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MY PHASE 2A MEDICINE > HAEM > Flashcards

HAEM Flashcards

1
Q

What are the constituents of blood?

A

55% plasma, 45% cells (RBC, WBC, platelets)

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2
Q

Where are RBC produced and destroyed?

A 
Erythropoiesis = bone marrow
Erypoptis = Liver, spleen, bone marrow
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3
Q

Which WBC are granulocytes?

A

Neutrophils
Basophils
Eosinophils

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4
Q

What are the distinctive features of neutrophils?

A
  1. Multi lobar nucleus
  2. Role in inflammation and infection
  3. Role in myeloid leukaemia
  4. Phagocytic
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5
Q

What are the distinctive features of eosinophils?

A
  1. Bi/tri lobar nucleus
  2. DIURNAL (more in the morning)
  3. numbers raised in parasitic infection
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6
Q

What are the distinctive features of basophils?

A
  1. Associated with hypersensitivity reactions

2. Similar role to mast cells -> secrete histamine

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7
Q

When do lymphocyte numbers decrease?

A

chemo / HIV

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8
Q

What is the general role of B/ T cells?

A

B cells = mediators in humeral immunity ( antibodies)

T cells = mediators on cellular immunity (cytotoxic CD8+ and T helper CD4+)

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9
Q

What are monocytes?

A

Immature cells that differentiate once they LEAVE the bloodstream

Many form macrophages

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10
Q

Where are platelets derived from and what is their function?

A
  • Derived from megakaryocytic in bone marrow

- Major role in clotting (platelet plug/coagulation cascade)

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11
Q

What is the purpose of the coagulation cascade?

A

Ultimately produces FIBRIN

- strengthens the platelet plug

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12
Q

What are the functions of thrombin?

A
  1. Converts fibrinogen to fibrin
  2. Activated factor XIII to factor XIIIa
  3. Positive feedback effect on further thrombin production
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13
Q

What clotting factors does warfarin/ heparin/ DOAC inhibit?

A 
Warfarin =  Factor 2, 7, 9 , 10 
Heparin/DOAC = Factor Xa
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14
Q

What is the purpose of plasmin?

A
  1. Cuts fibrin into fragments

2. Prevents blood clot growing and becoming problematic

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15
Q

Why is the liver important in clotting?

A
  1. The liver synthesises many clotting factors
  2. The liver produces bile salts which are needed for Vit K absorption
    …factors 2, 7, 9 , 10 are vit K dependent
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16
Q

Give examples of 5 pieces of information that could be obtained from collecting a Full Blood Count sample?

A
  1. Red blood cell volume
  2. White blood cell volume (of all types)
  3. Platelet volume
  4. Haemoglobin concentration
  5. Mean Corpuscular Volume
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17
Q

Why would you carry out a reticulocyte count?

A

Enables you to see how quickly the bone marrow is producing new RBCs. (Reticulocytes are immature RBCs)

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18
Q

What does a low/high reticulocyte count indicate?

A

Low = indicative that something is preventing RBCs from being produced e.g. a haematinic deficiency

High = - indicate that RBCs 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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19
Q

How would you measure the amount of iron in someones body? Why is it sometimes not accurate?

A

SERUM FERRITIN

  • Ferritin is an acute phase protein and so it’s levels can become falsely raised in inflammation and malignancy (much like PSA)
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20
Q

What is the purpose of a thick/thin blood film?

A

Thick = permits the examination of a large amount of blood for the presence of parasites.

Thin = allows for the observation of RBC morphology, inclusions, and intracellular and extracellular parasites.

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21
Q

Briefly describe the structure and function of haemoglobin

A
  1. 2 alpha chains + 2 beta chains
  2. Each haemoglobin can carry 4 x O2.
  3. carry and deliver oxygen to tissues
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22
Q

What is an INR test? What would normal values be?

A

International Normalised Ratio (Prothrombin time)

  • should be around 1.0
  • patients on warfarin should be between 2.0 and 3.0
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23
Q

How would you classify anaemia based on the mean corpuscular volume?

A

MCV<80 = MICROCYTIC
MCV 80-100 = NORMOCYTIC
MCV >100 = MACROCYTIC

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24
Q

Give 5 presenting symptoms of anaemia

A
  1. Fatigue
  2. Lethargy
  3. Dyspnoea
  4. Palpitations
  5. Headache
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25
Q

Give 3 signs of anaemia

A
  1. Pale Skin
  2. Pale mucous membranes
  3. Tachycardia (compensatory to meet demand)
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26
Q

What are the 3 main causes of microcytic anaemia?

