Physiology - Neuro Flashcards

1
Q

Describe the synthesis, release and action of acetylcholine at a nerve synapse and how is its action terminated

A
  • synthesised from choline and acetyl-coA by the enzyme choline acetyltransferase in the cytoplasm of the cell
  • choline is directly synthesised in neurons and taken up at synaptic cleft
  • acetylcholine then stored in small clear vesicles at cholinergic terminals (via VAT)
  • action potential causes influx of calcium at terminal and exocytosis of acetylcholine into synaptic cleft
  • acetylcholine then binds the the post-synaptic receptor
  • acetylcholine is then broken down via hydrolysis by acetylcholinesterase into choline and acetate
  • choline is taken back into the cell (there is no acetylcholine reuptake)
  • leaving synaptic cleft via diffusion, broken down in blood and liver by pseudocholinesterase
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2
Q

Describe the 2 types of acetylcholine receptors

A

Nicotinic = ion channels, 2 types, present in neuromuscular junction and brain
mimicked by nicotine and blocked by paralytics

Muscarinic = g proteins, 5 types, present in smooth muscle, glands and brain
mimicked by muscarine and blocked by atropine

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3
Q

Describe the synthesis, release and action of adrenaline at a nerve synapse and how its action is terminated

A
  • tyrosine (mostly dietary) enters cells, where it is converted to L-dopa by tyrosine hydroxylase
  • L-dopa is then converted to dopamine by aromatic L-aa decarboxylase AADC
  • dopamine enter small dense-cored vesicles, where it is converted to noradrenaline by dopamine beta-hydroxylase
  • noradrenaline is converted to adrenaline in adrenal medulla and parts of the brain by PNMT
  • released by exocytosis and acts on postsynaptic and to a lesser extent pre-synaptic terminals
  • removed from the synaptic junction by:
    1. binding to post-synaptic receptors
    2. binding to pre-synaptic receptors
    3. reuptake into presynaptic neurons by norepinephrine transporter NET
    4. catabolism to inactive form by COMT (in synaptic cleft) or MAO (inside cell)
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4
Q

What types of noradrenaline receptors are there

A

alpha (g proteins, 2 types)
beta (g proteins, 3 types)
dopamine (g proteins, 5 types)

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5
Q

What catecholamines act as neurotransmitters

A

noradrenaline, adrenaline, dopamine

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6
Q

How is serotonin synthesised, what are its functions and how is it broken down?

A
Serotonin is synthesised from tryptophan by hydroxylation (tryptophan hydroxylase) and decarboxylation (AADC)
it is found in platelets, GI tract and brain 

Functions:
- CNS: regulation of mood, sleep and cognition, cerebral and meningeal vasoconstriction
- GIT: nausea/vomiting, facilitate GI secretions and peristalsis
- platelet aggregation
- smooth muscle contraction

Catabolism:
- reuptake to presynaptic neurons from synaptic cleft by SERT, inactivated by MAO, excreted in urine

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7
Q

Draw the components of a muscle spindle

A

-muscle spindle is made of 3 parts and is purely sensory, does not contribute to overall strength

1) intrafusal fibers: consists of dynamic nuclear bag, static nuclear bag and nuclear chain fibers
2) myelinated afferent fibers: from central non-contractile part to synapse on spinal cord dorsal root
3) myelinated gamma efferent fibers: from spinal cord ventral root to polar contractile part of intrafusal fiber

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8
Q

Describe the sequence of events in a stretch reflex

A
  • monosynaptic reflex: muscle stretched, causing contraction of the same muscle as a response
  • sense organ intrafusal fiber sends afferent impulse to synapse on motor neurone in spinal cord (NT = glutamate)
  • efferent fibers travel to extrafusal fibers to cause contraction
  • inhibitor interneuron projects to antagonistic muscle
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9
Q

Describe the withdrawal reflex

A
  • polysynaptic reflex occurring in response to a painful stimulus where the sense organ is a nociceptor
  • crossed response = flexion and withdrawal of ipsilateral limb and extension of contralateral limb
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10
Q

What is meant by the term polysynaptic reflex and what are the effects

A
  • one or more interneurons interposed between the afferent and efferent neurons
  • prolonged effect due to different time for stimulus to reach the effector
  • may have reverberation circuit as some interneurons turn back on themselves and prolong the effect
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11
Q

What is the inverse stretch reflex

A
  • reflex that occurs when too much tension is generated and relaxation occurs instead of contraction via inhibition
  • modulated by the golgi tendon organ located at the origin and insertion sites of a muscle (NT is glycine)
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12
Q

What are upper motor neurons and lower motor neurons

A

-upper motor neuron: in cerebral cortex and brainstem, carry information down to activate lower motor neuron
lesion = initially weak and flaccid, then spastic and hypertonic and hyper-reflexic and upward plantars

-lower motor neuron: spinal and cranial motor neurons that directly innervate skeletal muscle
lesion = flaccid paralysis, muscular atrophy, fasiculations, hypo-reflexic

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13
Q

What is the physiological basis of clonus

A
  • clonus is the regular, repetitive, rhythmic contractions of a muscle subjected to sudden, sustained stretch
  • due to loss of descending cortical input to inhibitor neurons called Renshaw cells
  • leads to the loss of inhibition of antagonist muscle, causing repetitive contractions of ankle flexors and extensors
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14
Q

What are long term complications of spinal cord injury

A

ulcers
muscle atrophy
hypercalcaemia - renal stones
uti

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15
Q

How is pain transmitted and what are the different types of fibers

A

-primary afferent fiber:
sense organ = naked nerve ending peripherally, cell body in dorsal root ganglion
2 types of fibers = A delta and C, terminate in dorsal horn
A delta = myelinated, neurotransmitter is glutamate, fast pain
C = unmyelinated, neurotransmitter is substance p, slow pain

