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Haematology Flashcards

1
Q

What is the percentage of plasma in the blood?

A

55%

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2
Q

What does the other 45% consist of?

A
  1. Red blood cells
  2. Platelets
  3. White blood cells
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3
Q

What are 4 facts about Red blood cells?

A
  1. lifespans of 120 days
  2. They are biconcave and anucleated
  3. Produced in the bone marrow
  4. Eryptosis occurs in the spleen liver and bone marrow
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4
Q

What are the types of White blood cells?

A

Granulocytes
Lymphocytes
Monocytes

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5
Q

What are the types of granulocytes?

A

Neutrophils
Eosinphils
Basophils

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6
Q

What are neutrophils?

A

Phagocytic
Play a role in inflammation and myeloid leukaemia

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7
Q

What are eosinophils?

A

More common in the morning
Numbers raised in parasitic infections/ allergic reactions

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8
Q

What are basophils?

A

Associated with hypersensitivity reaction
Have a similar role to mast cells, when stimulated secrete histamine

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9
Q

What are the two types of lymphocytes?

A

T cells - mediator in cellular immunity
B cells - mediator in humeral immunity
Lymphocyte numbers increase in viral infection/ inflammation but decrease in HIV and Chemotherapy

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10
Q

What are the types of T helper cells?

A

Cytotoxic (CD8+)
T Helper (CD4+)

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11
Q

What are monocytes?

A

Immature cells that differentiate once they leave the blood stream
Go on to form macrophages

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12
Q

What are platelets?

A

Derived from megakaryocytes
Major role in clotting cascade and platelet plug

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13
Q

What does Factor Xa convert?

A

Prothrombin (II) to thrombin (IIa)

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14
Q

What is the function of thrombin?

A

Converts fibrinogen to fibrin
Activates XIII into XIIa
Positive feedback effect on further thrombin production

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15
Q

What does warfarin inhibit?

A

Inhibits vit K epoxide reductase
Factors 10, 9,7 and 2

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16
Q

What does Heparin do? Name a LMWH

A

Activates antithrombin 3 and inhibits X - dalteparin

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17
Q

What is the fibrinolytic system?

A

plasminogen converted to plasmin
Plasmin cuts fibrin into fragments
Prevents blood clots from growing and becoming problematic

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18
Q

What is a Full Blood Count?

A

Basic blood test that gives information about blood constituents
- RBC volume
-WBC volume
-Platelet volume
-Haemoglobin concentration
-Mean corpuscular volume

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19
Q

What is a reticulocyte count?

A

Enables you to see how quickly the bone marrow is producing new RBC’s

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20
Q

What does a low reticulocyte show?

A

Indicative that something is preventing RBC’s from being produced e.g haematinic deficiency

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21
Q

What does a high reticulocyte count show?

A

Indicative that RBC’s are being lost or destroyed (e.g bleeding/haemolytic anaemia) New RBC production is increased to act as a compensatory mechanism

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22
Q

What is Serum Ferritin?

A

Ferritin is the major iron storage protein of the body. Ferritin can be used to indirectly measure the iron levels in the body.
Ferritin is an acute phase protein and so its levels can become falsely raised in inflammation and malignancy.

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23
Q

What is a blood film?

A

Smears of blood are placed onto slides and then examined under a microscope

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24
Q

What is a thick blood film used for?

A

permits examination of a large amount of blood for the presence of parasites ( but not identification of species)

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25
Q

What is a thin blood film used for?

A

Allows for observation of RBC morphology, inclusions and intracellular and extracellular parasites.

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26
Q

What is PT/INR?

A

Prothrombin time - measure of the time taken for a blood clot to form via the extrinsic pathway.
INR- international normalised ratio is used for patients on anticoagulants.
They measure overall clotting factor synthesis

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27
Q

What disease affect PT/INR?

A

liver disease
DIC
Vit K deficiency
Warfarin levels

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28
Q

What are the normal PT/INR levels?

A

12-13seconds/ 0.8 - 1.2 seconds

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29
Q

What is APTT?

A

Activated partial thromboplastin time - measure of the time taken for blood clot via the intrinsic pathway
APTT indicated issues with factors VIII,IX,XI

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30
Q

What conditions are linked to aPTT?

A

Haemophilia A - VIII
Haemophilia B - IX
von willerbands disease- VII

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31
Q

What is the normal time for APTT?

A

35-45 seconds

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32
Q

What is bleeding time?

A

Assess overall platelet function and levels
Measure of how long it will stop a patient bleeding from a wound

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33
Q

What platelet specific disorders increase BT?

A

Von willerband’s disease
ITP
DIC
Thrombocytopaenia

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34
Q

What is the normal bleeding time?

A

1-6 mins

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35
Q

What is thrombin time?

A

Tests how fast fibrinogen is converted into fibrin by thrombin.
If time is prolonged it is caused by either a synthetic issue or a consumption time

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36
Q

What disease are linked to a prolonged Thrombin time?

A

DIC
Liver failure
Malnutrition
Abnormal fibinolysis

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37
Q

What is the normal thrombin time?

A

10-15 secs

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38
Q

What are the steps that lead to a platelet plug?

A
  1. Von Willebands factor adheres to vascular injury
    2.VWF then binds to GPIb receptors on surrounding platelets
    3.After binding, the ADP P2Y12 receptor on the platelet is activated leading to increased expression of GPIb/IIa
    4.These newly expressed receptors then finally bind to fibrinogen which leads to further platelet aggregation
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39
Q

What is haemoglobin?

A

Protein in the red blood cells that carry and delivers oxygen to tissues. Each adult Hb molecule is comprised of 2 alpha and 2 beta chain .Each Hb chain can carry 4 x 02.

