Acute inflammation

Sebastian Bassi
Flashcards by Sebastian Bassi , updated more than 1 year ago


2nd year Anat path Flashcards on Acute inflammation, created by Sebastian Bassi on 01/25/2016.

Resource summary

Question Answer
Define: acute inflammation A local response by living tissue to tissue injury resulting in the formation of a fluid rich -protein -cells (polymorphs , later macrophates)
Exudate accumulates at the site by: 1. An increase in blood flow to area under attack 2. An increase in permeability of the basement membrane of the blood vessels Achieved through chemical mediators released when injured
Vascular phase - Increased blood flow to the area - Slowing of blood flow in the distended blood vessels due to : >increased permeability of blood vessels > Loss of axial flow > Higher MWt proteins leak out of blood vessels( antibiotics too)
Cellular phase: Neutrophils - Attachment of neutrophils to walls of blood vessels - Movement of cells through vessel wall - Phagocytosis of debris/organisms by neutrophils - Intracellular killing/digestion by neutrophils
Local response by staph. aureus - Coagulase produced by the organism precipitates fibrin out around the lesion, containing it. - Boil of the skin (well circumscribed)
Local response by Strep. pyogenes - Hyaluronidase produced by organism which breaks down hyaluronic acid (component of CT in dermis. - Organism "digest pathway for self - Causing spreading superficial infection -poorly demarcated - Cellulitis/impetigo
Cardinal signs of acute inflammation 1. Rubor (redness) 2. Calor (heat) 3. Tumor (swelling) 4. Dolor (pain) 5. Loss of function
Tissues and acute inflammation 1) expansion of tissue (NB brain and bone) 2) Surface area covered by exudate (Shock) 3) Tissue release further dmg substances (chemical dmg) 4) Physiologically respond different (alveoli bv contract)
Beneficial effects of acute inflammation (fluid) 1. Dilutes toxins 2. Contain antibodies 3. Fibrin (localize) 4. Polymorphs (destroy pyogenic) 5. Macrophages (ingest proteins)
Possible outcomes of acute inflammation 1. Resolution 2. Suppuration 3. Healing by fibrosis 4. Progression to chronic inflammation 5. Spread 6. Death
Destroys harmful enzymes in neutrophils Alpha-1-antitrypsin (deficiency = emphysema)
Vascular phase steps - Transient, brief, vasoconstriction - Dilatation of blood vessels - Increased blood flow (active hyperaemia, prostaglandins) - Exudate into tissues - Slowing of blood flow - Increased lymphatic flow
Local responses A) various organisms B) Therapeutic intervention (local peritonitis) C) Toxins (gangrene)
Kinin and histamine lead to an immediate but transient increased vascular permeability through walls of VENULES ONLY
Endothelial cell injury Leads to a delayed but persistent vascular peermeability through both capillaries and venules
2 main cell types 1) Neutrophil : - definitive cell of acute inflammation - produced in bone marrow - initial phagocytosis 2) Macrophage : - Phagocytosis - Antigen presentation - Secrete factors which stimulate fibrosis - Production of complement components
Cellular phase 1) sloiwing of blood flow 2) Margination of leukocytes 3) Triggering 4) Strong adhesion (integrins) 5) Motility 6) Phagocytosis 7) Intracellular killing (superoxide, halides)
Consequences of acute inflammation - Resolution - Suppuration - Fibrosis - Progression (to chronic) - Death
Systemic effects 1) Fever 2) Leucocytosis 3) Alterations in serum proteins
Specific patterns - Suppuration - Cellulitis (phlegmon) - Pseudomembranous (fibrinopurulent) inflammation - Serous inflammation - Catarrhal inflammation - Ulceration
Local response implications - Low grade sensing system - Coagulation systems - Inflammatory mediators - Complement cascade - Cells of chronic inflammation
Treatment of Non-infective causes i) Antibodies to chemical mediators of inflammation ii) Suppression of immune response : steroids iii) Plasmapheresis iv) Antipyretics v) non-steroidal anti inflammatories
Prevention of sepsis i) Preparation of skin ii) Haemostasis iii) debridement iv) Prophylactic antibiotics
Suturing of laceration i) cleaning ii) haemostasis iii) needle iv) Thread v) threaded or not
Aftercare - Wound dressing + ointments - Antibiotics - analgesic - antipyretics - anti-inflamms. (NSAIDS)
Show full summary Hide full summary


Immune system(II)
Clare Yu
CD4 T cells: The Master Controllers of the Immune System
Ifeoma Ezepue
Why is immunology important?
Ifeoma Ezepue
Immune system
Clare Yu
enzymes and the organ system
GCSE AQA Biology - Unit 2
James Jolliffe
Biology AQA 3.2.5 Mitosis
GCSE AQA Biology 1 Quiz
Lilac Potato
Biology AQA 3.1.3 Osmosis and Diffusion
Using GoConqr to study science
Sarah Egan
Biology- Genes and Variation
Laura Perry