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Semester 2 - PathPro > 3. Acute inflammation > Flashcards

3. Acute inflammation Flashcards

1
Q

What is inflammation?

A

The response of living tissue to injury

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2
Q

What are the aims of inflammation?

A

Its purpose is to deliver defensive materials (white blood cells and fluid containing plasma proteins) to a site of injury.
It aims to protect the body against infection, particularly bacterial infection, and to clear damaged tissue and initiate tissue repair.

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3
Q

What are the features of acute inflammation?

A
  • Immediate
  • Short duration
  • Innate
  • Limits damage
  • Stereotyped (always same ie non specific)
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4
Q

What are the major causes of acute inflammation?

A

• Foreign bodies (splinters, dirt, sutures)
• Immune reactions
• Infections (bacterial, viral, parasitic) and microbial toxins
• Tissue necrosis (any cause)
• Trauma (blunt and penetrating)
• Physical and chemical agents (e.g., thermal injury, e.g., burns or
frostbite, irradiation, environmental chemicals).

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5
Q

What are the two phases of acute inflammation?

A

vascular phase

cellular phase

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6
Q

What is acute inflammation controlled by?

A

Chemical mediators

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7
Q

What is the disadvantage of acute inflammation?

A

Can cause local and systemic complications

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8
Q

What is the goal of the vascular and cellular phase of inflammation?

A

Vascular = accumulation of exudate (through changes in blood flow)

Cellular = delivery of neutrophils

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9
Q

What are the clinical signs of acute inflammation?

A 
Rubor - redness
Tumor - swelling
Calor - heat
Dolor - pain
Loss of function
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10
Q

Describe the changes in blood flow seen in the vascular phase?

A

1) Trigger
2) Vasoconstriction (seconds)
3) Vasodilatation (minutes ie more prolonged)—-> calor+rubor
4) Increased permeability (leaky) - fluid/proteins/cells escape

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11
Q

What is Starling’s Law in relation to movement of fluid?

A

Movement of fluid is controlled by the balance of hydrostatic and oncotic pressure. These pressures exist in the vessels and interstitum

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12
Q

What is interstitium?

A

Fluid outside blood vessels and between cells

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13
Q

What is the difference between hydrostatic and oncotic pressure

A 
Hydrostatic = pressure exerted on a vessel wall BY FLUID. Pushes fluid away.
Oncotic = pressure exerted BY PROTEINS. Draws fluid towards proteins.
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14
Q

What is the function of vasodilation?

A
  • increased blood flow so increased capillary hydrostatic pressure
  • forces fluid out into interstitium
  • Also increases the delivery of fluid and leucocytes to the area of injury
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15
Q

what is the function of increased vessel permeability?

A
  • Plasma proteins move into interstitium

* Increased interstitial oncotic pressure

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16
Q

what is the combined result of vasodilation and increased vessel permeability?

A
  • Fluid movement OUT of vessel INTO interstitium

* OEDEMA (swelling/tumor)

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17
Q

Describe the role that histamine has in inflammation

A
  • Histamine is a vasoactive mediator.
  • It’s already present within cells and tissues in around the damage site.
  • Histamine is stored in granules of mast cells, basophils and platelets.
  • It is released in response to many stimulation e.g physical damage, immune reactions and complement components.
  • In acute inflammation histamine is used to produce pain, arteriolar dilation and venule leakage ( increased permeability).
  • The fluid leakage occurs as histamine causes endothelial cells to contract and pull apart, this then creates the gaps through which plasma proteins can get through.
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18
Q

Describe the role that Serotonin has in inflammation

A

Serotonin is very similar to histamine.
It’s also a vasoactive mediator and is stored in the granules of platelets.
It also causes pain, arteriolar dilation and venular leakage

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19
Q

Provide the function of prostaglandins and bradykinins in acute inflammation

A
  • Prostaglandins are produced in inflammation from the phospholipids in cell membranes. These are also used to cause vasodilation.
  • They also make the skin more sensitive to pain and cause fever.
  • The production of prostaglandins can be inhibited by NSAIDs and aspirin. This can then reduce swelling and pain.

