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Year 2: Clinical Pathology > Haematology > Flashcards

Haematology Flashcards

1
Q

Haemopoiesis

A

Production of blood cells and plasma that occurs in the bone marrow

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2
Q

Multipotent haemopoietic stem cell - does what?

A

Can divide/ differentiated into any cell linage and produce mature blood cells

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3
Q

two Cell linages - and the mature cells they produce?

NOTE: ‘White (immune) blood cells’ come from 2 different linages

A

Myeloid - erythrocytes, platelets, monocytes, neutrophil, basophil and eosinophil

Lymphoid - Lymphocytes - T cells, B cells and natural killer cells

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4
Q

What are granulocytes? 4 Examples (what they do)

A

Myeloid linage cells with granules in the cytoplasm eg

Neutrophils - phagocytosis
Eosinophils - parasitic infection
Basophils - allergic/ innate reactions
Mast cells - release histamine in allergic reaction

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5
Q

What do monocytes do?

A

Myeloid linage.
Monocytes in the blood BUT macrophages in tissue
Antigen presenting Cells, Phagocytosis

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6
Q

Specialized monocytes in specific tissues?

A

Kupffer cells in the liver

Langerhan cells in the skin

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7
Q

Stem cells division methods (4) - what they produce + affect on stem cells pool?

Symmetrical
Asymmetrical
Lack of Self renewal
Lack of self renewal 2

A

Symmetric = self renewal of 2 stem cells = increase pool
Asymmetric = 1 Progenitor 1 stem cells = maintain pool
Lack of self renewal
= produce two Progentior cells = reduce pool
= don’t divide = maintain pool

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8
Q

Progenitor cell?

A

A pluripotent stem cells that are either common meyloid or common lymphoid progentior cell
Remain in blood for lifetime

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9
Q

Meylopoesis

A

Production of meyloid linage cells

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10
Q

Lymphopoesis

A

Production of lymphoid linage cells

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11
Q

Mature cells - lifespan in the blood?

A

Limited
Erythrocytes = 120 days
Neutrophils = 6 - 10 hours

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12
Q

Haemopoesis in the feotus? –> child?

A

Aortic gonad mesonephros –> Liver –> spleen

–> Bone marrow when born (production in liver and spleen stop)

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13
Q

Aneamia = ?

A

Reduced Erythrocytes

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14
Q

Raised erythrocytes?

A

polycythaemia

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15
Q

Reduced neutrophils ? (often due to drugs)

A

Neutropenia

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16
Q

Neutrophillia (usually due to inflammation and what type of infection?)

A

Raised neutrophils

Due to BACTERIAL infection

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17
Q

Increased eosinophils? - due to parasitic infection and allergies

A

Eosinophilia

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18
Q

Basophillia - is due to?

A

Increased Basophils

Due to chronic myeloid leukeamia

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19
Q

Raised Monocytes is called and occurs when?

A

Monocytosis - during TB infection

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20
Q

Reduced lymphocytes

Increased lymphocytes

A 
Reduced = Lymphopenia 
Increased = Lymphocytosis
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21
Q

Causes of increased lymphocytes?

A

Viral infection eg. glandular fever (EBV)

Lymphocytic leukaemia

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22
Q

Increased plasma cells - what called and why?

A

Plasmacytosis

Due to infection or myeloma

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23
Q

Thrombocytopenia?

A

Reduced platelets

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24
Q

What measurements does a full blood count include?

A 
Hb concentration
Mean cell volume
Mean cell Hb
White blood cell count
Platelet count
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25
Q

Testing blood cells includes? (4)

A

Full blood count
Blood film/ cultures - for pathogens in blood (sepsis
Coagulation screen - time taken to clot in certain agents
Bone marrow - aspirate and Trephine (core biopsy)

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26
Q

What is EDTA?

A

The preservative used to collect blood into

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27
Q

When are blood results outside the ‘normal ranges’ considered normal?

A

If they are normal for that patient in that clinical situation
eg. low WBCC due to recent bone marrow transplant

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28
Q

Microcytic hypochromic aneamia?
MCV ?
MCH
Causes (3)?

A

Small RBC low RBCC
Low MCV and low MCH

iron deficient, Thalasaemia - other blood disorders

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29
Q

Normocytic normochromic aneamia?
MCV ?
MCH
Causes (4)?

