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1. HUMAN & ANIMAL PHYSIOLOGY > kevin (L4) > Flashcards

kevin (L4) Flashcards

1
Q

HAEMATOLOGY

A

The study of blood & in particular the medical specialty concerned with disorders of the blood

Blood and the tissues in which it is formed represent - large single organ system.

Haematopoietic system basics:
- Many key paradigms underlying stem cell biology, cancer and thrombosis.
- Involved in every aspect of patient care from:
. routine blood counts
. blood transfusion
. specialised management of patients with leukaemia or haemophilia.

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2
Q

Blood

A 
CELLS
- white cells (leukocytes), 
- red cells (erythrocytes)  
- platelets (thrombocytes)
- very rarely other cells 
foetal cells, cancer cells.
- DNA

PLASMA
Plasma is water, electrolytes, dissolved gases, urea, proteins, lipids, glucose & lots of other things in trace quantities
- some of which really should not be there
- alcohol? cotinine?

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3
Q

cell types in blood

A

erythrocyte (red) / 4^-6 x 10^12 / 40-50% by volume
leukocyte (white) / 4^-11 x 10^9
thrombocyte (platelet) / 1^-4 x10^11

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4
Q

blood cell lineages

A

DIAGRAM IN L4 S7

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5
Q

lymphoid cells

A

Lymphoid from lymph
the clear fluid from the thoracic lymph duct
and by extension lymphoid tissue i.e. containing (large numbers of) lymphoid cells e.g. lymph nodes, spleen

Myeloid means from bone marrow.

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6
Q

Erythrocyte membranes

A

Adaptation of erythrocyte to carrying O2 through very fine blood vessels:

  • can deform to squeeze through fine (3 μm) vessels but springs back to usual shape;
  • (this gets screwed up in sickle cell anaemia);
  • the shape is maintained by the cytoskeletal system and allows for flexibility
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7
Q

erythrocytes diseases

A

Too few erythrocytes = anaemia
pallor, breathlessness, fatigue due to lack of O2 transport to tissues.

Too many = polycythaemia
raised blood viscosity & so strain on heart.

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8
Q

leukocytes are present in?

A
  • primary lymphoid tissues where they are produced
    bone marrow, thymus,
  • and also in secondary lymphoid tissues where they function
    (( spleen, lymph nodes, mucosa-associated lymphoid tissue (MALT: e.g. Peyer’s patches mostly in gut) tonsils. ))
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9
Q

leukocytes in other tissues for health

A

Generally (in health) few leukocytes are present in other tissues

a scattering of mast cells, macrophages dendritic cells especially in the gut and skin usually in the connective tissue underlying epithelium
sometimes lymphocytes in the epithelium (intraepithelial lymphocytes).

Infection - inflammation

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10
Q

Leukocyte recognition

A

Morphology/Size – compare to RBCs
Stains and dyes
Histochemistry
Antibodies to cell surface markers

(All are cells involved with the immune response:
on the whole, lymphocytes belong to adaptive immunity
leukocytes of the myeloid series belong to innate immunity.)

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11
Q

leukocytes morphology

A 
Cells in suspension are always round
in tissues may form a characteristic shape 
e.g. dendritic cells 
nuclei may have distinctive shape
size varies
granules in the cytoplasm
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12
Q

leukocytes stains

A

Most common H&E Haematoxylin & Eosin

eosin is a pink acidic dye, binds proteins stains cytoplasm pink

haematoxylin is a blue-purple basic dye which binds nucleic acids

colouring depends on the cell type.
Platelets are the dust looking particles in the back - they are not cells, they are fragments of cells

STAIN IMAGE IN L1 S16

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13
Q

Leukocyte Histochemistry

A

Staining characteristics:
Histochemistry:
Exploitation of specific enzymes (e.g. esterases, phosphatases) within cell types convert colourless substrate into coloured product

Non specific esterases important in defining monocytic lineage related leukemias. Label monocyte lineage – brown neutrophils not good!

