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Year 4/5 Revision > Haematology > Flashcards

Haematology Flashcards

1
Q

Anaemia = Hb < ?

A

<130 M
<120 F

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2
Q

Causes of Anaemia
Microcytic (5)
Normocytic (5)
Macrocytic (6)

A

Microcytic = TAILS (thalassemia, anaemia of chronic disease, iron deficiency, lead poisoning, sideroblastic)
Normocrytic= AAA-SH (aplastic, acute blood loss, anaemia of chronic disease, sickle cell disease, haemolytic)
Macrocytic= FATRBC (folate deficiency, alcoholism/CLD, hypothyroidism, reticulocytosis, B12 deficiency, cytotoxic drugs/anti-folate drugs)

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3
Q

Iron deficiency anaemia is a microcytic hypochromic anaemia from increased blood loss, reduced iron intake and malabsorption.
List 5 presenting features, 2 main investigations + inv considerations and 3 mngmnt options.
Findings from FBC (Transferrin, ferritin, TIBC)

A
  • Angular chelitis, atrophic glossitis, brittle hair, koilonychia, pica
  • FBC, blood film, iron studies
  • FBC - Low ferritin, low transferrin, raised TIBC
  • Blood film - target cells, poikolocytes (pencil)
  • investigate underlying cause (ca- colonoscopy?, OGD, bone marrow biopsy)
  • iron tables (Ferrous sulfate), iron infusion (IV Cosmofer), blood transfusion
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4
Q

2WW Guidelines for suspected malignancy in iron defiency anaemia
- Which people would you refer for endoscopy urgent review

A

Men Hb <11
Post menopausal women <10

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5
Q

Finding on blood film - iron def anaemia

A

Poikolocytes (pencil)

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6
Q

Thalaessemia (autosomal recessive) - types of alpha (4) and beta (2)

A

Alpha - gene deletions
* silent - affects 1 copy of alpha globin chain
* trait - “ 2
* HbH disease - “3
* fetal hydrops (Bart’s) - “4
* Beta- gene mutations
* minor trait
* major

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7
Q

Inv for thalaessemia = FBC, heamoglobin electrophoresis & genetic testing.
What are the findings from hb electrophoresis for beta thalessemia (3)

A

Increased HbA2 and HbF
Reduced/absent HbA

HbA is the most common form of Haemoglobin (made from 2x alpha chains, 2 x beta chains.)
Note in alpha thalassemia- hb electrophoresis is typically normal.

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8
Q

Mngmnt thalaessemia

A

Iron chelation - Desferroxamine
Blood transfusion

prevents the iron overload from repeated blood transfusions

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9
Q

Sideoblastic anaemia:
* type
* mechanism
* cause
* blood film finding
* iron, ferritin and transferrin sats?
* bone marrow finding?

treatment supportive/underlying cause or Pyroxidine

A
  • hypochromic microcytic
  • RBCs fail to incorporate iron into haem - ring of iron forms around nucleus; biosynthesis in mitochondrion
  • congenital or acquired (chemo, alcohol, myeloproliferative)
  • basophilic stippling of RBCs
  • high ferritin
  • high iron
  • high transferrin concentration
  • prussion blue staining shows ringed sideroblasts

raised iron because it is not being incorporated into haem (loose)

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10
Q

What causes basophilic stippling (in general)
typical causes

A

Presence of basophils within the RBC cytoplasm –>
Disturbed erythropoeisis
Can contain fragments of DNA/mitochondria
causes
thalassemia
sideroblastic anaemia
megaloblastic anaemia
lead poisoning
etcetc

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11
Q

Lead poisoning
- presentation
- blood film
- fbc
- mx
- differential

A
  • microcytic anaemia presenting with abdominal pain, peripheral neuropathy and blue stained gingiva.
  • also neuropsychotic features, constipation and fatigue
  • blood film = basophilic stippling and clover-leaf
  • FBC: microcytic anaemia
  • reqs chelation (DMSA, EDTA etc)
  • acute porphyria - also presents with abdominal pain and neurological signs (but normally raises delta aminolaevulinic acid levels)
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12
Q

Normocytic anaemias - AAASH.
Aplastic anaemia occurs due to a problem within the bone marrow itself. What are its two main presentations?

