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Haem Flashcards

1
Q

List the clinical features associated with anaemia

A

SYPMTOMS

  • Fatigue
  • Dysponea
  • Faintness
  • Palpatations
  • Headache

SIGNs

  • Pallor
  • Hyperdynamic circulation
  • Tacycardia
  • Flow murmur
  • Cardiac enlargement
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2
Q

Classify the different types of anaemia

A
  1. Microcytic
    - small hypo chromic red cells
    - decreased MCV
  2. Normochromic
    - low haematocrit
    - low haemoglobin
    - normal MCV
  3. Macrocytic
    - enlarged MCV
  4. Haemolytic
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3
Q

List the causes of microcytic anaemia

A
  1. Haem defect
    - IDA
    - ACD
  2. Globin defect
    - Thalasaemia
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4
Q

List the causes of normocytic anaemia

A 
Recent blood loss 
Bone marrow failure 
Renal failure 
Early ACD 
Pregnancy
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5
Q

List the types and causes of macrocytic anaemia

A
  1. Megablastic
    - Vit B12/ Folate deficiency
    - Anti folate drugs
    - Cytotoxics
  2. Non-megablastic
    - Reticulocytes
    - Alcohol and liver disease
    - Hypothyroidism
    - Myelodysplasia
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6
Q

List the causes of haemolytic anaemia

A

Increased RBC breakdown

  • Anaemia
  • Increased unconjugated BR
  • Increased urobilinogen
  • Bile pigment stone

Intravascular

  • Haemoglobinaemia
  • Increased haemoglobinuria
  • Increased haemosiderin
  • Methaem

Extravascular
- Splenomegaly

Acquired

  • Immune mediated
  • Mechanical
  • Infections
  • Burn
  • PNH
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7
Q

Causes of IDA

A
  1. Increase Loss
    - Menorrhagia
    - GI bleed
    - Hookworms
  2. Decreased intake
    - Poor diet
  3. Malabsorption
    - Coeliac
    - Chrohn’s
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8
Q

Findings on blood film for IDA

A

Haematinics

  • Decreased ferritin
  • Decreased TIBC
  • Decreased transferring saturation

FILM

  • Anisocytosis
  • Pencil cells
  • Poikilocytosis

May consider doing Upper and lower GI endoscopy

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9
Q

Treatment of IDA

A

Ferrous sulphate 200mg PO TDS

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10
Q

Explain the pathology of sideroblastic anaemia

A

Ineffective erythropoiesis
Increase iron absorption
Iron loading in the bone marrow - RINGED SIDEROBLASTS
Haemosiderosis

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11
Q

Causes of sideroblastic anaemia

A

Myelogysplastic/ myeloproliferative disease

Drugs ( chemo, anti TB, lead)

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12
Q

Treatment of sideroblastic anaemia

A

Pyridoxine

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13
Q

Explain the pathophysiology of thalassameia

A 
Point mutations (beta) and deletions (alpha)
Unbalanced production of global chains 
Precipitation of unmatched global 
Membrane damage
Haemolysis while still in the BM
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14
Q

Types of B thalassaemia

A 
1) Major
B0/B0 or B0/B+/ or B+/B+
Features (3-6mnth)
- Severe anaemia 
- Jaundice 
- Extramedullary erythropoiesis 
* Frontal bossing 
* Maxillary overgrowth 
* HSM 
- Haemochromatosis 
2) Trait 
B/B+ (decrease production) or B/B0 (no production)
- Mild anaemia 
- Decrease MCV
- Increase hBA2 and increase HbF
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15
Q

Findings on a blood film for B thalassaemia

A

Decrease Hb
Decrease MCV
Increased HbF
Increase HbA2 variable

FILM
Target cells and nucleated RBCs

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16
Q

Treatment of thalassaemia

A

Life long transfusions
SC desferrioxamine Fe chelation
BM transplant

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17
Q

Types of alpha thalassaemia disease

A

1) Trait
-/aa or a-/a-
Asymptomatic
Hypochromic microcytes

2)HbH disease
- -/a
Moderate anaemia
Haemolysis: HSM, Jaundice

3)Hb Barts
-/-
Hydrops fetalis
Death in utero

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18
Q

Findings for marcocytic anaemia on investigation

A

Film

  • B12/Folate
  • Hypersegmented PMN
  • Oval macrocytes
  • EtOH/ Liver
  • Target cells

