Week 1 Lecture 2- Inflammation Flashcards
(28 cards)
What is inflammation
Part of the innate defence mechanisms of the body against infectious or non infectious aetiologies (things that’s effect)
Any type of tissue damage or infliction that initiates a set of vascular and cellular events to clear out cellular deplores or pathogens, initiating repair
List causes OF inflammation
Genetic abnormalities
Nutritinal abnormalities
Immunologic reactions (damage caused by immune system)
Endocrine
Physical agents
Chemical agents
Infectious agents
Hypoxia (abnormality respiratory or circulatory function)
How long is acute inflammation
6 weeks (less than)
How long does chronic inflammation last
6 weeks <
List the 5 cardinal signs of acute inflammation
Redness
Heat
Swelling
Pain
Loss of function
Early tissue response followed by healing
Aims of inflammation (4)
Bring immune cells to the area
Destroy pathogens
Remove cellular debris
Begin repair
List defence cells
Neutrophil
Eosinophil (allergy in gIT)
Basophil
Monocyte
T-cell
B-cell
Natural killer
Macrophage
List acute phase protein
There is a sudden increase in plasma conc of certain protein in a self defence
C reactive protein (CRP) increase from 7 hours. Decrease after 48 hours
Elevated segmentation rate (ESR) increased of this from 7 days of defence
Ferritin
List acute inflammation phases (2)
Vascular phase
Cellular phase
Explain vascular phase of acute inflammation
-Vasodilation occurs
-Increasing the permeability of the vascular barrier
-Regulated by chemical mediators
-Exudation of fluid (to area fluid moves w plasma)
-Oedema- allows proteins such as immunoglobins to migrate through. Removes pathogens and cell debris through lymphatic drainage.
Explain cellular phase of acute inflammation
• Polymorphonuclear neutrophils migrate and adhere to swollen epithelial cells
through either:
Margination – cells line up against the endothelium
Rolling – close contact with and roll along the endothelium
Adhesion – connecting to the endothelial wall
Migration – cells move through the vessel wall to the affected area
• They push through the cell membranes passing into the area of damage through a
process called CHEMOTAXIS
.
• Phagocytosis of the foreign body (the pathogen is engulfed and contained with a
phagosome).
• The phagosome is then destroyed but release proteolytic enzymes
Explain extravasation
The movement of white blood cells and fluid from blood vessels to the surrounding tissues.
In response to injury, infection or other inflammatory stimuli.
Helps eliminate harmful agents
What do mast cells secrete through their glands
Histamine
Leukotreins
Protoglandins
(Inflammatory mediators located into the intra space)
When we have a fever, the PG3 protein stimulates the hypothalamus which gives us ab increase in temp. What is the purpose of this?
Cellular metabolism
Denature DNA of pathogens
Iron to area as hR increases so more blood is pumped too the area
What is the outcome of acute inflammation
- removal of the exudate
- resolution (restore to normal via replacing cells, chemical substances are neutralised, normalisation of vascular permeability, apoptosis of inflammatory cells, lymph drainage)
- healing by scar
-progression to chronic inflammation
List clinical examples of acute inflammation
Asthma
Sepsis
Vasculititis
Meningitis
Acute trauma
Causes of chronic inflammation
Sensitivity (external trigger that can be result in allergy)
Exposure (low-level exposure or irritants like chemicals)
Autoimmune disorders (immune system mistake attacks normal healthy tissues
Auto inflammatory disease (genetic factors)
List factors for chronic inflammation
Age
Obesity
Standard American diet
Smoking
Low sex hormones
Stress
Sleep problems
What does inflammation cause
Angiogenesis (formation of new blood vessels)
Mononuclear cell infiltration (macrophages, lymphocytes, plasma cells)
-fibrosis (scar)
Compare acute vs chronic inflammation
Acute inflammation onset is immediate whereas chronic is delayed.
Acute duration is a few days whereas chronic is up to months and years
Causative agents for acute is bacteria and injured tissues whereas chronic is persistent acute inflammation, viral autoimmune
Acute major cells are neutrophils, basophils, monocytes, macrophages whereas chronic is mononuclear, mono, lymphocytes, plasma cells, fibroblast
Acute primary outcomes are resolution, abscess formation and chronic inflammation. Chronic outcomes are tissue destruction, fibrosis, necrosis
What do cytokines release
(They are the Little messages released for an immune response )
The granules released are mainly histomines
Prostoglandins
Describe diapydesis
Process by leukocytes move from bloodstream into tissues.
Pass through blood vessel wall
Describe positive chemotaxis, what undergoes this?
Movement towards a higher conc of a chemical or a signalling molecules
Neutrophils undergo this when moving to the site of inflammation in response to cytokines sending signals.
Describe the process of innate immunity
Bacteria with antigen on surface releases endotoxins
Endotoxins act on mast cell nucleus to release inflammatory cytokines
Stimulating P-selectin on endothelial cells to initiate extravasation (leakage of blood or lymph)
Transmigration, margination, adhesion, diapedeasis and positive chemotaxis occurs
The inflammatory cytokines act on endothelial cells causing them to contract and increase permeability (swelling)
Smooth muscle cells are acted on and they relax leading to vasodilation and heat and redness
Neutrophils undergo exocytosis of free antigens. Apoptosis
Macrophages undergo phagocytosis forming a phagolysosome
MCH2 recombination and attach to specific antigen and present on cell membrane
Macrophage turns into antigen presenting cell
