Revision: Acute Inflammation Flashcards
main causes of acute inflammation
physical agents
chemicals
tissue necrosis
microbial infections
hypersensitivity rxns
purpose of an AIR
to protect the surrounding tissue and body
though it may lead to complications
characteristic macroscopic features of an AIR
Rubor: redness
Tubor: swelling
Calor: Heat
Dolor: Pain and loss of function
characteristic microscopic features of an AIR
1 Vasodilatation
2 Endothelia retract and gaps form in vessel wall
3 an exudate of water, salts and small plasma proteins leak through
4 margination (neutrophils adhere to swollen endothelial cells) and emigration (neutrophils migrate through the BM)
5 Macrophages and lymphocytes come in the same way as neutrophils
How do changes in an AIR combat injury?
1 Exudation: delivery of inflam. mediators, nutrients, fibrinogen, ABs, dilution of toxins, inc. lymphatic drainage which delivers pathogens to phagocytes and antigens to the IS
2 Vasodilatation: inc. delivery of exudation, inc. temperature (kills of harms pathogens)
3 Infiltration of cells: removes pathogenic organisms and necrotic debris
4 Pain and loss of function: enforces rest to reduce chance of further damage to the tiss.
Types of chem. mediators involved in an AIR
proteases: these are plasma prot.s made in the liver eg kinins, the complement system (C3/5a), coagulation/fibrinolytic system
prostaglandins/leukotrienes: metabolites of arachidonic acid and inflammatory intermediates, both are a class of eicosanoids
cytokines and chemokines: many and varied, made by WBCs, eg TNF-alpha, Interleukins
Roles of chem. mediators in an AIR
inc. blood flow: histamine, prostaglandin
inc. vascular permeability: histamine, leukotriene
neutrophil chemotaxis: LTB4, C5a, bacterial peptides
phagocytosis: C3b
pain: histamine
how do macro. changes result from micro. changes?
rubor: inc. vasodilatation
calor: inc. vasc. permeability
tubor: inc. vasodilatation
dolor: histamine
Overall neutrophil action in an AIR
1 Migration to site of infection by chemotaxis
2 phagocytose M-Os
3 May produce toxic metabolites or enz.s that cause damage to the host tiss.
Migration/infiltration of neutrophils steps
1 Margination (they line up along vessel edge)
2 Rolling (stick intermittently)
3 Adhesion (stick more avidly)
4 Emigration through vessel wall
Phagocytosis in neutrophils steps
Contact, recognition, internalisation
then degradation, either O2 dependent (H2O2, O2, HOCl.) or O2 independent (cationic prots - ‘defensins’, Bacterial Permeability Inc. prot - BPI)
systemic effects of an AIR
fever: from endogenous pyrogens such as TNF-alpha and IL-1 and prostaglandins (aspirin inhibits this, therefore inhibits a fever)
Leukocytosis (WBC count above normal range): IL-1 and TNF-alpha stimulate more WBC release, Macro.s and T-lymphocytes produce colony-stimulating factors, viruses stim. lymphoytes, bacteria stim. neutrophils
Acute phase response: decreased appetite, inc. HR, altered sleep pattern, changes in plasma conc.s on Acute phase prot.s:
Acute phase prot.s: C-reactive protein (induces the complement system to attach to dead cells, removing them), Haptoglobin, Fibrinogen, Serum Amyloid A, alpha-1 antitrypsin (protease inhibitor, protects tiss. from enz.s of inflam. cells)
Fever in an AIR cause
endogenous pyrogens eg TNF-alpha and IL1 and prostaglandins (aspirin inhibits this, therefore also fever)
leukocytosis in an AIR cause
IL-1 and TNF-alpha stim. the release of more WBCs
Macro.s and T-lymphocytes produce colony-stimulating factors
virus -> more lymphocytes
bacteria -> more neutrophils
Acute phase response in an AIR
dec. appetite, inc. HR, altered sleep pattern, changing plasma conc.s of Acute phase prot.s:
Acute phase prots: haptoglobins, fibrinogens, serum amyloid A, alpha-1 antitrypsin (protease inhibitor, protects tiss. from enz.s of inflam. cells), C-reactive prot. (induces the comp. system to bind to dead cells, removing them)
Resolution of an AIR
changes gradually reverse, vascular changes stop - vessel calibre and perm. return to normal, neutrophils no longer marginate - THEREFORE:
- neutrophils die, break up, carried away/phagocytosed
- exudate drains to the lymphatic system
- fibrin is degraded by plasmin and other proteases
- damaged tiss. COULD regenerate, though not if the tiss. architecture is destroyed
complications of an AIR
swelling -> blockage of tubes eg bile duct, intestines
pain and loss of function, esp. if prolonged
exudate -> serositis (inflam. of serous membrane), cardiac tamponade (pericardial eff. into pericardium)
loss of fluid -> burns
skin blisters
cause: sunlight, heat, chemicals
features: pain, profuse exudate (swelling)
fluid strips off overlying epithelia, relatively few inflamm cells are present so fluid is clear UNLESS bacterial infection
leads to resolution, or scarring
Lobar pneumonia
cause: streptococcus pneumoniae
features: prostration, fever, counghing, breathlessness, hypoxaemic
the alveoli contain exudate instead of air
acute appendicitis
NSExactly what causes it, can be a blockage form faeces of from Crohn’s disease or ulcerative collitis
pain spreads from middle of abdomen to bottom RHS, worsens
if appendix is not removed surgically, it can burst and infect other organs
alpha-1 antitrypsin deficiency
inherited Acute inflammatory disorder
alpha-1 antitrypsin inhibits elastase, w/o this elastase breaks down lung (-> emphysema) and liver (-> liver cirrhosis) tiss.
abscess
occurs in solid tiss
inflammatory exudate forces apart the tiss
liquefactive necrosis in centre
causes high pressure -> PAIN
may cause tiss. damage and squash adjacent structures
pericarditis
serositis in pericardium
pericardium becomes inflamed, inc. pressure on the heart, therefore dec. the cardiac output