A

PRCA
Pancytopenia

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13
Q

Aplastic can be acquired or inherited.
2 types of inherited and 2 causes of acquired?

A
  • Diamond Blackfan & Fanconi syndrome
  • Drugs (cytotoxics, antibiotics), infections (EBV, HIV), toxins (benzene).
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14
Q

Features of Fanconi syndrome (inherited aplastic anaemia) (6)

A
  • Facial & skin abnormalities (e.g. microcepahly, cafe au lait spots)
  • Absent thumb
  • Horsehoe kidney & prox tubule dysfunction
  • Aplastic anaemia - pancytopenia
  • Intellectual disablity
  • Short stature
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15
Q

General sx of haemolytic anaemia

A

Anaemia + jaundice + splenomegaly
?gall stones

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16
Q

Haemolytic anaemia can be hereditary (affecting membrane, metabolism & haemoglobin) and acquired (immune or non-immune). List 5 causes of hereditary haemolytic anaemia.

A
  1. Spherocytosis
  2. Elliptocytosis
  3. G6PD deficiency
  4. Thalassemia
  5. Si ckle Cell Disease
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17
Q

Key fact for
spherocytosis

A
  • splenomegaly, jaundice & gallstones
  • often presents in aplastic crisis during parvovirus inf
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18
Q

Key fact for
elliptocytosis

A

mostly asx

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19
Q

Triggers for H6PD deficiency (3) acute haemolytic episodes

A

Meds - sulfonylureas (Gliclazide), CIprofloxacin, and anti-malarials

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20
Q

key facts for
G6PD deficiency:
- genetics
- ethnicity
- haemolysis triggered by (3)
- findings on blood film (main + 3 others)
- reduced NADPH results in..
- ix: blood film & what else?
- management

A
  • X linked, affected African/Medit. newborn babies (M)
  • fava beans, certain drugs, infeection
  • Heinz bodies (+ ghost, bite, blisters)
  • reduced NADPH –> oxidative damage to RBC
  • test using G6PD assay and repeat after 3 months
  • treat underlying infection, avoid precipitants, transfusion may be needed
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21
Q

key facts for
Sickle cell anaemia

A
  • autosomal recessive
  • malaria protective
  • presentation = SICKLED: note splenomegaly, priapism and dactylitis (under 3)
  • crises & complications
  • req tranfusion, imms, hydroxycarbamide (increased fetal hb) long term for pain and prophylaxis for crises
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22
Q

point mutation for SCD, on chr 11

A

glu- val on beta globin gene

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23
Q

findings on blood film for SCD

A

Howell-Jolly bodies (sign of hyposplenism) & target cells

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24
Q

presentation: SCD

A

Splenomegaly
Infarction
Crises
Kidney disease
Liver & lung disease
Erection (priapism)
Dactylitis

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25
Q

Sickle cell crises (4)
General management
1. Thrombotic “vaso-occlusive”
2. Acute Chest Syndrome
3. Sequestration crisis
4. Aplastic

A

General
Analgesia + O2 + IV Fluids
1. Blockage in organs (lungs, brain, hip)
2. Blockage in pulmonary microvasculature –> infarction in lung parenchyma. Treat with O2, analgesia, Abx
3. Splenic sequestration - sickling of the blood causing pooling within spleen(or lungs) - acute emergency, fall in retics.
4. Triggered by parvovirus infection: fall in Hb, fall in retics

4 - note elliptocytosis can also present like this

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26
Q

The acquired haemolytic anaemias can be classed as immune (Coombs +ve) and non-immune (Coombs -ve).
Name 2 types of each.

A

Immune
* Cold, occurs <10degrees
* Warm, more common, at >37 degrees
* Non-immune
* Paroxysmal noctural haemaglobinuria
* Microangiopathic (e.g. 2ndary to HUS)

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27
Q

Feature of PNH (paroxysmal nocturnal haemaglobinuria)

A type of acquired haemoltyic anaemia (non-immune, Coombs -ve)

A

Red urine in morning

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28
Q

Macrocytic anaemias can be megaloblastic (folate & B12 deficiency) and non-megaloblastic.
Folate & B12 deficiency can be caused by malnutrition, malabsorption (Crohn’s, coeliac) or autoantibodies (pernicious).
In pernicious anaemia what antibodies are present? (2)
What Ca does it increase your risk of 3x?

