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MOD - Lecture 3 Flashcards

1
Q

Name 3 facts of acute inflammation

A

Evolves over hours or days
Innate
Stereotyped

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2
Q

How long does chronic inflammation take to evolve?

A

Weeks, months or years

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3
Q

What suffix is used to indicate inflammation of tissue or organ?

A

Itis e.g. Appendicitis

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4
Q

Describe acute inflammation

A

Rapid response that aims to deliver mediators of host defence
Most defensive agents circulate in the blood in active form
When needed, delivered and activated
Leave the blood at site of injury

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5
Q

Why is fluid delivered to site of injury before leucocytes?

A

Fluid - within seconds
Leuocytes - minutes

As leucocytes can’t just pour out of vessels

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6
Q

What causes acute inflammation? (6)

A 
Foreign bodies 
Immune reactions
Infections
Tissue necrosis 
Trauma 
Physical/chemical agents e.g burns, irritation
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7
Q

What are the clinical signs of acute inflammation? (5)

A 
Rubor = redness 
Calor = heat
Tumour = swelling
Dollar = pain
Loss of function - enforces rest and reduces chance of further damage
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8
Q

When does pain occur in acute inflammation?

A

When the specialised nerve endings are stimulated by mediators especially bradykinin

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9
Q

Why does swelling occur in inflammation?

A

Fluid and leucocytes take up space within the tissue

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10
Q

What forces are involved in Starlings Law equilibrium?

A

Capillary pressure
Interstitial free fluid pressure
Plasma colloid osmotic pressure
Interstitial fluid colloid osmotic pressure

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11
Q

Where is histamine stored?

A

Granules for mast cells, basophils and platelets

Histamine and serotonin are available immediately from preformed supplies

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12
Q

What does histamine produce in acute inflammation?

A

Pain
Arteriolar dilation
Venular leakage

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13
Q

How does histamine cause fluid leakage?

A

Causes endothelial cells to contract and pull apart.

This creates gaps through which plasma proteins can pass

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14
Q

How can you reduce pain and swelling?

Describe the mechanism.

What drugs are taken?

A

Block the production of prostaglandins

By inhibiting the enzyme (cyclo-oxygenase) that produces prostaglandins from arachadonic acid.

Aspirin
NSAIDs

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15
Q

What is the effect of bradykinin?

A

Pain

Increased vascular permeability

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16
Q

How does serotonin differ from histamine?

A

Serotonin produces fibroblasts

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17
Q

In relation to Starlings law, what is the main force driving fluid out of the vessels?

and back into the blood?

A

Hydrostatic pressure of the blood

Colloidal osmotic pressure of plasma proteins

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18
Q

How does excess fluid drain from the tissues?

A

Lympathics - excess fluid drawings from the tissues taking with it microorganisms and antigens which are presented to the immune system in the lymph nodes.

Lymph nodes draining a focus of inflammation can themselves become inflamed, swollen and painful. (Lympahedenitis)

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19
Q

What are the three defensive proteins in the exudate?

How do they work?

A

Opsonins - coat foreign material and make them easy to phagocytose.

Complement - proteins assembled locally to produce bacteria-perforating structure

Antibodies - bind to surface of microorganisms, also act as opsonins.

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20
Q

What is the protein rich and protein poor tissue fluid that develops in inflammation called?

A

Exudate - protein rich

Transudate - protein poor

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21
Q

Name the chemical mediators that induce vascular leakage?

A

Histamine & Serotonin (mast cells and platelets)
Bradykinin (formed from plasma precursor)
Complement components - C3a, C4a, C5a (formed form plasma precursors)

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22
Q

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

Where are they normally found?

What does their presence in the tissue indicate?

What type of cell are they?

A

Neutrophil
Blood or bone marrow
Invasion by bacteria or some other parasite or tissue injury
End cell - cannot multiply

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23
Q

What is chemotaxis?

A

Directional movement towards a chemical attractant

E.g. Clotting blood (fresh blood isn’t)
Activation of complement fragments C3a, C4a, C5a. All chemotactic - especially C5a.
Leukotriene produced by leucocytes

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24
Q

How does blood clot form? (3)

What enzyme breaks down a clot?

