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Phase 2 Medicine > Intro - Inflammation > Flashcards

Intro - Inflammation Flashcards

1
Q

Define inflammation

A

A local physiological response/reaction to tissue injury or infection involving cells such as neutrophils and macrophages
Not a disease, but a manifestation of disease

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2
Q

Acute inflammation involves what WBC?

A

Neutrophil polymorph

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3
Q

Chronic inflammation involves what WBC?

A

Macrophages and lymphocytes

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4
Q

Positives of inflammation

A
  • destroys invading/infecting microbes
  • Starts healing process as brings all essential cells to site
  • Walls off an abscess cavity so prevents spread of infection
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5
Q

Negatives of inflammation

A
  • Autoimmunity
  • Overreaction to stimulus
  • Swelling - an abscess (esp in brain) can act as a space occupying lesion and compress surrounding tissues
  • Fibrosis from chronic inflammation may distort tissues or permanently affect their function
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6
Q

Other cells involved in inflammation

A

Endothelial cells (line vessels in areas of inflammation and become sticky in these areas so cell adhere/allow cells to pass through thereby forming exudate/grow into damaged area to form new vessels) and fibroblasts (form collagen in areas of chronic inflammation and repair)

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7
Q

What is a granuloma?

A

A group of macrophages clumped together (but called epithelioid histocytes here) surrounded by lymphocytes.
Part of particular sorts of chronic inflammation

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8
Q

Which classes of drugs can treat inflammation and give examples and mechanisms?

A

NON-steroidal anti-inflammatories
- Ibuprofen / aspirin
- inhibit prostaglandin synthetase (prostaglandins are chemical mediators of inflammation)
Steroids (cortico-)
- Betnovate cream etc
- Bind to DNA and up-regulate inhibitors of inflammation and down regulate mediator. They are immune modulators

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9
Q

Steps of acute inflammation and how these relate to the 5 cardinal signs of acute inflammation

A
  • Smooth muscle precapillary sphincters relax
  • Dilation of capillaries (vascular component) = red/hot
  • Neutrophil polymorphs recruited to the site
  • Chemical mediators e.g. histamine/bradykinin/prostaglandins/NO/heat, cause vessels to become more permeable
  • these chemicals cause = pain
  • Vascular leakage of protein-rich exudate = swelling
    (hydrostatic pressure in the capillaries is increased due to loss of proteins, leading to fluid movement out of the vessels so more swelling)
  • Outcome may be resolution, suppuration (pus/abscess), organisation or progression to chronic inflammation
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10
Q

5 cardinal signs of inflammation

A

Red = rubor
Heat = calor (due to hyperaemia (more blood in that area) and some systemic fever
Swelling = tumour
Pain = dolor (due to stretching/distortion of tissues due to oedema and bradykinin/prostaglandin/serotonin release)
Loss of function (due to severe swelling -> immobilisation and pain -> restricted movement)

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11
Q

Causes of acute inflammation and why these cause inflammation

A

Microbes - bacteria and viruses
(viruses kill cells by intracellular multiplication/bacteria produce exotoxins or have endotoxins on their surfaces- this all leads to initiation of inflammation)
Hypersensitivity - parasites, TB, hay fever
(all types to consider (the chemical mediators for hypersensitivity reactions are very similar to those of inflammation))
Physical agents - trauma, UV or ionising radiation, cold (frostbite)
Irritant/corrosive chemicals - acids, bases, corrosives
(cause gross tissue damage or release specific irritants causing inflammation)
Tissue necrosis - ischaemic infarction
(inadequate blood flow -> infarction -> tissue death -> potent inflammatory stimulus)

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12
Q

Stages in neutrophil polymorph migration to the site

A
  • Migration
    (with loss of intravascular fluid and slower blood flow at the site, neutrophils flow in the peripheral zone of the vessel)
  • Adhesion
    (known as pavementing. Attach to endothelial cell surfaces)
    (histamine and thrombin upregulate adhesion molecules on the surface of endothelial cells)
  • Emigration
    (move between cells (usually in venules) using pseudopodia)
  • Diapedesis
    (= Passive movement of RBCs out of blood vessels dependent on hydrostatic pressure forcing them out)
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13
Q

Why is histamine implicated in acute inflammation?

A

It can be released immediately as is stored in pre-formed granules so can have an immediate effect.
It is stored in most cells but especially basophils, eosinophils, other leucocytes and platelets.

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14
Q

What mediators stimulate the release of the mediator histamine?

A

C3a and C5a (complement components) and lysosomal proteins from neutrophils

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15
Q

Which endogenous chemical mediators of acute inflammation cause… vascular dilation?

A

histamine
prostaglandins
NO

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16
Q

Which endogenous chemical mediators of acute inflammation cause… increased vascular permeability?

A 
histamine
prostaglandins (potentiates it)
NO
bradykinin
C5a
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17
Q

Which endogenous chemical mediators of acute inflammation cause… adhesion of WBCs?

A

the upregulation of adhesion molecules on the endothelial cell surfaces by IL-8, C5a, IL-1 and TNF-alpha

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18
Q

Which endogenous chemical mediators of acute inflammation cause… Neutrophil polymorph chemotaxis?

A

IL-8 and others

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19
Q

What is resolution? [an outcome of acute inflammation]

A

Complete restoration of the tissues to normal
e.g. acute lobar pneumonia does this
Requires: min. cell death, organ can regenerate, rapid destruction/drainage of causal agent and exudation

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20
Q

What is suppuration? [an outcome of acute inflammation]

A

Formation of pus.
Mix of living/dying/dead neutrophils and bacteria, cellular debris and sometimes lipid globules.
Stimulus is often pyogenic (pus causing) bacteria.
Can lead to abscess formation - collection of pus. Note the bacteria in the abscess cavity are relatively inaccessible to antibodies or antibiotics

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21
Q

What is organisation? [an outcome of acute inflammation]

A

Tissue replaced by granulation tissue (tissue forming in response to injury and contains new blood vessels/fibroblasts) leaving a scar due to fibrosis occurring here.
Occurs when there is damage to the connective tissue framework, excess fibrin and dead tissue that cannot be lysed, exudate that is hard to remove or cells cannot be regenerated. Dead cells are removed by macrophages etc then the space fills with granulation tissue and this tissue eventually forms a fibrous scar

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22
Q

What is the progression to chronic inflammation? [an outcome of acute inflammation]

A

If inflammatory agent is persisting/not removed the nature of the exudate/response can change.
Lymphocytes, plasma cells, macrophages, multinucleate giant cells (macrophages combining), fibroblasts all involved

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23
Q

Systemic effects of inflammation

A
  • Pyrexia (fever)
  • Constitutional symptoms
  • Weight loss
  • Reactive hyperplasia of the reticuloendothelial system (lymph node enlargement and splenomegaly)
  • Haematological changes
  • Amyloidosis
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24
Q

Why does pyrexia occur with inflammation?

A

Neutrophil polymorphs and macrophages produce endogenous pyrogens which act on hypothalamus and set the thermoregulatory mechanisms at a higher temp.
Interleukin-2 is the most effective pyrogen.
It is stimulated by phagocytosis, endotoxins and immune complexes

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25
Q

Why does weight loss occur with inflammation?

A

Negative nitrogen balance (due to energy required for inflammatory mediators) - common with extensive chronic inflammation

26
Q

What haematological changes occur with inflammation?

A

Increased neutrophils
- in pyogenic infections/tissue destruction/acute inflammation
Increased eosinophils
- in allergic disorder/parasitic infection
Increased Lymphocytes
- in chronic and viral infections
Increased monocytes
- in some bacterial infections
Anaemia
- may be due to blood loss into inflammatory exudate (diapedesis) or haemolysis due to toxins

27
Q

What does IL (in IL-8 or IL-1) stand for?

A

Interleukin

28
Q

What does TNF in TNF-alpha stand for?

A

Tumour necrosis factor

29
Q

How is the inflammatory exudate cleared up?

A

Neutrophils and macrophages release lysosomal enzymes into the ECF which digests the inflammatory exudate.
The lymphatic vessels also dilate so that oedema fluid of the inflammatory exudate can be drained from the area.

30
Q

Why are lymphatics important in acute inflammation?

A

Antigens are carried to the regional lymph nodes for recognition by lymphocytes which dictates the immune response. Therefore, as in acute inflammation the lymphatics dilate, the processes of inflammation and immune response are linked.

31
Q

What is the role of a neutrophil polymorph in acute inflammation?

A

Adhesion to the microorganism
- bacterial endotoxins activate complement via alternative pathway which generates component C3b
- Antibody-antigen complexes activate complement via classical pathway which also generates C3b
- enables opsonisation
Phagocytosis
- ingest, phagosome, fuse with lysosome, kill
Intracellular killing
- Hydrogen peroxide or lysozyme
Release of lysosomal products
- damage local tissues by proteolysis with elastase, collagenase etc
- damage activates coagulation factor XII
- this attracts other leucocytes to the area
- some of the compounds released increase vascular permeability, others are pyrogens (induce systemic fever)

32
Q

5 descriptive terms used to describe macroscopic appearances of inflammation

A 
Serous (lots of fluid release)
Suppurative (purulent) (pus)
Membranous
Pseudomembranous
Necrotising (gangrenous)
33
Q

Positive effects of the fluid exudate

A
  • dilutes the toxins
  • antibodies can enter ECF due to increased vascular permeability
  • transports drugs to area
  • fibrin formation from exuded fibrinogen can stop organisms moving/spreading and enable phagocytosis and is a matrix for granulation tissue to form on
  • delivers nutrients and O2 to neutrophils
  • stimulates immune response by lymphatic drainage of this fluid into lymph nodes
34
Q

How is excessive immune activation prevented?

A

At the site of the pathogen entry, there is relative tissue hypoxia so stimulation of the innate immune system is increased but the adaptive immune system is suppressed.

35
Q

Causes of chronic inflammation

A

Primary (i.e. it was never acute) e.g.Transplant rejection or glandular fever etc
Progression from acute (unresolved)
Recurrent episodes of acute inflammation e.g. chronic cholecystitis
Autoimmunity

36
Q

Reasons for primary chronic inflammation

A
  • resistance of infective agent to phagocytosis/intracellular killing e.g. TB, viruses
  • endogenous substances that are inert or resistant lysosomal enzymes e.g. uric acid crystals, necrotic bone
  • Inert exogenous materials e.g. asbestos, implanted prostheses (indigestible by body)
  • Autoimmune diseases e.g. Rheumatoid arthritis/pernicious anaemia
  • specific diseases of unknown aetiology e.g. chronic inflammatory bowel disease
  • primary granulomatous diseases e.g. crohns, sarcoidosis
37
Q

Which form of acute inflammation (using their descriptive terms to categorise them) is the most likely form to progress to chronic inflammation?

A

Suppurative
e.g. osteomyelitis (abscess in bone is difficult to eradicate due to poor macrophage access)
abscess forms in an area with inadequate drainage and develops thick walls (granulation and fibrous tissue).
Rigid walls fail to come together when eventually drained. Pus stagnates and becomes organised. Replaced by fibrous scar

38
Q

Macroscopic appearances of chronic inflammation

A 
chronic ulcer
chronic abscess cavity
thickening of wall of a hollow viscus
granulomatous inflammation 
fibrosis
39
Q

Does chronic inflammation form more or less exudate than acute inflammation?

A

Less (therefore less swelling)

40
Q

What may be occurring at the same time as continuing destruction in chronic inflammation?

A

Regeneration and repair

41
Q

How is granulation tissue formed (in chronic inflammation)?

A

Angiogenesis followed by fibroblast proliferation and collagen synthesis results in granulation tissue.
This process is regulated by low molecular weight proteins called growth factors.

42
Q

What does EGF do? [a growth factor]

A

epidermal growth factor causes the regeneration of epithelial cells

43
Q

What does TGF-alpha do? [a growth factor]

A

transforming growth factor alpha causes regeneration of epithelial cells (like EGF does)

44
Q

What does IGF-1 do? [a growth factor]

A

insulin-like growth factor 1 has a synergistic effect with other growth factors

45
Q

What does TNF do? [a growth factor]

A

tumour necrosis factor stimulates angiogenesis

46
Q

What kind of stimulation is occurring during healing when growth factors trigger cellular events in nearby cells?

