Session 2 - Acute Inflammation Flashcards
Name some causes of an acute inflammatory response
- Microbial infections
- Hypersensitivity reactions
- Physical agents
- Chemicals
- Tissue necrosis
Name the cardinal signs of acute inflammation
- Calor (Heat)
- Rubor (Redness)
- Tumor (Oedemma)
- Dolor (Pain)
And loss of function
Name the steps involved in acute inflammation
1 - Vasodilation
2 - Gaps form in endothelium
3 - Exudation
4 - Margination and Emigration of Neutrophils
Name the chemical mediators involved in vasodilation
Histamine, Prostaglandins, C3a, C5a
Name the chemical mediators involved in increasing vascular permeability
Histamine, Prostaglandins, Kinins
Name the chemical mediators involved in emigration of leukocytes
Leukotrienes, IL-8, C5a
Discuss the action of neutrophils
- Move to site of injury though chemotaxis
- Phagocytose micro-organisms by making contact, recognising and internalising them
- Then form with lysosomes to have contents destroyed
- Activated neutrophils may release toxic metabolites and enzymes that can cause damage to host tissue
Name some acute phase responses to acute inflammation
- Decreased appetite, increased heart rate, altered sleep patterns
- Changes in conc of acute phase plasma proteins;
e. g C-reactive protein (CRP), Fibrinogen and alpha1-antitrypsin
Name the three types of systemic consequences of acute inflammation
- Acute phase responses
- Fever
- Leukocytosis
What may occur following acute inflammation?
- Complete Resolution
- Continued acute inflammation with chronic inflammation (abscess)
- Chronic inflammation and fibrous repair
- Death
What features of chemical mediators allows them to have their actions stopped?
Short half lives
How may chemical mediators have their actions stopped?
Degradation, Dilution or Inhibition
When is complete resolution not possible?
If tissue architecture is damaged
Name some possible complications of acute inflammation
- Swelling
- Exudate
- Loss of fluid
- Pain and loss of function
Name some clinical examples of acute inflammation
- Skin Blisters
- Abscesses
- Pericarditis
What is Hereditary Angio Oedemma?
- Disorder caused by deficiency in C1 inhibitor
- C1 inhibitor also inhibits Bradykinin
- Uninhibited Bradykinin vastly increases vascular permeability -> Oedemma
- Treated with C1 inhibitor infusions or frozen fresh plasma
What is alpha1-anti trypsin deficiency?
- Disorder of acute inflammation
- Alpha1-anti trypsin usually inhibits elastase
- Without inhibition elastase breaks down liver and lung tissue
- causes emphysema and liver sclerosis
What is Chronic Granulomtaous Disease?
- recessive sex-linked disorder
- Immune phagocytes cannot form ROS
- some bacteria need ROS to destroy them
- Granulomas formed in an attempt to contain bacteria
What is Acute Inflammation?
The response of living tissue to injury, with the aim of limiting damage to tissue