A

Plasma enzymes activate Thrombin
Thrombin acts on fibrinogen, converting it to fibrin (insoluble protein)
RBC become trapped in insoluble fibrin mesh which forms a clot.

Clots resolve when fibrin is broken down by proteolytic enzyme plasmin

25
What happens during activation?
Within 5 seconds of chemotaxis binding to cell surface receptors Calcium and sodium ions rush into the cells Cell swells Reorganises its cytoskeleton Activated cells are more sticky than normal cells
26
What is margination and what happens during margination? What happens to the number of selectins and activation of integrins during inflammation?
Leucocytes assume marginal positions in the vessels Leucocytes stick to the walls of venules Roll along the wall and become trapped, stop and crawl out of the vessel. They are trapped when their receptors bind to adhesion molecules Increase by inflammatory mediators and chemotaxis
27
What is diapedesis and describe.
Leucocytes dig their way out of vessels as they don't use the endothelial gaps Produce collagenase to digest basement membrane Move towards their target by pulling along collagen fibres of other tissue structures.
28
What substances make it easier for phagocytes to recognise target? Give two examples
Opsonins - plasma proteins IgG antibody - not present when bacteria is encountered first time C3b complement
29
What happens is opsonins are not present on the molecule to be phagocytosed?
Phagocyte will recognise microbial surface antigens
30
Describe phagocytosis
Phagocyte forms a crater shape around particle to be phagocytosed Crater forms a cup shape around particle, edges of the cup come together, plasma membranes fuse. Phagosome digests the particle Degranulation can occur before particle is completely enclosed and cause some bactericidal enzymes to leak into surrounding tissue = local tissue injury.
31
What two mechanisms kill organisms that have been phagocytosed?
Oxygen dependent - using free radicals = oxidative burst Oxygen independent - using enzymes e.g. Proteases, nucleases, phospholipases and lysozyme
32
What six steps does a neutrophil go through to kill bacteria?
Chemotaxis - summoned to place of injury Activation - switch to higher metabolism Margination - stick to endothelial lining Diapedesis - crawl through endothelium Recognition/attachment - recognise bacteria and attach Phagocytosis - engulf bacterium
33
What is a chemical mediator?
Produced in a focus of inflammation and modulates the inflammatory response
34
What are the two most common responses to mediators?
Motion | Secretion
35
What must every mediator have to ensure the inflammatory response is not on-going? Why is the duration of inflammation also limited?
Inhibitors Mediators have short half lives
36
What are the seven groups of endogenous mediators?
Vasoactive amines - histamine and serotonin Vasoactive peptides - bradykinin Complement components - C3a, C5a, generated from complement forming into tube. Clotting and Fibrinolytic cascades - generate inflammatory mediators Mediators derived from phospholipids e.g. Prostaglandins. Leukotriene B4 very powerful chemotactic agent Cytokines and chemokines - tumour necrosis factor Exogenous mediators e.g. Endotoxin
37
What is the difference between a cytokine and chemokines?
Cytokines - polypeptides produced by many cells and act as messengers between cells Chemokines - a group of cytokines involved in chemotaxis. Both have local and systemic effects.
38
What are the five main roles of inflammatory mediators?
Vasoidlation - histamine and serotonin Increased vascular permeability - histamine and serotonin get (mast cells and platelets) Prostaglandins Chemotaxis - Leukotriene B4, C5a, C3a, Chemokines Phagocytosis - C3b Pain - bradykinin, prostaglandins
39
What are the local complications of acute inflammation? (4)
Damage to normal tissue - secondary to substances produced by neutrophils Obstruction of tubes e.g. Fallopian or intestine and compression of vital structures e.g. Fluid accumulation in the brain Fluid loss - fluid accumulates until a point where it prevents further exudate on. Can continuously leak from a surface wound e.g. Burns Pain and loss of function
40
What are the four main systemic effects of acute inflammation? Why do they occur?
