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Blood disorders Flashcards

1
Q

Causes of macrocytic

A 
B12
Folate
Alcoholic
Thyroid
High reticulocytes / haemolysis
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2
Q

Development of spherocytes

A

Systemic sclerosis > autoantibodies specific for RBCs > antibodies stick to RBCs > spleen will detect antibodies and spleen will bite off bits with antibodies on > no more biconcave, now like footballs = spherocytes

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3
Q

RBC with antibodies stuck on, a DAT test is where you add an antibody to the antibody (on the RBCs bad), causing RBCs to ?

A

Agglutinate

If DAT is positive then its likely to be autoimmune haemolysis

If DAT is negative then hemolysis is due to heart valve etc

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4
Q 
Hodgkins Lymphoma vs Non-Hodgkins Lymphoma
Age/Sex
Sx 
Dx
Extra
A

HL is usually younger male patients

HL features progressive lymph node enlargement that causes a mediastinal mass SVC/airway obstruction = cough

Extra-nodal involvement is more common in NHL - thus wider range of potential presentation - also more associated with autoimmune conditions

HL features mirror-image nuclei + Reed-Sternberg cells + raised ESR. Most common type is nodular sclerosing

NHL is more often B cell than T cell and can be Diffuse large B cell or Follicular

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5
Q

‘B’ symptoms in lymphoma and in which are they more common?

A

Fever, weight loss and night sweats

More common in HL
In NHL they signify disseminated disease (remember extranodal more common in NHL)

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6
Q

Diagnosis of Lymphoma

A
  1. Excision node biopsy
  2. Immunohistochemistry/ FISH to subtype
  3. Staging via CT

Blood film is useful for reed-sternberg cells
Bone marrow biopsy often needed in NHL (extranodal)
LDH is raised = poor prognosis + increased risk of tumour lysis

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7
Q

Which lymphoma is associated with HIV and is given Rituximab to target CD20 cells

Most aggressive NHL?

A

Diffuse large B-cell

Burkitt’s

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8
Q

Histopathological examination of an enlarged lymph node demonstrated prominent, well-defined para-cortical follicles with germinal centres, diagnosis?

A

Normal!

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9
Q

Ann Arbor staging

A

I: Single LN region
II: One side of diaphragm
III: Both sides of diaphragm
IV: Disseminated

A: No systemic symptoms
B: Fever, night sweats, weight loss

E: Extralymphatic site
S: Splenic disease

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10
Q 
Tumour lysis syndrome
Pathophysiology
Adverse effects
Risk factors
Prevention
Mx
A

Death and breakdown of a large number of tumour cells into toxic components which induce renal AKI

Hyperuricemia (nucleic acid breakdown)
Hyperkalemia (K from dead cells)
Hyperphosphatemia (dead cells)
Hypocalcemia (opposite to phosphate and renal failure)

AKI due to urate/uric acid
Arrhythmias due to metabolites

High LDH or chemo sensitive tumours - BURKITTS, leukemia, small cell, germ cell

Hydrate, correct elctrolytes and ALLOPURINOL / Rasburicase

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11
Q

Virchow’s triad

A

Stasis of blood flow
Endothelial injury
Hypercoagulability

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12
Q 
Factor V Leiden
Pathophysiology
Sx
Ix
Mx
A

Mutated Factor V lacks cleavage site with natural anticoagulant Protein C thus no anticoagulation of Factor V takes place

DVT, PE, risk of miscarriage

Normal PT/apTT
Activated protein C resistance Test
If positive, confirm with DNA testing

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13
Q

DVT
Wells score
Ix

Any unprovoked VTE do cancer screen

A 
Tender
swollen
Calf >3cm one side
Pitting oedema
Collateral superficial veins
Previous DVT
Cancer
Immobile/surgery
- if alternative Dx more likely
  1. Wells score
  2. D dimer
  3. Venous duplex USS (skip to here if wells score is >2)
  4. CT/MRI contrast venography is too invasive really
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14
Q

PE
Wells score
Ix

Any unprovoked VTE do cancer screen

A 
Haemoptysis
HR >100
Raised RR
Clinical signs of DVT
Previous DVT/PE
Surgery or immobilisation
Active cancer
Pleuritic chest pain
SoB
Collapse

Raised JVP
ECG - S1Q3T3
Respiratory alkalosis as hyperventilation

  1. ECG/CXR/ABG
  2. Wells score + D dimer
  3. CPTA - diagnostic
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15
Q 
DIC
Pathology
Cause
Sx
Ix
Mx
A

TF excess causes lots of clotting but then runs out and you get lots of bleeding

Sepsis, malignancy, trauma, liver disease

Prolonged PT + apTT
Low fibrinogen
Low platelet
High D-dimer

Tx underlying cause
Resus + blood transfusion

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16
Q

Test and clotting factors that assess intrinsic pathway?

