HAEM Flashcards

1
Q

What are the constituents of blood?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where are RBC produced and destroyed?

A
Erythropoiesis = bone marrow
Erypoptis = Liver, spleen, bone marrow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Which WBC are granulocytes?

A

Neutrophils
Basophils
Eosinophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the distinctive features of basophils?

A
  1. Associated with hypersensitivity reactions

2. Similar role to mast cells -> secrete histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

When do lymphocyte numbers decrease?

A

chemo / HIV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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+)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are monocytes?

A

Immature cells that differentiate once they LEAVE the bloodstream

Many form macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the purpose of the coagulation cascade?

A

Ultimately produces FIBRIN

- strengthens the platelet plug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What clotting factors does warfarin/ heparin/ DOAC inhibit?

A
Warfarin =  Factor 2, 7, 9 , 10 
Heparin/DOAC = Factor Xa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the purpose of plasmin?

A
  1. Cuts fibrin into fragments

2. Prevents blood clot growing and becoming problematic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Give 5 presenting symptoms of anaemia

A
  1. Fatigue
  2. Lethargy
  3. Dyspnoea
  4. Palpitations
  5. Headache
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Give 3 signs of anaemia
1. Pale Skin 2. Pale mucous membranes 3. Tachycardia (compensatory to meet demand)
26
What are the 3 main causes of microcytic anaemia?
1. Iron deficiency 2. Thalassaemia 3. Anaemia of chronic disease
27
Give 4 signs of IRON DEFICIENCY anaemia
1. Brittle hair and nails 2. Atrophic Glossitis (smooth tongue) 3. Kolionychia (spoon nails) 4. Angular stomatitis (inflamed corners of mouth)
28
Give 5 causes of iron deficiency anaemia
1. Blood loss (chronic - think periods) 2. Poor absorption. 3. Decreased intake in diet. 4. Hook worm! 5. Breastfeeding, low iron in breast milk.
29
What investigations would you do if you suspected iron deficiency anaemia?
1. FBC - Hypochromic microcytic anaemia 2. Serum Ferritin (careful!) - Low 3. Reticulocyte Count - REDUCED 4. Endoscopy - Possible GI bleed related cause?
30
What is the treatment for iron deficiency anaemia? Give 4 side effects of the treatment
Oral ferrous sulphate 1. Black stools 2. Constipation 3. Diarrhoea 4. Nausea
31
What are the 3 main causes of normocytic anaemia?
1. Acute blood loss / hemorrhage 2. Combined haematinic deficiency (e.g. iron and B12) 3. Anaemia of chronic disease
32
Where is iron absorbed?
In the duodenum
33
Give 4 chronic diseases that can cause anaemia
1. CKD 2. Rheumatoid arthritis 3. Lupus 4. Cancer
34
What are the 3 main causes of macrocytic anaemia?
1. B12 deficiency (Pernicious) 2. Folate Deficiency 3. Alcohol excess
35
What is megaloblastic anaemia?
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
36
What are the main causes of folate deficiency anaemia?
1. Poor folate diet 2. Malabsorption 3. Pregnancy 4. Anti-folate drugs (Methotrexate)
37
Where is folate absorbed?
Jejenum
38
Give 4 causes of pernicious anaemia
1. Atrophic gastritis 2. Gastrectomy 3. Crohn's 4. Coeliac disease
39
How and where is vit b12 absorbed?
1. Bound to intrinsic factor | 2. terminal ileum
40
What additional feature would you see with patients with B12 deficiency anaemia?
Neurological problems | /angina/heart failure
41
How do you treat pernicious anaemia?
Vitamin B12 (Hydroxocobalam) tablets/injections
42
What is haemolytic anaemia?
1. Occurs when RBCs are destroyed before 120 days | 2. Can be due to inherited or acquired cause
43
Give 4 signs and symptoms of haemolytic anaemia
Symptom = gall stones (excess bilirubin) Signs = - jaundice - splenomegaly - leg ulcers
44
Give 3 inherited causes of haemolytic anaemia
1. Membranopathies 2. Enzymopathies 3. Haemoglobinopathies
45
Give 3 acquired causes of haemolytic anaemia
1. Autoimmune 2. Infections 3. Secondary to systemic disease
46
What would you see on a blood film of a patient with haemolytic anaemia?
