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Phase 2a > Haemotology > Flashcards

Haemotology Flashcards

1
Q

Anaemia defenition

A
  • Low RBC mass
  • Increase plasma volume
    eg: Pregnancy
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2
Q

What does reticulocyte count indicate

A

Low - production issue

High - removal issue

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3
Q

MCV classification

A

MCV <80 - Microcytic

MCV 80-100 - Normocytic

MCV >100 - Macrocytic

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4
Q

Microcytic anaemia causes

A

Iron deficiency
- hypochromic

Chronic disease

Thalassaemia

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5
Q

Normocytic anaemia causes

A

Acute blood loss

Chronic disease

Combined haemanitic def
- Querey malabsorption

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6
Q

Macrocytic anaemia causes

A

Vit B12 def

Alcohol/liver disease

Hyperthyroidism

Folic acid def

Reticulocytosis

FAT RBC MD
D- drugs
AZT/Phenytoin

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7
Q

Serum ferritin

A

Major iron storage protein in the body
- directly measure iron levels in the body

  • Acute phase reactant so can be raised falsley in inflammand malignancy
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8
Q

Anaemia general presentation

A

Sx

  • fatigue
  • lethargy
  • dyspnoea
  • palpitations
  • headache

Signs

  • pale skin
  • pale mucous membranes
  • tachycardia (compensatory)
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9
Q

Iron deficiency causes

A 
Poor diet - low iron
Blood loss
- Menorrhagia
- GI bleeding
- Hookworm
Malabsorption - coeliac 
Pregnancy - increased requirements
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10
Q

Where is iron absorbed

A

Duodenum

*Coelaic disease - Inflamm and duodenal cell destruction

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11
Q

Iron deficiency anaemia signs

A
  • Brittle hair and nails
  • Atrophic glossitis
  • Kolionychia
  • Angular stomatitis
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12
Q

Iron deficiency anaemia investigations

A
  • Serum ferritin
  • Low serum ferritin confirms dx
  • Acute phase reactant
  • FBC
    Hypochromic microcytic anaemia
  • Reticulocyte count
  • Reduced
  • Transferrin saturation
  • LOW = Iron deficiency
    HIGH = Iron overload
  • Coeliac serology
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13
Q

Iron deficiency anaemia tx

A 
Ferrous sulphate 
S/E:
- Black stools 
- Nausea
- Constipation 
- Diarrhoea
- GI upset 
- Abdo discomfort

*Take with OJ

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14
Q

Why should you take ferrous sulphate with OJ

A

Increases acidity - helps with absorption

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15
Q

What are the promoting factors for intestinal iron absorption

A
  • Gastric acid
  • Iron def
  • Increase Erythropoeitc -activity
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16
Q

Anaemia of chronic disease

A
  • Shortening of RBC
  • RBC reduced cell production

CKD
RA
SLE
Cancer

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17
Q

Investigations for new iron def anaemia in an adult withhout a clear underlying cause

A

GI cancer investigations

  • Oesophago-gastroduodenoscopy (OGD)
  • Colonoscopy
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18
Q

What is the normal rise in iron levels for a pt recieving iron def anaemia tx

A

10 grams/ litre / week

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19
Q

Megaloblastic anaemia

A

B12 and folate

  • Inhibition of DNA synthesis
  • Continued growth without division
  • Macrocytosis
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20
Q

What are megaloblasts

A

Erythroblasts with delayed nuclear maturation due to delayed DNA synthesis

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21
Q

Folate deficiency

A
  • Anaemia

- Neural tube malformation

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22
Q

Folate sources

A 
Green leafy veg 
- Spinach 
- Brocolli 
Liver 
Kidney
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23
Q

How long is the folate store in the body + where is it basorbed

A

4 months

Jejunum

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24
Q

Causes of folate def anaemia

A
  • Poor folate diet
    Alcohol
    Poverty
  • Malabsorption
    Coeliac
    IBD - Crohns
  • Pregnancy
  • Anti flolate drug
    Methotrexate
    Phenytoin
  • Haemolysis
  • Malabsorption
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25
Q

