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Clinical investigation of disease > WEEK 4 > Flashcards

WEEK 4 Flashcards

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1
Q

erythropoiesis

A
  • stem cell - proerythroblast
  • uncommitted - committed
  • erythroblast - normoblast
  • ribosomes production - Hb accumulation
  • Reticulocyte -Rbc
  • Nucleus ejected - circulating
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2
Q

Haemoglobin

A
  • iron containing protein in red cells which carry oxygen from lungs to all cells in your body
  • low haemoglobin is called anaemia

-caused by bleeding, deficiencies of iron and vitamins B12 or folate

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3
Q

Normocytic anaemias

A

causes or normocytic anaemias (normal MCV)

  • Acute blood loss
  • anaemia of chronic disease
  • bone marrow 2o’s renal failure
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4
Q

Microcytic anaemia (Small RBC )

A

causes of microcytic anaemias (Low MCV)

  • iron Def
  • thalassaemia (genetic abnormality causing reduction in globin production)
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5
Q

clinical symptoms in iron deficiency

A
  • pallor
  • SOB
  • TATT
  • Glossitis
  • spoon nails
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6
Q

haemoglobin synthesis

A
  • haem synthesis - series of biochemical reactions in mitochondria leading to synthesis of protoporphyrin
  • iron is supplied from circulating transferrin
  • globin chains are synthesised on ribosomes
  • tetramer of 4 globin chains each with its own haem group makes up haemoglobin molecule
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7
Q

Iron

A
  • homeostasis regulated to avoid extremes - iron deficiency anaemia or iron overload
  • total body 3-5g 2/3 found in haemoglobin of red cells
  • average diet contains 10 - 15 mg per day
  • 1- 2 mg absorbed daily through intestine
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8
Q

causes of iron deficiency

A

increased requirements

  • chronic blood loss
  • growth
  • pregnancy and lactation
  • inadequate supply
  • malabsorption
  • poor diet
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9
Q

treatment of iron deficiency

A
  • underlying causes
  • oral ferrous sulphate
  • iron injection
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10
Q

laboratory diagnosis

A
  • blood film and red cell indices

-hypochromic microcytic anaemia

-anisocytosis

  • bone marrow
  • serum ferritin
  • serum iron and TIBC
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11
Q

Iron overload

A
  • excess iron absorbtion - hereditary haemochromatosis - genetic defect in iron metabolism where feedback control of dietary absorption is lost
  • regular blood transfusions
  • increased iron intake
  • liver disease
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12
Q

Clinical symptoms in B12 & folate deficiency

A
  • weight loss
  • fatigue
  • glossitis
  • jaundice
  • dementia
  • paraesthesia
  • neuropathy
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13
Q

Folates - sources and daily requirements

A
  • liver, eggs , yeast , whole grains, leaf beg mainly
  • very sensitive to heat
  • need 100ug per day. loss in faeces, sweat, urine
  • body stores 10 mg mainly in liver
  • body stores enough for 3-4 months
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14
Q

Vitamin B - sources and daily requirements

A
  • synthesised by microorganisms only
  • main source dietary - animal products
  • heat stable - little loss during cooking
  • lose between 1-4 ug daily (urine, faeces)
  • body stores 3-4 mg in liver
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15
Q

Tissue and neurological manifestations

A
  • affects dividing cells
  • disturbed neurological functions
  • neural tube defects
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16
Q

Haemolytic anaemias

A

Intravascular haemolysis

  • leads to Free Hb eventually entries urine = haemoglobinuria + haemosiderinuria
  • fragmented cells called schistocytes are seen in intravascular haemolysis
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17
Q

Extravascular haemolysis

A
  • haemolysis spleen and liver microphage Fc receptors bind immunoglobulin attached to RBCs and either ingest small portions of RBC membrane creating spherocytes or phagocytizing RBC
  • Spherocytes have less surface area, become spherical
  • eventually unable to pass through splenic microcirculation due to deformability
  • low glucose in spleen which ^ haemolysis
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18
Q

Other acquired causes

A
  • drug induced (immune) - usually drug specific antibodies which cross react
  • mechanical - physical damage to red cells by heart valves or microangiopathic haemolytic anaemia where red cells are damaged by fibrin strands due to DIC
  • Infections - wide variety of infections cause haemolysis through direct invasion of RBC
  • march haemoglobinuria - damage to Rbc in small bones of feet
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19
Q

Leukaemia

A
  • disease resulting from neoplastic proliferation of haemopoietic or lymphoid cells
  • ACUTE/ CHRONIC
  • Myeloid, lymphoid , biphenotypic (rare)
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20
Q

Acute leukaemia

A
  • over 50 % blasts in BM
  • often blasts in PB
  • AML or ALL
  • causes

-oncogenes

-retroviruses and viruses

-chemicals and radiation

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21
Q

blast cells

A
  • immature precursors of either lymphocytes or granulocytes
  • do not appear in peripheral blood
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22
Q

laboratory tests (AML)

