ic1 2013 - bed - bed revision lecture for moodle - updated

8/12/2019 IC1 2013 - BED - BED Revision Lecture for Moodle - UPDATED

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BED Revision Lecture

IC1 2013

Prof Mary LeaderBED

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Acute Inflammation

Definition response of tissue to cell damage

Professor Mary LeaderProfessor of Pathology

Royal College of Surgeons

Dublin and Bahrain

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Causes of Cell Necrosis

Ischaemia

Micro-organisms

Radiation

Hypersensitivity

Cold

Heat

Trauma

Chemicals

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Role of Inflammation

1. Contain and isolate injury

2. Destroy microorganisms

3. Inactivate Toxins

4. Prepare for tissue repair and healing

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Inflammation

Acute- minutes to days Immediate and early response to injury

Characterized by

fluid protein

Polymorphonuclear cells (neutrophils)

Chronic- weeks to years Cells (Lymphocytes and macrophages)

Granulation tissue

Define Granulation tissue? 6


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Acute inflammation Vascular & Cellular

Response

Components of acute inflammation

Vascular

Vasodilatation

Increased endothelial permeability. This allows

protein, fluid, polymorphs and monocytes into

the area of tissue damage

Cellular

Extravasation of neutrophils and monocytes

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Cellular response-

Leucocyte Function

Opsonisation-coating a bacterium or a particle

to facilitate its phagocytosis

Phagocytosis (to engulf and destroy cells and cell

constituents)

Release of leucocytes products/mediators with

effects on surrounding tissue (tissue injury)

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Exudate- Extravascular fluid with high protein

concentration

Exudate is the characteristic fluid of acuteinflammation

Transudate -Extravascular fluid with low proteinconcentration

Vascular permeability- osmotic

pressure

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Signals that attract leucocytes

Products of invading micro-organisms

Endogenous Compounds

4 plasma systems eg Complement, Kinin, Clotting,

Fibrinolytic

Vasoactive Compounds

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Chemical mediators of inflammation

Vasoactive amines eg histamine & heparin

Phospholipid-derived products

Arachnoid Acid metabolites

Platelet activating factor

Cytokines

Nitric oxide

Lysosomal enzymes

Oxygen derived free

radicals No need to know functionof each, just know they

are pro inflammatory 11


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Plasma Proteases:These are 4 interrelated

systems that are activated in inflammation

Complement system

Kinin system

Clotting system

Fibrinolytic System

What are the functions of complement and

kinins?

What activates complement?

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The Complement System

Cascade of 20 proteins activated by 2 Pathways

ClassicalAg/Ab

ComplexAlternate

1. Lipopolysaccharide from cell wall

2. Ig A

3. Ig E

4. Plasmin

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Functions of Complement proteins

Chemotaxis

Opsonization

PhagocytosisCell Lysis

Vascular permeability

Anaphalotoxins

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The Kinin System

Function: Change the tone of the blood vessel

wall

Cascade commences with activation of

Hageman Factor

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Beneficial effects of inflammation

Contain and isolate injury

Destroy microorganisms

Dilute toxins

Arrival of antibodies to the site ofinflammation

Drug transport

Delivery of nutrients and oxygen

Prepare for healing and repair

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Outcome of Acute Inflammation

Complete Resolution

Healing by Scarring

Abscess Formation

Progression to Chronic Inflammation

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Chronic Inflammation

Definition:

Inflammation of prolonged duration in whichactive inflammation, tissue destruction and

attempts at repair are proceeding

simultaneously.

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Chronic Inflammation

Tissue infiltrated by:

LymphocytesPlasma cells

Macrophages

Granulation tissue

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What is granulation tissue?

Newly formed blood vessels and chronicinflammatory cells.

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Causes of Chronic Inflammation

Progression from Acute Inflammation

Following repeated bouts of Chronic Inflammation

Primary Chronic Inflammation

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Macrophages

Central character in Chronic Inflammation.

Functions Phagocytosis

Secretion : oxygen metabolites,

proteases, cytokines, chemotacticfactors, growth factors.

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LymphocyteMacrophage Relationship

Lymphocytes are activated by antigen presentedby macrophages.

Lymphocytes consequently producelymphokines.

Lymphokines stimulate macrophages to further

stimulate macrophages to present antigen and

secrete mediators

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Granulomas

Localised collection of Histiocytes and macrophages.

Causes of granuloma formation.

o TB

o Fungal infections

o Sarcoidosis

o Foreign material

o Response to tumourso Type IV Hypersensitivity reactions.