A

Normal sized BUT low RBCC
Low MCV and normal MCH

Blood loss, kidney disease (other chronic disease), bone marrow failure

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30
Q

Macrotcytic aneamia?
MCV ?
Causes (3)?

A

Large RBC low RBCC
High MCV

Vit B12 or folate deficiency, Haemolytic anaemia, myelodysplasic syndrome

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31
Q

Myelodysplasia syndrome what is it?

A

Strain of cancers
Mutation in stem cells
Immature blood cells can’t mature or leave the bone marrow
Abnormal cells that do reach the blood = cytopenias

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32
Q

Characteristics of Myelodysplasia?

A 
Hypogranular neutrophils
Aneamia
Thrombocytopenia
Neutropenia 
Oval macrocytes
Increased cellular activity in bone marrow
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33
Q

Symptoms of myelodysplasia syndrome (4)

A

Fatigue
dysppnoea
Infections
bruising and bleeding

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34
Q

Refractory aneamia - blood test measurement?

A

High haemoglobin (MHC)
Normal WBCC and platelets
Low RBCC

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35
Q

Refractory aneamia (type of myelodysplasia) - what is it? results in what appearance of RBC? (4)

A 
Increased erythoid precursors in the bone marrow 
RBCs are 
Different shaped (dimorphic)
Different sizes (anisocytic)
Loss biconcave appearance
Stomatocytes - slit in them
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36
Q

Treatment for refractory aneamia

A

Iron chelation or frequent blood donation to reduce iron overload
Erythropoietin injections = normal RBC produced

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37
Q

Leucodepletion?

A

Removal of WBC from donated blood

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38
Q

Blood plasma from donations is separated and used in? (3)

A

Fresh frozen plasma
cryopercipitate
Fractionation - Forming factor concentrates (clotting cascade factors), immunogloblins and albumin

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39
Q

Packed Red blood cell donation - storage

A

4 degrees for 35 days

electrolyte solution

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40
Q

‘Group and screening’ of recipient before blood transfusion involves?

A

Grouping by ABO group and Rh

Screening = For antibodies against any specific antigens

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41
Q

‘Crossmatching’ of recipients and donors blood before transfusion involves?

A

Patients plasma + sample of donor blood –> agglutination? or haemolysis occur? (counter indication)

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42
Q

Transfusion threshold?

Values?

A

Level to which Hb most drops before a Packed RBC transfusion is required
<70 g/L = acute anaemia
<80 g/L for those with cardiovascular disease

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43
Q

Indicators for packed RBC trasnfusion for hemorrhage?

A

30-40% blood loss = transfusion considered

>40% blood loss = transfusion required

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44
Q

Objectives for transfusion in chronic aneamia?

Targets?

A

Due myeloid failure syndromes
Symptoms relief - fatigue
Prevent long term ischemic injury to organs

Hb 80-100 g/L - above which is iron overload

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45
Q

Objectives and risk of transfusion in Thalasameia?

Targets?

A

Supression of endogenous erythropoetin BUT Risk of iron overload
Hb 100-120 g/L

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46
Q

Counter indications for Pack RBC donations? (3)

A

Patients wishes and believes
Adverse effect and risk of cross reaction
Alternatives:
- correcting aneamia (iron or B12)
- Correcting anticoagulation - stopping medications

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47
Q

Platelet donations - storage

A

Room temp for 5 days

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48
Q

Adult Theraputic dose (for platelet donation?)

A

4 pooled donations (separated from full blood)

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49
Q

Indication for Platelet transfusion (3) plus examples

A

Thrombocytopenia, platelet dysfunction OR bleeding prevention
Eg.
Haemorrhage
Bone marrow dysfunction + complication (sepsis)
Prophylaxis for surgery

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50
Q

Counter indications for platelet transfusion (2)

A

Herparin induced thrombocytopenia

rare clotting disorders

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51
Q

Fresh Frozen plasma (FFP) donations - storage?

A

-30 degrees stored for 24 months - thawed before use

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52
Q

Indications for FFP?

A

Where clotting factors are required

Surgery, Haemorrhage AND rare clotting disorders

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53
Q

Counter indications for FFP?

A

Warfarin reversal

Single factor deficiencies

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54
Q

PCC - prothrombin complex concentrate - what is it? what is it used for?