Folate deficiency anaemia presentation

A 
Anaemia sx - 
Headache 
Pallour 
Lethargy 
Fatigue

Signs -
Glossitis
NO neuropathy

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26
Q

Folate deficiency anaemia investigations

A

Blood film -
Macrocytic anaemia
Hypersegmented neutrophil polymorphs

Red cell folate levels - LOW
*Indicates low body stores

SB biopsy only if hx does not suggest dietary deficiency - Looking for small bowel disease

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27
Q

Folate deficiency anaemia tx

A
  • Oral folic acid tablets
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28
Q

Sources of B12

A

Animal meats
Dairy
Milk

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29
Q

Length of B12 bodily stores

A

2-4 years

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30
Q

B12 deficiency anaemia

A

Prenicious anaemia

  • Megaloblastic
  • Low reticulocyte count
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31
Q

Where is B12 absorbed

A
  • Terminal ileum

- Binds to Intrinsic factor and absobed by enterocytes

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32
Q

What is prenicious anaemia

A

AI disease

  • Ab against parietal cells or Intrinsic factor
  • Prevents B12 absorption due to lack of Intrinsic factor
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33
Q

Prenicious anaemia causes

A

Atrophic gastritis
Gastrectomy
Crohns
Coeliac

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34
Q

Causes of B12 deficiency anaemia

A 
Prenicious anaemia
Ileal resection 
Crohns disease 
Gastric bypass 
- Food passes quickly (Pepsin can't act to release B12)
- Tapeworm
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35
Q

B12 def anaemia presentation

A 
Sx of anaemia
Glossitis
Angular stomatitis 
Neurological sx 
Lemon - Yellow tinge 
*pallour + mild jaundice 
*Excessive Hb breakdown as body tries to remove defective large RBC
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36
Q

Specific neurological sx of B12 def anaemia

A

Peripheral neuropathy

  • w/ numbness or paraesthesia
  • Weakness
  • Ataxia
  • Dementia
  • Hallucinations
  • Loss of vibration sense/propioception
  • Depression
  • Irritabilty
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37
Q

B12 deficiency anaemia investigations

A

Blood film

  • Macrocytic RBC
  • Hypersegmented neutrophils

Serum Ab screen
- Inrinsic factor Ab

Serum B12 Low

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38
Q

B12 def anaemia tx

A

Hydroxyxobalamin - B12

  • Tablets
  • Injections
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39
Q

B12 def anaemia complications

A

HF
Angina
Neuropathy

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40
Q

What is sickle cell disease

A

Disorder of Hb quality

  • Autosomal Recessive
  • Point mutation of the Beta globin gene resulting in a HbS variant
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41
Q

Whta is the codon chnage in sickle ell disease

A

Glutamic acid –> Valine

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42
Q

When does SCD manifest

A

After HbF levels decrease

- Approx 6 months

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43
Q

How does HbS affect oxygenation

A

HbS can carry O2 normally

  • changes shape when deoxygenated
  • allows aggregation with other HbS proteins
  • Insoluble and polymerises
  • polymerisation distorts RBC into a crescent shape
  • RBC fragile and easily haemolysed
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44
Q

Factors promoting sickling in SCD

A 
Acidosis 
Low flow vessels 
Infection
Dehydration 
Hypoxia 
Cold 
Stress
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45
Q

What does repeated sickling do to RBCs

A

Promotes premature destruction

  • Intravascular haemolysis
  • Anaemia
  • Hb spillage –> Jaundice

Impaired passage of RBCs in microcirculation due to sickling
- Small vessel obstruction
- Tissue infarction
PAIN

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46
Q

Sickle cell trait presentation

A 
Sx free with no disability unless in extreme conditions:
*Vaso-occlusive events 
- High altitude 
- Dehydration 
- Hypoxia 
Unpressured aircraft
Anasthesia
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47
Q

Benefit of sickle cell trait

A

Selective advantage of protection against Falciparum malaria

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48
Q

Sickle cell disease presentation

A 
Vaso-occlusion 
- Dactylitis 
- Avascular necrosis 
- Pain in long bones 
  spine/ribs/pelvis 
- stroke 
- seizures