A
  • FBC - low Hb and plts
  • morphology
  • cytochemistry
  • flow cytometry
  • cytogenetics
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23
Q

cytogenetcis

Study These Flashcards
A

AML incidence
MRD - minimal residual disease

relapse - disease returns

remission - disease free

BMT - bone marrow transplant

MUD - matched unreleased donor

SCT - Stem cell transplant

24
Q

All laboratory tests

Study These Flashcards
A

morphology

cytochemistry

  • MPX/SB neg
  • PAS block pos

immunophenotyping

  • CD19+ (b) CD10+ CALL
  • CD7 (T)

cytogenetics

  • hyperdiploidy common
25
Acute leukaemia - symptoms
- pallor, lethargy - fever, malaise, infections organ infiltrations causes - lymphadenopathy - splenomegaly - gum infiltration - CNS
26
CML (chronic myeloid leukaemia )
- CML is malignant disorder of haemopoietic stem cell - 3 recognisable phases : chronic, acerated, blastic transformation in which condition resembles acute leukaemia
27
CML lab finidngs
- WBC usually >50x10^9/l - morphology - ^ myeloid cells at all stages of development - predominantly myelos and neuts - B12^
28
CML incidence / symptoms
- more common in adults 40/60 years - 2600 people in UK - splenomegaly, hepatomegaly, anaemia, sweating , weight loss, bruising, epistaxis
29
Treatment for CML
historically has been - hydroxyurea - alpha - interferon - allogeneric BMT - sibling BMT < 55 years - MUD BMT < 20 years - PBSCT new treatment - intro of imatinib mesylate. imatinib occupies ATP binding sites of several tyrosine kinase molecules and prevents phosphorylation of substrates involved in regulating cell cycle
30
CLL (chronic lymphoid leukaemia - Lymphoprolif)
- neoplastic proliferation of mature looking lymphocytes - not usually aggressive disease - lymphoid mass often in blood, BM, spleen, lymph nodes
31
Symptoms/ incidence CLL
- elderly pateints - male female 2:1 - aneamia/ thrombocytopenia - infections
32
other haematological conditions
- myeloma - myeloproliferative disease - myelodysplasia - lymphoma
33
Antigens and antibodies
antigen - any substance which may be recognised as foreign antibody - product of immune system that react with corresponding antigen
34
what are blood group antigens
located in red cell membrane
35
blood gp antigens cont
- inherited structures - alleles on gene code via mRNA for proteins directly Rh or enzymes that cause production of carboydrates *=(ABO, lewis P, I) - different alleles arise as a result of spontaneous genetic mutations creating diversity
36
clinical significance of ABO gps
- ABO incompatible transufsion reactions -usually from A or B transfusion reactions -can cause acute intravascular haemolysis -severe efects, potientially fatal even when small volumes are transfused - pregnancy -HDN gp O mother
37
Rh system
rhesus positive - patients are DD or Dd rhesus negative - patients are dd
38
clinical significance of Rh system
- all Rh antibodies capablle of causing severe transfusion reactions - prevent stimulation of anti-D by accurately D typing all donors and patients - antibodies to Rh system, specifically anti - D and anti C capable of causing haemolytic disease of newborn (HDN)
39
antibody - antigen reactions
aggulation stage 1 - antibody binds to RBC stage 2 - lattice is formed
40
collection of blood components
2 different methods - processing of whole blood donation - obtaining components from apheresis
41
Leucocyte depletion
- BSE injected cows given rise to vCJD - vCJD can be transmitted through blood transfusion - prion in highest conc in white cells - all components passed through filters to removed white cells
42
blood and blood products
donation testing - blood grouping - presence of high titre ABO antibodies - micro(virology)
43
red cells
- storage at 4oc - shelf life 35 days - volume 220-300 - in aneamia investigate underlying - commenced with 30 minutes - transfused over 2-3 hours max 4 hours - 131.80 pounds
44
red cells - oxygen delivery
- difficult to measure - rely on haemoglobin or estimated blood loss
45
when to transfuse red cells
- red cells loss in surgery and trauma - >20% blood volume - symptomatic or critical aneamia that cannot be corrected by any other means - exchange transfusion
46
Fresh frozen plasma (FFP)
- plasma component - clotting factors - shelf life of 2 yeats at -30oc - dose 12-15ml/kg - stored at 4oc once thawed - cost 39.55
47
indications for platelet transfusions
- failure of production - bone marrow disease - dont work - function disorders - washed out - massive transfusion - destroying them - immune thrombocytopenias
48
Transfusion reactions
introduction - less than 1% of individuals receiving blood transfusions have an adverse effect, termed a transfusion reaction - transfusion reactions can be caused by immunological and non0immunological mechanisms - complications of transfusions can involve any blood component and can be fatal
49
immunological reactions
- antigens (Ags) in donor cell or plasma react with recipient antibodies (Ab) - Abs or lymphocytes in donor plasma react with Ag or cell in recipient
50
reactions to incompatible red cells
- Abs to red cells are most important in blood transfusion -large volume transfused -naturally occuring antibodies -immune antibodies, evoked by transfusion or pregnancy
51
Haemolytic transfusion reactions
- A haemolytic transfusion reaction (HTR) is the occurance of lysis or rapid removal of red cells in recipient - acute (immediate) HTRs occur during or within 24 hours of transfusion
52
Acute (immediate) HTR
- administration of ABO incompatible blood - symptoms include : -fever -pain at infusion site -chest and lumbar pain - physical signs include : hypotension , haemoglobinuria, bleeding and renal failure
53
delayed HTRs
- secondary immune responses following re-exposure toa given RBC ag - clinical features : -fever, fall in Hb, jaundice and haemoglobinuria -hypotension and renal failure and uncommon
54
febrile non -haemolytic reactions
- transfusion of blood components (RBC or plts) containing incompatible WBCs may provoke severe febrile reactions - clinical presentations
55
non - immunoligcal reactions
- transfusion - associated circulatory overload - transfusion - transmitted infections - bacterial contamination - variant Creutzfeldt jakob disease
56
transfusion - transmitted infections
- transmissibility of infectious agents -asymptomatic infection -present in blood stream -transmitted parenterally -able to survive during storage - viruses - hepatitis , HIV , HTLV, herpes , CMV, EBV - bacteria - syphilis, pseudomonas, staphylococcus - protozoa - malaria
57
SHOT Serious Hazard Of Transfusion
- improving safety of transfusion process - informing policy within transfusion services - improving standards of hospital transfusion practise

Clinical investigation of disease (5 decks)

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