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ESA2 - Mechanisms Of Disease > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

What is the difference between acute and chronic inflammation?

A
  • ACUTE evolves over hours/days

- CHRONIC evolves over weeks, months and even years

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2
Q

What suffix is used to indicate inflammation of an organ/tissue?

A

-ITIS e.g. inflammation of the appendix would be “appendicitis”

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3
Q

Why do chemical mediators (leukocytes, plasma proteins) need to be delivered to a site of injury?

A

Local defences are not enough to prevent against infection e.g. Epithelia

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4
Q

How are leukocytes and fluid signalled to leave the blood cappillary at a site f damage?

A
  • Epithelia release chemical mediators of inflammation (e.g. cytokines, chemokines)
  • These signal immune response cells and make the walls of capillaries more permeable so fluid and leukocytes can leak out
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5
Q

Name 6 causes of inflammation

A
  • Foreign bodies
  • Infections (bacterial, viral etc.)
  • Tissue necrosis
  • Trauma
  • Physical and chemical agents
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6
Q

What are the characteristic clinical signs of acute inflammation?

A
  • RUBOR (redness)
  • CALOR (heat)
  • TUMOUR (swelling)
  • DOLOR (pain)
  • LOSS OF FUNCTION (promotes rest)
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7
Q

What is inflammation?

A
  • Response to injury of a vascularised living tissue

- Delivers defensive materials to a site of injury

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8
Q

Describe how an area of inflammation can be come red and hot (RUBOR and CALOR)

A
  • Blood vessels in area of injury dilate
  • INCREASED PERFUSION at site of injury to transport chemical mediators and plasma proteins
  • Area becomes red from increased blood flow and hot from dilation (more heat loss)
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9
Q

What is the role of bradykinins?

A
  • Chemical mediators that stimulate specialised nerve endings at the site of injury causing PAIN
  • Increases permeability of vessel walls so exudate leaks out
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10
Q

What is the significant of vasodilation of arterioles following inflammation?

A
  • Arterioles dilate and increase perfusion into capillaries so CAPILLARY PRESSURE RISES
  • Increased delivery of fluid and plasma proteins to injured tissues
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11
Q

Explain how increased leakage of venule walls leads to decrease in perfusion rate upstream

A
  • Plasma proteins escape, leads to increased HAEMATOCRIT of venules and increased RESISTANCE of blood flow
  • Increased pressure as outflow is hampered, upstream vessel lumens dilate and blood flow slows
  • Increased pressure means greater exudate into tissues so more plasma proteins and fluid delivered
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12
Q

What are vasoactive amines? Give 2 examples

A
  • Group of chemical mediators that are the first to appear during inflammation
  • Examples are Histamine and Serotonin
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13
Q

Where is histamine found?

A
  • Mast cells
  • Basophils
  • Platelets
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14
Q

What can stimulate the release of histamine? (3)

A
  • Physical damage
  • Immune/hypersensitivity reactions
  • Complement components
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15
Q

What is the role of histamine in acute inflammation?

A
  • PAIN, arteriolar dilation and venular leakage
  • Causes endothelial cells in capillary walls to CONTRACT and pull apart, forming GAPS which allow plasma proteins and fluid to leak out into tissues (exudate)
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16
Q

What is the main difference between the action of histamine and serotonin?

A

Serotonin can STIMULATE FIBROBLASTS

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17
Q

What are prostaglandins and when are they produced?

A
  • Produced during inflammation by cell membrane phospholipids
  • Cause VASODILATION, make the skin more sensitive to pain and cause FEVER
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18
Q

Describe how NSAIDS such as aspirin work

A
  • Blocks production of prostaglandins from arachnodonic acid by inhibiting cyclo-oxygenase
  • This reduces pain and swelling
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19
Q

How can the release of histamine be stimulated?

A

In response to:

  • Physical damage
  • Immune response/hypersensitivity
  • Complement components
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20
Q

Explain how vasodilation of arterioles increases the delivery of exudate to an area of injury

A
  • Dilation causes flow to accelerate in capillaries so CAPILLARY PRESSURE RISES
  • Capillaries that are normally empty are filled so increases delivery of fluid and leucocytes
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21
Q

What is meant by haematocrit?

