Revision: Chronic inflammation Flashcards
chronic inflammation definition
chronic response to injury w/ associated fibrosis
How can a CIR arise?
1 It can take over from an AIR
-If damage is too severe to be dealt with in a few days
2 It can arise de novo
- some autoimmue conditions eg RA
- some chronic infections eg viral hepatitis
- chronic low level irritation
3 It can develop alongside an AIR
- from persistent/repeated/severe infections
list cells involved in a CIR
lymphocytes, eosinophils, myo/fibroblasts, macrophages (+ giant cells- Langhans, Foreign body type, Touton)
Lymphocytes in a CIR
aka Chronic Inflamm. Cells
Function: Complex, but mainly immunological
- B/Plasma (presence indicates high chronicity): differentiate and produce ABs
- T: Control (CD4/helper), Cytotoxic (CD8/killer)
eosinophils in a CIR
Allergic rxns, parasitic infestations, some tumours
Myo/fibroblasts in a CIR
recruited by macrophages, produce collagen
macrophages in a CIR
varied levels of activation, important in AIRs as well
Functions: -synthesis of clotting factors, cytokines, complement components, proteases
- control of other cells via cytokines
- processing and presentation of AGens to IS
- Phagocytosis and destruction of debris and bacteria
- Also fuse together to form multinucleate Giant Cells
Giant Cells
multinucleate cells formed from fusion of macrophages due to frustrated phagocytosis
Types: Langhans -> indicative of (though not specific to) TB (nuclei are arranged in a horseshoe-like pattern)
Foreign body type -> found especially in implants (nuclei are disorganisd)
Touton -> fat necrosis (ring of nuclei surrounded by foamy cytoplasm)
what is present here?
Langhans Giant Cell - indicative of TB
distinguished by horse-shoe arrangement of nuclei around cytoplasm
What is present here, in the centre?
Touton Giant cell -> indicative of fat necrosis
distinguished by circular arrangement of nuclei around foamy cytoplasm
What is present here?
Foreign body type Giant Cell -> usually from an implant, IS recognises it as foreign and attempts to remove it
Distinguished by disorganised nuclei in pockets, not in a pattern, unlike touton and langhans
Chronic colecystitis
Cause: repeated obstruction of gall bladder w/ gallstones
-> repeated AIR -> CIR & fibrosis of gall bladder wall
Treatment: surgical removal of gall bladder
Gastric Ulceration
Cause: Acute - alcohol, drugs Chronic - Helicobacter Pylori
-> ulceration due to an imbalance between acid production and mucosal defence - the acid eats into the lining of the GI tracts
Treatment - ‘triple therapy/treatment’:
- PPI (proton pump inhibitor) - inhibits the secretion of protons into the gastric lumen, attempting to increase the pH eg Omeprazole
- 2 antibiotics to combat the H. pylori eg clarithromycin, amoxicillin
Inflammatory Bowel Disease
Affects S and L intestine, presents w. diarrhoea, rectal bleeding and other symptoms
Ulcerative collitis: No known direct cause, combo. of factors, superficial
-Treatment: immunnosuppresants, colectomy (surgical removal of large intestine)
Chron’s Disease: Thought to be caused by a combo. of genetic and environmental factors
- Transmural (affects entire thickness of wall), Stricture (stenosis/narrowing), fistulae (abnormal connectons made between to epith. line organs)
- Treatment: lifestyle mod.s eg diet, hydration, immunosuppresants
Liver cirrhosis
cause: alcohol, HBV/HCV (hep. B/C), drugs eg paracetamol, toxins, immunological, fatty liver disease
CIR w/ fibrosis - disorganised architecture leading to an attempted regeneration - nodules of hepatocytes surrounded by bands of collagen -> cirrhosis
Cannot be reversed, treatment is either a lifestyle change to prevent further damage, or a liver transplant
Thyrotoxicosis
Hypermetabolic clin. syndroms w/ elevated serum levels of T3 and T4, commonly cause by Graves’ disease:
Cause: AImmune disease where ABs stim TSH receptors on follicle cells to produce and release more T3 and T4
Signs and symptoms (due to hyperthyroidism): inc. HR and metabolic rate, weight loss, exopthalmus, osteoporosis, anxiety, trouble sleeping, hyperactivity
Treatment: carbimazole - inhibits addition of iodine to thyroglobulin, this then reduces the amount of T3 and T4 made
Rheumatoid Arthritis
AImmune disease, w/ a localised CIR and a systemic Immune response
- Localised: joint destruction
- Systemic: can affect other organs, cause amyloidosis (sol. prots. become insol., deposited in EC space causing the disruption of normal function
Treatment: painkillers eg paracetamol, NSAIDs (Non Steroidal Anti Inflammatory Drugs) eg ibuprofen
Clinical examples of a CIR
Inflammatory bowel disease
-> Crohn’s disease, Ulcerative collitis
Liver cirrhosis
Thyrotoxicosis - Graves’ disease
RArthritis
Chronic Colecystitis
Gastric ulceration
how do CIRs and immune responses interact?
They overlap:
Immune responses cause pathology by CIRs, CIRs can stimulate immune responses
granulomas
epithelioid histiocytes (activated macrophages) surrond something it is unable to get rid of eg bacteria, fungi and other foreign material, normally also contain lymphocytes but can contain other cells eg neutrophils, eosinophils, Giant cells
Generally caused by persistent low grade AGenic stim. and hypersensitivity
The main causes are: -mildly irritating foreign material
- Infections: mycobacterium eg tuberculosis, leprosy
- >syphilis
- > some fungi
- Unknown cause: sarcoids (granulomas in multiple organs at once), Crohns’, wegener’s granolumatosis
TB
caused by mycobacterium, esp M. TB
makes no toxins/lytic enz.s, it causes disease by beign persistent and activating a CIR -> therefore, does not DIRECTLY cause harm
Outcomes: 1 Arrest -> fibrosis -> scarring
2 Erosion -> bronchus, bronchopneumoniae
3 TB empyema (collection of pus)
4 Erosion into bloodstream