-dorsal horn neurons: axons travel in lateral spinothalamic tract to thalamus

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16
Q

Differentiate between fast pain and slow pain fiber

A
  • fast pain: A delta, myelinated, 2-5um diameter, conduction rate 12-30m/s, NT is glutamate
  • slow pain: C, unmyelinated, 0.4-1.2um diameter, conduction rate 0.5-2m/s, NT is substance P
17
Q

What is referred pain and what is the theory involved

A

-irritation of a visceral organ causing pain in a distant somatic structure
-example: diaphragm projects to the shoulder, heart projects to the arm, ureter projects to the testicle
-convergence projection theory:
visceral pain referred to a distant somatic structure that shares the same embryonic origin or dermatome
somatic and visceral pain fibers converge on the same 2nd order neuron in the dorsal horn

18
Q

How is acute pain modulated

A
  • endogenous opioids
  • descending inhibition
  • gate control theory: non-painful stimulation of large touch/pressure afferents causes inhibition of pain pathways
  • perception and psychological factors
19
Q

What site do opioids act on

A

opioid receptors (mu, kappa, delta) in afferent nerve fibers, dorsal horn of spinal cord and brain

20
Q

Describe the neural connections of the visual pathways and describe visual field defects on the picture

A

-retina to optic nerve to optic chiasm to optic tract to lateral geniculate body in the thalamus
lateral geniculate body projects to:
occipital lobe = primary visual cortex
pretectal nucleus in midbrain = synapses on edinger-westphal nuclei, controls pupillary responses

21
Q

Why is the fovea important for visual acuity

A
  • fovea is the area where visual acuity is the greatest, it is positioned at the center of the macula
  • it is the area of the retina with the highest concentration of cones and no rods
22
Q

What ocular factors influence visual acuity

A
  • optical factors: cataracts, keratitis, astigmatism, myopia, hyperopia
  • retinal factors: retinopathies, optic neuritis
  • stimulus factors: illumination, brightness, contrast, length of time exposed to stimulus
23
Q

How is visual acuity measured

A
  • use of a Snellen chart viewed from a distance of 6 meters or 20 feet
  • numerator is the distance at which the chart is read, denominator is the smallest line that can be read
24
Q

What is nystagmus

A

-the vestibulo-ocular reflex is present to maintain eye position when the head moves
-nystagmus is the involuntary movement of eye during rotation and may be physiologic or pathologic
-physiological nystagmus is part of the VOR characterised by 2 phases
slow = smooth pursuit in the direction opposite of head rotation
fast = saccadic movement in direction of head rotation once limit of the slow component is reached
-pathologic nystagmus is characterised by excessive saccadic movement
causes: damage to a component of the vestibular system
-types: horizontal, vertical, rotational
-direction of eye movement is identified by the direction of the fast component

25
Q

What are the 2 main mechanisms of deafness and how are they differentiated

A

types:
- conductive - due to impaired sound transmission in external or middle ear
ex. wax, foreign body, otitis media/externa, perforated eardrum
- sensorineural - due to loss of cochlear hair cells or problems with CN 8 or central auditory pathways
ex. aminoglycoside damage, CN 8 tumours, medulla CVA

diagnosis:
-weber - tuning fork on vertex
sound loudest in bad ear = conductive
sound loudest in good ear = sensorineural
-rinne - tuning fork over mastoid then air
sound not heard in air after bone in bad ear = conductive
sound persists in air after bone in bad ear = sensorineural

26
Q

What is the pathogenesis of fever

A
  • the hypothalamus controls temperature regulation
  • fever occurs when the thermoregulatory mechanism is altered to maintain a body temperature above normal

1) bacterial toxin (endotoxin) cause monocytes/macrophages/kupffer cells to release cytokines (interleukins, TNF)
2) cytokines act as endogenous pyrogens and activate the pre-optic area of the hypothalamus
3) hypothalamus causes the release of PGE2, which increases the temperature set point
4) hypothalamus then regulates heat generating behaviours

27
Q

What is the body’s response to hot and cold environments

A

mechanism activated by cold: posterior hypothalamus
-increased heat production = shivering, hunger, increased voluntary activity, increased A and NA release
-decreased heat loss = cutaneous vasoconstriction, curling up, horripilation
mechanism activated by heat: anterior hypothalamus
-increased heat loss = cutaneous vasodilation, sweating, increased respiration
-decreased heat production = anorexia, apathy, inertia

28
Q

How is heat lost from the body

A

radiation, convection and conduction (70%), vaporisation of sweat (27%), respiration (2%), urination and defecation (1%)

29
Q

How is thirst regulated

A

-thirst is mainly controlled in the anterior hypothalamus diencephalon

increased thirst:

  • hypertonicity of plasma sensed by osmoreceptors in anterior hypothalamus
  • hypovolaemia sensed by baroreceptors in heart and blood vessels
  • physiological stress

decreased thirst:

  • hypothalamic disease
  • damage to diencephalon
  • altered mental state
30
Q

What is the purpose of the reticular activating system

A
  • regulates respiratory, cardiovascular and endocrine functions
  • increases consciousness and alert state and heightened sensory perception
  • sends signals to the thalamus, which is a gateway to the cerebral cortex
  • location: mid-ventral portion of the medulla, midbrain and 4th ventricle
31
Q

A nerve fibre types

A

alpha - somatic motor and proprioception

beta - touch/pressure

gamma - motor to muscle spindle

delta - fast pain response, temp (cold)