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Finals > Haematology > Flashcards

Haematology Flashcards

1
Q

What is used to diagnose anaemia

A

Low haemoglobin

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2
Q

If you have a patient with low haemoglobin, what would you then check

A

Mean cell volume

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3
Q

Normal haemoglobin? For women and men?

A

Women- 120-165 g/l
Men- 130-180 g/l

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4
Q

Normal mean cell volume

A

80-100 femtolitres

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5
Q

3 types of anaemia

A

Microcytic
Normocytic
Macrocytic

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6
Q

Microcytic anaemia causes

A

‘TAILS’
T- thalassaemia
A- anaemia of chronic disease
I- iron deficiency anaemia
L- lead poisoning
S- sideroblastic anaemia- enough iron but not used —> same effect as iron deficiency

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7
Q

Normocytic anaemia causes

A

‘3As and 2 Hs’
A- acute blood loss
A- anaemia of chronic disease
A- apastic anaemia
H- haemolytic anaemia
H- hypothyroidism

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8
Q

What type of anaemia can hypothyroidism cause?

A

Normocytic anaemia

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9
Q

Megaloblastic anaemia causes

A

B12 deficiency
Folate deficiency

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10
Q

Normoblastic anaemia causes

A

Alcohol
Reticulocytosis- usually from haemolytic anaemia or blood loss
Hypothyroidism
Liver disease
Drugs e.g. azathioprine

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11
Q

Two types of macrocytic anaemia and difference between them?

A

Megaloblastic and normoplastic

Megaloblastic- caused by impaired DNA synthesis meaning cell can’t divide normally, instead of dividing just grows

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12
Q

Symptoms of anaemia

A

Tiredness
SOB
headaches
Dizziness
Palpitations
Worsening other conditions e.g. angina, HF, peripheral vascular disease

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13
Q

Symptoms specific to iron deficiency anaemia

A

Pica- dietary cravings for abnormal things

Hair loss

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14
Q

Generic signs of anaemia

A

Pale skin
Conjunctival pallor
Tachycardia
Raised resp rate

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15
Q

Specific signs of iron deficiency anaemia

A

Koilonychia- spoon shaped nails
Angular chelitis- sores on side of mouth
Atrophied glossitis- smooth tongue due to atrophy of papillae
Brittle hair and nails

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16
Q

What type of anaemia would jaundice indicate?

A

Haemolytic anaemia

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17
Q

Investigations for anaemia

A

Haemoglobin
Mean cell volume
B12
Folate
Ferritin
Blood film

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18
Q

Where is iron absorbed

A

Duodenum and jejunum

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19
Q

Iron needs to remain in the Fe2+ form to be absorbed. What medication can alter this and why?

A

PPIs
Stomach acid keeps iron in Fe2+ form. Without iron turns to Fe3+ which can’t be absorbed. PPIs can reduce acid and reduce iron absorption

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20
Q

What inflammatory conditions can cause iron deficiency anaemia and why?

A

Iron absorbed in duodenum and jejenum so inflammation here can reduce absorption.

Coeliac disease
Crohn’s disease

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21
Q

General causes of iron deficiency anaemia

A

Insufficient dietary intake
Increased iron requirements e.g. pregnancy
Iron lost e.g. slow bleed e.g. colon cancer
Inadequate absorption e.g inflammation in Bowel

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22
Q

Most common causes of iron deficiency anaemia in adults and children

A

Adults- blood loss
1st- menstruating women
Then, GI tract
Most common: oesophagitis and gastritis
Consider: GI tract cancer, Crohn’s or UC

Children- dietary insufficiency

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23
Q

What carrier protein carries iron around the blood?

A

Transferrin

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24
Q

What is ferritin

A

Form iron takes when deposited and stored in cells

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25
Q

What causes increased ferritin in blood

A

Any form of inflammation e.g. infection or cancer

Low ferritin in blood highly suggestive of iron deficiency

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26
Q

What does high and low ferritin levels in blood indicate

A

Low: likely iron deficiency anaemia

High: likely related to inflammation rather than iron overload.

