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BII > Peter Browlett Lectures > Flashcards

Peter Browlett Lectures Flashcards

L2, 6, 7, 11

1
Q

what is haematopoesis

A

Process by which mature blood cells are generated

from stem cells in the bone marrow

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2
Q

Why do we need to study

haematopoiesis ?

A

blood tests are important part of management of patients

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3
Q

definition of haematopoetic tissue and 2 main examples

A

tissues generating non-lymphoid cells of the blood

  • bone marrow (mainly sternum)
  • spleen
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4
Q

what are the haematopoetic sites during development?

A

yolk sac, AGM endothelium and placenta –> fetal liver –> bone marrow

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5
Q

changes in bone marrow of distal bones with age

A

during childhood there is progressive fatty replacement of marrow thoughout the long bones, the fatty tissue can revert back to haematopoetic tissue

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6
Q

what is extramedullary haematopoiesis, when is this observed?

A

haematopoesis in the organs other than bone marrow, e.g. spleen or liver. Can be observed in diseased states

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7
Q

what is myelofibrosis

A

type of myeloproliferative neoplasm- abnormal clone of HPSC - resulting in fibrosis (or replacement wiht scar tissue)

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8
Q

what are the main constituents of bone marrow?

A

trabecular bone

fat cells (stromal cells)

HPSC

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9
Q

changes to the cellularity of bone marrow with age

A

decrease

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10
Q

decribe the hierachy of the haematopoesis

A

stem cells generate progenitor cells (lymphoid and myeloid)

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11
Q

what antigen is used to measure stem cells

A

CD34 antigen is expressed on the human HSC

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12
Q

3 sources of HSCs

A

Bone marrow

umbilical cord

peripheral blood

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13
Q

function of erythropoetin

A

stimulate RBC production

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14
Q

function of thrombopoetin

A

stimulates platelet production

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15
Q

function of granulocyte colony stimulating factor

A

stimulates neutrophil production

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16
Q

3 Assessment of Blood & Bone

Marrow

A

full blood count (automated, gives absollute nyumbers and cell types - impt to look at morphology)

bone marrow examination - HSC

stem cells - look for CD34 positive cells

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17
Q

what is acute myeloid leukemia

  • symptoms
  • diagnosis
  • treatment
A

cancer of the myeloid line of blood cells - rapid growth of abnormal cells.
- tiredness, bruising and easy infections

  • diagnosis by decrease RBC and platelets, bone marrow examination
  • treatment by chemotherapy and supportive care, antibiotics to prevent infections.
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18
Q

the shape of a RBC allows for

A

flexibility

increased area for gas exchange

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19
Q

function of RBC

A

Hb carriage

O2 transport

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20
Q

what is hereditary spherocytosis

A

abnormality in the membrane of RB causing shortened lifespan of the RBC

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21
Q

the RBC keeps the Hb in a ___ ____ and maintains _______ ________

A

reduced state

osmotic equilibrium

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22
Q

what is G6PD deficiency?

A

inherited defects in enzyme that prevents free radical build up pathways causing haemolysis (shortened RBC survival)

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23
Q

basic structure of haemoglobin

A

2 alpha globulin chains and 2 beta globulin chains and haem group

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24
Q

how does iron deficiency cause anaemia?

A

reduced production of haem due to low iron

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25
Q

how do thalassaemias cause anaemia

A

impaired production of globin chains- results in low Hb

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26
Q

what are the 4 morhological stages of erythroid precursor cell differentiation?

A

progressice increase in Hb

chromatin clumping

extrude nucelus

loss of RNA

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27
Q

average lifespan of RBC

A

120 days

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28
Q

main regulator of erythropoesis

  • where is this produced
  • what triggers production?
A

erythropoetin

  • produced in kidneys
  • responds to low O2 tensions (increase EPO production)
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29
Q

what are 4 effects of EPO?

A

binds to the EPO receptor

  • stimulates RBC progenitor cells
  • increased Hb synthesis
  • reduced RBC maturation time
  • increased reticulocyte release
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30
Q

when is clinical use of recombinant EPO?

A

anaemia of renal failure

- also myelodysplastic syndromes

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31
Q

process of RBC destruction- what are the end products?

A

RBC breakdown in the liver by macrophages

  • Hb is broken down into haem and globin chains

haem:

  • iron –> bone marrow
  • protoporphyrin - bilirubin (liver-bile)
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32
Q

definition of anaemia

A

low Hb than normal for the age and sex patient

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33
Q

cardiovascular responses to anaemia

A

increased cardiac output (right shift in Hb dissociation curve)
- makes O2 more readily available to tissues

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34
Q

difference between physiological and morphological classifications of anaemia?

A

physiological- impaired production or increased loss/reduced survival

morphological- based on the appearance and size of cells (microcytic/macrocytic)

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35
Q

2 categories of physiological anaemia?