• Bradykinin is also a vasoactive mediator, it’s used to produce pain and increased vascular permeability.

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20
Q

What are the consequences of fluid moving out of the vessels?

A

The movement of fluid out of the vessels and into tissues will mean that the blood left in the vessels sill be a lot thicker, you’ll have an increased viscosity of blood.

Due to this increase viscosity blood will have difficulty in flowing causing reduced flow through vessels. This is known as stasis.

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21
Q

What is the advantage of increased vessel permeability and vasodilation?

A

As well as delivering plasma proteins to the site of injury, the abundant tissue fluid has another important
function. Excess fluid drains from the tissues in the lymphatics taking with it micro-organisms and antigens which are thus presented to the immune system within the lymph nodes

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22
Q

What is exudate?

A
  • increased vascular permeability
  • protein rich fluid (delivers proteins to area of injury)
  • occurs in inflammation
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23
Q

What is transudate?

A
  • vascular permeability unchanged
  • low protein content
  • fluid movement due to increased capillary hydrostatic pressure and reduced capillary oncotic pressure
  • occurs in heart failure/ hepatic failure/ renal failure
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24
Q

What are the defensive proteins in exudate?

A
  • Opsonins – which coat foreign materials and make them easy to phagocytose.
  • Complement – a group of proteins that are assembled locally to produce a bacteria-perforating structure
  • Antibodies – bind to the surface of micro-organisms and also act as opsonins.
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25
Q

How does a vessel wall become permeable ?

A
  1. Retraction of endothelial cells due to the action of vasoactive mediators e.g histamine, NO, bradykinin
  2. Direct injury to the site e.g due to burns, toxins and direct trauma.
    The endothelial cells get damaged and allow proteins and vessels to escape.
  3. Leukocyte dependent injury
    Here there are enzymes/ toxic oxygen species released by activated inflammatory cells. This can then cause the increase in permeability of the vessel walls.
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26
Q

How is the vascular phase effective?

A
  1. Interstitial fluid
    The increase in interstitial fluid dilutes the toxins from the injury and reduces the risk of damage.
  2. The exudate
    This delivers proteins to the site of injury.
    One example would be fibrin which creates a mesh and limits the spread of the toxin.
    As well as this it also brings immunoglobulin(released by lymphocytes) proteins to the site which allows for targeted destruction of pathogens.
  3. Fluid drains to the lymph nodes
    This means that antigens and toxins will be delivered to the lymph nodes, detected and this stimulates the adaptive immune response. Proliferation of lymphocytes in lymph nodes
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27
Q

What are the chemical mediators that induce vascular leakage ?

A

histamine and serotonin, bradykinin and the complement components C3a, C4a and C5a

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28
Q

Give the features of neutrophils

A

Neutrophils are a primary type of leucocyte (WBC) and are involved in acute inflammation.

They have a trilobed nucleus in their structure. They’re granulocytes so contain granules in their cytoplasm.

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29
Q

What does the presence of neutrophils in tissue indicate?

A

Neutrophils are usually found in the blood and the bone marrow which means that their presence in the tissue will indicate invasion by bacteria and or tissue injury.

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30
Q

What is the lifespan of neutrophils?

A

They only have life span of 12-20 hours are an end cell meaning they can’t multiply.
Each neutrophil contains about 2000 granules which themselves contain bactericidal substances.

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31
Q

List the 6 process that must occur to allow a neutrophil to capture and kill a bacterium in tissue space

A
  1. Be summoned to the place of injury = chemotaxis
  2. Switch to a higher metabolic level = activation
  3. Stick to the endothelial surface = margination
  4. Crawl through the endothelium = diapedesis
  5. Recognise the bacterium and attach to it = recognition-attachment
  6. Engulf the bacterium = phagocytosis
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32
Q

How do neutrophils leave blood vessels?