Test and clotting factors that assess extrinsic pathway?

Vitamin K dependent clotting factors?

Correction/mixing study to prolonged apTT?

Bleeding time?

A

apTT
8,9,11
Hemophilia, vWB, Heparin or Lupus anticoagulant (actually prothrombotic in vivo, but prolongs aptt time when tested in vitro)

PT
7
Warfarin, Vit K def

2,7,9,10

If apTT is prolonged then add mixing study if it corrects then it was a clotting factor deficiency BUT if its still incorrect then it’ll be due to Lupus anticoagulant

Platelets/thrombocytopenia

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17
Q 
Haemophilia A
Pathophysiology
Sx
Ix
Mx
A 
X-linked thus often missed in families if females affected. Can be acquired.
Factor 8 (aaaight)

Young, bleeds after venepuncture or surgery, joint pain/swelling

apTT prolonged but then NORMAL after mixing study
Factor 8 assay determines severity

Replace with recombinant factor 8

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18
Q

Haemophilia B
Pathophysiology
Sx
Ix

A

X-linked Factor 9 deficiency

Presents similar to Haemophilia A but is far less common

Prolonged apTT
Factor 9 def

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19
Q

Acquired Haemophilia
Cause
Sx
Ix

A

Autoimmune Hx, Liver/renal disease (reduce platelets), Vit K def, drugs

Presents later in life

The APTT is not correctable because the patient has antibodies to the factors and therefore will continue to destroy the factors in a mix, unlike haemophillia A/B

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20
Q

If the question features a female, no specific factor deficiency just prolonged apTT AND asks for most common/likely bleeding disorder?

A

Von Willebrands

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21
Q 
Von Willebrands
Pathophysiology
Sx
Ix
Mx
A

Autosomal dominant
VWF binds platelets and stabilises factor 8

Platelet type picture - brusiing, epistaxis, prolonged bleeding

As it stabilises factor VIII it can mimic a factor VIII deficiency in blood results, so it is important to request a vWF study too

Desmopressin (DDAVP) stimulates VWF production

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22
Q

A 57 year old woman presents with an acute 2 day history of a swollen and painful right knee. The joint is red and extremely tender on examination.

Which is the most important initial Investigation?

A

Septic arthritis

Joint aspiration!

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23
Q

Trauma - most appropriate replacement fluid?

