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Phase 4 Medicine > Haematology > Flashcards

Haematology Flashcards

1
Q

Define anaemia

A

Anaemia describes a low haemoglobin concentration due to either a reduction in the proportion of circulating red blood cells or increased plasma volume (pregnancy).

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2
Q

Give 3 mechanisms in which anaemia can be caused by

A

Blood loss (acute or chronic)

Haemolytic anaemia

Deficient/defective erythropoiesis

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3
Q

Define MCV

A

Mean Cell Volume - Describes the average size of red blood cells in a sample

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4
Q

Define MCH

A

Mean Corpuscular Haemoglobin - Describes the average quantity of haemoglobin present in a single red blood cell

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5
Q

Define MCHC

A

Mean Corpuscular Haemoglobin Concentration

Describes a calculation of the amount of haemoglobin per unit volume in a single red blood cell

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6
Q

Describe the reticulocyte count

A

Describes a count of the number of immature RBCs in the bone marrow.

(if the cause if anaemia is a production issue, this will be low. If the cause is a removal issue, this will be high)

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7
Q

Describe the use of Ferratin in testing for anaemia

A

Ferritin is a blood protein that contains Iron.

Low ferritin indicates the body’s iron stores are low, which may indicate iron deficiency anaemia.

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8
Q

When may ferratin levels increase? Why?

A

May increase during inflammation.

As ferritin is an acute phase reactant

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9
Q

What types of anaemia present with a low MCV? (3)

A

Iron Deficiency Anaemia (most common)

Thalassaemia

Sideroblastic anaemia

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10
Q

What types of anaemia present with a normal MCV? (5)

A

Acute Blood Loss

Anaemia of chronic disease

Bone marrow failure

Hypothyroidism

Pregnancy

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11
Q

What types of anaemia present with a high MCV? (3)

A

B12/Folate deficiency anaemia

Alcohol excess

Antifolate drugs (phenytoin)

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12
Q

What effect does phenytoin have on blood cells?

A

Can cause folate deficiency, leading to macrocytic anaemia

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13
Q

Where in the intestine is iron absorbed? And how?

A

Duodenum

Iron ions are actively transported into duodenal intestinal epithelial calls by the intestinal haem transporter (HCP1).

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14
Q

What type of anaemia is iron deficiency anaemia?

A

Microcytic

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15
Q

Give 4 causes of iron deficiency anaemia

A

Blood loss (menorrhagia, GI bleeding, Hookworm)

Poor diet/poverty (reduced iron intake)

Malabsorption (coeliac disease)

Pregnancy

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16
Q

Give 5 clinical features of iron deficiency anaemia

A

Anaemic features (fatigue, dyspnoea, faintness)

Brittle nails/hair

Koilonychia (spoon-shaped nails)

Atrophic glossitis (smooth/glossy tongue)

Angular stomatitis/cheilosis (ulcers in corners of mouth)

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17
Q

If microcytic anaemia does not respond to iron therapy, what could it be? Describe this condition.

A

Sideroblastic anaemia

Describes condition characterised by ineffective erythropoiesis resulting in increased iron absorption in the duodenum and iron loading in the bone marrow.

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18
Q

Define anaemia of chronic disease and describe it’s cause.

A

Describes anaemia secondary to chronic disease.

Involves the polypeptide hepcidin (produced by the liver).

Hepcidin production increases in chronic diseases, inhibiting the release of iron from macrophages. Hepcidin ultimately inhibits iron transport and absorption.

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19
Q

Give 4 common conditions causing anaemia of chronic disease

A

Tuberculosis

Crohn’s disease

Rheumatoid Arthritis

SLE

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20
Q

How is anaemia of chronic disease treated? (2)

A

Treat underlying chronic condition.

Erythropoietin (EPO)

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21
Q

Describe 2 categories of macrocytic anaemia

A

Megaloblastic - Characterised by presence of megaloblasts (b12/folate deficiency)

Non-megaloblastics - Erythroblasts are normal (alcohol excess, pregnancy)

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22
Q

Where is vitamin B12 absorbed?

A

Ileum (small intestine)

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23
Q

What factor must be present for Vitamin B12 to be absorbed?

A

Intrinsic factor

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24
Q

Where is intrinsic factor (important for B12 absorption) produced?

A

Parietal cells of the stomach

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25
Q

Where is B12 stored?

A

Liver (for 4 years)

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26
Q

Describe the use of vitamin B12 and why it’s deficiency leads to anaemia.

A

B12 helps synthesise Thymidine and hence DNA.

Defiency results in impaired DNA synthesis > delayed nuclear maturation in cells undergoing erythropoiesis > generation of abnormally large RBCs + decreased RBC production.

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27
Q

In what foods can vitamin B12 be found? (3)

A

Meat, Fish, Diary products

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28
Q

Give 3 causes of vitamin B12 deficiency

A

Pernicious anaemia (most common)

Dietary deficiency (vegans not using supplements)

Malabsorption (post-gastrectomy - no intrinsic factors, Crohn’s disease)

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29
Q

Describe pernicious anaemia

A

Autoimmune condition in which atrophic gastritis affects the fundus of the stomach.

Plasma cell and lymphoid infiltration leads to destruction of parietal cells.

Leads to intrinsic factor deficiency which results in less B12 being absorbed in the ternimal ileum, leading to macrocytic anaemia.

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30
Q

What cells produce stomach acid?

A

Parietal cells

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31
Q

Give 5 risk factors for pernicious anaemia

A

Elderly

Female

Fair haired/Blue eyes

Blood group A

Hypothyroidism and Addison’s disease

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32
Q

Give 4 clinical features of pernicious anaemia

A

Insidious onset (progressively increasing symptoms of anaemia)

Lemon tinge to skin (pallor + jaundice)

Glossitis (red beefy tongue)

Angular cheilosis (stomatitis)

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33
Q

What system is distinctively effected in B12 deficiency anaemia? What features may be present?