A

ineffecitve production or decreased RBC survival

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36
Q

3 main causes of impaired RBC production

A

decifiencies (B12, folate, iron)

genetic defect in produciton (thalassaemia)

bone marrow failure (leukemia, irradiation or drugs)

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37
Q

2 cause so freduced RBC survival

A

blood loss (trauma or surgery)

haemolysis

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38
Q

what parameters are used to differentiate morphological anaemias?

A

MCV, Hb concentration and blood film observations

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39
Q

what is the haematocrit

A

the ratio of colume of RBC to the total volume of blood

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40
Q

3 causes of microcytic hypochromic (reduced Hb) anaemia

A

iron deficiency

chronic illness (iron block)

genetic - thalassaemia

41
Q

what are the 4 ways to diagnose iron deficiency?

A

measure serum iron, iron binding capacity (transferrin) and iron saturation, serum ferritin

42
Q

what does serum iron measure?

A

measures the amount of iron in the liquid portion of the blood

43
Q

what does transferrin measure?

A

directly measures the level of transferrin in the blood. Transferrin is the protein that transports iron around in the body. Under normal conditions, transferrin is typically one-third saturated with iron. This means that about two-thirds of its capacity is held in reserve

44
Q

what does serum ferritin measure?

A

reflects the amount of stored iron int he body

45
Q

what does TIBC measure?

A

(total iron-binding capacity)—measures the total amount of iron that can be bound by proteins in the blood. Since transferrin is the primary iron-binding protein, the TIBC test is a good indirect measurement of transferrin availability.

46
Q

what does UIBC measure?

A

(unsaturated iron-binding capacity)—The UIBC test determines the reserve capacity of transferrin, i.e., the portion of transferrin that has not yet been saturated with iron. UIBC also reflects transferrin levels.

47
Q

what does Transferrin saturation measure?

A

a calculation that reflects the percentage of transferrin that is saturated with iron (100 x serum iron/TIBC)

48
Q

Iron is normally absorbed from food in the ____ ______ and transported throughout the body by binding to ________, a protein produced by the _____. In healthy people, most of the iron transported is incorporated into the production of ________. The remainder is stored in the tissues as ______.

A

Iron is normally absorbed from food in the small intestine and transported throughout the body by binding to transferrin, a protein produced by the liver. In healthy people, most of the iron transported is incorporated into the production of hemoglobin. The remainder is stored in the tissues as ferritin.

49
Q

what is haemachromatosis?

A

rare genetic disease in which the body absorbs and builds up too much iron, even on a normal diet.

50
Q

serum iron, UIBC and serum feritin levels in iron deficiency

A

increased UIBC and decreased SF

51
Q

serum iron, saturation, TIBC and serum feritin levels in anaemia of chronic disease (inflammation)

A

ferritin is normal or high (ferritin is a acute phase protein)

normal or slightly decreased serum iron and TIBC

normal saturation

52
Q

why is ferritin known as a acute phase protein? why does this increase with chronic disease

A

increases with inflammation

  • liver damage can cause ferritin to leak out
  • also in hodgkins lymphoma
53
Q

4 causes of iron deficiency

A

diet (vegetarian)

malabsoprtion (proximal small bowel)

increased demands (pregnancy)

chronic blood loss (GI tract malignancy)

54
Q

what are the 2 forms of iron replacement therapy? example for each?

A 
oral= ferogradumet
IV= ferric carboxymatlose
55
Q

what is hepcidin, why is it high during inflammation and what are the downstream effects?

A

regulator of entry of iron into the bloodstream
- inflammation causes high hepcidin, serum iron falls due to iron trapping within the macrophages and liver cells + decreased gut iron absoprtion.

this causes iron deficiency and hence anaemia

56
Q

RBC cellular characteristics of beta thalassaemia

A

fragmented or irregular shaped RBC

Small or microcytic RBC

57
Q

diagnosis of thalassaemia

A 
blood counts (Hb, MCV and RBC counts)
- iron studies and phenotypic analysis
58
Q

5 main causes of macrocytic anaemia

A 
B12/folate def
alcohol
liver disease
primary bone marrow disorders
hypothyroidism
59
Q

example of macrocytic megaloplastic anaemia cause- what is the mechanism?

A

B12/folate deificiency

- impaired DNA synthesis

60
Q

causes of low B12/folate

A 
diet - vegans (B12 is in milk, eggs and meat)
malabsorption
- gastrectomy
- immune (pernicious anaemia)
- terminal ileum disease
61
Q

why do B12 deficiencies present late?

A

the body has stores of B12 for 3-4 years

62
Q

causes of low folate

A

lack of veges

coeliac

increased demands (pregnancy)

63
Q

2 types of haemolytic anaemia

A

intrinsic = inherited defect in the RBC membrane

extrinsic = autoimmune

64
Q

clinical presentation of haemolytic anaemia

A

anaemia

jaundice, splenomegaly

raised reticulocyte count (due to increased production)

65
Q

what are the 2 main types of leukocytes?

