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K-Medicine-Year 3 > Haematology > Flashcards

Haematology Flashcards

1
Q

What is microcytic anaemia?

A

Small red cells,

MCV( mean corpsular volume of red cells)

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2
Q

What could cause microcytic anaemias?

A

Iron deficiency
Chronic disease anaemia
Thalassaemia
Sideroblastic anaemia (rarer)

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3
Q

What is normocytic anaemia?

A

Normal sized red cells

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4
Q

What are some DDs for localised lymphadenomapthy?

A

Local infx,- pyogenic eg tonsilitis,
TB

Lympoma
2o carcinoma

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5
Q

What are some generalised DDs for lymphadenopathy?

A

Infx, Epstein Barr V(EBV), CMV, toxoplasmosis sp, TB, HIV,

Lymphoma
Leukemia
↪️ systemic disease, SLE, sarcoidosis, RA

Drug rctn- phenytoin

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5
Q

What is myeloablative therapy with Bone Marrow (BM) transplant?

A

Tx that employes high dose chemo or chemo + radiation
Aim: clearing BM completely.

Allogenic BMT( transplant) from another individual
HLA identical sibling.,

Autogenous: pt is his own source of stem cells.

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6
Q

What is the definition of anaemia?

What must you ensure for an accurate result?

A

When Hb ⬇️, men (130-180g/L)
Women (115-155g/L)

Avoid prolonged venous occlusion
Dont take it from arm w/IV infusion

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7
Q

What are some sx of anaemia?

A

Tiredness, lack of energy,
SOB on exercise
Palpitations
Iscahemic pain

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8
Q

What is ferritin?

A

Acute phase protein.
So Fe deficiency might be hard to diagnose on inflammatory disease so tissue dtores might need to be examined directly from bone marrow.
So will be high whenever CRP or ESR are high.

  • tissue stores of iron
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9
Q

What are some common causes of microcytic anaemia ?

A

Low MCV

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10
Q

Where is blood formed?

A

Emryonic yolk sac before the fetal liver becomes the major one at 5-8weeks. Remains, shorlty before BM takes over after birth.

Firts few years- all bone has red haematopoietic stemm cells, later…
BM, vertebrae, pelvis, sternum, prox ends of humerus and femur.

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11
Q

What happens in increased haematopoietic disorders?

A

Eg chronic haemolytic anaemias and chronic myeloproliferative disorders

Haematopoietic tissue will expand, and will accumulate in other tissues, like lover and spleen.

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12
Q

What happens in haemoatopoiesis?

A

Long term haemopoietic stem cells (HSCs) in BM are capable of 1. Self renewal
2. Differentiation into specialised progenitors of individual cell linage

Progenitors go further division amd differentiation–> single types of mature blood cells.

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13
Q

So what are HSCs?

A

Multipotent progenitor cells which have limited self renewal capacity but remain able to differentiate into all blood linages.

HSC- haemopoietic stem cell .

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14
Q

What do short term HSCs give rise to? (2)

A

Long term HSC–> short term HSCs—>

  1. Common Lymphoid progenitor
  2. Common myeloid progenitor
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15
Q

What does the COmmon lymphoid progenitor give rise to?

A
  1. Precursor B cell—> B cells, Plasma cells,
  2. Precurso T cell–> Thelpers, Cytotoxic
  3. NK cell precursor–> NK cell
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16
Q

What does the Common myeloid progenitor give rise to?

A
  1. GMP (granulocyte macrophage progenitor)

2. MEP (megakaryocyte/erythrocyte progenitor)

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17
Q

What does the MEP give rise to?

A
  1. Erythrocyte progenitor—> erythrocytes

2. Megakaryocyte —> platelets

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18
Q

What will the GMP five rise to?

A
  1. Neutrophil & monocyte precursor–> a) Neutrophil
    - -> b) Monocyte—> macrophage
  2. Eosinophil precursor–> eosinophil
  3. Basophil precursor–> basophil
19
Q

What happens As cells progress through differentiation?

A

they accure more functional specialisation and lose their multipotency.

20
Q

What are the granuloscytes and what is their function?

Neutrophils

A
  1. Ability to migrate to inflammation areas (chemotaxis) and primed by cytokines like TNF-a and IFN-gamma—> neutrophils are then 2. able to phagocytose opsonised microbes
  2. Respiratory burst- release of reactive O2 species- substrate for enzyme MPO–> generating Hydrochlorus acid- cytotoxic effects.
  3. Neutrophil granules also contain antimibrobial agents.
21
Q

What are eosinophils for?

A

(Bright pink granules)
Can also phagocytose BUt classicaly assc w/ immune respones to parasitic infx.

Found in large numbers in Allergy and Atopy ‼️

IL-5 appears to be crucial for their differentiation.

22
Q

What do Basophils do?