Anaemia

Splenic sequestriasation

Mesenteric ischaemia

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49
Q

Long term SCD complications

A

CKD
Pulmonary HTN
Poor growth
- avascular necrosis of bones results in shortened deformed bones in kids

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50
Q

Vaso-occlusive crisis

A
  • Sickled RBCs clog up capillaries
  • Distal ischaemia
  • Assosc with:
    dehydration
    Riased haematocrit

*PRIAPISM
trapping blood in penis causing painful and persistent erection
- UROLOGICAL EMERGENCY

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51
Q

Splenic sequestrian crisis

A
  • Sickled cells block blood flow to the spleen
  • Acute enlarged and painful spleen
  • leads to:
  • Severe anaemia
  • Hypovolemic shock
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52
Q

Aplastic crisis

A
  • Temp loss of new blood ell production
  • Triggered by parvovirus B19 infection
  • Leads to severe anaemia
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53
Q

Acute chest syndrome Sx and causes

A

Sx:

  • Fever / resp sx
  • New infiltrates seen on X-ray

Causes:
- Infection (pneumonia)
- Non infective cause
(pulmonary vaso-occlusion or fat emboli)

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54
Q

Acute sickle cell disease complications

A

Sickle cell crisis
Acute chest syndrome
Haemolytic
Mesenteric ischaemia

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55
Q

Sickle cell disease investigations

A

Screen neonates - Blood/Heel prick test

FBC -
Hb
Reticulocyte

Blood film -
Sickled erythrocytes

Hb electropharesis

  • HbSS present
  • HbA absent
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56
Q

Sickle cell disease management

A
  • Analgesia
  • Tx underlying cause: Abx
  • Fluids
  • Folic acid
  • Tranfuse when falling Hb
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57
Q

Disease modifying tx SCD

A

Hydroxycarbamide

  • Increase gamma and foetal globin
  • HbS cannot polymerise as HbF gets in its way so prevents sickling

Stem cell transplant

Blood transfusion
*Beware iron overload

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58
Q

Alpha - Thalassaemia

A

Deficiency in alpha chain synthesis in red cell precursors

  • Caused by gene deletions found on chromosome 16
  • Protection from falciparum malaria
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59
Q

Thalassaemia

A
  • Hb quantity disease
  • AR disease
  • Precipitation of globin chains on:
  • RBC precursors –> ineffective erythropoesis

*Mature RBC –> Haemolysis

Faulty production and premature destruction

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60
Q

Thalassaemia

  • Spleen
  • Bone marow
A

Splenomegaly
- filters blood to collect destroyed RBCs causing swelling

BM expansion

  • Compensate for chronic anaemia
  • Susceptibility to fractures
  • Prominent features:
  • Pronounced forehead
  • Malae eminences
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61
Q

Thalassaemia presentation

A

Sx:

  • Fatigue
  • Poor growth and development
  • Pronounced forehead and malar eminences

Signs:

  • Splenomegaly
  • Gallstones
  • Jaundice
  • Pallor
  • Microcytic anaemia
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62
Q

What is HbH disease

A

3 deleted alpha genes

  • Low HbA
  • Severe haemolyticanaemia
  • Splenomegaly
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63
Q

What disease is caused by 4 deleted alpha globin chain genes

A
  • Hb Barts Hydrops Fetalis
  • Cannot carry oxygen
  • Not compatible with life
  • Baby is:
    Pale
    Oedematous
    Big Liver
    Big spleen
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64
Q

Alpha thalassaemia investigations

A

Bloods - Microcytic

Blood smear:

  • Microcytic + Hypochromic
  • Target cells

Hb Electrophoresis

Genetic testing:
- Amniocentisis

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65
Q

Iron overload

  • Monitoring
  • Management
A

Serum ferritin

Chelating agents
- Deferiprone

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66
Q

Beta - Thalassaemia

A

Deficiency in Beta globin chain synthesis

  • Results in excess alpha chains which combine with gamma and delta chains
  • Increase HbA2 and HbF
  • Ineffective erythropoesis and haemolysis
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67
Q

