15,16-Basic Haemotology Flashcards

1
Q

standard blood smear ?

A

WBC-pink coloured cytoplasm adn purple coloured nuceli
RBC-no nuclei
Platelets-purple coloured cell fragments

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2
Q

Function of blood ?

A

Transport (/communication):
o Nutrients from (GI) tract, or hormones, to the tissues; (respiratory) gas transport between lungs &
tissues; removal of metabolic waste products
* Regulation:
o Homeostasis of the internal environment: maintaining body
temperature blood/fluid volume in the circulatory system.
* Protection:
o Preventing blood loss (→ clot formation → stop bloodloss); preventing infection : defends
the body against foreign organisms

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3
Q

Blood plasma and formed elements ?

A

o Include erythrocytes, i.e. red blood cells (RBCs), leukocytes, i.e. white
blood cells (WBCs) and thrombocytes, i.e. platelets.
* One can show the nature of the suspension via centrifugation → heavier RBCs are ‘packed’ at bottom; plasma seen as clear, pale-yellow fluid at top.

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4
Q

Plasma proteins in plasma ?

A

lbumins (~60% of total plasma protein):
o Synthesised by liver; aid lipid, and steroid hormone transport.
o Body fluid balance: provide most of the colloid osmotic pressure
o Many drugs bind to albumins: affects their ‘free’ concentration.
* Globulins (~40%):
o Further subdivided into α, β and γ-globulins: α & β are made in
liver, help transport lipids & fat-soluble vitamins in blood; γ are
antibodies (by lymphocytes) → defend body against infection.
* Clotting factors (<5%; involved in coagulation):
o Fibrinogen (factor I; accounts for 2-4%) produced by the liver.

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5
Q

What are RBC ?

A

most abundant cell type in blood:
o Small, circular, biconcave discs (7-8 μm diameter); have no nucleus.
* Chief function is to carry the respiratory gases around body; haemoglobin protein binds O2
Haematocrit ratio: proportion of total blood volume occupied by RBCs/erythrocytes:
* Blood viscosity (i.e. its resistance to flow)

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6
Q

What are 5 classes of WBC ?

A
  1. Neutrophils
  2. Eosinophil
  3. Basophil
  4. Lymphocytes
  5. Monocyte
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7
Q

2 main categories of WBC ?

A

Granulocytes: lobed nuclei; large cytoplasmic granules:
1. Neutrophils: granules stain with both acidic & basic dyes.
2. Eosinophils: granules stain red with acidic dyes (e.g. Eosin).
3. Basophils: granules stain dark purple with basic dyes.
Agranulocytes: nuclei that are not lobed; no granules
1. Lymphocytes (B- & T-lymphocytes).
2. Monocytes; largest WBC; long-lived (months).

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8
Q

What are the prinicples of diapedis ?

A

When infection triggers a mast cell or
macrophage to secrete chemicals,
translocate P-selectin to cell surface.
* Circulating neutrophil (or other WBC)
meets P-selectin (adhesion molecule),
it slows & meets the cytokine (red) →
activation of integrins (blue) →
neutrophil then attaches to the cell.
* Via amoeboid movement, neutrophil
migrates (in)to site of infection.

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9
Q

What are platelets ?

A

minute fragments of cells; consist of very little cytoplasm, surrounded by a plasma membrane:
o Formed in bone marrow; ‘bud’ off cytoplasm of megakaryocytes.
o Normal blood smear: appear as densely staining small particles.
o Normally do not contain a nucleus
important role in control of bleeding
Platlets aggregation and clot retraction

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10
Q

What is Haematopoiesis ?

A

formation of blood cells
continuously renewed by haematopoiesis:
o All blood cell types are generated from a common population of
multipotent stem cells in red bone marrow (adult):
o Erythropoiesis→ new erythrocytes (RBCs).
o Leucopoiesis → new leucocytes (WBCs).
o Thrombopoiesis → new thrombocytes (platelets).

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11
Q

RBC lifespan ?

A

120 days
Type II diabetes screening tests include: random or fasting blood glucose
levels and checking glycated haemoglobin, i.e. HbA1c levels

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12
Q

Major disorders of RBC ?