A
  1. Iron deficiency
  2. Thalassaemia
  3. Anaemia of chronic disease
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27
Q

Give 4 signs of IRON DEFICIENCY anaemia

A
  1. Brittle hair and nails
  2. Atrophic Glossitis (smooth tongue)
  3. Kolionychia (spoon nails)
  4. Angular stomatitis (inflamed corners of mouth)
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28
Q

Give 5 causes of iron deficiency anaemia

A
  1. Blood loss (chronic - think periods)
  2. Poor absorption.
  3. Decreased intake in diet.
  4. Hook worm!
  5. Breastfeeding, low iron in breast milk.
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29
Q

What investigations would you do if you suspected iron deficiency anaemia?

A
  1. FBC - Hypochromic microcytic anaemia
  2. Serum Ferritin (careful!) - Low
  3. Reticulocyte Count - REDUCED
  4. Endoscopy - Possible GI bleed related cause?
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30
Q

What is the treatment for iron deficiency anaemia? Give 4 side effects of the treatment

A

Oral ferrous sulphate

  1. Black stools
  2. Constipation
  3. Diarrhoea
  4. Nausea
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31
Q

What are the 3 main causes of normocytic anaemia?

A
  1. Acute blood loss / hemorrhage
  2. Combined haematinic deficiency (e.g. iron and B12)
  3. Anaemia of chronic disease
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32
Q

Where is iron absorbed?

A

In the duodenum

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33
Q

Give 4 chronic diseases that can cause anaemia

A
  1. CKD
  2. Rheumatoid arthritis
  3. Lupus
  4. Cancer
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34
Q

What are the 3 main causes of macrocytic anaemia?

A
  1. B12 deficiency (Pernicious)
  2. Folate Deficiency
  3. Alcohol excess
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35
Q

What is megaloblastic anaemia?

A
  1. Can be caused by folate/B12 deficiency
  2. Means that there has been an inhibition of DNA synthesis
  3. RBC cannot progress onto mitosis causing continuing growth without division
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36
Q

What are the main causes of folate deficiency anaemia?

A
  1. Poor folate diet
  2. Malabsorption
  3. Pregnancy
  4. Anti-folate drugs (Methotrexate)
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37
Q

Where is folate absorbed?

A

Jejenum

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38
Q

Give 4 causes of pernicious anaemia

A
  1. Atrophic gastritis
  2. Gastrectomy
  3. Crohn’s
  4. Coeliac disease
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39
Q

How and where is vit b12 absorbed?

A
  1. Bound to intrinsic factor

2. terminal ileum

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40
Q

What additional feature would you see with patients with B12 deficiency anaemia?

A

Neurological problems

/angina/heart failure

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41
Q

How do you treat pernicious anaemia?

A

Vitamin B12 (Hydroxocobalam) tablets/injections

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42
Q

What is haemolytic anaemia?

A
  1. Occurs when RBCs are destroyed before 120 days

2. Can be due to inherited or acquired cause

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43
Q

Give 4 signs and symptoms of haemolytic anaemia

A

Symptom = gall stones (excess bilirubin)

Signs =

  • jaundice
  • splenomegaly
  • leg ulcers
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44
Q

Give 3 inherited causes of haemolytic anaemia

A
  1. Membranopathies
  2. Enzymopathies
  3. Haemoglobinopathies
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45
Q

Give 3 acquired causes of haemolytic anaemia

A
  1. Autoimmune
  2. Infections
  3. Secondary to systemic disease
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46
Q

What would you see on a blood film of a patient with haemolytic anaemia?

A

Schistocytes

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47
Q

What is aplastic anaemia?

A

When bone marrow stem cells are damaged -> pancytopenia.

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48
Q

What stimulates EPO?

A

Tissue hypoxia.

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49
Q

Name a primary cause of polycythaemia.

A

Polycythaemia rubra vera - over reactive bone marrow.

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50
Q

Give 3 secondary causes of polycythaemia.

A
  1. Heavy smoking.
  2. Lung disease.
  3. Cyanotic heart disease.
  4. High altitude.
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51
Q

What is neutrophilia?

