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YEAR 3 & 5 CORE CONDITIONS > Haematology > Flashcards

Haematology Flashcards

1
Q

What are the four groups of causes of iron deficiency anaemia?

A
  1. Excessive blood loss
  2. Dietary inadequacy
  3. Iron malabsorption
  4. Excessive requirements
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2
Q

What condition can typically cause iron malabsorption?

A

Coeliac disease

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3
Q

What is the most common cause of iron deficiency anaemia in tropical countries?

A

Hookworm causing blood loss from the GI tract

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4
Q

What are some signs you see when examining an iron deficient patient?

A
  • Pallor
  • Pale palmar creases
  • Koilonychia (spooning of the nails)
  • Angular stomatitis
  • Atrophic glossitis
  • Dysphagia = Plummer-Vinson syndrome
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5
Q

What would a blood film look like in iron deficiency anaemia?

A

Hypochromic microcytic anaemia +/- anisocytosis and poikilocytosis

Hypochromia = low mean corpuscular Hb (MCH)
Microcytosis = low MCV
Anisocytosis = variation in size between RBCs
Poikilocytosis = abnormally shaped RBCs
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6
Q

Why is serum ferritin not always a very useful marker of iron levels?

A

It is an acute phase reactant

i.e. although it correlates with total body iron stores, it can be raised in infection/inflammation

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7
Q

What further investigations would you do in a patient with iron deficiency anaemia?

A 
Coeliac serology. 
If negative (and male or post-menopausal woman), refer for gastroscopy + colonoscopy to rule out GI bleed
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8
Q

What is the treatment for iron deficiency anaemia and how long do you treat for?

A

Ferrous sulphate 200-300mg 1-2 times a day

Once Hb levels are normal, continue treatment for a minimum of 3 months

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9
Q

What are the main side effects of iron replacement therapy?

A

Constipation or diarrhoea
Black stools
Nausea
Abdominal pain

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10
Q

What is the main reason that Hb levels do not rise despite iron replacement therapy?

A

Non-compliance due to GI upset side effects of iron. So always check compliance first and adjust dose if necessary.

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11
Q

Microcytic anaemia does not always mean iron deficiency. What are other causes of microcytic anaemia?

A
  1. Thalassaemia
  2. Sideroblastic anaemia (would see basophilic granules)
  3. Anaemia of chronic disease
  4. Lead poisoning
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12
Q

What is sideroblastic anaemia due to?

A

Impaired ability of bone marrow to produce normal RBC (ineffective erythropoiesis)

Iron levels are normal or high but not used properly

Can be caused by TB medications

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13
Q

What is a complication of sideroblastic anaemia?

A

Organ damage due to excess iron deposition

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14
Q

What MCV is macrocytosis defined by?

A

MCV > 96 fL

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15
Q

What is a megaloblast?

A

A cell in which the nuclear maturation is delayed compared with the cytoplasm due to defective DNA synthesis

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16
Q

What are the main causes of megaloblastic macrocytic anaemia and why?

A

Vitamin B12 and folate deficiency - they are required for normal DNA synthesis

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17
Q

What drugs can cause folate deficiency?

A

Methotrexate
Anti-epileptics
Trimethoprim

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18
Q

What surgical procedure commonly causes vitamin B12 deficiency?

A

Gastrectomy

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19
Q

What causes non-megaloblastic macrocytic anaemia?

A
  • Excess alcohol
  • Liver disease
  • Hypothyroidism
  • Reticulocytosis in haemolysis
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20
Q

Describe the difference between macrocytosis and microcytosis

A

Macrocytosis occurs when there is a problem with the synthesis of blood cells
Microcytosis occurs when there is a problem with haemoglobin production

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21
Q

What might a high MCV without anaemia suggest?

A

Myeloma

Hyperglycaemia

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22
Q

What vitamin is folate?

A

Vitamin B9

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23
Q

What do neutrophils look like in B12 and folate deficiency?

A

Hypersegmented. Normally there should be less than 5 segments.

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24
Q

When testing for folate levels, why is serum folate not always very reliable and what is a more reliable indicator?

A

Serum folate only indicates recent intake

Red cell folate is a more reliable indicator

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25
Q

What is pernicious anaemia?

A

Autoimmune condition where atrophic gastritis leads to lack of intrinsic factor secretion from parietal cells of stomach, therefore vitamin B12 cannot be absorbed in the terminal ileum.

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26
Q

What cells are characteristic of Hodgkin’s lymphoma?

A

Reed-Sternberg cells = multi-nucleated giant cells

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27
Q

Previous infection with what virus can cause Hodgkin’s lymphoma?

A

Epstein-Barr virus

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28
Q

What do the lymph nodes feel like in lymphomas?

