Inflammation Flashcards
3 lines of defence
1- skin and mucous membranes
Skin is physical barrier and waterproof
Mucous membranes secrete things and trap viruses and bacteria
Eg, tears wash away particles, eyelashes trap particles, blink reflex, enzymes neutralise harmful substances and skin stops entry of pathogens
2- inflammation
Non-specific, natural, innate immunity and rapid response
3- immunity
Specific, acquired immunity, adaptive and slow response
Define inflammation
Body’s non specific protective response to tissue damage, disease or injury in attempt to destroy, dilute or wall off injurious agent and injured tissue
5 cardinal signs of inflammation
Acronym: We See Really Painful Legs
Warmth / calor - increased blood flow, either specific or whole body (Pyrexia)
Swelling/ tumor- oedema, leaky fluid
Redness/ rubor- increased blood flow
Pain/ dolor - locally by compression of nerve endings + chemical release
Loss of function / function leasa
Why do we have inflammation?
Prevents minor infections from becoming unmanageable
Prepares damaged tissue for repair
5 factors that cause inflammation
Injury / trauma- physical (sports), thermal (ice burns), radiation (flash burns), electrical and chemical
Infection- virus, bacterium, rickettsiae, fungi, Protozoa or worms
Infarction- lack of oxygen to damaged tissue eg, MI leads to ischaemia
Immune reactions- foreign protein hypersensitivity like allergies and auto immune conditions like RA or ankylosing spondylitis or chrons disease
Nutrient deprivation
ITIS
Means inflammation
Eg Conjunctivitis - eye inflammation Arthritis- inflammation in joints Tendinitis- inflamed tendons Appendicitis - inflamed appendix Peritonitis - inflamed abdominal cavity Pericarditis- inflamed heart Capsulitis - inflamed capsules of joints
Mechanism of inflammation
Vicky Can’t Pick Lemons
Vascular response- changes in blood flow and protein rich exudation
Cellular response - leucocyte emigration
Phagocytosis - starts clear up process of causative agent
Lymphatic drainage - rid of excess fluid and gives protection
Steps in vascular response
TRANSIENT VASOCONSTRICTION- few seconds
MORE PROLONGED VASODILATION
INCREASE BLOOD FLOW AND HYDROSTATIC PRESSURE
OPENING OF CAPILLARY BEDS
INCREASED VASCULAR PERMEABILITY
BRADYKININ- amino acid so Capillary endothelium retracts (crenallation). Causes muscles in blood vessel walls to constrict so gaps are larger in vessels.
Leaking plasma- protein rich exudate
Oedema formation - fluid retention at injury site
Haemoconcentration - more proteins lost from blood , blood gets thicker and more concentrated
Stasis - blood flow slows and then stops
Cellular response
Basically, neutrophils get to site first, they are small and travel quickly in blood. Drawn by chemotaxis. Neutrophils also produce chemotactic chemicals.
then monocytes, which last longer but take longer to arrive as larger
Turns into macrophages
WBC travel on inside normally
Chemotaxis - WBCs to rim of vessel in MARGINATION
Endothelial cells positive charge and WBC negative
ROLL of WBCs as cant move smoothly
ADHESION- WBCs stick to vessel walls
PAVEMENTING- Flattens WBCs at walls
All due to chemotaxis
WBCs struggle to get through gaps in blood vessels and form projections called pseudopods
WBCs wriggle in amoeboid actions
WBCs pass through gaps by emigration and diapedesis cell walking (from blood vessel into extracellular fluid to site of injury)
Chemotaxis encourages more WBCs to area to destroy damaged cells or pathogen
Phagocytosis
Neutrophils and monocytes become macrophages at injury site
Macrophage ingests + destroys antigen, remove damaged tissue etc.
Macrophages die in process
This is non specific
Lymphatic drainage
Lymph system beside vascular, runs through lymph nodes like femoral triangle, popliteal fossa, cubital fossa etc.
Lymphatic system drains tissue fluid, products of inflammation and antigens not dealt with
Antigen presenting cells present to immunity - 3rd line of defence
WHY RUBOR?
Increased blood flow to area via vasodilation
Why calor?
More blood flow to area via vasodilation. It can be local or pyrexia (whole body increases in temperature)
Function leasa
Because of tissue damage, swelling and pain
Dolor
More vascular permeability and fluid = compressed tissue and compresses nerves. Chemical mediators elicit pain on nerve endings
Pain prevents more inflammation
Diabetics have reduced pain
Tumor
Increased vascular permeability of vessels
Extra cellular fluid accumulates in tissues to form an oedema
Blood tests that detect inflammation
HIGH WHITE BLOOD CELL COUNT (leucocytosis) above 10,000 mm2
WHITE BLOOD CELL DIFFERENTIAL- proportions of different WBCs . In inflammation proportion of immature neutrophils increases more than others,
ERYTHROCYTES SEDIMENTATION- red blood cells sediment. With inflammation, more fibrinogen causes clumping of RBCs. So RBCs sediment at faster rate. Above 100mmhr
C REACTIVE PROTEIN- protein produced by liver in acute inflammation more than 10mg/L
COMPLIMENT ACTIVITY- activation of compliment in inflammation. Over time this may decrease as compliment factors exhausted.
PROTHROMBIN TIME- increased prothrombin means reduced time to coagulate
FIBRINOGEN- elevated during inflammation to promote coagulation
CAUSE OF ACUTE INFLAMMATION
Often known like trauma, surgery or antigen invasion
CAUSES OF CHRONIC INFLAMMATION
Often unknown, like unresolved acute or persistent irritants
Onset of acute
Rapid onset
Onset of chronic
Slow
Deterioration of acute inflammation
Rapid acute response (VCPL)
Exudate formation
Deterioration of chronic
Slow and lack of acute response
Proliferation of fibroblasts
Resolution of acute
Fully resolved
Resolution of chronic
Fails to resolve
Course of acute
Definite course
Course of chronic
Slow unremitting
Main cells in acute
Neutrophils, monocytes and macrophages
Main cells I chronic
Macrophages and fibroblasts
Acute phagocytosis
Active phagocytosis
Phagocytosis of chronic
Irritant resistant to phagocytosis
Ongoing chemotaxis
Outcome of acute
Beneficial
Prevent invasion
1st stage of tissue repair
Outcome of chronic
Destructive scar tissue
Loss of movement
Examples of acute
Acute tonsillitis
Acute appendicitis
Acute sprain
Examples of chronic
Chronic bronchitis
RA
COPD
Ankylosing spondylitis
Medication for inflammation
Aspirin- suppresses inflammatory response. Prostaglandins
NSAIDS
Ibuprofen
Diclofenac sodium
Naproxen
Corticosteroids
Prednisolone- interrupts inflammation chronic. Stops chemical mediators
Suppresses phagocytosis
Immunosuppressants- methotrexate
Suppresses natural response but can make prone to other infections, non specific