A
  • Marginate to edge
  • Roll - weak intermittent binding
  • Adhesion - to endothelium
  • Emigration/ diapedisis - escape the endothelium
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33
Q

What is chemotaxis

A

Movement along an increasing chemical gradient of chemoattractants

34
Q

Describe the process of chemotaxis in acute inflammation

A
  • Neutrophils move up a chemotactic gradient
  • Chemotaxins include bacterial peptides, injured tissues, substances produced by leucocytes - inflammatory mediators (C5a, LTB4), and spilled blood(Fresh blood isn’t chemotactic but clotted blood is.).
35
Q

Describe the process of activation in acute inflammation

A
  • Within five seconds of the chemotaxin binding to the cell surface receptors, calcium and sodium ions rush into the cell, it swells and reorganises its cytoskeleton assuming a roughly triangular shape pointing in the direction of the chemotactic stimulus.
  • Within 5-10 seconds the cell sends out pseudopodia.
  • Activated cells are stickier than normal cells.
36
Q

Describe the process of marination, rolling and adhesion in acute inflammation

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.
• Leucocytes are trapped when their receptors bind to adhesion molecules (called selectins and integrins)
on the endothelium.
• When the leucocytes roll along the endothelium they are binding to selectins, when they adhere and stick firmly they are binding to integrins such as ICAM-1 (intercellular adhesion molecule-1).
• The number of selectins and the activation of integrins are increased by inflammatory mediators and chemotaxins.

37
Q

What are the 2 adhesion molecules? Describe their roles

A 
Selectins
• Expressed on activated endothelial cells
• Cells activated by chemical mediators
• Responsible for “rolling”
Integrins
• Found on neutrophil surface
• Change from low affinity to high affinity state
• Responsible for “adhesion”
38
Q

Describe the processes of diapedesis in acute inflammation

A
  • Leucocytes ‘dig’ their way out of the venules, they don’t use the endothelial gaps through which the exudate escapes.
  • They produce collagenase which digests the basement membrane.
  • Once in the extravascular space the leucocytes move towards their target by pulling themselves along collagen fibres of other tissue structures.
39
Q

What Do Neutrophils Do?

A

• Phagocytosis
- engulf pathogen and form Phagosomes which fuse with lysosomes and Produce secondary phagolysosomes, where the pathogen is degraded by enzymes and then released out by exocytosis as soluble debris - degranulation process
• Also release inflammatory mediators

40
Q

How Do Neutrophils Recognise What To Phagocytose?

A
  • Opsonins are substances which make it easier for phagocytes to recognise targets, attach to them and then phagocytise them.
  • Opsonins are plasma proteins.
  • They include:
  • IgG antibody – this is the most important opsonin but it will not be present when a bacterium is encountered for the first time.
  • C3b fragment of complement – this is released when complement system is activated.
  • Toxin covered in C3b and Fc (opsonins)
  • Receptors for C3b and Fc on neutrophil surface
  • If opsonins are not present then the phagocyte recognises microbial surface antigens.
41
Q

How Do Neutrophils Destroy Pathogens?

A

Organisms that have been phagocytised can be killed by two mechanisms:
• Oxygen-dependent – using oxygen derived free radicals (hydrogen peroxide (H2O2), superoxide anion (O2-) and hydroxyl (OH.)) which are released into the phagosome. This mechanism of killing is called the oxygen burst or respiratory burst.
• Oxygen-independent – using enzymes, e.g., proteases,
phospholipases, nucleases and lysozyme

42
Q

Do neutrophils only damage pathogens?

A

NO

activated neutrophils may also cause damage to host tissue

43
Q

How is the cellular phase effective?

A
  • Removal of Pathogens and Necrotic tissue

* Release Inflammatory Mediators

44
Q

What are chemical mediators?