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40
Q

What is the definition of Anaemia?

A

Anaemia is a lower than normal concentration of haemoglobin due to a reduction in cell mass or increased plasma volume. Also accompanied by a fall in red cell blood count and packed cell volume.

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41
Q

How is anaemia classified?

A

Based on the mean Corpuscular volume (MCV)

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42
Q

What is MCV?

A

Measure of the average size and volume volume of red blood corpuscle

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43
Q

What is microcytic?

A

MCV<80

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44
Q

What is normocytic?

A

MCV 80-100

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45
Q

What is macrocytic?

A

MCV >100

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46
Q

What are the consequences of Anaemia?

A
  • Reduced 02 transports
    -Tissue hypoxia
    -Compensatory changes
    (increased tissue perfusion, increased 02 transfer to tissues, increased RBC production)
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47
Q

What is Haemolytic?

A

Increased breakdown of RBC

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48
Q

What is Aplastic?

A

decrease in RBC,WBC,Platelets

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49
Q

What are the general symptoms of anaemia?

A
  • fatigue
    -lethargy
    -dyspnoea
    -palpitations
    -headcahe
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50
Q

What are the general signs of Anaemia?

A

Pale skin
Pale mucous membranes - nose and eyelids
Systolic flow murmur
Tachycardia - to meet demand

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51
Q

What are the 3 main causes of Microcytic Anaemia?

A
  1. Iron deficiency
  2. Thalassaemia - body makes an abnormal form or inadequate amount of HB
    3.Anaemia of chronic disease
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52
Q

What is Iron deficiency anaemia?

A

Iron is absorbed in the duodenum and is necessary for the formation of haemolytic. Less iron available for haemoglobin synthesis - less haemoglobin - lack of effective RBCs - Anaemia.
- mc anaemia worldwide

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53
Q

What are the causes of iron deficient anaemia?

A
  1. Low iron diet -malnutrition
    2.Malabsorption - coeliac disease
  2. Blood loss - menorrhagia, Gi bleeding, Hookworm
  3. Pregnancy
  4. Breastfeeding
    colon cancer in elderly - rare, red flag
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54
Q

What are the signs of Iron deficient anaemia?

A
  • Brittle hair and nails
    -Atrophic Glossitis - tongue inflammation with atrophy of papillae
    -Koilonychia - spoon shaped nails
    -Angular Stomatitis - inflammation of corners of mouth
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55
Q

What are the investigations for iron deficient anaemia?

A

-Reticulocyte count - reduced
FBC and blood film - hypo chromic microcytic anaemia
-anisocytosis - variation in size
-poikilocytosis- variation in shape
-Serum ferritin - low
-Endoscopy/ colonoscopy for possible GI bleed

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56
Q

What is the treatment for iron deficient anaemia?

A

Ferrous sulphate - oral iron
Ferrous fumarate

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57
Q

What are the side effects of Ferrous sulphate treatment?

A

Black stools
Constipation
Diarrhoea
Nausea
Epigastric abdominal pain

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58
Q

What are the causes of Normocytic anaemia?

A
  1. Acute blood loss/haemorrhage
  2. combined haematinic deficiency e.g iron and B12
  3. Anaemia of chronic disease
  4. Sickle cell disease
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59
Q

What is Anaemia of chronic disease?

A

Anaemia that is secondary to a chronic disease. Occurs in patients with a chronic inflammatory disease.

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60
Q

What are the causes of Chronic disease Anaemia?

A
  • Chron’s
    -RA
    -TB
    -Malignancy
    -CKD
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61
Q

What is the pathology of anaemia of chronic disease?

A

These conditions can cause either a shortening of RBC life or reducing RBC production.
- Decreased release of iron from BM to developing erythroblasts
-Less erythropoietin produced in response to anaemia
-High levels of hepcidin expression - inhibits duodenal iron absorption and macrophage release of iron
- decreased RBC survival

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62
Q

What is the presentation of Anaemia of chronic disease?

A

Anaemia symptoms and signs

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63
Q

What are the investigations of anaemia of chronic disease?

A

-FBC and blood film - Normocytic/microcytic and hypochromic (Pale)
- Low serum iron and low total iron binding capacity
-Increased or normal serum ferritin

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64
Q

What is the treatment for Anaemia of chronic disease?

A

Treat underlying cause
Recombinant erythropoietin

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65
Q

What are the main causes of Macrocytic anaemia?

A

Megaloblastic
1. B12 deficiency (pernicious anaemia)
2.Folate deficiency
Non- megaloblastic
3. Alcohol excess

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66
Q

What is megaloblastic?

A

B12 and Folate deficiency anaemia’s can be referred to as megaloblastic anaemias. Megaloblastic means that there has been an inhibition of DNA synthesis. The RBCs cannon progress onto mitosis causing continuing growth without division.

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67
Q

What is Pernicious anaemia?

A

Pernicious anaemia is an autoimmune condition in which the parietal cells are attacked and there’s a loss of Intrinsic factor production and therefore B12 malabsorption as B12 is absorbed count to IF. B12 is required for the formation of red blood cells.

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68
Q

What are other causes of B12 deficiency?

A
  • low dietary intake
    -atrophic gastritis
    -gastrectomy
    -chron’s
    -coeliac disease - malabsorption
    All affect If production or absorption at the terminal ileum
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69
Q

What are the symptoms of pernicious anaemia?

A
  • anaemia symptoms - fatigue, lethargy, palpitations, dyspnoea
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70
Q

What are the signs of pernicious anaemia?

A

Glossitis
Angular stomatitis+ glossitis
Jaundice - excess breakdown of Hb/ lemon below skin
Neurological symptoms - polyneuropathy - B12 def causes demyelination

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71
Q

What is polyneuropathy?