A

Paracrine

47
Q

What are some differences between macrophages and neutrophil polymorphs?

A

Macrophages are in chronic inflammation, neutrophils are in acute.
Macrophages can ingest a wider range of materials.
Macrophages are longer lived (neutrophils ingest microorganisms then bring about their own destruction so lifespan is limited)
Macrophages are part of the reticuloendothelial system (aka mononuclear phagocyte system)

48
Q

What do granulomas secrete - that can be used as a blood marker if someone has suspected systemic granulomatous disease (e.g. sarcoidosis)?

A

ACE

49
Q

What can happen to the centre of a granuloma?

A

Caseous necrosis (e.g. in TB)

50
Q

What can some of the epithelioid histocytes convert to in a granuloma?

A

Multinucleate giant cells

51
Q

What induces granuloma formation?

A

Indigestibility of matter by macrophages
Deranged immune response
Beryllium can also cause granuloma formation

52
Q

What is the sequence of macrophage development?

A

Hemopoietic stem cell -> monocyte (in the blood) -> macrophage (when in a tissue)

53
Q

Difference between granuloma and granulation tissue

A

Granuloma is an aggregation of epithelioid histocytes and lymphocytes and is a feature of some specific chronic inflammatory disorders.
Granulation tissue is a component of healing comprising small blood vessels (capillary loops that have proliferated into the area), connective tissue matrix and myofibroblasts (fibroblasts with muscle fibre filaments so they play a role in collagen synthesis and wound contraction)

54
Q

Fibrin vs Fibrous

A 
Fibrin = is deposited in blood vessels, tissues and on surfaces (e.g. in acute inflammation) and is a result of thrombin acting on fibrinogen.
Fibrous = describes the texture of a non-mineralised tissue of which the principle component is collagen (e.g. scar tissue)
55
Q

Stages of healing by 1st intention

A
  • Incision is clean (little damage to tissue either side apart from cut blood vessels)
  • Blood (platelets) is exposed to collagen so small clots form on surface (forms scab to keep wound clean)
  • Blood present also brings fibrin to site to form a fibrin network to create a weak joint
  • The platelets exposed also release chemotactic factors to attract inflammatory cells to remove debris
  • fibroblasts arrive and make collagen
  • Capillaries proliferate to bridge gap
  • Joint is now strong (and white as collagen now present)
    Only residual effect = failure to reconstruct elastic network in dermis
    (mechanical support from sutures and plasters may help while weak joint strengthens)
56
Q

Process of healing by 2nd intention

A
  • There is a deficit as there is tissue loss or wound margins cannot be opposed e.g. infection
  • Hair follicles have been lost so harder for regeneration to occur as stem cells have been removed
  • Phagocytosis to remove debris
  • Capillaries grow into area (proliferation of vascular endothelium - angiogenesis)
  • Fibroblasts produce and deposit collagen
  • This granulation tissue fills the defect
  • The process is slower and a bigger scar is left
  • Epithelial regeneration to cover the surfaces
  • Whole process = Repair not regeneration
57
Q

What are liable cells?

A

Cells with a good capacity for regeneration e.g. surface epithelium
always lost and replaced

58
Q

What are stable cell populations?

A

Divide at a slow rate normally and retain capacity to regenerate when needed e.g. hepatocytes and renal tubular cells

59
Q

What are permanent cells?

A

No effective regeneration e.g. nerve cells

60
Q

What is organisation?

A

Repair of specialised tissues by the formation of a fibrous scar

61
Q

What increases the amount of scarring from a wound?

A

Infection and inflammation - they stop the wound contraction and increase the size of the defect needing to be filled with granulation tissue

62
Q

Negatives of wound contraction

A
  • if the tissue damage is circumferential around a tube -> stenosis (narrowing) or obstruction due to a stricture
    e. g. gut or blood vessel
  • distortion and permanent shortening of a muscle = contracture
  • Burns can cause massive contraction -> cosmetic damage and impaired mobility

Phase 2 Medicine (6 decks)

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