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Inflammation Flashcards

1
Q

What is inflammation

A

The body’s response to any form of cellular injury. This is PROTECTIVE.

Cellular injury includes: infection, heat, trauma, hypoxia, radiation

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2
Q

What are the aims of inflammation

A
  • remove injurious agent
  • clear dead tissue
  • trigger healing
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3
Q

What is acute inflammation

A

A rapid, transient process involving vascular changes and neutrophil accumulation.

It is orchestrated by cytokines released by injured cells (histamine, serotonin, PG, LT and platelet-activating factor)

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4
Q

What is chronic inflammation

A

A more persistent form of inflammation in which there is on-going tissue destruction and attempted repair

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5
Q

What are the 2 main events in acute inflammation

A

Vascular changes

Neutrophil leukocytosis and accumulation in area of damage.

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6
Q

What are the vascular changes which occur in acute inflammation

A

Blood vessels dilate (trying to get the WBCs to the area of inflammation)

Endothelial cells activated = increased permeability of capillaries, resulting in the leaking of small proteins (fibrinogen) into the area of damage

Note this fibrinogen will get converted to fibrin as the activation of the coagulation cascade which will result in the production of thrombin (converts fibrinogen to fibrin)

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7
Q

What role does neutrophil leukocytosis and accumulation play in acute inflammation

A

Increased neutrophil production in bone marrow = NEUTROPHIL LEUKOCYTOSIS.

Endothelial cell activation = up-regulation of adhesion molecules on endothelial cells (ICAM-1/VCAM-1) and hence neutrophils migrate into the area of damage.

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8
Q

What is the result of vascular changes and neutrophil leukocytosis/accumulation in acute inflammation

A

Formation of acute inflammatory exudate in the area of damage

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9
Q

What does acute inflammatory exudate consist of

A
  • Fluid
  • Fibrin (acts as a scaffold - neutrophils use to move around the area of inflammation)
  • Neutrophils (phagocytose and kill microoganisms. Also release enzymes to break down damaged tissue)
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10
Q

What are the local effects of acute inflammation

A
  • calor (warmth) (due to + blood flow)
  • rubor (redness) (due to + blood flow)
  • tumour (swelling) (due to + permeability)
  • dolor (pain) (due to inflammatory mediators activating pain nerve endings)
  • loss of function (due to pain)
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11
Q

What are the systemic effects of acute inflammation

A

When injury is severe.

Due to inflammatory mediators (IL-1/6, TNF-alpha)

Effects:

  • Fever
  • Liver secretes acute phase proteins (CRP)
  • Hormone production = ADH, cortisol, adrenaline. This results in malaise, weakness and appetite loss
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12
Q

What is CRP

A

An acute phase protein and an opsonin.

For this reason it is an important part of the body’s inflammatory response to bacteria.

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13
Q

How is CRP produced

A

Made in the liver in response to IL-6 secreted by macrophages

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14
Q

What is opsonisation

A

The process of coating a particle (eg. microbe) to target it for phagocytosis.

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15
Q

In a patient with a CRP of 100, would you expect this to be due to viral or bacterial infection

A

Significantly raised CRP: Bacterial - bacterial infections are potent stimulators of CRP.

However raised CRP is not specific!

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16
Q

List reasons for high CRP

A
  • infection (bacterial > viral)
  • burns
  • trauma
  • polymyalgia rheumatica
  • giant cell arteritis
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17
Q

What is a raised CRP a risk factor for

A

Atherosclerosis

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18
Q

What are the possible outcomes of acute inflammation

A
  • Regeneration/resolution
  • Repair (with scarring)
  • Progression to chronic inflammation
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19
Q

What is regeneration (resolution) in the context of acute inflammation

A

The damaged cells are replaced with exactly the same cell type. Complete restoration of normal structure and function.

The tissue returns to normal. This is the best outcome.

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20
Q

How is the outcome of acute inflammation determined

A

Factors include:

  • Severity of injury (more severe = less likely regeneration is possible)
  • Type of cell damaged = continuously dividing / quiescent tissues are able to regenerate, whereas non-dividing tissue cannot
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21
Q

What factors make resolution a likely outcome of acute inflammation

A
  • limited tissue destruction without significant damage to the connective tissue framework
  • damaged cells are able to regenerate
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22
Q

What is repair in the context of acute inflammation

A

Repair results in fibrous scar formation.