A

Ratio of volume of erythrocytes to total volume of blood within the vessel

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22
Q

Explain how leaky venules can lead to an increase in resistance of blood flow within them

A
  • Plasma can escape through tiny gaps between endothelial cells
  • INCREASED HAEMATOCRIT within venules to blood is more viscous, leading to resistive flow
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23
Q

Explain the vascular changes that occur in acute inflammation

A
  • Vasodilation of arterioles to increase blood flow to site of injury
  • Increased permeability of venules leads to increased loss of exudate from vessel; blood is more viscous and flow slows at site of injury - STASIS
  • Reduced rate of outflow so exudate can be delivered
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24
Q

What 4 forces are involved in Starling’s Law?

A
  • Capillary pressure
  • Interstitial free fluid pressure
  • Plasma colloid osmotic pressure
  • Interstitial fluid colloid osmotic pressure
25
Q

What are the main forces involved in driving fluid IN and OUT of the capillary?

A
  • IN - Plasma colloid osmotic pressure of plasma proteins (e.g. increased plasma proteins inside capillary)
  • OUT - hydrostatic pressure of the blood (capillary pressure e.g. increased pressure of fluid)
26
Q

Describe the lymphatic role of the tissue fluid in acute inflammation

A
  • Exudate contains microorganisms and antigens, which are drained into the lymphatics
  • Foreign antigens are presented to the immune system within the lymph nodes which aids the immune response
27
Q

What do you call inflammation of the lymph nodes?

A

Lymphadenitis

28
Q

Name 3 plasma proteins present in the exudate

A
  • Opsonins
  • Complement
  • Antibodies
29
Q

What is the name given to tissue fluid that contains no plasma proteins? Where might this be seen?

A
  • TRANSUDATE (ultrafiltration of plasma that occurs in normal tissue)
  • Seen in HEART FAILURE due to increased hydrostatic pressure of capillaries
30
Q

Name 4 chemical mediators that induce vascular leakage

A
  • Histamine
  • Bradykinin
  • Serotonin
  • Complement C3a, C4a, C5a
31
Q

What is the primary type of leucocyte involved in acute inflammation?

A

NEUTROPHIL

32
Q

What does the presence of neutrophils in tissue suggest?

A
  • Normally ONLY found in the blood and bone marrow

- Indicates INVASION BY BACTERIA/PARASITE and/or TISSUE INJURY

33
Q

What is chemotaxis?

A
  • Directional movement towards a chemical attractant (chemotaxins) at the site of injury
  • These include bacterial products (e.g. ENDOTOXIN), injured tissues and substances released from leucocytes (CYTOKINES)
34
Q

What is the role of chemotaxins? Give 4 examples

A
  • Released by cells or bacteria to attract and recruit inflammatory cells at the site of injury
  • Complement C3a, C5a; Endotoxin; Thrombin and FDPs, Leukotriene B4
35
Q

What powerful chemotaxin is produced by leucocytes?

A

Leukotriene B4

36
Q

What is Endotoxin?

A

Lipopolysaccharide CHEMOTAXIN released from outer membrane of Gram Negative bacteria

37
Q

How do chemotaxins work to direct neutrophils to the site of injury?

A
  • Chemotaxin binds to receptors on neutrophils and stimulates influx of Na+ and Ca2+
  • Cell swells and cytoskeleton is reorganised into a triangular shape pointing in the direction of the chemotacic stimuli
38
Q

Briefly describe margination, rolling and adhesion of neutrophils

A
  • Endothelial wall is coated in adhesion molecules such as SELECTIN and INTEGRIN
  • Neutrophils marginate at periphery of vessel and stick to the wall, binding to integrins and roll along wall binding to selectins until they become trapped
39
Q

Describe the process of diapedesis

A
  • Leucocytes DIG their way out of venules as they cannot escape through the gaps which exudate flows (too big)
  • Produce COLLAGENASE which digests the basement membrane
  • Pull themselves along collagen fibres of other tissues to reach site of injury
40
Q

What is the role of opsonins? Give 2 examples

A
  • Substances which bind to foreign bodies and allow them to be recognised by phagocytes and phagocytosed
  • e.g. IgG antibody, complement C3b
  • When not present, phagocyte recognises surface antigens
41
Q

What is degranulation?

A

Digestion of a foreign body by granules of phagosomes - inject bactericidal substances into particle and destroys them

42
Q

Describe 2 ways (one O2 dependant, one O2 independent) by which phagocytes can kill phagocytosed organisms

A
  • OXYGEN DEPENDANT - production of ROS such as superoxide, H2O2 and OH- and release into phagosome
  • OXYGEN INDEPENDENT - use of ENZYMES such as proteases and lysozyme
43
Q

What is meant by an inflammatory mediator?