A

Caused by symmetrical damage to the peripheral nerves and posterior lateral columns of the spinal cord

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72
Q

What are the investigations for pernicious anaemia?

A

FBC and blood films - would show macrocytic RBC/ megaloblasts
-Autoantibody screening- check for IF and parietal cell antibodies -anti IF Ab’s
Serum B12 low

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73
Q

What are the treatments for pernicious anaemia?

A

Vitamin B12 (hydroxycobalamin)
NOT FOLIC ACID - causes fulminant neurological deficits
Dietary advice

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74
Q

What are the complications of PA?

A

CVD
Neuropathy

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75
Q

What is folate deficiency anaemia?

A

Folate is absorbed in the jejunum and is found in green vegetables and is essential for DNA synthesis. Without Folate RBC can’t undergo mitosis so they just grow - macrocytic

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76
Q

What are the causes of folate deficiency ?

A

-Poor folate diet - poverty, alcohol, elderly
-Malabsorption - crohns, coeliac
-Pregnancy
-Anti folate drugs - methotrexate

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77
Q

What is the presentation of folate deficient anaemia?

A
  • classic anaemia symptoms - fatigue, lethargy, headache, palpitations, dyspnoea
    -angular stomatitis/ glossitis
  • no neuropathy unlike B12
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78
Q

What are the investigations for folate deficient anaemia?

A

FBC and blood film - macrocytic / megaloblastic anaemia
low serum folate

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79
Q

What is the treatment for folate deficient anaemia?

A

Dietary advice
Folic acid supplementation -
maybe for pregnancy -prophylactic

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80
Q

What is Haemolytic anaemia?

A

Haemolytic anaemia occurs when RBCs are destroyed before 120 days

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81
Q

How are old RBCs removed?

A

removed from the circulation by macrophages present in the red pulp of the spleen

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82
Q

Where does haemolytic occur?

A

intravascular - within blood vessels
Extravascular - within reticuloendothelial system, by macrophages in spleen, liver and bone marrow

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83
Q

What are the causes of haemolytic anaemia?

A
  • inherited (haemoglobinopathies, membranopathies, enzymopathies)
  • acquired ( autoimmune haemolytic anaemia, infections- malaria, secondary to systemic disease)
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84
Q

What are the symptoms of haemolytic anaemia?

A
  • Gallstones (from excess bilirubin)
    -Jaundice ( from excess bilirubin)
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85
Q

What is bilirubin?

A

A yellowish substance made during your body’s normal process of breaking down old red blood cells.

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86
Q

What are the signs of haemolytic anaemia?

A
  • leg ulcers
    -splenomegaly
  • signs of underlying disease (malar rash)
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87
Q

What are the investigations of haemolytic anaemia?

A

FBC - reduced haemoglobin normocytic normochromic
Reticulocyte count - increased
Blood film - presence of schistocytes
High serum unconjugated billirubin
High urinary urobillinogen
High faecal stercobillinogen

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88
Q

What is the treatment for haemolytic anaemia?

A

Folate and iron supplementation
Immunosuppressives
Splenectomy

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89
Q

What are shistocytes?

A

RBC fragments

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90
Q

What are Haemoglobinopathies?

A

Group of recessively inherited genetic conditions affecting haemoglobin

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91
Q

What is sickle cell disease?

A

Autosomal recessive condition, where there is a single base mutation causing a production of abnormal beta globin chains.

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92
Q

What is the epidemiology of sickle cell disease?

A
  • more common in afro- Caribbean
  • 1 in 4 chance of disease
    -SCA is homozygous
    -SCA trait is heterozygous - protected from malaria
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93
Q

What is the pathology of sickle cell disease?

A
  • mutation of the B globin gene (glutamic acid to valine/ A to T) results in a HbS variant
    RBC more fragile therefore low surface area so less efficient
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94
Q

What does sickling of cells produce?

A

-Premature destruction of RBCs - intravasucalr haemolysis
-Obstruction of microcirculation (vast-occlusion) -> tissue infarction

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95
Q

What is the presentation of sickle cell disease?

A

-jaundice - due to Hb breakdown
-Anaemia symptoms
-Complications: - due to cold, hypoxia
Vaso-occlusion crisis - sickle cells polymerise and trap in long bone blood vessels
-Acute chest syndrome - vaso-occlusive crisis of pulmonary vasculature

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96
Q

What happens if the HB falls suddenly? Possible causes?

A

Splenic infarction- spleen is engorged in RBC
BM aplasia - destroys erythrocyte precursors
Further haemolysis - drugs, acute infection
Gallstones, leg ulcers. -avascular necrosis of femoral head

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97
Q

What are the investigations for sickle cell disease?

A

-Screen neonates - blood/heel prick test
-FBC - normocytic normochromic high reticulocyte count
-Blood film - sickled erythrocytes
-Hb electrophoresis - Hb SS present and absent Hb A confirms diagnosis of sickle cell disease

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98
Q

What is the management for sickle cell disease?

A

Acute attacks - IV fluid +analgesia(NSAIDs) +O2

Long term:
- avoid precipitants
-Drugs: hydroxycarbamide + folic acid supplements
-Transfusion + Fe chelation

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99
Q

What are the complications of sickle cell disease?

A

Pulmonary HTN and chronic lung disease = most common cause of death in adults with SCD
- sickle cell chest crisis
-Renal impairment

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100
Q

What is Thalassaemia?

A

Autosomal recessive condition where you have a decreased rate of production or no production of one or more globin chains in red cell precursors/ mature red cells.

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101
Q

Where is Thalassaemia most common?

A

Mediterranean, Middle East, Asia

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102
Q

What is the precipitation of imbalance globin chains?