Schistocytes
47
What is aplastic anaemia?
When bone marrow stem cells are damaged -> pancytopenia.
48
What stimulates EPO?
Tissue hypoxia.
49
Name a primary cause of polycythaemia.
Polycythaemia rubra vera - over reactive bone marrow.
50
Give 3 secondary causes of polycythaemia.
1. Heavy smoking. 2. Lung disease. 3. Cyanotic heart disease. 4. High altitude.
51
What is neutrophilia?
Too many neutrophils.
52
Give 3 causes of neutrophilia.
Reactive - infection/ inflammation/ malignancy Primary - CML.
53
Give 3 causes of lymphocytosis.
Reactive - Viral infections/ Inflammation/Malignancy. Primary - CLL.
54
What is thrombocytopenia?
Not enough platelets.
55
Give examples of two Haemoglobinopathies
1. Sickle cell disease (disorder of quality) | 2. Thalassemia (disorder of quantity)
56
Give examples of 2 membranopathies
1. Spherocytosis | 2. elliptocytosis
57
Give an example of an enzymopathy
Glucose 6 phosphate dehydrogenase deficiency
58
What is sickle cell disease?
A haemoglobin disorder of quality. HbS polymerises -> sickle shaped RBC.
59
What is the advantage of being a carrier of sickle cell disease?
Carriage offers protection against falciparum malaria.
60
Describe the inheritance pattern of sickle cell disease.
Autosomal recessive. Sickle cell disease is homozygous SS.
61
If both parents are carriers of the sickle trait. What is the chance that their first child will have sickle cell disease?
Their offspring have a 1/4 chance of being affected with a sickle cell disease. (50% chance of being a carrier).
62
How long do sickle cells last for?
5-10 days - this explains why sickle cell disease is described as haemolytic.
63
Give 4 acute complications of sickle cell disease.
1. Very painful crisis. 2. Stroke in children. 3. Cognitive impairment. 4. Infections.
64
Give 3 chronic complications of sickle cell disease.
1. Renal impairment. 2. Pulmonary hypertension. 3. Joint damage.
65
Describe the treatment for sickle cell disease.
1. Transfusion. 2. Hydroxycarbamide. 3. Stem cell transplant.
66
What is the mutation that causes sickle cell disease?
1. Point mutation of the Beta globin gene 2. Valine to Glutamine 3. Resulting in a HS variant.
67
What is the significance of parvovirus for someone with sickle cell disease?
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.
68
What is the affect of sickle cell anaemia on reticulocyte count?
Reticulocyte count is raised.
69
What can precipitate sickling in sickle cell anaemia?
Trauma, cold, stress, exercise.
70
Why does sickle cell anaemia not present until after 6 months of age?
HbF is not affected by sickle cell anaemia as it is made up of 2 alpha and 2 gamma chains.
71
What drug can be used to prevent painful crises in people with sickle cell anaemia?
Hydroxycarbamide
72
How would you detect the presence of sickle cell disease on investigation?
1. Hb ELECTROPHARESIS | 2. HbSS present and absent HbA.
73
What is thalassaemia?
A haemoglobin disorder of quantity. There is reduced synthesis of one or more globin chains with leading to a reduction in Hb -> anaemia.
74
If someone has beta thalassaemia do they have more alpha or beta globin chains?
They have very few beta chains, alpha chains are in excess.
75
What is the clinical classification of beta thalassaemia?
1. Thalassaemia major. 2. Thalassaemia intermedia. 3. Thalassaemia carrier/heterozygote.
76
Which clinical classification of thalassaemia relies on regular transfusions?
Thalassaemia major.
77
Which clinical classification of thalassaemia is often asymptormatic?
Thalassaemia carrier/heterozygote.
78
When do people with beta thalassaemia major usually present and why?
These patients usually present very young due to having severe anaemia and so a failure to feed/thrive.
79
Why is it important to monitor iron levels in someone with beta thalassaemia major?
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
What might you see on a blood count taken from someone with beta thalassaemia major?
1. Raised reticulocyte count. | 2. Microcytic anaemia.
81
Describe the inheritance pattern for membranopathies.
Autosomal dominant.
82
Briefly describe the physiology of membranopathies.
Deficiency of red cell membrane proteins caused by genetic lesions
83
What is the treatment for membranopathies?