Blood

  • LFT: mild increase bilirubin in B12/ folate deficiency
  • TFT
  • Se B12
  • Re cell folate: reflects body stores over 203 months

BM biopsy
Megaloblastic eythropoiesis
Giant metamyelocytes

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19
Q

Sources, stores and absorption of folate

A

Source: Green veg, nuts, liver
Stores: 4 mo
Absorption: proximal jejunum

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20
Q

Causes of folate deficiency

A

Decreased intake
- Poor diet

Increased demand

  • pregnancy
  • haemolysis
  • malignancy

Malsbsorption

  • Coeliac
  • Crohn’s

Drugs

  • EtOH
  • Phenytonin
  • Methotrexate
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21
Q

Treatment of folate deficiency resulting in macrocytic anaemia

A

1) B12 unless a normal level

3) Folate 5mg/d PO

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22
Q

Sources, stores, absorption of B12

A

Source: meat, fish and diary
Stores: 4yrs
Absorption: terminal ileum bound to intrinsic factor (released from the gastric parietal cells)
Role: DNA and myelin synthesis

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23
Q

Causes of B12 deficiency

A

Decreased intake
- Vegan

Decreased intrinsic factor

  • Pernicious anaemia
  • Post gastrectomy

Terminal ileum

  • Crohn’s
  • Ileal resection
  • Bacterial overgrowth
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24
Q

Features of B12 deficiency

A

General

  • Symptoms of anaemia
  • Lemon tinge: pallor and mild jaundice
  • Glossitis ( beefy, red tongue)

Neuro

  • Paraesthesia
  • Peripheral neuropathy
  • Optic atrophy
  • SACD
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25
Q

Discuss the features and pathology of SACD

A

Caused by pernicious anaemia
Combined synmmetrical dorsal column loss and corticospinal tract loss
Distal sensory loss, esp joint position and vibration
Ataxia, wide gait and +ve Romberg’s test

MIXED UPPER AND LOWER MOTOR NEURONES SIGNS 
- Spastic paraparesis
- Brisk knee jerls 
- Upgoing plantars 
Pain and temperature remain intact
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26
Q

Findings for pernicious anaemia on investigations

A

Decreased WCC and platelets if severe
Intrinsic abs +ve
Parietal cell abs

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27
Q

Outline the pathology of pernicious anaemia

A

Autoimmune atrophic gastritis caused by autos vs parietal cells or IF
>40yrs
Associated with thyroid disease, vitiligo, addison’s, decreased HPT
Ca: x3 risk of gastric adenocarcinoma

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28
Q

List the different types of haemolytic anaemia

A
  1. Autoimmune mediated
    - Warm
    - Cold
  2. Paraoxysmal nocturnal hemoglobinuria
  3. Haemolytic uraemic syndrome
  4. Thrombotic thrombocytopenia purpura
  5. Hereditary spherocytosis
  6. G6PD deficiency
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29
Q

List the types of AIHA and the features associated with each one

A

WARM

  • IgG mediated, bind at 37C
  • Extravascular haemolysis and spherocytes
  • Linked to SLE, RA
  • Rx: immunosuppression and splenectomy

COLD

  • IgM mediated, fix to complement (haemolysis intravascular)
  • Agglutination: acrocyanosis and Raynaud’s
  • Ix: complement alone
  • Rx: avoid cold, rituximab
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30
Q

Pathlogy PNH

A 
Absence of RBC anchor molecule (GPI) 
Decrease cell surface proteins complement degradations proteins 
IV lysis 
Affects stem cells 
Decrease platelets and PMV
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31
Q

Findings of PMH on investigations

A

Anaemia
Thrombocytopenia
Neutropenia

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32
Q

Treatment of PNH

A

Long term anticoagulation
Eculizumab prevetns complement MAC formation
IV haemolysis