A

Too many neutrophils.

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52
Q

Give 3 causes of neutrophilia.

A

Reactive - infection/ inflammation/ malignancy

Primary - CML.

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53
Q

Give 3 causes of lymphocytosis.

A

Reactive - Viral infections/ Inflammation/Malignancy.

Primary - CLL.

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54
Q

What is thrombocytopenia?

A

Not enough platelets.

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55
Q

Give examples of two Haemoglobinopathies

A
  1. Sickle cell disease (disorder of quality)

2. Thalassemia (disorder of quantity)

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56
Q

Give examples of 2 membranopathies

A
  1. Spherocytosis

2. elliptocytosis

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57
Q

Give an example of an enzymopathy

A

Glucose 6 phosphate dehydrogenase deficiency

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58
Q

What is sickle cell disease?

A

A haemoglobin disorder of quality. HbS polymerises -> sickle shaped RBC.

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59
Q

What is the advantage of being a carrier of sickle cell disease?

A

Carriage offers protection against falciparum malaria.

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60
Q

Describe the inheritance pattern of sickle cell disease.

A

Autosomal recessive. Sickle cell disease is homozygous SS.

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61
Q

If both parents are carriers of the sickle trait. What is the chance that their first child will have sickle cell disease?

A

Their offspring have a 1/4 chance of being affected with a sickle cell disease. (50% chance of being a carrier).

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62
Q

How long do sickle cells last for?

A

5-10 days - this explains why sickle cell disease is described as haemolytic.

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63
Q

Give 4 acute complications of sickle cell disease.

A
  1. Very painful crisis.
  2. Stroke in children.
  3. Cognitive impairment.
  4. Infections.
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64
Q

Give 3 chronic complications of sickle cell disease.

A
  1. Renal impairment.
  2. Pulmonary hypertension.
  3. Joint damage.
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65
Q

Describe the treatment for sickle cell disease.

A
  1. Transfusion.
  2. Hydroxycarbamide.
  3. Stem cell transplant.
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66
Q

What is the mutation that causes sickle cell disease?

A
  1. Point mutation of the Beta globin gene
  2. Valine to Glutamine
  3. Resulting in a HS variant.
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67
Q

What is the significance of parvovirus for someone with sickle cell disease?

A
  1. Parvovirus is a common infection in children.
  2. It leads to decreased RBC production and can cause a dramatic drop in Hb in patients who already have a reduced RBC lifespan.
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68
Q

What is the affect of sickle cell anaemia on reticulocyte count?

A

Reticulocyte count is raised.

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69
Q

What can precipitate sickling in sickle cell anaemia?

A

Trauma, cold, stress, exercise.

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70
Q

Why does sickle cell anaemia not present until after 6 months of age?

A

HbF is not affected by sickle cell anaemia as it is made up of 2 alpha and 2 gamma chains.

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71
Q

What drug can be used to prevent painful crises in people with sickle cell anaemia?

A

Hydroxycarbamide

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72
Q

How would you detect the presence of sickle cell disease on investigation?

A
  1. Hb ELECTROPHARESIS

2. HbSS present and absent HbA.

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73
Q

What is thalassaemia?

A

A haemoglobin disorder of quantity. There is reduced synthesis of one or more globin chains with leading to a reduction in Hb -> anaemia.

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74
Q

If someone has beta thalassaemia do they have more alpha or beta globin chains?

A

They have very few beta chains, alpha chains are in excess.

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75
Q

What is the clinical classification of beta thalassaemia?

A
  1. Thalassaemia major.
  2. Thalassaemia intermedia.
  3. Thalassaemia carrier/heterozygote.
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76
Q

Which clinical classification of thalassaemia relies on regular transfusions?

A

Thalassaemia major.

77
Q

Which clinical classification of thalassaemia is often asymptormatic?

A

Thalassaemia carrier/heterozygote.

78
Q

When do people with beta thalassaemia major usually present and why?

A

These patients usually present very young due to having severe anaemia and so a failure to feed/thrive.

79
Q

Why is it important to monitor iron levels in someone with beta thalassaemia major?

A

There is a risk of iron overload from the regular trasnfusions. Excess iron will be deposited in various organs e.g. the liver and spleen and cause fibrosis.

80
Q

What might you see on a blood count taken from someone with beta thalassaemia major?