Can still have normal ferritin with iron deficiency anaemia

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27
Q

What test is more commonly used to measure transferrin in blood

A

Total iron binding capacity

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28
Q

What happens to Total Iron Binding Capacity (TIBC) in iron deficiency

A

Increases
Indicates increased transferrin

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29
Q

What happens to TIBC and transferrin levels in iron overload

A

Decreases

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30
Q

What investigation is done for unclear cause of iron deficiency anaemia

A

Oesophago-gastroduodenoscopy (OGD) and colonoscopy to rule out cancer of GI tract

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31
Q

Management of iron deficiency anaemia

A

Depends on severity

Blood transfusion
Iron infusion e.g. cosmofer. Avoid in sepsis
Oral iron e.g. ferrous sulphate 200mg TDS. Expect 10g/l per week

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32
Q

What protein is needed for the absorption of vitamin B12?

A

Intrinsic factor

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33
Q

What is the Pathao physiology of pernicious anaemia?

A

Autoimmune condition. Antibodies against parietal cells or intrinsic factor. Therefore vit B12 can’t be absorbed

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34
Q

Symptoms of Vit B12 deficiency

A

Peripheral neuropathy- numbness and tingling in hands and feet
Loss of vibration sense or proprioception
Visual changes
Mood or cognitive changes

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35
Q

Diagnostic investigation for pernicious anaemia

A

Instrinsic factor antibody- 1st line
Gastric parietal cell antibody- sometimes also done

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36
Q

Management of dietary cause of B12 deficiency

A

Cyanocobalamin

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37
Q

Management of pernicious anaemia

A

Absorption problem!
Hydroxycobalamin 1mg IM, 3 times weekly, for 2 weeks. Then every 3 months

If neuro symptoms e.g. 1mg every other day til improvement in symptoms

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38
Q

If folate and B12 deficiency simultaneously, how would you treat it?

A

Treat B12 deficiency first- dietary cyanocobalamin or IM hydroxycobalamin
Then treat folate deficiency

If given folic acid with B12 deficiency, can cause subacute combined degeneration of cord

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39
Q

Two main types of haemolytic anaemia?

A

Inherited
Acquired

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40
Q

Types of inherited haemolytic anaemias? (5)

A

Hereditary spherocytosis
Hereditary elliptocytosis
Thalassaemia
Sickle cell anaemia
G6PD deficiency

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41
Q

Acquired haemolytic anaemias?

A

Autoimmune haemolytic anaemia
Alloimmune haemolytic anaemia (transfusionrractions and haemolytic disease of newborn)
Paroxysmal nocturnal haemoglobinuria
Microangiopathic haemolytic anaemia
Prosthetic valve related haemolytic

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42
Q

Features of haemolytic anaemias

A

Features of destroyed RBCs
- anaemia
- spenomegaly
- jaundice

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43
Q

What would a FBC and a blood film show in haemolytic anaemia?

A

FBC- Normocytic anaemia
Blood film- schistocytes- fragments of RBCs

( direct Coombs test is +ve in autoimmune haemolytic anaemia)

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44
Q

How is hereditary spherocytosis inherited?

A

Autosomal dominant
(Most common inherited haemolytic anaemia in Northern Europe)

Sphere shaped RBCs that easily break down when passing through spleen

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45
Q

How would hereditary spherocytosis usually present?

A

Jaundice
Gallstones
Splenomegaly
Often in an aplastic crisis due to parvovirus

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46
Q

How is hereditary spherocytosis diagnosed?

A

Clinical and family history
Spherocytes on blood film
FBC- raised MCHC (mean corpuscular haemoglobin conc)
Raised reticulocytes- rapid turnover of RBCs

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47
Q

Treatment for hereditary spherocytosis?

A

Folate supplements
Splenectomy
+/- cholecystectomy if gallstones problematic

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48
Q

Difference between hereditary spherocytos and hereditary elliptocytosis?

A

Presentation and management the same.
Elliptocytosis has ellipse shaped RBCs rather than sphere shaped

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49
Q

What is G6PD deficiency inheritance pattern?