A

A mediator is any molecule that is produced in a focus of inflammation and modulates the inflammatory response in some way. Motion (contraction or relaxation of vascular smooth muscle cells, contraction of venular endothelial cells, movement along a chemotactic gradient and phagocytosis by neutrophils) and secretion are common responses to mediators.

45
Q

What are the groups of chemical mediators?

A
  • Vasoactive amines, e.g., histamine and serotonin
  • Vasoactive peptides, e.g., bradykinin
  • Complement components, e.g., C3a, C5a.
  • Clotting and fibrinolytic cascades – both these processes generate inflammatory mediators
  • Mediators derived from phospholipids – prostaglandins, thromboxanes and leukotrienes
  • Cytokines and chemokines, e.g., interleukins, tumour necrosis factor (TNF), interferons
  • Exogenous mediators of inflammation, e.g., endotoxin produced by gram negative bacteria
46
Q

What is the function of complement components

A

The function of complement is to form a tube (called the membrane attack complex) which punches holes in bacteria thus causing them to die. It circulates in the blood as a number of disassembled proteins. When it assembles into its tube structure it generates, as by products , some powerful inflammatory mediators (C3a, C5a)
and also the opsonin C3b

47
Q

What are chemokines and cytokines?

A
  • Cytokines are polypeptides that are produced by many cells and act as messengers between cells.
  • Chemokines (short for chemotactic cytokines) are a group of cytokines which are involved in chemotaxis.
  • Many cytokines are produced by macrophages and they start to appear in the hours following injury.
  • They have both local and systemic effects.
48
Q

Where do chemical mediators originate from?

A
  • Activated inflammatory cells
  • Platelets
  • Endothelial Cells
  • Toxins
49
Q

Main roles and main sources of inflammatory mediators in acute inflammation?

A
  • Vasodilatation – histamine and serotonin (from mast cells and platelets), prostaglandins (from many cells).
  • Increased vascular permeability – histamine and serotonin, bradykinin (from the plasma precursor kininogen).
  • Chemotaxis – leukotriene B4 (from leucocytes), C5a and C3a (from complement plasma precursors), chemokines (from leucocytes and other cells), bacterial products (from bacterial metabolism).
  • Phagocytosis – C3b (from complement plasma precursor).
  • Pain – bradykinin, prostaglandins .
50
Q

What are Local Complications of Acute Inflammation?

A
  • Damage to normal tissue – secondary to substances produced by neutrophils and released during the process of phagocytosis.
  • Obstruction of tubes, such as the intestine or Fallopian tubes, and compression of vital structures – secondary to the swelling produced by the inflammatory exudate.
  • Loss of fluid – in tissue spaces as fluid accumulates the tissue pressure increases until it reaches a level that prevents further exudation. However, fluid can continuously leak from a surface wound. For this reason, extensive skin wounds, such as burns, result in the loss of very large amounts of fluid.
  • Pain and loss of function
  • Exudate- Compression of organs E.g. cardiac tamponade
51
Q

What are systemic Complications of Acute Inflammation?

A
  1. Fever
  2. Leucocytosis
  3. The Acute Phase Response
  4. Septic Shock
52
Q

Describe how acute inflammation can lead to fever

A

Macrophages when they are stimulated to do so by exogenous (bacterial) pyrogens (particularly endotoxin) produce pyrogenic cytokines, e.g., TNF, interleukin-1. These cytokines cause an increase in synthesis of prostaglandin E2 within the anterior hypothalamus which alters temperature

53
Q

Describe how acute inflammation can lead to Leucocytosis

A

In leucocytosis the number of circulating leucocytes increases. Neutrophilia is seen during bacterial infection. Macrophages and endothelial cells in injured tissues produce colony stimulating factors and
these stimulate the bone marrow to produce more neutrophils.
Bacterial = neutrophils
Viral = lymphocytes

