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Year 1 Semester 2 Pathological Processes > S2) Acute Inflammation > Flashcards

S2) Acute Inflammation Flashcards

1
Q

What is inflammation?

A

Inflammation is a response to injury of vascularised living tissue (indicated by the suffix -itis)

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2
Q

Identify 4 purposes of inflammation

A
  • Deliver defensive materials (blood cells and fluid) to a site of injury
  • Protect the body against infection
  • Clear damaged tissue
  • Initiate tissue repair
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3
Q

In terms of time, distinguish between acute and chronic inflammation

A
  • Acute inflammation evolves over hours or days (innate and stereotyped)
  • Chronic inflammation evolves over weeks, months or even years
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4
Q

What is acute inflammation?

A

Acute inflammation is a rapid response to an injurious agent which aims to deliver mediators of host defence (leucocytes and plasma proteins) to the site of injury

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5
Q

In acute inflammation, leucocytes and plasma proteins need to be delivered because local defences are not adequate.

Describe the mechanism of delivery of these defences

A
  • Most defensive agents circulate in the blood in inactive form and when needed, they are delivered and activated
  • They leave the blood vessels at the site of the injury without interrupting blood flow to other tissues
  • This process is controlled by chemical mediators
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6
Q

Identify 5 major causes of acute inflammation

A
  • Foreign bodies e.g. splinters, dirt, sutures
  • Immune reactions
  • Infections e.g. bacterial, viral, parasitic
  • Tissue necrosis
  • Physical and chemical agents e.g. burns, frostbite, irradiation
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7
Q

What are 5 cardinal signs of acute inflammation?

A
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8
Q

Describe the initial tissue change in acute inflammation, how it is achieved and result of this

A
  • Brief period of arteriolar vasoconstriction (lasting a few seconds)
  • Vasodilatation of the arterioles occurs due to vasoactive mediators e.g. histamine
  • Resultantly, flow accelerates in the capillaries and capillary pressure rises

Result = increased fluid and leucocyte delivery to the area of injury

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9
Q

What follows vasodilation in acute inflammation?

A
  • Venular leakage (increased permeability)
  • Plasma escapes through gaps between endothelial cells
  • Resultantly, an increased haematocrit within the venules increases resistance to blood flow within them
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10
Q

In 5 steps, outline the effects of vasodilation and increased venular permeability in acute inflammation

A
  • Hampers blood outflow from the area of injury
  • Increases pressure upstream causing vasodilation of upstream vessels
  • Blood flow slows down
  • Thus, there’s greater exudation of fluid into the tissue spaces
  • Greater delivery of plasma proteins to the site of injury
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11
Q

Outline the properties, location, action and effects of histamine in acute inflammation

A
  • Properties: vasoactive amine, readily available in cells/platelets
  • Location: stored in granules of mast cells, basophils and platelets
  • Action: released in response to stimuli such as physical damage, immune reactions and complement components
  • Effects: pain, arteriolar dilatation and venular leakage
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12
Q

Outline the properties, location and effects of serotonin in acute inflammation

A
  • Properties: vasoactive amine, readily available
  • Location: stored in the granules of platelets
  • Effects: similar vascular effects as histamine
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13
Q

What are prostaglandins and what do they do in inflammation?

A
  • Prostaglandins are substances produced in inflammation from cell membrane phospholipids
  • They cause vasodilatation, fever and increase pain sensitivity
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14
Q

Describe how the production of prostaglandins can be blocked to reduce pain and swelling

A
  • Production can be blocked by aspirin and NSAIDs
  • These drugs inhibit cyclo-oxygenase (the enzyme that produces prostaglandins from arachadonic acid)
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15
Q

Identify 2 other substances with vasoactive properties

A
  • Leukotrienes
  • Bradykinin
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16
Q

Acute inflammation throws off the equilibrium of fluid exchange in the microcirculation. Starling’s law describes the forces involved in this equilibrium.

What are the forces?

A
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17
Q

Discuss the roles of endothelium in acute inflammation

A
  • The endothelium of the capillaries and venules acts as a semipermeable membrane
  • This allows the escape of water and electrolytes but retains plasma proteins
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18
Q

The exchange between the blood and tissue spaces depends on the four forces below.

Describe this

A
  • The main force driving fluid out of the vessels is the hydrostatic pressure of the blood
  • The main force driving fluid back into the blood is the colloidal osmotic pressure of the plasma proteins
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19
Q

What is the impact of the altered vascular elements (vasodilation and venular leakage) on the forces in Starling’s law?

A
  • Arterioles dilate increasing capillary pressure, hence, driving more fluid out of the blood
  • Plasma proteins escape into the tissue spaces, raising the osmotic pressure there and reducing colloid osmotic pressure
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20
Q

What is the significance of vasodilation and increased permeability in acute inflammation?

