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Medicine Unit 9 UoS > Unit 9 - Inflammation and repair > Flashcards

Unit 9 - Inflammation and repair Flashcards

1
Q

What are the clinical features of inflammation?

A

Calor - heat
Rubor - redness
Tumor - swelling - vasodilation, increasing blood flow, increased vascular permeability, vascualr stasis
Dolor - pain - action of inflammatory mediators on free nerve endings
Functio laesa - loss of function - damage to cells necessary for function

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2
Q

What is acute inflammation?

A

Rapid and short lived response to injury
Develops in mins/hours
Persists for few days

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3
Q

What are the physiological mechanisms of acute inflammation?

A

Vasodilation
Increased vascular permeability
Vascular stasis
Pain
Leuckocyte extravasation

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4
Q

Vasodilation

A

Occurs rapidly
Histamine acts on smooth muscle of small blood vessels - arterioles
New capillary beds open

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5
Q

Increased vascular permeability

A

Histamines, bradykinin, prostaglandins and leukotrienes increase vascular permeability.
Endothelial cells contract and tight junctions between are disrupted

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6
Q

Vascular stasis

A

Slowing/cessation of blood flow
Movement of fluid out of blood increases viscosity
Fibrin clots contribute to stasis

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7
Q

Pain in inflammation

A

Action of prostaglandins, growth factors and cytokines on free nerve endings - activating or sensitising

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8
Q

Leukocyte extravasation

A

Leukocytes are recruited to the site of inflammation by migrating from the vascular lumen into the tissue, then to site of injury

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9
Q

How do cells stop and adhere to capillary endothelium?

A

Stasis allows cells to line up near endothelium - margination
Leukocyte chemokine signalling allows adhesion molecules to have high affinity state

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10
Q

What is this cell involved in acute inflammation?

A

Neutrophil
predominant first 6-24 hours before replaced by monocytes
Nucleus has 2-5 lobes
Phagocytose microbes, dying cells, cell debris, produce NETs, secrete cytokines

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11
Q

What is this cell involved in acute inflammation? What are its identifying features

A

Monocyte
Large, pale staining cytoplasm, bean shaped nucleus
differentiates into populations of macrophages and dendritic cells to regulate cellular homeostasis

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12
Q

What cell is this involved in acute inflammation? Identifying features?

A

Macrophages
Large, pale staining cytoplasm, bean shaped nucleus, more cytoplasm than monocytes
Phagocytic, secrete lots of pro-inflammatory cytokines, can activate T cells

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13
Q

What are some non-cellular effectors in acute inflammation?

A

Complement - Components C3a and C5a are peptide mediators of local inflammation, act on leukocytes and endothelial cellsfacilitate the uptake and destruction of pathogens by phagocytic cells.
Enzymes - eg matrix metalloproteinases from macrophages, break down extracellular matrix
NETs - extruded nuclear chromatin and antimicrobial proteins. Immobilise and destroy pathogens

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14
Q

How may systematic inflammation present?

A

Tachycardia
Hypotension
Leukocytosis
Fever

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15
Q

How do cytokines act to cause systematic inflammation?

A

Longer lasting than histamine
Act on:
Hypothalamus to cause fever
Sympathetic nervous system to induce CV changes
Liver to produce acute phase proteins e.g. CRP
Bone marrow to produce leukocytes

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16
Q

What are types of acute inflammation?

A

Serous
Fibrinous
Purulent
Ulcerative

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17
Q

What is serous inflammation?

A

Accumulation of exudate in a cavity e.g. peritoneal/space created by injury
Exudate from plasma or mesothelium
Exudate is sterile and free of leukocytes

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18
Q

What is fibrinous inflammation?

A

Large deposition of fibrin
Typically at lining of body cavities e.g pleural/pericardial
High vascular leakage + procoagulant stimuli - fibrin deposition
Scar forms if unresolved

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19
Q

What is purulent inflammation?

A

Formation of pus - necrotic debris (dead neutrophils, tissue cells and usually bacteria) and tissue fluid
Abscess is localised collection of pus buried in tissue
If chronic, may replace with fibrotic connective tissue
Often caused by pyogenic bacteria

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20
Q

What is ulcerative inflammation?