A

phagocytes

lymphocytes

66
Q

sub-categories of phagocytes and examples

A

granulocytes (neutrophils-90%, eosino and basophils)

monocytes

67
Q

describe teh kinetics of granulocyte production?

  • maturation time
  • circulating time
A

7-10 day maturation

6-10 hours circulation before entering tissues for phagocytosis

68
Q

main regulators of granulopoiesis

A

haematopoetic growth factors

IL3, stem cell factor, G-CSF

69
Q

what is G-CSF, (brand name) and effects- who is it used for?

A

granulocyte colony stimulating factor (filgastrim)

- used in patients with neutropenia (bone marrow failure, chemotherapy)

70
Q

3 functions of neutrophils

A

chemotaxis

phagocytosis

killing bacteria
- (non)/oxidative

71
Q

what is Neutrophil leucocytosis

A

increased number of neutrophils usually due to inflammation or infection

72
Q

what is neutropenia, what are the risks (what is this called?)

A

patients with a low neutrophil count

  • have an increased risk of infection
  • -> febrile neutropenia
73
Q

which of the phagocytes are granulocytes?

A

neutrophils
eosinophils
basophils

74
Q

process of monocyte development

A

circulate for 1-3 days

- enter tissues (transform into macrophages)

75
Q

what are the main phagocytic functions of monocytes?

A

chemotaxis
opsonisation
phagocytosis (and ingestion)

76
Q

what are the 3 main roles of the monocytes?

A

phagocytosis
synthetic functions (complement, interferon)
antigen presentation

77
Q

what is monocytosis? what are the 2 types? examples?

A

monocytosis- increased
- reactive= chronic infections (TB)

  • malignant- acute/chronic myeloid leukemia (monoblastic type)
78
Q

what is Eosinophilia and when is this observed?

A

increase in eosinophils- allergy/hypersensitivity reactions

also parasite infections

79
Q

effects and function of basophils

A

close relationship to mast cells
- allergic symtpoms
granules contain histamine (vasoldilation)

80
Q

what is the normal make up of citculating lymphocytes? (%)

A

75% ish T cells
10% B cells
NK cells

81
Q

what are primary lymphoid organs and examples for B cells and T cell?

A

where lymphocytes are formed and mature
B= Bone marrow
T= Thymus

82
Q

what are Secondary Lymphoid Organs

and examples?

A

where lymphocytes are activated
- lymph nodes
spleen
bone marrow

83
Q

what are the 2 potential classifications of causes of lymph node enlargement?

A

reactive - viral/bacterial infection

malignancy- lymphomas or metastatic spread

84
Q

causes of Lymphocytosis

A

reactive - viral (infectious mononucelosis)

malignant - chronic lymphocytic leukemia

85
Q

Lymphopenia causes?

A 
HIV infections (CD4 T cell deficit)
- steroid therapy, bone marrow failure
86
Q

define Polycythaemia

A

state of disease where haematocrit is increased

87
Q

4 mains types of blood and bone marrow cancers

A

leukemia

myeloproloferative neoplasms

lymphomas

myeloma

88
Q

what is the pathological process of leukemia

A

proliferation of immature bone marrow cells (lose abiloity to differentiate beyond “blast” cells)

  • expand tha replace normal cells
  • abnormal leukemic cells spill into the blood.
89
Q

4 pathogenesis causes of leukemia?

A

congenital/inherited

viral infections

radiation

chemical/DNA changing drugs

90
Q

2 subtypes of acute leukemia?

A

acute myeloid leukemia (AML)

Acute lymphoblastic leukemia (ALL)

91
Q

2 types of leukemia?

A

acute, chronic

92
Q

what are the 3 main clinical symptoms of Acute leukemia?

what are some less common symptoms?

A

loss on normal cells (RBC, platelets and neutrophils)
- fatigue (anaemia), bleeding (thrombocytopenia) and infections (neutropenia)

liver and spleen enlargement
bone pain (marrow infiltration)
93
Q

what ages are acute leukemia likely to present?

A

occur over all ages
- ALL - mainly childhood
AML - mainly adults

94
Q

how is leukemia diagnosed?

A

full blood count

bone marrow biopsy

95
Q

blood count results of leukemia

A

full blood count

  • anaemia
  • WBC increase
  • usually severe thrombocytopenia
96
Q

bone marrow biopsy indications of leukemia

A

over 20% blasts (myeloid or lymphoid)

97
Q

treatment for acute leukemia

A

general/supportive care:
- infusion (RBC and platelets)
managing infections (antibiotics)

chemotherapy

HSC transplant

98
Q

what are the 3 steps of acute leukemia chemotherapy?

A

Induction therapy- lower the number of plasma cells in bone marrow (induce remission)

consolidation- to mop up residual leukaemia
cells

maintainance therapy (only ALL)- keep patients in remission

99
Q

what is autologous and allogenic HSC transplant?

A

autologous- own stem cells are taken in remission

allogenic- matched sibling or unrelated donor

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