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Systematic Effects of Inflammation.

o Pyrexiapolymorphs and macrophagesproduce pyrogens which act on thehypothalmus

o Constitutional symptomsmalaise, anorexia,nausea

o Weight Loss

o Reactive hyperplasia of mononuclearphagocytic systemnodes

o Haematological changesincreased ESR,wcc, anaemia, amyloidosis.

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Morphologic patterns in acute and

chronic inflammation

Serous inflammation

Fibrinous inflammation

Suppurative inflammation Ulcers

Sinus

Fistula

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Serous inflammation

Accumulation of thin fluid derived from the blood

serum or secretion of mesothelial lining

Effusion

Peritoneal Pleural

Pericardial

Skin blisters

Viral infection

Burn

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Fibrinous inflammation

Accumulation of fluid and fibrin

Body cavities

May be removed by fibrinolysis (resolution) Organisation

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Suppurative inflammation

Characterised by large amounts of pus

Can be seen in association with certain

organisms (staphylococcus)

May lead to abscess formation

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Abscess

Localised collection of pus

Dead and degenerate leucocytes

Dead and degenerate host tissue cells

Oedema fluid

Dead microorganisms

Empyema

Localised collection of pus in a cavity eg pleura,

gallbladder

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Ulcer

Local defect in an epithelial surface

They are distinguished from erosions by the

extent of tissue loss

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Sinus

Is a tract lined by granulation tissue leading

from a chronically inflamed cavity to a surface

eg

Sinuses associated with osteomyelitis

Pilonidal sinus

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Fistula

Is a track open at both ends, with abnormal

communication between two surfaces

Gastrointestinal fistula in Crhons disease

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Wound healing

Types of wound healing

Primary intention

Secondary intention

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Wound with apposed edges Minimal loss of tissue

Surgical incision or clean wound

Primary intention

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Large gaping wound

Extensive loss of cells

Infarction Ulcer

Abscess

Secondary intention

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Pathologic aspects of wound healing

Deficient scar formation

Wound rupture

Excessive scar formation

Keloid

Contracture deformity

Malignant transformation (v. very rare)

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Factors that influence healing

Local factors

Systemic factors

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Factors which impair bone healing

Movement

Poor approximation

Poor blood supply

Infection

Steroids

Poor nutrition Interposition of soft tissue

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Systemic factors

Age

Nutrition (protein, Vit. C)

Metabolic status (Diabetas Mellitus)

Hormones (steroids)

Malignancy

Chemotherapy Radiotherapy

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Steps in Repair

Formulation of new vessels, migration andproliferation of fibroblasts.

Deposition of extra cellular matrix.

Maturation and organisation of fibrous tissue.

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Necrosis

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Necrosis

Definition: cell death in living tissue

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Atoptosis

Programmed cell death in living tissue

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Causes of Necrosis

Ischaemia

Microorganisms

High or low temperature

Chemicals

Hypersensitivity

Radiation Drugs

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Inflammation is the bodys response to

Necrosis

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Types of Necrosis

Coagulativecell outlines visible

Caseousno cell outlines

Liquifactivebrain

Fibrinoidassociated with fibrin deposition

Fat Necrosis

Gangrenous (ischaemia and anaerobic organisms)

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Bodys response to Apoptosis no

inflammation

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Ischaemia Reperfusion Injury

Causes

Oxygen radicals during reoxygenation damage

the mitochondrial membrane Xss Oxygen radicals are toxic to the cell

Cytokines from adjacent dead cells attract

polymorphs

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OEDEMA (EDEMA)

Definition is an increase in interstitial water.

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ECF

l m

3 litres 9 litres of

Intravascular fluid Interstitial fluid

(plasma high ) (low protein

content) content)

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ECF contains practically all body sodium,

whereas intracellular fluid has a high

potassium and magnesium concentration.

Interstitial fluid has a low colloidal osmotic

pressure.

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Fluid collections in body cavities

Hydrothorax

Hydropericardium

Hydroperitoneum (ascites)

More commonly referred to as effusions

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Hydrostatic pressure pushes fluid out of vessel

Oncotic pressure -due to high protein in vessel

-pulls fluid into vessel. Lymphatics also play a

role in removal of interstitial fluid.

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Factors which cause oedema

Inflammation

Increased Hydrostatic Pressure in Vessels

Local or generalised venous obstruction

Na & Water retention

Lymphatic Obstruction

Low intravascular protein levels

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Reduced plasma osmotic pressure

Liver Failure

Nephrotic Syndrome

Protein losing enteropathy

Starvation

Malabsorption

Burns

ic1 2013 - bed - bed revision lecture for moodle - updated

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