A

Neurological system

Symmetrical paraesthesia (fingers/toes)

Early loss of vibration and proprioception

Progressive weakness and ataxia

Dementia, irritability, depression or psychosis.

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34
Q

Give 3 clinical neurological signs of B12 deficiency

A

Positive babinski (UMN)

Absent knee jerk (LMN)

Absent ankle jerk (LMN)

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35
Q

Give 3 diagnostic tests used for B12 deficiency

A

Blood film (Macrocytic RBCs, Oval Macrocytes)

FBC (Raised MCH, Low Hb, Low B12)

Serology (parietal cells Abs, intrinsic factor Abs)

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36
Q

Presence of what is specific for pernicious anaemia diagnosis?

A

Intrinsic factor antibodies

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37
Q

What IM injection can be given to malabsorption patients with pernicious anaemia?

A

Hydroxocobalamin (synthetic B12)

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38
Q

What type of anaemia does folate deficiency cause?

A

Macrocytic anaemia

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39
Q

What foods contain folate? (3)

A

Fruits, Leafy Green vegetables, Liver

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40
Q

Where is folate absorbed in the intestine?

A

Duodenum/Proximal Jejenum

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41
Q

Give 4 causes of folate deficiency

A

Poor diet (main cause)

Pregnancy

Malabsorption (coeliac/Crohn’s)

Antifolate drugs - Methotrexate/Trimethoprim)

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42
Q

Give 3 antifolate drugs

A

Phenytoin

Methotrexate

Trimethoprim

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43
Q

Give 4 risk factors for folate deficiency

A

Elderly

Alcoholics

Pregnant

Crohn’s/Coeliac

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44
Q

What type of anaemia may present with neuropathy?

A

B12 deficiency anaemia

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45
Q

What is the treatment for folate deficiency anaemia? (2)

A

Treat underlying cause

Folic acid OD for 4 months
(Never give without B12, unless pt is known to have normal B12, as low B12 states can precipitate/worsen subacute combined degeneration of the spinal cord)

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46
Q

Define aemolysis

A

Describes the premature breakdown of RBCs.

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47
Q

Describe 2 types of haemolytic anaemia

A

Uncompensated and Compensated Haemolytic Anaemia

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48
Q

Where can haemolysis occur? (2)

A

Intravascular - Occurs in circulation

Extravascular - Occurs in reticuloendothelial system (macrophages of bone marrow, liver and spleen)

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49
Q

Describe what happens in the bone marrow during haemolytic anaemia (2)

A

To compensate for increase in haemolysis, bone marrow increases output be increasing proportion of cells committed to erythropoiesis (RBC production).

Reticulocytes are also released prematurely, these are larger than mature cells (macrocytic) and stain blue on peripheral blood film.

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50
Q

Give 2 causes of haemolytic anaemia

A

Acquired (inflammatory, infection, blood transfusion rejection, hypersplenism)

Hereditary (G6PD/Pyruvate Kinase Deficiency, Sickle Cell, Spherocytosis)

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51
Q

Give 3 hereditary causes of haemolytic anaemia

A

Enzymopathies (G6DP or Pyruvate Kinase Deficiency)

Haemoglobinopathies (Sickle Cell, A/B thalassaemia)

RBC membrane defects (elliptocytosis or spherocytosis)

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52
Q

Describe autoimmune haemolytic anaemia

A

Anaemia characterised by autoimmune destruction of RBCs

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53
Q

What test is used to diagnose autoimmune haemolytic anaemia?

A

Coombs Test (positive direct antigloblin test)

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54
Q

Describe 2 classifications of autoimmune haemolytic anaemia

A

Warm (AIHA);
- Caused by IgG
- Haemolysis occurs in extravascular sites (spleen)
- Causes - Autoimmune disease (SLE), Neoplasia, Methyldopa

Cold AIHA
- Caused by IgM
- Haemolysis mediated by compliment, occurs intravascular
- Features include; Raynaud’s and acrocyanosis

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55
Q

How is autoimmune haemolytic aneamia managed?

A

Steroids - Prednisolone

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56
Q

How is Glucose 6 Phosphate Dehydrogenase Deficiency inherited?

A

Heterogenous X-linked condition (more common in males)

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57
Q

What is the pattern of inheritance of spherocytosis?

A

Autosomal Dominant

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58
Q

Describe inherited spherocytosis

A

Describes deficiency in RBC membrane protein Spectrin.

Deficiency results in loss of RBC membrane stability > Spherocytosis > reduced MCH and Increased MCHC.

Spherocytes are more rigid and les deformable therefore unable to pass through the spleen. Resultantly are destroyed via extravascular haemolysis

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59
Q

Describe the clinical presentation of inherited spherocytosis (2)

A

Jaundice at birth (delayed and asymptomatic)

Splenomegaly

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60
Q

How is inherited spherocytosis treated?

A

Splenectomy
(Relieves symptoms of anaemia or splenomegaly and prevents recurrent gall stones).

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61
Q

Describe the composition of normal Hb (HbA)

A

Haem + 2 Alpha Chains + 2 Beta Chains

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62
Q

Describe the composition of foetal Hb (HbF)

A

Haem + 2 Alpha Chains + 2 Gamma Chains

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63
Q

Describe the composition of delta (HbA2)

A

Haem + 2 Alpha Chains + 2 Delta Chains

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64
Q

Describe thalassaemia

A

Describes genetic conditions of unbalanced HB synthesis, with underproduction (or no production) of one globin chain.

Unbalanced globins precipitate within mature RBCs leading to haemolysis.