A

X linked recessive

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50
Q

What often can cause a G6PD deficiency crisis? (Key info for exams is G6PD triggers)

A

Infections
Medications - primaquine (antimalarial), ciprofloxacin, sulfonyureas, sulfasalazine, other sulphonamide drugs

Fava beans- broad beans

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51
Q

How does G6PD deficiency usually present?

A

Jaundice- usually neonatal
Gallstones
Anaemia
Splenomegaly
HEINZ BODIES on blood film

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52
Q

How is G6PD deficiency diagnosed?

A

G6PD enzyme assay

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53
Q

Two types of autoimmune haemolytic anaemia?

A

‘Warm type’ and ‘Cold type’ autoimmune haemolytic anaemia
Due to the antibodies having different effects at different temps.

Warm more common

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54
Q

What is cold type autoimmune haemolytic anaemia often secondary to?

A

Aka- cold agglutin disease

Lymphoma, leaukaemia, lupus, infections e.g. mycoplasma, EBV, CMV, HIV

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55
Q

Management of autoimmune haemolytic anaemias?

A

Blood transfusions 🩸
Prednisolone/ steroids
Rituximab- monoclonal antibody against B cells
Splenectomy

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56
Q

What causes alloimmune haemolytic anaemia?

A

Blood transfusions or haemolytic disease of the newborn.
Due to foreign RBCs or antibodies in blood

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57
Q

How does paroxysmal nocturnal haemoglobinuria usually present?

A

Red urine in morning (containing haemoglobin and haemosiderin)
Or thrombosis: PE, DVT, hepatic vein thrombosis
Smooth muscle dystonia e.g. oesophageal spasm or erectile dysfunction

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58
Q

Management of paroxysmal nocturnal haemoglobinuria

A

Eculizumab- monoclonal antibody targets complement component 5 in complement system
Or bone marrow transplant

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59
Q

What’s the pathophysiology of paroxysmal nocturnal haemoglobinuria?

A

A genetic mutation in haematopoietic stem cells in bone marrow occurs in patients lifetime
Results in loss of proteins on surface of RBCs that inhibit the complement system

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60
Q

What is the pathophysiology of microangiopathic haemolytic anaemia? (MAHA)

A

Structural abnormalities in small blood vessels cause haemolysis of RBCs. Usually secondary to an underlying condition

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61
Q

What conditions is microangiopathic haemolytic anaemia often secondary to?

A

Haemolytic uraemia syndrome
DIC
TTP- thrombotic thrombocytopenia purpura
SLE
Cancer

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62
Q

Management of prosthetic valve haemolysis?

A

Monitor
Oral iron
Blood transfusion if severe
Revision surgery if needed

63
Q

What chains does normal haemoglobin consist of?

A

2 alpha chains
2 beta globin chains

64
Q

What are the 2 types of thalassaemia?
How are they inherited?

A

Alpha thalassaemia- defects in alpha-globin chains
Beta thalassaemia- defects in beta-globin chains

Both autosomal recessive

65
Q

Pathophysiology of thalassaemia?

A

Altered alpha or beta chains meaning RBCs are more fragile so break down easily and collect in spleen
Bone marrow expands to produce more RBCs so more susceptible to fractures and prominent features e.g. forehead and cheekbones (malar eminences)

66
Q

Signs and symptoms of thalassaemia?

A

Microcytic anaemia- low mean corpuscular vol
Generic anaemia sx- fatigue, pallor
Jaundice
Gallstones
Spenomegaly
Poor growth
Pronounced forehead and malar eminences (cheek bones)

67
Q

How is thalassaemia diagnosed?

A

FBC- microcytic anaemia
Haemoglobin electrophoresis- ?globin abnormalities
DNA testing

Pregnant women offered screening

68
Q

What’s a common long term problem seen in treated thalassaemia patients?

How is this monitored?

How is it managed?

A

Iron overload- due to faulty RBCs, transfusions and increased iron absorption in response to anaemia

Serum ferritin

Iron chelation

69
Q

How does iron overload present?

