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Haem Flashcards

1
Q

Signs / Symptoms Anaemia

A

Fatigue
Dyspnoea
Faintness
Palpitations
Headache
Tinnitus
Anorexia
Pallor
Hyperdynamic circulation e.g. tachycardia, flow mumurs, cardiac enlargement

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2
Q

Big consequences of anaemia

A

↓O2 Transport
Tissue hypoxia
Compensatory changes - (↑tissue perfusion, ↑O2 transfer to tissue, ↑RBC production)

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3
Q

Pathological consequences of anaemia

A

Myocardial fatty change
Fatty change in liver
Aggravate angina
Skin and nail atrophic changes
CNS cell death (cortex and basal ganglia)

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4
Q

State causes of macrocytic anaemia

A

B12/Folate def
+ HLARD

Hypothyroidism
Liver disease
Alcohol
Reticulocytes - haemolysis
Drugs - Azathioprine

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5
Q

State causes of normocytic anaemia

A
  1. Acute blood loss!
  2. Anaemia of Chronic disease
  3. BM failure
  4. Renal failure
  5. Hypothyroidism
  6. Haemolysis
  7. Pregnancy
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6
Q

Is haemolytic anaemia microcytic or macrocytic?

A

Neither - bc it can be normocytic or macrocytic

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7
Q

Define anaemia
State values

A

Low haemoglobin conc
< 135 g/L for men
< 115g/L for women

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8
Q

Investigations for anaemia

A

FBC + film
Reticulocyte count
U&Es, LFTs, TSH

Iron def - ferritin, iron studies, look for cause
Chronic disease - clinical Ix, lab investigation, renal failure?
B12 def - IF antibodies, schilling test, coeliac ab

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9
Q

Define FBC
What does one consist of?

A

Basic blood test that gives info on blood constituents

RBC vol
WBC vol (all types)
Platelet vol
Haemoglobin conc
Mean corpuscular volume (MCV)

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10
Q

Why is the GS Ix for IDA limited?

A

Because ferritin is an acute phase protein

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11
Q

What does reticulocyte count show?

A

How quickly new RBCs are being formed

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12
Q

What are reticulocytes?

A

Immature RBCs

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13
Q

What does a low reticulocyte count show?
Give an example of a cause

A

Something is preventing new RBCs from being produced
e.g. Haemantinic deficiency

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14
Q

What does a high reticulocyte show?
Give an example of a cause

A

RBCs are being lost or destroyed & ↑Reticulocyte as a compensatory mechanism
e.g. Bleeding or Haemolytic anaemia

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15
Q

What is ferritin?

A

Major iron storage protein of the body

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16
Q

What can ferritin be used to measure?

A

Used to indirectly measure iron levels in body

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17
Q

When and why can ferritin be falsely raised?

A

In inflammation and malignancy
Because it is an acute phase protein

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18
Q

What does a thick blood film permit?

A

Examination of a large amount of blood for presence of parasites (NOT identification of species)

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19
Q

What does a thin blood film permit?

A

Observation of RBC morphology, inclusions and intracellular/extracellular parasites

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20
Q

What does each haemoglobin molecule consist of?

A

2 alpha and beta chains

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21
Q

State the value ranges for micro, normo and macrocytic anaemia

A

MCV < 80 = Microcytic
MCV 80 - 100 = Normocytic
MCV > 100 = Macrocytic
UNITS - femtolitres 2

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22
Q

Where is iron absorbed?

A

Duodenum

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23
Q

Pathophysiology of Iron-Def anaemia

A

↓Iron available for haem synthesis
∴ ↓ Haemoglobin
∴ ↓ Effective RBCs
∴ Anaemia

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24
Q

Causes IDA

A

Low iron diet
Blood loss - menorrhagia, GI bleeding, Hookworm
Malabsorption - coeliac disease
Pregnancy
Breastfeeding

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25
Q

Signs/Symptoms more specific to IDA

A

Brittle hair and nails
Atrophic glossitis
Angular stomatitis
Koilonychia

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26
Q

DDx IDA

A

Anaemia of chronic disease
Thalassaemia

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27
Q

Ix IDA

A

FBC & Blood film - hypochromic microcytic RBCs
Also, anisocytosis and poikilocytosis

Serum ferritin - low
↑ Total iron binding capacity

↓Reticulocyte count

Endoscopy/Colonoscopy - to see if upper/lower GI bleed

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28
Q

Tx IDA

A

Treat cause!
Ferrous sulphate - oral iron
Ferrous fumarate

Continue for 3 months until Hb is normal

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29
Q

If a patient is responding to iron treatment, what should you find?

A

An increase in reticulocyte count
then gradual increase in Hb until normal

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30
Q

S/E of ferrous sulphate / fumarate

A

Black stool (melaena) ! (DDx for upper Gi bleed)

Constipation
Diarrhoea
Nausea
GI upset
Epigastric abdo pain

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31
Q

Microcytic Anaemia Causes

A

TAILS
Thalassaemia
Anaemia of Chronic Disease
Iron def
Lead poisoning
Sideroblastic anaemia

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32
Q

What is Plummer Vinson Syndrome?

A

TRIAD OF :
1. Dysphagia
2. Iron def
3. Oesophageal webs

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33
Q

What is Thalassaemia?

A

Inherited disease
↓ Rate of production or NO production
of one or more globin chains (α or β̞)
in red cell precursors OR mature RBCs

∴ in red cell precursors = ineffective erythropoiesis
& in mature RBCs = haemolysis

∴ ↓Production and ↑premature destruction of RBCs

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34
Q

Where is Thalassaemia most common?

