Acute Inflammation Flashcards
What is inflammation
Response of living tissue to injury
Compare the vascular and cellular phase
How is inflammation controlled
Cellular: Delivery of neutrophils
Vascular: Blood flow changes, accumulation of exudate
Chemical mediators
Name 5 major causes of acute inflammation
Microbial infections Hypersensitivity reactions Physical agents (trauma) Chemicals Tissue necrosis
Name 5 clinical signs of acute inflammation
Rubour Tumour Calor Dolor Loss of Function
How does vascular flow change during acute inflammation
Vasoconstriction in first few seconds
Vasodilation in first few minutes
Increased vessel permeability
Regarding fluid movement, what is Starling’s Law?
Movement of fluid is controlled by the balance of Hydrostatic Pressure and Oncotic Pressure
How does inflammation cause swelling by altering vascular flow
- Vasodilation increases hydrostatic pressure
- Increased vessel permeability allows plasma proteins to enter interstitium, thus increased interstitial oncotic pressure
- Fluid moves out of vessel, into Intersitium
How does fluid leaving vessel affect the contents that remain
Increased viscosity of blood Reduced flow (Stasis)
Compare Exudate and Transudate
- Vascular permeability
- Protein content of fluid
- When do they occur
Exudate:
- Increased vascular permeability
- Protein rich fluid
- In inflammation
Transudate:
- Unchanged vascular permeability
- No protein in fluid
- Heart/ hepatic/ renal failure
State 3 ways vascular permeability can be increased
- Direct injury (Burns, trauma)
- Retraction of endothelial cells
- Leukocyte dependent injury (Enzymes/ toxic oxygen species released by inflammatory cells)
How is the vascular phase effective
Give 3 ways
More interstitial fluid= Toxins diluted
Exudate delivers proteins such as antibodies and fibrinogen (Mesh limits toxins spread)
Fluid drains to lymph nodes, antigens presented to immune system
How do Neurophils leave vessels in 4 steps
- Margination (Move towards endothelia)
- Rolling (Move along endothelia via weak bonds)
- Adhesion (Tight bonds formation)
- Diapedesis/ Emigration (Move through endothelia)
Compare the 2 adhesion molecules response for “rolling” and “adhesion” in Neutrophil Emigration
- Selectins on Activated endothelial cells are responsible for Rolling
- Integrins on Neutrophil surface change from Low to High affinity state, responsible for Adhesion
What is Chemotaxis
How do neutrophils move in this way
Movement along an increasing chemical gradient of chemoattractants
Re-arrangement of cytoskeleton
How do Neutrophils recognise pathogens
Give an example
Opsonins
Pathogen covered in C3b and Fc opsonins
Neutrophil surface has C3b and Fc receptors
How is the cellular phase effective in 3 ways
Removal of pathogens
Removal of necrotic tissue
Release of inflammatory mediators
What are inflammatory mediators
Name 4 ways they originate
Chemical messengers that control and co-ordinate inflammatory response
Activated inflammatory cells
Platelets
Endothelial cells
Toxins
Name 4 Mediators that cause vasodilation
Histamine
Serotonin
Prostaglandins
Nitric Oxide
Name 5 mediators that increase vascular permeability
Histamine Serotonin Bradykinin Leukotrienes Nitric Oxide
Name 4 mediators that stimulate chemotaxis
C3a, C5a
IL-1
TNF-Alpha
Leukotrienes
Name 3 mediators that cause pain
Bradykinin
Histamine
Prostaglandins
Name 3 pyrogens (Mediators cause fever)
Prostaglandins
IL-1
IL-6
Mediators;
Name 2 vasoactive amines
name 1 vasoactive peptides
Name 2 complement proteins
Amines: Histamine, Serotonin
Peptides: Bradykinin
Complement: C3a and C5a
Mediators;
Name 2 derived from phospholipids
Name 1 Cytokines/ chemokine
Name 1 exogenous mediator
Prostaglandins and Leukotrienes
TNF (Tumour Necrosis Factor)
Endotoxins from pathogens
What are the 2 types of Complications from Acute Inflammation
Name 4 examples of each
Local
- Obstruction of tubes/ compression of organs
- Loss of fluid
- Pain
- Normal tissue damaged
Systemic
- Fever
- Leucocytosis (Increased WBC production)
- Acute Phase Response (Malaise, Lethargy, Altered sleep) induces rest
- Septic shock (Huge release of mediators)
What are NSAIDs
How do they work?
Non-Steroidal Anti Inflammatory drugs
Block mediators that cause fever
What are Acute Phase Proteins
Name one that is measured as a marker for inflammation
Name 1 protein made in smaller amounts during Acute Phase Response. Name 2 made in larger amounts
Proteins released due to inflammation
C-Reactive Protein
Albumin- made less
Alpha-1 antitrypsin and Fibrinogen- made more
Name 4 outcomes of Septic Shock
Hypotension
Tachycardia
Multi-organ failure
Death
What are the 3 possible outcomes of Acute Inflammation
- Complete resolution
- Fibrosis (Repair with connective tissue)
- Chronic inflammation (With repair)
When does Acute Inflammation result in Fibrosis
When does it result in Chronic Inflammation
Fibrosis- If there is substantial tissue destruction
Chronic- When Acute isn’t enough to combat cause
Regarding Complete Resolution,
- What happens to Mediators
- Vessel diameter and permeabilty
- Neutrophils
- Exudate
- Tissue structure
- Degraded/ inactivated/ diluted (Short half lives)
- Return to normal
- Apoptosis and Phagocytosed
- Drained via lymphatics
- If preserved, undergoes regeneration
Name 4 types of Exudate and their appearance
- Pus/ Abscess- White/ creamy
- Haemorrhagic- Bloody
- Serous- Clear
- Fibrinous- Strands visible
What is a Pus/ Abscess exudate
What is a Seroma
Accumulation of dead/ dying neutrophils associated with Liquefactive necrosis
Accumulation of serous fluid in a body cavity
Hereditary Angio-oedema is an inherited Acute Inflammation Disorder.
What is the biochemical basis
Identify 3 symptoms
Deficiency of C1-Esterase inhibitor
Non-itchy cutaneous oedema
Recurrent abdominal pain
Family history of sudden death involving laryngeal involvement
Alpha-1 Antitrypsin deficiency is an inherited Acute Inflammation Disorder.
What is the biochemical basis
Identify 2 symptoms
Low Alpha-1 Antritrypsin levels
Emphysema (Damaged alveoli)
Hepatocyte damage-> Cirrhosis
Chronic Granulomatous Disease is an inherited Acute Inflammation Disorder.
What is the biochemical basis
Identify 3 symptoms
Phagocytes can’t make superoxide, so pathogens are Phagocytosed but NOT killed.
Granulomas
Skin/ lymph node abscesses
Many chronic infections in first year of life
Describe the process of Appendicitis in 3 steps
What organism causes it
- Lumen becomes blocked with Faecolith
- Accumulation of bacteria + Exudate
- Increased pressure-> Perforation
E. coli
Describe Pneumonia?
Which 2 organisms cause it
Exudate build up in lungs
H. influenazae + Strep pneumoniae
Describe Meningitis
What 2 organisms cause it
Identify 3 symptoms
How fatal is it
Exudate accumulation in meningeal space
N. mengitidis, E. coli
Headache
Neck stiffness
Photophobia
Rapidly fatal
What is Ascending Cholangitis, how is it related to Bile Abscess
What organism causes it
Bile duct inflammation caused by bacteria ascending from junction with Duodenum - Can cause a liver abscess
Caused by E. Coli