A

Least common of granulocytes

Immunity and inflammation.

23
Q

What is the function of Monocytes?

A

Immune roles
1. Precursors of a) macrophages & b) dendtritic cells
Phagocytosis, APCs.

Abs expose antigens at Fc fragments,
Again O2- dependent or i dependent ,echanisms.

24
Q

What do platelets and megakaryocytes do?

A

Megakaryocytes–> platelets, driven by TPO, there is replication of DNA w/o cell division –> ⬆️⬆️⬆️ amounts of mononucleate cells- polyploid.
So large #s of platelets are produced from 1 megakaryocyte. –> marrow sinusoids. The residual left, is phagocytosed.

Platelets:
1o haemostasis via von Willebrand factor + exposed collagen of damaged endoepithelial surfaces.

25
Q

Whats TPO? How is the Negative feedback loop working?

A

Thrombopoietin.
Key regulator of normal platelet production.
Produced by Liver, binds on TPO receptors on megakaryocyte.
↪️ signalling and maturation.

Tpo can also bind to platelets surface itself, so when their numbers are too high, tpo stays there, to leave less available TPO to bind to their receptors. –> Negative feedback loop

26
Q

Erythropoiesis + red cell function

A

Erythropoetin- expressed mostly in cortical interstitial cells of the kideny, where its trabscription is modulated in response to hypoxaemia. HIF-1 is induced in cells exposed to hypoxaemic conditions and enhances the epo gene.

⬆️⬆️EPO interacts with epo receptor on red cell progenitor membranes– erythro specific signalling cascade–>

  1. Enhanced proliferation
  2. Terminal differentiation of erythroid cells.

Reticulocyte- released in p. Blood. Larger than mature ones .

27
Q

What happens in Lymphopoiesis?

A

Pre B precursors in fetal blood. B cell maturation requires antigen exposure in the lymph nodes.

T cells formed in thymus. (Lymphocyte progenitors from fetal liver migrate to in earlt gestation.
Immature T cells do not express CD4 or CD8 receptors so…
↪️ undergo rearrangement of t recptr genes to permit surface expression of TCR (T cell receptor). Like b cells, maturations consists of being able to identify self and non self antigens.

During maturation, T cells aquire both CD4 + CD8 cell surface markers (double positibe thymocytes) –> undergo +ve selection to ensure only those who interact with MHC molecules.

T cells that interact with MHC I become CD8 +ve only, while those that interact with MHC class II down regulate their CD8 expression and become CD4 T cells.

Negative selection- T cells that interact steongly with self antigens in the thymous undergo apoptosis.

28
Q

What do CD4 + lymphocytes do?

A

T helpers
Majority
1. Production of cytokines to provoke inflammatory rcts in presensce of antigen. –> interferon gama,( from Th1 of cd4) and ILs 4,5,13 ( from Th2) .

29
Q

What are the effects of the cytokines produced from the Th cells?

A
  1. Activation pf monocyte/ macrophage system
  2. Promotion of granulocyte maturation
  3. Induction of Abs synthesis by B cells.
30
Q

What do CD8+ lymphocytes do?

A

Are T suppressor/cytotoxic cells–> 1/4th of T cell population in peripheral blood.
1. Destroy any cells expressing a peptide to which TCR can bind e.g. Virally infected cels.

31
Q

What are NK cells?

A

Natural killer cells (lymphocyes)
WBC
+ innate immune system.

Host rejection in tumours and viral,y infected cells.

32
Q

What happens in Hodgkins lympoma?

A

Definition: lympomas: neoplasms of lymphoid cells, originating in lymph nodes. HL (16%) dx histologically by Reed-Stenberg cells (B cell linage)
EBV genome detected in 50%

Peaks: 20-30, >50Yrs,

Hx: painless enlarging mass, usually neck,axilla, groin. May bcm painful after alcohol ingestion.
B symptoms

33
Q

What are B symptoms?

A

Fevers >38

Night sweats 🌙⭐️
Wt loss >10% of body wt in last 6months

Other: pruritus, cough, dyspnoea w/ intrathoracic disease

O/E :
NON-Tender rubbery lymphadenopathy: Cervical, axillary or inguinal.
Hepato

34
Q

How would you investigate HL?

A

Bloods:
1. FBC: anaemia of chronic disease- microcytic, leukocytosis⬆️, neutrocytosis ⬆, ️eosinophils ⬆️.
Lymphopenia w/ advanced disease (cx those undunctional ones accumulate so BM cannot form new ones)

  1. ⬆️ESR/CRP, LFTs ⬆️( LDH- dying cells, AST/ALT, if lover involved)
  2. Lymph node biopsy
  3. Bone marrow aspirate and trephine biopsy : advanced maybe
  4. Imaging
    CXR, CT thorax, abdo + pelvis, gallium scan, PER scans
    Staging (Ann Arbor)
  5. Single LN, 2. 2 or more, 3. LNs in both sides of Diaphragm,
  6. Extranodal invoclemtn, liver, BM, a) absence, b) B sx…
35
Q

Howmdo you manage HLs?