A

Mediterranean
Middle East
Asia

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35
Q

How is Thalassaemia inherited?

A

Autosomal recessive

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36
Q

Types of Thalassaemia

A

α-Thalassaemia
β̞-Thalassaemia

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37
Q

What globin chains are found in the majority of adult haemoglobin?

A

2x alpha globin chains
2x beta globin chains

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38
Q

Where the gene for alpha-globin chains found?

A

On both chromosome 16s

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39
Q

Cause Alpha Thalassaemia

A

Gene deletions

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40
Q

How does alpha Thalassaemia present with 1 gene deletion?
(-a/aa)

A

Usually normal blood picute
Asymptomatic

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41
Q

How does alpha Thalassaemia present with 2 gene deletions?
(–/aa)

A

Asymptomatic with possible mild microcytic anaemia
Carrier for alpha thalassaemia

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42
Q

How does alpha Thalassaemia present with 3 gene deletions?
(–/-a)

A

Common in parts of Asia!
↓↓ Reduction of alpha chain synthesis ∴ HbH disease

Severe haemolytic anaemia & features of haemolysis = splenomegaly, jaundice, leg ulcers

Sometimes transfusion dependent

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43
Q

How does alpha Thalassaemia present with 4 gene deletions?
(–/–)

A

NO a-chain synthesis
Only Hb Barts present - not compatible w life bc cannot carry oxygen

Death in utero
Infants stillborn - pale, oedematous with huge livers and spleen

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44
Q

What chains does Hb Barts have?

A

4x gamma chains
Not compatible with life!

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45
Q

What is an evolutionary advantage of carriers of alpha thalassaemia?

A

Protected from falciparum malaria

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46
Q

Cause of B Thalassaemia?

A

Point mutation causing - transcription, RNA splicing and translation mutations

∴ Unstable and unusable B chains

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47
Q

Pathophysiology B Thalassaemia

A

Genetic defects
∴ little/no normal B chain production
∴ XS a chain production
∴ a-chains combine with whatever is available - B, gamma or delta chains

∴ ↑ Production of HbA2 and HbF
∴ Result in ineffective erythropoiesis and haemolysis

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48
Q

What chains does HbA contain?

A

2 alpha
2 beta

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49
Q

What chains does HbA2 contain?

A

2 alpha
2 delta

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50
Q

What chains does HbF contain?

A

2 alpha
2 gamma

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51
Q

Where are B-globin genes found?

A

Chromosome 11

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52
Q

What mutations occur in B-Thalassaemia?

A

Point mutations ?

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53
Q

Describe how B-Thalassaemia minor presents

A

Asymptomatic
Carrier state
Mild micro and hypochromic anaemia
Iron stores and ferritin normal

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54
Q

Describe how B-Thalassaemia intermedia presents

A

Moderate anaemia - Patients don’t require transfusion
Splenomegaly, bone abnormalities, recurrent leg ulcers & gallstones

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55
Q

Describe how B-Thalassaemia major presents

A

Presents in 1st year of life - Cooley’s anaemia (severe) - with :
Failure to thrive
Recurrent infections
Listless (lacks energy)
Crying
Pale

Bony abnormalities (bc hypertrophy of ineffective BM) e.g. skull bossing, thalassaemic faces w enlarged maxilla + prominent frontal and parietal bones, hair on end sign on skull XR

Hepatosplenomegaly (bc haemolysis)

Will require lifelong transfusion if develop to adulthood

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56
Q

Ix B-Thalassaemia

A

Blood film - microcytic hypochromic anaemia
Target cells visible!

Increased reticulocytes and nucleated RBCs in periph circulation

GS!! Hb electropheresis! - shows ↑ HbF and absent/low HbA

Skull XR - hair on end sign, enlarged maxilla

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57
Q

Tx B-Thalassaemia

A

Blood transfusions regularly (~2-4x per week)
HbA has time to replenish

Long term folic acid supplements

Histocompatible marrow transplant could cure!!

nB - risk of iron overload!!
∴ give iron chelation (SC desderrioxamine, oral deferiprone) to decrease iron loading
& Ascorbic acid to ↑urinary excretion of iron
–
Things to consider : bone health, endo supplements, psych support

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58
Q

Why is there a risk of iron overload with blood transfusions?

A

Repeat transfusions = deposition of iron in major organs

e.g. *liver, spleen (cirrhosis and fibrosis)
pancreas, heart and endocrine glands (DM, HF, premature death)

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59
Q

What should be monitored in a patient with B-Thalassaemia?
Why?

A

Ferritin
Cardiac & liver MRI
Endo testing - gonadal function, DM screening, growth and puberty
–
bc blood transfusions can lead to complications in major organs

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60
Q

What is sideroblastic anaemia?

A

BM produces ringed sideroblasts instead of healthy RBCs

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61
Q

Causes Sideroblastic anaemia

A

Congenital - rare, X-linked
Chemotherapy
Anti-TB drugs
XS alcohol

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62
Q

Ix Sideroblastic anaemia

A

Increased ferritin
Blood film - hypochromic RBCs

GS!! - Sideroblasts in BM

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63
Q

Tx Sideroblastic anaemia

A

Remove cause
Pyridoxine

Repeated transfusions for severe anaemia
(& ∴ iron chelation and ascorbic acid)

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64
Q

3 Main Causes Normocytic anaemia

A
  1. Acute blood loss
  2. Combined haematinic def e.g. iron and B12 def - balances out micro and macro
  3. Anaemia of chronic disease
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65
Q

Causes Anaemia of Chronic disease

A

*Crohn’s
*RA

TB
SLE
Malignancy
CKD

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66
Q

Ix Anaemia of Chronic disease

A

FBC and blood film - normocytic/microcytic and hypochromic

Low serum iron
Low total iron binding capacity (TIBC)

↑ or normal serum ferritin

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67
Q

Tx Anaemia of Chronic disease

A

Treat underlying cause
Recombinant erythropoietin

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68
Q

What 2 groups can macrocytic anaemia be divided into?