A

Often seen in thalassaemia patients

Similar to haemochromotisisn:

Fatigue
Liver cirrhosis
Infertility and impotence
Heart failure
Arthritis
Diabetes
Osteoporosis and joint pain

70
Q

Where are the genes for alpha and beta thalassaemia coded?

A

Alpha- chromosome 16
Beta- chromosome 11

71
Q

What are the 3 types of beta thalassaemia?

A

Thalassaemia minor
Thalassaemia intermedia
Thalassaemia major

Gene defect can be abnormal copies and retain some function or deletion with no function.

72
Q

What is the pathophysiology and therefore presentation of thalassaemia minor?

A

Only 1 abnormally functioning gene (no deletion) and 1 normal —> mild microcytic anaemia

Monitor

73
Q

What is the pathophysiology and therefore presentation of thalassaemia intermedia?

A

2 abnormal genes or 1 abnormal with 1 deletion.

More severe microcytic anaemia

Monitoring, possible blood transfusion

74
Q

What is the pathophysiology and therefore presentation of thalassaemia major?

A

Homozygous deletion (rather than just abnormal)

… severe microcytic anaemia (often failure to thrive young)
Splenomegaly
Bone deformities

Regular transfusions
Iron chelation
Splenectomy
Bone marrow transplant- ?curative

75
Q

How is sickle cell anemia inherited.

A

Autosomal recessive. Genetic advantage for carrier for malarial resistance.

Abnormal gene on beta globin chain on chromosome 11

76
Q

Complications of sickle cell anaemia

A

Anaemia
Increased risk of infection
Stroke
Avascular necrosis in larger joints e.g. hip
Pulmonary hypertension
Priapism- painful persistent erection
CKD
SSickle cell crisis
Acute chest syndrome

77
Q

What are known triggers of a sickle cells crisis?

A

Infection
Dehydration
Cold
Stress

78
Q

What is a splenic sequestration crisis? How is it managed?

A

Sickle cells blocking blood flow to spleen —> enlarged painful spleen —> pooling in spleen —> severe anaemia and hypovolaemic shock

Supportive, blood transfusions, fluid resus for anaemia and shock.
Splenectomy preventative

79
Q

What is an aplastic crisis?
How is it managed?

A

Temporary pause in creation of new blood cells
Most often caused by parvovirus B19

Significant anaemia

Supportive: blood transfusions if needed. Often resolves within a week

80
Q

What is Acute chest syndrome?

A

Diagnosis:
Fever or resp symptoms with
New infiltrates on X-ray

Due to infection or noninfection e.g pneumonia, bronchiolitis, pulmonary vasoocclusion, fat emboli

81
Q

How is Acute chest syndrome managed?

A

Treat underlying cause
Medical emergency with high mortality

Antibiotics or antivirals for infections
Blood transfusion for anaemia
Incentive spirometry - machine encourages better breathing
Artificial ventilation ?intubation

82
Q

What are the four main types of leukaemia?

A

Acute myeloid leukaemia
Acute lymphoblastic leukaemia
Chronic myeloid leukaemia
Chronic lymphocytic leukaemia

83
Q

What are the two cell lines that are affected in leukaemia?

A

Myeloid
Lymphoid

84
Q

What is leukaemia?

A

Cancer of line of stem cells in bone marrow leading to excessive production of a type of abnormal white blood cell.

Excess production can lead to suppression and underproduction of other cell lines leading to PANCYTOPENIA (anaemia, leukopenia, thrombocytopenia)

85
Q

Most common ages for the different leukaemias

A

“ALL CeLLmates have CoMmon AMbitions” - ages from 45 to 75 in 10year jumps.

ALL- (under 5s) and over 45
CL- over 55
CM- over 65
AM- over 75

86
Q

What are some typical features of leukaemia?

A

Fatigue
Fever
Failure to thrive in children
Pallor (anaemia)
Petechiae and bruising (thrombocytopenia)
Abnormal bleeding
Lymphadenopathy
Hepatospenomegaly

87
Q

Differentials of petechiae?

A

Caused by thrombocytopenia

Leukaemia
Meningococcal septicaemia
Vasculitis
HSP
Idiopathic thrombocytopenia purpura (ITP)
Non accidental injury

88
Q

Diagnosis of leukaemia?