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65
Q

What are the 2 most common types of thalassaemias

A

Alpha thalassaemia (reduced A chain synthesis)

Beta thalassaemia (reduced B chain synthesis)

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66
Q

Define beta thalassaemia

A

Caused by mutation on chromosome 11 leading to decreased/no B chain Production.

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67
Q

Name 3 types of beta thalassaemia

A

Beta thalassaemia minor (trait/carrier)

Beta thalassaemia intermedia

Beta thalassaemia major

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68
Q

Describe beta thalassaemia minor (3)

A

Trait/carrier - heterozygous beta thalassaemia

Asymptomatic (anaemia is mild/absent)

Hb electrophoresis shows raised HbA2 and raised HbF

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69
Q

Describe beta thalassaemia intermedia (2)

A

Intermediate symptomatic state with moderate anaemia

Splenomegaly, bone deformities, gallstones, infections

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70
Q

Describe beta thalassaemia major

A

Presents in children with homozygous B-thalassaemia within the first year of life with;

Failure to thrive and recurrent bacterial infections

Severe anaemia from 3-6 months (when switch from gamma to beta chain occurs)

Extramedullary haematopoiesis > hepatosplenomegaly)

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71
Q

What skull x-ray sign may be seen in a patient with beta thalassaemia major?

A

Hair on end sign (increased marrow activity)

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72
Q

Describe the size of RBCs in beta thalassaemia major

A

Blood film = Large and Small irregular hypochromic RBCs

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73
Q

Give 3 complications of blood transfusions

A

Iron overload;

Mainly deposits in liver and spleen resulting in liver fibrosis and cirrhosis

Deposits in endocrine glands and heart, resulting in diabetes, hypothyroidism, hypocalcaemia and premature death.

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74
Q

Define sickle cell anaemia

A

Describes an autosomal recessive disorder in which production of abnormal haemoglobin leads to vaso-occlusive crisis.

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75
Q

Sickle cell anaemia has which pattern of inheritance?

A

Autosomal recessive

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76
Q

Sickle cell anaemia protects against which form of malaria?

A

Falciparum malaria

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77
Q

Describe vaso-occlusive crisis in terms of sickle cells

A

Sickle cells have a strong adherence to the endothelium. This can cause obstruction of small vessels, resulting in tissue infarction and pain.

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78
Q

Give 5 triggers of sickle cell vaso-occlusive crisis

A

Hypoxia

Cold weather

Infection

Dehydration

Stress

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79
Q

How may homozygous sickle cell anaemia present? (6)

A

Vaso-occlusive crisis

Mesenteric ischaemia (mimics acute abdomen)

CNS infarction

Acute chest syndrome

Pulmonary hypertension

Anaemia

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80
Q

Describe vaso-occlusive crisis (3)

A

Common due to microvascular occlusion

Affects marrow causing severe pain

Presents as dactylitis in children <3

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81
Q

Describe acute chest syndrome (sickle cell)

A

Occurs in 30% of patients. Describes vaso-occlusive crisis of the pulmonary vasculature.

Caused by; Infection, fat embolism, sequestration of sickle cells in pulmonary vasculature > pulmonary infarction.

Causes; dyspnoea, chest pain, hypoxia

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82
Q

Give 2 ways sickle cell causes anaemia

A

Splenic sequestration (sickle cells get trapped in spleen = acute, painful splenomegaly)

Bone marrow aplasia (aplastic crisis) (commonly follows infection with erythrovirus B19)

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83
Q

What infection commonly causes bone marrow aplasia (aplastic crisis) in Sickle Cell?

A

Erythrovirus B12

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84
Q

What test is used to diagnose sickle cell anaemia?

A

Hb Electrophoresis

Distinguishes HbSS and HbAS states

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85
Q

How is sickle cell anaemia treated? (6)

A

Avoid precipitating factors (cold, dehydration, infection)

Oral Hydroxycarbamide (increases HbF levels)

Antibiotic and Immunisaiton prophylaxis

Analgesia (morphine, codine, paracetamol, NSAIDS) for acute pain

Blood transfusions for anaemia

Bone marrow transplantation

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86
Q

Describe lymphomas

A

Lymphomas describe disorders caused by the spread/proliferation of malignant lymphocytes.

These accumulate in lymph nodes, causing lymphadenopathy.

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87
Q

Describe the difference between lymphoma and leukaemia

A

Lymphoma cancer cells are predominantly present in lymph nodes and other tissues, while leukaemia cancer cells are present in bone marrow and blood.

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88
Q

In which type of lymphoma would you find Reed-Sternberg Cells?

A

Hodgkin’s Lymphoma (derived from B lymphocytes)

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89
Q

What is a key hallmark of Hodgkin’s Lymphoma?

A

Reed-Sternberg Cells

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90
Q

Describe the incidence of Hodgkin Lymphoma

A

2 peaks;

Young adults (most common malignancy in 15-24 yr olds)

Elderly people (males)

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91
Q

Give 5 risk factors for Hodgkin’s Lymphoma

A

An affected sibling

Immunocompromised (wiskott-aldrich syndrome)

Infection (EBV, HIV)

Autoimmune disease (SLE)

Post transplantation

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92
Q

Describe Wiskott-Aldrich Syndrome. What condition is it associated with?

A

Associated with Hodgkin’s Lymphoma.

Characterised by microthrombocytopenia. Decrease in size and number of platelets, leading to easy bruising, prolonged bleeding and bloody diarhoea.