A

Megaloblastic
Non-Megaloblastic

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69
Q

What is a megaloblast?
When does one form? Why?

A

Cell where nuclear maturation is delayed but cytoplasm is not
∴ Lots of cytoplasm, tiny nucleus

Forms with B12 and folate deficiency
Bc both are required for DNA synthesis

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70
Q

What is a non-megaloblast?
When does one form?

A

Not a megaloblast
XS alcohol, reticulocytosis, liver disease, hypothyroidism

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71
Q

Other than causes for megaloblastic and non-megaloblastic, what are some causes for macrocytic anaemia?

A

Myelodysplasia
Myeloma
Myeloproliferative disorderes
Aplastic anaemia

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72
Q

What is folate found in?

A

Green vegetables, nuts, yeast and liver

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73
Q

What is folate synthesised by?

A

Gut bacteria

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74
Q

What is folate essential for?

A

DNA synthesis

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75
Q

Where is folate absorbed?

A

Jejunum

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76
Q

What does maternal folate deficiency cause?

A

Foetal neural tube defects

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77
Q

Causes of Folate Deficiency

A

Poor diet e.g. poverty, alcoholics, elderly
↑ Demand e.g. pregnancy or ↑cell turnover
Malabsorption e.g. coeliac disease, Crohn’s
Alcohol
Drugs - anti-epileptics, methotrexate

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78
Q

Ix Folate Deficiency

A

Blood film - anisocytosis and poikilocytosis w/ large oval macrocytes
Serum & red cell folate assay

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79
Q

Tx Folate Def

A

Assess for underlying cause (poor diet, malabsorption etc)

Folic acid (5mg/day PO for 4 months)

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80
Q

Prophylaxis for folate deficiency if pregnant
What does it prevent?

A

400mcg/day are given until 12 weeks
Helps prevent spina bifida

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81
Q

What is pernicious anaemia?

A

Autoimmune condition
Parietal cells are attacked
∴ atrophic gastritis AND ↓IF production

∴ ↓ B12 absorbed by iluem

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82
Q

Causes B12 Def

A

Diet - vegans
Pernicious Anaemia
Atrophic Gastritis
Malabsorption - Crohn’s, coeliac etc
Gastrectomy
Congenital metabolic errors

Basically anything that affects IF production by parietal cells in stomach
OR
anything that affects absorption in ileum

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83
Q

Where is B12 absorbed?

A

Terminal ileum
Bound to intrinsic factor (IF)

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84
Q

What produces B12?

A

Parietal cells

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85
Q

Signs / Symptoms Pernicious anaemia

A

Normal anaemia ones
+
Jaundice - XS breakdown of Hb
Neurological Sx - Polyneuropathy
Tongue Sx
Lemon yellow tinge

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86
Q

What is polyneuropathy caused by?
(Specifically relating to pernicious anaemia)

A

Symmetrical damage to peripheral nerves and posterior + lateral columns of spinal cord

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87
Q

How can you differentiate between B12 and folate deficiency?

A

Folate def does not have neuropathy but B12 does!

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88
Q

B12 and folate deficiency anaemias are what type of anaemia?

A

Megaloblastic macrocytic

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89
Q

Why are B12 and folate deficiency anaemia megaloblastic?

A

B12 and folate help with DNA synthesis

∴ deficiency = less DNA synthesis
∴ little nucleus + lots of cytoplasm

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90
Q

Ix Pernicious anaemia

A

FBC - ↓ Hb, ↑ MCV obvs
If severe, ↓WBC + platelets

Blood film - macrocytic RBCs

Megaloblasts in BM
Maybe ↓ Reticulocytes - production impaired

↓ Serum B12

MORE SPECIFIC TESTS :
Autoantibody screen for IF and parietal cells (present in 50% and 90% of cases respectively)

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91
Q

Tx Pernicious anaemia

A

Vitamin B12 (hydroxocobalamin) IM injections

NOT EVER FOLIC ACID !! - will cause fulminant neuro deficits

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92
Q

Comps Pernicious anaemia

A

HF
Angina
Neuropathy

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93
Q

A carrier of sickle cell disease (heterozygous) is protected from?

A

Falciparum malaria!

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94
Q

What is sickle cell disease?

A

Autosomal recessive normocytic haemolytic disease

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95
Q

Where is sickle cell disease more common?

A

In Afro-Caribbean ethnicities

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96
Q

Pathophysiology Sickle Cell disease

A

B globin gene mutation (glutamic -> valine)
∴ HbS variant is formed

When ↓O2, Hb variant polymerises and forms rod-like aggregates
∴ RBC becomes sickle-shaped + rigid

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97
Q

What triggers RBCs to turn sickle-shaped in sickle cell anaemia?