1. Folic acid | 2. Splenectomy
84
Why does a deficiency in glucose-6-phosphate dehydrogenase lead to shortened red cell lifespan?
G6PD protects cells against oxidative damage.
85
How is G6PD deficiency inherited?
X linked | but women can be effected
86
What would you see on a blood film of a Pt with G6PD deficiency?
1. Bite cells | 2. Blister cells
87
Give 3 signs of G6PD deficiency.
Crises characterised by: 1. Haemolysis. 2. Jaundice. 3. Anaemia.
88
What is the normal HB range for males/females?
Male Hb = 131 – 166 g/L | Female Hb = 110 – 147 g/L
89
What is anaemia?
Reduced red cell mass | +/- reduced haemoglobin concentration
90
If a patient presents with combined haematinic deficiency what is the most likely cause?
Malabsorption!
91
What is the difference between alpha and beta thalassaemia in terms of mechanism?
1. BOTH = Insufficient globin chains cause precipitation of dominant chain 2. Deletional (B thal) Mutational (a thal)
92
What is polycythaemia?
Too many RBC's, an increase in Hb.
93
What 3 blood test values would be increased in someone with polycythaemia?
1. Hb. 2. RCC. 3. PCV (packed cell volume/ haematocrit)
94
Give 3 symptoms of polycythaemia.
1. Itching. 2. Headache. 3. Dizziness. 4. Visual disturbance.
95
What is the main cause of Polycythaemia rubra vera?
JAK2 mutation (95%)
96
What is the treatment for polycythaemia rubra vera?
1. ASPIRIN | 2. venesection
97
What are the causes of severe neutropenia?
UNDERPRODUCTION Marrow failure Marrow infiltration Marrow toxicity e.g. drugs INCREASED REMOVAL Autoimmune Felty’s syndrome Cyclical
98
How does warfarin work?
It antagonises vitamin K and so you get a reduction in clotting factors 2, 7, 9 and 10.
99
How does heparin work?
It activates antithrombin which then inhibits thrombin and factor Xa.
100
What is disseminated intravascular coagulation (DIC)?
1. Clotting occurs inappropriately and diffusely, until clotting factors are exhausted. 2 At this point uncontrolled bleeding occurs.
101
Give 3 causes of disseminated intravascular coagulation (DIC).
1. Sepsis 2. Major trauma 3. Malignancy
102
What is the affect on fibrinogen in someone with disseminated intravascular coagulation (DIC)?
Decreased!
103
What blood results would a patient with DIC show?
1. Thrombocytopenia 2. prolonged PT + APTT (activated prothrombin time) 3. low fibrinogen 4. high d-dimers +/- evidence of organ failure
104
Name 2 things that are increased and 2 that are decreased in DIC.
Increased: PTT and APTT. Decreased: fibrinogen and platelets.
105
Give 2 causes of thrombocytopenia.
1. Production failure e.g. marrow suppression, marrow failure. 2. Increased removal e.g. immune response (ITP), consumption (DIC), splenomegaly.
106
What is the most common cause of thrombocytopenia?
Immune thrombocytopenic purpura (ITP)
107
What is Immune thrombocytopenic purpura?
Autoimmune destruction of platelets often triggered by VIRAL infection/malignancy
108
How would you treat Immune thrombocytopenic purpura?
1. Corticosteroids - prednisolone 2. Splenectomy 3. IV Ig
109
What is Thrombotic thrombocytopenic purpura?
Extensive microvascular clots form in small vessels in the body, resulting in a low platelet count and organ damage.
110
What are clinical features of platelet dysfunction?
MUCO-CUTANEOUS PATTERN 1. Mucosal bleeding 2. Epistaxis, gum bleeding, menorrhagia 3. Easy bruising 4. Petechiae, purpura 5. Traumatic haematomas (inc subdural)
111
How would you treat Thrombotic thrombocytopenic purpura?
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
What is haemophilia?
X-linked recessive disorders, deficient in clotting factors
113
What are the main 2 types of haemophilia?
``` Haemophilia A (most common) - reduction in factor 8 ``` Haemophilia B - reduction in factor 9
114
What would the PTT be like of a Pt with haemophilia?
1. Normal PTT (prothrombin time) 2. PROLONGED APTT (activated partial thromboplastin time) PTT → Extrinsic pathway APTT → intrinsic pathway
115
Give 5 risk factors for DVT.
1. Increasing age. 2. Obesity. 3. Pregnancy. 4. OCP (hyper-coagulability). 5. Major surgery. 6. Immobility. 7. Past DVT.
116
Give 3 symptoms of DVT.
Unilateral warm, tender, painful, swollen leg.
117
What forms the differential diagnosis for a DVT?
Cellulitis
118