A

1-2 Radiotherapy, with or without chemo,

3-4 cyclical chemo, .+- radiotherapy.

Autogenous and allogenous stem cell transplant.

36
Q

What are the complications and prognosis of HLs?

A

2o malignancy after tx, : AML, (1% at 10years) , NHLs, or solid tumours.

Inverted Y irradication: infertility, premature menopause, skin cancers.

Prognosis:
1-2 :80-90% cure rate
3-4 : 50-70% cure rate.

Prognosis less good with B sx, older, lymphocytes- depleted type.

37
Q

What happens in NHL?

A

NHLs- 85% B cell , 15% cell

38
Q

How do you investigate NHL?

A

Bloods: FBC( anaemia, neutropenia, thrombocytopenia if BM involvment)
U&Es- ⬆️ uric acid, ⬆️ ESR/CRP, ⬆️LDH, LFTs(⬆️AST/ALT), Ca2+ may be ⬆️. HIV, HBV, amd HCV serology.

Blood film: lympoma cells visible.
BM aspirate and biopsy.

Imaging: CXR, Ct thorax, abdomen, pelvis, CT plus PET for extranodal involvment.

LN biopsy: histopathologic evaluation, immunophenotyping, cytogenetics .

Class: as Hodgikns.

39
Q

Howmwould you manage NHLs?

A

Aggressive: early stages I-II or localised: locoregional radiation therapy. + chemo- on the high grades. + rituximab for CD20+.

Low grades: not as rapid cell dividing, so chemo doesnt work.
Short courses: rituximab.
Indolent: watch and wait. Careful.

Relapse: Autologous or allogenic stem cell transplantation.
Baseline ECHO + discuss fertility issues. And pulmonary function studies.

Complications: resulting from treatment: BM supression, N+ V, mucositis (infections), infertility, Tumor lysis syndrome, 2o malignancy.

Prognosis:
Dependdent on histological type. other factors: increasing age, stage, extranodal sites, LDH level.

40
Q

Whats multiple myeloma?

A

Haem malignancy characterised by proliferation of plasma cells resulting in bone lesions !! And prodcution of monoclonal immunoglobulin (paraprotein, usually IgG or IgA. )

Aetiology: unknown. Postulated viral trigger. Frequent chromosomal mistakes.
Assc w/ ionizing radiation, agricultural work or occupational chemical exposure (benzene) .

Epidimiology: 4 in 100,000. Peak: 70years old.
Afro-Caribeans> white ppl> Asians

Hx: found incidentaly on routine blood tests.
Bone pain: back, ribs. Sudden and severe if caused by pathological fracture or vertebral collapse.
Infections: often recurrent.
General: tirdness, thirst, polyuria, nausea, constipation, mental change (resulting from hypercalacaemia.)

Hyperviscosity: Bleeding, headaches, visual disturbance.

O/E: pallor, tachycardia, flow murmur, signs of HF, dehyrpdration, purpura, hepatosplenomgealy, macroglossia, carpal tunnel synrome and peripheral neuropathies.

41
Q

How would you Investigate Multiple myeloma?

A

Blood: FBC ( ⬇️Hb , normochromic normocytic) ⬆️ESR/CRP, U&Es (⬆️creatinine, ⬆️Ca 2+ in 45%)typically AlkPhosph.

Blood film: rouleaux formation with bluish backround.
Serum electrophoresis: 2/3 IgG and 1/3 IgA.
Bone marrow aspirate & biopsy:
⬆️ plasma cells- blue cytoplasm. >20%
CXR, pelvic or vertebral Xray. : osteolytic lesions w/o surrounding sclerosing. Pathological fractures.

42
Q

How would you manage multiple myeloma?

A

Emergency: rehydration. Consider dialysis and or plasmapharesis. Radiotherapy if there is bone pain, or cord compression. Treat fractures.

Medical: monitoring and bisphosphates.
Sx disease: chemo and renal support.
Prednisolone.
IFN-a may prolong remission after chemo.

BM or stem cell transplantation. Combined with chemo.

43
Q

What are some complications and thenprognosis of multiple myeloma?

A

Pathological fractures, renal F( accumulation at glomerulus) , spinal cord compression, carpal tunnel syndrome and polyneuropathies (amyloidosis).

Prognosis:
Median survival from dx: 4-6 years.
Markers:!CRP, CReatinine, age.

44
Q

What isnthe Durie-Salmon staging for multiple myeloma?

A

Based on serum Hb, immunoglobulins, Ca2+, creatinine levels, + # of radiographical bone lesions on the skeletal survey.

K-Medicine-Year 3 (3 decks)

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