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Y1 TP2 Pathological Processes (topic 3 Onwards) > 3. Chronic Inflammation > Flashcards

3. Chronic Inflammation Flashcards

1
Q

Duration of chronic inflammation

A

• Unlike acute inflammation, chronic inflammation is long-lived
– >3 weeks – May persist for many weeks, months, even years!

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2
Q

Chronic inflammation - definition

A

—> “Chronic response to injury with associated fibrosis”

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3
Q

Acute Inflammation - overview

A
  1. Acute insult e.g. papercut, low level bacterial infection
    1. Acute inflammation
    2. Small amounts of damage ??
      • yes = resolution
        - no (repair is inefficient) = chronic damage
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4
Q

Chronic inflammation - overview

A

repair is inefficient and leads to scarring

1. Chronic insult e.g. large burn, trauma – not localized 
2. Chronic damage 
3. Repair and scarring – replace damage tissue with collagen etc.
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5
Q

Aim of chronic inflammation

A

—> aim to repair something that is damaged

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6
Q

3 ways chronic inflammation can arise

A
  1. ‘take over’ from acute inflammation
    …if damage is too severe to be resolved within a few days
  2. May arise de novo
    – Some autoimmune conditions (e.g. RA)
    – Some chronic infections (e.g. viral hepatitis – virus replicates faster than immune system can clear it)
    – “chronic low-level irritation” (e.g. allergy to dust, repeated exposure of dust = continuous irritation)
  3. May develop alongside acute inflammation
    – In severe persistent or repeated irritation
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7
Q

What does chronic inflammation look like

A
  • Large number of cells involved
    • Characterized by the microscopic appearances which are much more variable than acute inflammation. (acute inflammation = neutrophil laden tissue)
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8
Q

Macrophage - what is it

A

—> phagocytes derived from blood monocytes (myeloid cells) - monocytes differentiate into mature macrophage only when they enter the tissue
• They are tissue resident – Sense infection within tissues
• Important in acute and chronic inflammation

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9
Q

Macrophage - functions

A

• Initial identification of pathogens
• Some early clearance of pathogen
• Phagocytosis and destruction of debris & bacteria
• Processing and presentation of antigen to immune system
• Synthesis of not only cytokines, but also complement components, blood clotting factors and proteases – use cell signaling IL8, TNF alpha
• Control of other cells by cytokine release
• Resolution of inflammation
○ Clearance of dead neutrophils
○ Release of anti-inflammatory cytokines such as IL10 – tells neutrophils to stay away

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10
Q

2 types of macrophages

A
  • M1 – pro inflammatory = sense damage, kickstart process

* M2 – second stage = clearing up neutrophils

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11
Q

Lymphocytes - what is it

A
  • • Any cells present resident in lymph: T cells and B cells

• Sometimes called ‘chronic inflammatory cells’
• Produce things to maintain inflammatory response until damage is cleared up
○ e.g. opsonins, immunoglobin (bind to and activate neutrophil and complement)
– But are a normal component of many tissues

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12
Q

Lymphocyte function

A
  • Complex, mainly immunological. - immunological memory
    • T lymphocytes involved in control & some cytotoxic functions.
    • B lymphocytes differentiate to produce antibodies
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13
Q

Plasma cells

A

– Differentiated antibody-producing B lymphocytes. Usually implies considerable chronicity.

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14
Q

Eoisinophils

A

– Allergic reactions, parasite infestations, some tumours.

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15
Q

Fibroblasts / Myofibroblasts:

A

– Recruited by macrophages; make collagen – act as a scaffold to make new tissue
○ This just fills in the gap with collagen but doesn’t serve the same function

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16
Q

Damage + immune response

A

• Release of things in from the cell that neutrophil has never seen before
More damage, more activation of immune system, more inflammation

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17
Q

Giant cells - definition

A

• Multinucleate cells made dervied by fusion of macrophages
○ Used to deal with large scale problems
○ Macrophages fuse together (giant body) to try and encapsulate something, surround the bad thing so it can’t spread

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18
Q

3 giant cell types

A

Langhans

Foreign Body Type

Touton (Fat necrosis) -

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19
Q

Langhans giant cells

A

(tuberculosis- forms biofilms, covering across large area and granuloma grows on top of it and tries to destroy it with ROS and enzymes but biofilms are hard to kill)
○ Langhans try to destroy and encapsulate bio film but it is difficult as bio film sits on the surface of tissue

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20
Q

Foreign Body Type giant cell

A

e.g. splinter and metal

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21
Q

Touton (Fat necrosis) - giant cell

A

encapsulate areas of necrotic tissue

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22
Q

Cell types in chronic inflammation

A 
Macrophages
Lymphocytes
Plasmacells
Eiosinophils
Fibroblasts/myofidroblasts
Giant cells
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23
Q

4 effects of chronic inflamonation

A
  • Fibrosis
    • e.g. gall bladder (chronic cholecystitis), chronic peptic ulcers, cirrhosis
  • Impaired function – loss of function
    • e.g. chronic inflammatory bowel disease
    • Rarely increased function due to chronic inflammation e.g. mucus secretion, thyrotoxicosis
  • Atrophy
    • gastric mucosa, adrenal glands
    • Loss of structures – e.g loss of vili and surface area
  • Stimulation of immune response
    • Macrophage - lymphocyte interactions
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24
Q

Fibrosis – chronic cholecystitis

A
  • Repeated obstruction by gall stones
  • Repeated acute inflammation (constantly happening) leads to chronic inflammation –> abscess
  • Fibrosis of gall bladder wall
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25
Q

Inflammatory bowel disease

A
  • Lost definition of vili
    • Idiopathic inflammatory disease affecting large and small bowel
    • Patients present with diarrhoea, rectal bleeding and other symptoms
    • Ulcerative colitis and Crohn’s disease (bulbous structures within gut lumen)

Prevent passage of things through gut, build up of things in gut —> inflammation

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26
Q

Ulcerative colitis

A

superficial
• Diarrhoea, bleeding
• Ulcers can be caused by infection with H.pylori

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27
Q

Crohn’s disease

A

ransmural

• Strictures, fistula (abnormal connection between two eputhelieum lined organs)

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28
Q

Common causes of cirronsis

A
  • Alcohol
  • Infection with HBV, HCV
  • Immunological
  • Fatty liver disease
  • Drugs and toxins
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29
Q

Liver cirrhosis - impaired function

A
  • Nodules seen on the surface that actually pass through the liver seen on the scan below
    • Nodules of heathy tissues surrounded by unhealthy fibrosis tissues – limiting distribution of things in and out of healthy tissues
    • Irreversible
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30
Q

Fibrosis

A
  • Chronic inflammation with fibrosis… (disorganisation of architecture, attempted regeneration) …leads to Cirrhosis
    • No more neat structures – no more proper function
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31
Q

Thyroxicosis - increased function

A
  • Enlarged thyroid – grave’s disease
    • More cells present
    • Too much thyroxin
    • Lump on neck can be seen where thyroid becomes enlarged
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32
Q

Atrophy

A

gastric mucosa

Normal
• Neat organsiation of mucosa layers
• Vili

Abnormal
• vilus processes with loss definition

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33
Q

Autoimmune disease

A

– constant activation of adaptive immune system to try and clear something that it can never clear
• Autoimmunity is almost always characterised by chronic inflammation
○ Treatment = immunocompromise patient – dampen down immune response

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34
Q

Granulomatous inflammation

A

—> = chronic inflammation with granulomas!

35
Q

Granuloma - what is it

A
  • Could have foreign body penetrate skin that stays there
    • Characterisitc encapsulation of area by immune cells
    • Lose structure and organisation of surrounding tisses
36
Q

Cells involved in a granuloma

A

• T and b cells
• macrophages
• Neutrophils – clear it up
• Dendritic cells (antigen presenting cells)
• Giant cells can form part of the granuloma
○ See the immune system at work, as the cells would normally work

37
Q

Why do granulomas arise

A
  • Persistent, low-grade antigenic stimulation e.g. bio film
  • Hypersensitivity – collection of conditions that are allergic reaction that cause an abhorrent not normal immune respsonse
38
Q

3 main causes of granulomatous infection

A

• Mildly irritant ‘foreign’ material

• Infections
– Mycobacteria: Tuberculosis, leprosy
– Other infections e.g. some fungi

• Unknown causes
– Sarcoid
– Wegener’s granulomatosis
– Crohn’s disease

39
Q

Foreign material from breakdown of artificial joint

Cause of a granuloma

A
  • Metal on metal hip implants – metal grind against each other the metal acetabulum and femurla head rub against each other
    • But this causes metal to drop off = form granulomas in surrounding tissue (damage to surrounding tissue is bad as this is what supports the implant
40
Q

Tuberculosis

Infection cause of granuloma

A

• Caused by Mycobacteria
– Especially M.tuberculosis.
– Difficult & slow to culture.