A
  1. Raised reticulocyte count.

2. Microcytic anaemia.

81
Q

Describe the inheritance pattern for membranopathies.

A

Autosomal dominant.

82
Q

Briefly describe the physiology of membranopathies.

A

Deficiency of red cell membrane proteins caused by genetic lesions

83
Q

What is the treatment for membranopathies?

A
  1. Folic acid

2. Splenectomy

84
Q

Why does a deficiency in glucose-6-phosphate dehydrogenase lead to shortened red cell lifespan?

A

G6PD protects cells against oxidative damage.

85
Q

How is G6PD deficiency inherited?

A

X linked

but women can be effected

86
Q

What would you see on a blood film of a Pt with G6PD deficiency?

A
  1. Bite cells

2. Blister cells

87
Q

Give 3 signs of G6PD deficiency.

A

Crises characterised by:

  1. Haemolysis.
  2. Jaundice.
  3. Anaemia.
88
Q

What is the normal HB range for males/females?

A

Male Hb = 131 – 166 g/L

Female Hb = 110 – 147 g/L

89
Q

What is anaemia?

A

Reduced red cell mass

+/- reduced haemoglobin concentration

90
Q

If a patient presents with combined haematinic deficiency what is the most likely cause?

A

Malabsorption!

91
Q

What is the difference between alpha and beta thalassaemia in terms of mechanism?

A
  1. BOTH = Insufficient globin chains cause precipitation of dominant chain
  2. Deletional (B thal)
    Mutational (a thal)
92
Q

What is polycythaemia?

A

Too many RBC’s, an increase in Hb.

93
Q

What 3 blood test values would be increased in someone with polycythaemia?

A
  1. Hb.
  2. RCC.
  3. PCV (packed cell volume/ haematocrit)
94
Q

Give 3 symptoms of polycythaemia.

A
  1. Itching.
  2. Headache.
  3. Dizziness.
  4. Visual disturbance.
95
Q

What is the main cause of Polycythaemia rubra vera?

A

JAK2 mutation (95%)

96
Q

What is the treatment for polycythaemia rubra vera?

A
  1. ASPIRIN

2. venesection

97
Q

What are the causes of severe neutropenia?

A

UNDERPRODUCTION
Marrow failure
Marrow infiltration
Marrow toxicity e.g. drugs

INCREASED REMOVAL
Autoimmune
Felty’s syndrome
Cyclical

98
Q

How does warfarin work?

A

It antagonises vitamin K and so you get a reduction in clotting factors 2, 7, 9 and 10.

99
Q

How does heparin work?

A

It activates antithrombin which then inhibits thrombin and factor Xa.

100
Q

What is disseminated intravascular coagulation (DIC)?

A
  1. Clotting occurs inappropriately and diffusely, until clotting factors are exhausted.
    2 At this point uncontrolled bleeding occurs.
101
Q

Give 3 causes of disseminated intravascular coagulation (DIC).

A
  1. Sepsis
  2. Major trauma
  3. Malignancy
102
Q

What is the affect on fibrinogen in someone with disseminated intravascular coagulation (DIC)?

A

Decreased!

103
Q

What blood results would a patient with DIC show?

A
  1. Thrombocytopenia
  2. prolonged PT + APTT (activated prothrombin time)
  3. low fibrinogen
  4. high d-dimers

+/- evidence of organ failure

104
Q

Name 2 things that are increased and 2 that are decreased in DIC.

A

Increased: PTT and APTT.

Decreased: fibrinogen and platelets.

105
Q

Give 2 causes of thrombocytopenia.

A
  1. Production failure e.g. marrow suppression, marrow failure.
  2. Increased removal e.g. immune response (ITP), consumption (DIC), splenomegaly.
106
Q

What is the most common cause of thrombocytopenia?

A

Immune thrombocytopenic purpura (ITP)

107
Q

What is Immune thrombocytopenic purpura?

A

Autoimmune destruction of platelets often triggered by VIRAL infection/malignancy

108
Q

How would you treat Immune thrombocytopenic purpura?

A
  1. Corticosteroids - prednisolone
  2. Splenectomy
  3. IV Ig
109
Q

What is Thrombotic thrombocytopenic purpura?

A

Extensive microvascular clots form in small vessels in the body, resulting in a low platelet count and organ damage.

110
Q

What are clinical features of platelet dysfunction?