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93
Q

Name 2 infections that can cause Hodgkin’s Lymphoma

A

EBV (glandular fever - infectious mononucleosis)

HIV

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94
Q

Give 6 clinical features of Hodgkin’s Lymphoma

A

Painless, cervical lymphadenopathy (rubbery on examination)

B-symptoms (fever, weightloss, nightsweats)

Mediastinal lymphadenopathy +/- cough

Cachexia (muscle wasting)

Anaemia

Hepato-splenomegaly

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95
Q

Give 1 clinical complication of Hodgkin’s lymphoma

A

Spinal cord compression (rare)

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96
Q

How is Hodgkin’s Lymphoma diagnosed?

A

Lymph node biopsy (presence of reed-sternberg cells)

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97
Q

What is the treatment for Hodgkin’s Lymphoma?

A

Combination chemotherapy ABVD;

Adriamycin
Bleomycin
Vinablastine
Dacarbazine

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98
Q

Give 4 complications of radiotherapy

A

Increased risk of second malignancies (in lung, breast, stomach, thyroid)

Increased risk of IHD

Increased risk of lung fibrosis

Increased risk of hypothyroidism

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99
Q

Give 4 side effects of chemotherapy

A

Myelosuppression > Infection

Nausea

Alopecia (hair loss)

Infertility

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100
Q

How is Hodgkin’s Lymphoma staged?

A

Lugano Classification (Uses PET scans to determine staging)

I - Confined to single lymph node

II - involvement of 2 or more nodal area on SAME side of diaphragm

III - involvement of nodes on both sides of diaphragm

IV - Spread beyond lymph nodes (e.g to bone marrow or liver)

A - no systemic symptoms other than pruritis
B- presence of B symptoms

101
Q

Give 3 B Symptoms

A

Fever

Weight loss

Nightsweats

102
Q

Describe non-hodgkin lymphoma

A

Describes all lymphomas without Reed-Sternberg Cells

103
Q

What is non-hodgkin lymphoma strongly linked to? (2)

A

Epstein Barr Virus (EBV)

Burkitts Lymphoma

104
Q

Give 4 clinical features of Non-Hodgkin Lymphoma

A

Superficial Lymphadenopathy

Extra-nodal diseases

B Symptoms

Pancytopenia

105
Q

Give 3 extra-nodal diseases associated with non-hodgkin lymphoma

A

Gut (most common);
Gastric MALT lymphoma (H.pylori)
Non-MALT gastric lymphoma
Small bowel lymphoma

Skin (2nd most common);
Mycosis fugoides

Oropharynx;
Waldeyer’s ring lymphoma (sore throat/obstructed breathing)

106
Q

How is non-hodgkin’s lymphoma categorised? Give examples;

A

Low/indolent grade (slow growing, incurable);
Includes;
- Follicular lymphoma
- Marginal Zone Lymphoma/MALT

High grade (more aggressive but curable)
Includes;
- Burkitt’s lymphoma
- Acute Lymphoblastic Leukaemia
- Diffuse large B cell lymphoma (most common)

107
Q

What test is used to classify non-hodgkin lymphoma?

A

Lymph node excision/marrow biopsy
(will show no presence of Reed-Sternberg Cells)

108
Q

What test is used for staging non hodgkin lymphoma?

A

CT/MRI or Chest x-ray (Ann arbor)

109
Q

What drug is used to maintain remission in low grade non-hodgkin lymphoma? What is it’s MOA?

A

Rituximab

Monoclonal antibody, binds CD20 on surface of b cells.

Bindings initiates cytotoxicity +/- apoptosis

110
Q

What is the treatment for high grade non-hodgkin’s lymphoma?

A

R-CHOP Regimen for 3 months

Rituximab
Cyclophosphamide
Hydroxy-Daunorubicin
Vincristine (oncovin)
Prednisolone

111
Q

Define leukaemias

A

Describes cancer of bone marrow characterised by the dysfunctional development of leukocytes.

112
Q

What are the 4 main subtypes of leukaemia

A

Acute Lymphoblastic Leukaemia (ALL)

Acute Myeloid Leukaemia (AML)

Chronic Myeloid Leukaemia (CML)

Chronic Lymphocytic Leukaemia (CLL)

113
Q

What is the most common paediatric leukaemia?

A

Acute Lymphoblastic Leukaemia

114
Q

What chromosome is commonly found in chronic myeloid leukaemia?

A

Philadelphia Chromosome (t9:22)
(Chromosome 22)

115
Q

What type of mutation is present on the Philadelphia chromosome?

A

BCR-ABL gene fusion

116
Q

Describe ALL

A

Acute Lymphoblastic Leukaemia

Describes arrested maturation and uncontrolled proliferation of immature lymphocyte precursor cells (lymphoblasts/blast cells) with bone marrow and tissue infiltration.

117
Q

Describe the prognosis of ALL in children

A

Philadelphia chromosome - T(9:22) Bad prognosis

T(12:21) - Hyperdiploidy - Good prognosis

118
Q

Give 2 factors associated with the development of ALL

A

Ionizing radiation (X-rays) during pregnancy

Down’s Syndrome (Trisomy 21)

119
Q

Give 7 clinical features of ALL

A

Acute onset and rapid progression (days/weeks)

Fever, nightsweats, unexplained weightloss

Marrow failure (anaemia, Infection, Bruising/bleeding)

Bone pain

Hepatosplenomegaly

Painless Lymphadenopathy

Infections

120
Q

What investigations would be worth performing on a patient with ? ALL (4)

A

Blood film (may show blast cells)
FBC (Low Hb, Low Platelets, Low WCC)
Chest X-ray/CT scan (mediastinal/abnormal lymphadenopathy)
Lumbar puncture (CNS infiltration)

121
Q

How is ALL managed? (6)

A

Supportive (blood/platelet transfusions)

Allopurinol (prevents tumour lysis syndrome)

Prophylactic antivirals, antifungals or antibiotics)

IV fluids

Chemotherapy

Marrow transplantation

122
Q

What dangerous complication can be triggered by combination chemotherapy?

