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FoM - principles of disease > acute + chronic inflammation > Flashcards

acute + chronic inflammation Flashcards

1
Q

acute inflammation:

A

a series of protective changes occurring in living tissue as a response to injury.

  • it is a dynamic homeostatic mechanism
  • done by higher organisms
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2
Q

inflammation cardinal signs:

A

rubor - redness

calor - heat

tumor - swelling

dolor - pain

  • loss of function
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3
Q

6 causes of acute inflammation:

A

Micro-organisms → bacteria, fungi, viruses, parasites

Mechanical → trauma & injury to tissue

Chemical → upset stable environment
* acid or alkaline

Physical → extreme condition
* heat - sunburn
* cold - frostbite

Dead tissue
* cell necrosis irritates adjacent tissue

hypersensitivity

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4
Q

acute inflammation process:

A
  • Series of microscopic events
  • Localised to affected tissue
  • Takes place in the microcirculation
  • Results the cardinal signs
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5
Q

microcirculation

A

circulation of blood in the smallest blood vessels, capillary beds, fed by arterioles and drained by venules.

includes the extracellular space with its content and the lymphatic channels.

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6
Q

starling forces:

A

forces that control the flow of fluid between the capillaries and the interstitial fluid

dynamic balance between hydrostatic and colloid osmotic pressures

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7
Q

Steps of pathogenesis in acute inflammation: (how it happens):

A

1- blood vessel radius changes - alteration of flow

2- Change in the permeability of the vessel wall - exudation
(movement of fluid and protein from vessel to extravascular space)

3- Movement of neutrophils from the vessel to the extravascular space.

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8
Q

Local changes in vessel radius and blood flow when acute inflammation starts:

A
  1. Transient arteriolar constriction → few moments, probably protective
  2. Local arteriolar dilation → (active hyperaemia)
  3. Relaxation of vessel smooth muscle → (ANS or mediator derived)

Triple Response → flush, flare, wheal
→ shows how quickly we respond to injury

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9
Q

Why does increased radius of the blood vessel (vasodilation) increase flow?

A

Poiseuille’s law

Q = ΔP x Pr4 / 8hL

(Q fluid flux, ΔP pressure gradient, r radius, h viscosity, L length)

flow is proportional to radius to the power of four

  • Increased arteriolar radius causes increased local tissue blood flow
  • Results in observed redness and heat
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10
Q

How does increased permeability occur in acute inflammation?

A

it is a localised vascular response

happens in the microvascular bed
- produced by chemical mediators.

leads to an endothelial leak

depending on the size of the holes/pores you get fluid and more protein leakage.

example of imbalance of Starling forces.

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11
Q

effects of increased permeability in capillaries:

A

[1] Exudation → the net movement of plasma from capillaries to extravascular space.

Leakage of:
- Fluid rich in protein
- Plasma (immunoglobulin and fibrinogen)

[2] Increased viscosity
→ fluid loss into extravascular space = more concentrated fluid in capillaries with blood cells and plasma proteins

causes a slow rate of flow - stasis

Poiseuille’s law

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12
Q

swelling of tissue due to acute inflammation:

A

1- Vascular/Endothelial leak (imbalance of Starling forces)

2- Change in pressure (hydrostatic & colloid osmotic)

3- Movement of fluid across the membrane into extravascular space (Exudation)

Oedema due to exudation
- it is an accumulation of fluid in the extravascular space.

tissue swelling in acute inflammation
(causes pain & reduces function)

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13
Q

difference between normal laminar and inflammatory blood flow:

A

Normal laminar (non-newtonian fluid)
- from endothelium to center of vessel
→ small to large molecules

Inflammatory blood flow (loss of normal laminar flow)
- from endothelium to center of vessel
→ (large to small molecules)

neutrophil - most important cell

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14
Q

characterisation of inflammatory blood flow:

A

1- Loss of normal laminar flow

2- rouleaux formation of erythrocytes
→ RBC aggregation in the centre of the lumen

3- neutrophil margination
→ neutrophils in the edge near endothelium

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15
Q

phases of neutrophili emigration:

A
  1. Margination
    - neutrophils move to endothelial aspect of lumen
  2. Pavementing
    - neutrophils adhere to endothelium
  3. Emigration
    - neutrophils squeeze between endothelial cells (active process) to extravascular tissues
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16
Q

diapedesis:

A

passive process

cells e.g. RBC, may follow a neutrophil when
it emigrates (active process) to extravascular tissue.