A

MUCO-CUTANEOUS PATTERN

  1. Mucosal bleeding
  2. Epistaxis, gum bleeding, menorrhagia
  3. Easy bruising
  4. Petechiae, purpura
  5. Traumatic haematomas (inc subdural)
111
Q

How would you treat Thrombotic thrombocytopenic purpura?

A
  1. Urgent plasma exchange (replaces ADAMTS 13 and removes antibody)
  2. Immunosuppression
  3. Do NOT give platelets –increases thrombosis
    90% mortality, 10 – 20% if treatment started promptly
112
Q

What is haemophilia?

A

X-linked recessive disorders, deficient in clotting factors

113
Q

What are the main 2 types of haemophilia?

A 
Haemophilia A (most common) 
 - reduction in factor 8

Haemophilia B
- reduction in factor 9

114
Q

What would the PTT be like of a Pt with haemophilia?

A
  1. Normal PTT (prothrombin time)
  2. PROLONGED APTT (activated partial thromboplastin time)

PTT → Extrinsic pathway
APTT → intrinsic pathway

115
Q

Give 5 risk factors for DVT.

A
  1. Increasing age.
  2. Obesity.
  3. Pregnancy.
  4. OCP (hyper-coagulability).
  5. Major surgery.
  6. Immobility.
  7. Past DVT.
116
Q

Give 3 symptoms of DVT.

A

Unilateral warm, tender, painful, swollen leg.

117
Q

What forms the differential diagnosis for a DVT?

A

Cellulitis

118
Q

What investigations might you do in someone to see if they have a DVT?

A
  1. D-dimer in those patients with a low clinical probability.
  2. US compression.
119
Q

What is the name of the score used to determine someones probability of having a DVT?

A

Wells score

120
Q

The Wells score determines someones clinical probability of having a DVT. Give 3 factors the score takes into account.

A
  1. Active cancer.
  2. Recently bedridden or major surgery.
  3. Tenderness along deep venous system.
  4. Swollen leg/calf.
  5. Unilateral pitting oedema.
121
Q

Describe the management for a DVT.

A

Aim of management is to prevent a PE!

- Anticoagulants - LMWH, warfarin

122
Q

What is the most important medical treatment for DVT prophylaxis?

A

LMWH

123
Q

How is malaria transmitted?

A
  1. Protazoal infection by Plasmodia falciparim

2. female Anopheles mosquito (Vector)

124
Q

What are the stages of the plasmodia life cycle in the human called?

A

Exo-erythrocytic and endo-erythrocytic stages

125
Q

What happens in the stages of the plasmodia life cycle that occur inside the human?

A

Exo-erythrocytic: Hepatcoytes become infected by sporozoites, the cells mature and develop and are released as tropozites.
Endo-erythrocytic: tropozites invade RBC’s. Parasite numbers expand rapidly with a sustained cycling of the parasite population.

126
Q

What signs and symptoms might you see in someone who has been infected with malaria?

A
  1. Chills/sweats
  2. Jaundice/ Hepatosplenomegaly
  3. Anaemia/fatigue
  4. Black urine (Black water fever)

FEVER + EXOTIC TRAVEL= MALARIA (until proven otherwise)

127
Q

Malaria diagnosis: what can thick and thin films tell you?

A
  • Thick films: sensitive but low resolution, tell you if you have malaria.
  • Thin films: tell you species and parasite count.
128
Q

What is the pathophysiology of malaria?

A
  1. Parasite matures in RBC → Knobs in RBC surface → Infected cells binds to each other (Rosetting) and receptors on endothelial cells walls
  2. Sequestration in small vessels becoming trapped.
  3. Micro circulation obstruction= tissue hypoxia.
129
Q

Give 4 complications of malaria

A
  1. Cerebral malaria
  2. ARDs
  3. Hypoglycemia
  4. Renal failure
  5. Shock
130
Q

What investigations should you carry out on a patient with suspected malaria?

A
  1. Blood film
  2. PREGNANCY TEST
  3. Rule out meningitis!!
131
Q

How do you treat malaria?

A

Quinine and doxycycline

132
Q

What is leukaemia?

A

A malignant proliferation of haemopoietic stem cells.

133
Q

What is acute myeloid leukaemia?

A

Neoplastic proliferation of blast cells.

134
Q

What can increase the risk of developing AML?

