Inflammation And The Three I’s Flashcards
Outline the bodies three lines of defence
1st - skin and mucous membranes. Epidermis ( outer layer ) - primary barrier
Mucous membranes try to stop it getting any further if skin is breached
2nd - inflammation. Non-specific, natural, innate and rapid response
3rd - immunity - specific, aquired immunity, adaptive and slow response.
Describe and explain inflammation and the five cardinal signs -
Inflammation is the bodies no-specific protective response to tissue disease injury in attempt to destroy/dilute or wall off both the injurious agent and injured tissue.
Result - cardinal signs
Redness - increased blood flow ( rubor )
Swelling - more fluid to area ( tumor )
Warmth - specific/non ( calor )
Pain - due to compression of nerve endings ( function laesa)
What is the purpose of inflammation ?
Prevent minor infections becoming overwhelming
Prepare damaged tissue for repair.
Factors that cause inflammation -
Injury/trauma - physical sport, an accident, radiation, electrical or chemical ( burn )
Infection - viruses/ bacteria, fungi /worms
Infarction - lack of o2 to an area
Immune reactions - foreign protein hypersensitivity eg allergies and autoimmunity eg gluten interolerence
Nutrient deprivation - high fatty processed diet trigger inflammatory response.
What suffix helps to identify when referring to inflammation ?
ITIS
Conjunctivitis - eyes
Appendicitis - appendix
Pericarditis - pericardium
Osteoarthritis - joint
Mechanism of inflammation
1) vascular response
Changes with blood flow - vasoconstriction, short time period. Blood vessels near affected area constrict allowing blood to clot and localise harmful agents.
Prologned vasodilation - they re-open therefore increasing blood flow and increase hydrostatic
Opening of capillary beds and increased vascular permeability.
Bradykini ( protein ) released and causes capillary endothelium to retract ( crenellation )
This creates gaps so plasma can leak
Oedema formation
Therefore heamoconcentration -> statis - slowing of blood in an area.
Mechanism of inflammation
2) cellular response -
Neutrophils are first ( not long lasting, smaller and quicker ) to emigrate to injury site followed by monocytes then macrophages. They squeeze through endothelial gaps by diapedesis.
Mechanisms of inflammation
2) cellar response - diapedesis stages:
Margination - chemical mediators attract WBC’s and their movement
Not smooth - WBC’s roll and get stuck ( adhesion ) towards endothelial cells.
They flatten out across blood vessels ( pavementing ) and move along as best they can and move through gaps in blood vessel - only some of cell will get through ( pseudopod formation )
Amoebiod action - try move itself through so it can emigrate outside blood vessel.
Diapedesis - ‘cell walking’ from inside blood vessel to outside
Happens due to chemotaxis response to injury.
Mechanism of inflammation
3) phagocytosis -
4) lymphatic drainage -
3) Process of ingestion of forgein material or particular matter
4) lymphatic system assists in tissue fluid drainage. Inflammation means lymphatic vessels open up therefore aiding drainage of excess fluid and any antigens not dealt with by inflammatory processes.
APC’s present to immune system, triggers. 3rd line of defence - specific immune system.
Common blood tests used to detect acute inflammation:
WBC count -
WBC differential -
WBC count - reference value: 5,000 - 10,000/mm^3
With inflammation value increases way above reference.
WBC differential - neutrophils higher than 75% suggest bacterial infection
Lymphocytes higher than 46% suggests viral infection
Eosinphils higher than 8% suggests worms
This test helps break down into type of WBC and therefore helps guide treatment.
Common blood tests used to detect acute inflammation
Erythrocyte sedimentation rate -
This is how long it takes RBC’s to fall to bottom of test tube
0-17mm/hr for men
1-25mm/hr for women
Common blood tests used to detect acute inflammation
Erythrocyte sedimentation rate -
This is how long it takes RBC’s to fall to bottom of test tube
0-17mm/hr for men
1-25mm/hr for women
Characteristics of acute inflammation:
Usually a known cause eg trauma
Onset is rapid
Deterioration is rapid
Full resolution and follows a definite course
Neutrophils involved first, followed by monocytes to macrophages
Involves active phagocytosis
Beneficial outcome, prevents invasion and restoration of full function.
Characteristics of chronic inflammation-
Often cause is unknown eg unresolved acute inflammation/ complications of it.
Slow insidious onset
Slower deterioration as lack of an acute response
Fails to resolve and follows a slow, self perpetuation course.
Macrophages and fibroblasts are cells involved
Persistent irritants therefore resistant to phagocytosis
Results in destructive scar tissue formation and loss of function.