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17
Q

ideal outcome of acute inflammation:

A

Inciting agent isolated & destroyed

Macrophages move in from blood and phagocytose debris; then leave

Epithelial surfaces regenerate

Inflammatory exudate filters away

Vascular changes return to normal

Inflammation resolves

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18
Q

benefits of acute inflammation:

A
  • Rapid response to non-specific insult
  • Cardinal signs and loss of function → transient protection of inflamed area
  • Neutrophils destroy organisms and denature antigens for macrophages
  • Plasma proteins localise process → through fibrinogen - clotting
  • Return to normal
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19
Q

4 possible outcomes of acute inflammation:

A
  • Resolution → ideal outcome return to normal
  • Suppuration → pus formation
  • Organisation → tissue repair
  • Chronic inflammation → inflammatory stays
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20
Q

suppuration:

A

Characterized by:

1- pus formation

– dead tissue, organisms, exudate, neutrophils, fibrin, red cells, debris

2- pyogenic membrane around pus

– capillary sprouts, neutrophils, fibroblasts
– walls off pus

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21
Q

empyema and pyaemia:

A

Empyema is a pus in a hollow viscus.
e.g. gallbladder & pleural cavity

Pyaemia is a pus discharged in the blood stream

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22
Q

abscess:

A

a collection of pus (suppuration) under pressure.

e.g. pimple

  • Single locule or multiloculated
    → points as ‘yellow head’ then discharges → healing and repair of skin
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23
Q

organisation:

A

Characterized by:

  • Granulation tissue
  • Healing and repair
  • fibrosis and formation of a scar
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24
Q

granulation:

A

Granulation tissue is the body’s repair kit for all damage, it is new connective tissue and microscopic blood vessels that form on the surfaces of a wound during the healing process

Formed of:

– new capillaries → angiogenesis
– fibroblasts and collagen
– macrophages

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25
Q

neutrophils:

A

mobile phagocytes
– recognise foreign antigen
– chemotaxis: move towards chemical, gets widely expressed
(sniffs it out like a dog)
– adhere to organism and start phagocytosis

  • Granules possess oxidants (e.g. H2O2) and enzymes (e.g. proteases)
  • Release granule contents
  • Phagocytose & destroy foreign antigen
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26
Q

consequences of neutrophile action:

A
  • theydie when granule content is released
  • produce fluid with bits of cell, organisms, endogenous protein [pus]
  • Might extend to other tissues and progress inflammation
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27
Q

plasma proteins:

A

Fibrinogens:
→ coagulation factor
→ forms fibrin and clots exudate
→ localises inflammatory process

Immunoglobulins:
→ found in plasma specific for antigen (humoural immune response)

28
Q

cell surface mediators:

A

adhesion molecules, i.e. sticky tapes, that appear on endothelial cells.

e.g.

ICAM-1 → help neutrophils stick to endothelium wall

P-selectin → interacts with neutrophil surface

29
Q

mediator molecules released from cells, histamine:

A

Histamine is preformed in mast cells near vessels, platelets and basophils.

released as a result of local injury

IgE mediated reactions

– causes vasodilatation, increased permeability

– acts via H1 receptors on endothelial cells

30
Q

mediator molecules released from cells (50hydroxtryptamin[serotonin]):

A

5-hydroxytryptamine (serotonin) is preformed in platelets.