A

Enlarged, non-tender, rubbery, superficial lymph nodes

Mostly cervical

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29
Q

What staging system is used for lymphomas?

A

Ann Arbor staging

  1. Single lymph node region
  2. Involvement of 2+ nodal areas on same side of diaphragm
  3. Involvement of nodes on both sides of diaphragm
  4. Spread beyond lymph nodes

Each stage has A (no systemic symptoms except pruritis) or B (systemic symptoms present)

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30
Q

What blood test results indicate a worse prognosis in Hodgkin’s lymphoma?

A

High ESR

Low Hb

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31
Q

What lymphomas does Non-Hodgkin’s lymphoma include?

A

All lymphomas without Reed-Sternberg cells

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32
Q

What is the most common Non-Hodgkin’s lymphoma?

A

Diffuse large B-cell lymphoma

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33
Q

What is the most common area for extranodal disease in Non-Hodgkin’s lymphoma?

A

GI tract

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34
Q

What are the 3 types of GI tract Non-Hodgkin’s lymphomas?

A
  1. Gastric MALT
  2. Non-MALT gastric lymphoma
  3. Small bowel lymphomas
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35
Q

What is Gastric MALT caused by?

A

H. Pylori

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36
Q

In LFTs, what indicates a poorer prognosis in Non-Hodgkin’s lymphoma?

A

Raised LDH because it indicates increased cell turnover

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37
Q

In terms of treatment/prognosis, what is the difference between low and high grade lymphomas?

A

Low-grade - slow-moving but incurable and widely disseminated

High-grade - aggressive but often curable

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38
Q

What symptom is uncommon but specific to Hodgkin’s lymphoma?

A

Alcohol induced pain

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39
Q

If there is major bleeding when a patient is on warfarin, what is your management? When can you restart warfarin?

A

Give prothrombin and vitamin K

Restart warfarin when INR < 5.0

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40
Q

If you see a high INR, what should you check for in the patient?

A
  • Bruising
  • Epistaxis
  • GI bleed
  • Cerebral bleeds
41
Q

What pathways are INR and APTT linked to?

A 
INR = PT = extrinsic pathway - used to monitor warfarin
APTT = intrinsic pathway - used to monitor heparin
42
Q

What is Plummer-Vinson syndrome?

A

Triad of:

1) Post-cricoid dysphagia
2) Upper oesophageal webs (thin membranes that go across the inside of upper part of oesophagus)
3) Iron deficiency anaemia

43
Q 
Name the ABO antigen present on RBC and the antibodies in plasma in these blood types:
O
A
B
AB
A

O:

  • No antigens
  • A and B antibodies in plasma

A:

  • A antigen
  • B antibodies

B:

  • B antigen
  • A Antibodies

AB:

  • A and B antigens
  • No A or B antibodies
44
Q

Which blood types are universal donors and which are recipients?

A

O negative are universal dOnOrs

AB positive are universal recipients

45
Q

List the types of immune related transfusion reactions that can occur (7)

A

1) Acute haemolytic transfusion reaction
2) Acute non haemolytic febrile transfusion reaction
3) Minor allergic reactions
4) Anaphylaxis
5) TRALI
6) Post transfusion purpura
7) Delayed haemolytic transfusion purpura

46
Q

What causes an acute haemolytic transfusion reaction?

A

ABO incompatibility results in severe destruction of donor RBCs by recipient antibodies

47
Q

How may an acute haemolytic transfusion reaction present?

A 
Rapid onset
Fever, chills, nausea, flushing
Pruritis, urticaria
Flank pain
Dyspnea
Burning at IV site
48
Q

What are some complications of an acute haemolytic transfusion reaction?

A

Renal failure
DIC
Jaundice

49
Q

How should an acute haemolytic transfusion reaction be managed?

A

Stop transfusion
Coombs test - detects antiglobulins showing autoimmune haemolytic anaemia
IV fluids
Vasopressors to maintain perfusion - obstruction of vessels by haemolytic debris and hypotension can decrease perfusion
ECG - hyperkalaemia secondary to severe haemolysis can occur
If DIC develops - FFP and platelets

50
Q

What causes a nonhaemolytic febrile transfusion reaction to occur?

A

After periods of long storage of blood products, cytokines may leak from donor RBCs and subsequently cause a mild immune reaction in the recipient

Also pre-formed antibodies in recipient lead to lysis of the few remaining leukocytes within donor RBC concentrates, leading to an inflammatory reaction

51
Q

How has the incidence of nonhaemolytic febrile transfusion reaction reduced?

A

Using leukoreduced RBC concentrates

52
Q

How does a nonhaemolytic febrile transfusion reaction present?

