leading to B12 deficiency anaemia.

45
Q

How does pernicious anaemia present?

A 
Anaemia
Peripheral neuropathy
Loss of vibration sense or proprioception
Visual changes
Mood or cognitive changes
46
Q

How is pernicious anaemia diagnosed?

A

1st line - intrinsic factor antibodies

2nd line - gastric parietal cell antibodies.

47
Q

How is pernicious anaemia managed?

A

1mg IM hydroxycobalamin (B12) 3 times a week for 2 weeks, then every 3 months. Can give daily if neuro sx.
Need to correct b12 before folate to avoid SCD

48
Q

What is haemolytic anaemia?

A

Destruction of RBCs (haemolysis) leadng to anaemia, splenomegaly (full of dead RBCs) and jaundice (bilirubin release from RBCs). Can be due to inherited or acquired conditions.

49
Q

Give 3 inherited and 3 acquired causes of haemolytic anaemia.

A 
Inherited:
Hereditary Spherocytosis - northern europeans
Hereditary Elliptocytosis
Thalassaemia
Sickle Cell Anaemia
G6PD Deficiency
Acquired:
Autoimmune haemolytic anaemia
Alloimmune haemolytic anaemia (= transfusions reactions and haemolytic disease of newborn)
Paroxysmal nocturnal haemoglobinuria
Microangiopathic haemolytic anaemia
Prosthetic valve related haemolysis
50
Q

What 3 investigations would you do for haemolytic anaemia and what would they show?

A

FBC - normocytic anaemia
Blood film - schistocytes (split RBCs)
Direct Coombs test - positive in AUTOIMMUNE haemolytic anaemia

51
Q

What is hereditary spherocytosis and how does it present?

A

Most common inherited haemolytic anaemia in northern europeans. Presents with anaemia, jaundice, splenomegaly and gallstones, aplastic crisis in presence of parvovirus.
Spherocytes on blood film, raised MCHC, raised reticulytes due to rapid turnover of RBCs.
Autosomal dominant inherited.
Treatment with folate and splenectomy, cholecystectomy if gallstones.

52
Q

What is hereditary elliptocytosis and how is it inherited?

A

Anaemia, jaundice, splenomegaly and gallstones, aplastic crisis in presence of parvovirus (same as spherocytosis)
Ellipse shaped RBCs on blood film, raised MCHC, raised reticulytes due to rapid turnover of RBCs.
AD inheritance.

53
Q

How does G6PD deficiency present?

A

Mediterranean and African patients
X linked recessive.
Neonatal jaundice, anaemia, splenomegaly, gallstones, crises triggered by infections, medications or fava beans (broad beans).

54
Q

How is G6PD deficiency diagnosed?

A 
G6PD enzyme assay
Heinz bodies (think heinz= beans) on blood film
55
Q

What is autoimmune haemolytic anaemia and how does it present?

A

Antibodies created against patients RBCs.
Warm type: Idiopathic, more common, CLL
Cold type: Cold agglutinin disease, only at low temps, secondary to lymphoma, leukaemia, SLE, infections eg EBV
Mx: transfusion, steroids, rituximab, splenectomy

56
Q

What is alloimmune haemolytic anaemia? Describe the 2 types.

A

=Antibodies against RBCs causing haemolysis.

  1. Haemolytic transfusion reactions: The immune system produces antibodies against antigens on the transfused RBCs (body produces the antibodies against foreign RBCs).

2 Haemolytic disease of the newborn: antibodies cross the placenta from the mother to the fetus which target antigens on the RBCs of the fetus (fetus receives the antibodies against their own RBCs are attacked).

57
Q

What is paroxysmal nocturnal haemoglobinuria?

A

Genetic mutation in the haematopoietic stem cells in the bone barrow occurs during the patients lifetime (rare). –> loss of the proteins on the surface of red blood cells that inhibit the complement cascade. Leads to uninhibited activation of the complement cascade on the surface of red blood cells and destruction of the red blood cells.

Red urine in the morning containing haemoglobin and haemosiderin. The patient becomes anaemic due to the haemolysis. Risk of thrombosis (e.g. DVT, PE and hepatic vein thrombosis) and smooth muscle dystonia (e.g. oesophageal spasm and erectile dysfunction).

Management: Eculizumab - mab against C5 –> suppression of the complement system. Bone marrow transplantation curative.

58
Q

What is microangiopathic haemolytic anaemia?

