1.3, 4.1, 6.1 Healing & repair, haemodynamic disorders

1.3 Cell biology
Molecular techniques to study DNA/RNA
1. Polymerase chain reaction (PCR)
2. Gel electrophoresis
3. In-situ hybridisation (ISH)
Molecular techniques to study protein
1. Enzyme-linked immunosorbent assay (ELISA)
2. Western blotting
3. Immunohistochemistry (IHC)
4. Immunofluorescence

4.1 Healing & Repair
3 types of cell regenerative capacity
1. Labile – Divide throughout life, constantly replaced e.g. epithelial cells
2. Stable – Divide when necessary e.g. Hepatocytes
3. Permanent – Divide only during fetal life e.g. Nerve cells
where are stem cells
1. Epidermis – adjacent to basement membrane in basal layer
2. Intestinal mucosa – bottom of crypts
1. The healing/regeneration process
1. Cells proliferate & spread out as a thin sheet until wound covered
2. Stop proliferating when they meet (contact inhibition)
3. Epidermis then built up from base
4. Covered by scab – layer of fibrin
The organisation/repair process
1. Granulation tissue forms (composed of capillary loops & myofibroblasts)
2. Dead tissue removed by neutrophil polymorphs and macrophages
3. Granulation tissue contraction (and accumulates collagen = scar forms)

1. Skin healing
1st intention – Incisions, close approximation of edges = fast healing
1. Edges joined by fibrin (scab_
2. Neovascularisation
3. Fibroblasts secrete collagen
2nd intention – tissue loss, not close approximation
1. Phagocytosis of debris
2. Granulation tissue fills defects
3. Epithelial regeneration to cover surface
Cytokines involved in healing/repair
1. Epidermal growth factor (EGF) – Epithelial regeneration
2. Vascular Endothelial growth factor (VEGF) – angiogenesis
3. Transforming growth factor beta (TGF-beta) – Control myofibroblasts and collagen formation
2. Gastric mucosal ulcers
1. Bleeding & fibrin covers surface
2. Phagocytosis of debris
3. Granulation tissue at base
4. Epithelial regeneration from ulcer edges
3. Bone fracture
1. haematoma – From ruptured vessels, debris removed
2. Callus – Woven bone (irregular)
3. Lamellar bone replaces woven bone
Factors affecting bone healing
1. Mobility – excess callus
2. Misalignment – Risk of degeneration
3. Interposed soft tissue – Risk of non-union
4. Liver
3 sources of cells for repair
1. Hepatocytes
2. Liver progenitor cells
3. Bone-marrow derived stem cells
5. Muscle
1. Cardiac & smooth = permanent cells (scar forms)
2. Vascular smooth muscle can form new vessels
-Voluntary muscle has limited regeneration by satellite cells
6. nerve
IAN damage
1. Mandible fractures
2. Lower 8’s
3. Rejection of neoplasms
3 types of peripheral nerve damage
1. Neurapraxia – Contusion, no loss of axon/endoneurium, recovery in days-weeks
2. Axonotmesis – lsos of axon contiuity, no endoneurium loss, 2-6 months, nerve dysfunction
3. Neurotmesis – Complete loss of continuity, poor prognosis
Nerve healing
1. Segmental demyelination – Myelin sheath dissolves in segments
2. Wallerian degeneration – Axons, myelin sheath, distal degen
3. Regeneration – New fibres grow down schwann cell tube
7. Alveolar socket
0 days – Clot retraction + clot stabilisation, fibrin cross linking
2 days – Clot lysis + Emigration of inflammatory cells
4 days – Granulation tissue grows into clot, macrophages demolish clot, gingival hyperplasia to cover clot
8 – Socket filled w granulation tissue + Epithelial migration complete
18 days – Woven bone formation around socket periphery
6 weeks – Woven bone beginning to remodel -> lamellar
8. Factors affecting wound healing
1. Age – Delayed healing e.g. angiogenesis, neutrophil, macrophage
2. Diabetes – Impaired wound healing, foot ulcers
3. Immunosuppression – increased susceptibility to infection
4. Alcoholism & smoking – decreased phagocytosis & neutrophil recruitment
5. Cushing’s syndrome/steroid therapy – interferes with granulation tissue formation

6.1 Haemodynamic disorders
1. Vasovagal syncope sequence
1. Stress induced increase in catecholamines = decreased peripheral vascular resistance, tachycardia, sweating. Generalised warmth, nausea, palpitations
2. When blood pools in periphery = drop in arterial BP, cerebral blood flow, dizzy & weak
3. Compensatory mechanisms to lower BP = bradycardia, if too low = syncope
Management
1. Stop treatment
2. Supine
3. Check breathing
(If not – life support, 000)
4. Crush ammonia under nose, oxygen, monitor vitals, have pt escorted home, future anxiety control
2. Edema – Excess fluid in intercellular compartment of tissue
5 causes of edema
1. Increased hydrostatic pressure
2. Increased vascular permeability
3. Lymphathic obstruction
4. Sodium retention
5. Physiological
5 types of oedema pathogenesis
1. Normal = hydrostatic pressure forces water out arterial end
2. Inflammatory edema = Gaps between endothelial cells
3. Venous edema = increased venous pressure
4. Lymphatic edema – lymphatic obstruction = no water drainage
5. Hypoalbuminaemic edema – Low plasma albumin
3. Atherosclerotic lesions
1. Starts with fatty streaks
2. Mature plaques have central lipid core + fibrous cap (macrophages, lymphocytes, mast cells)
How do they form
1. Injury to endothelial cells
2. Inflammatory cells & lipids migrate to intima & form plaques
3. As it matures, macrophages die, spilling liquids into core
4 clinical manifestations of atherosclerosis
1. Narrowing (stenosis)
2. Atherothrombotic occlusion
3. Embolism
4. Ruptured abdominal atherosclerotic aneurysm
4. Calcifications
1. Dystrophic calcifications – local precipitations of calcium
e.g. Atheromatous plaques, fat necrosis
2. Psommoma bodies – Lamellated calcified bodies
3. Metastatic calcification – widespread hypercalcaemia
5. Thrombus
1. Virchow’s triad
1. Change in intima
2. Change in blood flow
3. Change in blood constituents
Venous thrombosis
1. Mostly in leg, because blood going to heart is reliant on calf contraction
2. Immobile elderly pts
3. Tender, swollen, red
Arterial thrombosis formation & effects
1. Athermoatous plaque deposit
2. Loss of endothelial cells
3. Platelet adhesion
4. Occlusion by multilayered thrombus
Cold, pale, painful
Sequelae of thrombi
1. Resolve
2. Organised into a scar
3. Recanalised -ingrowth of new vessels
4. Embolism – Thrombus breaks off into circulation
6. Infarcts
Red infarcts – occurs in previously congested tissues, venous occlusions, flow not re-established after previous infarcts
White infarcts – arterial occlusion in solid organs e.g. heart, kidney
7. Embolism
-Embolus is a mass able to lodge in vessel & block lumen
-95% in leg veins, some pelvic veins, some intracranial venous sinuses
8. Vascular insufficiency
6 types of vascular insufficiency
1. Atheroma – Plaques narrow lumen
2. Spasm – Smooth muscle contraction
3. External compression
4. Vasculitis
5. Steal – diversion of blood
6. Hyperviscosity
9. Shock
3 types of shock
1. Cardiogenic – low cardiac output from heart unable to pump sufficient blood
2. Hypovolemic- low blood volume e.g. wound
3. Septic – Microbial

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