What investigations might you do in someone to see if they have a DVT?
1. D-dimer in those patients with a low clinical probability. 2. US compression.
119
What is the name of the score used to determine someones probability of having a DVT?
Wells score
120
The Wells score determines someones clinical probability of having a DVT. Give 3 factors the score takes into account.
1. Active cancer. 2. Recently bedridden or major surgery. 3. Tenderness along deep venous system. 4. Swollen leg/calf. 5. Unilateral pitting oedema.
121
Describe the management for a DVT.
Aim of management is to prevent a PE! | - Anticoagulants - LMWH, warfarin
122
What is the most important medical treatment for DVT prophylaxis?
LMWH
123
How is malaria transmitted?
1. Protazoal infection by Plasmodia falciparim | 2. female Anopheles mosquito (Vector)
124
What are the stages of the plasmodia life cycle in the human called?
Exo-erythrocytic and endo-erythrocytic stages
125
What happens in the stages of the plasmodia life cycle that occur inside the human?
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
What signs and symptoms might you see in someone who has been infected with malaria?
1. Chills/sweats 2. Jaundice/ Hepatosplenomegaly 3. Anaemia/fatigue 4. Black urine (Black water fever) FEVER + EXOTIC TRAVEL= MALARIA (until proven otherwise)
127
Malaria diagnosis: what can thick and thin films tell you?
- Thick films: sensitive but low resolution, tell you if you have malaria. - Thin films: tell you species and parasite count.
128
What is the pathophysiology of malaria?
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
Give 4 complications of malaria
1. Cerebral malaria 2. ARDs 3. Hypoglycemia 4. Renal failure 5. Shock
130
What investigations should you carry out on a patient with suspected malaria?
1. Blood film 2. PREGNANCY TEST 3. Rule out meningitis!!
131
How do you treat malaria?
Quinine and doxycycline
132
What is leukaemia?
A malignant proliferation of haemopoietic stem cells.
133
What is acute myeloid leukaemia?
Neoplastic proliferation of blast cells.
134
What can increase the risk of developing AML?
1. Preceding haematological disorders. 2. Prior chemotherapy. 3. Exposure to ionising radiation. 4. Downs syndrome
135
Give 5 symptoms of leukaemia.
1. Anaemia. 2. Infection. 3. Bleeding. 4. Hepatomegaly. 5. Splenomegaly.
136
Why are anaemia, infection and bleeding symptoms of leukaemia?
Bone marrow failure
137
Why are hepatomegaly and splenomoegaly symptoms of leukaemia?
Tissue infiltration
138
What investigations might you do on someone who you suspect has leukaemia?
1. Blood film. 2. Bone marrow biopsy. 3. Lymph node biopsy. 4. Immunophenotyping. 5. Cytogenetics.
139
What is histologically characteristic of AML?
AUER RODS (indicative of myeloblasts)
140
What is a distinctive presenting feature of AML?
Swollen gums
141
What is ALL?
Acute lymphoid leukaemia. There is uncontroleld proliferation of immature lymphoblast cells.
142
What are 3 characteristic features of ALL?
1. Lymphadenopathy 2. Hepatosplenomegaly 3. CNS symptoms
143
Which cell proliferation is most commonly seen in ALL?
B cell
144
How would you treat ALL/AML?
1. Chemo 2. Bone marrow transplant 2. Steroids
145
Why would you also prescribe Allopurinol?
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
What is CML?
Chronic myeloid leukaemia, there is uncontrolled clonal proliferation of basophils, eosinophils and neutrophils.
147
What would the FBC from someone with CML look like?
High WBC's.
148
What chromosome is present in >80% of people with CML?
Philadelphia chromosome
149
What is the treatment for CML?
IMATINIB - tryosine kinase inhibitor
150
How would a typical patient with CML present?
Mostly asymptomatic BUT can have B symptoms and hepatosplenomegaly
151
What are the risk factors for CML?
- middle aged | - ionising radiation
152
What is CLL?
Chronic lymphoid leukaemia. Proliferation of B lymphocytes leads to the accumulation of mature B cells that have escaped apoptosis.
153
What would you see on a blood film for a patient with CLL?
Smear cells
154
What can be used as a good prognostic tool for survival in patients with CLL?
Telomere length
155
What is the epidemiology of CLL?
Old, white, men (often accidental finding and people die with the disease)