A
  • in red cell precursors causes ineffective erythropoiesis ( reduced production of RBC)
    -in mature red cells causes haemolysis (premature destruction of red blood cells)
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103
Q

What are the two types of Thalassaemia?

A

Alpha thalassaemia - decreased alpha chain synthesis
Beta thalassaemia - decreased beta chain synthesis

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104
Q

What is Alpha thalassaemia caused by?

A

caused by gene deletions, the more deletions the more symptomatic the anaemia

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105
Q

What is the presentation of 1 deletion?

A

Blood picture normal

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106
Q

What is the presentation of 2 deletions?

A

Asymptomatic with possible mild microcytic anaemia

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107
Q

What is the presentation of 3 deletions?

A

Common in parts of Asia. Patients have low levels of HbA and high levels of HbH Parts. Severe haemolytic anaemia and splenomegaly. Sometimes transfusion dependent -marked anemia

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108
Q

What is the presentation of 4 deletions?

A

No a-chain synthesis, only Hb Barts. Hb Parts cannot carry oxygen and is incompatible with life. (infants stillborn; they are pale, with huge spleen and livers. - Hydrops fetalis - 100% HbH Barts

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109
Q

What is Beta Thalassaemia?

A

In homozygous B-thalassaemia there is little or no normal beta chain production therefore EXCESS alpha chain production. Alpha chains bind with whatever, beta, gamma, delta. Leading to increased production of HbA2 and HbF resulting in ineffective erythropoiesis and haemolysis

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110
Q

What causes beta thalassaemia?

A

mutations

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111
Q

What forms HbA?

A

2 alpha and 2 beta chains

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112
Q

What forms HbA2?

A

2 alpha and 2 delta chains

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113
Q

What forms HbF?

A

2 alpha and 2 gamma chains

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114
Q

What are the 3 clinical syndromes?

A

B- thalassaemia minor, intermedia and major

115
Q

What is Beta thalassaemia minor?

A

Asymptomatic heterozygous carrier state
-mild/absent anaemia - low MCV and hypo chromic
-iron and ferritin normal

116
Q

What is beta thalassaemia intermedia?

A

Moderate anaemia - patients don’t require transfusions
- splenomegaly, bone abnormalities, recurrent leg ulcers and gallstones

117
Q

What is Beta thalassaemia major?

A

Homozygous
-presents in 1st year of life with severe anaemia - failure to survive and recurrent infections
-bone abnormalities due to hypertrophy of ineffective bone marrow - skull bossing
-hepatosplenomegaly. -due to haemolysis

118
Q

What is the presentation of thalassamia?

A

Beta thalassemia - major Px in first year of life = general anemia + chipmunk facies and failure to thrive

119
Q

What are the investigations for thalassaemia?

A

-Diagnosis by Hb electrophoresis - shows increased HbF/ HbA2 and absent/low HbA
FBC and blood film -hypochrmoic and microcytic
-irregular and pale RBCs
-incraesed reticulocytes
-Skull XR - hair on end sign, enlarged maxilla

120
Q

What is the treatment for Thalassaemia?

A
  • Blood transfusions (replenishing HbA levels to normal) - risk of iron overload
    -Give iron chelation -oral deferiprone to decrease iron overloading
    -Ascorbic acid - increase iron urine excretion
    -splenectomy
    -folate supplements
121
Q

What is membranopathy?

A

Disease of a membrane

122
Q

What are the two types of membranopathy?

A

1.spherocytosis
2. elliptocytosis

123
Q

What is the pathology of spherocytosis?

A

Autosomal dominant condition that causes a defect in the RBC membrane increasing its permeability to sodium. Rbc become more rigid and spherical in shape and are mistaken by the spleen and prematurely destroyed

124
Q

What is the most common cause of Spherocytosis?

A

deficiency in red cell structural membrane protein spectrin

125
Q

What is spherocytosis?

A

Vertical deformity

126
Q

What is elliptocytosis?

A

Horizontal deformity?

127
Q

What are the symptoms of spherocytosis?

A

-neonatal jaundice
-excess bilirubin - gallstones
-leg ulcers

128
Q

What are the investigations of spherocytosis?

A

-Blood film - presence of spherocytes and reticulocytes
-FBC - raised reticulocyte count

-Direct ant-globulin test/ Coombs - will be negative, rules out autoimmune haemolytic anaemia

129
Q

What is the treatment for spherocytosis?

A

Splenectomy
Folic acid

130
Q

What is the pathology of glucose-6-phosphate dehydrogenase deficiency?

A

G6DP is vital in glutathione synthesis. Glutathione protects the RBC from oxidative crisis. With a G6DP reduction rbc have a shorter life span.

131
Q

What is the epidemiology of G6DP deficiency?

A
  • X-linked recessive condition
    -affects Mediterranean, Africa and middle east
  • protects from malaria
132
Q

What is the presentation of G6DP deficiency ?

A

Asymptomatic until exposed to oxidative stresser
- neonatal jaundice - excess bilirubin
-Back pain
-Dark urine

133
Q

What are oxidative triggers?

A
  • infections
    -food
    -medications
134
Q

What are the investigations for G6DP deficiency?

A

Blood film - Bite and blister cells, Heinz bodies

raised reticulocytes
normocytice normochromic RBC
Low G6PD levels

135
Q

What is the management of G6DP deficiency?

A

Avoid precipitants e.g henna
Transfuse if severe

136
Q

What is Bone marrow failure (Aplastic Anaemia)?

A

In BM failure, a reduction in the number of pluripotent stem cells causes a lack of haemopoiesis (production of blood cells and platelets). The reduced number of new RBCs produced to replace the old ones causes anaemia

137
Q

What are the causes of aplastic anaemia?

