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Clinical Biomedicine > W2: WBCs > Flashcards

W2: WBCs Flashcards

1
Q

how are WBCs split into 2 categories?

A

polymorphonuclear (granulocytes)
mononuclear

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2
Q

granulocytes include…

A

neutrophils (phagocytes)
eosinophils
basophils

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3
Q

mononuclear WBCs include…

A

lymphocytes
monocytes (phagocytes)

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4
Q

order smallest to largest WBC counts

A

basophils
eosinophils/monocytes
lymphocytes
neutrophils

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5
Q

neutrophils are elevated in…

A

bacterial infection
stress
exercise
myeloproliferative diseases e.g. leukaemia

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6
Q

lymphocytes are elevated in…

A

viral infection
lymphoproliferative diseases (e.g. lymphocytic leukaemia)

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7
Q

monocytes are elevated in…

A

infection
inflammation
tissue damage
monocytic leukaemia

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8
Q

eosinophils are elevated in…

A

allergy
intestinal parasites
hypereosinophilic syndrome
eosinophilic leukaemia

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9
Q

basophils are elevated in…

A

some myeloproliferative diseases
(esp chronic granulocytic leukaemia)

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10
Q

which 2 cell types can monocytes mature into?

A

macrophage
dendritic cell

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11
Q

neutrophil staining

A

granules are neutral-staining

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12
Q

eosinophil staining

A

granules stain w/ eosin (orange)

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12
Q

basophil staining

A

granules stain intensely w/ methylene blue

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13
Q

granulocyte maturation stages (neutrophils)

A

blasts
promyelocytes
myelocytes
metamyelocytes
‘band form’ neutrophils
neutrophils

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14
Q

granulocyte turnover

A

50-320 x 10^9/day

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15
Q

lifespan of a neutrophil

A

usually spend ~7h in peripheral blood (circulating & marginal pools)

migrate into tissues – last for ~20h, after which motility lost. Destruction by monocytes/macrophages.

Many also lost in GI tract.

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16
Q

marginal pools

A

stuck on inside of BVs

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17
Q

lifespan of eosinophils

A

8–12 h in circulation then 8–12d in tissues (thymus, lower GI tract,ovary, uterus, spleen & lymph nodes)

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18
Q

lifespan of basophils

A

few hrs-few days

19
Q

function of neutrophils

A

destruction of invading bacteria & some fungi

20
Q

how does a neutrophil perform its function? (2 steps)

A
  1. location by chemotaxis - motility up a conc grad
  2. phagocytosis = engulfing + killing
21
Q

chemotaxis requires…

A

*vessel wall adhesion
*mmt up conc grad

22
Q

motility of neutrophils

A

crawl

Amoeboid via pseudopodia.

Mechanism: chemotactic receptor-ligand binding followed by interaction of contractile proteins (e.g. actin & myosin)

23
Q

phagocytosis is accompanied by a ‘respiratory burst’ in which there is…

A

Incr O2 consumption
Incr glycolysis
Uprating of bactericidal processes e.g. Myeloperoxidase (MPO) activity
Increased expression of some constituents, e.g. Alkaline phosphatase

24
Q

stages of phagocytosis

A

1) Opsonisation w e.g. IgG /IgM Abs or complement.
2) Particle attachment, via a receptor for the opsonin
3) Pseudopodia enclose particle, which is ingested > phagosome
3) Fusion of granules into phagosome.
4) Microbial killing w/in 20m.

25
Q

how do neutrophils trap & kill bacteria extracellularly?

A

prod web of DNA & proteases

helps prevent spread of infection

26
Q

neutrophil nucleus structure

A

lobulate to aid deformability & motility

27
Q

primary granules of neutrophils

A

discharge into phagosomes. Contain microbicidal proteins (eg MPO, hydrolases & lysozyme) for oxidative & non-oxidative killing

28
Q

secondary granules of neutrophils

A

discharge into phagosomes and extracellularly. Contain hydrolases + chemotactic, opsonic & adhesion protein receptors e.g. Alkaline phosphatase, lysozyme & collagenase

29
Q

tertiary granules of neutrophils

A

Contain e.g. alkaline phosphatase, gelatinase (involved in destruction of collagen), cathepsin (a protease)

30
Q

defects of microbial killing: myeloperoxidase deficiency

A

Fairly common.
Partial or total.
Only 20% pts are immunocompromised. Oxygen free radicals (O-) & lysozyme
compensate.
Fungal infections are biggest prob.

31
Q

other neutrophil disorders

A

Neonate neutrophils have only 20 – 27% chemotactic activity of adults , less in premature neonates.

Neutrophil function declines w age – chemotaxis and phagocytosis significantly impaired in elderly.