HbF chains

A

2 x alpha

2 x gamma

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68
Q

HbA2 chains

A

2 x aplha

2 x delta

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69
Q

HbA chains

A

2 x alpha

2 x Beta

70
Q

Beta - Thalassaemia aetiology

A

Point mutation in splice sites or promoter sequence on chromosome 11
- Decrease Beta chain production or absence

71
Q

Beta Thalassassaemia phenotypes

A

B0 , B0 - Major

B+ , B+ - Intermedia

B , B+ - Minor

B0 = none 
B+ = Reduced
72
Q

What does extravascular haemolysis lead to in beta thalassaemia

A
  • Hypoxia
  • Secondary haemochromatosis
  • Jaundice
73
Q

Beta thalassaemia minor presentation

A

Mild anaemia

- Iron stores + ferritin normal

74
Q

Beta thalassaemia intermedia presentation

A

Moderate anaemia - NO TRASFUSSIONS REQUIRED

  • splenomegaly
  • Bone abnormalities
  • Leg ulcers
  • Gallstones
75
Q

Beta thalassaemia major presentation

A
  • Severe anaemia
  • Failure to thrive
  • chronic infections
  • Hepatosplenomegaly
  • Osteopenia
  • Bone abnormalities
  • Skull bossing
76
Q

Why does Beta thalassaemia present within the first year

A

HbF uses up free alpha chains until it runs out in the first 6m

77
Q

Beta thalassaemia major - investigations

A

FCB:
- high reticulocyte count

Blood film:
- Hypochromic + microcytic anaemia

Target cells

X Ray:
- Hair on end

Dx: Hb electrophoresis
- Increase HbF and ansent HbA

78
Q

What is anisocytosis

A

Variation in RBC size

- Iron deficiency anaemia

79
Q

What is poikilocytosis

A

Variation in RBC shape

- Iron deficiency anaemia

80
Q

Beta thalassaemia tx

A
  • Blood transfusion
  • Replenish HbA levels
  • Long term folic acid supplements
  • endocrine supplements
  • Promote fitness and healthy lifestyle
81
Q

How to monitor iron overload

A

MRI

  • Cardiac
  • Liver

Dexa scan

82
Q

Complications of iron overload

A

Liver fibrosis + cirrhosis
Hypothyroidism
Hypocalcaemia
Hypogonadasim

83
Q

Inherited haemolytic anaemias

A 
Heriditary sperocytosis 
Hereditary elliptocytosis 
Thalassaemia 
Sickle cell disease 
G6PD deficiency
84
Q

Acquired haemolytic anaemias

A
  • AI haemolytic anaemia
  • Infections
  • Secondary to systemic disease
  • Prosthetic valve related haemolysis
85
Q

what is haemolytic anaemia

A

Anaemia due to premature RBC destruction

86
Q

Haemolytic anaemia general presentation

A 
Anaemia 
Splenomegaly 
Jaundice 
Gallstones 
Leg ulcers
87
Q

What is hereditary elliptocytosis

A
  • RBC epilleptical in shape
  • Horizontal interactions
  • AD condition
88
Q

What is hereditary spherocytosis

A
  • RBC sphere shaped

- AD condition

89
Q

Membranopathy investigations

A

FBC:

  • Anaemia
  • Reticulocytosis

Blood film:
Sherocytes and Reticulocytes

90
Q

Membranopathy tx

A

Folate supplements

Splenectomy

91
Q

What is G6PD deficiency

A

X - linked recessive disease

  • Glucose -6 - phosphate dehydrogenase deficiency
92
Q

What does G6PD do

A
  • Enzyme for hexose monophosphate shunt
  • Maintains glutathione in reduced state
  • Glutathione protects RBCs from oxidatine injury
  • Shortened RBC lifespan due to oxidative injury
93
Q

Precipitants of oxidative crisis

A
  • Primaquine - Anti malarial
  • Ciprofloxacin
  • Sulfonylureas
  • Sulfasalazine

Broad beans
Fava beans
Infection

94
Q

Enzymeopathies presentation

A

Jaundice - neonatal
Gallstones
- anaemia
- splenomegaly

95
Q

Enzymeopathies investigations

A

Blood film:

  • Bite cells
  • Blister cells
  • Heinz bodies

G6PD enzyme Assay
- may be normal if taken immediately after an attack

96
Q

What should you avoid in G6PD deficiency

A

Henna

97
Q

What is cold AIHA secondary to

A
  • Lymphoma
  • Leukemia
  • SLE
  • EBV
  • CMV
  • HIV
98
Q

How does cold AIHA occur

A
  • Ab bind to RBC and cause agglutnation
  • Immune system activated
  • Filtration and destruction in the spleen
99
Q

AIHA tx

A

Blood transfusions
Prednisolone
Rituximab
Splenectomy

100
Q

Bone marrow failure

A
  • Reduction in number of pluripotent stem cells causes lack of haemopoesis
  • Reduced number of RBCs to replace old ones causing anaemia
101
Q

Bone marrow failure causes

A 
Congenital 
Acquired - Aplastic anaemia
Cytotoxic drugs 
Radiation 
Infections
102
Q

Bone marrow failure presentation

A 
Pancytopenia 
- Increase susceptibility to infections 
- Bruising 
- Bleeding 
Nose + gums
103
Q

Aplastic anaemia investigations

A

Bloods:

  • Pancytopenia
  • Decreased reticulocytes

BM biopsy:

  • Increase fat spaces
  • Hypocellular marrow
104
Q

DVT presentation

A 
Pain 
Swelling 
Redness
warmth 
Ankle oedema - Pitting
105
Q

DVT investigations

A

D - Dimer - exclusion only
US Doppler
Bloods
Wells score

106
Q

What causes an increase in D-dimers

A

post op
cancer
pregnancy
DVT

107
Q

DVT management

A
  • LMWH (Enoxaparin)
  • Warfarin
  • DOAC (Apixiban)

Prevention

  • compression stockings
  • mobilisation
  • leg elevation
108
Q

MOA LMWH

A

Enoxaparin

  • Inactivation of factor Xa
  • weight adjusted dose
109
Q

MOA Unfractioned heparin

A 
Binds to antithrombin 
Inhibits:
- Xa
- Thrombin 
- IXa
110
Q

What is APTT

A

Activated partial thromboplasmin time

- Monitered when ot is on Heparin

111
Q

MOA Warfarin

A

Prevents activation of clotting factors - 10,9,7,2
- Narrow therpautic range
Target = (2-3)
- Prolongs PT time

112
Q

What is leukemia

A

Malignant neoplasm of blast cells (haemopoetic stem cells)
- Excessive production of a single type of abnormal white cell
- excessive production leads to suppression of all other cell lines
(PANCYTOPENIA)
- Excessive production leads to blast cells spilling over into the blood from BM

113
Q

Leukemia aetiology/assosc

A
  • Chemicals (Benzene)
  • Alkylating agents
  • Radiation damage
  • Viruses
  • Genetics
  • Downs syndrome
114
Q

What is Acute lymphoblastic Leukemia

A

Malignancy of lymphoid cells affecting B/T cell lineages

- Proliferation of Lymphoblasts

115
Q

ALL assosciations + age

A
  • Downs syndrome
  • Ionising radiation during pregnancy

Under 5 and over 45

116
Q

Commonest childhood cancer

A

ALL

- Assosc with Down syndrome

117
Q

Common infection is ALL patients

A
  • Chest
  • Measels
  • CMV
  • Pneumocytisis pneumonia
  • Candidiasis
118
Q

ALL investigations

A

Bloods:
FBC
- Blast cells
- High WCC

BM aspirate
- Blast cells

CXR:

  • Abdo lymphadenopathy
  • Mediastinal lymphadenopathy

LP:
- Check for CNS involvement

119
Q

What is tumour lysis syndrome

A
  • release of uric acid from cells being destroyed by chemo
  • can cause AKI

Tx:
Allopurinol

120
Q

ALL management

A
  • blood/platelet transfusion
  • Neutropenic regimen
  • Prophylactic antivirals/fungals/biotics
  • Pt specific chemo regimens
  • BM transplants
121
Q