A

Local surface defect in tissue caused by sloughing off/disintergration of inflamed necrotic tissue
near a surface or Where inflammation and necrosis can occur
Acute and chronic inflammation may occur simultaneously

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21
Q

What are the outcomes of acute inflammation?

A

Resolution:
cause of inflammation eliminated, no lasting tissue damage, regeneration, returns to normal
Repair by fibrosis:
cause may be eliminated, extensive damage, cannot regenerate, connective tissue replaces
Progression to chronic inflammation:
cause persists

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22
Q

How may acute inflammation be treated?

A

COX inhibitors:
e.g. aspirin, paracetamol
inhibits prostaglandin synthesis
Steroids:
e.g. dexamethasome
binds to glucocorticoid receptors in innate immune cells, inhibiting inflammation

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23
Q

What is chronic inflammation?

A

May follow acute, or begin gradually
Weeks or months
Charaterised by simultaneous inflammation, tissue damage, repair

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24
Q

What are example of chronic inflammation?

A

CVD, neurological disease, autoimmune disease, rheumatoid arthritis, cancer, fibromyalgia

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25
Q

What are causes of chronic inflammation?

A

Persistent infection e.g. H pylori
Unresolved acute inflammation after injury
Continuing exposure to stimulus
Hypersensitivity diseases

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26
Q

What are the features of chronic inflammation?

A
  • Tissue infiltration
  • Destruction of normal tissue architecture
  • Angiogenesis and fibrosis
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27
Q

What cells infiltrate tissue in chronic inflam?

A

Mononuclear cells - monocytes, macrophages, dendritic cells and lymphocytes incl plasma cells

28
Q

What destroys normal tissue architecture in chronic inflam?

A

Persisting offending agent or immune cells.
Potential functio laesa

29
Q

What does angiogenesis and fibrosis consist of?

A

Characteristic of ongoing repair process
Production of new blood vessels
Excessive deposition of collagen and other ECM = connective tissue - contributing to loss of function

30
Q

What cell is this thats involved in chronic inflam?

A

Lymphocyte
Small
Thin edge of cytoplasm
Secretes cytokines

31
Q

What cell is this that is involved in chronic inflam?

A

Plasma cells
Random placed nucleus
Secrete antibodies

32
Q

What are the outcomes of chronic inflam?

A

Repair by fibrosis ->can cause further issues e.g. bile duct strictures, constrictive pericarditis

33
Q

What may cause chronic inflam?

A

Genetics
Acquired conditions e.g. cancer, metabolic and infectious disease
Character of immune-mediated inflammatory disease

34
Q

How can chronic inflammation be treated?

A

NSAIDs e.g. naproxen
Corticosteroids e.g. budesonide
Immunosuppressants e.g. methotrexate
Biologics e.g. adalimumab

35
Q

What is granulomatous inflammation? What are the features?

A

Chronic inflammation
Response to agent difficult to eradicate
-Organised collection of immune cells and others
- Aggregation of activated macrophages

36
Q

Foreign-body granuloma

A

Reaction to inert foreign material
No T cell mediated immune response

37
Q

Immune granuloma

A

Caused by agents that can cause T cell mediated response
Can be caused by mycobacterial, fungal and parasitic infections

38
Q

What are examples of granulomas without foreign bodies in non-infectious disease?

A

Chron’s disease
Sarcoidosis

39
Q

What cell types are found in granulomatous inflammation?

A

Macrophages/monocytes
Multinucleate giant cells
Lymphocytes

40
Q

What are caseating granulomas?

A

Granulomas with necrotic centre - looks soft and ‘cheesy’
Free radical mediated injury and hypoxia -> death by necrosis

41
Q

What is the outcome of granulomatous inflammation?

A

Heal by fibrosis
= Tissue and organ damage
Can calcify in certain tissues - type of scarring

42
Q

What are the outcomes of tissue repair?

A

Regeneration - after mild, superficial injury -stem cells regenerate epithelium
Scar formation - after severe injury
Or combination of both

43
Q

What are the stages to repair? (4)

A

-Hemostasis: immediate, blood vessels constrict, clotting activated
- Inflammatory: Starts quickly, lasts few days
- Proliferative: fibroblasts and endothelial cells prolif. Collagen produced
- Remodelling: ECM reorganises, variable replacement of normal tissue

44
Q

What are the different tissue type that regenerate to different degrees?