Abnormal neutrophils (e.g.hypogranular or agranular) found in myelodysplasia (“pre-leukaemia”), common in elderly

32
Q

eosinophils

A

Eliminate helminth (= parasitic worm) infections by antibody-dependant cell-mediated toxicity (IgE) and are key mediators of allergic inflammation

Elevated in helminth infections and allergy

Normally found in thymus, lower GI tract, ovary, uterus, spleen and lymph nodes, but not usually in thelung except in the case of airborne allergy. Tissue eosinophils are several 100 x more numerous than blood eosinophils

33
Q

Ab-dependent cell-mediated toxicity

A

a mechanism ofcell-mediated immune defence
effector cell of theimmune systemactivelylysesa target cell, whose membrane-surface Ags have been bound by specificAbs (IgE in the case of eosinophils)

34
Q

Eosinophils – some constituents and their functions

A

Eosinophil cationic protein creates pores in mems of target cells allowing potential entry of other cytotoxic molecules to the cell & has anti-viral activity

Major Basic Protein (toxic to parasites & epithelial cells, causes release of histamine & heparin from basophils & mast cells)

Eosinophil-derived neurotoxin (has antiviral properties)

Eosinophil peroxidase is active against micro-organisms

Eosinophil degranulation causes significant local tissue damage

35
Q

Eosinophil disorders

A

Hypereosinophilic syndrome – sustained unexplained eosinophilia > 1.5 x 109/l > 6 months.
Organ dysfunction due to eosinophilic infiltration (heart failure, skin & CNS disease etc)

Some cases are clonal (=Eosinophilic leukaemia)
In most cases the eosinophils are independent of GF control, = a myeloproliferative syndrome
A monoclonal pop of activated T lymphocytes may be found, producing excess IL5
Treatment attempts to limit organ damage by control of eosinophils using hydroxyurea, cytotoxic therapy, steroids.
Most cases are fatal

36
Q

basophils

A

Mature in marrow for 2-7d, circulate for 2 weeks

mature in marrow and circulate in blood, mast cells mature in tissues.

major growth factor for basophils is IL-3, mast cells require Stem Cell Factor (SCF). Both contain heparin & histamine.

Basophils degranulate into internal phagosomes, mast cells discharge granules.

37
Q

basophils - function

A

Basophils & mast cells orchestrate local immunologic & inflammatory reactions, esp. those involving parasitic infections. Secrete:
Histamine - chemotactic agent for eosinophils & is a vasodilator
Heparin - anticoagulant

Accum at site of allergic reactions, esp tick bites

key mediators of immediate hypersensitivity reactions e.g. asthma, urticaria & anaphylaxis

stim by e.g. IgE, IL-3, C5a, GM-CSF & insect venoms to release granule contents, esp histamine.

Basophil activation > release of numerous cytokines, e.g. IL-3, TNF-α & GM-CSF, IL-5,
IL-4.

38
Q

Disorders of basophils

A

Marked basophilia common in CML

Basophilia to a lesser extent is found in other myeloproliferative disorders, e.g. myelofibrosis & Primary Proliferative Polycythaemia.

Basophil leukaemia vrare. Treatment difficult due to release of histamine and other granule contents.

39
Q

Granulocyte function testing

A

Almost entirely limited to neutrophil function tests.

May be indicated in cases of:
Chronic bacterial infection
Increased susceptibility to bacterial infections
Therapy-resistant infections
Recurrent infections with nonpathogenic microorganisms
Abscesses of liver or lung

Rarely performed

Granulocytopenia (esp cyclic neutropenia) and defects of B cells or complement must be excluded first

Primary neutrophil dysfunction significant enough to cause clinical disease accounts for less than 6% of all primary immune deficiency

Nitroblue tetrazolium (NBT) dye reduction for Chronic Granulomatous disease.

Test of neutrophil respiratory burst (production of active oxygen species e.g. O-). Reduction of NBT to an insoluble blue compound by active neutrophils. Visual assessment (microscopy) of results.

Largely superceded by direct measurements of respiratory burst products using flow cytometry.

Can also test:

Motility by assessing ability to penetrate a filter membrane or observed movement across a glass slide
Phagocytosis:
Ingestion, e.g. by observing reduction in the number of free bacteria in a bacteria + neutrophil suspension
Killing, e.g. by observing the fall in numbers of ingested bacteria.
These functional assays are increasingly superceded by flow cytometry

40
Q

monocyte structure

A

Kidney-shaped nucleus
Abundant grey-blue cytoplasm filled
w fine reddish granules
Many cytoplasmic enzymes, esp lysosyme,
peroxidase, esterases
Cytoplasmic vacuoles are evidence of phagocytosis
Amoeboid motility, exhibit chemotaxis
Accum at the site of inflammation

41
Q

monocyte function

A

prod diff adhesins (adhesive glycoproteins) which facilitate adhesion to various surfaces, e.g. endothelial cells

APCs

Can phagocytose opsonised and non-opsonised particles (unlike neutrophils)

Can kill infected host cells (antibody-mediated cellular toxicity)

release many cytokines that stim other cells in IS

42
Q

monocyte lifespan

A

Several months. Can differentiate into macrophages and dendritic cells (& are the only blood cell that can do this)

43
Q

monocyte disorders

A

Lipid storage diseases, e.g. Gaucher’s disease, Niemann-Pick disease result from an accum of debris w/in macrophages – inherited impairment of degrad.
Cause permanent cellular and tissue damage, esp in brain, PNS, liver, spleen, and BM.

An increased number of monocytes (=monocytosis) occurs in chronic infections and inflammatory conditions, e.g. tuberculosis & Crohn’s disease

Monocytic leukaemia (Acute or Chronic)

44
Q

defects of microbial killing: respiratory burst failure - esp NADPH oxidase

A

Inherited, metabolic failure of microbial killing
Some organisms live in the phagosome > persistent infections.
Non-oxidative killing partially compensates (= Chronic Granulomatous Disease (CGD).

45
Q

defects of microbial killing: inherited/acquired defects in neutrophil adhesion/migration

A

Inherited defects v rare.
Acquired, e.g. leukaemia, diabetes, renal failure, > varying degrees of susceptibility to sepsis.

Clinical Biomedicine (23 decks)

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