– it is released when platelets degranulate in coagulation

– causes vasoconstriction

31
Q

mediator molecules released from cells (prostaglandins):

A

prostaglandins are arachidonic acid metabolites formed via cyclo-oxygenase pathway

  • released from many cells & many promote histamine effects and inhibit inflammatory cells
  • thromboxane A2 promotes platelet aggregation and vasoconstriction

→ NSAIDs are effective against them

32
Q

mediator molecules released from cells (cytokines adn chemokines):

A

e.g. TNFα, IL-1

small molecules produced by macrophages, lymphocytes, endothelium
in response to inflammatory stimuli.

– pro-inflammatory and anti-inflammatory effects

– stimulate intracellular pathways and signalling

33
Q

mediator molecules released from cells (nitric oxide and oxygen-free radicals):

A

nitric oxide (NO) cause smooth muscle relaxation, anti-platelet, regulate leukocyte recruitment to inflammatory focus

plays a role in regulation of blood pressure.

oxygen free radicals are released by neutrophils on phagocytosis, they amplify other mediator effects

e.g. (H2O2, OH-, O2-)

34
Q

mediator molecules inside cells for signalling:

A

Pattern associated molecular groups:
microbial antigen - genetically hardwired to recognise:
→ production of innate & adaptive immunity

Danger associated molecular groups:

substances released in response to stimulus

  • These molecules stimulate pattern recognition receptors on cell membranes
    → activation of inflammatory response
35
Q

intracellular inflammatory pathways:

A

[1] NF-κB (nuclear factor kappa-B) pathway

[2] MAPK (mitogen-activated protein kinase) pathway

– Stimulated in inflammation via surface receptors e.g. toll-like receptors (TLRs)

– Regulates pro-inflammatory cytokine production and inflammatory cell recruitment

[3] JAK-STAT (Janus kinase – signal transducer and activator to transcription)}} pathway

– Direct translation of extracellular signal to molecular expression

36
Q

Interaction of four enzyme cascades in Plasma:

A

[1] Blood coagulation pathways

– clots fibrinogen in exudate
– interacts widely with other systems

[2] Fibrinolysis

– breaks down fibrin, helps maintain blood supply
– fibrin breakdown products are vasoactive

[3] Kinin system

– bradykinin: pain

[4] Complement cascade

– ties inflammation with immune system

– active components stimulate increased permeability, chemotaxis, phagocytosis, cell breakdown

37
Q

immediate systemic effects of acute inflammation:

A

[1] Pyrexia - raised temperature

– endogenous pyrogens from white cells act centrally on brain

[2] Feel unwell

– malaise, anorexia, nausea
– abdominal pain and vomiting in children

[3] Neutrophilia - raised white cell count

release/produce from bone marrow

38
Q

long term effects of acute inflammation:

A

[1] lymphadenopathy - regional lymph node enlargement
– immune response

[2] weight loss - catabolic process

[3] anaemia

39
Q

effects of systemic infection:

A

Shock - inability to perfuse tissues

  • Clinical picture of early septic shock

– peripheral vasodilatation

– tachycardia - high heart rate

– hypotension - low blood pressure

– often pyrexia

– sometimes haemorrhagic skin rash

40
Q

how does septic shock happen?

A

systemic release of chemical mediators from cells into plasma

– Mediators cause vasodilation causing loss of systemic vascular resistance (SVR) - BP = CO x SVR

– Results in catecholamine release e.g. adrenaline

– Tachycardia → increased Heart Rate (HR) follows to maintain Cardiac Output (CO) because

       → Increased Heart Rate compensates the. loss in SVR - CO = SV x HR
  • Bacterial endotoxin released

– Interleukin-1 released
– Acts on hypothalamus - pyrexia

  • Activation of coagulation

– Disseminated intravascular coagulation
– Vasoactive chemical - vasodilatation
– Haemorrhagic skin rash

41
Q

What happens when raised HR fails to compensate for the loss in SVR?