A

FBC- pancytopenia
Blood film- abnormal cells?
Lactate dehydrogenase (LDH)- often raised but not specific
!!Bone marrow biopsy- definitive diagnosis
Chest X-ray- infection or lymphadenopathy?
Lymph node biopsy- involvement or lymphoma?
LP- if CNS involvement?
CT, MRI, PET for staging

89
Q

Which type of leukaemia is linked with Down’s syndrome?

A

Acute lymphoblastic leukaemia (ALL)

90
Q

What would be seen on a blood film in ALL

A

Blast cells

91
Q

What gene mutation is associated with ALL? Although less strongly associated than CML

A

Philadelphia chromosome- t(9:22) translocation
30% adults
3-5% children

92
Q

What type of lymphocyte is usually abnormally proliferating in ALL and CLL

A

Often B lymphocytes

93
Q

Warm autoimmune haemolytic anaemia can be caused by ….. leukaemia

A

Chronic lymphocytic leukaemia

94
Q

Chronic lymphocytic leukaemia can transform into …..
This is called ….. transformation

A

Into high grade lymphoma
Called Richter’s transformation

95
Q

What is Richter’s transformation?

A

CLL transforms into a high grade lymphoma

96
Q

What’s seen on blood film in CLL?

A

Smear and smudge cells
Occurs when blood is smeared, fragile WBCs rupture leaving the smudge/smear appearance

97
Q

What are the three typical phases of CML?

A

Chronic phase- can last 5 years, often asymptomatic, often incidental finding

Accelerated phase- take up 10-20% of bone marrow and blood. Symptomatic: anaemia, thrombocytopenia, immunocompromised

Blast phase- >30% blast cells in bone marrow and blood. Severe symptoms and pancytopenia. Often fatal

98
Q

Characteristic genetic association with CML?

A

Philadelphia chromosome. Translocation between chromosome 9 and 22. A t(9:22) translocation

99
Q

Most common leukaemia in adults?

A

AML

100
Q

AML can result from a myeloproliferative disorder such as…

A

Polycythaemia rubra vera
Myelofibrosis

101
Q

What will a blood film show in AML?

A

High proportion of blast cells
AUER RODS in cytoplasm

102
Q

What type of leukaemia is associated with Auer rods

A

Acute myeloid leukaemia

103
Q

What malignancy type is most often associated with Philadelphia chromosome?

A

Chronic myeloid leukaemia

104
Q

What are the mainstay treatment options for leukaemias?

A

Chemotherapy
Steroid
+/-
Radiotherapy
Bone marrow transplant
Surgery

105
Q

Complications of chemotherapy?

A

Failure
Stunted growth in children
Infections due to immunodeficiency
Neurotoxicity
Infertility
Secondary malignancy
Cardiotoxicity
Tumour lysis syndrome

106
Q

What is tumour lysis syndrome?

A

Caused by release of uric acid from cells destroyed by chemo —> form crystals in interstitial tissues and kidney tubules —> AKI

Can also release potassium and phosphate (phosphate can reduce calcium. All monitored

107
Q

Two main types of lymphoma?

A

Hodgkin’s - a specific disease
Non-hodgkins -all other lymphomas

1 in 5 lymphomas are Hodgkins

108
Q

What age is Hodgkin’s lymphoma normally seen?

A

Bimodal distribution
~20yo and 75yo

109
Q

Risk factors for Hodgkin’s lymphoma?

A

HIV
EBV
Autoimmune e.g. RA, sarcoidosis
Family history

110
Q

Presentation of lymphomas?

A

Lymphadenopathyx- non tender, rubbery feel. Pain with alcohol!
B symptoms- fever, weight loss, night sweats
Other generic: fatigue, itching, cough, SOB, abdo pain, recurrent infections

111
Q

Investigations for lymphoma

A

Lactate dehydrogenase- raised but non specific
Lymph node biopsy- DIAGNOSTIC
REED STEINBERG CELLS- IN HODGKINS
CT, MRI, PET diagnosis and staging

112
Q

What staging system is used for lymphoma and what are the stages?