33
Q

Cause of haemolytic uraemic syndrome

A

E.coli 0157:H7

Undercooked meat

34
Q

Features of HUS

A

Bloody diarrhoea
Abdominal pain
Thrombocytopenia
Renal failure

35
Q

Features of thrombotic thrombocytopenia purpura

A 
Fever 
CNS signs 
MAHA 
Thrombocytopenia 
Renal failure
36
Q

Treatment of TTP

A

Plasmapheresis
Immunosuppression
Splenectomy

37
Q

Pathology of G6PD deficiency

A

X-linked disorder of pentose phosphate shunt
Decrease EADPH production
RBC oxidative damage
Med and Middle/ Far East

38
Q

Findings on a blood film in cases of G6PD deficiency

A 
Irregularly contracted cels 
Bite cells 
Ghost cells 
Blister cells 
Heinz bodies
39
Q

Clinical features of polycythaemia vera

A 
Hyperviscosity 
- Headaches
- Visual disturbances 
- Tinnitus 
- Thrombosis 
(arterial, strokes, TIA, peripheral emboli) (venous, DVT, PE, Budd Chiari)
Histamine release
Erythromelalgia (sudden sever burning in the hands and feet with redness of the skin 
Splenomegaly 
Hepatomegaly 
Gout
40
Q

Invesitgations you would request in a patient presenting with features of polycthaemia vera

A 
JAK2 +ve 
FBC: increase RBC, Hb and Hct 
Increase WCC 
Increase platelets 
BM hyper cellular with erythroid 
Decreased EPO 
Increase RBC mass on isotope studies
41
Q

Treatment of polycthaemia vera

A

Hct <0.45 to decrease thrombosis
Aspirin 75mg OD
Venesection if young
Hydroxycarbamide

42
Q

List potential differentials for polycthaemaia

A

True polycthaemia: total volume of red cells
Primary: PV
Secondary: Hypoxia, altitude, COPD and smoking

Pseudopolycthaemia 
(decrease plasma volume) 
Acute 
- Dehydration 
- Shock 
- Burns

Chronic

  • Diuretics
  • Smoking
43
Q

Pathology of sickle cells disease

A 
Point mutation in B globin gene 
glu- val 
SCA: HbSS
Trait: HbAS 
Cells have a decreased life span 
Haemolysis 
Thrombosis
44
Q

Findings on investigation sickle cells disease

A 
Low Hb 
Increased reticulocytes 
Increased bilirubin 
Sickle cells and target cells 
Hb electrophoresis
45
Q

A patient presents with long term leg ulcers complaining of bone pain. His renal function tests of off and you notice he has dactylics.
His Hb is 6 with high BR. Blood film reveals target cells
What is the dx?
How would you treat this patient in the short and long term

A

Sickle cells disease

Acute 
- Analgesia ( opioids IV) 
- Good hydration
O2
- Keep warm

Chronic

  • Pen V BD + immunisations
  • Folate
  • Hydroxycarbamide
46
Q

Describe the pathogenesis of myeloma

A

Clonal proliferation of plasma cells
Raised monoclonal IgG or IgA
Increased production of free light chains
Urinary BJP
Clones produce IL6 which inhibits osteoblasts and activate osteoclasts

47
Q

Symptoms of multiple myeloma

A 
Calcium: Hypercalcaemia of malignancy 
R: Renal Impairment 
- Light chains 
- Increase Ca 
- AL amyloid 
Anaemia 
- Bone marrow infiltration 
- Neutropenia 
- Thrombocytopenia 
Bone
- Bone lesions 
- Backache and bone pain 
- Pathological #
- Vertebral collapse
48
Q

An elderly man in his 90’s presents complaining of back ache. He says it has been getting worse over the past 3 months. He says he has also just been feeling a bit off, tummy aches and down in himself. He has also been lacking in energy and breathless when climbing the stairs.
What is your working dx?
What investigations would you order to support this diagnosis