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14
Q

Leukocytes - Immunocytochemistry and Immunohistochemistry

A

IMMUNOLOGICAL DETECTION

  • Antibody Binding of extracellular/intracellular antigens
  • Antibodies linked to fluorescent chromophores = cyto
  • Antibodies linked to enzymes to convert substrates = histo
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15
Q

types of markers and what lineage it comes from

A

DIAGRAM TO LEARN IN L4 S19

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16
Q

Flow cytometry

A

The different “coloured cells” are counted and the intensity of their fluorescence measured. The data is presented in a variety of formats, most usually “dot plots” (as here) where each dot represents one cell and the axes are fluorescence intensity.

Two colour flow cytometry of bone marrow aspirate from patient with myeloma showing excess of plasma cells (white blood cells, effector B cells) CD38+CD138+ (region R2)

17
Q

Monocyte morphology

A

platelets have markers but they are not cells
monocytes are at least 3 times bigger than a red blood cell with a lot of cytoplasm in it, a lot of granules and a c-shaped nucleus
its marker is CD14+ is a protein that sits on the external surface of these cells and can be detected by antibodies

as the monocytes move out of the blood cells into the tissues they change shape

18
Q

Thrombocytes = Platelets

A

platelets are produced by fragmentation of Megakaryocytes in the bone marrow
they attach to a site where blood vessels are forming and the membrane is pushed through holes in these blood vessels to be sheared off into platelets
that are smaller than red blood cells

19
Q

plasma

A

Plasma is the fluid component of blood

Electrolytes, acid/base etc

Proteins: ~70 g/L classified as albumin, α globulins (1 and 2), β globulins and γ globulins

All except γ-globulins (aka immunoglobulins, Ig, = antibodies) are synthesised by the liver.

20
Q

serum VS plasma

A

Serum is the fluid that is left after blood has clotted.
It contains all the proteins of plasma
e.g. antibodies
except those that are involved in the clot.

21
Q

plasma proteins

A 
Why are γ globulins in e.g. patients 8, 9 & 10 diffuse but in e.g. 2 & 7 clear prominent bands?
Myeloma results in the production of ONE class of gamma globulin – rather than the normal diffuse band
Make sure you don’t confuse Myeloid and Myeloma
The examples in 2 and 7 and even 1 here are likely producing Myeloma Protein as above the ONE class of gamma globulin. Number 5 might have a leukemia – as gamma globulins are lost and therefore susceptible to infection.

DIAGRAM IN L4 S26

these are taken from patients who might have myeloma
the gamma globulin bands are diffused because you produce a lot of different types of antibodies each of a unique size
Patients 2/4/7 have cancer because they are producing only one type of gamma globulin
Patient 5 is immunodeficient because that is not producing any type of gamma globulin and so do not have any antigen resistance

22
Q

plasma proteins concentrations

A

albumin 35-50 g/L

alpha-globulins 5-15 g/L

  • alpha-anti-trypsin 1-2 g/L
  • haptoglobulin 1-2 g/L

beta-globulin 5-12 g/L

  • coagulation factors 2-4 g/L
  • complement 1-3 g/L
  • lipoproteins 1 g/L

gamma-globulins 6-17 g/L

TOTAL 60-80 G/L

23
Q

plasma protein roles

A

What are they for?
Many proteins are present in low concentrations and have specialised functions

polypeptide hormones (e.g. ?) 
regulators of blood pressure (e.g. ?) 
some enzymes (e.g. ?)
24
Q

albumin

A

Albumin: a carrier for many substances with low solubility in plasma:

  • especially lipids: hormones (e.g. ?), fatty acids
  • binds Ca2+
  • helps maintain osmolarity of blood.

High concentration of albumin in serum makes this protein a major carrier of steroids and lipophilic hormones and a regulator of their access to receptors.

Albumin is a sink for xenobiotics, diminishing the binding of xenobiotics to hormone receptors and other cellular proteins. This protects animals from endocrine disruption by xenobiotics.