A

“Stress” e.g.
Cold
Infection
Dehydration
Hypoxia
Acidosis

Causes microvascular occlusion

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98
Q

Signs / Symptoms Sickle Cell disease

A

Can be Asx
Anaemia symptoms
Acute pain in hands + feet (dactylitis)
Jaundice (breakdown of Hb)

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99
Q

Ix Sickle cell anaemia

A

FBC - Normocytic normochromic with ↑reticulocyte count

Blood film - sickled erythrocytes
Howell-Jolly bodies

Hb electrophoresis
If 90% of Hb = HbS, then diagnostic!
–
NEONATAL SCREENING

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100
Q

Tx Sickle Cell disease

A

ACUTE ATTACKS :
IV fluid + Analgesia + O2

LONG TERM :
Avoid precipitants
Hydroxycarbamide + Folic acid supps
Transfusion (+ Iron chelation + Ascorbic acid)

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101
Q

What is the most common cause of death in adults with Sickle cell disease?

A

Pulmonary HTN
Chronic lung disease

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102
Q

Comps Sickle cell disease

A

Splenic sequestration - autosplenectomy !
Vaso-occlusive crisis

Osteomyelitis (In sickle cell patients, caused by salmonella!!!)

ACUTE CHEST CRISIS = pulmonary vessel vaso-occlusion!! can cause resp distress!!! EMERGENCY!!!

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103
Q

Type of haemolysis in Sickle Cell Anaemia

A

BOTH - Intravascular (inside vessels) && Extravascular (inside spleen)

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104
Q

How is spherocytosis inherited?

A

Autosomal dominant

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105
Q

Pathophysiology spherocytosis

A

↓ Spectrin
∴ ↑ RBC membrane permeability to Na+
∴ RBCs become rigid and spherical

∴ Spleen believes RBCs are damaged are they are prematurely destroyed
= Extravascular haemolysis

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106
Q

Signs / Symptoms Spherocytosis

A

General anaemia
NEONATAL JAUNDICE
Splenomegaly
Gallstones!

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107
Q

Ix Spherocytosis

A

FBC & reticulocyte count - ↑↑Reticulocytes!
Blood film - shows spherocytes

Osmotic fragility tests - RBCs fragile in hypotonic solution

Coombs’ test! (Direct anti-globulin test) = NEG !!
Rules out autoimmune haemolytic anaemia! (spherocytes are often seen in AHA)

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108
Q

What is the most common cause of spherocytosis or elliptocytosis ?

A

↓ Spectrin

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109
Q

What is spectrin?

A

RBC structural membrane protein

110
Q

What is the structural difference between spherocytosis and elliptocytosis?

A

Spherocytosis - vertical deformity
Elliptocytosis - horizontal deformity

111
Q

Signs / Symptoms Elliptocytosis

A

Same as spherocytosis i think

112
Q

Tx Spherocytosis

A

Splenectomy!
Wait until 6 years old at least - otherwise very high sepsis risk!

113
Q

Tx Neonatal Jaundice

A

Phototherapy

114
Q

Comps of untreated Neonatal jaundice

A

Kernicterus!
Where bilirubin accumulates in basal ganglia
∴ CNS dysfunction and death!!

115
Q

Ix Autoimmune Haemolytic Anaemia

A

Direct Coomb’s test +VE

116
Q

How is Glucose-6-phosphate dehydrogenase deficiency inherited?

A

X-linked recessive

117
Q

Pathophysiology of G6PD deficiency

A

G6PD essential in hexose monophosphate shunt - maintains glutathione in reduced state

Glutathione protects RBC from oxidative crisis

∴ without G6PD, RBCs will undergo oxidative crisis!

118
Q

What type of individuals does G6PD deficiency mostly affect?

A

Mediterranean
Africa
Middle/Far East

119
Q

What does G6PD deficiency protect against?

A

Falciparum malaria

120
Q

Signs / Symptoms G6PD Def

A

Neonatal jaundice
Chronic haemolytic anaemia
–
Acute haemolysis - Rapid anaemia, Jaundice (dark urine)
Back pain

121
Q

What can G6PD def be caused by?

A

Ingestion of fava beans !!!
Henna
Illness
& common drugs - quinine, sulphonamides, quinolones and nitrofurantoin

122
Q

Ix G6PD Def

A

FBC - anaemia, raised reticulocytes

Blood film - Bite and blister cells, Heinz bodies!!
Confirmed with enzyme assay!

123
Q

Tx G6PD Deficiency

A

Avoid precipitants e.g. Henna
Transfuse if severe

124
Q

When should you assume malaria until proven otherwise?

A

FEVER + EXOTIC TRAVEL

125
Q

3 stages of Malaria

A

Exo-erythrocytic
Endo-erythrocytic
Hypnozoite stage

126
Q

Causes Malaria

A

Parasites from plasmodium family

Plasmodia falciparum - MC !!!
P. Ovale & P. Vivax - latent!!
P. Malariea

127
Q

How is Malaria transmitted?

A

Infected female Anopheles mosquito
OR contaminated needle OR transfusion

128
Q

Describe the stages of transmission of malaria

A
  1. Mosquito bites human host, spreads plasmodium sporozoites into blood stream
  2. Travels to liver
    Maturation occurs, forms schizonts
  3. After few days, infected hepatocytes rupture
    Releases merozoites into blood
    Merozoites taken up by erythrocytes
  4. They develop further inside erythrocytes, then rupture (contributes to anaemia) and release pyogens (causes fever)
  5. If RBCs are infected w/ P. Falciparum, they adhere to endothelium in small vessels
    ∴ vascular occlusion
    ∴ severe organ damage (esp in gut, kidney, liver, brain)

If RBCs are infected w/ P. Ovale or P. Virax, remain latent in liver as hypnozoites
These are the reason for any relapses that occur

129
Q

DDx Malaria

A

Dengue
Typhoid
Hepatitis
Meningitis
Encephalitis
Viral haemorrhagic fever

130
Q

What does a thick and thin blood film show with malaria?