A

Plasma derived clotting factors plus vit K

reversal of life threatening over anti-coagulation (bleeding)

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55
Q

Acute transfusion reactions - immunological cause? (4) + timings after transfusion

A

Heamolytic transfusion reactions (ABO incompatibility) - 15 mins
Tranfusion related acute lung injury (TRALI) - 72-90 hours
Allergies - urticarial rash
Anaphylaxis

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56
Q

Acute non immunological transfusion reactions? (2)

A

Transfusion associated circulatory overload (TACO)

Febrile non-haemolytic transfusion reaction (FNHTR)

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57
Q

Long term immunological transfusion reactions *3 - 14 days

A

Delayed haemolytic reactions

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58
Q

Long term non immunological transfusion reactions

examples

A

Transfusions transmissible infections (TTI)

eg. Hep B and C, HIV, prion disease

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59
Q

Symptoms of acute ABO incompatibility?

Cause?

A 
Acute renal failure, microvascular thrombosis and vasodilation
Fever
Chills 
Back pain
Shock - hypotension

Human error

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60
Q

TRAIL - cause and effect?

Main donations

A

Transfusion related acute lung injury

Activated WBC against HLAs of donors blood –> lung infiltrates (seen on Xray)

FFP and platelets

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61
Q

Risk factors for overload (TACO)

A

Elderly, children and those Left ventricle dilations

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62
Q

Delayed haemolytic reactions - what its it? how presents?

A

IgG against ABO blood groups

Presents as jaundice, fatigue and fever with low Hb

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63
Q

Heritable bleeding disorders?

A

Often one defect

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64
Q

Von Willeband factor?

A

Stimulates the production of a fibrin clot

Interacts with vessel wall and platelets

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65
Q

Clinical presentation of Von Willeband disease

A

Petechiae - non blanching, non palpable rash
Superfical bruise
Bleeds are prolonged but not recurrent

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66
Q

Von willebane disease is?

A

Hereditary bleeding disorder with varying penetrance

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67
Q

3 types of Von willeband disease

A

Type 1 = mild. (dominant) Reduced amount (not made or quickly destroyed)
Type 2 = normal amount BUT defective
Type 3 = completely absent (recessive)

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68
Q

Treatment for Von willeband disease (4)

A

Antifibrolytics eg. tranexamic acid
Desmopressin - stimulates vWF production
Plasma derived vWF from donors
OCP - for menorrhagia

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69
Q

Co-agulation defects ?

A

Deficiency in one of the co-agulation factors

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70
Q

Clinical presentation of co-agulation defects? (5)

A 
Deep muscular bleeds - haematomae
Joint bleeds - Haemarthrosis
Retroperintoneal bleeds
Prolong and recurrent bleeds 
After trauma Spontaneous bleeds
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71
Q

Haemophillia - two types? inheritance?

A

Type A = VIII deficient
Type B = IX deficient or christmas disease

Both X linked recessive
Abnormal activated partial prothrombin time

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72
Q

Treatment of haemophillias

A

Replace clotting factors with FFP
Desmopressin
antifibrolytic
Icing and rest

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73
Q

Acquired bleeding disorders

A

Often defects in many factors

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74
Q

Vit K deficiency - what factors affected?

A 
Vitamin K dependent factors 
II
VII
IX
X
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75
Q

Causes of vitamin K deficiency ? (4)

A

Antibiotics
Neonates
Obstructive jaundice
Prolong nutritional deficiency

76
Q

Massive Transfusion syndrome - what cause it (2)? what it results in?

A

Transfusion of blood volume equivalent to total volume in less then 24 hours
loss of 50% of blood volume in 3 hours

Dilation depletion of clotting factors

77
Q

DIC - what does it stand for?

A

Disseminate intravascular coagulation

78
Q

What is disseminate intravascular coagulation?

A

General disruption to the physiological balance of procoagulative and anticoagulant mechanism
eg. excessive use of platelets and clotting factors

79
Q

Acute causes of DIC (4)

A

Sepsis
Trauma
Acute heamolysis (ABO mismatch)
Tissue necrosis

80
Q

Chronic causes of DIC (3)

A

Malignancy
Liver disease
Retained dead feotus

81
Q

Treatment for DIC

A

Treat underlying cause (Eg. chemo, antibiotics)

Supportive treatment = maintain profusion, folic acid and vit K supplements

82
Q

Indicators for emergency management of DIC (3)

A

Platelet <50 g/L = platelet transfusion
PT or APTT ratio >1.5 = FFP given
Fibrinogen <1g/L = antifibrolytics

83
Q

APTT - Activated partial thromboplastic times - what does it test?