A

Tumour Lysis Syndrome

123
Q

How does Tumour Lysis Syndrome present biochemically?

A

High Uric Acid - Hyperuricaemia

High Potassium - Hyperkalaemia

High Phosphate - Hyperphosphatemia

Low calcium - Hypocalcaemia

124
Q

How is Tumour Lysis Syndrome managed? What is it’s MOA?

A

Allopurinol

Xanthine oxidase inhibitor (inhibits production of uric acid)

125
Q

What is the most common acute leukaemia in adults?

A

Acute Myeloid Leukaemia

126
Q

Describe Acute Myeloid leukaemia

A

Describes a neoplastic proliferation of blast cells derived from myeloid lineages (give rise to basophils, neutrophils, eosinophils).

127
Q

Give 3 cells derived from myeloid lineages

A

Basophils
Neutrophils
Eosinophils

128
Q

Give 4 risk factors for Acute Myeloid Leukaemia

A

Long term complication of chemotherapy

Myelodysplastic syndromes

Radiation

Down’s Syndrome (trisomy 21)

129
Q

Give 4 clinical features of AML

A

Marrow failure (Anaemia, Infection, Bleeding)

Hepato-splenomegaly

Gingival Hyperplasia (first sign of AML)

Disseminated intravascular coagulation

130
Q

Define Disseminated Intravascular Coagulation

A

A condition where blood clots form throughout the body due to abnormal excessive generation of thrombin and fibrin in the circulating blood.

131
Q

The presence of what may be found on a bone marrow biopsy of a patient with AML?

A

Auer rods

132
Q

Describe chronic myeloid leukaemia

A

Myeloproliferative disorder characterised by an uncontrolled clonal proliferation of myeloid cells.

133
Q

In whom does CML present?

A

Adults ONLY

Commonly presents between ages of 40-60

134
Q

Give 5 clinical features of CML

A

Symptomatic anaemia (fatigue, dyspnoea ect)

Abdominal discomfort (due to splenomegaly)

Weight loss

Fever and sweats in absence of infection

Bleeding

135
Q

What would a blood count show in a patient with CML? (3)

A

Very high WCC (with a whole spectrum of myeloid cells)

Low Hb (normochromic and normocytic)

Variable platelets

136
Q

How is CML treated? (2)

A

Oral Imatinib (BCR/ABL tyrosine kinase inhibitor)

Stem cell transplant (only in younger patients)

137
Q

Describe Chronic Lymphocytic Leukaemia (CLL)

A

Most common form of leukaemia, predominantly occurring later in life.

Characterised as the progressive accumulaiton of clonal dysfunctional malignant B cells.

138
Q

What is the most common genetic abnormality leading to CLL?

A

Deletion in the long arm of chromosome 13

139
Q

What can CLL develop into?

A

Richter’s syndrome - Aggressive Lymphoma

140
Q

Give 3 clinical features of CLL

A

Often asymptomatic (appearing on routine FBC)

Anaemia or infection

Rubbery Lymphadenopathy

141
Q

Give 3 complications of CLL

A

Autoimmune haemolysis

Increased infection risk (due to low IgG)

Bone marrow failure

142
Q

What may be present on a blood film of a patient with CLL?

A

Smear cells

143
Q

What may a blood count show for a patient with CLL? (2)

A

Raised WCC (with very high lymphocytes)

Signs of marrow failure (low Hb, platelets and neutrophils)

144
Q

What is the 1st line medical treatment for CLL?

A

Fludarabine + Rituximab +/- Cyclophosphamide

145
Q

Define myelodysplasia. What can it become?

A

Describes a clinical disorder of haematopoetic stem cells leading to dysplasia and ineffective haematopoesis in bone marrow.

Can become acute myeloid leukaemia

146
Q

What can cause myelodysplasia

A

Carcinogenic agents;
Benzene
Radiation
Chemotheraputic agents

147
Q

What cells can lymphoid stem cells differentiate into? (2)

A

T Lymphocytes

B Lymphocytes (eventually plasma cells)

148
Q

What cells can myeloid stem cells become? (7)

A

Erythrocytes (RBCs)
Platelets
Mast Cells
Eosinophils
Polymorphs
Monocytes
Osteoclasts

149
Q

What is the cellular precursor to a platelet?

A

Megakaryocyte

150
Q

What is the cellular precursor to erythrocytes?

A

Reticulocytes

151
Q

What is the cellular precursor to monocytes, basophils, neutrophils and eosinophils?

A

Myeloblasts

152
Q

Define multiple myeloma. How is it characterised?

A

Describes a type of bone marrow cancer involving several areas of the body, including the spine, skull pelvis and ribs.

Multiple myeloma is characterised by the uncontrolled proliferation of clonal plasma cells (B lymphocytes)

153
Q

Give 3 histological features of plasma cells in multiple myeloma

A

Plasma cells are 2-3 times larger

Plasma cells have eccentric nuclei (located on one side) that are round or oval

Plasma cells have a perinuclear halo (clear area around the nucleus)

154
Q

How do plasma cells evade apoptosis in multiple myeloma?

A

Overexpression of BCL-2 allows cells to escape apoptosis.

155
Q

Give 5 clinical features of multiple myeloma

A

Unexplained bone pain (in lower back/thorax)

Fatigue

Symptoms of hypercalcaemia (bone pain, abdo pain, depression, constipation ect)

Weight loss

Hepato-splenomegaly/Lymphadenopathy

156
Q

Give 4 pathophysiological features of multiple myeloma

A

Progressive bone marrow failure (pancytopenia)

Destructive bone disease (malignant cells inhibit osteoblasts and stimulate osteoclasts)

Kidney failure (nephropathy - Tamm-Horsfall proteins)

Bacterial infections (2nd to neutropenia)

157
Q

Give 3 severe complications of multiple myeloma

A

Spinal cord compression (urgent MRI if suspected)

Hyperviscosity (due to increased circulating immunoglobulins)

Acute renal injury

158
Q

What test is used to diagnose multiple myeloma? What will it show?

