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MEDICINE > NAS W5 > Flashcards

NAS W5 Flashcards

1
Q

INHIBITORY NEURONE

A

when active, produces neurotransmitters which inhibit neurones it makes synaptic contact with

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2
Q

INHIBITED NEURONE

A

one which is firing less because inhibitory neurotransmitter has been released from neurones it synapses with

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3
Q

REFLEX

A
  • stereotyped (always same response) involuntary reactions of CNS to specific sensory input
  • brings about rapid response
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4
Q

CLINICAL RELEVANCE OF REFLEX

A
  • stereotyped so we can test for a known reflex to see issue

- e.g. autonomic (involuntary) pupillary reflex - shine light in eye & expect pupil to constrict

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5
Q

FUNCTIONS OF REFLEX

A

protective, postural control, homeostasis

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6
Q

INTEGRATION CENTRE

A

contains interneurons (between sensory & motor & are in CNS & take info from reflex arc & relay it to other interneurons)

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7
Q

HYPERFLEXIA

A

when communication between brain (CNS) & integration centre is damage so there is unregulated reflex arc

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8
Q

TYPES OF PROPRIOCEPTORS

A

muscle spindles & golgi tendon organs

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9
Q

MUSCLE SPINDLE8

A
  • stretch exceeds threshold = AP firing = depolarisation = sensory neurone releases neurotransmitter (excitatory) to increase motor activity (AcH released leads to contraction to prevent damage to skeletal muscle)
  • monosynaptic (no interneurones)
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10
Q

CROSS-EXTENSOR REFLEX

A

we can simultaneously extend one muscle (extensor) & relax another (flexor) to get reflex (excitatory neurotransmitter leads to contraction but also releases inhibitory neurotransmitter which stops firing of excitatory so muscle relaxes)

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11
Q

GOLGI TENDON ORGANS

A
  • prevent damage due to overwork
  • polysynaptic (have interneuron (it is inhibitory)
  • we lift something heavy = activates muscle spindles= muscle contracts & applies compression to nerve endings = golgi tendon organ activated so AP form in sensory afferent = AP depolarise synaptic terminal & release neurotransmitter (excitatory so causes interneuron to fire more AP) but interneuron releases inhibitory neurotransmitter so no AP in motor neurone & no AcH in muscle so no contraction (called reverse myotatic reflex)
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12
Q

SKELETAL MUSCLE NEURONE SUPPLY

A

somatic nervous system (voluntary)

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13
Q

SMOOTH MUSCLE NEURONE SUPPLY

A

autonomic nervous system (modifies muscle by increasing or decreasing myogenic activity not generating it)

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14
Q

GLANDS

A

autonomic nervous system (NS modifies secretions of glands to get effect)

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15
Q

TYPES OF DAMAGE TO NERVE (ENDO, PERI, EPINEURIUM)

A
  • NEUROPRAXIA (least severe) - nerve loses ability to function normally due to myelination damage BUT only temporary
  • AXONOTMESIS (mid-severe) - axons & myelin sheaths damaged but endo, peri & epi neurium stay intact (in renervation, Schwann cells provide adjacent segment with protection as guide endo, peri, epi on where to attach nerve sprouts)
  • NEUROTMESIS (most severe) - entire nerve completely severed so there is no complete recovery
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16
Q

HOW NEURONES REACT TO INJURY

A

MINUTES - neurone stops conducting AP beyond site of injury & 2 cut ends of axon pull apart, seal themselves & swell at same time
HOURS - degeneration of synaptic terminal (leads to accumulation of vesicles) & astroglia pull terminals away from postsynaptic cell
DAYS/WEEKS - proximal segment to cell body undergoes chromatolysis & in distal segment, distal stump of axon degenerates

17
Q

FATE OF PROXIMAL SEGMENT OF SEVERED NERVE (CHROMATOLYSIS)

A
  • cell body becomes active & produces lots of proteins for repairing cell so cell body volume increases & gets bloated so nucleus displaced from centre to periphery.
  • injured nerve seals wounded stump (form neuroma) so this segment of nerve doesn’t die & could regenerate to innervate peripheral structures
18
Q

FATE OF DISTAL SEGMENT OF SEVERED NERVE

A

axon dies due to loss of nutritional support from cell body (Wallerian digestion) & is digested by phagocytes but they save myelin, epi, peri, endo to form hollow tubes that guide new growth of axon in proximal end

19
Q

FATE OF DENERVATED MUSCLE (ACUTE (now) & CHRONIC (later))

A

ACUTE - muscle paralysed & can’t do reflex & immediately starts fasciculation but this ends if no re-innervation
CHRONIC- as fasciculations die down, muscle loses bulk due to denervation (denervation atrophy) or lack of use (disuse atrophy) so dies & goes muscle tissue replaced with connective

20
Q

TREATMENTS TO NERVE INJURY

A

nerve repair (remove damaged section & reconnect healthy ends), nerve graft, pain relief meds, electrical stimulation

21
Q

SUMMARY OF HOW NEURONS IN PNS REGENERATE AXONS

A
  1. after degeneration of distal axon & myelin, macrophages clean up debris & induce schwann cells to divide
  2. myelin-forming schwann cells repopulate nerve sheaths
  3. macrophages induce Schwann cells to make nerve growth factor & axons sprout & some enter new Schwann cell tubes
  4. Axonal growth cones successfully grow

MEDICINE (27 decks)

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