A
  • Auto-abs against gastric parietal cells & intrinsic factor.
  • reduced IF and reduced HCl.
  • Gastric adenoca

B12 requires intrinsic factor to be absorbed

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29
Q

Presentation of B12 deficiency (3)

A
  • Peripheral neuropathy
  • Visual changes - reduced colour vision
  • Mood changes (e.g. irritability)
  • Anaemia sx - note glossitis
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30
Q

B12 deficiency can lead to SACDC. What tracts does this affect, and how does it present?

A
  • Combined = both lateral corticospinal and dorsal columns.
  • Sensory loss but preserved pain/temperature sensation
  • Mixed UMN and LMN signs (e.g. spastic paresis)
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31
Q

Treatment for B12 deficiency
Can it reverse SACD?

A
  • B12 supplementation (hydroxycobalamin - parenteral, or cyanocoblamin - oral)
  • No.
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32
Q

Main difference between acute & chronic leukaemias

A

Acute - present with acute symptoms, with cytopenia
Chronic - often asx initially and gradual onset, with cytosis

33
Q

Where are folate and B12 absorbed from?

A

Small intestine:
folate (prox jejenum)
B12 (term ileum)

34
Q

Acute Leukaemias
* what is the main pathophysiology resulting in bone marrow failure in ALL and AML?
* 3 features of bone marrow failure

A
  • impaired differentiation
  • excessive proliferation of immature cells (blast cells)
  • which compete with healthy bone marrow cells
  • resulting in cytopenia
    E.g.
  • AML - myeloblasts, thrombocytopenia
  • ACL - lymphoblasts, neutropenia
    Features of BMF
  • Anaemia - pallor, fatigue, Neutropenia - frequent infections, Thrombocytopenia - easy bruising, bleeding. Bone marrow failure affects all blood cells except lymphocytes (which are formed in the thymus/bone marrow and mature in lymph nodes).
35
Q

AML
* age affected?
* risk factors (2)?
* prognosis?
* blood film findings (2)?

A
  • Adults - most common adult leukaemia
  • myelodysplastic syndrome and myeloproliferative disroder
  • worst
  • blast cells & auer rods
36
Q

ALL
* age affected?
* risk factors (2)?
* prognosis?
* blood film findings (2)?

A
  • children - most common childhood cancer
  • Down’s syndrome, Philedelphia chromosome (in some)
  • 3/4 children complete recovery
  • blast cells
37
Q

Chronic leukaemias
Mechanism behind the cytosis seen on blood film

A
  • Excess proliferation of (more) mature cells (further down the line) than acute leukaemias.
  • the mature cells have partial functionality
  • but because more mature, no competiton in bone marrrow
  • aka on blood film - absence of blast cells
  • also anaemia due to myelofibrosis
38
Q

CML - ALL CML have the philedelphia chromsome
Philedelphia chromosome translocation?
what does it code for?
what drug targets it?

A
  • t(9:22)
  • results in BCR:ABL gene
  • codes for tyrosine kinase
  • Imatinib - tki, for CML
39
Q

CML
* age affected?
* risk factors (2)?
* prognosis?
* blood film findings (2)?

A
  • adult
  • Philedelphia chrom(95% of CML have it)
  • poor
  • excess cells from myeloid lineage: thrombocytosis + increase in granulocytes at different stages of maturation (eosniophilia and basophilia)
  • and anaemia
40
Q

CLL
* age affected?
* risk factors (2)?
* prognosis?
* blood film findings (2)?
* complications (2)

hint (sudden transformation, type of anaemia, reccurent infections)

A
  • Adults - most common of all leukaemias
  • TP53, Trisomy 13
  • good
  • smudge cells
  • Richter transformation (to NHL), hypogammaglobulinaemia, warmAIHA
41
Q

Lymphoma = Hodgkin’s-
most common subtype: nodular sclerosing

  • blood film finding
  • age
  • risk factors (2)
  • common presenting symptom
  • rx
A
  • Reed-Sternberg cells
  • 20s and 60s (bimodal)
  • infection (EBV) and autoimmune
  • tender lymphadenopathy after alcohol
  • chemo (ABVD) and radio x
42
Q

Which is more common - HL or NHL?

