case 2 Flashcards

1
Q

in dorsal columns, where soea cuneatus end and gracilis start

A

gracilis monitors lower limbs starting at T6

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2
Q

drug abuse

A

substance used in a manner that doesnt conform to social norms

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3
Q

drug dependance

A

depends for normal physical functioning. withdrawl symptoms.

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4
Q

drug addiction

A

behavioural symdrome. compulsive use.

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5
Q

substance use disorder

A

2-3 mild, 4-5 moderate 6-7 severe

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6
Q

malingering

A

conscious fabrication of symptoms to achieve some
form of benefits such as attention, to be relieved of undesirable activities, to obtain
prescription medication, or to qualify for disability compensation.

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7
Q

development of the vertebral column

A

mesoderm-paraxial intermediate and lateral plate mesoderm. Paraxial goes around notochord. vesicles in LP, seperates into somatic and splanich. Paraxial into somatic mesoderm into blocks called somites 44 pairs.
somite splits into sclerotome which forms bone cartilage tendons meninges. dermatome forms skin over VC. myotome forms deep back and neck muscles.
sclerotomal into anterior loose and posterior densly packed cells. some dense move cranially where form IVD. notochord becomes nucleus pulposus. anulus fibrosus surrounds. in 6th week condrification centres appear, fuse in centrum, ossification occurs.
spindal cord finishes l2 conus medullaris then cauda equina.

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8
Q

machanoreceptors

A

usually Ab fibres. 1. Merkel’s Disks - Highest spatial resolution, allows them to resolve tiny spatial details. Ideal for processing information about form and texture.

  1. Meisenner Corpuscle – Account for 40% of hand machanosensory information. Efficient in processing information about low-frequency vibration that occurs when objects move across the skin.
  2. Ruffini Endings – essential to internally generated stimuli (e.g. finger movements).
  3. Pacinian Corpuscle – detecting vibrations transmitted through objects that contact the hand.
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9
Q

exteroreceptors

A

superficial in the skin. Respond to nociceptive stimuli, temperature, touch and pressure

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10
Q

nociceptors

A

Aδ group of myelinated axons, or into the C fiber group of unmyelinated axons. free nerve endings. continued stimulus can dec threshold-sensitisation.
polymodal when detect thermal mechanical and chemical stimuli.
neurotransmitter is glutamate. activate AMPA receptors. substance P also released from C fibres.
epicritic pain is fast, protopathic is slow pain.

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11
Q

pain pathways

A

often spinothalamic, synapse lamina I V.
spinomesencephalic tract projects to PAG matter and superior colliculi. connects limbic system. when to SC influence eye movement and direct gaze to site of injury.
spinoreticular tract-emotional arousal aspects of pain and slow pain.
trigeminal in head.
spinoparabrachial: hypothalamus and amygdala affects appetite sleep and mediates learning

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12
Q

transduction

A

cell damage causes release of chemical mediators like ATP bradykinin histamine from mast cells, seratinin from platlets, leukotreines, lactic acid prostaglandins substance P. bind and open Na channels cause noxious stimulus into electrophysiological.

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13
Q

axon reflex

A

C fibres cause AP to CNS and back towards skin where vasoactive substances CGRP and substance P released. causes histamine release and vasodilation.

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14
Q

sensory discriminative component

A

location intensity and quality of pain. first pain. spinothalamic pathway.

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15
Q

affective motivational component

A

projections to reticular formation midbrain thalamus hypo and limbic system. emotional and visceral responce. second pain.

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16
Q

hyperalgesia and allodynia

A
  1. Thresholds are lowered so that stimuli that would normally not produce pain now begin to (allodynia).
  2. Responsiveness is increased, so that noxious stimuli produce an exaggerated and prolonged pain (hyperalgesia).
17
Q

peripheral sensitisation

A

a reduction in threshold and an increase in responsiveness. 1. Protect the injured area – this occurs as a result of painful perceptions produced by ordinary stimuli close to the site of damage.
2. Promote healing and guard again infection – this occurs by means of local efforts such as increased blood flow and the migration of white blood cells to the site. decreased pain threshold directly at the core of the site of injury (primary hyperalgesia), it also decreases the threshold at areas surrounding the site of injury (secondary hyperalgesia).

18
Q

central sensitisation

A

increase in the excitability of neurons within the central nervous system, so that normal inputs begin to produce abnormal responses. The increased excitability is typically triggered by a burst of activity in nociceptors, which alter the strength of synaptic connections between the nociceptor and the neurons of the spinal cord (so-called activity-dependent synaptic plasticity).
 Low-threshold sensory fibres (e.g. for very light touch), begin to activate neurons in the spinal cord (for inputs from the body) or in the brainstem (for inputs from the head) that normally only respond to noxious stimuli. As a result, an input that would normally evoke an innocuous sensation now produces pain.
• Nociceptive pain results from direct activation of nociceptors.
• Neuropathic pain results from direct injury to nerves

19
Q

perception

A

reticular system-autonomic and motor response. looking at injury.
somatosensory-intensity type and location. relates to past memory.
limbic system-emotional and behavioural responce.