A
  • congenital

-infections
-idiopathic

138
Q

What are the signs of aplastic anaemia?

A
  • anaemia
    -increased susceptibility to infections
    -increased bruising
    -incraesed bleeding
139
Q

What are the investigations for aplastic anaemia?

A

FBC - would show pancytopenia (low levels of all bloods)
Reticulocyte count - low or absent
BM biopsy - hypocellular marrow with increased fat spaces

140
Q

What are the treatments for aplastic anaemia?

A
  • remove causative agent
    -blood/platelet transfusion
    -BM transplant
    -immunosuppressive therapy - ciclosporin
141
Q

What are the haematological malignancies?

A

-leukaemia
-lymphoma
-myeloma

142
Q

What is leukaemia?

A

Neoplastic proliferation of immature blast cells (precursor of WBC, RBC or platelets) which build up in the blood. Result in low production of other haematopoetic cells therefore functional pancytopenia

143
Q

What is Acute myeloid leukaemia ?

A

neoplastic myeloblast proliferation, so other blood cells in the BM are crowded out.

144
Q

What is the epidemiology of AML?

A
  • t15;17
    Usually older people -65
    -Associated with Downs syndrome and radiation
    -3year survival = only 20%
145
Q

What is the presentation of AML?

A

General leukaemia Sx = BM failure -bone pain, bleeding, infections, anaemia

+gum infiltration
+hepatosplenomegaly

146
Q

What are the investigations for AML?

A

FBC and blood film -pancytopenia, Auer rods
BM Biopsy - 20% myeloid blasts

147
Q

What is pancytopenia?

A

Deficiency of all 3 cellular components

148
Q

What is the treatment for AML?

A

-Chemotherapy
-All-Trans-retnoic Acid (ATRA) ( used for subtype of AML = promyelocytic leukaemia)
-Abx prophylaxis for neutropenia, transfusion to correct anaemia
-Allopurinol if doing chemo-
prevent tumour lysis syndrome
-Last resort - BM transplant

149
Q

What is tumour lysis syndrome?

A

When Chemotherapy given→ Chemo releases uric acid from cells -> can accumulate in the kidneys → damage/ loss of function.
o To prevent give Allopurinol (Xanthine oxidase inhibitor)
- to treat = IV fluid and correct electrolytes

150
Q

What is promyelocytic leukemia?

A

A subtype of AML. The mutation that causes acute promyelocytic leukemia involves two genes, the PML gene on chromosome 15 and the RARA gene on chromosome 17

151
Q

What is CML?

A

neoplastic myelocyte proliferation - base/neuto/eosinphils

152
Q

What causes Chronic myeloid leukaemia?

A

t9:22 Philadelphia chromosome. BCR-ABL gene fusion causing tyrosine kinase irreversibly switched on = increases cell proliferation

153
Q

What is the pathology of CML?

A

The mutation in Philadelphia chromosome t(9:22) activates tyrosine kinase causing increased cell (myelocyte) proliferation.BM crowded, cytopenia.

154
Q

What is the epidemiology of CML?

A

-60
-associated with exposure to ionising radiation

155
Q

What are the symptoms of CML?

A
  • fever, fatigue
    -bleeding, bruising, infection
    -anaemia
    -hepatosplenomegaly
156
Q

What are the investigations for CML?

A

FBC - Pancytopenia/ blood blast cell % shows severity of CML
BM biopsy- high granulocytes
Philadelphia chromosome genetic test

157
Q

What is the treatment of CML?

A

-Chemo + imatinib

158
Q

What is the risk of CML?

A

progression to AML if no treatment or late diagnosis - if blast cells >20% on biopsy

159
Q

What is acute lymphoblastic leukaemia?

A

Neoplastic lymphoblast proliferation, BM becomes crowded, cytopenia

160
Q

What is the pathology of ALL?

A

Mostly B-cell lineage - t(12;21) = good prognosis
most common childhood malignancy
Associated with downs +radiation

161
Q

What is the epidemiology of ALL?

A
  • Most common childhood malignancy - 75% cases >6y.o
    -Associated with downs and radiation
162
Q

What are the symptoms of ALL?

A

General leukaemia symptoms except 6y.o with downs , hepatosplenomegaly

163
Q

What is the diagnosis for ALL?

A

FBC - pancytopenia
Blood film = increased in lymphoblasts
BM biopsy = >20% lymphoblasts = diagnostic
Immunofluorescence - TdT positive lymphoblasts (terminal deoxynucleotdyl transferase)

164
Q

What is the treatment for ALL?

A

Chemo + maybe allopurinol - usually good prognosis

165
Q

What is Chronic lymphocytic leukaemia?

A

Neoplastic proliferation of lymphocytes, mostly mature B lymphocytes that have escaped apoptosis and don’t die. BM too crowded - cytopenia.

166
Q

What is the epidemiology of CLL?

A
  • Incidence increases with age
    -Typically affects older people
    -multifactorial
    -75% 5 year survival
167
Q

What are the symptoms of CLL?

A
  • 70 y/0 men
  • general anaemia
    -lymphadenopathy (non-tender)
    -Hepatosplenomegaly
168
Q

What is the diagnosis of CLL?

A

FBC - pancytopenia (except lymphocytes)
Blood film - shows small lymphocytes of mature appearance with ‘smear or smudge cells’
hypogammaglobulinemia as no plasma cells (Ig producing cells)

169
Q

What is the treatment for CLL?

A

Progressive = palliative and chemo if old
IV - Ig

170
Q

What is a complication of CLL?

A

Ritcher’s transformation - B-cell massively accumulates in lymph nodes - massive lymphadenopathy and transformation from CLL to aggressive lymphoma

171
Q

What is lymphoma?