A

NHL

43
Q

Lymphoma - Non-Hogkins - subtypes:
B cell
* Slow growing mass, often multiple sites?
* similarto above
* Common childhood cancer worldwide, causing “starry sky appearance on biopsy”, and associated with EBV?
* Associated with H.pylori?
T cell
* As?sociated with Coeliac disease?

A
  • Diffuse large B cell
  • Follcular
  • Burkitt’s
  • MALT
  • T cell lymphoma of intestine

note starry sky als a finding on renal biopsy for post-strep GN

44
Q

Investigation = typical haem ones like FBC & blood film. What other lymphoma specific inv are of use? (3)
+ Treatment (HL/NHL)

A
  • Lymph node biopsy, PET scan (extra-nodular disease), CT-TAP/Neck for staging
  • Chemo/radio
  • HL- ABVD
  • NHL - R-CHOP
45
Q

What is myeloma, describe its hallmark feature, and how it presents (CRABBI)?

A
  • cancer of the plasma cells (type of b cell that produced Abs & cytokines)
  • proliferation of monoclonal antibodies (IgG or IgA)
  • hypercalcaemia, renal failure, anaemia, bone pain/#s - back. bleeding, recurrent infection
  • also causes hypercoaguable stae (risk of stroke) - due to inflammation from cancer and from paraproteinaemia (clot aggregation)

hypercalcaemia and bone lesions due to cytokines –> osteoclastic activity, mobilisation of calcium from bone to blood

46
Q

Myeloma investigations
* electrophoresis:
1. urine
2. serum
* Bloods - serum immunoglobulins; U&E, Calcium, FBC
* Blood film
* Bone marrow aspiration
* Imaging - what is first line?
* what finding may be present from xrays?

Diagnostic criteria: 1 major and one minor or 3 minor.
Major = bone marrow aspiration shows plasmacytoma (biopsy) and >30% plasma cells; and raised M proteins (serum electrophoresis)
Minor - 10-30% plasma cells, minor elevations of M protein, osteolytic lesions, low levels of other antibodies (non-cancerous) in blood

A
  • Bence-Jones proteins
  • M protein
  • monoclonal paraprotein (IgG and IgA); renal failure, hypercalcaemia, anaemia, thrombocytopenia
  • roleaux formation (stacked RBCs)
  • confirms diagnosis - excess plasma cells
  • whole body MRI
  • rain drop skull (similar to pepperport skull of hyperparathyroidism)

Both are due to light chain deposition

47
Q

Myleoma - management (4)

A
  • Chemo
  • Bisphosphonates
  • Radio - bone lesions
  • Autologous stem cell transplant
48
Q

Myeloproliferative disorders are when there is chronic prolfieration in the myeloid cell lines (RBCs, granulocytes, thromboyctes).

Which leukaemia are they risk factors for?

A

Acute myeloid leukaemia (AML)

49
Q

What condition is caused by proliferation of the following cells:
- RBC
- Megakaryocyte
- Thrombocyte

A
  • Polycythaemia vera (=erythrocytosis)
  • Myelofibrosis
  • Primary thrombocythaemia
50
Q

Primary polycythaemia vera mutation

A

JAK-2

51
Q

What condition presents with massive hepatosplenomegaly, and 1 in 2 patients are JAK 2 +VE?
What is this caused by?
What accompanies this?

A

Massive –>
mega (karyocyte) proliferation –>
primary myelofibrosis
. Note DRY TAP!
Myelofibrosis= scar tissue develops in bone marrow –> extra-medullar haematopoesis –> splenomegaly
Symptoms of hypermetabolism - weight loss/ night sweats

52
Q

Patients with PV and thrombocythaemia have increased risk of thrombosis and erythromelagia - what is this?