  • Nature of organism
    • Wall lipids (Mycosides).
  • Produces no toxins or lytic enzymes
  • Causes disease by persistence and induction of cell-mediated immunity.
    • Biofilm product

Necrosis in centre = loss of integrity of underlying tisue

41
Q

Sarcoidosis

Granuloma unknown cause

A

Variable clinical manifestations

  • young adult women
  • non caseating granulomas = don’t cause necrosis
42
Q

Crohn’s disease

Granuloma unknown cause

A

Regional enteritis

Patchy full thickness inflammation throughout bowel

43
Q

Granulomatosis with polyangitis .

Granuloma unknown cause

A

Causes grandlomatious inflammation in the vasculature

44
Q

Wound

A
  • A wound is an injury to the skin with/without underlying tissues/organs
45
Q

Causes of wounds

A
  • surgery
  • a blow, a cut
  • heat/cold
  • friction/ shear force, pressure
  • chemicals
  • disease, such as ulcers or carcinomas
46
Q

Examples of wounds

A
  • Skin cut
    • Burn
    • Ulcer caused by inflammation or diseases
    • Very severe trauma injuries including skin, underlying structures even organs and bones
47
Q

Timings of wound healing

A

• Seconds-minutes: haemostasis
○ A lot of red blood cells and clot

• Minutes-hours: acute inflammation
○ Inflammatory cells migrate into wound

• 1-2 days: chronic inflammation

• 3 days: regeneration or repair → unique granulation tissue and epithelial cell growth
○ Cells and other moleculre accumulate

  • 7-10 days = early forming of scar
  • Weeks – 2 years = scar maturation or scar disappears in successful regeneration
48
Q

4 cell types in healing

A
  1. Inflammatory cells
    • neutrophils, macrophages, lymphocytes
  2. Endothelial (+progenitor) cells proliferation
  3. Fibroblasts and myofibroblasts
  4. Parenchymal cells- epithelial cells (basal cells)
49
Q

Function of inflammatory cells

neutrophils, macrophages, lymphocytes

A

○ Phagocytosis of debris

○ Production of chemical mediators

50
Q

Function of Endothelial (+progenitor) cells proliferation

A

• Angiogenesis = form new blood vessels

51
Q

Function of Fibroblasts and myofibroblasts

A

• Produce collagen and contract to help close wound

1. Fibroblasts and myofibroblasts
2. Accumulate in granulation tissue
3. Secret collagen 
4. Form framework for granulation tissue
52
Q

Function of Parenchymal cells- epithelial cells (basal cells)

A

• Proliferate and restore skin structure

53
Q

Aim of wound healing

A

> aims to restore damage structure

54
Q

4 stages of wound healing

A
  1. Haemostasis
    • as vessels are open → clot/scab to seal wound
  2. Inflammation
    • as there has been tissue injury → cytokines and phagocytosis
  3. Proliferation
    • as structures have been injured/lost → regrowth by stem cells → regeneration and repair
  4. Remodelling → functional regaining (scar disappearing and regeneration complete)
    • Tissue restoration, recover function
55
Q

haemostasis

A

• as vessels are open → clot/scab to seal wound

56
Q

Granulation tissue - definition

A

= special tissues that form in the wound

  • Proliferation of the repair tissue
  • Has a granular appearance and texture (red)(rich angiogenesis)
57
Q

Cells in granulation tissue

A
  1. Endothelial cells form new capillaries
  2. Fibroblasts and myofibroblasts – produce collagen and contract wound
  3. Type I collagen
  4. Chronic inflammatory cells
58
Q

Functions of granulation tissue

A
  1. Fills the gap
  2. Angiogenesis (red) to supply oxygen, nutrients and cells
  3. Contracts and closes the wound
  4. Help lost tissue to restore – skin cell re growth
59
Q

4 Diseases due to defects in collagen synthesis

A
  • Scurvy
    • Ehlers- danlos syndrome
    • Osteogenesis imperfecta
    • Alport syndrome
60
Q

Scurvy

A

○ Vitamin C deficency – lysol oxidase
○ Bleeding, delayed wound healing
○ Collagen synthesis requires vitamin c

61
Q

Fibrous repair

A

—> Fibrous repair is scar formed by fibrovascular connective tissue that replaces lost tissue after an injury

62
Q

When does fibrous repair occur

A
  • Occurs when extensive lost of tissue or/and local infection/persistent harmful agent
  • Forming by overgrowth of granulation tissue into dense collagen fibres
  • Associated with loss of function: flexibility, sweating, sensation…
63
Q

