Acute inflammation 1+2 Flashcards
Define acute inflammation
It is a fundamental response which maintains the integrity of organism and involves a series of protectivve changes occurring in living tissueas a response to injury.
Name the cardinal signs of inflammation
rubor - redness, darkening
calor - heat
tumor - swelling
dolor - pain
loss of function
List the causes of acute inflammation
> micro-organisms - bacteria, fungi, viruses, parasites (pathogenic organisms cause infection)
> mechanical - trauma - injury to tissue (all injuries even sterile (eg surgery))
> chemical - upset stable environment (acid or alkali - upset pH, bile and urine - irritation when in inappropriate place e.g. peritoneum)
> physical - extreme conditions
(heat - sunburn, cold - frostbite, ionising radiation)
> dead tissue (cell necrosis irritates adjacent tissue)
> hypersensitivity (several classes of reaction)
Describe the sequence of events constituting acute inflammation
Injury or Infection: The process begins when tissues are damaged due to injury, infection, or harmful stimuli.
Vascular Response: Blood vessels in the affected area undergo changes:
Vasodilation: Blood vessels widen, increasing blood flow to the area, causing redness and warmth.
Increased Permeability: The blood vessel walls become more permeable, allowing proteins and leukocytes (white blood cells) to move into the tissue, leading to swelling (edema).
Cellular Response:
Leukocyte Recruitment: White blood cells, primarily neutrophils, are attracted to the site of injury through chemical signals (chemokines).
Adhesion: Neutrophils adhere to the endothelium of blood vessels and migrate through the vessel walls into the tissue (diapedesis).
Phagocytosis: Neutrophils and other phagocytes engulf and digest pathogens and debris in the affected area.
Release of Mediators: Activated immune cells release inflammatory mediators (e.g., cytokines, prostaglandins) that promote inflammation and further recruit more immune cells.
Resolution of Inflammation: Once the threat is eliminated, anti-inflammatory signals are activated, leading to the cessation of the inflammatory response. This may involve the apoptosis (programmed cell death) of neutrophils and the clearance of debris by macrophages.
Healing and Repair: The tissue begins to heal, with the formation of new tissue and restoration of function.
Describe the benefits and outcomes of acute inflammation
Benefits:
> rapid response to non-specific insult
> cardinal signs and loss of function
(transient protection of inflamed area)
> neutrophils destroy organisms and denature antigen for macrophages to phagocytose
> plasma proteins localise process
> resolution and return to normal
Outcomes:
> resolution
> suppuration
> organisation
> chronic inflammation
Use correctly the terminology of acute inflammation
“structure”-itis
peritoneal cavity = peritonitis
meninges = meningitis
appendix = appendicitis
lungs = pneumonia
pleural cavity = pleurisy
Describe the role of neutrophil and the consequences of their action
> mobile phagocytes; recognise foreign antigen, move towards it - chemotaxis, adhere to organism
> granules possess oxidants (eg H2O2) and enzymes (eg proteases)
release granule contents
> phagocytose & destroy foreign antigen
Consequences:
- neutophils die when granule contents released
- produce a “soup” of fluid, bits of cell, organisms, endogenous proteins - pus
- might extend into other tissues, progressing the inflammation
List the mediators of acute inflammation and describe functions
Mediators include:
> molecules on endothelial cell surface membrane
> molecules released from cells
> molecules in the plasma
> molecules inside cells
Collective effects:
> vasodilatation
> increased permeability
> neutrophil adhesion
> chemotaxis
> itch and pain
Explain the systemic effects of acute inflammation
Immediate;
> pyrexia - raised temperature, endogenous pyrogens from white cells act centrally.
> feel unwell - malaise, anorexia, nausea, abdominal pain and vomiting in children
> neutrophilia - raised white cell count, bone marrow releases/produces
Longer term effects;
> Lymphadenopathy - regional lymph node enlargement, immune response
> weight loss - catabolic process
anaemia
Explain the outcomes of acute inflammation
> resolution; everything is fixed :)
> suppuration:
- pus formation; dead tissue, organisms, exudate, neutrophils, fibrin, red cells, debris
- pyogenic membrane surrounds pus; capillary sprouts, neutrophils, fibroblasts, walls off pus
> organisation:
- granulation tissue is the central to organisation
- results in healing and repair
- leads to fibrosis and formation of a scar
> dissemination (sepsis):
- usually has a microbial cause,
- spread to bloodsteam - patient “septic”
- bacteraemia - bacteria in blood
- septicaemia - growth of bacteria in blood
- toxaemia - toxic products in blood
> chronic inflammation
What are the effects of systemic infection?
> shock - inability to perfuse tissues
~ clinical picture of sepsis
- peripheral vasodilatation
- tachycardia - high heart rate
- hypotension - low blood pressure often pyrexia
- sometimes haemorrhagic skin rash
