1inflammation is seen in infection acute and chronic etc

1inflammation.ppt

1. InflammationInflammation
Jan Laco, M.D., Ph.D.

2. InflammationInflammation
complex protective reaction
caused by various endo- and exogenous
stimuli
injurious agents are destroyed, diluted or
walled-off
without inflammation and mechanism of
healing could organism not survive
can be potentially harmfull

3. TerminologyTerminology
Greek root + -itis
metritis, not uteritis
kolpitis, not vaginitis
nephritis, not renitis

4. MechanismsMechanisms
local - in cases of mild injury
systemic
3 major:
1. alteration
2. exsudation - inflammatory exsudate
–liquid (exsudate)
–cellular (infiltrate)
3. proliferation (formation of granulation and fibrous
tissue)
usualy - all 3 components - not the same intensity

5. ClassificationClassification
several points of view
length:
–acute × chronic (+ subacute, hyperacute)
according to predominant component
–1. alterative (predominance of necrosis - diphtheria)
–2. exsudative (pleuritis)
–3. proliferative (cholecystitis - thickening of the wall by
fibrous tissue)

6. ClassificationClassification
according to histological features
–nonspecific (not possible to trace the etiology) - vast
majority
–specific (e.g. TB)
according to causative agent
–aseptic (sterile) - chemical substances, congelation,
radiation - inflammation has a reparative character
–septic (caused by living organisms) - inflammation has
a protective character

7. Acute inflammationAcute inflammation
important role in inflammation has
microcirculation!
supply of white blood cells, interleukins,
fibrin, etc.

8. Local symptomatologyLocal symptomatology
classical 5 symptoms (Celsus 1st c. B.C.,
Virchow 19th c. A.D.)
1. calor - heat
2. rubor - redness
3. tumor - swelling
4. dolor - pain
5. functio laesa - loss (or impairment) of
function

9. Systemic symptomatologySystemic symptomatology
fever (irritation of centre of thermoregulation)
–TNF, IL-1
–IL-6 – high erythrocyte sedimentation rate
leucocytosis - increased number of WBC
–bacteria – neutrophils
–parasites – eosinophils
–viruses - lymphocytosis
leucopenia - decreased " "
–viral infections, salmonella infections, rickettsiosis
immunologic reactions - increased level of some
substances (C-reactive protein)

10. Vascular changesVascular changes
vasodilation
–increased permeability of vessels due to widened intercell.
junctions and contraction of endothelial cells (histamin,
VEGF, bradykinin)
protein poor transudate (edema)
protein rich exsudate
leukocyte-dependent endothelial injury
–proteolysis – protein leakage
 platelet adhesion  thrombosis

11. Cellular eventsCellular events
leukocytes margination  rolling  adhesion  transmigration
emigration of:
–neutrophils (1-2 days)
–monocytes (2-3 days)
chemotaxis
–endogenous signaling molecules - lymphokines
–exogenous - toxins
phagocytosis - lysosomal enzymes, free radicals, oxidative burst
passive emigration of RBC - no active role in inflamm. -
hemorrhagic inflammation

12. PhagocytosisPhagocytosis
adhesion and invagination into cytoplasm
engulfment
lysosomes - destruction
in highly virulent microorganisms can die
leucocyte and not the microbe
in highly resistant microorganisms -
persistence within macrophage - activation
after many years

13. Outcomes of acute Outcomes of acute
inflammationinflammation
1. resolution - restoration to normal, limited injury
–chemical substances neutralization
–normalization of vasc. permeability
–apoptosis of inflammatory cells
–lymphatic drainage
2. healing by scar
–tissue destruction
–fibrinous inflammtion
–purulent infl.  abscess formation (pus, pyogenic membrane,
resorption - pseudoxanthoma cells - weeks to months)
3. progression into chronic inflammation

14. Chronic inflammationChronic inflammation
reasons:
–persisting infection or prolonged exposure to
irritants (intracell. surviving of agents - TBC)
–repeated acute inflamations (otitis, rhinitis)
–primary chronic inflammation - low virulence,
sterile inflammations (silicosis)
–autoimmune reactions (rheumatoid arthritis,
glomerulonephritis, multiple sclerosis)

15. Chronic inflammationChronic inflammation
chronic inflammatory cells ("round cell" infiltrate)
–lymphocytes
–plasma cells
–monocytes/macrophages activation of macrophages by
various mediators - fight against invaders
lymphocytes  plasma cells, cytotoxic (NK) cells,
coordination with other parts of immune system
plasma cells - production of Ig
monocytes-macrophages-specialized cells
(siderophages, gitter cells, mucophages)

16. Morphologic patterns of Morphologic patterns of
inflammationinflammation
1. alterative
2. exsudative
–2a. serous
–2b. fibrinous
–2c. suppurative
–2d. pseudomembranous
–2e. necrotizing, gangrenous
3. proliferative
–primary (rare) x secondary (cholecystitis)