Scar

A

• See bundles of collagen formed in granulation tissues
• If something goes even more wrong = leloid overgrowth of scar – scar overgrows above skin levels
○ Increased bundles of collagen
○ Definitley damaged function

64
Q

6 complications of fibrosis repair

A
  • Insufficient fibrosis
    • Formation of adhesions
    • Loss of function (in heart)
    • Disruption of complex tissue relationships within an organ
    • Overproduction of fibrous scar tissues
    • Excessive scar contraction
65
Q

Insufficient fibrosis

A

○ Insufficient repair, danger of wound being open = hernia and ulcers

66
Q

Formation of adhesions

A

○ Occurs in abdominal surgery
○ Fibrosi repairs Compromising organ function or blocking tubes, e.g., intestinal obstruction following abdominal surgery

67
Q

Loss of function in heart

A

○ Due to healed myocardial infarction with non-contracting area scar
○ Connective tissue may replace some muscle of the heart – loss fo function in blood pumping

68
Q

Disruption of complex tissue relationships within an organ

A

○ Distortion of architecture interfering with normal function, e.g., liver cirrhosis, connective tissues form scar between liver unit, destroy normal liver function

69
Q

Overproduction of fibrous scar tissues

A

Keloid scar

70
Q

Excessive scar contraction

A

○ Can cause obstruction of tubes, disfiguring scars following burns or joint contractures (fixed flexures)

71
Q

Regeneration (functional repair)

A

• is the growth of cells and tissues to replace lost structures, in which new growth completely restores portions of damaged tissue and recovers normal function (eventually no scar)

72
Q

Repair (fibrous repair)

A

• a process when severely damaged or non-regenerable tissues are replaced by the connective tissue –scar, with loss of specialised function

73
Q

2 Clinical classification of healing

A
  • Primary intention

* Secondary intention

74
Q

Primary intention

A

• Wound surfaces have been closed, with very little tissue loss and no infection (clean).
• Intact connective tissue scaffold. (e.g skin sharp cut, surgical incision, sutured wound)
→Regeneration

75
Q

Secondary intention

A

• A wound that is extensive and involves considerable tissue loss, and in which the edges cannot be brought together (e.g. ulcer, burn), infected wound
→Fibrous repair

76
Q

Tertiary intention healing

A
  • Delayed secondary intention

* Try and solve this problem with rescuing method for better healing

77
Q

Healing of bone fractures

A
  1. Haematoma (process haemostasis) : fills gap and surrounds injury. Inflammation occurs.
  2. Granulation tissue forms (regernation stage) : Capillaries develop, cytokines activate osteoprogenitor cells
  3. Soft callus: at 1 week, fibrous tissue and cartilage
  4. Hard callus: after several weeks, initial woven bone forms–weaker and less organised than lamellar bone but can form quickly
  5. Lamellar bone: (normal bone structure) replaces woven bone,
  6. Remodelling to mechanical stress, and bone not physically stressed is resorbed, bone structure is re-established, weeks -2 years
78
Q

Peripheral nerve regernation and repair

A
  • Axons are myelinated by schwann cells
    • Injury to peripheral nevres = damage
    • Schwann cells can efficiently regenerate
    • Neuron is recovered – axons can regenerate (but not cell body)
79
Q

If regeneration goes wrong – and nerves can’t become reconnected

A
  • Neuroma formation
    • Lack of long distance regernation
    • Lost innervation
80
Q

Neuroma

A

• Traumatic neuroma is a benign growth (tumor) of nerve tissue (nerve fibers and myelin), that occurs in response to injury or surgery, when normal growth is interrupted.

81
Q

Factors influencing regeneration and repair

Systemic factors

A
  1. Age - stem cell aging
  2. Disease/health
    • Diabetes/Obesity, Genetic disorders
  3. Oxygen delivery-anaemia, hypoxia
  4. Drugs - steroids (cortisol, immunosuppressive and inhibit collagen synthesis), cytotoxics…
  5. Malnutrition
    • Protein loss or lack of essential
    • Vitamin C deficiency
82
Q

Factors influencing regeneration and repair

Local factors

A
  1. Type, size, location of wound
  2. Blood supply
  3. Local infection
  4. Necrotic tissue or denervation
  5. Mechanical stress or Physical factors:
    • Protection (dressings)
    • Surgical techniques
83
Q

Synovitis

A

Synovium of joint becomes inflamed (swollen)

Y1 TP2 Pathological Processes (topic 3 Onwards) (9 decks)

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