A

Lymphocytic accumulation in lymph nodes

172
Q

What are the two types of lymphomas?

A
  1. Hodgkin’s lymphoma
  2. Non-Hodgkin’s lymphoma
173
Q

What is Hodgkin’s lymphoma?

A

Typically a disease of young adults - peaks in teens and later in life. Previous infection with Epstein-Barr Virus is thought to play a role.

174
Q

What HL be classified in to?

A

Classical Hodgkin’s lymphoma - Reed-Sternberg cell
-Nodular lymphocyte predominant Hodgkin’s lymphoma - Reed- sternburg ‘ popcorn’ variant

175
Q

What is the presentation of Hodgkin’s lymphoma?

A
  • B symptoms
  • painless rubbery lymphadenopathy ( painful after drinking alcohol)
176
Q

What are the B-symptoms?

A

Fever
Night sweat
unintended weight loss

177
Q

What is the diagnosis of Hodgkin’s lymphoma?

A

Lymph node biopsy - Reed-Sternberg cells positive
Low Hb, raised ESR +lactate dehydrogenase
CT/MRI chest/ abdo/ pelvis for staging

178
Q

What is Ann Arbor staging?

A

staging of HL and NHL from 1-4

179
Q

What is AA stage 1?

A

single lymph node

180
Q

What is AA stage 2?

A

2 or more lymph nodes on same diaphragm side

181
Q

What is AA stage 3 ?

A

lymph nodes on both diaphragm sides?

182
Q

What is AA stage 4?

A

Widespread disease outside of lymph nodes

183
Q

What does it mean if it is prefixed with A or B?

A

A - absence of B symptoms
B - presence of B symptoms

184
Q

What is the treatment of HL?

A

ABVD (Chemo) - Adriamycin, Bleomycin, Vincristine, Dacarbazine

185
Q

What are the side effects of chemotherapy?

A

alopecia, n+v, myelosuppression, BM failure, infection

186
Q

What is febrile Neutropenia?

A

Massive risk in patients who had recent high does of chemo
- Fever, tachycardia, sweats,rigors,tachypnoea
Treat - immediate broad spec Abx (amoxicillin)

187
Q

What is non - Hodgkin’s lymphoma?

A

MC type - diffuse large B cell (80%)
Burkitt’s
Follicular

188
Q

What is the presentation of NHL?

A
  • more varied as many subtypes
    -B symptoms
    -painless rubbery lymphadenopathy (not affected by alcohol)
189
Q

What is the diagnosis of NHL?

A

Lymph node biopsy - diagnostic - no reed-sternberg or popcorn cells/ and confirms NHL subtype (Burkitt’s = starry sky biopsy)
-CT abdo/pelvis/chest for staging

190
Q

What is a sub-type of NHL?

A

Burkitt’s lymphoma

191
Q

What is the treatment for NHL?

A

R-CHOP Chemo : Rituximab , cyclophosphamise, Hydroxy- daunorubicin, Vincristine, prednisolone

192
Q

What is Multiple Myeloma?

A

Neoplastic monoclonal proliferation of plasma cells

193
Q

What is the epidemiology of multiple myeloma?

A

M>W
70y.o african- caribbbeans

194
Q

What is the pathology of myeloma?

A

Malignant plasma cells produce an excess of IgG - 55% and IgA -20%

195
Q

What is the presentation of multiple myeloma?

A

OLD CRAB
1. Old
2. C - hypercalcaemia (increased osteoclast bone resorption) - (causing weak bones, kidney stones, abdo moans and psychedelic groans)
3.Reanl failure- immunoglobulins deposit in kidneys - Bence jones protein in urine)
4. Anaemia - BM infiltration
5. Bone lesions(painful, new onset back pain in elderly)

196
Q

What is the diagnosis of multiple myeloma?

A

-FBC + Blood film= normocytic nomochromic and increased ESR (Rouleaux formation - aggregations of RBC)
- Urine dipstick -bence jones protein in urine
-U+E = renal failure, kidney stone
-Serum electrophoresis= paraprotein ‘ M spike’
-XR Skull -pepper pot skull due to osteolytic lesions

197
Q

What is a precursor to myeloma?

A

MGUS - monoclonal gammopathy of undetermined significance
<10% BM plasma cells
-Asymptomatic

198
Q

What is the treatment for myeloma?

A

Chemotherapy
Bisphosphonates (alendronate)
BM stem cell transplant

199
Q

What is thrombopoietin?

A

Produced in the liver - stimulates the production of platelets by megakaryocytic

200
Q

What does thromboxane A2 do?

A

Platelet receptor - synthesised in platelets via COX-1
Induces platelet aggregation

201
Q

What are P2Y12?

A

platelet receptors - amplifies platelet activation
- important for clopidogrel

202
Q

What are GPIIB/IIIa?

A

Platelet receptors - receptor for von Willeband factor - essential for platelet adhesion to vessels

203
Q

What are the causes of decreased platelet production?

A

-leukaemia, myeloma, lymphoma
-Low B12, Folate
-Liver disease =decreased TPO
-HIV/TB

204
Q

What are the causes of increased platelet destruction?

A

-ITP
-Drug induced -heparin
-DIC
-TTP

205
Q

What are the causes of reduced platelet function?

A

-congenital abnormality
-Aspirin
-VW disease
-uraemia

206
Q

What is thrombocytopenia?

A

Deficiency of platelets in bloods

207
Q

What are the causes of thrombocytopenia?

A
  • reduced platelet production
    -Excess peripheral destruction of platelets
    -problems of enlarged spleen
208
Q

What is Immune thrombocytopenia purpura?