A

Serum/urine gel electrophoresis followed by immunofixation electrophoresis (IE)

Shows presence of monoclonal band

159
Q

What will a blood film show in a patient with multiple myeloma?

A

Rouleaux formations

160
Q

What will a bone marrow biopsy show in a patient with multiple myeloma?

A

Elevated plasma cell count

161
Q

What would an x-ray/MRI show in patients with multiple myeloma?

A

Lytic bone lesions in spine, pelvis, skull or ribs.

162
Q

What criteria is used to describe the phenotype of multiple myeloma? (4)

A

CRAB criteria

C - Calcium Elevation
R - Renal dysfunction
A - Anaemia
B - Bone disease

163
Q

What immunoglobulins are predominantly produced by multiple myeloma cells?

A

IgG (2/3 of cases)

IgA (1/3 of cases)

164
Q

How is multiple myeloma treated?

A

Bisphosphonates (clodronate, zolendronate, pamidronate)

Immunomodulatory drugs (Thalidomide, Lenalinomide)

Corticosteroids (dexamethasone, prednisolone)

Anti CD38 monoclonal antibodies (Daratumumab)

165
Q

Name 2 bisphosphonates and describe their moa

A

Clodronate and Zolendronate

Function by inhibiting osteoclast proliferation and inducing osteoclast apoptosis.

166
Q

Give 2 complications of lenalidomide (Immunomodulatory drug). What is it important to monitor for?

A

Neutropenia and thromboembolism.

Monitor for sepsis and consider aspirin for anti-coagulation.

167
Q

Give 4 differentials for multiple myeloma

A

Diabetes mellitus

Polymyalgia Rheumatica

Waldenstrom’s macroglobulinaemia (high levels of IgM not IgG)

Amyloid light chain amyloidosis.

168
Q

What does a PTT blood test test?

A

Partial Thromboplastin Time

Intrinsic pathway

169
Q

Give 2 causes for a prolonged PTT

A

Factor VIII deficiency (Haemophilia A or Von-Willebrand disease)

Factor IX deficiency (Haemophilia B)

170
Q

What does PT measure?

A

Prothrombin time

Extrinsic pathway

171
Q

What can cause a prolonged PT time

A

Factor VII deficiency (early sign of DIC)

172
Q

What can cause both a prolonged PTT and PT? (4)

A

Vitamin K deficiency

Severe DIC

Liver disease

High dose heparin or DOAC

173
Q

How would haemophilia present with regards to PTT, PT and bleeding time?

A

PTT - Increased
PT - Normal
Bleeding time - Normal

174
Q

How would Von Willebrand’s disease present with regards to PTT, PT and Bleeding time?

A

PTT - Increased
PT - Normal
Bleeding time - Increased

175
Q

How would vitamin K deficiency present with regards to PTT, PT and Bleeding time?

A

PTT - Increased
PT - Increased
Bleeding time - Normal

176
Q

Name 2 Low Molecular Weight Heparins

A

Enoxaparin and Dalteparin

177
Q

What is the moa of heparin?

A

Binds to antithrombin III, increasing it’s activity.

Antithrombin III inhibits activated factor X, factor II (thrombin) and factor IX.

178
Q

What can be used to reverse the effects of heparin?

A

Protamine Sulfate

179
Q

What is the MOA of Warfarin?

A

Inhibits vitamin K reductase.

Thus inhibits factors II, VII, IX, X (1972)

180
Q

What factors are dependent on vitamin K?

A

Factors II, VII, IX, X (1972)

181
Q

What can be used to reverse the effects of warfarin?

A

Vitamin K

182
Q

Name 2 DOACS

A

Direct Oral Anti Coagulants

Rivaroxaban and Apixaban

183
Q

What type of drugs are Rivaroxaban and Apixaban? What is their moa?

A

Direct Oral Anti Coagulants

Direct factor X inhibitors

184
Q

What class of drugs are dabiatran and Agatraban and what is their moa?

A

Direct Oral Anti Coagulants

Direct thrombin inhibitors

185
Q

What substances produced by the body maintain blood vessels in a non-clotting state? (3)

A

Prostacyclin (inhibits platelet activation)

Nitrous Oxide (inhibits platelet adhesion + dilates vessels)

Endothelial ADPase (inhibits ADP which is a platelet activator)

186
Q

Describe Deep Vein Thrombosis

A

Describes the development of a blood clot, within a vein deep to the muscular tissue planes.

187
Q

Where do DVTs commonly develop?

A

Lower leg, thigh or pelvis

188
Q

Give 6 risk factors for DVT

A

Immobility (surgical patients, long haul fights)

Oral contraceptive pill

Age

Pregnancy

Trauma

Cancer

189
Q

How does the Oral Contraceptive Pill increase risk of DVT?

A

Synthetic oestrogen increases plasma fibrinogen and the activity of coagulation factors VII and X

190
Q

Give 5 clinical features of DVT

A

Unilateral presentation

Pitting oedema

Signs of inflammation (swelling, redness, hot, throbbin pain)

Tenderness

Prominent (dilated/distended) superficial veins

191
Q

What score is used to assess the probability of DVT?

A

Wells’ Score

192
Q

Describe the use of the Wells’ Score and state what factors it considers. (9)

A

Scoring system used to assess probability of DVT.

DVT likely if a score of 2 or more is achieved.