A
  • Increased flow of fluid (with its plasma proteins) out of the vessels into the tissue spaces
  • Delivery of plasma proteins to the site of injury
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21
Q

What happens to the excess fluid in the tissue spaces during acute inflammation?

A

Excess fluid drains from the tissues in the lymphatics taking with it micro-organisms and antigens which are presented to the immune system within the lymph nodes

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22
Q

Identify the three main types of defensive proteins in the exudate and describe their actions

A
  • Opsonins – coat foreign materials to enhance phagocytosis
  • Complement – a group of proteins locally assembled to produce a bacteria-perforating structure
  • Antibodies – bind to the surface of micro-organisms and also act as opsonins
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23
Q

Compare and contrast exudate and transudate

A
  • Exudate is the protein-rich tissue fluid that develops in inflammation
  • Transudate is the protein-poor ultrafiltrate of plasma occurring in normal vessels
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24
Q

Identify the chemical mediators involved in vascular leakage

A
  • Histamine
  • Serotonin
  • Bradykinin
  • C3a, C4a and C5a
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25
Q

What are neutrophils?

A

Neutrophils are the primary type of leucocyte involved in acute inflammation

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26
Q

Describe the structure, function and location of neutrophils

A
  • Structure: contains about 2,000 granules containing bactericidal substances
  • Function: escapes from blood vessels into tissue spaces in response to chemical ‘calls’ from bacteria, injured cells or other inflammatory cells
  • Location: normally only found in the blood and bone marrow, and in tissue during inflammation
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27
Q

In 6 steps, outline the processes that occur when a neutrophil captures and kill a bacterium in the tissue space

A

⇒ Chemotaxis: be summoned to the place of injury

⇒ Activation: switch to a higher metabolic level

⇒ Margination: stick to the endothelial surface

⇒ Diapedesis: crawl through the endothelium

⇒ Recognition-attachment: recognise the bacterium and attach to it

⇒ Phagocytosis: engulf the bacterium

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28
Q

What is a cytokine?

A

Cytokines are polypeptides that are produced by many cells and act as messengers between cells

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29
Q

What is chemotaxis?

A

Chemotaxis is directional movement towards a chemical attractant (chemotaxin)

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30
Q

What are chemokines?

A

Chemokines (short for chemotactic cytokines) are a group of cytokines which are involved in chemotaxis

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31
Q

Identify some chemotaxins

A
  • Bacterial products e.g. endotoxin
  • Injured tissues
  • Substances produced by leucocytes
  • Spilled blood
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32
Q

What is an endotoxin?

A

An endotoxin is a lipopolysaccharide from the outer membrane of gram negative bacteria

33
Q

Fresh blood isn’t chemotactic, why is clotted blood chemotactic?

A
  • When blood clots a cascade of plasma enzymes is activated resulting in the formation of thrombin and fibrin
  • Both thrombin and fibrin degradation products are chemotactic, therefore clotting blood is chemotactic
34
Q

What happens when a complement is activated?

A
  • Release of fragments of C3, C4 and C5 called C3a, C4a and C5a
  • All of these are chemotactic (especially C5a)
35
Q

Activated cells are stickier than normal cells.

Why is this?

A
  • Within five seconds of the chemotaxin binding to cell surface receptors, Ca2+ and Na+ rush into the cell
  • The cell swells and reorganises its cytoskeleton
  • It assumes a triangular shape pointing in the direction of the chemotactic stimulus and sends out pseudopodia
36
Q

Leucocytes can also produce chemotaxins.

Identify one

A

Leukotriene B4 is the most powerful chemotaxin from leucocytes

37
Q

What is margination?

A

Margination is the process whereby leucocytes assume marginal positions in the vessels

38
Q

Outline rolling and adhesion

A
  • Leucocytes stick to the walls of venules as they heed the chemotactic ‘call’
  • They roll along the wall but then become ‘trapped’ (adhesion), stop and crawl out of the vessel
39
Q

Distinguish between rolling and adhesion

A

The number of selectins and the activation of integrins are increased by inflammatory mediators and chemotaxins:

  • When the leucocytes roll along the endothelium, their receptors are binding to selectins
  • When they adhere and stick firmly, their receptors are binding to integrins such as ICAM-1
40
Q

What is diapedesis?

A
  • Diapedesis is when leucocytes ‘dig’ their way out of the venules as they don’t use the endothelial gaps through which the exudate escapes (takes 3-9 minutes)
  • They produce collagenase which digests the basement membrane
41
Q

What is recognition-attachment?