A

Multiple myeloma

1) ESR and se electrophoresis if >50 with back pain

2) Bloods
- FBC; normocytic normochromic anaemia
- Film; rouleaux and plasma cells and cytopenias
- Increased ESR, Increased U&Es
- Increased Ca
- Normal ALP

3) Urine electrophoresis BJP

4) XRAY skeletal survey
- Punched out lytic lesions
- Pepper pot skull
- Vetebral collapse
- Fractures

5) Bone marrow biopsy
- Clonal BM plasma cells >10%

49
Q

Treatment of multiple myeloma

A

Supportive

  • Analgesia and bisphosphonates for the bone pain
  • Anaemia: transfusion and EPO
  • Renal impairment: adequate hydration
  • Infections: broad spec abx

Complications

  • Hypercalcaemia: hydrations, frusemide and bisphosphonates
  • Cord compression: MRI, dexamethasone, local radiotherapy
  • Hyperviscosity: Plasmapheresis (remove the light chains)
  • AKI: rehydration

Specific:

  • Fit: induction chemo
  • Allogeneic BMT

Unfit

  • Chemo only
  • Bortezomib
50
Q

List the key features of acute lymphoblastic leukaemia

A
  1. BONE MARROW FAILURE
    - Anaemia
    - Thrombocytopenia
    - Leukopenia
  2. INFILTERATION
    - Lymphadenopathy
    - Orchidectomy
    - Thymic enlargement
    - Bone pain
51
Q

A young child aged 21/2 years presents to A7E for the third time in a month with a bad infection and a high fever. The on call consultant worries he may have ALL.
What investigations would you order and what would they show if this was the case?

A

Bloods

  • FBC
  • Increased WCC
  • Low RBC, low PMN

Bone marrow aspirate
- >20% blast cells

CXR
- mediastinal and abdo lymph

52
Q

Outline the complications associated with chronic lymphocytic leukaemia

A

Autoimmune hepatitis
Evan’s: AIHA + ITP
Marrow failure

53
Q

Discuss the link between CML and the philadelphia chromosome

A

Reciprocal translocation
Formation of BCr- ABL fusion gene
>80% CML

54
Q

Treatment of CML

A

Imatinib
- Tyrosine kinase inhibitor

Aloogenic stem cells transplant

55
Q

Key features of the non hodgkin’s lymphoma lymphadenopathy

A

Painless
Symmetrical
Spreads discontinuously

56
Q

Classify non Hodgkin’s lymphoma

A 
B-cell 
- low grade 
Follicular 
Small cell 
Marginal zone
  • high grade
    Diffuse large B cell
    Burkitts

T CELL
Adult T cell
Enteropathy assoc
Anaplastic

57
Q

Treatment of non hodgkins lymphoma

A

R-CHOP regimen

58
Q

Features of hodgkin’s lymphoma lymphadenopathy

A

Painless
Asymmetrical
Continous

Mass affect such as SVC obstruction and bronchial obstruction

59
Q

Features of hodgkin’s lymphoma seen on LN biopsy

A

Reed stein burg cells

60
Q

Treatment of hodgkin’s lymphoma

A

ABVD regimen

61
Q

Discuss the types of thrombophillias

A

INHERITED

1) Protein V leiden/ APC resistance
- Deactivates proteins and thrombomodulin cofactors
- Don’t develop thrombosis

2) Prothrombin Gene Mutation
- Increase in prothrombin levels
- Increase in thrombosis due to decrease fibrinolysis by thrombin-activated fibrinolysis inhibitor

3) Protein C and S deficiency
- Increase of thrombosis
- Skin necrosis ( esp with warfarin)

4) Antithrombin III Deficiency
- Thrombin inhibition

ACQUIRED

  • Progesterone in OCPs
  • Anti phospholipid syndrome
62
Q

Systems involved in anti-phospholipid syndrome

A

“CLOTS”

  • Coagulation defect, increase APTT
  • Livido reticularis
  • Obsteric complication (recurrent 1st trimester abortion)
  • Thrombocytopenia
63
Q

