Inflammatory response/repair Flashcards
(26 cards)
4 signs of inflammation
- Swelling
- redness
- heat
- pain
What is the first things cells release when injured (+ ex)
- Injured cell releases Alarmins (DAMPs)
- -histone pros, uric acid, heat shock pros, s100, HMGGB1)
What do the Alarmins bind to (+ ex)
Bind to non specific receptors found on surfaces of surounding cells (TLRs, RAGE, TREM1)
When alarmins bind to receptors what do they release
release proinflammatory mediators
- Cytokines (IL1, TNFa)
- Lipid chem mediators
- Vasoactive amines
What do pro inflammatory mediators cause
- muscle relazation (vasodialation)
- increased blood delivery
- Flushing action
- increased vessel leakiness (opens tight junctions allowing swelling)
- activate selection adhesions
Steps of Extravasion of Leukocytes (what causes rolling adhesion and tight binding)
-Selections expressed by activated endothelial cells
- S-lex expressed by white blood cells willl come in contact w selectins and cause rolling adhesion
- ICAMS further aid in slowing down white blood cell causing tight binding
What is diapedesis and chemotaxis
diapedis- binding causes conformational change that allows white blood to squeeze bw capillary endothelial cells
Chemotaxis- Once in, the white blood cells will follow cehmokine gradiants to migrate to site of injury
What percentage of Leukocytes is made of granulocytes and what are the sub cats
70%
basophils- <1% (helps regulate clotting)
Monocytes- 5%
macrophages
What processes indicated there is chronic inflamation
fibrous, angiogenesis and granuloma are signs of chronic inflammation
S+s of systematic inflamatin
-prescence of elevated lvls of inflammatory mediators n peripheral blood
- Fever, peripheral blood leukocytes, headache, chills
- can cause net mvmt of fluids into tissues causing risk of shocj
What are ex of acute phase pros and why are they produces
- produced in response to systemic inflammation
- Il6, c reactive pro, fibrinogen, plasminogen, ferritin, alpha 1 anti trypsin + mannan
What triggers regerneration of tissues
Growth factors (EGF, VEGF, TGF, granulocyste macrophage stim factro)
Epidermal growth factor function
Binds to receptors resulting in various signaling paths (RAS, RAF, MEk)
-activation of genes/pros that favour entery into cell cycle/proliferation
Vascular Endothelia growth factor function (what else can it be produced by)
- induce proliferation of endothelia cells
- can also be produced by platlets
transforming GF beta function
Stims deposition of collegen + ECM components
Granulocyte marcrophage stim factor
Stims stem cells to produce monocytes and granulocytes
Labile, stabile and perminent tissues; amount of stem cells and regeneration ability, ex
Labile- many active stem cells, high regen (bone marrow, skin, gut)
Stabile- only enter cell cycle as needed (prox tubules of kid, liver)
Perminent- can only be replaced w scar/fibrous tissue
Steps of fibrous repair
- Inflamation (macrophages/fibroblasts)
2. Proliferation (angiogenesis, granulation, remodeling, epithelization)
What happens in inflammation stage of fibrous repair
inflamation- injury induces inflammatory response which leaks to recruitment of active leukocytes + fibroblasts
What are the pro inflammatory and anti inflamatory macrophages
M1- pro inflamatory
M2- anti inflammatory ( clearence of dead cells, secrete GFs)
What happens in the prolifeation stage of fibrous repair
fibroblasts lay down collegen/elastin, angiogenesis, granulation and wound contracture happens
What happens in angiogenesis (what causes it)
Increased blood delivery to injured area
-Angiogenic GFs (VEGF, PDGF) produced by M2 macrophages
When does granulation start to occur
72 hours post injruy
What happens in remoddeling
Type 3 collagen replace by type 1
-myofibril a smooth mm actin contracts to better tolerate forces