1 point is given to each of the following;

  • Active cancer or within last 6 months
  • Paralysis, paresis or recent plaster immobilisation
  • Recently bedridden for > 3 days or major surgery in last 12 weeks
  • Localized tenderness along back of the calf
  • Entire leg is swollen
  • Calf swelling by >3cm compared to other leg
  • Pitting oedema confined to the symptomatic leg
  • Collateral superficial veins (non-varicose)
  • Previous DVT
193
Q

If a Wells’ score of ≤1 is given, what does this indicate and what should be subsequently done?

A

Indicates DVT is unlikely

Perform D-dimer test;
- If Negative - Exclude DVT
- If Positive - Offer Proximal Leg Vein USS

194
Q

If a Wells’ score of ≥2 is given, what does this indicate and what should be subsequently done?

A

Indicated DVT is likely

Perform D-Dimer and USS within 4 hours
- If both negative - Exclude DVT
- If USS positive - Treat as DVT
- If D-dimer is positive but USS is negative, repeat USS in 1 week

195
Q

What should be done is a proximal leg USS cannot be carried out within 4 hours?

A

Conduct a D-Dimer Test and give DOAC (interim therapeutic anticoagulation)

196
Q

What is given as interim therapeutic anticoagulation if a proximal vein USS cannot be performed within 4 hours (pt has a Wells’ score of >2)

A

DOAC (Apixaban or Rivaroxaban)

(LMWH previously used)

197
Q

For a patient with ?DVT, if an USS is negative but a D-dimer is positive, what are the next steps? (2)

A

Stop interim therapeutic anticoagulation

Offer a repeat proximal leg vein USS 6-8 days later

198
Q

What is D-Dimer?

A

D-Dimer is a fibrin degradation product (Fibrin is used to provide a scaffold for platelets during clot formation - haemostasis)

199
Q

Describe the treatment of confirmed DVT

A

1st line - Apixaban or Rivaroxiban
2nd line - LMWH followed by Dabigatran or edoxaban OR LMWH followed by Warfarin

200
Q

How is DVT treated for patient with severe renal impairment (<15/min)?

A

LMWH, Unfractioned heparin or LMWH followed by Warfarin

201
Q

If a patient with antiphosphilipid syndrome has DVT, how should they be treated?

A

LMWH followed by Warfarin

202
Q

For how long should DVT patients have anticoagulation?

A

At least 3 months

203
Q

What is the classic triad for PE presentation?

A

Pleuritic chest pain

Dyspnoea (breathlessness)

Haemoptysis (coughing blood)

204
Q

Give 4 common clinical findings for PE

A

Tachypnoea (resp rate >20/min)

Crackles on auscultation

Tachycardia (HR >100bpm)

Fever

205
Q

What initial imaging investigation should be conducted in all patients with suspected PE? Why?

A

Chest X-ray - To exclude pneumothorax

206
Q

What score is used to assess the likelihood of PE? What is the criteria for this?

A

PE Wells Score

PE Likely if score >4
PE unlikely if score <4

207
Q

What criteria are used in a PE Wells’ score? (7)

A

Clinical signs/symptoms of DVT (3 points)

Alternative diagnosis less likely than PE (3 points)

Heart rate >100bpm - (1.5 points)

Immobilisation for >3 days or surgery in last 4 weeks (1.5 points)

Previous DVT/PE (1.5 points)

Haemoptysis (1 point)

Malignancy (on treatment or in last 6 months) (1 point)

208
Q

If PE Wells’ score is >4 what are the next steps

A

Score > 4 = PE Likely

Arrange immediate CTPA
If positive - Diagnose PE
If negative - Consider Proximal Leg Vein USS if DVT is suspected

209
Q

If PE Wells’ score is <4 points, what are the next steps?

A

Score <4 = PE Unlikely

Arrange D-Dimer test
If positive - Arrange CTPA
If negative - Stop anticoagulation and consider alternative diagnosis

210
Q

If PE Wells’ score is >4 (PE likely) and CTPA is not immediately available, what should be done?

A

Commence interim therapeutic anticoagulation with DOAC (rivaroxaban or apixaban)

211
Q

What score is used to exclude PE in patients known to have a low pre-test probability (<15%)

A

PERC - Pulmonary embolism rule out criteria

212
Q

What are the criteria for PERC? (8) How is it interpreted?

A

Pulmonary Embolism Rule Out Criteria (PERC)

Age >50
Heart rate >100
Oxygen saturations <94%
Previous DVT or PE
Recent surgery or trauma in the past 4 weeks
Haemoptysis
Unilateral leg swelling
Oestrogen use (HRT, contraceptives)

If all of the above are absent the post-test probability of PE is <2%

213
Q

What is the imaging tool used to diagnose PE?

A

CTPA

214
Q

What may be seen on an ECG for a patient with PE?

A

S1Q3T3

Large S wave in lead I

Large Q wave in lead III

Inverted T wave in Lead III

215
Q

Describe the management of PE

A

1st line - Apixaban or Rivaroxiban
2nd line - LMWH followed by Dabigatran or edoxaban OR LMWH followed by Warfarin

216
Q

How long should a patient have anticoagulation treatment if their VTA was provoked (i.e following immobilisation due to major surgery)?

A

Stopped after initial 3 months.
(3-6 months for patient with active cancer)

217
Q

How long should a patient have anticoagulation treatment if their VTA was unprovoked?

A

Continue for 6 months.

218
Q

Define polycythemia vera

A

Describes a myeloproliferative disorder caused by clonal proliferation of marrow stem cells, leading to an increase in red cell volume.

Often accompanied by overproduction of neutrophils and platelets

219
Q

A mutation in what is present in 95% of polycythemia vera patients?