A

Anaemia: variety of blood disorders characterised by a reduced
number of RBCs (reduced haematocrit), reduced [haemoglobin], or
both → reduction in O2-carrying capacity of blood.
Sickle cell anaemia: defect in 1 of the haemoglobin chains; sickle haemoglobin (HbS) is transmitted by
recessive inheritance:
o Homozygotes: HbS becomes ‘sickled’ when deoxygenated → deformation of RBCs.
* Deformed RBCs clump together; obstruct blood flow → tissue hypoxia (lack of O2); pain.
* The ↑ risk of blood clot formation primarily will affect the liver, spleen, heart and kidneys.

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13
Q

What is Haemostasis ?

A

prevents blood loss
Platelets are essential for the clotting process: they ‘stick’ to the damaged site (in/on plasma side) → ‘sticking’ action helps forms a temporary plug

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14
Q

What are the 3 steps involved in Haemostasis ?

A
  1. Vascular spasm / vasoconstriction: when vascular endothelium is damaged, causes blood vessel to narrow; short duration.
  2. Platelet aggregation & plug formation: Within seconds of injury, platelets begin to accumulate & adhere to the damaged site: platelets become attached to extracellular matrix via integrin receptors (activated by e.g. collagen) → platelets get activated → change their morphology: become more elongated, filopodia present → stick to each other & to damaged site: this requires
  3. Blood coagulation :fibrinin stands ceate a mesh–>blood components form a clot
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15
Q

What are clotting factors ?

A

are normally
present in plasma, in their
inactivated form.
* In general, have many names
and/or roman numerals..!
1 activated clotting factor goes on
to activate another, as shown:
Activated factor

Inactive factor → Active factor

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16
Q

What are the 2 pathways for blood coagulation ?

A

Extrinsic pathway: activated when blood
comes in contacts with tissue factor (III).
* Intrinsic pathway: slower; is activated when
blood contacts the damaged vessel wall.

17
Q

What is the termination of clotting cascade ?

A
  1. Tissue Factor Pathway Inhibitor (TFPI):
    * Protein synthesised by endothelial cells.
    * Extrinsic pathway is inhibited/terminated when factor Xa
    forms a complex with TFPI→ inhibits factor VIIa and TF.
  2. Activity of thrombin is kept in check by several inhibitors:
    * Notably antithrombin (plasma protein, produced by liver):
    * Prevents spread away from clotting site.
  3. Protein kinase C (PKC) system:
    * Activated when thrombin binds thrombomodulin on surface
    of endothelial cells → complex activates PKC system →
    breaks down factors Va and VIIIa (in to inactive peptides).
18
Q

Healing process ?

A

Blot clots formed at inappropriate sites (within the circulation) can be lethal:
o Thrombus: clot at an inappropriate site, that may block a/the vessel; embolism: small clot ‘breaks off’ and travels… May block small blood vessels
In the case of inappropriate blood clotting, this can be prevented by
endogenous (i.e. made in body) anticoagulants:
o Prostacyclin: antagonises thromboxane A2
(latter causes platelet aggregation)…

19
Q

What is the immune system dividied into ?

A

2 division
Natural & Adaptive
Natural: provides innate immunity;
recognises molecular features characteristic of common infecting organisms → mounts an immediate (fast) defence.- Leukocytes, macrophages, mast cells, etc.
Adaptive :s specific and has memory; provides a mechanism for responding to any infections not previously encountered (/seen).

20
Q

What is inflammation ?`

A

physiological, non-specific response to tissue damage /injury, infection, or cellular necrosis (i.e. cell death).
acute= lasts for few days
chronic

21
Q

What is imflammatory response ?

A

The inflammatory response includes (when e.g. skin is damaged):
1. Local vasodilation (i.e. ↑ in blood flow).
2. Increased capillary permeability to plasma proteins.
3. WBC infiltration into damaged tissues
The triple response (‘stages of inflammation’): reddening of skin at site of injury (acute vascular response) → quickly followed by local oedema (i.e. tissue swelling due to fluid accumulation in those affected) → surrounding skin area
becomes ‘flushed’: the flare

22
Q
A