M2 L9 Flashcards
(30 cards)
what determines a tissue response to injury
- nature of damaging agent
- tissue type damaged
- damage severity
what is the broad response to injury?
acute inflammation
what happens after acute inflammation
- if the tissue can regrow it does
- if the tissue cannot regrow it is repaired
- if the damaging agent persists there is chronic inflammation
-> if this is not overcome chronic inflammation persists
-> if it is overcome repairs take place
how is inflammation described
redness
swelling
heat
pain
loss of function
what are the stages of acute inflammation
- very brief constriction (few secs)
- vascular dilation
- endothelial contraction
- neutrophil activation and migration
what happens during vasodilation ( in acute inflamm)
- increased blood flow
- chemical mediators released from damaged tissue eg. histamines
- mediators act on blood vessels
what happened during endothelial contraction (acute inflamm)
- endothelial cells swell and retract
- increased permeability to water, salts, proteins eg. fibrogen, immunoglobulins
- causes swelling
what happens during neutrophil activation and migration (acute inflamm)
- damage replaced with exudate components
- neu adhere to endothelium (margination) then actively migrate towards damage
- fibrin is polymerised from fibrinogen in tissue
outcomes of acute inflammation
- regeneration (if connective tissue is intact)
- organisation and repair
- chronic inflammation persists
what are the five stages of tissue repair
- organisation and repair
- vascular granulation
- fibrous granulation
- collagen scar formation
- fibrous scar formation
organisation and repair (tissue repair)
- macrophages enter and clear debris
- granulation tissue laid down
vascular granulation (tissue repair)
- damaged area replaced by complex of interconnecting capillaries, macrophages and support cells
- macrophages secrete angiogenic factors to guide cap growth
- fibroblasts also attracted
fibrous granulation
- fibroblasts proliferate
- collagen layers replace capillaries
- few remaining lymphocytes
collagen scar formation
- fivrovlasts allign to deposit collagen for max strength
- fibroblasts -> cytes
- vascularity reduced
fibrous scar formation
- permanent scar formed
- contraction can result in scar size reduction
- overproduction of collagen = keloid
why do surgical cuts heal better
- less damage to epi -> less inflammation and fibrin
- less granulation tissue -> less angiogenesis
- collagen fibres can meet horizontally with less space to fill
what do connective tissue diseases result from?
- infection
- injury
- genetics
- unknown cause
what are three collagen defect disorders
- Osteogenesis imperfecta
- Ehlers danlos
- Alport syndrome
what causes osteogenesis imperfecta?
- type I collagen deficiency (less or poorer quality)
-> poorer quality = more severe disorder
-autosomal dominant - mutations in COL1A1 and COL1A 2
what are two symptoms of OI
- brittle bones
- blue sclera
- etc
what are the first three types of OI
I
- produce less collagen (milder)
- most common
II
- produce poor collagen (severe)
- less common
- perinatal lethal
III
- poor collagen
- less common
- severe deformation
what is EDS
- group of heritable connective tissue disorders
- affects skin, ligaments and organs
how is EDS characterised
- loose joints
-stretchy skin - abnormal scarring
what does eds inc risk of
- dislocations
- scoliosis
-osteoarthritis