A

Thick - v sensitive but low res, shows IF parasite is there

Thin - shows type of parasite

131
Q

What is neutropenic sepsis?

A

Temp > 38
AND absolute neutrophil count > 1x10^9

132
Q

How do you treat neutropenic sepsis?

A

ABX IMMEDIATELY

133
Q

How do you treat acute sickle cell crisis?
i.e. Painful crisis

A

Pain relief
IV fluid

134
Q

How do you treat Chest crisis?

A

IV fluid
Abx
Closely monitor

135
Q

How do you treat spinal cord compression?

A

Steroid e.g. high dose dexamethasone and MRI

136
Q

What is tumour lysis syndrome?

A

When chemo is given, cancer cells are broken down and contents are released (e.g. hyperkalaemia, nucleic acid)
Produce crystals and get deposited in kidneys
Causes damage and loss of function

137
Q

How do you prevent tumour lysis syndrome?

A

Allopurinol

138
Q

How do you treat tumour lysis syndrome?

A

ALLOPURINOL
IV fluids
Correct electrolytes

139
Q

What is DVT?

A

Blood clot in a deep vein in body, usually leg

140
Q

Causes DVT

A

Surgery
Immobilisation! - bed rest
Long haul flights
-
Factor V Leiden
Anti-thrombin def
-
Anti-phospholipid syndrome
Lupus anticoagulant

141
Q

RF DVT

A

Same as for PE

Age
Obesity
Pregnancy, OC Pill, HRT
Varicose veins
Long haul travelling often
Plasminogen def
Thrombophilia - predisposition towards caucasians

142
Q

Signs / Symptoms DVT

A

Usually vague

Pain, Swelling (Calf)
Warmth
Redness
Ankle oedema

143
Q

Ix DVT

A

D-dimer - normally excludes diagnosis!
BUT positive doesn’t confirm diagnosis

Doppler US
Compression US - tests proximal veins
Find popliteal vein, if CANNOT be squashed = DVT!!!!!!!!

Venogram - for calf
FBC - incl. platelets
–
If low Well’s score, do D dimer as initial
If high Well’s score, go straight to Doppler US

144
Q

What things can produce a positive D-dimer?

A

Surgery
Pregnancy
Infection
Cancer

145
Q

DDx DVT

A

Cellulitis

146
Q

What is the main aim of treatment for DVT?

A

To prevent PE

147
Q

Tx DVT

A

LMW heparin
e.g. SC enoxaparin

Warfarin - PO, target INR = 2-3

DOACs e.g. apixaban

148
Q

Why are DOACs now preferred to warfarin?

A

Don’t need to be monitored!

149
Q

Mechanism for Warfarin

A

Antagonises vit K dependent clotting factors -> 10, 9, 7, 2
(1972)

150
Q

Prevention DVT

A

Compression stockings
Early mobilisation
Leg elevation

151
Q

Comps DVT

A

PE
Post-thrombotic syndrome
Recurrence of thrombosis

152
Q

Which is more common - ITP or TTP?

153
Q

RF Acute Myeloid Leukaemia

A

Age
Down’s syndrome
Chemo
Irradiation

154
Q

Define Leukaemia

A

WBC’s lose ability to differentiate but maintain ability to replicate

155
Q

What age group is AML usually found in?

A

Elderly (65 - 75 years avg)
but really might not be

156
Q

Signs / Symptoms AML

A

Cancer B symptoms
Fatigue - anaemia
Easier bleeding & bruising - thrombocytopenia
Infection - leukopenia
Bone pain - ↑Cell production ∴ BM expansion
Fever
GUM SWELLING
Hepatosplenomegaly

157
Q

What are Cancer B symptoms?

A

Unexplained weight loss
Night sweats
Anorexia
Fatigue
Haemoptysis

158
Q

Name a subtype of AML
What can occur in this subtype?

A

Acute promyelocytic Leukaemia
DIC

159
Q

~ Cause AML

160
Q

Ix AML

A

FBC + Blood film - pancytopenia
Myeloperoxidase +ve
AUER RODS

GS!! - BM BIOPSY ≥ 20% myeloid blasts

161
Q

Tx AML

A

Chemo - to induce remission
+ Allopurinol - to prevent tumour lysis syndrome

Supportive - blood/platelets/Abx
IV fluids
BM transplant + steroids - maintain remission

–
Subtype of AML = Acute promyelocytic leukaemia
Tx = All-Trans-Retinoic-Acid !!

162
Q

In AML, how would you give IV Abx/fluids?
Describe and Why do we do this?

A

Hickman line!
Permanent cannula into main vessel, tunnelled under SC fat
∴ harder for infection!!

163
Q

Describe progression of AML

A

Rapid progression unless treatment asap!

164
Q

What is tumour lysis syndrome?

A

Chemo releases uric acid from cells!
Can accumulate in the kidneys!

165
Q

What age group does ALL affect?
Describe the prognosis

A

Children :( below 6 years
But good prognosis!! :)

166
Q

Cause ALL

167
Q

What is ALL?

A

Proliferation of immature lympho

168
Q

Most common childhood malignancy?