A

Onset 1-6hrs after transfusion
Fever
Chills
Malaise

53
Q

How is a a nonhaemolytic febrile transfusion reaction managed?

A

Stop transfusion until an acute haemolytic transfusion reaction has been ruled out

Paracetamol

54
Q

How does anaphylaxis occur following transfusion?

A

Occurs when an individual has previously been sensitised to an allergen present in the blood, and on re-exposure, releases IgE or IgG antibodies

Individuals with severe IgA deficiency may develop an IgG antibody against IgA on the surface of donor RBCs

Triggers mast cell degranulation

55
Q

How may anaphylaxis present following transfusion?

A

Sudden onset
Shock
Hypotension

56
Q

What is the management of anaphylaxis following transfusion?

A 
Adrenaline 0.5-1mg IM and repeat every 10 mins until improvement occurs
O2
IV fluids
Nebulised salbutamol may be needed
Airway management - get anaesthetist
57
Q

What is a TRALI?

A

Transfusion related acute lung injury

58
Q

What occurs in a TRALI?

A

Soluble factors (antibodies and certain lipids) in the donor blood leads to activation of the recipients granulocytes

59
Q

Transfusion of which products is most likely to cause a TRALI?

A

FFP

Platelets

60
Q

How does a TRALI present?

A 
Within 6hrs
Non productive cough
Breathlessness
Hypoxia
Frothy sputum
Fever
Hypotension due to hypovolaemia
61
Q

What does a CXR show in a TRALI

A

Multiple perihilar nodules with infiltration of the lower lung fields

62
Q

How is a TRALI managed?

A

Stop transfusion
O2
IV steroids for anti inflammatory therapy

63
Q

What is Graft-vs-host disease?

A

Almost always fatal

Donated bone marrow or peripheral blood stem cells view recipients body as foregin and attack the body

64
Q

How does GvHD present?

A 
Day 4-30 post transfusion
High fever
Diffuse erythematous skin rash progressing to erythroderma, diarrhoea and abnormal liver function
Pt deteriorates with bone marrow failure
Death from overwhelming infection
65
Q

How is GvHD prevented?

A

Irradiation of cellular blood products

66
Q

What is TACO?

A

Transfusion associated circulatory overload

67
Q

How does TACO present?

A

Symptoms of hypervolaemia:

  • SOB
  • S3 gallop
  • Jugular venous distension
  • HTN
68
Q

What does a CXR show in TACO?

A

Signs of pulmonary oedema

69
Q

What is the treatment of TACO?

A

Diuretics (furosemide)
O2
Assisted ventilation if severe

70
Q

What electrolyte imbalances can occur following a transfusion?

A

Hyperkalaemia - esp rapid transfusions causing mechanical damage of RBC

Hypocalcaemia - formation of complexes with the added citrate (anticoagulant in the bag the blood is donated in)

71
Q

What is DIC?

A

Disseminated intravascular coagulation

Systemic activation of the clotting cascade with micro thrombi formation, platelet consumption and subsequent exhaustion of all the clotting factors

72
Q

What are some causes of DIC?

A

STOP Making Trouble

Sepsis / snakebites
Trauma
Obstetric complications
Pancreatitis
Malignancy
Transfusion
73
Q

What obstetric complications lead to DIC?

A

Amniotic fluid embolism
Pre-eclampsia
Placental abruption
Retained products of conception

74
Q

What malignancies are associated with DIC?

A

Acute promyelocytic leukaemia (rare subtype of AML)
Pancreatic, ovarian or gastric adenocarcinomas
NSCLC

75
Q

How may DIC present?

A

Bleeding

  • Petechia, purpura, ecchymoses
  • Oozing from wounds
  • Haematuria
  • Blood in body cavities eg haemoperitoneum

Thrombosis

  • Acute renal failure (oliguria)
  • Hepatic dysfunciton (jaundice)
  • ARDs (dyspnoea, crackles)
  • PE (dyspnoea, chest pain, haemoptysis)
  • DVT
  • Neurodysfunction (altered mental status, stroke)
  • Purpura fulminans (extensive skin necrosis)
  • Waterhouse Friderichsen syndrome
76
Q

What is Waterhouse Friderichsen syndrome?

A

Adrenal infarcts leading to adrenal insufficiency

77
Q

How does adrenal insufficiency present?

A 
Postural hypotension
Nausea + vomiting
Weight loss
Anorexia
Lethargy
Depression
Hyponatraemia
78
Q

Describe the course of DIC depending on the cause

A

Acute eg following trauma / sepsis

Subacutely eg following malignancy

79
Q

What findings on bloods suggest DIC?

A

Low platelets
High D-dimer
High PT and APTT
Low fibrinogen

80
Q

Which coagulation factors are decreased in DIC?