54
Q

Describe how acute inflammation can lead to Acute phase reaction

A

• The acute phase response is a change in the levels of some plasma proteins that is seen because the liver changes its pattern of protein synthesis.
• Some proteins are produced in smaller amounts by the liver, e.g., albumin, and others are produced in larger
amounts(acute phase proteins), e.g., FIBRINOGEN (needed for blood coagulation), ceruloplasmin (a free radical scavenger), C3 (a protein of the complement system), alpha-1 ANTITRYPSIN (a protease inhibitor), C-REACTIVE PROTEIN (CRP, an opsonin).
• The acute phase response is produced by cytokines released during inflammation.
• The sleepiness, lack of appetite, tachycardia, Malaise that are seen in serious injury are a result of the acute phase response - induces rest

55
Q

Describe how acute inflammation can lead to septic shock

A

If bacterial products or inflammatory mediators spread around the body in the blood stream inflammation can occur throughout the body. This results in shock. Shock is a dramatic drop in blood pressure (Hypotension, tachycardia) due to widespread vasodilatation and increase in vascular permeability with resultant fluid exudation. It is often fatal as multi organ failure.

56
Q

What happens after acute inflammation?

A

1 - Complete resolution
2 – Repair with connective tissue (fibrosis)
If there has been substantial tissue destruction
3 – Progression to chronic inflammation
Prolonged inflammation with repair

57
Q

How does complete resolution occur?

A
  • Mediators have short half lives
  • Diluted/inactivated/degraded
  • Vessel calibre and permeability returns to normal
  • Neutrophils undergo apoptosis and get phagocytosed
  • Exudate drained via lymphatics
  • If tissue architecture is preserved, can undergo regeneration
58
Q

What are the 3 types of exudate?

A
  1. Pus/abscess
  2. Haemorrhagic exudate
  3. Serous exudate
  4. Fibrinous exudate
59
Q

Describe pus/abscess

A

exudate is creamy/white as it is rich in neutrophils - typical of infections by chemotactic bacteria

60
Q

Describe Haemorrhagic exudate

A

A haemorrhagic exudate contains enough red blood cells to appear bloody to the naked eye. It indicates that as well as inflammation significant vascular damage has also occurred. It is seen in destructive infections or when the exudate is a result of infiltration by a malignant tumour

61
Q

Describe Serous exudate

A

Serous exudates contain plasma proteins but few leucocytes suggesting that there is no infection by micro-organisms. They are clear and are seen typically in blisters, e.g., after a mild burn. Note serous exudates differ from transudates because they contain plasma proteins and they differ from plasma because they don’t contain fibrinogen.

62
Q

Describe fibrinous exudate

A

In a fibrinous exudate there is significant deposition of fibrin (i.e., a blood clot without the red blood cells). When fibrinous exudates occur in the pericardial or pleural spaces the fibrin that is deposited means that the serosal surfaces no longer slide smoothly over each other. This results in friction between the serosal surfaces which can be heard as a rubbing sound.

63
Q

How does the appendix appear in acute appendicitis?

A
  • swollen
  • discoloured red/ yellow
  • pus due to exudate
  • can see vasculature of vessels
64
Q

Why can a perforation in the wall of the appendix occur in acute appendicitis?

A

As inflammatory cells (neutrophils) release enzymes to attack bacteria, these enzymes can attack own body tissue to form a hole

This can lead to peritonitis as faecal matter can leak into the peritoneum

65
Q

What do NSAIDS do?

A

Non- steroidal anti-inflammatory drugs that block cyclo-oxygenase enzymes involved in the production of prostaglandins e.g aspirin

66
Q

What happens in appendicitis?

A
  • Blocked lumen by faecolith
  • accumulation of bacteria + exudate
  • increased pressure —> perforation
67
Q

What are the main causative organisms of pneumonia?

A

Streptococcus pneumoniae

Haemophilus influenzae

68
Q

What are the symptoms of pneumonia?