A

Mmall blood vessels have structural abnormalities that cause haemolysis of the blood cells travelling through them. Like mesh inside the small blood vessels shredding the red blood cells. Secondary to:

Haemolytic Uraemic Syndrome (HUS)
Disseminated Intravascular Coagulation (DIC)
Thrombotic Thrombocytopenia Purpura (TTP)
Systemic Lupus Erythematosus (SLE)
Cancer

59
Q

What is prosthetic valve haemolysis and how is it treated?

A

Prosthetic valves case turbulence around the valve and collision of red blood cells with the implanted valve. Basically the valve churns up the cells and they break down.

Management:
Monitoring
Oral iron
Blood transfusion if severe
Revision surgery may be required in severe cases
60
Q

What is thalassaemia?

A

2 autosomal recessive conditions causing genetic defect in the protein chains that make up haemoglobin.
Normal haemoglobin consists of 2 alpha and 2 beta-globin chains.
Chromosome 16 - Alpha globin chains –> alpha thalassaemia
Chromosome 11 - Beta globin chains –> beta thalassaemia
Makes cells fragile and break down more easily. Spleen collects the destroyed RBCs which leads to splenomegaly.

61
Q

How does thalassaemia present?

A

Splenomegaly due to buildup of dead RBCs
Bone marrow proliferation to compensate for anaemia –> susceptibility to fractures, pronounced forehead and malar eminences (cheekbones), poor growth and development
Microcytic anaemia, fatigue, pallor
Jaundice, splenomegaly, jaundice

62
Q

How is thalassaemia diagnosed? Give 1 initial blood test and what you would see.

A

Full blood count shows a microcytic anaemia.
Haemoglobin electrophoresis is used to diagnose globin abnormalities.
DNA testing can be used to look for the genetic abnormality
Pregnant women in the UK are offered a screening test for thalasseamia at booking.
Measure serum ferritin for iron overload.

63
Q

Give 5 signs of iron overload.

A

Fatigue, liver cirrhosis, infertility, impotence, HF, arthritis, diabetes, OP and joint pain

64
Q

How is alpha thalassaemia managed?

A 
Monitoring the full blood count
    Monitoring for complications
    Blood transfusions
    Splenectomy may be performed
    Bone marrow transplant can be curative
65
Q

What is thalassemia minor and what is the management?

A

Type of beta thalassaemia in which one beta globin gene is abnormal and one is normal. Only needs monitoring, mild microcytic anaemia

66
Q

What is thalassemia intermedia and what is the management?

A

Type of beta thalassaemia in which two copies of the beta globin gene are defective, or one defective and one deletion gene. Needs monitoring and occasional transfusions for microcytic anaemia. Consider iron chelation to prevent iron overload.

67
Q

What is thalassemia major and what is the management?

A

Patients with beta thalassaemia major are homozygous for the deletion genes. They have no functioning beta-globin genes at all. This is the most severe form and usually presents with severe anaemia and failure to thrive in early childhood.

Thalassaemia major causes:
Severe microcytic anaemia
Splenomegaly
Bone deformities
Management involves regular transfusions, iron chelation and splenectomy. Bone marrow transplant can potentially be curative.
68
Q

What is sickle cell anaemia? Explain the pathophysiology.

A

Sickle cell anaemia is a genetic condition that causes sickle (crescent) shaped red blood cells. This makes the red blood cells fragile and more easily destroyed leading to an haemolytic anaemia.

Hb transports oxygen in RBCs. Fetal haemoglobin (HbF) is usually replaced by haemoglobin A (HbA) at around 6 weeks of age. Patients with sickle-cell disease have an abnormal variant called haemoglobin S (HbS). HbS causes red blood cells to be an abnormal “sickle” shape.

AR inherited abnormal beta-globin on chromosome 11. One copy of the gene results in sickle-cell trait. Two abnormal copies are required for sickle-cell disease.

69
Q

Why is sickle cell more common in patients from Africa, India, Middle East and Carribean?

A

Reduced severity of malaria in people with sickle cell trait. These countries are traditionally affected by malaria - selective advantage.

70
Q

How is sickle cell disease diagnosed?

A

Tested for in pregnancy in at-risk people

Tested for on newborn screening heel prick test

71
Q

Give 5 complications of sickle cell disease.

A 
Anaemia
Increased risk of infection
Stroke
Avascular necrosis in large joints such as the hip
Pulmonary hypertension
Painful and persistent penile erection (priapism)
Chronic kidney disease
Sickle cell crises
Acute chest syndrome
72
Q

How is sickle cell disease managed?