A

Autoimmune destruction of platelets (IgG antibodies to platelets and megakaryocytes). Often triggered by a viral infection.

209
Q

What is the epidemiology of ITP?

A

-ITP in children often follows a viral infection, rapid onset which is usually self limiting
-ITP in adults, usually young women with malignancy , HIV other autoimmune diseases , is usually more chronic
ITP more common than TTP

210
Q

What is the presentation of ITP?

A
  • well systemically
    -purpuric rash
    -Easy bleeds
    -menorrhagia
211
Q

What are the investigations for ITP?

A

FBC - thrombocytopenia
Increased megakaryoblasts on BM examination

212
Q

What is the treatment for ITP?

A
  • corticosteroids - prednisolone
    IV IgG
    -splenectomy
213
Q

What is thrombotic thrombocytic purpura?

A

AdamTS13 deficiency
-VWF normally cleaved into fragments
-here, remain as multimers +aggregate at endothelial injury sites :
Adult females, malignancy,HIV

214
Q

What is the cause of TTP?

A

occurs due to deficiency of ADMATS 13, a protease which is normally responsible for degradation of VWF

215
Q

What is the presentation of TTP?

A

purpuric rash
menorrhagia
AKI
Fever
Anameia
Neurological Sx
not well

216
Q

What are the investigations for TTP?

A

FBC - reduced platelets , shistocytes
ADAMATS 13 low

217
Q

What is the treatment for TTP?

A

1- plasmapheresis
2- prednisolone + rituximab

218
Q

What is Disseminated intravascular crisis?

A

Wide spread clotting and bleeding ( all platelets and clotting factors used for blood clots)

219
Q

What is the pathology of DIC?

A
  • involves widespread generation of fibrin within the blood vessels caused by initiation of coagulation pathway. Also secondary activation of fibrinolysis which contributes to bleeding followed by thrombosis.
220
Q

Why does DIC occur?

A

occurs when the balance between forming new clots and breaking down clots is tipped in favour of clots- widespread clotting (organ ischaemia) - depleted clotting factors - bleeding

221
Q

What are the causes of DIC?

A

Activation of CC:
-Malignancy -lekaemia t(15:17) translocation
-Trauma
-Infections - meningitis
-Liver Disease

222
Q

What is the presentation of DIC?

A
  • bleeding (typically from venepuncture/IV sites/nose and mouth)
    -bruising
    -SOB
    -Haemoptysis
223
Q

What are the investigations for DIC?

A
  • Prolonged PTT/APTT/TT
    -Decreased fibrinogen and increased fibrin degradation products
    Blood film - shows fragmented cells
224
Q

What is the treatment for DIC?

A

-Treat underlying cause - maintain blood volume and tissue perforation
-May need transfusions - platelets, RBCs and fresh frozen plasma - replace clotting factors

225
Q

What is Polycythaemia?

A

Defined as an increase in haemoglobin, packed cell volume and RBC’s
Erythrocytosis of any cause

226
Q

What is the primary cause of Polycthaemia?

A
  • Polycthaemia ruba vera -mutation in JAK2 v617 gene
227
Q

What is the secondary cause of polycthaemia?

A

Chronic hypoxia
Inappropriate increase in erythropoietin - renal/ livertumours
Dehydration

228
Q

What are the symptoms of polycthaemia?

A

Itchy after a bath, burning in fingers and toes, reddish plethoric complexion, blurred vision, headache, hepatosplenomegaly, erythromelalgia

229
Q

What is the diagnosis of polycthaemia?

A

FBC - high WCC, platelets, RBC
High Hb
Genetic test - JAK2 gene positive

230
Q

What is the treatment for Polycthaemia ?

A

Venesection + aspirin (procedure to reduce red blood cells)

231
Q

What is Haemophilia?

A

X-linked recessive disorders- Factor deficiency
mainly affects men
Haemophilia A is more common

232
Q

Whta is Haemophilia A?

A

Factor 8 deficiency

233
Q

What is Haemophilia B?

A

Factor 9 deficiency

234
Q

What is the presentation of Haemophilia?

A

spontaneous bleeds, easy bruising, epistaxis, haemarthrosis - bleeding into joint spaces

235
Q

What are the investigations of Haemophilia?

A

Normal PT and increased APTT (as only intrinsic pathway affected)
F8 and F9 low assay

236
Q

What is the treatment for haemophilia?

A

A = IV F8 and desmopressin ( releases F8 stored in vessel walls)
B =IV F9

237
Q

What is Von Willerbrand’s disease?

A

Most common inherited bleeding disorder.Autosomal dominant mutation of vWf gene on chromosome 12 leading to a vhf deficiency.

238
Q

What is the pathology of VWF disease?

A

VWF is responsible for basis of platelet plug, deficient VWF means more spontaneous bleeds and bruising.

239
Q

What is the presentation of VWF disease?

A

Bleeding
bruising
Menorrhagia
Epistaxis

240
Q

What is the diagnosis for VWF disease?

A

Normal PT and increased APTT, normal F8/9 assay
Low VWF

241
Q

What is the treatment for VWF?

A

Non curable
Desmopressins. -increase VWF release from endothelial webel parade bodies

242
Q

What is the triad for thrombosis?

A

Vessel wall injury
Stasis
Hypercoagubility

243
Q

What is deep vein thrombosis?

A

Occlusion in normal vessels, most commonly deep veins of the leg. Commonly occur after long periods of immobilisation.

244
Q

What are the causes of DVT?

A

surgery, immobility, leg fracture, contraceptive pill, long haul flights, pregnancy

245
Q

What are the risk factors of DVT?