A

Time for blood clot via the intrinsic pathway (when reacted with silica)

84
Q

PT/INR - prothrombin time/ internalised normal ratio

A

Assess the extrinsic pathway (Tissue factor is added)

85
Q

TCT - Thrombin clotting time

A

Time till clot forms when thrombin added

86
Q

Warfarin - what kind of anticoagulant. How monitored?

A

Vit K antagonist

Monitored by PT/ INR –> aka verse the average time

87
Q

Warfarin drug interactions - what increase bleeds (6)(potentiate)

A 
Ampicillin
Erythromycin
NSAIDs
Anti -acids
Corticosteroids
Amidodarone - AF treatment
88
Q

Warfarin drug interactions - that increase clotting (antagonist) (5)

A 
Rifampicin 
Carbamazepine (epilepsy)
Cholesterol lowering
Kidney failure (K+ sparing)
Vit K
89
Q

Reversing Warfarin
Life threatening?
Non life threatening?

A

WITH HOLD warafin and give vit K

Life threatening = also give Factor IV and Prothrobin complex concentrate (PCC)

90
Q

Heparin - how does it work?

A

Stimulates exogenous fribolytic mechanisms

91
Q

Heparin - over anti-coagulation reversal treatment?

A

Stop heparin

Administer Protamine

92
Q

LMWH - low molecular weight heparin –> advantages?

A

More predictable = monitor less
Longer half life = administer less
better bioavaiability

93
Q

Examples of LMWH (3)

A

Deltaparin
tinzaparin
enoxaparin

94
Q

Myeloproliferative disorder that results in ‘thick blood’?

A

Polycytheamia vera - increased RBC, (platelets and neurtophils)

95
Q

HCT? - in a blood test and EPO in a blood test?

A 
HCT = the % of RCB out of total blood cells
EPO = amout of erythropoetin in the blood
96
Q

What are secondary polycytheamias?

What are relative polycytheamias?

A

Secondary = to another disease eg. kidney failure, COPD, chronic hypoxia

Relative = due to normal RBC but low plasma levels due to dehydration

97
Q

Signs and symptoms of polycythemai vera (10)

A 
Plethora - excessive bodily fluid
Itching - when in hot water 
Splenomegaly 
Engorged retinal vessels
Headache
Malaise
Tinnitus
gout
Gangrene
peptic ulcer
98
Q

Cause of Polycytheamia - with elevate EPO?

with normal EPO

A 
Elevate = kidney disorders
Normal = JAK2 gene mutation and Polycytheamia vera
99
Q

Essential thrombocytosis

A

Myeliodproliferative disease –> increased platelets

Increased thrombotic risk

100
Q

Essential thromocytosis - differential diagnosis for raised platelets? (7)

A 
Surgery
Infections
Inflammation
Malignancy
iron deficient
hyposplenism
Drugs
101
Q

Diagnosis of Essential Thrombocytosis?

Genes that cause?

A

Exclude other causes
Persistent platelets over >450x10^9/L

Genes 
JAK2 (50% of cases)
CALR (45% of cases - JAK2 negative)
102
Q

Treatment of thrombocytosis?

A

Assess clotting risk

Aspirin 75 mg daily

103
Q

Idiopathic myelofibrosis - presents as?

A 
Many cytopenias
Large spleen (splenomegaly)
104
Q

Genetic involved in myelofibrosis

A

JAK2 and CALR

105
Q

Treatment and prognosis for myelofibrosis?

A

JAK2 inhibitors
Bone marrow transplant

5 years - not good

106
Q

What is chronic myeloid leukaemia ? - myleoproliferative disorder
Mutation?

A

Pluripotent stem cell disorder
T(9:22) or Philadelphian translocation on BCR-ABL fusion gene
Too many Mature WBC in the blood

107
Q

Presentation and symptoms of myeloid leukaemia (5)

A 
Leucocytosis
Aneamia 
Splenomegaly - due to infarction
Venous occlusion (renal and DVT)
Gout
108
Q

Treatment of Myeloid leukaemia?

