Neutrophils Flashcards

1
Q

peripheral blood circulation half-life

A

7 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

main function of neutrophils

A

phagocytosis

- energy dependent process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Phases of neutrophil phagocytosis

A
  • migration and extravasation
  • recognition and attachment
  • ingestion
  • killing (O2-dependent and O2-independent)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Different types of migration

A
  • chemotaxis
  • locomotion
  • chemokinesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is chemotaxis?

A

directed movement of phagocytic cells to a site of injury via a concentration gradient of chemostatic substances (chemoattractants)

  • picks up low conctn - follows until high conctn
  • stimulates change in morph (pseudopods)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Locomotion

A

random and non-directional

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Chemokinesis

A

non-directional but increases migration speed when chemoattractants are released

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

migration of neuts out of the circulation and into the site of tissue damage or infection

A

extravasation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Phases of extravasation

A
  • rolling: along endothelial cells lining blood vessels; contact between neut selectins and endothelial cell adhesive molecules
  • adhesion: release of chemokines immobilizes neuts
  • transmigration: migration of neuts through the blood vessel wall and into tissues (between or through endothelial cells)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

“to prepare for dining”

A

opsonization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

types of granules in neuts for degranulation

A
  • primary: azurophilic, non-specific (lysozyme, myeloperoxidase, proteases, defensins)
  • secondary: lilac, specific to neut function (lactoferrin, cytochromes)
  • tertiary: electron microscopy (gelatinase, collagenase, membrane glycoproteins)
  • secretory: alk phosphatase, complement receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

oxygen independent killing

A
  • phagosome change in pH (alkaline to neutral)
  • degranulation (1 and 2 granules)
  • digestive enzymes from granules released = bactericidal molecules and hydrolytic enzymes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

hydrolytic enzymes and bactericidal molecules

A

digestive enzymes from granules released

  • lysozyme: hydrolyzes bacterial cell wall
  • lactoferrin: removes iron, inhibits bacterial growth
  • defensin: kills bacteria, viruses and fungi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Leukocyte Adhesion Deficiency (LAD)

A
  • defect in cell adhesion molecules CD11 and CD18
  • unable to stick to endothelial cells of blood vessels and migrate to tissues
  • type I, II, and III (degree of severity depends on mutation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Chediak Higashi

A
  • abnormally large lysosomes (especially in cells that contain granules; melanocytes = albinism)
  • WBC have abnormal chemotaxis and degranulation (incr risk of infection)
  • large platelet granules (prolonged bleeding)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Chronic Granulomatous Disease (CGD)

A
  • chronic granulomas (tumor-like phagocytes) formed during inflammation
  • due to failure of resp burst (O2 dep killing)
  • can degranulate at site but can’t kill (little to no O2-, H2O2 or HOCl)
  • incr susceptibility to deep tissue and pulmonary infection
  • detectable at birth and can be fatal!
  • rare; inherited
17
Q

Myeloperoxidase deficiency

A
  • absence of myeloperoxidase
  • impaired killing but benign and mostly asymptomatic (enhances intracellular killing but not absolutely needed)
  • autosomal recessive
  • function abnormal but infection not serious
18
Q

severe G6PD def

A
  • decreased NADPH production
  • required for O2 dependent killing
  • increased susceptibility to severe infections
19
Q

how do neuts exit circulation?

A

through diapedesis

20
Q

Diapedesis

A
  • passage of cells through intact vessel walls

regulated by integrins and selectins on neuts and endothelial cell on the surfaces of blood vessels

21
Q

Lifespan of neuts in tissues

A

varies depending on whether infectious or inflammatory agents are present

22
Q

neutrophil roles as WBC

A
  • innate immune system = protects against infectious agents

- inflammatory response = cytokine + histamine release; increased blood flow and WBC migration

23
Q

opsonin

A

any molecule in he plasma which acts on a particle to induce phagocytosis (IgG, IgM, C3b)

24
Q

T or F. Opsonization is part of the recognition and attachment phase

A

T!

25
Q

oxygen-dependent killing

A
  1. respiratory burst: after phagosome forms, NADPH oxidase through the HMP shunt generates superoxides
  2. myeloperoxidase: H2O2 => HOCl/bleach oxidizes bacterial components by halogenation of bacterial cell wall and decarboxylation into an amino acid
  3. antioxidant mechanisms: to prevent damage to neuts; superoxide dismutase, glutathione peroxidase, catalase
26
Q

nitroblue tetrazolium stain

A
  • chronic granulomatous diseae
  • indirectly detects production of superoxide anion (neut killing ability)
  • yellow => blue (when formazan precipitate binds to anions)
  • no blue means CGD