A

All of them

81
Q

What are some ddx of DIC?

A

Severe hepatic dysfunction

Thrombotic thrombocytopenic purpura

Heparin induced thrombocytopenia

82
Q

How can severe hepatic dysfunction be differentiated from DIC?

A

FVIII assay

Would be low in DIC (all are low)

But normal in chronic liver disease as not only made by hepatic cells (also sinusoidal endothelial cells)

83
Q

How can thrombotic thrombocytopenic purpura be differentiated from DIC?

A

No consumption coaguloptahy - so normal PT and aPTT in thrombotic thrombocytopenic purpura

In DIC both are prolonged

84
Q

What is the management of DIC?

A

Underlying disease management
Transfusions
Synthetic protease inhibitor (blocks thrombin and plasmin) preventing activation of coagulation factors eg Gabexate mesilate

Antifibrinolytic therapy eg tranexamic acid

85
Q

What transfusions are offered in DIC?

A

Platelet concentrate:
- if platelets are <10,000 in an asymptomatic individual, or <50,000 with active bleeding or a surgery planned

FFP:
- If PT or aPTT >1.5 normal value

Cryoprecipitate if fibrinogen <150mg/dL

Packed RBC if massive haemorrhage without response to fluids or if Hb <7g / dL

86
Q

Haemolytic anaemia can be divided into intrinsic (increased destruction of RBC due to a defect within RBC) and extrinsic haemolytic anaemia (abnormal breakdown of normal RBC).

What can cause intrinsic haemolytic anaemia?

A

Membrane defects

  • Hereditary spherocytosis
  • Paroxsymal nocturnal hemoglobinuria

Enzyme defects:
- G6PD deficiency

Hemoglobinopathies:

  • Sickle cell
  • Thalassaemia
  • Hb C disease
87
Q

What can cause extrinsic haemolytic anaemia?

A

Mechanical destruction eg prosthetic heart valves

Shearing of RBC due to occlusion of small vessels by microthrombi

Immune reactions to infections (eg mycoplasma) or tumours (CLL)

Infections
Isoimmune reactions eg ABO/Rh
Increased degradation by the spleen eg hypersplenism

88
Q

What can lead to shearing of RBC due to occlusion of small vessels by microthrombi?

A

HUS (haemolytic uraemic syndrome)

TTP (thrombotic thrombocytopenic purpura)

89
Q

How do haemolytic anaemias present?

A

Anaemia:
- Pallor, fatigue, exertional dyspnoea

Haemolysis:

  • Jaundice
  • Pigmented gallstones due to the build up of indirect bilirubin in bile
  • Splenomegaly
  • Back pain and dark urine in severe haemolysis with haemoglobinuria (nephrotoxic)

Sings of increased haemoposis (mostly in chronic eg thalassaemia)

90
Q

What are signs of increased haematopoeisis?

A

Bone marrow expansion - widening of diploic space of skull, biconcave deformity in vertebral bodies

Cortical thinning and softening of bone leading to increased risk of pathological fractures

Extramedullary hematopoiesis (RBC production outside of bone marrow - pathological) - hepatosplenomegaly

91
Q

What are findings on bloods of haemolytic anaemia?

A

Low Hb
Low haematocrit
Low RBC count

92
Q

What is a reticulocyte?

A

Immature RBC that develops in bone marrow during erythropoiesis

Circulates in blood for 1-2 days before becoming mature RBC

93
Q

What happens to reticulocyte counts in haemolytic anaemia and why?

A

Increases

Loss of erythrocytes leads to a reactive increase in erythropoiesis

This leads to an increase in reticulocytes in peripheral blood

94
Q

What is the MCV in haemolytic anaemias?

A

Normal in most

Decreased in thalasseamia / anaemia of chronic disease

Can rarely be increased in severe reticulocytosis (when bone marrow becomes highly active to compensate for the RBC loss) - reticulocytes are larger than RBC

95
Q

What does LDH imply? Is it increased or decreased in haemolytic anaemia?

A

Cellular breakdown

Raised

96
Q

When are Heinz bodies seen on a blood smear?

A

G6PD deficiency

RBC with damaged haemoglobin

97
Q

When are target cells seen on a blood smear?

A

Sickle cell
Thalassaemia
HbC disease

98
Q

When are teardrop cells seen on a blood smear?

A

Thalassaemia

99
Q

What test is used to differentiate between autoimmune and non-autoimmune haemolytic anaemias?

A

Coombs test

  • Coombs positive = autoimmune
  • Coombs negative = non-autoimmune

Direct Coombs test - detects antibodies on surface of RBCs

Indirect Coombs test - detects antibodies in serum

YEAR 3 & 5 CORE CONDITIONS (30 decks)

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