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23
Q

What factors make repair a likely outcome of acute inflammation

A
  • substantial tissue destruction (significant damage to connective tissue framework)
  • damaged cells unable to regenerate
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24
Q

Which cells are able to regenerate

A

CONTINUOUSLY DIVIDING CELLS = epithelia, haematopoetic, fibroblasts, smooth muscle

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25
Which cells are unable to regenerate
NON-DIVIDING = neurons, skeletal muscle, cardiac muscle
26
What are the steps of repair in the context of acute inflammation
- Organisation = replacement of inflammatory exudate by granulation tissue. - Scar formation = granulation tissue is replaced by a scar - laid down by fibroblasts (scar is mainly composed of fibrous tissue)
27
What is granulation tissue
A fragile complex of proliferating capillaries, macrophages and fibroblasts. Capillaries give granulation tissue its distinctive red colour.
28
What is the main component of fibrous tissue
Collagen fibres
29
Why is repair less desireable than resolution as an outcome of acute inflammation
Repair results in scar formation. The scar is mechanically strong, but lacks the specialised function of the original tissue leading to a loss of specialised function.
30
What is an abscess
A localised collection of pus within a newly formed cavity
31
What causes an abscess
Pyogenic bacteria - eg. staph A inflammatory response to these organisms encompasses a massive emigration of neutrophils which then die following phagocytosis of the organism and release large amounts of lysosomal enzymes. Together with the exotoxins (from the bacteria) it results in the formation of a cavity - which contains pus.
32
What are the zones of an abscess
(1) A cavity that contains pus (2) Layer of living neutrophils and fibrin at the periphery of the pus (3) Wall / membrane (a) An inner layer of granulation tissue (b) An outer layer of fibroblastic tissue - laying down scar tissue
33
What is pus
Pus contains necrotic (liquefied dead) tissues with dead and dying neutrophils, fibrin and oedema fluid.
34
Why is the wall of an abscess both helpful and unhelpful
Wall represents attempt to repair area. It also acts as a barrier to prevent further spread of infection. However by keeping everything trapped inside it means that healing cannot occur. Will usually require I+D.
35
What are most common sites for abscess formation
Skin and tooth
36
What is an empyema
Accumulation of pus in a pre-exsisting cavity. This is different to an abscess - which is in a newly formed anatomical cavity.
37
List examples of chronic inflammation
- persistent infection (H. pylori / TB / Hep C) - AI disease - Non-living material eg. asbestos
38
What are 3 processes occuring in chronic inflammation
- persistent tissue injury and destruction - on-going inflammatory response to limit the damage - attempts to organise and heal by fibrosis
39
What are the main inflammatory cells in chronic inflammation
Macrophages, lymphocytes, plasma cells
40
What are the consequences of chronic inflammation
- Scarring (fibrosis) (= can lead to problems eg. obstruction) - Tissue destruction (= gastric ulcer causing perforation / haemorrhage) - Development of cancer - Diversion of nutrients (demand to maintain inflammation = weight loss, anaemia of chronic disease, decreased host resistance) - Amyloidosis - reactive systemic amyloid (AA amyloid)
41
What is granulomatous inflammation
A specific type of chronic inflammation | An aggregate of activated (epithelioid) macrophages.
42
What are the main causes of granulomatous inflammation
- infections (TB) - sarcoidosis - Crohn's disease
43
What is the most common infectious disease in the world
TB
44
How would you describe mycobacterium tuberculosis
Small rod-shaped bacillus with a thick lipid-rich cell wall.
45
How does TB spread
Respiratory route - from a patient with 'smear positive' active TB
46
Where does TB infection begin
Although it is spread through the respiratory route, as the respiratory mucosa is very resistant to invasion the infection begins in the terminal air spaces at the periphery of the lungs - just beneath the pleural surface.
47
Describe pathophysiology of initial TB infection
TB infection begins in the terminal air spaces. They are engulfed by alveolar macrophages - the alveolar macrophages are unable to destroy the mycobacteria because their thick cell wall resists attack. Survival of the organism allows it to multiply within the macrophages - eventually leads to cell death and the release of more microorganisms. Over weeks the mycobacteria spread in macrophages via the blood to the apices of the lungs and multiple other organs (eg. kidneys/adrenals/bones/meninges) asymptomatic in 95% of pts
48
A few weeks after initial TB infection, T cell mediated immunity is established. What does this involve
- macrophages (APCs) activate mycobacteria-specific CD4+ T helper cells via MHC class II - Th1 produce IFN-gamma, a powerful activator of macrophages = promotes intracellular killing The activated macrophages aggregate around mycobacteria and form granulomas - an anoxic and acidic environment = centre of the lesion becomes necrotic (CASEOUS NECROSIS - "soft cheese") and so most of the TB dies Lesion becomes quiescent and sealed off by scar tissue - can calcify. Some bacilli survive in dormant form and reactivate later
49
What are giant cells
Formed by the fusion of many activated macrophages.
50
What is the Ghon complex
In TB - the calcified scar of the granuloma in the lung parenchyma and the hilar lymph node
51
What is active tuberculous disease
An infection with mycobacterium tuberculosis where mycobacteria are growing and causing symptoms/signs of disease.