A

Avoid dehydration and other triggers of crises
Ensure vaccines are up to date
Antibiotic prophylaxis to protect against infection with penicillin V (phenoxymethypenicillin)
Hydroxycarbamide can be used to stimulate production of fetal haemoglobin (HbF). Fetal haemoglobin does not lead to sickling of red blood cells. This has a protective effect against sickle cell crises and acute chest syndrome.
Blood transfusion for severe anaemia
Bone marrow transplant can be curative

73
Q

What is sickle cell crisis and how is it managed?

A

Umbrella term for acute crises related to SSD, range from mild to life-threatening, may be triggered by infection, dehydration, cold or stress.
Managed supportively - admit for IV fluids, analgesia (start with paracetamol, avoid NSAID in renal impairment), keep warm, treat trigger eg infection, penile aspiration in priapism.

74
Q

What is vaso-occlusive crisis?

A

Sickled RBCs clogging capillaries causing distal ischaemia. It is associated with dehydration and raised haematocrit.
Symptoms are typically pain, fever and those of the triggering infection. It can cause priapism in men by trapping blood in the penis causing a painful and persistent erection. This is a urological emergency and is treated with aspiration of blood from the penis.

75
Q

What is splenic sequestration crisis?

A

RBCs blocking blood flow within the spleen. This causes an acutely enlarged and painful spleen. The pooling of blood in the spleen can lead to a severe anaemia and circulatory collapse (hypovolaemic shock).

Splenic sequestration crisis is considered an emergency. Management is supportive with blood transfusions and fluid resuscitation to treat anaemia and shock.

Splenectomy prevents sequestration crisis and is often used in cases of recurrent crises. Recurrent crises can lead to splenic infarction and therefore susceptibility to infections.

76
Q

What is aplastic crisis?

A

Temporary loss of the creation of new blood cells, usually triggered by infection with parvovirus B19. It leads to significant anaemia. Management is supportive with blood transfusions if necessary. It usually resolves spontaneously within a week.

77
Q

What is acute chest syndrome?

A

Fever or respiratory symptoms with new infiltrates seen on a chest xray.
Can be due to infection (e.g. pneumonia or bronchiolitis) or non-infective causes (e.g. pulmonary vaso-occlusion or fat emboli).
Emergency - high mortality
Mx: prompt supportive management and treatment of the underlying cause:
Antibiotics or antivirals for infections
Blood transfusions for anaemia
Incentive spirometry using a machine that encourages effective and deep breathing
Artificial ventilation with NIV or intubation may be required

78
Q

What is leukaemia?

A 
Cancer of bone marrow stem cells.
Acute Myeloid
Acute LymphoBLASTIC
Chronic Myeloid
Chronic LymphoCYTIC
Causes pancytopaenia
79
Q

What is the epidemiology of leukaemia?

A 
ALL CeLLmates have CoMmon AMbitions:
ALL <5, Down's
CLL >55, Common, smudge cells
CML >65, Philadelphia Chromosome
AML >75, Auer rods
80
Q

Give 4 signs and 4 symptoms of leukaemia.

A

Signs: FTT, pallor, petechiae, lymphadenopathy, hepatosplenomegaly
Symptoms: fatigue, fever, bruising, bleeding, rash, SOB (anaemia), infections

81
Q

Give 6 causes of non-blanching petechial rash and bruising in children.

A 
Leukaemia
Meningococcal septicaemia
Vasculitis
Henoch-Schonlein Purpura (HSP)
Idiopathic Thrombocytopenia Purpura (ITP)
Non-accidental injury
82
Q

What are the two types of bone marrow biopsy?

A

Aspirate = Liquid sample of cells from bone marrow. Can be examined immediately
Trephine - solid core sample. Takes longer to assess in lab but provides better assessment of cells and structure

83
Q

What is bone marrow biopsy and how is it done?

A

Taken from iliac crest

Involves local anaesthetic and specialist needle.

84
Q

Give 6 complications of chemotherapy.

A 
Failure
Stunted growth and development in children
Infections due to immunodeficiency
Neurotoxicity
Infertility
Secondary malignancy
Cardiotoxicity
Tumour lysis syndrome
85
Q

What is Richter’s transformation?

A

CLL transforms into high-grade lymphoma.

86
Q

Explain tumour lysis syndrome.

A

Cells destroyed by chemo and release uric acid

Uric acid forms crystals in the interstitial tissue and tubules of the kidneys and causes acute kidney injury.

87
Q

What is the management of tumour lysis syndrome?

A

Allopurinol or rasburicase are used to reduce the high uric acid levels.
Other chemicals such as potassium and phosphate are also released so these need to be monitored and treated appropriately. High phosphate can lead to low calcium, which can have an adverse effect, so calcium is also monitored.

Phase 4 (11 decks)

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