A

Sudden burning pain in hands and feet + red skin

53
Q

What are MDS (myelodysplastic syndromes)?
Risk factors?
Like myeloproliferative disorders what can they also progress to?
How do they present?
Blood film shows blasts; bone marrow biopsy diagnostic.
Mx - supportive, immunosuppressive, disease modifying therapy, growth factors, or haemaotopeotic stem transplant

A
  • Ineffective haematopoeisis due to mutations in haematopoetic stem cells.
  • Age; chemo/radio. 90% primary, 10% secondary to chemo/radio therapy.
  • Risk of progression to AML
  • Sx of bone marrow failure
54
Q

Amyloidosis (a paraproteinanaemia) - key points(3)

A
  • depositon of amyloid protein in multiple organs (kidneys, heart, nerves, GIT)
  • problem within bone marrow due to dysfunction in plasma cells –> production of light chains
  • congo-red staining?
  • sx depend on which organ is affected
  • similar treatment to myeloma
55
Q

Bleeding disorders
Factors involved in the
- intrinisic pathway
- extrinsic pathway
- final common pathway
of the clotting cascade

A
  • Intrinsic = 12, 11, 9, 8
  • Extrinsic = 7
  • Common = 10 (Factor X), 5, 2 (prothrombin), 1 (thrombin)
56
Q

Coagulation tests
APTT
PT

A
  • APTT: detects problems in clotting factors in the intrinsic cascade + final common pathway (12, 11, 9, 8 + 10, 5, 2, 1)
  • PT: extrinsic + FCP (7 + 10, 5, 2, 1)
57
Q

Von-Willebrand disease is the most common acquired clotting disorder.
- What is the function of the VWF protein?
- how do the three types of VWD differ from eachother?
- Majority of VWD are autosomal recessive or dominant?

A
  • VWF stabilises Factor 8 (intrinsic pathway) and promotes platelet adhesion
  • Types 1-3 from least to most severe VWF is either reduced, abnormal or absent.
  • Majority are autosomal dominant (types 1 and 2)
58
Q

Blood findings from coag screen for VWD

A
  • Increased APTT (dysfunctional intrinsic pathway)
  • Increased bleeding time (PFA-100)
59
Q

Bleeding disorders can be classified broadly into vascular, platelet, and coagulation (clotting factor) disorders.
Name 3 types of inherited coagulation disorders and 2 acquired?

A

Inherited:
* VWF disease (technically affects clotting factors AND platelets)
* Haemophilia A - Factor 8 deficiency (intrinsic)
* Haemophilia B - Factor 9 deficiency (intrinsic)
Acquired
* Liver disease
* Vitamin K deficiency
* Warfarin/anticoagulant use

60
Q

List 4 types of vascular disorders

A
  • Ehlers-Danlos
  • Vitamin C deficiency
  • Hereditary haemorrhagic telangiectasia (HHT)
  • Infection, steroids, vasculitis
  • Senile purpura
61
Q

4 diagnostic features of HHT

A
  1. Epistaxis
  2. Telangiectases at multiple sites
  3. Visceral lesion (e.g. GI bleed or AVM)
  4. FHx
62
Q

Classify platelet disorders and give 2 examples for each

A
  • Reduced quantity: ITPP, essential thrombocytopenia, dilutional, bone marrow failure (aplastic anaemia/drugs), megaloblastic anaemia, auto-immmune processes
    Reduced quality - congenital causes (rare) e.g. Gp1b deficiency (Bernard-Souler) or GPIIb (Glanzmann’s)
63
Q

Which clotting factors do haemophilia A and B affect?
How does haemophilia A (more common) present?

A

A - Factor 8 - haemarthroses, post-op bleeding
B -Factor 9

64
Q

Rx for VWD/haemophilia (3)

A

Desmopressin
Tranexamic acid
Infusion of VWF/F8

65
Q

What is disseminated intravascular coagulation (DIC)?
Finding on blood film?
Finding on FBC/coags?
What is its medical treatment?
Example patient: pt presents with episataxis post op, low plt and fibrinogen, raised APTT/INR, raised D-dimer

A
  • Extensive clot production AND bleeding triggered by trauma/surgery/infection
  • low plt, prolonged pt/aptt, low plasma fibrinogen, elevated d dimer
  • Schistocytes: due to microangiopathic haemolytic anaemia
  • Caused by sepsis, malignancy, trauma, obs etc
  • Main contributor is tissue factor (TF)
  • Reqs FFP/Plt & heparin
66
Q

Typical blood picture for DIC
- PT and APTT
- FIbrinogen
- Fibrinogen degradation products

Thrombin time = fibrinogen function

A
  • Increased
  • Decreased (as being used to make fibrin)
  • Increased
67
Q

What is thrombophilia?