169
Q

RF ALL

A

Down’s syndrome
Radiation
Neurofibromatosis

170
Q

Signs / Symptoms ALL

A

Cancer B symptoms - more common than AML
Fatigue - anaemia
Easier bleeding & bruising - thrombocytopenia
Infection - leukopenia
Bone pain - ↑Cell production ∴ BM expansion
Fever
Hepatosplenomegaly
Swollen testicles
Lymphadenopthy

171
Q

Ix ALL

A

FBC - pancytopenia
Blood film - ↑Lymphoblasts

Immunofluorescence - TdT +ve lymphoblasts
(terminal deoxynucleotidyl transferase)

GS!! BM BIOPSY ≥ 20% lymphoblasts

172
Q

Tx ALL

A

Chemo
+ Allopurinol

Usually good prognosis! :)

173
Q

Which is the most common leukaemia?

174
Q

What age group does CLL tend to affect?

175
Q

RF CLL

A

FHx of ALL and CLL
Caucasian
Male

176
Q

What might be a trigger for CLL?

177
Q

What is CLL?

A

Chronic Lymphocytic Leukaemia
Accumulation of mature B cells that have escaped apoptosis

178
Q

CLL Pathophysiology

A

Too many mature B cells that have escaped apoptosis
∴ too many premature cells which accumulate in BM
∴ crowding out
∴ Cytopenia

179
Q

Signs / Symptoms CLL

A

Symptomatic patient assoc with later stage of cancer !
Usually incidentally found on FBC etc
–
General anaemia Sx
Lymphadenopathy (non-tender)
Hepatosplenomegaly
Infection - low IgG

180
Q

Ix CLL

A

FBC - pancytopenia (but not lymphocytes), anaemia
Blood film - SMUDGE CELLS

Immunophenotyping - HYPOGAMMAGLOBULINAEMIA
(B cells don’t differentiate into plasma cells! ∴ no Ig!)

181
Q

Progression CLL

A

Rules of 3s!
1/3 never progress
1/3 progress slowly
1/3 progress actively

Might tranform into aggressive lymphoma - RICHTER’S SYNDROME

182
Q

Comps CLL

A

RICHTER’S TRANSFORMATION
B cells massively accumulates in lymph nodes - Huge lymphadenopathy !
Becomes aggressive lymphoma!

183
Q

How can Hepatosplenomegaly present?

A

Abdo fullness

184
Q

Tx CLL

A

If late stages - chemo + allopurinol

IV Ig - hypogammaglobulinaemia

Palliative if old

185
Q

Cause + Pathophysiology CML

A

t (9;22)
PHILADELPHIA CHROMOSOME

BCR-ABL gene fusion - causing tyrosine kinase irreversibly switched on!
∴Granulocytes prolif!
∴ XS premature cells
∴ Accumulate in BM
∴ Crowding out
∴ CYTOPENIA etc

186
Q

Signs / Symptoms CML

A

Cancer B symptoms
Fatigue - anaemia
Easier bleeding & bruising - thrombocytopenia
Infection - leukopenia
Bone pain - ↑Cell production ∴ BM expansion
Fever
MASSIVE Hepatosplenomegaly

187
Q

Ix CML

A

FBC - pancytopenia (but granulocytosis)!

Blood blast cell % - severity (WHO)
≥ 10 - Chronic (BEST)
10-19 Accelerated
20 ≤ Blast crisis!! (WORST)

BM Biopsy = ↑ Granulocytes
Taken from iliac crests

PHILADELPHIA CHROMOSOME genetic test! - Fluorescent in situ hybridisation (FISH)

188
Q

Tx CML

A

Chemo + Allopurinol

Imantinib - TK inhibitor
Only if Philadelphia chromosome POS

189
Q

Comps CML

A

Risk of progression to AML if untreated/late Dx!!

190
Q

What is the Staging used for Lymphoma?

A

Ann-Arbor
For HL + NHL

191
Q

What is Lymphoma?

A

Malignant proliferation of lymphocytes which accumulate mostly in lymph nodes
Can be in blood, BM, liver + spleen too!

192
Q

Types of Lymphoma

A

Hodgkin’s Lymphoma
Non-Hodgkin’s Lymphoma
Burkitt’s Lymphoma

193
Q

What age group do you expect to see Hodgkin’s Lympma?

A

BIMODAL - Teens and elderly!

194
Q

What is Hodgkin’s Lymphoma assoc with?

A

Epstein Barr Virus

195
Q

Signs / Symptoms Hodgkin’s Lymphoma

A

B symptoms
Painless, rubbery, non-tender lymphadenopathy - often cervical LN
Lymph pain caused by alcohol !!!
Cachexia
Hepatosplenomegaly

Some young women present w cough (bc mediastinal lymphadenopathy) - Kinda rare tho!
Also can be SVC obstruction

196
Q

How are Hodgkin’s Lymphoma and Non-Hodgkin’s Lymphoma divided?

A

Histologically

197
Q

Ix Hodgkin’s Lymphoma

A

GS!!!! LN BIOPSY
REED-STERNBERG CELLS = diagnostic!!!!