A

Any molecule produced during inflammation that modulates an inflammatory response

44
Q

Name 3 common responses of cells to chemical inflammatory mediators

A
  • Chemotaxis
  • Phagocytosis
  • Contraction/Relaxation (e.g. smooth muscle cells, venous endothelial cells)
45
Q

Give 5 examples of groups of endogenous mediators of inflammation

A
  • Vasoactive amines (histamine)
  • Vasoactive peptides (bradykinin)
  • Complement (C3a, C3b, C5a)
  • Clotting factors and fibrinolytic cascades
  • Cytokines and chemokines
46
Q

What are the main sources and roles of inflammatory mediators?

A
  • Vasodilation of arterioles
  • Increased vascular permeability
  • Chemotaxis
  • Phagocytosis
  • Pain
47
Q

List 4 local complications of acute inflammation

A
  • DAMAGE TO NORMAL TISSUE due to substances released by neutrophils
  • OBSTRUCTION OF TUBES AND COMPRESSION caused by swelling and fluid accumulation
  • LOSS OF FLUID due to increased tissue pressure so fluid leaks from surface wound
  • PAIN/LOSS OF FUNCTION to enforce rest
48
Q

Explain how a fever occurs in acute inflammation

A
  • Macrophages stimulated by exogenous pyrogens and produce PYROGENIC CYTOKINES
  • Stimulates production of PROSTAGLANDIN E2 from anterior hypothalamus which causes fever, pain and increased vascular permeability
49
Q

What systemic effects can arise from acute inflammation? (4)

A
  • Fever
  • Leucocytosis
  • Change in level of plasma proteins (acute phase response)
  • Shock
50
Q

Describe how neutrophilia can lead to leucocytosis

A
  • Occurs during bacterial infection
  • Colony stimulating factors produced by macrophages and endothelial cells stimulate bone marrow to produce more neutrophils
  • Number of circulating leucocytes increases, causing leucocytosis
51
Q

What is the acute phase response and what are the resulting symptoms?

A
  • Change in level of plasma proteins produced by the LIVER within hours of injury
  • Produced by CYTOKINES released during inflammation and cause tiredness and lack of appetite
52
Q

Give examples of proteins which have an altered synthesis during the acute phase response

A
  • DECREASED PRODUCTION - Albumin

- INCREASED PRODUCTION - fibrinogen, complement C3, ceruloplasmin, α-1 antitrypsin, C-reactive protein (CRP)

53
Q

Explain how shock can occur in acute inflammation

A
  • Spread of bacteria products and mediators around systemic circulation
  • Leads to inflammation throughout body
  • DRAMATIC DROP IN BLOOD PRESSURE due to widespread vasodilation and increased vascular permeability with resultant fluid exudate
  • Often FATAL
54
Q

Describe how acute inflammation is resolved

A
  • Mediators and neutrophils have SHORT LIFESPAN so do not persist
  • Once removed, vascular permeability returns to normal and exudate is reabsorbed or drained into lymphatics
  • Neutrophils undergo apoptosis and are phagocytosed (along with necrotic debris) by macrophages
55
Q

Name the 4 types of exudate and explain their appearance

A
  • PUS/ABSCESS - creamy/white (rich in neutrophils)
  • HAEMORRHAGIC - red (where vascular damage has occurred)
  • SEROUS - clear (contains plasma proteins but no leucocytes)
  • FIBRINOUS - friction between serosal surfaces (due to deposition of fibrin) e.g. bread and butter pericarditis
56
Q

What is hereditary angio-oedema and what are the symptoms?

A
  • Rare autosomal dominant deficiency of C1-ESTERASE INHIBITOR (complement protein)
  • Attacks of non-itchy cutaneous angio-oedema and recurrent abdo pain (intestinal oedema)
57
Q

Explain the consequences of α-1 antitrypsin disorder

A
  • Deficiency in protease so enzymes released from neutrophils cannot be broken down
  • Neutrophil enzymes can damage parenchymal tissue causing emphysema, liver disease or cirrhosis
58
Q

Explain the pathophysiology of chronic granulomatous disease

A
  • Genetic condition where phagocytes are unable to produce ROS superoxide so CANNOT GENERATE A RESPIRATORY BURST
  • Chronic infections (as bacteria cannot be destroyed) and numerous granulomas formed

ESA2 - Mechanisms Of Disease (8 decks)

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