CO = SV x HR

BP = CO x SVR

A

Raised HR is insufficient to maintain cardiac output

SVR low → so BP falls (BP = CO x SVR)

This leads to reduced perfusion of tissues:

  • Tissue hypoxia (less oxygen delivery)
  • Loss of cell tissue and organ function
42
Q

outcomes of septic shock:

A

Rapidly fatal

Tissue hypoxia → cell death

Haemorrhage

  • Requires urgent intervention and support

– awareness and early recognition
– ability of young people to compensate
– admit to hospital and intensive care

43
Q

chronic inflammation meaning:

A

inflammation that tends to be long term in which the cell population is:

Lymphocytes
Plasma cells → production of antibodies
Macrophages → phagocytosis & antigen presenting cells

It may follow from an ongoing acute inflammation
– “acute on chronic inflammation”

or arise as primary pathology

44
Q

features of chronic inflammation;

A

[1] malaise and weight loss

e.g.

  • tuberculosis (lung, lymph node, bone, kidney, skin)
    • systemic effect

[2] gradual loss of function

e.g.

  • autoimmune thyroiditis (functional gland destruction)
    • hypothyroidism
  • Crohn’s disease (GI tract ulceration and fibrosis)
    • pain, diarrhoea, gut obstruction
  • leprosy (cutaneous nerve destruction)
    • loss of sensation
45
Q

angiogenesis;

A

Angiogenesis - the formation of new vessels.

Hypoxia stimulates the release of {{c1::Vascular Endothelial Growth Factor (VEGF)}} for proliferation.

Blood supply enters damaged tissue and aids in healing & granulation

46
Q

angiogenesis generic nature:

A

Angiogenesis and organisation in thrombosis
– limits thrombus propagation
– reinstatement of flow

Angiogenesis in malignant tumours
– angiogenesis occurs as tumour grows (hypoxic cells & VEGF)
– potential for therapeutic control

Fibrosis and scarring in atherosclerosis
– similarities with chronic inflammation

47
Q

granulation:

A

Capillaries grow into inflammatory mass
→ access of plasma proteins & macrophages & fibroblasts from blood and tissue

  • fibroblasts lay down collagen to repair damaged tissue
    → collagen replaces inflammatory exudate
  • Patches tissue defects
  • Replaces dead or necrotic tissue
  • Contracts and pulls together
48
Q

scar:

A

a small firm blemish on skin made from fibrous tissue as a product of granulation tissue.

It can be a problem in the loops of bowel following peritonitis.

49
Q

primary chronic inflammation:

A

(i.e. not arising after an acute inflammation)

Features:
* lymphocytes, plasma cells, macrophages, fibrosis

Occurs because of:

[1] Autoimmune disease
– autoantibodies directed against own cell and tissue components – autoantigens
– damage organs, tissues, cells, cell components

e.g.
– thyroiditis, rheumatoid disease, pernicious anaemia (chief/parietal cells)
– systemic lupus erythematosis (nuclear antigen)

[2] Material resistant to digestion
– mycobacteria, Brucella, viruses
– cell wall resistant to enzymes

[3] Exogenous substances
– sutures, metal and plastic e.g. joint replacements, mineral crystals, glass,
– do not produce immune response (not antigenic)

[4] Endogenous substances
– necrotic tissue, keratin, hair
– cannot easily be phagocytosed

[5] Granulomatous inflammation

50
Q

plasma cell:

A

differentiated B-cells that are responsible for antibody production

B-cell mechanisms

[1] Differentiation to plasma cells
→ production of antibodies (facilitates immune response)

[2] Interaction with macrophages
(Antigen presenting cells - APC)
→ immune memory

51
Q

t cell mechanisms:

A

T-cell mechanisms:

[1] Production of cytokines

– attract and hold macrophages
– activate macrophages & lymphocytes
– alter permeability of endothelial cells

[2] Production of interferons

– antiviral effects
– attract and stimulate other cells

[3] Lysis - specific antigen response

– chemical mechanisms - toxic granule proteins

52
Q

natural killer cells:

A

cells of the innate immunity similar to neutrophils

they destroy antigens and cells.
→ chemical mechanisms - granule proteins

53
Q

macrophages:

A

cells that remove debris, have a role in immune system - antigen presenting cells (APCs).

come from bone marrow, blood and tissues.