↑Lactate dehydrogenase
↓Hb
↑ESR

(NB: Nodular Lymphocyte Predominant Hodgkin’s lymphoma produces Popcorn cells - variant of RS cells)

198
Q

Describe Ann-Abor Staging

A

STAGE 1 - LN in one region

STAGE 2 - 2 or more LN regions but same side of diaphragm

STAGE 3 - Affects LN both sides of diaphragm

STAGE 4 - Widespread disease outside LN in bone, liver, lung etc

A - Absence of B symptoms
B - B symptoms

199
Q

Tx Hodgkin’s Lymphoma

A

ABVD
Adriamycin
Bleomycin
Vincristine
Dacarbazine

Stage 1-2a - shorter course, then radiotherapy
Stage 2b-4b - longer course

200
Q

S/E Of Chemo

A

Alopecia
N+V
Myelosuppression
BM failure
INFECTION
Infertility
TUMOUR LYSIS SYNDROME

201
Q

Describe Reed-Sternberg cells

A

“Owl eye” nuclei cells

202
Q

Bigboi comp of Chemo
Signs / Symptoms
Tx

A

Febrile Neutropenia! - huge risk if recent/high dose chemo

Fever (38+), Tachycardia, sweats, rigors, tachypnoea

IV Beta lactam - Piperacillin + Tazobactem !!!

203
Q

Name some differences between HL + NHL

A

HL :
Reed-Sternberg cells
Skin excoriations(?)
Neutrophillia

NHL :
NO Reed-Sternberg cells (usually)
Skin rashes e.g. mycosis fungoides
Neutropenia

204
Q

Comp of Bleomycin

A

Lung damage

205
Q

Types of Non-Hodgkin’s Lymphoma

A

Low grade - Follicular
High grade - Diffuse B ** - MC (80%)
VV High grade - Burkitt’s

206
Q

Signs / Symptoms NHL

A

B Symptoms
Painless, rubbery, non-tender Lymphadenopathy
NOT AFFECTED BY ALCOHOL

Extranodal involvement MC than HL :
GI - bowel obstruction
BM - fatigue, easy bruising
Spinal cord - loss of sensation
Skin involvement - mycosis fungoides

207
Q

RF Hodgkin’s Lymphoma

A

EBV
Affected sibling
SLE
Obese
Post-transplant

208
Q

Ix Non-Hodgkin’s Lymphoma

A

GS!!!! LN BIOPSY
No Reed-Sternberg/Popcorn cells
Burkitt’s - “starry sky” biopsy

STAGING - CT/MRI chest/abdo/pelvis

209
Q

Tx Non-Hodgkin’s Lymphoma

A

R-CHOP

Rituximab
Cyclophosphamide
Hydroxydanorubicin
Oncovin (brand name) - Vincristine
Prednisolone

210
Q

MOA Rituximab

A

Targets CD20 on B cells

211
Q

Describe Low grade NHL

A

Slow growing
Usually advanced at presentation
Incurable
Median survival = 9-11 years

212
Q

Describe High grade NHL

A

Usually has nodal presentation
1/3 have extranodal involvement

213
Q

Why does ↑Lactose dehydrogenase reflect worse prognosis in malignancies usually?

A

Bc sign of increased cell turnover
∴ cell proliferation ! :/

215
Q

Alongside the normal lymphoma signs/symptoms, how might Burkitt’s Lymphoma present?

A

Jaw lymphadenopathy in children

216
Q

Pathophysiology Multiple Myeloma

A

Neoplastic monoclonal proliferation of plasma cells
∴ XS production of one type of Ig - monoclonal paraprotein (usually IgA or IgG)

217
Q

Signs / Symptoms Multiple Myeloma

A

Old CRAB

Old - 75+

Ca2+ ↑↑ - Bones, Stones, Abdo moans, Psychedelic groans
Renal failure - nephrotic + Ig light chains deposit in kidney - BJ proteins !!
Anaemia (BM failure)
Bone lesions - new onset back pain in elderly

218
Q

What chromosome abnormalities are assoc with Multiple Myeloma?

A

T (11;14) - MC
13q - poorer prognosis & Tx resistance

219
Q

RF Mutiple Myeloma

A

Afro-Caribbean
Elderly
HIV

220
Q

Ix Multiple Myeloma

A

FBC - normocytic normochromic anaemia, ↑ESR
ROULEAUX FORMATION

Urine dipstick - BENCE JONES PROTEINS

U&E - Renal failure, consider XR KUB (stones)

Bone profile - Hypocalcaemia + ↑ALP

Serum electrophoresis - IgX spike! Hypergammaglobuliaemia for IgX

XR - Skull - Pepper pot
Osteolytic lesion in long bones - “Punched out holes”

BM BIOPSY ≥ 10% plasma cells

221
Q

What is a Rouleaux Formation?

A

Abnormal aggregation of RBCs

222
Q

Tx Multiple Myeloma

A

Chemo
Bisphosphonates e.g. alendronate
Dialysis
Analgesia
Treat infections w Broad spec Abx

Consider BM stem cell transplant!

223
Q

DDx Multiple Myeloma
How to differentiate

A

MGUS - Monoclonal Gammopathy of Undetermined Significant
PRECURSOR, not actual myeloma

< 10% BM plasma cells
No/Little paraprotein spike
ASx

224
Q

Quick!!!!
Malaria Presentation?

A

Fever!!!! + Travel to malarial area

225
Q

Signs / Symptoms Malaria

A

FEVER + EXOTIC TRAVEL
Headache
Malaise
Myalgia
Diarrhoea
Cough
BLACKWATER FEVER !!!!
HEPATOSPLENOMEGALY
ANAEMIA

Delayed diagnosis - jaundice, confusion, seizures

226
Q

Ix Malaria

A

Immediate blood testing - Mandatory in UK
Detailed travel history

Microscopy of thick AND thin blood smear w/ Giemsa stain
If 1st comes back neg, serial blood films should be done at 12-24 hrs and then 24 hrs after

Rapid diagnostic test detection of parasite antigen

227
Q

Tx Malaria

A

Quinine + Doxycycline

If severe, IV artesunate
Primaquine for latent

228
Q

Polycythaemia vera assoc gene?