A

Labile tissue: continually dividing in normal state, easily regenerate if stem cells are still present
Stable tissue: capable of regeneration in response to injury
Permanent tissue: terminally differentiated, unable to regenerate

45
Q

How does regeneration occur?

A

Surviving functional cells proliferate
Stem cells located in specific niches in tissue differentiate
Growth factors produced by macrophages, epithelial cells and fibroblasts drive regeneration

46
Q

TGF-B

A

Transforming growth factor beta
Function:
Fibroblast migration, collagen synthesis, monocyte migration

47
Q

PDGF

A
48
Q

VEGF

A
49
Q

EGF

A
50
Q

FGF

A
51
Q

What role does ECM have in tissue repair?

A

Needed for full regeneration
Damaged ECM -> scarring
Cells use integrins to bind to ECM
Interaction signals cells -> cell survival and proliferation

52
Q

Scar formation

A

When damage is severe, tissue unable to regenerate
No return to full function
Granulation tissue forms within 3-5 days

53
Q

What are the stages of scar formation?

A

Angiogenesis - vascular endothelial cells proliferate in response to GF, new blood vessels sprout
Fibroblast migration and proliferation - stimulated by GF and cytokines
Deposition of ECM - fibronectin dominates first, then collagen
Decreased cellularity, progressive vascular regeneration - macrophages, fibroblasts and vascularity decline
Myofibroblast differentiation, contraction of scar
Remodelling of new connective tissue - Organisation of collagen. MMPs

53
Q

What are histological features of scars?

A

Dense fibrous tissue
No adnexal structures e.g. glands
Re-epithelialisation

53
Q

What factors influence tissue repair?

A

Infection
Disease
Nutritional status
Glucocorticoids
Mechanical factors
Perfusion
Foreign bodies
Injury type and extent

53
Q

Why does infection and disease affect tissue repair?

A

Infection: prolongs inflammation and may increase damage
Disease: poor perfusion, impaired leukocyte function, ongoing low level systemic inflammation

54
Q

Why does nutritional status and glucocorticoids affect tissue repair?

A

Nutritional status: protein deficiency, vitamin C deficiency (collagen synthesis)
Glucocorticoids: reduce inflammation and impact repair process

55
Q

Why do mechanical factors, poor perfusion foreign bodies and injury type and extent affect tissue repair?

A

Mechanical factors: physical disruption of repairing tissue
Poor perfusion: reduced delivery of materials/cells
Foreign bodies: persistence of stimulus
Injury type and extent: extensive injury will result in at least partial loos of function

56
Q

What are different types of scars?

A

Hypertrophic scar, keloid, excess granulation tissue, wound rupture/ulceration, contracture

57
Q

What type of scar is this? why is it formed?

A

Hypertrophic scar
Due to excessive collagen generation and accumulation

58
Q

What type of scar is this? why is it formed?

A

Keloid
Due to excessive collagen generation and accumulation

59
Q

What type of scar/wound is this? Why is it formed?

A

Excess granulation tissue
Can block further healing re-epithelialisation

60
Q

What type of scar/wound is this? Why is it formed?

A

Wound rupture or ulceration
After inadequate formation of granulation tissue/scar
Due to repeated trauma/continuing infection

61
Q

What type of scar is this? Why is it formed?

A

Contracture
Excessive contraction of a scar leads to restricted movement or deformity

62
Q

What are some causes of systemic chronic inflammation (low-grade)?

A

Ageing: immunosenescence and mitochondrial dysfunction likely to contribute
Poor diet: alteration of gut microbiome and excess adipose tissue
Stress: prolonged cortisol levels promotes inflammation and attenuates tissue repair

63
Q

What are some consequences of low grade systemic chronic inflammation?

A

Sickness behaviours and physiological responses: fatigue, raised BP
Breakdown of tolerance leading to autoimmune disease and IMID
Dysregulation of normal cellular and tissue physiology, predisposing to metabolic diseases and cancer

Medicine Unit 9 UoS (11 decks)

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