A

Oral cytotoxic drugs eg. busulphan
Interferons
Allogenic bone marrow transplant (50% curative)
Imatinib = Tyrosine kinase inhibitors for BCR-ABL genes

109
Q

IgM - what is it released?

A

When a B cells is exposed to an antigen in the blood

initial immune response

110
Q

Class switching of IgM –> another Ig.
When/ where does it happen?
What cells can express all the Igs

A

Class switching occurs when naivee B cells are exposed to antigen in primary lymphoid tissue and they mature into PLASMA or MEMORY cells

Therefor Plasma cells are monoclonal and express Ig G, E, D, A, and M

111
Q

Plasma cell differentiation pathway (4)

  • in the lymph tissue
A

Proliferation - only those with highly specific receptors = monoclonal
Immunoglobin somatic hypermutation and class switching - heavy chains change
Selection - only those with high affinity for the antigen
Differentiation –> mature cell

112
Q

Immunogloblins
Light chains =
heavy chains =
- held together by disulphide bonds

A 
Light = kappa or lambda
Heavy = A, G, E, M or D
113
Q

Plasma Dyscrasias - caused by?

A

Disorders of plasma cells

Abnormal proliferation of monoclonal plasma cells

114
Q

Detecting plasma cells and Igs

A

Serum Protein electrophoresis (ablumin, Ig alpha 1 and 2, Ig Beta and Ig gamma)

Immunofixation - to find specific monoclonal Igs

115
Q

Detection of the a Plasma Dyscrasia

A

‘M spike’

Protein electrophorsis shows that M protein is being released by the defective monoclonal plasma cells

116
Q

Most common Plasma Dyscrasias

A

MGUS - monoclonal gammopathy of uncertain significance

117
Q

Diagnosis myeloma?

  • MRE criteria = test
  • CRAB criteria = symptoms
A 
Bone marrow biopsy + blood test + MRI
= MRE myeloid defining events
>60% clonal plasma cells in biopsy
>1 bone lesion on MRI over 5mm
>100 mg/L of serum light chains

C- hypercalceamia
R - renal insufficiency
A - anaemia
B - bone lesions

118
Q 
Symptoms of CRAB
Hypercalceamia
Kidney insufficiency 
Anaemia
Bone lesions
A

C = constipation, confusion, anorexia and polyuria

R = confusion, oliuria

A = fatigue

B = bone pain back an ribs

119
Q

MGUS -monoclonal gammopath of uncertain significance

diagnosis?
% progression to Myeloma?

A

Serum M protein <30 g/L

30% progress to myeloma (others can progress lymphoproliferary disorders)

120
Q

Amyloid Light chain Amyloidosis - what is it?

A

Defective genes = missfolding of Ig light chains –> aggregate = beta plated fibrils

121
Q

Affect of AL Amyloidosis?

A

Proteinuria 3g/day
Liver and cardiac symptoms

Fibrils seen in urine by urine PCR

122
Q

Non hodgkins lymphoma - what is it?

Causes?

A

Enlargement of LN in certain patterns + splenomegaly

Malignant or non malignant (infection, inflammation) - most rule out

123
Q

2 types of non-hodgkins lymphoma?

A

High grade + acute onset - systemic symptoms (weight loss)
eg. Burkitts Lymphoma

Low grade + chronic onset - clinically well, clear bloods, relapsing patterns
eg. Follicular lymphoma

124
Q

Follicular lymphoma? - causes

A

Type of non hodgkins - gradually increasing size of LN

Genetic component - T(14:18) BCL2 protooncogene = neoplastic cells aren’t apoptosed

125
Q

Prognosis of Folliucular lymphoma? - what is it called (5) aspects

A

FLIPI - follicular lymphoma internation prognostic index

Age >65
Ann Arbor staging 
4 + nodules
low Hb
LDH levels
126
Q

Hodgkin’s Lymphoma - what is it?

A

Neoplastic lymphocytes called Hodgkin Reed-sternberg (HRS) cells - specific histology

127
Q

Hodgkins lymphoma - affects? (3)

85% 5 year survival

A

LN sclerosis
Reduction in number of lymphocytes
Mixed cellular presentation

128
Q

Chronic Lymphocytic leukamia - what is it?

Presents with?

A

Disorder of mature B cells
Lymphadenopathy and splenomegaly
Lymphocytosis in blood tests
Bone marrow failure –> systemic symptoms

129
Q

Grading system and Complications (5) of Chronic Lymphocytic leukamia?