A

Ann Arbor staging
Stage 1- only 1 region of lymph nodes
Stage 2- >1 region but same side of diaphragm
Stage 3- lymph nodes on both sides of diaphragm
Stage 4- widespread outside of lymphatics

113
Q

Management of lymphoma and their risks?

A

Chemotherapy- risk of leukaemia and infertility
Radiotherapy- risk of cancer, tissue damage and hypothyroidism

114
Q

Other more common types of non Hodgkin’s lymphoma?

A

Burkitt lymphoma- associated with EBV, malaria, HIV

MALT lymphoma- associated w H.pylori (mucosa associated lymphoid tissue, usually around stomach)

Diffuse large B cell lymphoma- rapidly growing painless mass in patients over 65

115
Q

Risk factors for non Hodgkin’s

A

HIV
EBV
H.pylori (MALT lymphoma)
Hep B and C infection
Exposure to pesticides, TRICHLOROETHYLENE used in some industrial processes
Family history

116
Q

Monoclonal antibodies can be used to treat some non Hodgkin’s lymphomas such as…

A

Rituximab

117
Q

What is myeloma?

A

Cancer of plasma cells. Type B lymphocytes (that produce antibodies)
Results in abnormal cell proliferation of one type of B cell —> high quantity of a single antibody.
Accounts for 1% of all cancers

118
Q

What’s the difference between myeloma and multiple myeloma?

A

Multiple myeloma is myeloma affecting multiple parts of the body

119
Q

What is Monoclonal gammopathy of undetermined significance (MGUS)?

A

Excess of single type of antibody with no other features.
May later progress
Monitored

Can lead to smouldering myeloma. Progression of MGUS, higher levels, premalignant.

Waldenstrom’s macroglobulinemia- a smouldering myeloma specifically excess IgM

120
Q

What are the 5 main types of immunoglobulin (antibody)

A

IgA, IgG, IgM, IgD, IgE

121
Q

What antibody most commonly is affected/raised in myeloma?

A

IgG, in >50% of cases
When the single antibody is overproduced in by the identical cancerous B/plasma cells, they’re called monoclonal paraproteins

122
Q

What protein is often seen in the urine of patients with myeloma?

A

Bence Jones proteins.
They’re a subunit of antibodies called light chains

123
Q

What disease are Bence Jones proteins seen in and where are they found?

A

Myeloma
In urine

124
Q

What areas are more commonly affected by myeloma?
What occurs at these bony areas?

A

Skull, spine, long bones, ribs.

Infiltration of bone marrow can cause osteolytic lesions —> pathological #s

125
Q

Why is hypercalcaemia often see in myeloma?

A

Bone marrow infiltration. Causes increased osteoclast activity and reduced osteoblast activity. More bone break down —> increased release of calcium from bone —> hypercalcaemia

126
Q

How does myeloma sometimes lead to myeloma renal disease?

A

High immunoglobulin levels can block tubules
Hypercalcaemia impairs renal function
Dehydration
Treatment medications e.g. bisphosphonates can damage kidneys

127
Q

Four key features to remember for my myeloma?

A

CRAB

C - Calcium elevated
R - Renal failure
A - Anaemia- Normocytic normochromic from replacement bone marrow
B - Bone lesions/pain

128
Q

Risk factors for myeloma

A

Older age
Male
Black African
Family history
Obesity

129
Q

Acronym for remembering myeloma investigations?

A

BLIP

B - Bence jones protein- request urine electrophoresis
L - serum free light chain assay
I - serum immunoglobulins
P - serum protein electrophoresis

Bone marrow biopsy- DIAGNOSTIC

130
Q

Imaging looking for bone lesions? And preferred order

A

Whole body MRI
Whole body CT
Skeletal survey- full body xrays

131
Q

X-ray signs in multiple myeloma

A

Punched out lesions
Lyric lesions
‘Raindrop skull’- due to lyric lesions on skull

132
Q

First line treatment for myeloma?