A
  1. Preceding haematological disorders.
  2. Prior chemotherapy.
  3. Exposure to ionising radiation.
  4. Downs syndrome
135
Q

Give 5 symptoms of leukaemia.

A
  1. Anaemia.
  2. Infection.
  3. Bleeding.
  4. Hepatomegaly.
  5. Splenomegaly.
136
Q

Why are anaemia, infection and bleeding symptoms of leukaemia?

A

Bone marrow failure

137
Q

Why are hepatomegaly and splenomoegaly symptoms of leukaemia?

A

Tissue infiltration

138
Q

What investigations might you do on someone who you suspect has leukaemia?

A
  1. Blood film.
  2. Bone marrow biopsy.
  3. Lymph node biopsy.
  4. Immunophenotyping.
  5. Cytogenetics.
139
Q

What is histologically characteristic of AML?

A

AUER RODS (indicative of myeloblasts)

140
Q

What is a distinctive presenting feature of AML?

A

Swollen gums

141
Q

What is ALL?

A

Acute lymphoid leukaemia. There is uncontroleld proliferation of immature lymphoblast cells.

142
Q

What are 3 characteristic features of ALL?

A
  1. Lymphadenopathy
  2. Hepatosplenomegaly
  3. CNS symptoms
143
Q

Which cell proliferation is most commonly seen in ALL?

A

B cell

144
Q

How would you treat ALL/AML?

A
  1. Chemo
  2. Bone marrow transplant
  3. Steroids
145
Q

Why would you also prescribe Allopurinol?

A

Prevents tumour lysis syndrome

(fast growing tumours have faulty metabolism, break down and release potassium – causes heart problems such as arrhythmias, and also the release of DNA (renal problems)

146
Q

What is CML?

A

Chronic myeloid leukaemia, there is uncontrolled clonal proliferation of basophils, eosinophils and neutrophils.

147
Q

What would the FBC from someone with CML look like?

A

High WBC’s.

148
Q

What chromosome is present in >80% of people with CML?

A

Philadelphia chromosome

149
Q

What is the treatment for CML?

A

IMATINIB - tryosine kinase inhibitor

150
Q

How would a typical patient with CML present?

A

Mostly asymptomatic BUT can have B symptoms and hepatosplenomegaly

151
Q

What are the risk factors for CML?

A
  • middle aged

- ionising radiation

152
Q

What is CLL?

A

Chronic lymphoid leukaemia. Proliferation of B lymphocytes leads to the accumulation of mature B cells that have escaped apoptosis.

153
Q

What would you see on a blood film for a patient with CLL?

A

Smear cells

154
Q

What can be used as a good prognostic tool for survival in patients with CLL?

A

Telomere length

155
Q

What is the epidemiology of CLL?

A

Old, white, men (often accidental finding and people die with the disease)

156
Q

What is the most common form of leukaemia?

A

Chronic lymphoid leukaemia

157
Q

What is lymphoma?

A

A malignant growth of WBC’s predominantly in the lymph nodes.

158
Q

Although predominantly in the lymph nodes, lymphoma is systemic. What other organs might it effect?

A
  1. Blood.
  2. Liver.
  3. Spleen.
  4. Bone marrow.
159
Q

Give 4 risk factors for lymphoma.

A
  1. Primary immunodeficiency.
  2. Secondary immunodeficiency e.g. HIV.
  3. Infection e.g. EBV, HTLV-1.
  4. Autoimmune disorders e.g. RA.
160
Q

Give 4 symptoms of lymphoma.

A
  1. Enlarged lymph nodes in arm/neck.
  2. Symptoms of compression syndromes.
  3. General systemic ‘B’ symptoms e.g. weight loss, night sweats, malaise.
  4. Liver and spleen enlargement.
161
Q

What are B symptoms?

A
  1. weight loss
  2. night sweats
  3. malaise
162
Q

What investigations might you do in someone who you suspect has lymphoma?

A
  1. Blood film.
  2. Bone marrow biopsy.
  3. Lymph node biopsy.
  4. Immunophenotyping.
  5. Cytogenetics.
163
Q

What are the symptoms of Hodgkins lymphoma?

A
  1. Painless lymphadenopathy.

2. Presence of ‘B’ symptoms e.g. night sweats, weight loss.

164
Q

What is needed for diagnosis of Hodgkins lymphoma?