A

Grading = Binet’s System

Complications =
Progression to higher grade leukemias
Recurrent infections
Haemolytic aneamia
Neutropenia 
Thrombocytopenia
130
Q

Haemoglobin switches at birth?

Chromosomes 16 and 18 involved

A

Feotus = HB-F

At birth = HB-F (50%): HB-A (50%)

Neonatial = HB-A

Adult = HB-A2

131
Q

Why HB-F haemoglobin in utrio?

A

Higher affinity for Oxygen so can compete with mothers HB-A2

132
Q

Difference in RBC structure in children VS adults?

A 
Larger RBC
higher Haemocrit (% RBC/ total cells)
133
Q

Lymphocytes in the feotus

  • Passive immunity
  • Own immune system?
A

IgG - crosses the placenta
IgA, D, E, G, M - in breast milk

Own antibodies not made til 2 - 3 months
Satisfactory immune response at 6 months

134
Q

Platelets in the fetus - when do they reach adult level

any differences VS adults?

A

18 weeks gestation

Less responsive to some agents BUT more responsive to vWF

135
Q

Coagulation factors in feotus?

Vit K in the feotus?

A

Do not cross placenta - prevents clotting in the embillicus
Reach adult levels by 6 months
Vit K = only 10% of mothers –> require supplements

136
Q

Causes of congential anemia (7) + examples

A

Haemoglobin sysnthesis issues eg. thalassaemia and sickle cell

Bone marrow failure

Peripheral destruction - auto antibodies (RHs incompatibility)

Membrane defects eg. Hereditary spherocytosis

Enzyme defects eg. G6DP

Twin - twin transfusion (shared placenta) = blood loss in one

Fetomaternal haemorrhage on deliver = blood loss

137
Q

Causes of Acquired anemia in neonates? (4)

A

iron B12 and folate deficient (malnutrosed)
Bone marrow failure
Haemolytic anemia
Blood loss + bleeding disorders (rare)

138
Q

Changes in RBC during pregnancy? (3)

at 32 weeks gestation

A

Plasma volume and MCV increases by 50%
Haemodilation (red cell mass) increase by 25% = macrocytic
Anaemia is common

139
Q

Leucrocytic changes in pregnacy?

2nd trimester

A

Neutrophillia (increase)

140
Q

Gestational platelet count?

A

Raises till 20 weeks
Falls again (thrombocytopenia) - should always check this is not for a pathological reason
Recovers rapidly after birth

141
Q

Coagulation in pregnancy?

A

Prothrombotic or hypercoagulative state
Decreases in Anticoagulants and fibrolysis
Increase in coagulation factors

142
Q

Testing for blood disorders in pregnancy? (3)

A

Genetic screening - Paternal testing
Antenatal screening - amnio and villus for those high risk patients
Post natal - heal prick test for Haematopathologies (SC and thalaseamia)

143
Q

Testing for haemoglobinopathologies (3)

A

Hb electrophoresis
Heat instability + O2 dissociation curve
DNA analysis

144
Q

Sickle Cell - what is it/ what goes?

A

Single point mutation in beta globin = HBS.

Polymerises in low O2 = tactoids –> distort the shape of cell

145
Q

Affect of Sickle cell

A

HbS = charged –> seen on electrophoresis
Reduced life span of cells = haemolytic aneamia
Reduced O2 delivery
Haemostatic activation = microvascular thrombosis and inflammatory style disorders

146
Q

Compliactions of sickle cell

A

Vasculooclusion - Dactylitis, chest and ab pain
Septiceamia
Aplastic crisis - sudden stop in production of RBC = aneamia
Hyposplenism
Renal disease
Avascular necrosis (femoral head)
Leg ulcers, gall stones, rentinopathy

147
Q

Treatment/ management (3)

A

Hydroxycarbomide - revert some HbS –> HbF prevents some aggregations
Transfusions, hydration and analgesics - for acute crisis
Penicillin prenatally for 6 months

148
Q

Thalasaemia - what is it?

A

Genetic mutation - heterogeneous

Reduced synthesis of certain Hb chains = imbalance of chains –> pathology

149
Q

Types of Thalaseamia
Based on what chain is not produced
- And severity

A

Alpha
Beta

  • Minor = Carriers looks like iron deficient - small pale RBC
  • Intermediate = clinical symptoms BUT variable genotype
  • Major = life threatening
150
Q

Affects of Thalaseamia B

A

Excessive alpha chains - ineffective erythropoiesis + reduced RBC life span –> aneamia

Increases bone marrow activity - skeletal deformities, increased iron absorption, organ damage

Enlarged/ overactive spleen - increased transfusion requirements

151
Q

Other symptoms of thalaseamia B
Intermedia (5)
Major (presentation)

A

intermediate = Anaemia, pulmonary hypotension, bone changes, leg ulcers, hypothyroidism

Major = presents as aneamia 1st/ 2nd year of life

152
Q

Treatment of Thalasemia (5)

A 
Transfusion
Iron chelation (Desferrioxamine)
Hormone replacements
Monitoring
Genetic counselling and screening
153
Q

Arterial VS Venous thrombotic event

A

Arteriole = plaque rupture –> endothelial injury and platelet aggregation

Venous = Virchows triangle (hypercoagubility, statis and endothelial injury) –> Coagulation response

154
Q

Arterial VS Venous thrombotic conditions?

A

Arteriole = MI or ischemic stroke - Treat with anti platelets

Venous = VTE including DVT and PE. Treat with anti-coagulants

155
Q

Pro -coagulant produces (2) anticoagulant reagents (5)

A

Pro = Clotting factors and platelets

Anti = Protein C
Protein S
Fibrinogenolytic system
Anti-thrombin

156
Q

VTE - PE and DVT - percentage of each condition that also has a silent version of the other?

A

VTE = venous thromboembolism

50% DVT have an asymptomatic PE

80% of PE have a silent DVT

157
Q

Characteristics of VTE

A

Recurrent
Post thrombotic syndrome - damage valves and swelling
Mainly hospital acquired - due to hypercoagulative state

158
Q

Risk factors for VTE (11)

Past medical
Current conditions
Drugs

A 
Active/ past cancer
Family history
Major trauma/ surgery
recent pregnancy
Dehydration
Obesity
Varicose veins
OCP - oestrogen
Periods of immobility
Hormone replacement therapy
Thrombophilias
159
Q

Prophylaxis prevention of VTE
(all patients assessed for clotting risk when admitted to hospital)
- Non-pharmacological
- Pharmacological

A

Non pharma = TED stockings + encourage early mobility after surgery

Pharma = LMWH - low molecular weight heprin
Eg. Fondaparinux
Rivaroxaban and Apixaban - inhibitor factor Xa
Dabigatran - inhibit thrombin

160
Q

3 Step diagnosis

A

1) Wells score = at high risk? Risk factors, signs and symptoms
2) D-dimer = if a fibrin clot has been formed
3) Ultrasound
DVT = duplex scan + compression
PE = chest CT + dye to color vessels

161
Q

Treatment of VTE (3)

A

Start on stronger dose LMWH for 5 days
eg. Trinzaparin
Overlap with Warfarin - monitor Prothrombin time
Continue Warfarin for 3 - 6 months till IMR 2.5

162
Q

Thrombophillia - what is it?

Signs: get a VTE when … (4)?

A

Famillia or acquired haemostatic mechansim –> predisposes someone to a thrombotic event

Patient will get a VTE
Spontaneously
At a young age
Of disproportionate severity
Recurrent
163
Q

3 hereditary Thrombophillias

A

Activate C reactive protein OR FV Ledien - polymorphims reacts with envrio factors –> Protein C isn’t broken down

Prothrombin - point mutation = deficient in antithrombin

Dysfibrinogenaemia - misfolded fibrinogen

164
Q

Autoimmune Thrombophillia?
Seen in which conditions?

Affects

A

Antiphospholipid syndrome (APS) or Hugh’s syndrome- antibody against negatively charged phosolipids

Lupus, Vasculitis, Syphilis, connective tissue disorders

Venous thrombotic events and miscarriages

165
Q

Pernicious aneamia

  • What causes
  • What it results in
A

Autoimmune disease that destroys gastric parietal cells and intrinsic factor
RESULTS IN no uptake of B12 –> megablastic aneamia

166
Q

Reasons for Iron deficiency ?

A

Bleeding - GI, malignant, menstruation
Increased demand - pregnancy and puberty
Decreases intake/ absorption - Coeliac disease

167
Q

Test for iron deficiency?