A

Chemotherapy with
- bortezomoid
- thalidomide
- dexamthasone

For myeloma bone disease —> bisphosphonates
Bone pain/lesions —> radiotherapy
Orthopaedic surgery to stabilise #s
Cement augmentation

133
Q

What are the three most common myeloproloferative disorders?
And what are each of the cell lines affected?

A

Primary myelofibrosis- haemopoietic stem cells

Polycythaemia vera - erythoid cell line

Essential thrombocytopenia - megakaryocytic cell line

134
Q

What disease develops from the following proliferating cell lines

A

Haemopoetic stem cells —> primary myelofibrosis

Erythoid cells —> polycythaemia vera

Megakaryocyte —> essential thrombocytopenia

135
Q

What type of malignancy to myeloproliferative disorders have the potential to develop into?

A

Acute myeloid leukaemia

136
Q

What mutations are associated with myeloproliferative diseases?

A

JAK2 -remember this one!
—> Can be targeted by JAK2 inhibitors e.g. ruxolitnib
MPL
CALE

137
Q

What is myelofibrosis?

A

Where proliferation of a cell line leads to fibrosis of the bone marrow, replaced by scar tissue
Due to response to cytokines released from proliferating cells e.g. fibroblast growth factor

138
Q

If bone marrow is fibrotic, haematopoiesis (blood cell making) can start to occur in which areas?
What’s this process called?

A

Liver and spleen

Extramedullary haematopoiesis

Can lead to hepatospenomegaly and portal hypertension
Can lead to spinal cord compression if around spine

139
Q

Key signs of polycythaemia vera?

A

Conjunctival plethora (red in conjunctiva of eyes)
‘Ruddy’ complexion
Splenomegaly

140
Q

What abnormality on FBC would be seen in polycythaemia vera?

A

Raised haemoglobin
>185g/l in men
> 165 g/l in women

141
Q

What blood test results would be raised in primary thrombocythaemia?

A

Raised platelet count >600x10(9) /l

142
Q

What might you see on a blood film of someone with myelofibrosis?

A

Teardrop shaped RBCs
Poikilocytosis- varying sized RBCs
Blasts- immature red and white cells

143
Q

Management of primary myelofibrosis?

A

Mild- monitored

Allogenic stem cell transplant? Curative but risky
Chemotherapy- not curative but controls sx
Supportive mx of anaemia, splenomegaly and portal hypertension

144
Q

Management of polycythaemia vera?

A

Venesection- 1st line
Aspirin- reduced thrombosis risk
Chemotherapy- controlling disease

145
Q

Management of essential thrombocythaemia

A

Aspirin- reducing thrombus risk
Chemotherapy

146
Q

What is thrombocytopenia?

A

Low platelet count
Normal platelet 150 to 450 x10(9)/L

147
Q

What are some causes of thrombocytopenia?

A

Production problems:
Sepsis
B12 or folate deficiency
Liver failure so less thrombopoietin made
Leukaemia
Myelodysplastic syndrome:

Destruction problems:
Medications e.g. sodium valproate, methotrexate, isotrentinoin, antihistamines, PPIs
Alcohol
ITP
Heparin induced thrombocytopenia
Haemolytic uraemia syndrome

148
Q

What would a platelet count of 50x10(9) likely present with?

A

Easy bruising
Prolonged bleeding
E.g. nosebleeds, bleeding gums, heavy periods, blood in urine or stool

149
Q

What could more likely occur with a platelet count of 10x10(9)

A

High risk of haemorrhaging stroke and GI bleeds

150
Q

Key differentials fro abnormal or prolonged bleeding

A

Thrombocytopenia (low platelets)
Haemophilia A and B
Von Willebrand disease
DIC, often 2nd to sepsis

151
Q

What is ITP?

A

Immune/idiopathic/autoimmune/primary thrombocytopenic Purpura

Antibodies against platelets

152
Q

Management of ITP

A

Prednisolone
IV immunoglobulins
Rituximab- monoclonal antibody against B cells
Splenectomy

153
Q

What type of cancer is predisposed by pernicious anaemia?

A

Gastric cancer

Finals (13 decks)

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