A

Whole blood

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24
Q

Febrile neutropenia
Criteria
Ix
Mx

A

Neutrophil <1.0 + FEVER

FBC, U&Es, cultures, CXR - search for source

IVT + broad spectrum antibiotics - Tazocin/Gentamycin

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25
``` Thrombocytosis Cause Ix DDx Complication ```
More likely to have blood clot/stroke Splenomegaly Associated with JAK2 but if that is negative then do bone marrow biopsy to look for MEGAKARYOCYTES as may be serious cause > aspirin DDx: Polycythaemia rubra has raised haematocrit Can progress to myelofibrosis
26
Haptoglobin during hemolysis?
Low as all used up to mop up RBCs ``` High LDH High reticulocytes High bilirubin DAT scan for antibodies if its autoimmune Blood film for spherocytes ```
27
To know whether high platelets is due to reactive/infection or myeloproliferative disorder, do ?
CRP Hx Trend of patlets is it in keeping with onset of illness?
28
Low platelets, what do next?
Redo test as often platelet clumping can cause this!
29
``` Polycythaemia rubra vera Cause Sx Ix Mx Complication ```
60s 1': JAK2 mutation = Abnormal BM = erythropoiesis 2': EPO due to hypoxia (smoke/alcohol) ITCH after bath, burning pain in hands and feet, headache, vertigo, hepatosplenomegaly, CLOTS! (DVT + Budd-Chiari) Red/blue skin High Hb + haematocrit >0.55, high platelets + WCC, Low EPO 2': Only Hb/haematocrit is raised and EPO is high not low! TEST FOR JAK2 (tyrosine kinase) mutation Venesection Aspirin + Hydroxycarbamide (only in 1') Can progress to myelofibrosis
30
``` Acute Lymphoblastic Leukemia (ALL) Demographic Pathophysiology Sx Ix ```
ALL = Little people/CHILDREN Accumulation of lymphoid blast cells in the bone marrow leads to failure of production of normal blood cells/Bone Marrow Failure Lymphadenopathy CNS involvement + Extramedullary (parotid/gonad) involvement > AML 1. FBC is pancytopenic 2. Blood film >30% lymphoblasts 3. Bone marrow biopsy: All nucleus
31
Sx relevant to all leukaemias?
Anaemia – weakness, tiredness, SOB Thrombocytopenia – bleeding, bruising Neutropenia – Recurrent infection, fever Anorexia Back / joint pain
32
``` Acute Myeloid Leukaemia (AML) Demographic Pathophysiology Sx Ix Associations ```
Down syndrome adults (M for Men) Myeloid blast cells replace normal cells in bone marrow >20% blasts (<20% = MDS) Auer Rods (Rod Stewart, upside down W is M) BM biopsy: Primitive cells - NO well differentiated WBCs (unlike CML) Can arise from myelodysplastic syndrome (MDS) CML (common in elderly) DIC + bone marrow failure = AML
33
``` Chronic Myeloid Leukaemia (CML) Demographic Pathophysiology Sx Ix Mx ``` Wrestler CM Punkedelphia
30-50yrs 3 phases: Chronic > accelerated > blast crisis (Sx+Tx as AML) ``` Extremely high BASOPHILS and platelets! Splenomegaly Gout Itching Headaches due to hyperviscosity ``` 95% positive for Philadelphia Chromosome (Translocation 9,22) - identify with FISH 22 deletion, 9addition = BCR-ABL gene fusion - active all the time = uncontrolled MATURE WBC proliferation Blood film is HYPERCELLULAR Cytogenetics for Ph-Ch as tyrosine kinase inhibitor - IMATINIB! Imatinib can cause pleural effusion
34
``` Chronic Lymphocytic Leukaemia (CLL) Presentation Sx Ix Mx ``` smudge CeLLs
Insidious onset so diagnosed incidentally Male with asymptomatic high WCC Mature but defective lymphocytes infiltrate bone marrow + SMUDGE CELLS Only consider chemo if symptomatic
35
Multiple myeloma Pathophysiology Sx
Malignancy of pasma cells: 1. Immunoglobulins + light chains in serum/urine + PARAPROTEINS pumped out by plasma cell 2. Lytic bone changes via osteoclasts 3. Excess plasma cells in bone marrow - CD138+ Bone pain/fractures Renal failure due to light chain filtration Hypercalcemia High ALP Pancytopenia Recurrent infections - low functioning Igs Diagnosis: 1. Paraproteins: Plasma electrophoresis - gamma proteins OR Bence-Jones protein in urine 2. Excessive bone marrow plasma cells 3. Lytic bone lesions or renal impairement +ESR and rouleax RBCs (on top of each other) Since lots can cause high calcium+alp+bone pain (prostate mets) look at protein level - high rotein+low albumin Associated with amyloidosis + hyperviscosty (extra protein = thicker blood)
36
Differentiating the leukemias
ALL is children + >30% lymphoblasts + CNS/testes involvement + small nucelus AML is auer rods + down syndrome + DIC + >30% myeloblasts CML is philadelphia + v high baso/eosinophils + hypercellular + splenomegaly + blast crisis CLL is asymptomatic high WCC + incidental + mature lymphocytes + SMUDGE cells + most common
37
Anaemia
Conjuctival pallor Angular stomatitis Koilonychia Glossitis - beefy red in B12
38
``` Sideroblastic anaemia Pathophysiology Cause Presentation Iron panel ```
