Session 2 Acute Inflammation Flashcards
(26 cards)
What is meant by acute inflammation?
Immediate response to injury in living tissue
Give 5 causes of acute inflammation
- microbial infections
- hypersensitivity reactions/ immune reactions
- physical agents: cuts/burns/physical injury
- chemicals
- tissue necrosis
What are the clinical features of acute inflammation?
- rubor : redness
- tumor : swelling
- calor: heart
- dolor: pain
(And loss of function)
Real talk calzones dominate
What changes in blood flow occur with acute inflammation?
1) vasoconstriction for the first few seconds
2) vasodilation of arterioles and then capillaries = increase in blood flow (calor and rubor)
3) increased permeability of blood vessels = exudation of protein rich fluid into tissues and slowing of circulation = tumor
4) concentration of RBC in small vessel and increases viscosity of blood = STASIS (= INFECTION)
What is the main chemical mediators of acute inflammation?
histamine
- released from mass cells, basophils and platelets
- cause vascular dilation
How does the exudation of fluid into tissues occur?
Arterial dilation leads to increased hydrostatic pressure
Increased permeability of vessel walls leads to loss of protein into interstitium.
What is a consequence of vascular leakage?
Oedema
What’s the difference between exudate and transudate?
Exudate = high protein content Transudate = low protein content
What cells will you find in acute inflammation?
Neutrophils mainly (also Called polymorphs because they’re nuclei take lots of shapes)
So if you have neutrophils = acute inflammation, you’ll see neutrophil migration to tissue. No neutrophil, no acute inflammation
Also macrophages but not as important
How do neutrophils infiltrate a cell?
1) stasis causes neutrophils to line up at the edge of a blood vessel along the endothelium = marination
2) neutrophils then roll along endothelium, sticking to it intermittently = rolling
3) then stick more avidly = adhesion
4) followed by emigration of neutrophils through blood vessel wall
How do neutrophils escape from the vessel?
- relaxation of inter-endothelial cell junctions
- digestion of vascular basement membrane
- movement
What is the role of complement proteins?
Attach to tissue/bacteria, to allow them to be more recognisable by a polymorphism
What do neutrophils do and how do they do it?
Phagocytosis
Facilitated by opsonins (chemical compounds that attach to parts of tissue/immunoglobulin)
Done with o2
- superoxide and hydrogen peroxide
Done without o2
- lysozyme and hydroplanes
How to neutrophils move to the site of injury?
Along a chemotaxis
What are the chemical mediators of acute inflammation?
- proteases: complement system, kinins, etc.
- prostaglandins
- cytokines e.g interleukins
How does exudation of fluid combat injury?
- delivers plasma proteins to area of injury immunoglobulin
- inflammatory mediators
- dilutes toxin by increasing volume of fluid in tissue
- increases lymphatic drainage = delivers micro organisms to phagocytes and antigens to immune system
How does vasodilation combat injury?
- removes pathogenic organisms and necrotic debris
How does pain/loss of function combat injury?
- enforces rest, reduces chance of further traumatic damage
What are the systematic consequences of acute inflammation?
- fever: interleukin 1 and tumour necrosis factor a produced by endogenous pyrogens increases body temp
- leukocytosis
- acute phase response: decreased appetite, raised pulse rate
- change in one of acute phase proteins
- shock: a clinical syndrome of circulatory failure
What can happen after the developement of acute inflammation?
- resolution
- chronic inflammation = abscess
- chronic inflammation and fibrous repair
- death
What happens in resolution?
- exudate drains into lymphatic
- fibrin is degraded by plasmin and other proteases
- neutrophils die, break up and are carrier away or are phagocytosis
- damaged tissue might be able to regenerate if tissue architecture isn’t destroyed.
What is the causative organisms of lobar pneumonia and what is the clinical course?
Caused by streptococcus pneumoniae
Course = fever, prostration, hypoxaemia, dry cough and breathlessness
What happens in skin blistering?
Causes: heat, sunlight and chemicals
Get paint and profused exudate
- collection of fluid strips off overlying epithelium
- exudate clear unless bacterial infection develops
- get resolution or scaring
What is an abscess?
Solid tissue
Inflammatory exudate forces tissue appart
Liquefactive necrosis in centre
Cause high pressure = pain
Basically a spot