Indications for doing a thrombophilia screen

A 
Arterial thrombosis <50 
Venous thrombosis < 40 
Familial VTE 
Unexplained recurrent VTE 
Unusual site ( portal/mesenteric) 
Recurrent foetal loss 
Neonatal 
Investigations 
FBC 
Clotting 
Fibrinogen concentration 
Factor V leiden / APC resistance 
Lupus anticoagulant and anti-cardioliin 
Assay for AT, protein C and s deficiency
64
Q

Treatment of patients with thrombphillia

A 
Rx acute thrombosis 
Anticoagulate INR 203 
Consider life long warfarin 
Note the increase VTE risk with OCP and HRT 
Prophylaxis in high risk situations
65
Q

Classify the types of vascular bleeding disorders

A

CONGENITAL

  • HHT
  • Ehler’s Danlos (easy bruising)
  • Pseudoxanthoma elasticum

ACQUIRED

  • Senile purpura
  • Vit C deficiency
  • Infection
  • Steriods
  • Vasculitits (HSP)
66
Q

Classify platelet disorders

A

Thrombocytopenia ( low platelets)

DECREASED PRODUCTION

  • BM failure, aplastic, infiltration, drugs (EtOH, cyto)
  • Megloblastic anaemia

INCREASED DESTRUCTION

  • Immune (ITP, SLE, CLL, heparin, viruses)
  • Non immune (DIC, TTP, Hus, PNH, anti-phospho)
  • Splenic pooling ( Portal HTN, SCD)
67
Q

List possible coagulation disorders

A 
Haemohilia A ( F8 Deficiency) 
Haemophillia B (F9 Deficiency) 
Von Willebrands deficiency
68
Q

Discuss the pathology and treatment of haemophilia A

A

Deficiency in F8
X-linked (affects males, more common than haemophilia B)
Presents with haemoarthroses, bleeding after surgery

Increased APTT
Normal PT
Decreased F8 assay

Treatment

  • Avoid NSAIDS and IM injections
  • Minor bleeds ( desmopressin and transexamic acid
  • Major bleeds (hF8)
69
Q

Discuss the pathology and treatment of von Willibrand disease

A

Commonest inherited clotting disorder
Stablises F8
Binds platelets to Gplb to damaged endothelium

  • Increased APTT, bleeding time, normal plat, decreased vWF AG

Treatment

  • Desmopressin
  • Transexamic acid
70
Q

List the causes of pancytopenia

A

CONGEITAL
- Fanconi’s anaemia

ACQUIRED

  • Idiopathic aplastic anaemia
  • BM filteration
  • Leukaemia
  • Lymphoma
  • Myelofibrosis
  • Megaloblastic anaemia
  • Infection
  • Radiation
  • Drugs
71
Q

Features of aplastic anaemia

A 
Rare stem cell disease 
Pancytopenia 
Hypocellular marrow 
Anaemia 
Infections 
Bleeding 
15-24yrs
>60yrs
72
Q

Causes of aplastic anaemia

A

Inherited
- Fanconi’s anaemia

Acquired

  • Drugs
  • Viruses (parovirus)
  • Autoimmune (SLE)
73
Q

Investigation of aplastic anaemia

A

Bone Marrow

- Hypocellular marrow

74
Q

Treatment of Aplastic anaemia

A

Tranfusion
Immunosupression
Allogeneic BMT

75
Q

Pathophysiology of myelodysplastic syndrome

A

BM failure
Clone of stem cells with abnormal development
Chemo or radiotherapy

Cytopenia
Hypercellular BM
Ringed sideroblasts
Can lead to AML

76
Q

Treatment of myelodysplastic syndromes

A 
Supportive 
- transfusions 
- EPO 
Immunosuppression 
Allogenic BMT
77
Q

Define amyloidosis

A

Grape of disorders characterised by extracellular deposits of protein in an abnormal fibrillar form that is resistant to degradation

78
Q

Features of AL amyloidosis

A

Proteinuria and nephrotic syndrome
Restrictive cardiomyopathy - sparkling appearance on echo
Nerves peripheral and autonomic neuropathy
GIT macroglossia, malabsorption, haemorrhage and obstruction
Vascular periorbital purpura

Very short median survival

Haematology (1 decks)

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