File - Dr.Muhammad Hamad

advertisement
Chronic Inflammation
Dr Rezaur Rahman
dr.reza2006@gmail.com
Learning objectives for PMDC in
Chronic Inflammation

Chronic inflammations/ Granulomatous diseases.

The systemic effects of acute and chronic inflammation and their
possible outcomes.
Significance of ESR.
Examples of induced hypothermia in medicine.




Pathogenesis, clinical features and lab. Diagnosis of Gout.
Management of acute and chronic Gout.
dr.reza2006@gmail.com
Definition of Chronic Inflammation
Inflammation of prolonged duration (weeks or
months) in which active inflammation, tissue
destruction and attempts at repair are
proceeding simultaneously
dr.reza2006@gmail.com
Acute Vs Chronic Inflammation
dr.reza2006@gmail.com
Exudate Vs Transudate
dr.reza2006@gmail.com
Aetiology: Onset & Causes
A. Chronic inflammation from onset (de novo)
1. Persistent infection by certain microorganism
2. Prolonged exposure to toxic/aggressive agent
3. Autoimmunity: RA, SLE, Hashimoto’s thyroiditis,
Chronic gastritis of pernicious anaemia
4. Unknown cause: Sarcoidosis, Crohn disease,
ulcerative colitis
B. Chronic inflammation developing from acute
inflammation(Acute to Chronic)
dr.reza2006@gmail.com
A. Chronic inflammation from onset (de
novo)
1.
2.
3.
4.
Persistent infection by certain microorganism
Prolonged exposure to toxic/aggressive agent
Autoimmunity: RA, SLE, Hashimoto’s thyroiditis,
Chronic gastritis of pernicious anaemia
Unknown cause: Sarcoidosis, Crohn disease,
ulcerative colitis
dr.reza2006@gmail.com
1.Persistent infection by certain
microorganism


Mycobacterium tuberculosis, Mycobacterium lepri,
Treponema pallidum, certain viruses, fungi, parasitelow toxicity, delayed hypersensitivity and
granulomatous inflammation
Helicobacter pylori- Chronic gastritis, gastric ulcer,
duodenal ulcer
dr.reza2006@gmail.com
2.Prolonged exposure to toxic/aggressive
agent





Aggressive action of acid pepsin in gastric juice
causing peptic ulcer
Cigarette smoking causing Chronic bronchitis
Toxic plasma lipid components- atherosclerosis
Talc, suture, other nondegradable material
Silica- silicosis of lung
dr.reza2006@gmail.com
B. Chronic inflammation
developing from acute
inflammation(Acute to Chronic)




Persistence of injurious agent, eg, organism in abscess
Interference in healing process, eg, sequestrum(dead
bone) in chronic suppuratve osteomyelitis
Drainage is delayed or inadequate, eg, lung abscess
Recurrent bouts of acute inflammation, eg, chronic
pyelonephritis, chronic cholecystitis, chronic gout.
dr.reza2006@gmail.com
Histological types of Chronic
Inflammation
1.
2.
Specific Chronic Inflammation: histologically
distinctive. Granulomatous inflammation is
specific inflammation
Nonspecific Chronic Inflammation: not
histologically distinctive
dr.reza2006@gmail.com
Granuloma:

Granuloma is a microscopic aggregation of
macrophages and epitheloid cells which are
modified macrophages, surrounded by a collar
of mononuclear leucocyte, principally
lymphocyte.
Usually giant cells and occasionally plasma
cells are present.
dr.reza2006@gmail.com
dr.reza2006@gmail.com
dr.reza2006@gmail.com
dr.reza2006@gmail.com
dr.reza2006@gmail.com
dr.reza2006@gmail.com
dr.reza2006@gmail.com
Giant cell of Granuloma:
Large cell with more than one nucleus.
 Formed by fusion of macrophages or epitheloid cell. 20 or more
small nuclei are present.
 Types:
1. Langhans’ giant cells- nuclei are arranged in horse-shoe
pattern. Found in tuberculosis and sarcoidosis
2. Foreign body giant cells- haphazardly scattered nuclei. Found
in foreign body granuloma.
3. Aschoff giant cell- rheumatic lesion
4. Giant cell of ‘Giant cell tumor of bone’- osteoclast type
5. Tuton giant cell- in Xanthoma
6. Giant cell to reaction to sodium urate crystal in gout
dr.reza2006@gmail.com
** Physiological Giant cell- Osteoclast, megakaryocyte
etc

Malignant giant cell:
Found in Anaplastic tumor
 Hodgkin’s disease: Reed-Stenberg giant cell
 Choriocarcinoma
 Poorly differentiated astrocytoma
dr.reza2006@gmail.com
Difference between:
dr.reza2006@gmail.com
Classification of Granulomatous
inflammation

1.
2.
3.
4.

1.
2.

1.
2.
3.
4.
Aetiological classification
Infectious agent- bacteri, helminth, fungi
Physical & chemical agents- exogenous & endogenous
Autoantigen: Wegener’s grnulomatosis, Giant cell arteritis
Unknown: Sarcoidosis, Crohn’s disease
Classification on Pathogenesis
Immune granuloma
Foreign body granuloma
Histological classification
Non caseating granuloma
Caseating granuloma
Suppurative granulomatous inflammation
Diffuse granulomatous inflammation
dr.reza2006@gmail.com
A. Infectious agent

1.
2.
3.

1.
2.
3.



Bacteria:
Mycobacterium tuberculosis- tubercle- noncaseating/hard &
caseating/soft
Mycobactrium lepri- tuberculoid & lepromatous
Treponema pallidum- Gumma
Helminth:
W. bancrfti
A. lumbricoides
Schistosoma
Fungi:
Rhinosporidiosis seeberi
Cryptococcus neoformans, Coccidioido immitis & Histoplasma
capsulatum
dr.reza2006@gmail.com
Tubercle Vs Gumma
dr.reza2006@gmail.com
Immune Vs Non-immune
granuloma
dr.reza2006@gmail.com
Histological classification:
dr.reza2006@gmail.com
Nonspecific chronic Inflammation





Chronic inflammatory ulcer- peptic ulcer
Chronic suppuratve inflammation- chronic abscess,
chronic pyelonephritis, chronic osteomyelitis
Chronic fibrinous, serous or serofibrinous inflammation
following acute inflammation
Chronic catarrhal inflammation- chronic allergic rhinitis
Chronic necrotizing inflammation- chronic amoebiasis
dr.reza2006@gmail.com
Systemic effects of Acute
Inflammation




Fever:
Leucocytosis, specially neutrophilic leucocytosis- due to
stimulation of bone marrow leading to release of immature cells in
the circulation(shift to the left)
Synthesis of ‘acute phase protein’- liver synthesizes acute phase
protein like C reactive protein(CRP), Fibrinogen and Serum
Amyloid A(SAA).
CRP is a marker of activity and very useful prognostic test
for active Rheumatic fever and other conditions where there is
increased tissue necrosis like MI. As it is not influenced by other
factors, so it is more useful than ESR.
Increased Fibrinogen level is responsible for high ESR. SAA is
responsible for deposition of amyloid in different tissues
Others- lethargy, anorexia, sweating, tachycardia,
hypotension, hypoglycaemia leading to shock due to liberation
of different cytokines, particularly IL1, TNF.
dr.reza2006@gmail.com
Systemic effects of Chronic
Inflammation
 Fever




Anaemia
Leucocytosis- lympho or monocytosis
ESR- elevated
Amyloidosis
dr.reza2006@gmail.com
dr.reza2006@gmail.com
Download