20
Q

modulation of pain-gate control theory

A

• Pain signals are blocked when the ‘gate is closed’.
• Pain signals pass from the spinal cord to the brain when the ‘gate is open’.
• According to the gate control theory, we can be distracted from the pain by the release of endorphins (neurotransmitters).
• Our spinal cord has large (Aβ) and small (C) nerve fibres:
 Aβ fibres - these close the pain gate.
 C fibres – these activate and open the pain gate.
can be closed via TENS machine as stim Ab fibres to close gate as activate inhibitory interneurons.

21
Q

modulation of pain-supraspinal

A

parts of the brain can send signals to stop pain. contain enkephalinergic neurons which secrete encephalin. met or leu. delta opiod receptors inhibit GABAergic interneurons . can cause closure of Ca channels, opening K channels, hyperpolarise cell stop noxious stimuli.

22
Q

catastrophising

A

rumination - a focus on threatening information, both internal and external; (2) magnification - overestimating the extent of the threat; and (3) helplessness - underestimating personal and broader resources that might mitigate the danger and disastrous consequences.

23
Q

prolapsed intervertebral disc

A

nucleus pulposus usually ectends posterolaterally where anulus fibrosus is thin. most common in L4/5/S1. acute pain from pressure on longditudinal ligaments and inflamation,. chronic pain compression nerve-refered pain. seen on MRI as dec IVD and IVS. , it usually compresses the nerve root numbered one inferior to the herniated disc.• Root pressure is suggested by limitation of flexion of the hip on the affected side if the straight leg is raised (Lasègue’s sign). bed rest doesnt help. early mobilisation.
with spinal cord compression, decompression surgery needs to be prompt before irreversible damage.

24
Q

disc level and symptoms

A

L3/4 so L4 root, sensory loss in inner calf, weakness sof inversion of foot and loss knee reflex.
L5 root, sensory lokk in outer calf and dorsum foot, weakness in dorsiflexion.
S1 root sensory loss in sole foot weakness in plantar flexion and ankle reflex lost.

25
Q

surgical approaches

A
  • Discectomy: surgical removal of part (partial discectomy) or all (total discectomy) of a diseased or damaged intervertebral disc. It is performed for the relief of neurological symptoms arising from a displaced intervertebral disc or as part of a more extensive procedure.
  • Laminectomy: surgical cutting into the backbone to obtain access to the vertebral (spinal) canal.
26
Q

opioid receptor mechanism

A
  1. Inhibition of adenylyl cyclase – opioids reduce the intracellular cAMP content. This affects protein phosphorylation pathways and hence cell function.
  2. Opiates promote the opening of potassium channels – this reduces synaptic transmission as it causes the axon membrane to be in a state of hyperpolarisation.
  3. Inhibit the opening of calcium channels – this reduces the amount of neurotransmitter released into the synaptic cleft, thus reducing synaptic transmission.
27
Q

NSAIDs

A
  1. Anti-inflammatory effect – modification of the inflammatory reaction.
    o This occurs as a result of a decrease in prostaglandin E2 and prostacyclin (PGI2).
    o It reduces vasodilatation and, indirectly, oedema.
    o Accumulation of inflammatory cells is not reduced.
  2. Analgesic effect – reduction of certain types of (especially inflammatory) pain.
    o It occurs as a result of a decrease in the production of prostaglandins that sensitise nociceptors (ORL1) to inflammatory mediators such as bradykinin.
    o They are therefore effective in all conditions that are associated with increased local prostaglandin synthesis.
  3. Antipyretic effect – lowering of body temperature when this is raised in disease.
    o IL-1 releases prostaglandins in the CNS, where they elevate the hypothalamic set point for temperature control, thus causing fever.
    o NSAIDs prevent this.
28
Q

MRI`

A

T1 weighted image:
• This image weighting is useful for assessing the cerebral cortex, identifying fatty tissue, characterising focal liver lesions and for post-contrast imaging.
• In T1-weighted images, water appears dark, while fatty tissues appear bright.
 Thus, T1-weighted images have the appearance of anatomical brain sections, with CSF appearing dark, gray matter appearing gray (higher water content), and white matter appearing white (higher lipid content).
• The resolution of fine anatomical detail can usually be seen better with T1-weighted images.
T2 weighted image:
• This image weighing is useful for detecting oedema, revealing white matter lesions and assessing zonal anatomy in the prostate and the uterus.
• In T2-weighted images, on the other hand, water appears bright, and lipid appears dark.
 Thus, CSF appears very bright; areas of brain oedema, gliosis and gray matter are bright but somewhat less so than CSF; and myelinated areas appear dark.
• T2-weighted images usually make regions of brain abnormalities appear bright and easier to see than on T1.
• However, one pitfall of T2-weighted images is that bright-appearing CSF can obscure pathology located in the parenchyma adjacent to the ventricles or pia.