A

Jack2

220
Q

Give 6 clinical features of polycythemia vera

A

Pruritus, typically after a hot bath

Splenomegaly

Hypertension

Hyperviscosity (arterial/venous thrombosis)

Low ESR

Haemorrhage (2d to abnormal platelet function)

221
Q

What tests should be performed in a patient with suspected polycythaemia vera? (4)

A

FBC/Blood film (raised haematocrit, neutrophils, basophils and platelets)

JAK2 mutation

Serum ferritin

Renal/Liver function tests

222
Q

What criteria is required to diagnose JAK2-positive polycythemia vera?

A

Both A1+A2;

A1 - High haematocrit OR raised red cell mass
A2 - Mutation in JAK2

223
Q

Give 4 causes of secondary polycythemia

A

COPD

Altitude

Obstructive sleep apnoea

Excessive erythropoietin; cerebellar haemangioma, hypernephroma, hepatoma.

224
Q

Name 2 blood film findings suggestive of hyposplenism

A

Howell-Jolly bodies and Siderocytes

225
Q

Outline the key points for using Packed Red Cells

A

Used for transfusion in chronic anaemia and cases where infusion of large volumes of fluid may result in cardiovascular compromise

226
Q

Outline the key points for using Platelet Rich Plasma

A

Given to patients who are thrombocytopaenic and are bleeding or who require surgery.

227
Q

Outline the key points for using Fresh Frozen Plasma (4)

A

Prepared from single units of blood

Contains clotting factors, albumin and immunoglobulin

Used in correcting clotting deficiencies in patients with hepatic synthetic failure who are due to undergo surgery

It should NOT be used as a first line therapy for hypovolaemia

228
Q

Outline the key points for using Cryoprecipitate (3)

A

Formed form supernatant of FFP

Rich source of Factor VIII and fibrinogen

Allows large concentration of factor VIII to be administered in small volume

229
Q

Outline the key points of using SAG-Mannitol Blood

A

Removal of all plasma from a blood unit and substitution with:

Sodium chloride
Adenine
Anhydrous glucose
Mannitol

230
Q

Give 2 examples for when you would use Cryoprecipitate

A

Disseminated Intravascular Coagulation

von Willebrand disease

231
Q

Describe what Irradiated blood products are and why they are used

A

Describes blood products depleted of T-lymphocytes.

Used to avoid Transfusion Associated Graft Versus Host Disease (TA-GVHD) caused by engraftment of viable donor T-lymphocytes

232
Q

Give 5 situations in which Irradiated blood products are required

A

Bone marrow/stem cell transplants

Immunocompromised (chemotherapy/congenital)

Hodgkin lymphoma

Intra-uterine transfusions

Neonates up to 28 days post expected date of delivery

233
Q

Describe the use of Prothrombin Complex Concentrate (2)

A

Used for the emergency reversal of anticoagulation in patients with either severe bleeding or a head injury with suspected intracerebral haemorrhage

Can be used prophylactically in patients undergoing emergency surgery depending on the particular circumstance.

234
Q

Give 5 classifications of blood product transfusion complications

A

Immunological: acute haemolytic, non-haemolytic febrile, allergic/anaphylaxis

Infective

transfusion related acute lung injury (TRALI)

transfusion-associated circulatory overload (TACO)

Other; hyperkalaemia, iron overload, clotting

235
Q

Describe the cause of non-haemolytic febrile reaction and describe how it may present

A

Caused by antibodies reacting with white cell fragments in the blood product and cytokines that have leaked from the blood cell during storage.

Presentation; Fever, chills

236
Q

How is non-haemolytic febrile reaction managed? (3)

A

Slow/stop the transfusion

Paracetamol

Monitor

237
Q

Describe the cause of a minor allergic reaction to blood products and describe how it may present

A

Caused by foreign plasma proteins

Presentation; Pruritus, urticaria

238
Q

How is a Minor Allergic Reaction to blood products managed? (3)

A

Temporarily stop the transfusion

Antihistamines

Monitor

239
Q

Describe what causes Anaphylaxis in response to blood products and state how it may present.

A

Caused by patients with IgA deficiency who have anti-IgA antibodies

Presentation; Hypotension, Dyspnoea, Wheezing, Angioedema

240
Q

What antibody is responsible for causing Anaphylaxis in response to blood products?

A

IgA

241
Q

How is Anaphylaxis in response to blood products managed? (3)

A

Stop the transfusion

IM adrenaline

ABC support (oxygen, fluids)

242
Q

What causes an Acute Haemolytic Reaction to blood products and how may this present?

A

Caused by ABO-incompatible blood (human error)

May present as; Fever, abdominal pain, hypotension

243
Q

How is Acute haemolytic reaction in response to blood products managed? (3)

A

Stop transfusion

Confirm diagnosis;
Check pt name on blood product
Send blood for direct Coombs test, repeat typing and cross-matching

Fluid resuscitation with saline solution

244
Q

What antibody drives Acute Haemolytic Transfusion reaction to blood products?

A

IgM antibodies

245
Q

State the cause of Transfusion associated circulatory overload (TACO) and describe it’s presentation

A

Caused by excessive rate of transfusion or pre-existing heart failure

Presentation; Pulmonary oedema, Hypertension

246
Q

How is Transfusion Associated Circulatory Overload (TACO) managed? (2)

A

Slow/stop transfusion

Consider IV loop diuretics (furosemide) and oxygen

247
Q

Describe the cause of Transfusion Related Acute Lung Injury (TRALI) and describe it’s presentation

A

Non-cardiogenic pulmonary oedema occurring secondary to increased vascular permeability caused by host neutrophils that become activated by substances in donated blood

Presentation; Hypoxia, pulmonary infiltrates on chest x-ray, fever, hypotension

248
Q

How is Transfusion Related Acute Lung Injury (TRALI) managed? (2)

A

Stop the transfusion

Oxygen and supportive care

Phase 4 Medicine (15 decks)

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