A

SOB, cough, sputum, fever

Due to build up of exudate in lungs

69
Q

What are risk factors for pneumonia?

A

Smoking, pre- existing lung condition e.g. COPD, asthma, malignancy

70
Q

What is meningitis caused by?

A

Accumulation of exudate in meningeal space

Many causative organisms: inc Group B streptococcus, E.Coli and neisseria meningitides

71
Q

What is meningitis?

A

Inflammation of meninges

72
Q

What are symptoms of meningitis?

A
  • Headache
  • Neck stiffness
  • Photophobia
  • Altered mental state
73
Q

What are the four stages of lobar pneumonia?

A

1) Congestion (24 hours): lots of bacteria, increase in neutrophils , proteinacious exudate makes lung heavy, vascular dilation to let in WBCs so lung looks more red than usual
2) Red hepatization (2-3 days): lots of RBCs, further increase in neutrophils , fibrin starts accumulating, exudate on pleura outside of lung - red, firm lobe(liver like)
3) Gray hepatization (4-6 days): firm grey lung, inflammation turned chronic, exudate containing neutrophils and fibrin, RBCs start to break down
4) Resolution: looks back to normal, exudate has been broken down/ digested/ reabsorbed by enzymes (sometimes coughed up as sputum)

74
Q

What is Hereditary angio-oedema?

A
  • rare autosomal dominant condition
  • sufferers have an inherited deficiency of C1-esterase inhibitor (a component of the compliment system). - can be reduced levels or normal levels but reduced function
  • Reduced C2 and C4 levels but normal C3
  • No uriticaria or hives
  • Patients have attacks of non-itchy cutaneous angiooedema (rapid oedema of the dermis, subcutaneous tissue, mucosa and submucosal tissues).
  • They also experience recurrent abdominal pain which is due to intestinal oedema.
  • There is often a family history of sudden death which is due to laryngeal involvement
75
Q

What is chornic granulomatous disease?

A
  • In this genetic condition phagocytes are unable to generate the free radical superoxide as genetic deficiency in one of the components of NADPH oxidase responsible for generating superoxides
  • Bacteria are phagocytised but the phagocytes cannot kill them as they can’t generate an oxygen burst.
  • This results in many chronic infections in the first year of life.
  • Numerous granulomas and abscesses affecting the skin, lymph nodes, and sometimes the lung, liver and bones occur, however they are ineffective at eliminating the infectious agents
  • Can be X-linked or autosomal recessive
76
Q

What is alpha-1 antitrypsin deficiency?

A

• autosomal recessive disorder with varying levels of severity
• there are low levels of alpha-1 antitrypsin, a protease inhibitor which deactivates enzymes released from neutrophils at the site of inflammation.
• Patients with the disorder develop emphysema as proteases released by neutrophils within the lung act unchecked and destroy normal parenchymal tissue.
• Liver disease also occurs as the hepatocytes produce
an abnormal version of the protein which is incorrectly folded.
• It polymerises and cannot be exported from the endoplasmic reticulum.
• This causes hepatocyte damage and eventually cirrhosis.

77
Q

What is an abscess?

A
  • Accumulation of dead and dying neutrophils
  • With associated liquefactive necrosis
  • Can cause compression of surrounding structures:
  • Pain
  • Blockage of ducts
78
Q

What are the names when Exudate pours into serous cavities?

A
  • Pleural space - Pleural effusion
  • Peritoneal space- Ascites
  • Pericardial space - Pericardial effusion

• variety of causes

79
Q

How can gallstones lead to an abscess?

A
  • cause obstruction of bile duct
  • stagnant bile can become infected with bacteria from the bowel
  • results in inflammation of bile ducts
  • infection and inflammation can spread up the bile ducts to the liver where an abscess can form!
80
Q

What is peritonitis?

A

acute inflammation of the peritoneum

Semester 2 - PathPro (16 decks)

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