Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Immunology > Chronic tissue injury and infection > Flashcards

Chronic tissue injury and infection Flashcards

1
Q

How do recognise chronic inflammation?

A

injury, inflammation, repair
Macrophages and granulation tissue, new blood vessels
Usually adaptive response
e.g. gallbladder- red pus lining, cholesterol gallstones, thick and pale with fibrosis tissue wall

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

What is granulation tissue?

A

New connective tissue- (formed by) fibroblasts, vessels (allows circulation to continue delivering exudate), lymphatics, collagen eventually
Surround dead tissue, pus or irritants- protects and delivers

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

What are the types of monocytes?

A

Sentinel- (CD16+) patrol in vessels, survey and support endothelium
Migratory- emigrate steadily

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

What occurs to monocytes during inflammation?

A

Enhanced migration, activation- activated interstitial monocytes acquire APC ability, secrete TNF and NO (antimicrobial)
Become interstitial monocytes- initially pro-inflammatory, later restorative
Monocytes exit by lymphatics/ death

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

How are macrophages created?

A

Monocytes in blood (from yolk sac/ bone marrow) enlarge and undergo mitochondrial, lysozyme and ER changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why are macrophages useful?

A

Highly plastic and capable cells- enhanced killing (IFN gamma), immune modulation (cytokine, chemokines, antigen presentation), acute phase reaction, clearance, new or remodelled tissue
Homeostatic and metabolic functions

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

How is NET associated with autoinflammation?

A

Gout (urate crystal) arthritis

Reaction of crystals activates monocyte inflammasomes, triggers NET release, localised pain

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

How is NET associated with allergy?

A

Asthma- neutrophil inflammation, rhinovirus increases Netosis, NET DNA intensifies allergic type 2 immune responses in asthmatic airways

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

How is NET associated with autoimmunity?

A

Systematic lupus erythematosus

NET major source of antigens, immune complexes trigger more NET release, NET injure endothelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are inflammasomes?

A

Caspase-rich multiprotein complexes

Assembled by PRR signals in myeloid cells

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

What do caspase enzymes produce?

A 
Inflammatory cytokines (IL-1 beta and IL-18)
Programmed lytic cell death (pyroptosis)- liberates cytokines and inflammasomes, traps bacteria in the corpse, glucocorticoid resistance (cleaves receptor)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Why are inflammasomes important?

A

Antimicrobial defence, inflammatory cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Name the special types of inflammatory lesions

A 
Inflammatory sinus and fistula
Erosion and ulcer
Abscess and cellulitis
Granuloma
Amyloid deposition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is an inflammatory sinus?

A

Infected hair follicle, abscess, lined by granulation tissue
Characterised by blind ending pit and tracking
Small hole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is a fistula?

A

Fistula hole between two surfaces
Painful
Surgical intervention can lead to more
Abnormal link between different epithelial surfaces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is an erosion and ulcer?

A

Localised defect in epithelial surface
Sloughing of inflammatory necrotic tissue
Full thickness- all the way through surface
Exposes tissue under epithelial
Dermis/ lining of stomach
Not quick fix- no basement membrane
Exposed to acidic juices- expand ulcer, digest submucosa (ulcer deeper/ erosion has basal membrane so potential to regenerate)
Erode through wall of artery- haemorrhage
Perforating gastric ulcer

17
Q

What is an abscess?

A

Pus accumulates in newly formed cavity- avascular so poor drug penetration
Pus- neutrophil and potassium rich, excretory enzymes- damage tissues. Swarm pushes aside connective tissue
Granulation tissue surrounds to deliver exudate

18
Q

What are abscess outcome?

A

Persists- scars/ fibrosis (burst)
Discharges- sinus and fistula
Fascial inelastic- tissue swelling limit, pressure increase, same as blood coming in, no blood supply- strangle itself
Drained to relieve pressure

19
Q

What is cellulitis?

A

Unlocalised subcutaneous spready infection- Strep pyogenes, staph aureus

20
Q

What are granulomas?

A

Organised clusters of mature macrophages in response to persistent stimuli

21
Q

What are the characteristics of granulomas?

A 
Larger, more organelles, ruffled membranes, avascular
Low turnover (foreign body- inert indigestible material like suture)
High turnover (immune- toxic inciting agent, continual replenishment and Tell cells migrate in then retained)
22
Q

Describe non- immune granulomas

A

Foreign body reaction to poorly antigenic material
Larger, non-phagocytosable material
Aspirated cooked cellulose food molecule

23
Q

What does a tuberculosis granuloma looks like?

A

Lots of nuclei, merged cytoplasm, contain mycobacteria

24
Q

What occurs during mycobacterium tuberculosis infection?

A

Manipulates macrophage response
Granulomas form and spread the infection unrestricted
Specific T cells are required to arrest infection

25
Q

How do they manipulate macrophage responses?

A

Inhaled bacteria are imported into lung tissue in macrophages
Renders them insensitive to T cell help
Promotes its phagocytosis (avoiding lysosomes)
Promotes m0 chemotaxis and phagocytosis of apoptotic m0/ Mimics complement system/ Waxy coat so cant digest- survives in cytoplasm/ Suppresses adaptive

26
Q

How do granulomas form and spread the infection unrestricted?

A

Phagocytosis of apoptotic infected m0 infects arriving m0, migration of infected m0 initiates secondary granulomas, m0 necrosis permits exuberant extracellular proliferation- soft caseous necrosis

27
Q

What is the impact of specific T cells being present?

A

TNF and IFN gamma produced. TNF not necessary for granulomas but increases microbicidal capacity
Contribute to lung destruction (cavitation) and so transmission
Bacterial population stabilise- some proliferate, others go dormant until immunity dips

28
Q

How is chronic kidney inflammation diagnosed?

A

Enlarged on ultrasound scan, proteinuria, failed glomerulus, amyloid-fibrils in tissues

29
Q

What is amyloid?

A

Extracellular accumulation of insoluble fibrils made from a misfolded peptide (plus amyloid P protein)
Polymerise- beta pleated sheet
Misfolded proteins self-associate- either aggregation-prone mutant or simple overproduction of normal protein (+/- defective degradation)

30
Q

What are the causes of amyloid?

A

Different disease proteins- local/ multiorgan

amyloid AA/ serum amyloid A in chronic inflammatory disease

31
Q

What are the outcomes of chronic inflammation?

A

Focal scarring to protect- ulcer, abscess
Widespread scarring destroys; organ failure- cirrhosis, chronic pyelonephritis, ischaemic heart disease
Persistence promotes cancer- osteomyelitis, cirrhosis

Immunology (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions