Pathology if inflammation.causes, manifestation, types Flashcards
definition of inflammation
complec local mesenchymal and vascular reaction of living tissue on different types of damage
systemic manifesarions of local inflammation
nausea, ^temp, headache, fatigue, enlarged LN, leukocytosis
long lasting chriniz–>AA amyloidosis
SIRS-systemic inflammatory response syndrome
pathogenesis of sepsis
leads to MODS
physiological role of inflammation
- eliminate cause of inflammation and minimize tissue dmaage
- stop spreading of the cause of inflammation (surrond it)
- activate processes of regeneration and repair(healing
pathological role of inflammation
excessive or long lastin reaction leading to tissue damage
role in pathogenesis of many diseases
factors determining inflammatory responese
- features of pathogen
- response of host organism
feature of pathogenbi
- type and mechanism of tissue
- virulence
- infectious dose
- portal of entrance
- products of pathigen
response of host organism
- systemic disaese (dm, Chronic renal insufficency-CHRI, cirrhosis, alcholism, BM failure)
- tumors
- function status of IS-psecific and nonspeficific
- type and localization of damaged tissye
- local host factors
components of inflamamtion
1 cellualr
2. humoral
cellular compinent of inflammation
- neutrophils
-eosinophils - monocytes/macrophagesa dn tissue macrophages (histiocytes)
- lymphocytes and plasma cells
- mast cells
-thromocytes
-endothelial cells
-fibroblast/fibrocytes
humoral component of inflammaiton
- cell derived:
- histamine, serotonin: vasoactive
- prostagladnins, leujotrines: arachionic acid
- free oxy radical, nitric oxide, cytokines, neuropeptides
- plasma derived
- liver
1.components of complement
2. factor X11 (hageman factor) : vessle dia
3. processes of hemostasos, including blood coagualtion and fibrinolysis
- liver
macroscopical features of inflammaiton
typical for acute inflammaiton
1: Calor=Heat (^temp)
- VASODILATION AND HYPEREMIA=HIGHER BLOOD PERFUSION
- hitg metabolic rate=heat
2: Rubor=redness
- dilated vv full of blood
3: tumor=swelling
- leaking water form vv–>acc in interstitium–>inflammatory edema
- exsudate
4: dolor=pain
- inflammatory mediator stimulate nerve fibers–>pain
5: functio leasa=loss of fucntion
- tissue damaged–>not normal funciton
microscopical feature of inflammation types
alteration, exsudation, proliferation
1/2 are increased/advanced
signs (Features) of inflammaiton-histologically
- VASCUALR CHNAGES (sec to minutes)
- infiltrattion of tissue with the inflammatory cells=inflammatory infiltarte/7celluzation (hours-days)
- biochemical, metabolic and morphological changes in involved tissye, even in severe distant organs-liver, spleen, ln
- act of IS
What is altera5ion and what is ti caused by
to alter=damage
- represented by development of dystrophies and necrosis
caused by presence of microorganism, their toxins and immunopathological mechnaism: unfectionys inflammations
where can it be seen
- microscopic-monocellular necrosis in vrial hepatitis
- macroscopic: casefication in granulomas of TB
examples of alteration
- Viral encephalitits
- viral heptatitis
- deiphteric myocarditic: by corynebacterium diptheria
what is exsudation
leakage of fluid, proteins, blood cells from vv to interstitium, on mucosal surfaces or into cavities (pleural, peritoneal, pericardial cavitiies)
exsudate leakage is produced after fullfillment of which processes
- Vasodilation
- lead to redness and increased temp - increaseed vascular permeability
- bc of mediaters or direct damage to vv wall
- opening of gapes btw endothelial cells - exsudation + leukocyte emigration
- vascular stasits
what is transudate
- when filtrattion of fluid is higher that reabsoprtion into vv.
- permeability of vv is NOT CHNGES: only fluid escapes
hypostattic tissue edema due to heart failure
what is proliferation and what does it include
Proliferation is the development of granulation tissue which is vascularized pink tissue with granular apperanc
includes:
- multiplication of inflamamotry cells in inflammed tissue
- prolif of vv/endothelial cells(angiogenesis)
- prolif of interstitial cells-fibroblasts
- formaiton and remodeltation of new tissue
what is non-specific grnaulation tisuse and what is it compised of
-typically seen in chronic inflammaiton and healing
-responsible for healing and repair
- composed of
1. new forming vv: proliferation of ENDOTHELIAL CELLS
2. FIBROBLASTS
- make collagen and EM
what will nonspecific granuation tissue turn into
collagenous, hypocellualr, hypovascular tissue; aka SCAR
by healing, scarificaiton and fibrotization
what is specific granulation tissue
- not a tissye visible in process of healing
- NOT PROLIFERATING VV, NO VV
- composed of:
- histiocytes whcih get cahnged into epitheloid cells: epitheloid hitstiocytes
-
- histiocytes whcih get cahnged into epitheloid cells: epitheloid hitstiocytes
type of inflammation axx to time
peracute: days-week
acute: 1-3e
subacute: 3-6w
chronic: m-y
tyoe of inflammaiton acc to cells
acute: polymorphonuclears-nucleus and macrophages
chronic: lymphocytes, plasma, macro, fibrobalst
if we have allergic /parasitic etiology we can se
macro and eosinophils
if we have viral etiology
lymohocytes
what are liable cells
cells able to regenerate,
what is stabile cells or permanent cells
no ability to proliferate (musclem nervoys tissue)
- striated, cardiac muscle and most smooth muscle(not uterus)
- damage fixed only by repair–>non-specific grnaulation tissye–>fibrous scar
what is exacerbation
where acute inflammation may be reactivated, chronic–>acute