A

Endothelial injury - smoking, trauma, surgery

Virchow’s triad -Immobility, long haul flights

Hypercoagubility - preggo, coco,obesity, malignancy

246
Q

What is the presentation of a DVT?

A

Unilateral swollen calf with engorged leg veins
Typically warm and oedematous

247
Q

What are the investigations for a DVT?

A

Wells DVT score 1< likely DVT
D-dimer - coagulation screen, fibrinogen degradation product
Negative = no DVT if raised :
Doppler/compression ultrasound - find popliteal vein, if cannot be squashed = DVT - diagnostic

248
Q

What is a D-Dimer?

A

A D-dimer test looks for D-dimer in blood. D-dimer is a protein fragment (small piece) that’s released when a blood clot dissolves in your body.

249
Q

What is the treatment for a DVT?

A

Dual anticoagulation :
Apixiban - antifactor XA
LMWH if above CI

250
Q

What are the complications of a DVT?

A

Pulmonary Embolism

251
Q

How can you prevent a DVT?

A

Compression stockings
Early mobilisation
Leg elevation

252
Q

What is a pulmonary embolism?

A

DVT embolises and lodges in pulmonary artery circulation

253
Q

What does a PE present like? How would you treat it?

A

Pleuritic chest pain
Dyspnoea
Tachycardia
Evidence of DVT

If massive PE = IV ateplase
or
Anticoagulation - apixaban

254
Q

What is Malaria?

A

A Notifiable protozoal infection

255
Q

What are the causes of malaria?

A
  • protozoa infection by plasmodia falciparum, p.ovale and p.Virax
  • Transmitted by females Anopheles mosquito (vector)
256
Q

What is the pathology of malaria?

A
  • Sporozoites in mosquito saliva inoculate into host human
  • multiply inside hepatocytes as merozoites ( some merozoites lay dormant in p.ovale and virax)
    -Then into RBCs; merozoites ->trophozoites->schizont-> new merozoites
    RBC rupture- cause systemic infection
257
Q

What is the presentation of malaria?

A

-FEVER and EXOTIC TRAVEL
- anaemia
-Black water fever( malarial haemoglobinuria)
Hepatosplenomegaly

258
Q

What is the presentation of malaria in children?

A

Convulsions, Increase in ICP, hypoglycaemia. = so need to rule out meningitis - CSF analysis

259
Q

What is the diagnosis for malaria?

A

Blood film - thick (Malaria) and thin (species) = 3 separate readings negative before declared negative

260
Q

What is the treatment for Malaria?

A

Quinine and doxycycline
Artesunate IV - if severe

261
Q

What is neutropenia?

A

Lower than normal neutrophil count - <2.0 x10^9/L

Malignancy - myeloma/ lymphoma

262
Q

What is Neutrophila?

A

High neutrophil count >7.5x10^9/L

acute bacterial infection

263
Q

What is Lymphopenia?

A

Low lymphocyte count
<1.3x10^9/L
Causes: steroids, anorexia

264
Q

What is Lymphocytposis?

A

High lymphocyte count
>3.5x10^9/L
chronic infection

265
Q

What is monocytosis?

A

High count of monocytes
>0.8 x10^9/L

Causes:Malaria, typhoid, TB

266
Q

What is thrombocytopenia?

A

Low platelets
<150x10^9/L

Causes: HIV,TB infection
NSAIDs, alcohol, liver and renal disease

267
Q

What is Eosinphilia?

A

High count of eosinophils
>0.44x10^(/L
- check travel and drug history
Causes: asthma, paratactic infections, smoking

268
Q

What is thrombocytosis?

A

High platelet count
>400x10^9/L
Causes: iron deficiency, reactive inflammation

269
Q

What are two anti platelets?

A

Aspirin
Clopidogrel

270
Q

What is the action of aspirin?

A

Inhibits COX-1 which causes low thromboxane A2 - which activates platelets

271
Q

What is the action of clopidogrel?

A

Binds to P2Y12 receptos to stop platelet activation

272
Q

What are the uses of anti platelets?

273
Q

What are the anticoagulants?

A

Warfarin, LMWH - heparin, DOAC - apixaban

274
Q

What is the cation of warfarin?

A

Inhibits vit K epoxide reductase and therefore the VIT K clotting factors 10,9,7,2

275
Q

What is the action of heparin?

A

activates antithrombin3 and inhibits X - dalteparin

276
Q

What is the action of a DOAC?

A

inactivates factor Xa

277
Q

What is the use of IV Ateplase?

A

activates plasmin to degrade fibrin.

278
Q

What is the difference between arterial and venous thrombosis?

A

-Arterial (PVD) - low pulse, cool thin skin, intermittent claudication

-Venous(DVT) - high pulse, rubber , tumour, painful

279
Q

What is HIV?

A

retrovirus, sexual transmission, sharing needles

280
Q

What is the pathology of HIV?

A
  1. HIV gp120 binds to CD4 on TH
  2. Endocytoses RNA + enzymes
  3. Reverse transcriptase ;RNA to DNA
  4. Viral DNA integrates into hosts
  5. Protein synthesis
  6. Viral proteins and RNA exocytose and take part of CD4
281
Q

What is the diagnosis HIV?

A

Anti HIV Ig/ p24 Ab - ELISA test
Monitor progression - CD4 count, HIV RNA copies

282
Q

What is the treatment for HIV?

A

Highly active antiviral therapy - 3 reverse transcriptase drugs

283
Q

What is the 4 step progression of HIV?

A
  1. Primary infection - CD4+ dip
  2. Clinical latency - years
  3. Sx - fever, diarrhoea, night sweats
    4.AIDs - CD4+ <200/mm^3
    CMV- owl eyes
    Pneumocystitis jiroveci pneumonia

Phase 2a (9 decks)

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