156
What is the most common form of leukaemia?
Chronic lymphoid leukaemia
157
What is lymphoma?
A malignant growth of WBC's predominantly in the lymph nodes.
158
Although predominantly in the lymph nodes, lymphoma is systemic. What other organs might it effect?
1. Blood. 2. Liver. 3. Spleen. 4. Bone marrow.
159
Give 4 risk factors for lymphoma.
1. Primary immunodeficiency. 2. Secondary immunodeficiency e.g. HIV. 3. Infection e.g. EBV, HTLV-1. 4. Autoimmune disorders e.g. RA.
160
Give 4 symptoms of lymphoma.
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
What are B symptoms?
1. weight loss 2. night sweats 3. malaise
162
What investigations might you do in someone who you suspect has lymphoma?
1. Blood film. 2. Bone marrow biopsy. 3. Lymph node biopsy. 4. Immunophenotyping. 5. Cytogenetics.
163
What are the symptoms of Hodgkins lymphoma?
1. Painless lymphadenopathy. | 2. Presence of 'B' symptoms e.g. night sweats, weight loss.
164
What is needed for diagnosis of Hodgkins lymphoma?
Presence of Reed-sternberg cells.
165
Describe the staging of Hodgkins lymphoma
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
What is the epidemiology for Hodgkin's lymphoma?
Bimodal incidence - young and old (20s and over 50) | risk inc. with EBV/HIV/AIDS
167
What is the treatment for stage 1 - 2A Hodgkins lymphoma?
Short course combination chemotherapy followed by radiotherapy.
168
What is the treatment for stage 2B - 4 Hodgkins lymphoma?
Combination chemotherapy.
169
What are the possible complications of treatment for Hodgkins lymphoma?
1. Secondary malignancies. 2. IHD. 3. Infertility. 4. Nausea. 5. Alopecia.
170
Describe low grade non-hodgkins lymphoma.
Slow growing, advanced at presentation, often incurable. Median survival is 10 years.
171
What is the treatment for low grade non-hodgkins lymphoma?
If symptomless - do nothing. | Radiotherapy, combination chemotherapy and mAb may be used if symptomatic.
172
Describe high grade non-hodgkins lymphoma.
Aggressive. Nodal presentation, patient unwell. Often curable.
173
Describe the treatment for high grade non-hodgkins lymphoma.
- Early: short course chemotherapy and radiotherapy. | - Advanced: combination chemotherapy and mAb.
174
Give 2 signs of non-hodgkins lymphoma
1. enlarged painless lymph nodes | 2. face oedema -> obstructed SVC
175
What is myeloma?
Malignancy of plasma cells leading to progressive bone marrow failure. It is associated with production of characteristic paraprotein, bone disease and renal failure.
176
When might nodal pain be worse in patients with lymphoma?
When drinking alcohol!
177
In order to make a diagnosis of myeloma, there must be evidence of mono-clonality. What is mono-clonality?
Abnormal proliferation of a single clone of plasma cell leading to immunoglobulin secretion and causing organ dysfunction especially to the kidney.
178
In approximately 2/3 of people with myeloma, what might their urine contain?
Ig light chains - BENCE JONES protein
179
Give 4 signs of myeloma.
CRAB! 1. Calcium is elevated. 2. Renal failure. 3. Anaemia. 4. Bone lesions (lytic)
180
Why is calcium elevated in myeloma?
There is increased bone resorption and decreased formation meaning there is more calcium in the blood.
181
Why might someone with myeloma have anaemia?
Crowding out! | The bone marrow is infiltrated with plasma cells. Consequences of this are anaemia, infections and bleeding.
182
Why might someone with myeloma have renal failure?
Due to light chain deposition.
183
What investigations might you do in someone who you suspect has myeloma?
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
What would you expect to see on the blood film taken from someone with myeloma?
Rouleaux formation (aggregations of RBC's).
185
What are you looking for on a bone marrow biopsy taken from someone with myeloma?
Increased plasma cells
186
What are you looking for on electrophoresis in a patient with myeloma?
Monoclonal protein band.
187
What are you looking for on an X-ray taken from someone with myeloma?
Lytic bone lesions - ( long bones, pelvis and spine) Pepperpot skull!
188
Describe the treatment for symptomatic myeloma.
Chemotherapy, analgesia and bisphosphonates. Radiotherapy and bone marrow transplant can also be done.