A

Presence of Reed-sternberg cells.

165
Q

Describe the staging of Hodgkins lymphoma

A

Ann Arbor

  1. Stage 1: confined to a SINGLE lymph node region.
  2. Stage 2: Involvement of two or more nodal areas on the SAME side of the diaphragm.
  3. Stage 3: involvement of nodes on BOTH sides of the diaphragm.
  4. Stage 4: Spread BEYOND the lymph nodes e.g. liver.

Each stage is either ‘A’ - absence of ‘B’ symptoms or ‘B’ - presence of ‘B’ symptoms.

166
Q

What is the epidemiology for Hodgkin’s lymphoma?

A

Bimodal incidence - young and old (20s and over 50)

risk inc. with EBV/HIV/AIDS

167
Q

What is the treatment for stage 1 - 2A Hodgkins lymphoma?

A

Short course combination chemotherapy followed by radiotherapy.

168
Q

What is the treatment for stage 2B - 4 Hodgkins lymphoma?

A

Combination chemotherapy.

169
Q

What are the possible complications of treatment for Hodgkins lymphoma?

A
  1. Secondary malignancies.
  2. IHD.
  3. Infertility.
  4. Nausea.
  5. Alopecia.
170
Q

Describe low grade non-hodgkins lymphoma.

A

Slow growing, advanced at presentation, often incurable. Median survival is 10 years.

171
Q

What is the treatment for low grade non-hodgkins lymphoma?

A

If symptomless - do nothing.

Radiotherapy, combination chemotherapy and mAb may be used if symptomatic.

172
Q

Describe high grade non-hodgkins lymphoma.

A

Aggressive. Nodal presentation, patient unwell. Often curable.

173
Q

Describe the treatment for high grade non-hodgkins lymphoma.

A
  • Early: short course chemotherapy and radiotherapy.

- Advanced: combination chemotherapy and mAb.

174
Q

Give 2 signs of non-hodgkins lymphoma

A
  1. enlarged painless lymph nodes

2. face oedema -> obstructed SVC

175
Q

What is myeloma?

A

Malignancy of plasma cells leading to progressive bone marrow failure. It is associated with production of characteristic paraprotein, bone disease and renal failure.

176
Q

When might nodal pain be worse in patients with lymphoma?

A

When drinking alcohol!

177
Q

In order to make a diagnosis of myeloma, there must be evidence of mono-clonality. What is mono-clonality?

A

Abnormal proliferation of a single clone of plasma cell leading to immunoglobulin secretion and causing organ dysfunction especially to the kidney.

178
Q

In approximately 2/3 of people with myeloma, what might their urine contain?

A

Ig light chains - BENCE JONES protein

179
Q

Give 4 signs of myeloma.

A

CRAB!

  1. Calcium is elevated.
  2. Renal failure.
  3. Anaemia.
  4. Bone lesions (lytic)
180
Q

Why is calcium elevated in myeloma?

A

There is increased bone resorption and decreased formation meaning there is more calcium in the blood.

181
Q

Why might someone with myeloma have anaemia?

A

Crowding out!

The bone marrow is infiltrated with plasma cells. Consequences of this are anaemia, infections and bleeding.

182
Q

Why might someone with myeloma have renal failure?

A

Due to light chain deposition.

183
Q

What investigations might you do in someone who you suspect has myeloma?

A
  1. Blood film.
  2. Bone marrow aspirate and trephine biopsy.
  3. Electrophoresis.
  4. X-ray.
  5. CT scan.
  6. MRI scan.
  7. Chromosomal abnormalities.
184
Q

What would you expect to see on the blood film taken from someone with myeloma?

A

Rouleaux formation (aggregations of RBC’s).

185
Q

What are you looking for on a bone marrow biopsy taken from someone with myeloma?

A

Increased plasma cells

186
Q

What are you looking for on electrophoresis in a patient with myeloma?

A

Monoclonal protein band.

187
Q

What are you looking for on an X-ray taken from someone with myeloma?

A

Lytic bone lesions - ( long bones, pelvis and spine)

Pepperpot skull!

188
Q

Describe the treatment for symptomatic myeloma.

A

Chemotherapy, analgesia and bisphosphonates.

Radiotherapy and bone marrow transplant can also be done.

MY PHASE 2A MEDICINE (14 decks)

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