Treatment for iron deficiency (3)?

A

Blood film for ferritin levels (GOLD STANDARD)
Low Ferritin = low iron
% hypochromic cells

Treat = oral iron (GI issues), IV iron, IM iron (painful)

168
Q

Haemolysis? what is it?

A

Shortened red cell life span

169
Q

Cause of haemolysis

  • in side cell
  • in cell membrane
  • outside cell
A

Inside cell = haemoglobinpathology (sickle cell) or enzyme defect (G6PD)

Cell mem = Spherycytosis (hereditary)

Outside = Antibodies (autoimmune), drugs, toxins, heart valves

170
Q

Thrombocytopenias ??

Disorders that cause them = ITP and TTP

A

Low platelet count

ITP = immune thrombocytopenia Purpura
TTP = Thrombotic Thrombocytopenia Purpura
171
Q

ITP - immune thrombocytopenia

- what is it associated with?

A

Autoimmune disorder against the bodies platelets

Associated with autoimmune diseases, lymphoma and HIV

NOTE: Chronic = seen in adults
Acute = seen in children (following a viral
infection)

172
Q

Presentation of ITP

Treatment of ITP (4)

A

Bruising and petechiae

Steriods, immunosupressive drugs, splenectomy, Thrombomimic drugs

173
Q

TTP - thrombotic thrombocytopenia - what is it?

A

Autoantibody immune inhibition of ADAMTS 13 due to gene mutation = vWF deficiency

174
Q

TTP - signs and symptoms (5)

A 
Fever
neurological symptoms
Haemolysis
Microvascular occlusions
Kidney problems
175
Q

TTP - treatments (3)

A

Plasma exchange FFP
Steriods
Monitor ADAMTS-13 for relapse and control

176
Q

ACUTE myeloid leukaemia - what is it?

A

Mutation in a clone of the myeloid progenitor cells in the bone marrow
–> Blast (immature) cells in the blood (holes in their nucleus)

177
Q

Signs and symptoms of acute myeloid leukeamia

A

Aneamia
Recurrent overwhelming infections - gram negative
Easy bruising
Gum hypertrophy and gingivitis

178
Q

Classification of Myeloid leukamias by?

Subtypes?

A

Morphology

Subtypes = M1 M3 M5 and M6

179
Q

Treatment of Acute Myeloid leukamia

A

Induction treatment - using chemo to send disease into remission
Bone marrow transplant - in the young

180
Q

Acute Lymphoblastic leukemia - what is it?

A

mutation in the lymphoid progenitor cells in the bone marrow

–> lymphoblastic cells in the blood (large cytoplasms)

181
Q

Presentation of acute lymphoblastic leukemia?

A

Aneamia
easy bleeding/ bruising
Organ infiltration of organs - eg. spleen, liver, meninges, skin
Severe Infections - oral candida

182
Q

Management of Acute lymphoblastic leukamia?

Specific for meningeal effects?

A

Induction therapy - chemo
Bone marrow transplant - in poor prognosis patients
For Meningeal effects = intrathecal methotrexate and cranial irradiation

183
Q

Diagnosis and monitoring of AML and ALL (4)

Genetic analysis techniques

A

Morphology - from blood films

Cytochemistry - staining proteins to determine linage
Immunological markers - Fluorescence activating short cell (FASC)

Cytogenetic - FISH: abnormalities that correlate to prognosis + response to treatment

Molecular techniques (future) - PCR to track the changes in genes post treatment (check effectiveness)

184
Q

Complications of AML and ALL treatments ?

How managed? (2)

A

Post chemo neutropenia –> infection risk
= Neutropenic Sepsis (very low neutrophils)

Broad spectrum antiB - Tazocin and Gentamicin
Prophylaxis Anti B (levofloxacin) and isolation

185
Q

C1 protein deficiency (compliment system)?

A

Hereditary angioedema

186
Q

Gene that is mutation in hereditary angioedema?

A

SERPING1 gene - auto dom

187
Q

Sings and symptoms of hereditrary angioedema?

Attacks triggered by ? (3)

A

Episodic attacks of oedema in the face, genitals, extremities, GI tract and airways
Swelling in intestinal mucous membranes = coelic-like pain and vomitting
Triggered by trauma, viral infections, surgery

Year 2: Clinical Pathology (10 decks)

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