What is CLL

A

Chronic lymphocytic leukemia
- Chronic proliferation and accummulation of mature B-lymphocytes (non functional)

  • > 55 years old
122
Q

What is the commonest leukemia

A

CLL

123
Q

What influences the risk of CLL development

A

Mutations
Triosmies
Deletions

124
Q

CLL presentation

A

Often Asx

  • suprise finding on routine FBC
  • Anaemic
  • Infection prone
  • Sweats
  • Weight loss
125
Q

CLL signs

A
  • Enlarged rubbery non tender nodes

- Hepatosplenomegaly

126
Q

CLL investigations

A

FBC:

  • Lymphocytosis
  • Increase WCC

Blood smear:
- Smudge/ smear cells

BM biopsy:
- BM infiltration

127
Q

What can CLL transform to

A

High grade lymphoma

- Richter syndrome

128
Q

CLL complications

A
  • Warm AIHA
  • Hypogammaglobinaemia (Low IgG) –> Infection
  • Herpes zoster
  • BM failure
129
Q

What is AML

A

Acute myeloid leukemia
- Neoplastic proliferation of blast cells derived from marrow myeloid elements

  • Commonest leukemia in adults
  • > 75 y/o
130
Q

What can AML be the result of

A

Result from a transformation from a myeloproliferative disorder

  • PCRV
  • Myelofibrosis
131
Q

what is AML a long term complication of

A

Long term chemo for lymphoma

132
Q

AML presentation -

A

Similar to ALL

  • Anaemia
  • Infection
  • Bleeding
  • Hepatosplenomegaly

Gum hypertrophy - Infiltration

DIC - Thromboplastin release

133
Q

AML investigations

A

Blood smear:
- blast cells w/ AUER RODS

BM biopsy:
- blast cells

134
Q

Differentiating AML from ALL

A

Microscopy
Immunophenotyping
Molecular methods

135
Q

What is CML

A

Chronic myeloid leukemia
- uncontrolled clonal proliferation of myeloid cells

  • (40-60 y/o)
136
Q

CML cytogenetic changes

A

Philadelphia chromosome

  • t(9;22) –> BCR/ABL
  • tyrosine kinsae activity
  • stimulates cell division
137
Q

CML investigations

A
  • Cytogenic analysis of blood/BM for Ph chromosome
138
Q

CML Tx

A
  • IMATINIB
    specific BCR/ABL tyrosine kinase inhibitor
    chronic phase tx
  • Chemo
  • Stem cell transplant
139
Q

What is Lymphoma

A

B and T cell malignancies of the lymphoid system

- Accumulate in lymph nodes leading to lymphadenopathy

140
Q

What is Hodgkin’s lymphoma

- Age

A

Proliferation of lymphocytes

  • Bimodal age distribution
    peak = 20
    peak = 75
141
Q

Hodgkin’s lymphoma RF

A 
HIV
EBV
Family hx
AI condition - RA/SLE
Post transplantation
142
Q

Hodgkin lymphoma presentation

A

Lymphadenopathy

  • Neck
  • Axilla
  • Inguinal

B symptoms

  • fever
  • weight loss
  • night sweats
  • fatigue
  • pruritus
  • Hepatosplenomegaly
  • cough
  • S.O.B
  • Abdo pain
  • Recurrent infections
143
Q

Hodgkin lymphoma lymphadenopathy presentation

A
  • Non tender
  • Rubbery
  • Pain when drinking alcohol
144
Q

Hodgkin lymphoma investigation

A

Bloods:

  • high ESR
  • LDH

LN biopsy: DIAGNOSTIC
- Reed sternberg cells

CXR:
- Mediastinal widening from enlarged lymph nodes

CT/PET:
- Staging

145
Q

What are reed sternberg cells

A
  • Abnormally large B cells
  • Multiple nuclei that have nucleoli in them
  • Apperance of an owl with large eyes
146
Q

Differential diagnosis of lymphadenopathy

A
  • Tonsillitis
  • TB
  • HIV
  • EBV
  • CMV
  • Leukemia
  • SLE
  • Rheumatoid arthiritis
  • SLE
  • Sarcoidosis
147
Q

