Revision: Chronic inflammation Flashcards

1
Q

chronic inflammation definition

A

chronic response to injury w/ associated fibrosis

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2
Q

How can a CIR arise?

A

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
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3
Q

list cells involved in a CIR

A

lymphocytes, eosinophils, myo/fibroblasts, macrophages (+ giant cells- Langhans, Foreign body type, Touton)

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4
Q

Lymphocytes in a CIR

A

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)
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5
Q

eosinophils in a CIR

A

Allergic rxns, parasitic infestations, some tumours

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6
Q

Myo/fibroblasts in a CIR

A

recruited by macrophages, produce collagen

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7
Q

macrophages in a CIR

A

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
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8
Q

Giant Cells

A

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)

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9
Q

what is present here?

A

Langhans Giant Cell - indicative of TB

distinguished by horse-shoe arrangement of nuclei around cytoplasm

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10
Q

What is present here, in the centre?

A

Touton Giant cell -> indicative of fat necrosis

distinguished by circular arrangement of nuclei around foamy cytoplasm

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11
Q

What is present here?

A

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

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12
Q

Chronic colecystitis

A

Cause: repeated obstruction of gall bladder w/ gallstones

-> repeated AIR -> CIR & fibrosis of gall bladder wall

Treatment: surgical removal of gall bladder

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13
Q

Gastric Ulceration

A

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
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14
Q

Inflammatory Bowel Disease

A

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
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15
Q

Liver cirrhosis

A

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

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16
Q

Thyrotoxicosis

A

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

17
Q

Rheumatoid Arthritis

A

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

18
Q

Clinical examples of a CIR

A

Inflammatory bowel disease

-> Crohn’s disease, Ulcerative collitis

Liver cirrhosis

Thyrotoxicosis - Graves’ disease

RArthritis

Chronic Colecystitis

Gastric ulceration

19
Q

how do CIRs and immune responses interact?

A

They overlap:

Immune responses cause pathology by CIRs, CIRs can stimulate immune responses

20
Q

granulomas

A

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
21
Q

TB

A

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