229
Q

What is polycythaemia vera?

A

Abnormal increase of circulating RBCs

230
Q

Pathophysiology Polycythaemia Vera

A

Clonal prolif of myeloid stem cells in BM
cells can still differentiate
∴ XS RBCs

231
Q

Cause Polycythaemia Vera

A

Somatic mutation in single haematopoietic stem cell

232
Q

Signs / Symptoms Polycythaemia Vera

A

Can be ASx

Vague - headache, dizziness, tinnitus, visual disturbance

Characteristic !!! :
ITCHING AFTER HOT BATH
Erthromelalgia
Burning sensation in fingers and toes

233
Q

Comps of Polycythaemia Vera

A

Gout
Splenomegaly
Can progress to AML !!!

234
Q

Ix Polycythaemia Vera

A

FBC - ↑↑RBC, ↑Hb, ↑PCV
↑Haematocrit !!!

JAK-2 TESTING

BM - hypercellularity

235
Q

Tx Polycythaemia Vera

A

Aim : Keep haematocrit < 0.45
so thrombosis doesnt happen!

If low risk (i.e. Young) - venesection
If > 60 and high risk - HYDROXYCARBAMIDE

236
Q

What is ITP?

A

Immune Thrombocytic Purpura
Autoimmune platelet destruction!!! - IgG !

237
Q

Types of ITP and who they affect

A

T1 - Children, 2-6 years, post viral infection. Acute, Severe.

T2 - Adult women! W/ malignancy, HIV + Other autoimmunes. Chronic, Mild.

238
Q

Signs / Symptoms ITP

A

PURPURIC RASH
otherwise, systemically well!

239
Q

Tx ITP

A

1st Line - Prednisolone
+ IV Ig - to decrease splenic platelet destruction!!

2nd Line - Splenectomy

240
Q

What is TTP?

A

Thrombotic Thrombocytic Purpura
ADAMTS13 DEFICIENCY

241
Q

What does ADAMTS13 do?
Hence Pathophysiology of TTP

A

VWF cleaving enzyme
∴ When deficienct, remain as Multimers + aggregate at endothelial injury sites !!!

242
Q

RF TTP

A

Adult Females
Malignancy
HIV
Autoimmune conditions

243
Q

Signs / Symptoms TTP

A

PURPURIC RASH
Menorrhagia
AKI !!!
Fever
Haemolytic anaemia
Schistocytes!

244
Q

Ix TTP

A

Thrombocytopenia
Fragmented RBCs - Schistocytes!
Haemolytic anaemia

↓ ADAMTS13

245
Q

Tx TTP

A

1 - Plasmapharesis

2 - Prednisolone + Rituximab

246
Q

Tx Haemophilia A

A

Desmopressin
+ IV Factor 8

247
Q

Tx Haemophilia B

248
Q

Signs / Symptoms Haemophilia

A

Joint and soft tissue bleeds

249
Q

Signs / Symptoms Thrombocytopenia

A

Petechial rash
Mucosal bleeding
Easy bruising

250
Q

Generall, when are eosinophils elevated?

A

Parasitic infection

251
Q

Generally, when are monocytes elevated?

A

Myelodysplastic syndromes

252
Q

Generally, when is there neutrophila?

A

Acute bacteria infection

253
Q

PT/INR is a measurement of:

A

Coag speed through EXTRINSIC PATHWAY
10-13.5 seconds

254
Q

Normal INR?
On Warfarin?

A

0.8-1.2

On warfarin = 2-3 !

255
Q

Why might INR be ↑ ?

A

Anti-coags
Liver disease
Vit K def
DIC !

256
Q

What does APTT measure?

A

Coag speed through INTRINSIC PATHWAY

257
Q

Pathophysiology vWF

A

vWF is normally responsible for platelet plug
∴ when not functional, easier bleeding and bruising

258
Q

APTT time?
On Heparin?

A

35-45 seconds
60-80 on heparin

259
Q

Ix vWF disease

A

Normal PT
↑ APTT
Normal F8/9

↓ vWF obvs !!

260
Q

What might APTT be affected by?

A

Haemophilia A
Haemophila B
VWF disease

^ all of these = PT normal + Prolonged APTT !!

261
Q

Tx vWF

A

No cure
Desmopressin -

262
Q

What does Thrombin Time and Bleeding time measure?

A

Conversion of fibrinogen to fibrin

263
Q

MOA Desmopressin for vWF disease

A

Releases vWF from Weibel–Palade bodies

264
Q

Cause vWF disease

A

Auto-dom mutation of vWF gene on chromosome 12

265
Q

What is DIC?

A

Massive activation of coag cascade

266
Q

Triggers of DIC

A

Trauma
Sepsis - Meningococcal meningitis!
Malignancy

267
Q

Ix DIC

A

↓ Fibrinogen
↓ Platelets
↑ D-Dimer

268
Q

Tx DIC

A

Replace clotting factors
Cyroprecipitate - replace fibrinogen
Platelet transfusion

RBC transfusion if bleeding

269
Q

Ix Haemophilia

A

Normal PT
↑ APTT

& then obvs ↓ factor 8 (A) or ↓ factor 9 (B)

Phase 2 Quick (18 decks)

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