BM produces ringed sideroblasts instead of healthy RBCs - contain granules if iron surrounding nucleus - unable to incorporate iron into haemoglobin Reversible deficiency (alcohol etc) OR Irreversible Myeloproliferative disease Microcytic unresponsive to iron supplementation Iron often high Prussian blue stain of RBC in marrow shows ringed sideroblasts.
39
Which anaemia is skull bossing and hair on end sign seen?
Thalassaemia | Microcytic
40
Haemolytic anaemia
Premature brakdown of RBCs - autoimmune Raised LDH + potassium Blood film: Spherocytes, reticulocytes, fragments, bite cells Direct coomb's +ve autoiimune -ve inherited spherocytes or prosthetic valve disease
41
Thrombocytopenia causes
Decreased production: Haematinic deficiency Acute leukaemia/MDS Increased consumption: DIC Sepsis Immune mediated (ITP) - antibodies attach to RBC and make spleen kill them
42
High WCC due to?
Reactive due to infection OR leukemia
43
Both Polycythaemia vera and essential thrombocytosis and CML can develop into? Pathophysiology Presentation Ix
Myelofibrosis BM filled with fibrous tissue - associated with JAK2 Sweats, splenomegaly, cytopenia Blood film: Leukoerythroblastic = secondary mets affecting bone or myelofibrosis Pokilocytes = abnormally shaped RBCs Dacrocytes = teardrop shaped Nucleated RBCs = immature BM biopsy = Collagen fibrosis
44
Aplastic anaemia
Often autoimmune destruction of BM Drugs - Chemo Anaemia - tired Neutropenia - infections Thrombocytopenia - purpura All blood cells low - replaced with FAT - hypocellular BM
45
Richters transformation
CLL > Lymphoma
46
Bone marrow failure algorithm
1. Rule out sepsis or massive splenomegaly with USS, check drugs, B12/folate, abdo us for spleen 2. Do BM biopsy: Hypocellular = aplastic anaemia Hypercellular = BM cancer, either metastasis OR acute leukemia, myeloma, myelofibrosis infiltration into BM
47
Bone marrow failure/pancytopenia algorithm
1. Rule out sepsis or massive splenomegaly with USS, check drugs, B12/folate, abdo us for spleen 2. Do BM biopsy: Hypocellular = aplastic anaemia Hypercellular = BM cancer, either metastasis OR acute leukemia, myeloma, myelofibrosis infiltration into BM
48
Myeloproliferative disorders
Philadelphia +ve = CML (v high WCC) Essential thrombocytosis Polycythemia vera Myelofibrosis Can turn into AML
49
Difference between iron def anaemia and thallasemia
Both have low MCV but thalasemia has an almost normal hemoglobin
50
Clues for haemochromatosis
Chondrocalcinosis Liver cancer/cirrhosis Diabetes Testicular atrophy
51
Sequlae of B12 def
High MCV Low Hb Peripheral neuropathy/pin and needles Megaloblastic pancytopenia! 100!!!
52
MCV over ? = macrocytic Causes
100 ``` Alcohol B12 Folate Hemolysis Liver disease Chemo Thyroid ```
53
Major haemorrhage Mx
``` IV fluids Group&save 0-ve until then Stem bleeding/treat cause Warm whole blood ```
54
What can a high reticulocyte show?
That the bone marrow is actually working well and just trying to compensate for loss of RBCs
55
Hereditary hemolytic anaemias
Sickle cell - painful crisis Hereditary spherocytosis - remove spleen and the circular RBCs stop being killed All hemolytic anaemias can cause gallstones
56
Low Hb normal MCV high ESR?
Think anaemia of chronic disease
57
Blood film: Leukoerythroblastic =
Secondary mets affecting bone or myelofibrosis
58
Nucleated RBCs and myelocytes =
Cancer in the blood
59
Prolonged PT causes
Extrinsic: Liver disease Vit K def Warfarin DIC has apTT raised too Give vitamin K
60
Infectious mononucleosis Presentation Ix
``` Cervical lymphadenopathy Sore throat Malaise Rash after amoxicillin Splenomegaly (can rupture) Post-viral fatigue ``` Blood film: Mononuclear cells +ve monospot test IgM antibodies against EBV
61
Less than 9 months + Blasts =
Acute leukaemia
62
Gout is associated with cancers via
Tumour lysis syndrome / | Release of urate etc
63
Immune thrombocytopenia will show a normal bone marrow biopsy of:
Plentiful megakaryocytes Thus no need for platelet transfusion, just give steroids (treat cause)
64
Hilar lymphadenopathy
Lymphoma Sarcoidosis (usually bilateral) TB
65
``` Anaemia Rouleaux High ESR High calcium High urea and creatinine High protein ``` Dx?
Myeloma Check paraproteins and bence jones in urine
66
21 year old with fever and widespread bruises Neutropenia Blasts with auer rods Deranged clotting and d-dimer Dx?
AML > DIC
67
Back pain + difficulty peeing + constipation? DDx?
Spinal cord compression Prostate ca Myeloma MRI asap
68
Fast growing tumour/Burkitt Goiive chemo What are the risks?
Tumour lysis: Raised urate, K, phosphate, urea and creatinine = renal failure WATCH K FOR HEART DEATH Use allopurinol as prophylaxis
69
Prolonged apTT causes?
Intrinsic: Hemophilia Lupus anticoagulant if Asx - repeat with mixing study Heparin
70
``` Hemorrhagic or infarct stroke? Dysphasia Hemiparesis Warfarin AF ``` What do?
Urgent CT + INR Beriplex to reverse warfarin

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