MoD week 4-7 Flashcards
what is fibrous repair?
inflammatory, endothelial & fibroblasts cells infiltrate
blood clot forms (cytokines)
acute inflammation becomes chronic
clot is digested and replaced by granulation tissue
local hypoxia initiates angiogenesis (VEGF)
fibro/myofibroblasts produce ECM causing a scar
maturation is long lasting, cell population falls, collagen increases
myfibroblasts contract to reduce size
blood vessel differentiate and reduce
what are the 3 types of regeneration?
labile e.g. epithelial, in active cell division ATT
stable e.g. hepatocytes, enter cell cycle when required
permanent e.g. nerves, no stem cells to mitose
what is regeneration controlled by?
GF, hormones, proteins, contact between BM (e-cadherin) and between cells (integrin) - contact inhibition (cells stop growing when they meet)
what is healing by primary intention?
clean incised wound, apposed edges, minimal granulation & bleeding, loss of contact inhibition, epidermis regenerated, dermis undergoes fibrous repair
the wound closes first (epidermis) before dermis so can trap bacterial / infection
what is healing by secondary intent?
large skin defect, infarct or ulcer unopposed edges granulation tissue from wound edges loss of contact inhibition epidermis repairs from base up more myofibroblasts large scar takes longer
what are local factors which affect healing?
type, size, location apposition blood supply infection foreign material radiation surgery mechanical stress necrosis protection
what are general factors which affect healing?
age, drugs, diet, anaemia, obesity, general health, malignancy, genes, CVS status
how does the cardiac system heal?
limited, forms scar
how does the liver heal?
regeneration
enlargement of loves to compensate growth + replication of cells
How does a peripheral nerve heal?
schwann cells 1-3mm/day
regenerates proximal axon (elongate)
distal axon degenerates (wallerian degeneration)
use vacated schwann cells to guide axon growth
how does CNS heal?
gliosis
no healing as it is permanent
when damaged, support cells proliferate (glial cells)
how does muscle regenerate?
satellite cells (support)
what are some of the complications of healing?
- insufficient fibrosis
- excessive fibrosis (keloids)
- excessive contraction - contracture (pull on muscle) / stricture (narrowing of opening)
what is haemostasis?
body’s response to blood loss
cessation of bleeding, halting of blood loss
what are the stages of haemostasis?
- severed artery contracts to decrease pressure downstream
- platelet plug forms
- platelet plug stabilised by fibrin
- organisation and replaced by granulation tissue
how is haemostasis regulated? (think about thrombin, what stimulates and what inhibits)
positive feedback from thrombin (prothrombin –> thrombin –> fibrinogen –> fibrin)
thrombin inhibited by: antithrombin III & a-1 antitrypsin & protein C
what is haemostasis regulated by? (breakdown of fibrin)
plasmin breaks downs fibrin clots
plasminogen –(t-PA),(streptokinase)–> plasmin –> fibrin –> fibrin fragment
heparin enhances antithrombin III
warfarin –> antagonises vit K (needed for clotting)
what is thrombosis
formation of a solid mass in the blood stream during life
what is thrombosis caused by?
virchow’s triad, abnormalities in:
blood flow
blood component
endothelium wall (vessels)
what do arterial thrombosis look like?
pale, granular, lines of zhan, low cell content
what do venous thrombosis look like?
deep red, soft, gelatinous, high cell content
what are the fates of thrombus?
PORER
Propagation: thrombus spread and travel in direction of blood flow
Organisation: ingrowth of fibroblasts
Resolution: break down
Embolism: break off to lodge at different location
Recanalisation: blood vessels go through thrombus - supply
what is DIC?
clots everywhere - widespread around the body
what is embolism?
blockage of a blood vessel by a solid, liquid or gas at a site distant from its origin