52
In what circumstances will active TB occur
- A small minority who are unable to contain the initial infection (due to an inadequate T cell immune response = progress immediately to active TB) - Reactivation of latent disease (often the underlying cause for reactivation is clear (immunosuppression) - but not always)
53
What groups of people are at risk of active TB
- immunocompromised (HIV) = low CD4 count = impaired cell mediated immunity = reactivation - immigrants from countries with high rates of TB - elderly - alcoholics - DM
54
What is the pathophysiology behind active TB
Inappropriate Th cell response. Strong Th1 = protective immunity = granuloma (contains infection) If the IR is more Th2 driven = inappropriate immune cells recruited (lots of cells but the wrong ones) = extensive tissue destruction and survival of organism
55
What are the symptoms of active pulmonary TB
- Feeling unwell for weeks / months - Persistent cough - Constitutional symptoms
56
What makes a patient with TB infectious
When they have "open" TB - this happens when an enlarging focus erodes into an airway and the bacilli can enter the sputum
57
What is cavitating TB
An enlarging focus can erode into an airway and the bacilli can enter the sputum. In cavitating TB a major airway is involved and the necrotic material drains away and the focus transforms into a cavity.
58
Why is cavitating TB dangerous
These patients are very infectious! Their sputum contains large numbers of mycobacteria and they cough frequently.
59
What is latent TB infection
Infection with M. tuberculosis where mycobacteria are alive by not currently causing active disease.
60
How do you diagnose active TB
A combination of - Compatible Hx - Radiological findings - Lab features (microscopy and culture)
61
What are the radiological findings in active pulmonary TB
CXR / CT showing infiltrates involving upper lobes +/- cavitation.
62
What are the laboratory features seen in active pulmonary TB
(a) 3 respiratory samples (preferably spontaneously produced, deep cough sputum samples OR induced sputum/bronchoscopy) (b) microscopic examination of samples stained with Ziehl-Neelsen stain - shows ACID FAST BACILLI (c) Culture is the gold standard but it takes 3-6 weeks for result!
63
When is NAAT indicated as an investigation for TB
- Clinical suspicion of TB - Pt has HIV - Rapid information about mycobacterial species would alter patient care THIS TEST IS A REALLY FAST WAY TO GET SPECIFIC INFORMATION.
64
What is the gold standard investigation for TB
Culture. But because the bacteria are slow growing it takes so long for the result (3-6 weeks) - pt generally started on treatment long before result
65
In what groups is extra-pulmonary TB more common
Children and immunocompromised adults
66
What is the pathophysiology behind extra pulmonary TB
During the initial infection, there is sometimes haematogenous dissemination of bacilli to a number of organs. The localised infections then Gell walled off as granulomas and remain dormant. They can reactivate later = extra pulmonary TB
67
What sites are most commonly involved in extra pulmonary TB
- lymph nodes (cervical + supraclavicular) | - kidney
68
What is milary TB
Progressive disease with wide dissemination - results in numerous small foci of infection developing in any organs.
69
Who gets miliary TB
Patients with severely impaired immunity can develop this form of TB.
70
What is the management of TB
Antituberculous therapy (4 drugs for 2 months and 2 for 4 months) RIPE - rifampicin, isoniazid, pyrazinamide, ethambutol. MONITOR PATIENT COMPLIANCE. TB is a notifiable disease + contact tracing should be undertaken.
71
What is atherosclerosis
A chronic inflammatory process affecting the intima of arteries. It is characterised by the formation of lipid-rich plaques in the vessel wall.
72
What are the main modifiable risk factors for atherosclerosis
- Smoking - HTN - DM - Dyslipidaemia (abnormal lipoprotein levels - high ratio of LDL:HDL) These all damage the endothelium
73
What happens when endothelial cells of a vessel become damaged
They become dysfunctional: (1) increased permeability (2) production of adhesion molecules and cytokines (3) recruitment of inflammatory cells (monocytes + T cells) - adhere to the endothelium and migrate into the intima
74
What happens to monocytes when they enter the intima
They differentiate into macrophages.
75
What happens to macrophages in the pathogenesis of atherosclerosis
(1) produce free radicals - drive LDL oxidation to form oxidised LDL (2) engulf oxidised LDL and cholesterol crystals - becoming foam cells
76
What are foam cells
A macrophage containing abundant lipid in it's cytoplasm giving it a "foamy" appearance microscopically - hence the name.
77
What role do foam cells play in the pathogenesis of atherosclerosis
foam cells produce growth factors that stimulate the migration of smooth muscle cells from the media to to intima
78
What are the main non-modifiable risk factors for atherosclerosis
- FHx | - Male
79
What is a fatty streak
Collections of macrophages filled with oxidised LDL within the intima may be visible as a fatty streak. It may progress to an atherosclerotic plaque
80
How is an atherosclerotic plaque formed
Progresses from a fatty streak. A core of lipid debris forms as the foamy macrophages die and the lipid in their cytoplasm is released. Smooth muscle cells proliferate and change their behaviour - secreting collagen and extracellular matrix proteins = fibrous cap (attempt to repair via scarring) forms over the core. (NB: the core contains oxidised lipid and inflammatory cells)

Cellular pathology (8 decks)

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