Lymphoma staging

A 
Ann Arbor Classification Stage:
1
2
3
4

Stage A or B
A - No systemic sx other than pruritus

B - Presence of B sx in the last 6m

  • fever (>38)
  • sweats (change of clothes)
  • loss of weight
148
Q

Hodgkin lymphoma tx

A

Chemo
Radio

  • Ris of relapse
149
Q

Chemo risks or S/E

A 
Leukemia 
Infertility 
Alopecia 
Infection 
AML
NHL
Myelosuppression
150
Q

Radiotherapy risks

A 
Secondary malignancies
- lung 
- breast 
- melanoma
-sarcoma 
Damage to tissues 
Hypothyroidism
151
Q

What is Non-hodgkins lymphoma

A 
Lymphomas without charecteristic cells 
- Burkitt
- MALT
  Assoc with H-pylori 
   infection
- Diffuse large B cell 
   lymphoma
152
Q

Non hodgkin lymphoma risk factors

A
  • HIV
  • EBV
  • Hep B/C infection
  • Family hx
  • H.pylori infection
153
Q

Non hodgkin lymphoma presentation

A 
- Painless peripheral node enlargement 
Extra nodal:
- Bowel obstruction 
- Spinal cord compression 
- Pancytopenia
154
Q

Why is a high LDH a bad indicator of prognosis

A

Indicates high cell turnover therfore increase proliferation

155
Q

Non hodgkin lymphoma classification

A

Low grade

  • incurable
  • follicular lymphoma

High grade

  • aggressive but curable
  • diffuse large B cell
  • Burkitts
156
Q

Features of Burkitts lymphoma

A
  • Jaw lymphadenopathy
  • Childhood disease
  • Assosc with EBV infections
157
Q

When should you suspect malaria

A

Fever + Exotic travel

158
Q

MOA for anti-emetic Onadansetron

A

5HT3 antagonist

- Centrally acting for drug induced vomitting

159
Q

Actions for pt with febrile neutropenia

A

Emergency –> ABC
Perform cultures
Broad spectrum Abx
- Gentamicin + Tazosin

160
Q

When should you consider myeloma

A

Pt’s > 50y/o with bone or back pain and unexplained features

161
Q

What is myeloma

- and what is majorly produced

A

Malignancy of plasma cells

- IgA + IgG majorly produced

162
Q

What is found on urine/serum electrophoresis

A

Monoclonal paraprotein
- Bence Jones proteins
- Free IgG light chains
filtered by the kidney

163
Q

Myeloma anaemia pathophysiology

A

Bone marrow infiltration

- Pancytopenia

164
Q

Myeloma bone disease pathophysiology

A

Increase osteoclast activity and decrease osteoblast activity
- Increase RANKL from plasma + stromal cells

Osteolytic lesions
- Patchy bone metabolism

Hypercalcaemia
- Increase osteolytic activity

165
Q

Myeloma renal disease pathophysiology

A

Light chain deposition
- Loop of henle
- PCT
toxic inflammatory effect

Hypercalcaemia

166
Q

Myeloma key features

- acronym

A

C - hypercalcaemia
R - Renal failure/ AKI
A - Anaemia
B - Bone lesions

167
Q

Myeloma investigations

A

B - Bence jones protein
*Urine electrophoresis

L - Lytic bone lesions
*MRI –> CT –> X-Ray

I - Increased ESR

P - Pancytopenia
*FBC –> Increased Ca2+

Bone marrow biopsy

168
Q

Myeloma X ray findings

A

Punched out lesions
Lytic lesions
Raindrop skull

169
Q

Myeloma tx

A
  1. Chemotherapy + High dose dexamethasone (bone pain)
  • Stem cell transplant
  • EPO transfusions
  • Hydration (AKI)
  • Bisphosphonates
  • Avoid NSAIDs
170
Q

Pancytopenia defenition

A 
Decreased blood cells 
Anaemia 
Thrombocytopenia
- Easy bleeding 
- Easy bruising 
Low WCC
- infection prone

Phase 2a (11 decks)

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