9: chronic inflammation II Flashcards
pattern of chronic inflammation seen in a limited number of infectious and non-infectious conditions
granulomatous inflammamtion
aggregates of activated macrophages having a squamous cell-like epitheliod appearance
granulomatous inflammation
granulomatous formation setting
persistent T cell response to certain microbes and fungi leads to macrophage activations (injury); insoluble particles produce cell-mediated response
facaol area of granulomatous inflammation
granuloma
what does a granuloma contain
microscopic aggregation of macrophages that are transformed into epitheliod cells; epitheliod cells surrounded by a collar of mononuclear leukocytes, prinicpally lymphocytes and occasionally plasma cells
epitheliod macrophages, langhans giant cell, peripheral rim of lymphocytes
granuloma
granuloma v. granulation tissue:
granulation tissue: proliferation of fibroblast and new thin-walled, delicate capillaries in loose ECM
fibroblasts surrounded by abundant extracellular matrix, newly formed blood vesels and scattered macrophages
granulation tissue (think of the picture!!!)
epitheliod cells with pale, pink granular cytoplasm;a ggregates of macrophages with collar of lymphocytes, occasionally plasma cells. surrounding rim of fibroblasts and connectie tisseu
granuloma
peripheral arrangements of multinucleated giant cells
langans type
haphazarrd arrangement of multinucleated giant cells
foreign body type
forms when material too large to be phagocytosed by single macrophage
foreign body granuloma
granulomatous inflammation with extensive tissue destruction (caseous necrosis) numerous confluent granulomas in lung
TB
what is our second line of defense (first is skin)?
lymphatics which filter and police extracellular fluid
inflammation of lymphatic channels
lymphangitis
“blood poisoning”
red streaks up the arm- this is actually lymphangitis
if infection overwhlems LB, may gain access to vascular circulation:
bacteremia –> sepsis
inflammation of draining LN
reactive lymphadenitis
clincial hallmark of acute phase inflammation
fever because cytokine stimulate PG synthesis in hypothalamic thermoregulatior center and reset body temp.
where are plasma proteins synthesized
liver
what are teh acute phase proteins
CRP (c reactive prtn)
Fibrinogen
SAA (serum amyloid A protein)
what upregulate the synthesis of acute phase prtns
IL1
IL6
TNF alpha
what is higher WBC leukocytosis or leukemoid reaction
leukemoid reaction is extrememly high, like leukemia
why do you see a shift to the left in WBC as a systemic effect of inflammation?
increase in immature WBC due to accelerated release from bone marrow and increased bone marrow production
increase in absolute number of PMN seen in most BACTERIAL infection
neutrophilia
increase in absoulte number of lymphs; seen mostily in VIRAL infections
lymphocytosis
increase in absolute number of esoinophils seen in asthma hay fever and parasites
eosinophilia
DECREASE in absolute number of WBC seen in overwhelming infection
leukopenia
systemic inflammation effect on autonomic system
- increase pulse and BP
- decrease sweating
behavioral effect of systemic inflammation
shivering, chills, anorexia, somolence, and malaise
pathogenesis of sepsis
severe bacterial infections (large number organisms and toxins) lead to large quantities of cytokines TNF and IL-1
- cardiovascular decompensation
- increased TNF leads to DIC, microthrombi
- liver injury due to lack of gluconeogenesis and overproduction of NO
septic shock triad
DIC
hypoglycemia
CV failure
net result: multisystem organ dysfunction and death
primary cause of tissue injury in allergies and autoimune dieseaes
inflammation
association between chronic inflammatory conditions and cancer
STRONG
the longer an inflammation persists the higher the risk of associated carcinogenesis