A

A disorder predisposing to (venous) thrombosis, inh/acq

68
Q

Most common cause of inhr thrombophilia

A

Factor V Leiden (deactivation of 5 and 8)

69
Q

Prevalence of thrombosis with Factor V Leiden disease (heterozygous form)

A

5%
(homozygous 0.05%)

70
Q

acquired cause of thrombophilia (2)

A
  • anti-phospholipid syndrome
  • progesterone in OCPs
71
Q

Complications of haematological malignancies
The umbrella term for conditions causing:

A raised RBC/Hct >05
Raised WCC >100
Raised plasma proteins

A

Hyperviscosity syndrome:
e.g. polycythaemia vera
leukaemia
myeloma/Waldenstrom’s

72
Q

Complications of haem malignancies
- caused by chemotherapy (rarely- steroids) or lymphoma/leukaemia without chemo
- breakdown of tumour releases chemicals
- raised K+, raised PO4-, AKI evidence from Urea&Cr
- prevent: Iv Rasburicase and IV fluids or Allopurinol
-

A

Tumour lysis syndrome

73
Q

What is the MOA for the DOACS Rivaroxaban/Apixaban/Edoxaban?
How can they be reversed (except Edoxaban)?

A
  • Factor Xa Inhibitors
  • Andexanet alfa (recombinant human form factor xa)
74
Q

MOA of Dabigatran (DOAC) &
Reversal agent

A

Direct thrombin inhibitor
Idarucizumab

75
Q

Indication/contra-indication for different blood products
1. Packed Red Cells
2. Fresh Frozen Plasma
3. Cryoprecipitate
4. VWF concentrate
5. Platelets
6. SAG-Mannitol blood

A
  • Anaemia; malignancy (solid tumour). When a smaller volume of blood is rewd (to prevent CVS compromise).
  • Contains clotting factors, Immunoglobulins and albumin. Corrects coagulopathies; e.g. liver disease/malnutrition.
  • Supernantant of FFP. Contains Factor VIII and fibrinogen; for Haemophilia A or severe Fibrinogen deficiency.
  • For VWF deficiency
  • For thrombocytopenia (acute leukaemia/chronic low plt). Does not require cross-matching. Risk of NHFR. Highest risk of bacterial contamination ((e.g. contraindicated if immunocompromised).
  • Serum removed; red cells washed and replaced in solution ( sodium chloride, adenine, mannitol etc). Long shelf life / pts at risk of severe allergic reactions?
76
Q

Blood transfusion reactions
1. Non-hemolytic febrile reaction
2. Minor allergic reaction
3. Anaphylaxis
4. Acute haemolytic reaction
5. TACO
6. TRALI
What is the main difference between TACO and TRALI?

A
  1. Temp rise during administration of product. Due to host’s antibodies against WC fragments in donor blood; and leaked cytokines. Slow/stop/monitor.
  2. Due to foreign plasma proteins. Pruritus & urticaria. Slow/stop/monitor.
  3. Type 1 hypersensitivty. Stop/IM adrenaline.
  4. Due to ABO incompatability. Fever, abdo pain, hypotension. Stop, identity check, send blood for Coombs test.
  5. Transfusion associated circulatory overload - due to rapid rate of transfusion or exisitng HF. Stop –> ?furosemide.
  6. Transfusion related acute lung injury - non-cardiogenic lung injury; host neurtrophils –> increased vascular permeability. Stop infusion - titrate O2, give IV fluids and consider escalation of care. Bilateral coarse crepitations =noncardiogenic pulmonary oedema.

TACO = raised BP, requires diuretics. TRALI = low BP - hypotension, requires IV fluids, O2

77
Q

patients with NHL must receive what to prevent taGVHD?

A

irradiated blood products

78
Q

Signs of hyposplenism -e.g. post splenectomy, coeliac disease

A

Target cells
Howell-Jolly bodies
Pappenheimer bodies
Siderotic grtanules
Acanthocytes

79
Q

Myelofibrosis
a myeloproliferative disorder
Blood findings:
- FBC
- Blood film
- Bone marrow biopsy (alternative?)
- Urate levels and LDH

A
  • Anaemia
  • high WCC and thrombocytosis
  • tear drop poikolocytes
  • dry tap - need trephine biopsy
  • raised urate and raised LDH (high bone turnover)

Year 4/5 Revision (21 decks)

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