Proliferation of blood physiology
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Proliferation of Blood Physiology. nathan. RBC prolif. SCA Autosomal rec. Mutation of Hb gene Carriers res. To malaria Life exp  40s. Microcytic, hypochromic an. Reticulocyte Count: Inc: Bleeding compensation Haemolytic anaemia Haemolytic disease of newborn Dec Fe def anaemia

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Rbc prolif
RBC prolif.

  • SCA

  • Autosomal rec.

  • Mutation of Hb gene

  • Carriers res. To malaria

  • Life exp  40s

Microcytic, hypochromic an.

  • Reticulocyte Count:

  • Inc:

  • Bleeding compensation

  • Haemolytic anaemia

  • Haemolytic disease of newborn

  • Dec

  • Fe def anaemia

  • Pernicious anaemia

  • Aplastic anaemia

  • Radiation therapy

  • Marrow failure – inf/ca

  • HDN

  • (maternal IgG fetus rbc)

  • Death from HF

  • Intrauterine transfusion – early induction if app.

Megaloblastic an.

Platelet prolif
Platelet prolif

X1000 plt count

Normal range 150-450

<20 transfusion

20-50 monitoring

50+ ok, conservative monitoring

  • ET

  • 1 of 4 myeloprolif disorders

  • More sensative to growth factors

  • JAK2

  • Plt count >600 for 2+ mnths

  • Rx – interferon

  • ITP

  • Autoimmune attack of platelets

  • Rx with steroids



  • Myeloprolif disorders (often assoc with JAK2 mutation)

  • ET – inc platelets

  • Myelofibrosis – fibrotic BM - pancytopaenia

  • Polycythaemia vera – inc RBC

  • CML – inc myeloid progenitors and products

Myeloid prolif
Myeloid prolif.

Occurs in red bone marrow (red vs yellow; foetus vs adult)

  • Myeloblasts

  • Myeloblastic leukaemia

    • Failure of haemopoeisis

    • Continual prolif of myeloblasts w/o diff.

    • Pancytopaenia and hypoplasia BM


1, myeloblast;

2, promyelocyte;

3, megakaryocyte;

4, neutrophilmyelocyte;

5, young neutrophilmetamyelocyte;

6, "band" neutrophilmetamyelocyte;

7, polymorphonuclearneutrophil;

8, eosinophilmyelocyte;

9, eosinophilmetamyelocyte;

10, polymorphonucleareosinophil;

11, basophilmyelocyte;

12, polymorphonuclearbasophil;

13-16, stages of monocyte formation.

  • Neutropaenia

  • Febrile vsafebrile

    • Severely predisposed to infection

    • Common post-chemo

    • Dec production, inc destruction

    • Aplastic anaemia, cancers, VitB12,folate def

    • Autoimmune, chemo

Neutrophil eosinophil basophil monocyte – .......................................... macrophage in tissues

Neutrophils and macrophages physiology
Neutrophils and Macrophages Physiology

  • Invading viruses and bacetria are mainly destroyed by these.

  • Nuetrophils are mature cells that can attack bacteria in blood

  • Macrophages enter blood as monocytes (ineffective), mature in tissue (5x); can fight bacteria in tissues.

  • WBC enter tissue spaces by diapedesis

    • Squishing through smaller than cell size whole in cappilaries.

  • WBC are attracted to areas by chemotaxis.

    • Bact or viral toxins

    • Biproducts of degen. Inflam. Tissue

    • Complement

    • Biproducts of clotting

Neutrophils and macrophages physiology1
Neutrophils and Macrophages Physiology

  • How do they kill – phagocytosis then intracellular destruction

    • Rough cell surface

    • Dead +foreign tissues lack protect, protein coat

    • a/b + c complex attracts eating cells to the right plc

  • Neutrophilvs Macrophage phagocytosis

    • Netrophil– pseudopodia, around and fuse to create a chamber, invaginates into cyto, vesicle. Can handle 3-20 bac.

    • Macrophage - >100 bac; engulf larger particles (RBC, protozoa), can survive way longer

  • Destruction

    • Vesicles of lysosymes and other enzymes/bacteriocydes fuse with evil vesciles for a deadly combination.

Inflammation what do the neutrys and monoys do
Inflammation – what do the neutrys and monoys do?