Albumin will bind things with low affinity so they can bind and be removed very easily
it is both a transporter and a sink for foreign chemicals (like things you want to take to your liver to be metabolised)

25
Q

plasma proteins

A

complements
γ globulins
α-antitrypsin
haptoglobulin

26
Q

functions of plasma proteins

A 
- Complement:
When activated performs various functions.
Opsonisation
Chemotaxis
Lysis
Clumping
  • γ globulins:
    serum antibodies.
  • α-antitrypsin
    inhibits trypsin
  • Haptoglobulin
    binds free haemoglobin
27
Q

α- antitrypsin deficiency

A

α- antitrypsin deficiency is a genetic disease that results in the degradation and buildup of the protease inhibitor α- antitrypsin within the endoplasmic reticulum of the hepatocytes. This creates tangles within the cells that cannot be removed, and eventually lead to cirrhosis in childhood. Transplantation yields good outcomes for those with metabolic disorders such as α- antitrypsin deficiency.

diseases controlling our trypsin can be advantages because it regulates lots of other hormones and proteins
people who have too little antitrypsin can build up cirrhosis in their liver
capital globulin don’t last forever so they have to be degraded in the spleen

28
Q

Clotting Cascade Proteins

A

with damaged blood vessels, you get the release of signalling factors that cleave thrombin (which will drive the formation of fimbrin)

some enzymes found in the blood will activate the platelets and lead to the clotting of blood through the intrinsic pathway
the extrinsic pathway - the signal comes from the outside and cause some damage, which will drive the activation of tissue factors and leads to the cleavage of thrombin and the formation of fibrin

29
Q

Haemostasis and coagulation

A

Haemostasis - mechanisms which maintain the blood fluid within the circulatory system.

Clotting often starts off with damage to the endothelium
the lining of blood vessels.

Vasoconstriction
Platelet activation
Haemostatic plug
Coagulation
Stable Clot
Clot dissolution
30
Q

platelet membrane integrins and vW factors

A

Platelet membrane integrins mediate adherence to ECM:
integrin α2β1 binds to collagen
integrin α2bβ3 (aka glycoprotein GPIIA/III) binds to other ECM proteins (fibronectin & vitronectin)

Another protein, von Willebrand factor (vWF), binds to platelets and to collagen and is important in fixing platelets to the site of endothelial injury.

31
Q

binding of the integrins

A

Binding of the integrins results in activation of platelets

  • which release ADP which further activate platelets via their ADP receptors
  • and thromboxane A2 (TXA2) which also activates platelets.
  • (TXA2 is also a potent vasoconstrictor which will also help limit blood loss by reducing blood flow.)
  • Tissue factor (below) also activates platelets.
32
Q

activated platelets functions

A

Activated platelets bind more avidly to everything and release a range of protein factors.
These include
coagulation factors
growth factors to promote wound healing.
In addition phospholipids are up-regulated on the platelet surface: these are pro-thrombotic (i.e. stimulate clotting).

33
Q

plasma coagulation

A

Plasma coagulation is principally activated by tissue factor (aka factor III or thromboplastin): this is widely present in tissues but ABSENT from circulation.

Hence blood clots if it comes into contact with tissues i.e. as a consequence of injury to the endothelium.

This is described as the extrinsic pathway since it requires a factor from outside the circulation.

34
Q

mechanisms to prevent excessive clotting

A

There are mechanisms to prevent excessive clotting

  • thrombomodulin on endothelium binds thrombin & this complex activates protein C which inactivates factors Va and VIIa
  • antithrombin in plasma inactivates thrombin.
  • the protease ADAMTS13 degrades vWF.

So clotting is a balance between pro- and antithrombotic processes.

35
Q

haemostasis and coagulation

A

There are fibrinolytic mechanisms to remove clots.
These depend on digestion of fibrin by the protease plasmin.
this is present in plasma as the inactive precursor plasminogen which is activated by a range of factors particularly tissue plasminogen activator tPA.
In turn, tPA is controlled by other factors …

1. HUMAN & ANIMAL PHYSIOLOGY (8 decks)

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