17. Morphologic patterns of Morphologic patterns of
inflammationinflammation
2a. serous - excessive accumulation of fluid, few
proteins - skin blister, serous membranes - initial
phases of inflamm.
modification - catarrhal - accumulation of mucus
2b. fibrinous - higher vascular permeability -
exsudation of fibrinogen -> fibrin - e.g. pericarditis
(cor villosum, cor hirsutum - "hairy" heart
fibrinolysis  resolution; organization  fibrosis 
scar

18. 2c. suppurative (purulent) - accumulation of neutrophillic
leucocytes - formation of pus (pyogenic bacteria)
interstitial
–phlegmone – diffuse soft tissue
–abscess - localized collection
acute – border – surrounding tissue
chronic – border - pyogenic membrane
Pseudoabscess – pus in lumen of hollow organ
formation of suppurative fistule
accumulation of pus in preformed cavities - empyema
(gallbladder, thoracic)

19. complications of suppurative inflamm.:
bacteremia (no clinical symptoms!; danger of
formation of secondary foci of inflamm. (endocarditis,
meningitis)
sepsis (= massive bacteremia) - septic fever, activation
of spleen, septic shock
thrombophlebitis - secondary inflammation of wall of
the vein with subsequent thrombosis - embolization -
pyemia - hematogenous abscesses (infected infarctions)
lymphangiitis, lymphadenitis

20. 2d. pseudomembranous - fibrinous
pseudomembrane (diphtheria - Corynebacterium,
dysentery - Shigella) - fibrin, necrotic mucosa,
etiologic agens, leucocytes
2e. necrotizing - inflammatory necrosis of the
surface - ulcer (skin, gastric)
–gangrenous - secondary modification by bacteria - wet
gangrene - apendicitis, cholecystitis - risk of
perforation - peritonitis

21. Granulomatous inflammationGranulomatous inflammation
distinctive chronic inflammation type
cell mediated immune reaction (delayed)
aggregates of activated macrophages 
epithelioid cell  multinucleated giant cells
(of Langhans type x of foreign body type)
NO agent elimination but walling off
intracellulary agents (TBC)

22. Granulomatous inflammationGranulomatous inflammation
1. Bacteria
–TBC
–leprosy
–syphilis (3rd stage)
2. Parasites + Fungi
3. Inorganic metals or dust
–silicosis
–berylliosis
4. Foreign body
–suture (Schloffer „tumor“), breast prosthesis
5. Unknown - sarcoidosis

23. Tuberculosis – general Tuberculosis – general
pathologypathology
1. TBC nodule – proliferative
Gross: grayish, firm, 1-2 mm (milium)  central
soft yellow necrosis (cheese-like – caseous) 
calcification
Mi: central caseous necrosis (amorphous
homogenous + karyorrhectic powder) +
macrophages  epithelioid cells  multinucleated
giant cells of Langhans type + lymphocytic rim
2. TBC exsudate – sero-fibrinous exsudate
(macrophages)

24. LeprosyLeprosy
M. leprae, Asia, Africa
in dermal macrophages and Schwann cells
air droplets + long contact
rhinitis, eyelid destruction, facies leontina
1. lepromatous – infectious
–skin lesion – foamy macrophages (Virchow cells) + viscera
2. tuberculoid – steril
–in peripheral nerves – tuberculoid granulomas - anesthesia
death – secondary infections + amyloidosis

25. SyphilisSyphilis
Treponema pallidum (spichochete)
STD + transplacental fetus infection
acquired (3 stages) x congenital
basic microspical appearance:
–1. proliferative endarteritis (endothelial hypertrophy 
intimal fibrosis  local ischemia) + inflammation
(plasma cells)
–2. gumma – central coagulative necrosis + specific
granulation tissue + fibrous tissue

26. SyphilisSyphilis
1. primary syphilis - contagious
chancre (ulcus durum, hard chancre)
M: penis x F: vagina, cervix
painless, firm ulceration + regional painless
lymphadenopathy
spontaneous resolve (weeks)  scar

27. SyphilisSyphilis
2. secondary syphilis - contagious
after 2 months
generalized lymphadenopathy + various
mucocutaneous lesions
condylomata lata - anogenital region, inner
thighs, oral cavity

28. SyphilisSyphilis
3. tertiary syphilis
after long time (5 years)
1) cardiovascular - syphilitic aortitis (proximal a.)
–endarteritis of vasa vasorum  scaring of media  dilation 
aneurysm
2) neurosyphilis – tabes dorsalis + general paresis
–degeneration of posterior columns of spinal cord  sensory +
gait abnormality
–cortical atrophy  psychic deterioration
3) gumma – ulcerative lesions of bone, skin, mucosa –
oral cavity

29. Congenital syphilisCongenital syphilis
1) abortus
–hepatomegaly + pancreatitis + pneumonia alba
2) infantile syphilis
–chronic rhinitis (snuffles) + mucocutaneous lesions
3) late (tardive, congenital) syphilis
–> 2 years duration
–Hutchinson triad – notched central incisors + keratitis
(blindness) + deafness (injury of n. VIII)
–mulberry molars + saddle nose