Fever - thermostat of the body is switched higher. Aspirin inhibit cyclo-oxygenase reducing fever Leucocytosis - Increase in no. Of circulation Leucocytes Acute Phase Response - change in level of some plasma proteins. Some produced in small amounts e.g. Albumin and others in larger amounts fibrinogen. Sleepiness and lack of appetite are a result of APR Shock - Blood stream inflammation can occur if bacteria or inflammatory mediators spread around body Inflammatory mediators enter the blood stream in significant amounts. Effects seen within one day
41
What is shock? Causes Effects Outcome
Inflammatory mediators spread around the body in the blood stream = inflammation throughout body Dramatic drop in BP due to widespread vasodilation Increase in vascular permeability - resultant fluid exudation Often fatal.
42
What is resolution of acute inflammation?
Vascular permeability returns to normal Neutrophils undergo apoptosis and phagocytosed Exudate is reabsorbed into venules or drained away in lymphatics Fibrin is degraded
43
What happens to tissue in resolution?
If damaged parenchymal cells can regenerate tissue will return to normal If regeneration cannot occur an extensive fibrous scar will form
44
What are the four types of exudate?
Pus/abscess - exudate creamy white rich in neutrophils Haemorrhagic - RBC's make it appear bloody to naked eye. Indicates as well as inflammation significant vascular damage has occurred Serous - Plasma proteins but few leucocytes suggest there is no infection. Clear - seen in blisters Fibrinous - Significant deposition of fibrin
45
How do serous exudates differ from transudates?
Serous - contain plasma proteins. Also differ from plasma as they don't contain fibrinogen Transudates - don't contain plasma proteins
46
What are the clinical examples of inflammation?
``` Bacterial meningitis Lobar pneumonia Ascending colangitis Liver abscess Acute appendicitis ```
47
What are the three disorders of acute inflammation?
Hereditary angio-oedema Alpha1-anti trypsin deficiency Chronic granulomatous disease
48
Describe hereditary angio-oedema
Rare autosomal dominant disorder Inherited deficiency of C1-esterase inhibitor Patients have non itchy cutaneous angio-oedema. Recurrent abdo pain Often a family history of sudden death
49
Describe alpha1-antitrypsin deficiency.
Autosomal recessive disorder with varying levels of severity Low levels of alpha-1-antitrypsin = a protease inhibitor which deactivates enzymes released from neutrophils at site of inflammation Develop emphysema - proteases released by neutrophils in the lungs act unchecked and destroy normal lung tissue Liver disease - hepatocytes produce abnormal version of protein which is incorrectly folded. Polymerises cannot be exported from ER - hepatocyte damage and eventually cirrhosis
50
What is chronic granulomatous disease?
Genetic condition Phagocytes unable to generate the free radical superoxide Bacteria is phagocytosed but phagocytes cannot kill them as they cannot generate an oxygen burst Results in formation of chronic infections in first year of life
51
What is a response to injury of living tissue? What is its purpose?
Inflammation - deliver defensive materials To protect body from infection Clear damaged tissue Initiate tissue repair
52
What type of respiration do neutrophils use?
Aerobic and anaerboic
53
How many nuclei do neutrophils have?
Single nuclei
54
What are all inflammatory cells derived from?
Bone marrow precursors
55
What do macrophages produce?
Interleukin - 1
56
What would happen to the CRP levels and plasma viscosity in acute inflammation?
CRP - Increase CRP is an acute phase reactant Plasma viscosity - increase in acute phase reaction
57
What are the causative organisms of: 1. Lobar pneumonia 2. Acute appendicitis 3. Bacterial meningitis 4. Ascending cholangitis/ Liver abscess
1. Pneumococci 2. Intestinal worms, foreign bodies trauma 3. Streptococcus. Young adults = Neisseriae meningitidis. Neonate a = Group B streptococci 4. Entercoli/Ecoli
58
What is ascending cholangitis?
Bacterial infection on an obstruction of the biliary tree commonly from a gall stone. Organisms migrate backwards up the bile duct as a result of partial blockage Symptoms - yellow discolouration of skin, fever, abdo pain Can be life- threatening Treatment - IV fluids and antibiotics
59
Why does acute inflammation occur?
To limit the tissue damage

Semester 2 (26 decks)

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