Types:

(altered antigen presenting capacities)
* monocyte, histiocyte, activated macrophage, epithelioid cell, giant cell

Mechanisms:
* contain enzymes e.g. lysozyme
* produce interferons – destroy, influence process

54
Q

fibroblasts:

A

motile cells & metabolically active.

Make structural proteins e.g. various types of collagen.

55
Q

granulmatous inflammation:

A

characterised by the presence of granulomas (granulomata) in tissues and organs, which is a collection of macrophages.

stimulated by indigestible antigen, causes serious infections and idiopathic diseases.

aggregates of epithelioid macrophages in tissue that occur in response to indigestible antigen.

56
Q

granulomas:

A

aggregates of epithelioid macrophages in tissue that occur in response to indigestible antigen.

Many are type IV hypersensitivity reactions.

May contain giant cells, surrond dead material, or be surrounded by lymphocytes

Occasionally contains neutrophils and eosinophils

57
Q

giant cells:

A

may be a result of a fusion of macrophages.

Granuloma not needed for their presence but usually is present with them.

[1] Langhans type
- found in tuberculosis, with a peripheral rim of nuclei and a large cytoplasm.

[2] Foreign body type
- associated with pyogenic granulation tissue e.g. pilonidal abscess
→ acute inflammation with neutrophils, pus (organisation) and giant cells.

[3] Silicone associated
- ruptured silicone implants (usually in breasts)

[4] Warthin-Finkeldy type
- rarely seen in measles & central cluster of nuclei

58
Q

Infectious granulomatous diseases:

A
  • tuberculosis
    – Mycobacterium tuberculosis
  • ziehl neelsen stain
  • leprosy – Mycobacterium leprae
  • syphilis – Treponema pallidum
59
Q

Caseous necrosis:

A

dead tissue surrounded by macrophages, giant cells, lymphocytes.

No neutrophil presence & TB common in HIV

60
Q

non infective granulomas”

A

Rheumatoid disease
- tissue specific auto-immune disease
- ? cause

  • Sarcoidosis – classical clinical picture, ? cause
  • Crohn’s disease – chronic inflammatory bowel disease, ? cause
61
Q

surgical wound vs larger defect healing:

A

Surgical wound healing:

  • Healing by primary intention

→ minimal gap – blood clot

→ small amount of granulation tissue

→ small linear scar

Larger defect healing:

  • Healing by secondary intention

→ lots of granulation tissue ingrowth

→ contraction and scarring

62
Q

wound healing steps:

A

Injury, blood clot, acute inflammation, fibrin

  • Many growth factors and cytokines involved
  • Granulation tissue growth - angiogenesis
  • Phagocytosis of fibrin
  • Myofibroblasts move in and lay down collagen
  • Contraction of scar
  • Re-epithelialisation
63
Q

support wound healing:

A

cleanliness

  • apposition of edges (no haematoma - no blood clot)
  • sound nutrition
  • metabolic stability and normality
  • normal inflammatory and coagulation mechanisms
  • balanced local mediators
64
Q

impairing wound healing:

A
  • Dirty, gaping wound, large haematoma
  • Poor nourishment, lack of vitamins C, A
  • Abnormal CHO metabolism, diabetes, corticosteroid therapy
  • Inhibition of angiogenesis
65
Q

fracture healing:

A

healing of bone and the soft tissue around it.

Sequence:

  • Trauma, fracture, haematoma
    → Causes bits of dead bone and soft tissue
  • Acute inflammation, organisation, granulation tissue, macrophages remove debris
  • Granulation tissue contains osteoblasts as well as fibroblasts
66
Q

callus formation:

A

Osteoblasts lay down woven bone

Nodules of cartilage present

Followed by bone remodelling

  • osteoclasts remove dead bone
    – progressive replacement of woven bone by lamellar bone
    – reformation of cortical and trabecular bone

FoM - principles of disease (17 decks)

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