Pathophysiology

Subdecks (4)

Cards (30)

  • Phantom Limb Pain (peripheral nerve changes).
    Limbs full of sensory neurons, most pathways remain after amputation
    At site of amputation there are severed nerve endings -> endings can thicken & become more sensitive -> transmit distress signals (even in response to mild pressure) - normally inhibited by dorsal horn
    In somatosensory cortex, representation of amputated is still present -> increased representation (phantom limb pain)
    Overtime area of cortex representing amputated limb may shrink & pain stops
  • What is compartment syndrome?
    Increased pressure within a muscle compartment leading to reduced blood flow and tissue damage.
  • What is reperfusion injury?
    Can be called ischaemia reperfusion injury (IRI)
    Tissue damage caused when blood supply returns to tissue after a period of ischemia or lack of O2
    Return of O2 & inflammatory cells may lead to free radical generation -> further damages myocytes
  • What are the damaging substances produced from anaerobic respiration?
    Histamine
    Lactic acid
    NO
    Potassium
    Thromboplastin
  • What is released into systemic circulation in crush syndrome?
    Myoglobin
    Creatine kinase
    Potassium
    Magnesium
    Phosphorus
    Uric acid
  • How is histamine damaging (related to crush syndrome)?
    Vasodilator = exacerbates hypovolaemic shock
    Bronchoconstriction = exacerbates hypoxaemia
  • What is crush syndrome?
    Significant metabolic derangement
    Develops when crushed extremities or body parts remain trapped for prolonged period
    Can lead to renal failure & death
    When body part is released, floods with toxins
  • How can potassium be damaging when released in excess?
    Hyperkalaemia -> arrthymia
  • What is phantom limb pain?
    Ongoing painful sensations that seem to be coming from part of limb that is no longer there
    Limb is gone, pain is real
  • What is a major complication of crush syndrome?
    Compartment syndrome
  • How is lactic acid damaging?
    Metabolic acidosis
  • When is the onset of phantom limb pain most often?
    Soon after surgery
  • Crush injuries
    Trauma to blood vessels -> transudation of fluid, interstitial bleeding -> ischaemia & hypoxia
    Cells no longer able to maintain metabolic function -> oedema & third spacing of fluid
    If oedema occurs in a closed space -> increased pressure will collapse microcirculation, eliminate O2 transfer across capillary endothelium & further contribute to hypoxic insult
  • What are the 4 theories behind phantom limb pain?
    Not fully understood
    • Peripheral nerve changes
    • Spinal cord changes
    • Brain changes
    • Psychogenetic changes
  • Phantom limb pain (spinal cord changes)
    Central sensitisation - increase in DNMA receptor expression in dorsal horn
    Any incoming sensation can drive a disproportionate response -> conscious perception
  • Phantom limb pain (brain changes).
    Cortical reorganisation - areas of cortex that previously represented the amputated limb become invaded by neighbouring somatosensory & motor cortex
    Signals are still being sent & received to & from that are of cortex that belonged to missing limb