Examples of medication used for inflammation:
Aspirin
Non-steroidal anti-inflammatory drugs ( NSAIDs )
- ibuprofen
- naproxen
Corticosteroids
- predinsolone ( often used for chronic )
Immunosuppressants also used but are non- specific therefore leads patients prone to other infections
Basic idea of the immune response -
Host defence system - how the body protects itself from injury/harmful agents.
It’s the 3rd line of defence
There are two types: cell mediated and humoral immunity - these occur together
Immunity
Bone marrow -
Thymus gland -
Bone marrow - found in long bones.
Two types: yellow - found in long bone shaft
Red - found at bone ends. Produces white and red RBC’s
Thymus - produces T lymphocytes. Thymus is larger in children than in adults
Immunity
Lymph nodes -
Spleen -
Tonsils -
Lymph - holding areas for immune cells near blood vessels
Spleen - RBC recycling and stores WBC’s and platelets
Tonsils - 1st line of defence, holding areas for immunity cells.
* you can live without your spleen and tonsils
Cell mediated immunity -
This is how we fight intracellular pathogens eg viruses and how we keep track of cancer cells
Involves B and T lymphocytes formed in red bone marrow
B and T released imaturely from bone marrow to the thymus via bloodstream
Leave thymus mature - come out as CD8+T cell or CD4+T cell
They both activate and form killer T cells
Eat forgein matter - can cause problems for transplants patients
CD8 T cells - natural killer cells release peforin autolysis
Release lymphotoxin ( DNA ) apoptosis
CD4 T cells - manage and coordinate immune response. Increase production of T+B cells. Activate CD8 into killer T cells. Activate B cells to mature plasma cells.
Act as a suppressor cells - slow immune response.
Humoral immunity - ( antibody mediated )
Extracellular pathogens eg bacteria
Mature B lymphocytes released from red bone marrow and enter lymphatic tissue
B lymphocytes have antibodies that will bind to specific antigens
Recognise specific antigens and will bind to promote phagocytosis
CD4/8 cells help release these antibodies when we need them
B cells are activated by T helper cells and mature into plasma cells
Plasma cells produce immunoglobulin that interact with specific antigens.
What do both immunity processes produce ?
Both produce memory cells.
Antibodies ( immunoglobulin ) - the stages:
Agglutination - makes forgein body stick together so it cannot cause damage.
Precipitation - antibody and antigen combine and become insoluble therefore can’t do damage
Neutralisation - antibody combines to forgein body itself
Lysis - direct killing of cell by antigen
Opsonisaiton - antibody gives it a mark so then cells involved in phagocytosis recognise it quicker
Activation of complement cascade - series of enzymes that will cause the above to happen and act as chemotaxis.
Infection -
Infectious disease -
Infection - an extension of inflammatory and immune processes. Is a complication of immune function
Infectious disease - state of tissue destruction resulting from invasion by micro-organisms.
Types of pathogens -
Bacteria, viruses, fungi, protozoas ( mobile organisms that can invade )
Rickettsiae ( intracellular )
Helminths ( worms )
Mycoplasma - extracellular
elements of infection control:
Assess infection risk
Hand hygiene
Respiratory and cough hygiene
PPE
Safe management of care equipment
Safe management of healthcare linen
Safe management of bodily fluids and blood
Safe disposal of waste
Occupational safety/managing prevention of exposure.
What is considered one of the most important ways to reduce the transmission of infectious agents ?
Good hand hygiene.
Outline the chain of infection -
Infectious agent - reservoirs ( people, equipment) - portal of exit ( skin, excretions ) - means of transmission ( direct contact, airborne ) - portal of entry ( mucous membrane, respiratory tract ) - susceptible host ( surgery, burns, elderly )
At each stage things such as good hygiene can break the cycle to prevent transmission.
What is sepsis ?
Defined as life-threatening organ dysfunction caused by a dysregulated host response to an infection.
Bodies defence mechanism goes wrong, it attacks ‘itself’ instead of foreign matter
Sepsis
Describe the dysregulated systemic inflammatory response -
Increased capillary permeability/oedema ( become too permeable )
WBC’s block vessels
Tissue ischaemia ( blocked areas in circulatory system ) / hypoxia / necrosis
Endotoxins released therefore toxicity and cell death
Leads to organ dysfunction
Sepsis is always started by an infection eg UTI and pneumonia
How to sport sepsis in adults:
S -
E -
P -
S -
I -
S -
Slurred speech
Extreme shivering or muscle pain
Passing no urine ( in a day )
Severe breathlessness
It feels like you’re going to die
Skin mottled or discoloured