  • Inflammation – clinical signs, tissue changes

    • Vasodilation, inc permeability, clotting, mig of N and M, swelling

  • Walling off process – prevents spread of toxins through lymphatics and tissue spaces

  • MACROPHAGE INVASION!!!!! (immediate)

    • Eat as much bad stuff as quickly as possible

  • NEUTROPHIL INVASION!!!! (1-2hrs) (neutrophilia)

    • Margination – cap. Endo. Altered so N’s stick

    • Diapedesis

    • Chemotaxis

  • More macrophages - takes ages cos BM +blood supplies are depleted

  • Inc production of G + M in BM


  • 2%

  • Insignificant

  • Role in chemotaxis and phagocytosis

  • Eosinophilia in parasitic infections

  • Cant eat them but attach to parasites and release toxins to kill them

    • Hydrolytic enzymes

    • Reactive O2

    • Major basic protein

  • Accumulate in areas of allergic reactions

Neutrophil eosinophil basophil monocyte

Basophils mast cells
Basophils/Mast Cells

  • Release histamine during inflammation

  • Allergies – caused by IgE

  • The Ig attaches to these cells, and when the antigen (allergen) comes to bind to IgE, it explodes the basophils/mast cells that release:

    • Histamine, bradykinin, serotonin, heparin, slow-reacting substance of anaphylaxis, lysosymes

    • Responsible for most of allergic manifestations

Lymphocytic prolif
Lymphocytic prolif.

Prolif – thymus gland processes T-cell, liver B-cell

found in lymph tissue; spleen; thymus; tonsils; nodular tissue

  • Innate immunity

  • Non-specific destruction of non-self materials

  • Phagocytosis

  • Gastric acid secretions

  • Skin

  • Blood compounds, C, NK cells (recognise and destroy foreign cells, tumour cells and inf. Cells.)

  • Acquired/Adaptive

  • A/bs/bcell/humoral imm.

  • Tcell (cell-mediat.) imm.

  • Specifically targeted to antigens


B – cell CD20

Bmemory cells

NK cell CD16

T - cell


Plasma cell

T-cytotoxic CD8

Plasma cells make Ig’s

T-helper CD4

Lymphocytic mechanism of action descr. G+H Ch 34 pp439-450

What do lymphocytes do
What do lymphocytes do

  • Millions of diff. antigen specific t and b cells live in he lymphoid tissue, when activated it clones itself; with a view to creating lots of ab’s or antigen-spec. Circ. T cells.

  • B Activation – antigen is eaten by macrophage which presents it to b-cells; when it finds the right a/b ; also the t’s see the antigen and make helper t’sb cell. lymphoblastsplasmablasts

    • Plasma cells make their specific activating Ig

    • As well as making the plasmablasts, duplicate b cells are created (memory cells) which circulate around the body in the lymph as to allow for secondary (more effective if reexposed) response. [immunisation]


  • Variable portion

    • – specific to antigen

  • Constant –

    • proprties of ab, like C binding capacity.

  • Classes M G A D E

    • M – high in primary response, lots of binding sites but few in number

    • G-bivalent - 75%

    • E – allergies

  • What do a/bs do?

    • Directly attack evil things

      • Agglutination

      • Precipitation – molecular complex becomes too large to be eff.

      • Neutrilisation – cover off virulent surface areas of toxin/pathogen

      • lysis

    • Get complement to do the dirty work (classic pathway)

      • Next slide

A bs activate c
A/bs activate C

  • Opsonization and phagocytosis – makes the phagocytes more attracted >100x

  • Lysis

  • Agglutination – changes invading cell surface so they bind to eachother

  • Neutrilization of viruses

  • Chemotaxis – phagocytes

  • Activate mast cells and basophils

  • inflammation

T cells

  • Activation is similar to b cells but instead of producing ab’s they produce more t cells, and memory t cells which can circulate in blood and lymph for mths/yrs.

  • T-cells, unlike B, only recognise antigens when presented on MHC protein on APC (dendritic) in lymph.

    • MHC1- Tc; MHC2- Th

  • Helpers – form lymphokines-act on BM and imm. Cells (Ils, interferon, GMCSF)

    • Of vital importance, nearly no acq. Imm. Without them. Destroyed by HIV

    • Stimulates growth of Tc and Ts cells.

    • Stimulate B-cell diff

    • Activates macrophage sys.

    • Feedback on themselves


  • Cytotoxic – after binding to evil cell, release hole-forming proteins (perforins), cause fluid to rush into cell pop. Also, Tc cells can release toxins into cells. They can pull away from evil cells before they die (leaving them to die) and go kill other ones. They can last for months killing evil cells.

    • Especially lethal to virally inf. Cells; also roles in killing cancer cells and other non-self

  • TSurpressor. – surpressTc and Th. Proposed that these cells prevent excessive destruction of self by Tc cells. Also maybe a role in immune tolerance.

  • Immunisations and allergies.