acute inflammation Flashcards
what is inflammation
complex, non-specific tissue reaction
2 purposes of inflam
- remove necrotic/damaged tissue
2. elim. foreign invaders
2 times of inflammatiokn
acute, chronic, or acute on chronic
3 main features of inflammation
- blood flow (vasodilation)
- vascular permeability
- recruitment and activation of leukocytes
2 types of fluid in swelling
- tranudate
2. exudate
what is mech of transudate
fluid leaks out by osmosis due to lack of plasma proteins
3 features of transudate fluid
- low protein
- low cellularity
- low specific gravity
mech of exudate
increased vascular permeability means everything leaks out
3 features of exudate fluid
- high protein
- high cellularity
- high specific gravity
4 mechs of vasc. permeability
- endothelial retraction (NO and histamine) - rapid and shortlived
- direct endothelial injury - rapid and possibly long lived
- leukocyte-induced endo injury - delayed onset, long lived
- transcytosis - interconnected, uncoated vessicle and vacuoles
what does type of fluid tell you
tranudate - no inflammation
exudate - inflammation
what is acute lymphangitis
when inflammation affects lymph nodes
5 cardinal signs of inflammation
- rubor
- calor
- tumor
- dolor
- loss of function
what are steps of leukocyte reactions in inflammation
- injury activates macrophages to secrete TNF and IL-1
- leukocytes bind lightly to selectins on cell wall
- chemikine activation leads to integrin binding on cell wall (tight)
- diapedis occurs, where leukocyte squeezes through vessel wall
- chemotaxis - causes migration of leukocytes along chemokine gradient in interstitial tissues
3 examples of chemokines
- bacterial products
- leukotrine B4
- complement 5a
what is goal of chemotaxis
bring leukocyte close to offending agents
what are steps to phagocytosis
- binding of agent to membrane wall
- engulfment into lysosome
- destruciton of microbes
2 ways to destroy microbes
- digestion by lysosomal enzymes
2. free radicals
3 deficits of leukocyte function
- chediak-higashi syndrome - failure to fuse with lysosome leads to accumulation in vacuoules
- chronic granulomatous disease - failure of oxidative burst leading to accumulation
- myeloperoxidase deficiency - deficient halogenation
what are qualities of a neutrophil
early response
- lower phagocytic activity
- more lysosomal enzymes
- enzymes secreted into interstitial space causing further tissue damage
what are qualities of a macrophage
- later response
- lower quantitiy of lysosomal enzymes
- more phagocytic activity
- would repair and clean up
2 types of macrophages and their jow
M1 - via micorbes and IFN-G - inflammation
M2 - via IL13 and IL4 - anti inflammatory
2 types of inflammatory mediators and their features
- preformed, stored in granules for rapid release and action
- synthesized de-novo - delayed onset of action
3 features of pro-inflammaroty mediators
- activated by wide variety of stim with lots of crosstalk
- short lived and quick to decay
- present in bloods ad inactive precursors
2 types of preformed mediators
- vasoactive
2. lysosomal contsituents of leukocytes
2 types of vasoactive mediators and their funct
- histamines - mast cells - vasodilation and endothelial retraction
- serotonin - platelets and neuroendocrine cells - endothelial contraction - link between clotting and inflammation
what are lysossomal constituents of leukocytes
enzymes stores in neutrophils and macrophages that activate C3 and C5
what are de novo snythesized mediators
- arachndonic acid metabolites - eiconasoids
4 key actions of eiconasoids
- vasodilation - prostcyclin, PGE1 and2
- vasoconstriciton - thromboxane
- vasc. permeability - leukotrienes C4 E4 D4
- chemotaxis and cellular adhesions - leukotiene B4
3 classes of de novo made mediators
- arachnadonic acids
- NO
- cytokines
where is NO from and what is the function
- from endothelium, macrophages
2. microbial killing, vasodilation, anti-inflammatory
what are cytokines
proteins produced by many cell types that madulate the functions of other cell types
2 main cytokines
TNF and IL1
what are local and systemic effects of cytokines
- local - activation of leukocytes
2. systemic, fever, leukocytosis, acute phase proteins, sleep
what are 2 main systems of plasma protein derived inflammation
- complement system
2. coagulation and kinin systems
what are complement proteins
C3 an C5 - involved in innate and adaptive immunity - circulate in inactive form
what are 3 ways to activate complement proteins
- from microbes (alternate path)
- antibody mediated (classical path)
- mannose binding (lectin path)
4 possible outcomes of active complement proteins
- recruitment of leukocytes to destroy microbes
- bind to microbe to imporve recognition for phag.
- form a membrane attack complex (MAC) which cause fluid filling an explosion
- C5a activates lipoxygenase pathway - anti-inflammatory
what is coagulation and kinin system
hageman factor (factor XII) activated intrisic clotting pathway, kinin cascade - activates COX and get proinflammatory
what is main product of kinin cascade activation
bradykinin - mediated pain - hyperalgesia
3 major mediators of vasodilation
- protaglandin
- NO
- histamine
3 major mediators of permeability
- H and 5 HT
- leukotiens
- C3a and C5a
4 major mediators of chemotaxis and activation
- TNF
- IL-1
- C3and 5a
- leukotriene B4
2 mediators of fever
- TNF
2. IL-1
mediator of pain
bradykinin
3 mediators of tissue damage
- NO
- lysosomal enzymes
- ROS
2 morphological hallmarks of acute inflammation
- dilation of vessels
2. exudation
3 morphological patterns acute inflammation
- serous
- fibrinous
- pruulent (abscess)
3 morphological patterns acute inflammation depends on
- nature of injury
- severity of injury
- site of injury