A

Recognition attachment is when the phagocyte (leucocyte – neutrophil) recognises a pathogen and attaches to it through means of opsonisation/ PAMPs & PRRs

42
Q

What is phagocytosis?

A

Phagocytosis is when a phagocyte engulfs a pathogen/ necrotic tissue by extending its membrane around the particle and engulfing it

43
Q

Explain the 2 pathways in which phagocytosed organisms can be killed

A
  • Oxygen-dependent: respiratory burst using oxygen derived free radicals e.g. hydrogen peroxide (H2O2), superoxide anion (O2-) and hydroxyl (OH-)
  • Oxygen-independent: using enzymes e.g. proteases, phospholipases, nucleases and lysozyme
44
Q

What is a mediator?

A

A mediator is any molecule that is produced in a focus of inflammation and modulates the inflammatory response in some way

45
Q

What are the common responses to mediators in acute inflammation?

A
  • Motion:

I. Contraction/relaxation of vascular smooth muscle cells

II. Contraction of venular endothelial cells

III. Movement along a chemotactic gradient

IV. Phagocytosis by neutrophils

  • Secretion
46
Q

Inflammation needs to be controlled otherwise it would be on-going and spread around the body.

Describe its control

A
  • Inhibition of mediators
  • Mediators have short lives (seconds to minutes)
  • Effects of mediators last minutes to hours
47
Q

Endogenous mediators are supplied by the plasma, leucocytes and local tissues

How can mediators be grouped?

A

- Vasoactive amines e.g. histamine and serotonin

- Vasoactive peptides e.g. bradykinin

- Complement components e.g. C3a, C5a

- Mediators derived from phospholipids e.g. prostaglandins, leukotrienes

- Cytokines and chemokines e.g. interleukins and tumour necrosis factor (TNF)

- Exogenous mediators of inflammation e.g. endotoxin

48
Q

Identify the main roles of inflammatory mediators

A

- Vasodilatation (histamine and serotonin)

- Increased vascular permeability (histamine, serotonin and bradykinin)

- Chemotaxis (leukotriene B4, C5a, C3a, chemokines and endotoxins)

- Phagocytosis (C3b)

- Pain (bradykinin and prostaglandins)

49
Q

Acute inflammation can result in problems locally within the tissues.

Identify 5 local complications involved

A
  • Damage to normal tissue ​
  • Obstruction of tubes & compression of vital structures
  • Loss of fluid
  • Pain
  • Loss of function
50
Q

Explain how acute inflammation can lead to fluid loss

A
  • Fluid accumulates in tissue spaces as the tissue pressure increases until it reaches a level that prevents further exudation
  • However, fluid can continuously leak from a surface wound, resulting in large amounts of fluid loss
51
Q

Explain how acute inflammation can lead to damage of normal tissue

A

Secondary to substances produced by neutrophils are released to the surroundings during the process of phagocytosis, resulting in damage

52
Q

Explain how acute inflammation leads to the obstruction and compression of structures

A

Vital structures, intestinal/fallopian tubes can be obstructed or compressed secondary to the swelling produced by the inflammatory exudate

53
Q

Although produced locally, inflammatory mediators can enter the blood stream in significant amounts and have systemic effects.

What are the four main systemic effects of acute inflammation?

A
  • Fever
  • Leucocytosis
  • The Acute Phase Response
  • Shock
54
Q

Describe how fever occurs as a systemic effect of acute inflammation

A
  • Fever occurs when the thermostat of the body (situated in the anterior hypothalamus) is switched to a higher setting
  • Macrophages produce pyrogenic cytokines (TNF, interleukin-1) when stimulated by exogenous pyrogens
  • These cytokines cause an increase in synthesis of prostaglandin E2 within the anterior hypothalamus, resulting in fever
55
Q

What is leucocytosis?

A
  • In leucocytosis, the number of circulating leucocytes increases
  • Neutrophilia is seen during bacterial infection
56
Q

Describe how the acute phase response occurs as a systemic effect of acute infammation

A
  • The acute phase response is a change in the levels of some plasma proteins, triggered by cytokines, seen because the liver changes its pattern of protein synthesis
  • Some proteins are produced in smaller amounts e.g. albumin and others are produced in larger amounts e.g. fibrinogen, C3, alpha-1 antitrypsin, C-reactive protein
57
Q

What is shock?

