SBAs/ DONT KNOW WELL

• What is Botox? Why is it used to help manage patients with spastic CP?

  Injected botulinum toxin - usually produced by clostridium botulinum - highly neurotoxic Prevents the release of Ach from the alpha LMN into the synaptic cleft --> less excitation of muscle --> less contraction --> dec tone and spasticity as heightened stretch reflex is unable to occur
• describe the ascending pathway of pain modulation

  damaged tissue releases prostaglandins ->stimulates noiceptors -> transduction of pain through dorsal horn (1st order n) -> release of substance P when it synapses with 2nd order n. 2nd order n decussation and passes up spinothalamic tract -> eventually synapses with third order in thalamus -> 2rd order travels to specific part of somatosensory cortex in post central gyrus which correlates with that body part
• describe the descending pathway of pain modulation

  Neurons from the periaqueductal grey matter pass through the raphe magnus and synapse with a 2nd order n. that passes to the dorsal horn. The 2nd order n releases serotonin and NE into the substantia gelatinosa which bind to the presynaptic neuron (in the ascending path) inhibiting the release of substance p And stimulate an interneuron that releases enkephalin. Enkephalin also inhibits the presynaptic neuron from releasing substance p, as well as inhibiting the post-synaptic neuron (in the ascending path) ->prevents transmission to brain
• describe the process of fracture healing

  haematoma forms - stabilise the fracture 

  • Vasodilation, increase in vascular permeability -> Leucocyte extravasation and PIC. Debris is removed allowing granulation tissue to form and osteoprogenitor cells are recruited
  • Soft callus begins to form. Chondrocytes lay down cartilage and capillaries connect to the callus 
  • The soft callus is reabsorbed and replaced by a hard callus made from woven bone 
  • The callus begins to remodel as the woven bone is resorbed by osteoclasts and osteoblasts deposit new lamellar bone 
• describe the process of wound healing

  Haemostaisis - arteriole constriction and production vasoactive metabolites due to hypoxia and acidosis causing dilation. Histamine release for vasodilation - PICs can enter

  inflammatory phase -complement activation, neutrophils infiltrate (cause netosis and phagocytosis). Increase in M1 (antimicrobial) and M2 (tissue repair) macrophages which produce TGF-b and EGF -> angiogenesis and granulation tissue formation. Lymphocytes enter, Tregs supress IFN-gamma, dendritic cells stop T cells from decreasing collagen deposition
• describe the proliferative and remodelling phase of tissue repair

  Proliferative: angiogenesis once hemostatic plug formed. VEGF release due to hypoxia -> repairs bvs. GFs activate fibroblasts and they proliferate and migrate to lay down ECM proteins. Once matrix formed fibroblasts change to myofibroblast phenotype, assist in wound closure and epithelial cells migrate from edge to form a complete sheet. Remodelling phase: development of normal epithelium, followed by scar degradation (balance of synthesis and degradation of collagen and proteins)