A

Shock is a dramatic drop in BP due to widespread vasodilatation and increased vascular permeability with resultant fluid exudation

58
Q

Describe how shock occurs as a systematic effect of acute inflammation

A

Shock occurs when bacterial products or inflammatory mediators spread around the body in the blood stream inducing inflammation throughout the body

59
Q

In 5 steps, outline the resolution of acute inflammation

A
  • Inflammation mediators degrade
  • Normal vascular structure returns
  • Exudate is reabsorbed into the venules / lymphatics
  • Fibrin is degraded
  • Neutrophils undergo apoptosis and are phagocytosed
60
Q

Outline the sequelae of acute inflammation

A
  • Pus/abscess (purelent exudate)
  • Haemorrhagic exudate
  • Serous exudate
  • Fibrinous exudate
61
Q

What is purelent exudate?

A

- Pus is the cream/white exudate found in an abscess thatis rich in neutrophils

  • It is typical of infections by chemotactic bacteria
62
Q

What is haemorrhagic exudate?

A

- Haemorrhagic exudate is a type of exudate that is bloody because of the large component of red blood cells released from ruptured blood vessels

  • It indicates that inflammation and significant vascular damage have occurred and is seen in destructive infections/malignant tumours
63
Q

What is serous exudate?

A

- Serous exudate is a clear exudate which contains plasma proteins but few leucocytes suggesting that there is no infection by micro-organisms

  • They are seen typically in blisters e.g. after a mild burn
64
Q

How do serous exudates differ from transudates and plasma?

A
  • Serous exudates differ from transudates because they contain plasma proteins
  • Serous exudates differ from plasma because they don’t contain fibrinogen
65
Q

What is a seroma?

A

A seroma is a tissue space filled with clear, sterile fluid that occurs as a post-operative complication

66
Q

What is fibrinous exudate?

A
  • Fibrinous exudate is a type of exudate where there is significant deposition of fibrin i.e. a blood clot without the RBCs
  • Can occur in the pericardial/pleural spaces preventing the serosal surfaces from sliding smoothly over each other creating a rubbing sound
67
Q

Identify 4 clinical examples of acute inflammation

A
  • Bacterial meningitis
  • Lobar pneumonia
  • Liver abscess
  • Acute apendicitis
68
Q

What is hereditary angio-oedema?

A

- Hereditary angio-oedema is an extremely rare autosomal dominant condition in which sufferers have an inherited deficiency of C1-esterase inhibitor

  • Patients have attacks of non-itchy cutaneous angio-oedema and experience recurrent abdominal pain due to intestinal oedema
69
Q

What is α1-antitrypsin deficiency?

A

- α1-antitrypsin deficiency is an autosomal recessive disorder resulting in low levels of alpha-1 antitrypsin, a protease inhibitor which deactivates enzymes released from neutrophils at the site of inflammation

  • Patients develop emphysema as proteases released by neutrophils within the lung destroy normal parenchymal tissue
70
Q

Explain how α1-antitrypsin deficiency can also present with liver disease?

A
  • Hepatocytes produce an abnormal version of the protein which is incorrectly folded
  • It polymerises and cannot be exported from the ER causing hepatocyte damage and eventually cirrhosis
71
Q

What is chronic granulomatous disease?

A
  • Chronic granulomatous disease is a genetic condition wherein phagocytes cannot form superoxide and initiate a respiratory burst
  • This results in many chronic infections in the first year of life as well as the formation of numerous granulomas and abscesses affecting the skin, lymph nodes, lung, liver and bones
72
Q

What is the difference between lobar and bronchopneumonia?

A
  • Lobar pneumonia affects all or part of a lobe with other areas generally normal
  • Bronchopneumonia has a patchy distribution and generally involves more than one lobe and often both lungs (seen in young & old patients)
73
Q

Identify the four pathological stages of lobar pneumonia

A
  • Congestion
  • Red hepatisation
  • Grey hepatisation
  • Resolution
74
Q

Identify 5 complications which can arise following lobar pneumonia

A
  • Bacteraemia (resulting in meningitis, arthritis or endocarditis)
  • Lung abscesses
  • Empyema
  • Pleural effusion
  • Lung fibrosis
75
Q

Outline congestion in lobar pneumonia

A
  • Vascular congestion
  • Lobe is heavy, red and boggy
  • Alveoli contains fluid, scattered neutrophils and many bacteria
76
Q

Outline red hepatisation in lobar pneumonia

A
  • Occurs after a few days
  • Affected lung has a liver-like consistency
  • Alveolar spaces are packed with neutrophils, red cells and fibrin
  • Fibrinous/fibropurulent exudate on the adjacent pleura
77
Q

Outline grey hepatisation in lobar pneumonia

A
  • Lung tissue is dry, grey and firm
  • Red cells get lysed
  • Fibrous exudate persists within alveoli
78
Q

Outline resolution in lobar pneumonia

A
  • Exudate is enzymatically digested and resorbed or expectorated
  • Basic architecture of the lung is left intact

Year 1 Semester 2 Pathological Processes (15 decks)

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