Physiology of analyzers

1
Physiology of analyzers
2
Characteristic of optical system of
eyeComponents of eye

• Sclera gives shape to eyeball and protect its
  inner structures.
• Cornea transmits and refracts light.
• Choroid supplies blood to eyeball.
• Ciliary body supports lens through suspensory
  ligament and determines its thickness secretes
  aqueous humor.
• Iris regulates diameter of pupil, and hence the
  amount of light entering the vitreous chamber.
• The function of retina is photoreception
  transmits impulses.
• Lens refracts light and focuses onto fovea
  centralis.

3
Circulation of inner eye fluid

• Aqueous humor, a clear liquid, is produced in the
  ciliarys body by diffusion and active transport
  and flows through the pupil to fill the anterior
  chamber of the eye. It is normally reabsorbed
  through a network of trabeculae into the canal of
  Schlemm, a venous channel at the junction between
  the iris and the cornea anterior chamber angle.

4
Circulation of inner eye fluid
5
Physical refraction, formation of representation
in reduced eye

• Refraction is a bent of light rays when they pass
  from one medium into a medium of a different
  density, except when they strike perpendicular to
  the interface. Refractive index is a ratio of
  speed of light ray in air to corresponding
  transparent medium.
• Reducted eye is the model of eye in which all
  mediums have one index of bent. It need for value
  of bent force of eye. In this case formed less,
  overturn and real pictures.

6
(No Transcript)
7
Clinical refraction, their kinds

• There are three kinds of refraction myopia
  (nearsightedness), emetropia (norm),
  hypermetropia (hyperopia or farsightedness).

8
Emetropia

• When the main focus of eye is onto retina and
  we have clear picture we say about emetropia.

9
Myopia

• When the ray come together in front of retina
  we say about myopia.

10
Hyperopia

• When the ray come together at the back of retina
  we say about hyperopia.

11
Kinds of aberration. Astigmatism

• Astigmatism is a common condition in which the
  curvature of the cornea is not uniform. When the
  curvature in one meridian is different from that
  in other, light rays in that meridian are
  refracted to a different focus, so that part of
  the retinal image is blurred.

12
Concept of accommodation, its mechanism and
regulation

• The process by which the curvature of the lens is
  increased is called accommodation. At rest the
  lens is held under tension by the lens ligaments.
  Because the lens substance is malleable and the
  lens capsule has considerable elasticity, the
  lens is pulled into a flattened shape.

13

• When the gaze is directed at a near object, the
  ciliary muscle constricting. This decreases the
  distance between the edges of the ciliary's body
  and relaxes the lens ligaments, so that the lens
  springs into a more convex shape. The relaxation
  of the lens ligaments produced by contraction of
  the ciliary's muscle is due partly to the
  sphincter like action of the circular muscle
  fibers in the ciliary's body and partly to the
  contraction of longitudinal muscle fibers that
  attach interiorly, near the corneoscleral
  junction.

14
Protective mechanisms of eye Role of cornea and
conjunctive

• Conjunctiva protects the eyeball by preventing
  object.
• Pupils reactions
• When light is directed into one eye, the pupil
  constricts (pupillary light reflex). The pupil of
  the other eye also constrictes (consensual light
  reflex).

15

• Eye tonometry is basis on ability of ocular apple
  to deformation under pressure on the outside. The
  more deformation of eyes by respective power of
  pressure- the lower quantity of intraocular
  pressure.
• The tonometer of A.M.Maclakov is small cylinder
  with parts, which finish grounds with milk glass
  diameter 10 mm. At first 1-2 gums of solution of
  anaesthetic substance (0,5 solution of dykayn)
  are dripped in the eye. Grounds of tonometer is
  greased by thin layer of dye-stuff (colargol,
  methylene blue) after cylinder is free
  accommodated on the cornea of research eye such,
  that it flattens it its weight approximately
  during 1 second. In the place of flatten dye
  leaves on the cornea, the light spot is replied
  its on the ground of tonometer. The imprint of
  this spot on the slightly moist paper is named
  tomogram. The more intraocule pressure- the
  lesser size of imprint and conversely.
• The quantity of area of flatten is connected with
  level of intraocular pressure by mathematical
  dependence, that made it possible for
  S.S.Golovina worked tables of remitting of
  diameter of circle of flatten in tonometric
  indexes.
• The complete consists of 4 tonometers with mass 5
  g 7,5 g 10 g 15 g that widen range of
  measuring of intraoular pressure.
• The intraocular pressure is 16-26 mm of mercury
  post in the norm.

16
Mechanism of vision sensitiveStructure of retina

• It is organized in 10 layers and contains the
  rods and cones, which are the visual receptors,
  plus 4 types of neurons bipolar cells, ganglion
  cells, horizontal cells, amacrine cells. Layers
  pigment epithelium, rod and cone (outer and inner
  segments), outer nuclear layer, outer plexiform
  layer, inner nuclear layer, inner plexiform
  layer, ganglion cell layer, optic nerve fibers.
  In the center of retina is present fovea
  centralis, which has only cones and blind spot
  a place of exit of optic nerve, where absent
  visual receptors.

17
(No Transcript)
18
Physiological properties of pigment layers and
photoreceptors of retina

• The light perceived by receptor cells of retina.
  There are near 120 million of rods and 6 million
  of cones. The rods are extremely sensitive to
  light and are the receptors for night vision
  (scotopic vision). The cones are responsible for
  vision in bright light (photopic vision) and for
  color vision. The maximal density of cones is in
  fovea centralis, but the fovea contains no rods.
  The maximal density of rods is in parafoveal
  place.
• Each receptor has outer (light-like) segment,
  where are present photosensitive pigment, and
  inner segment, which are rich in mitochondria.
  The photosensitive pigments in the rods is called
  rhodopsin or visual purple. There are 3 different
  cone pigments iodopsin, photopsin, chlorolab.
  The photosensitive pigments have different
  sensitivity to different length of waves.
• In pigment layer of retina present pigment
  melanin which take place in securing the clear
  vision. Vitamin A takes place in resynthesis of
  photosensitive pigments and present in melanin.

19
(No Transcript)
20
Photochemical reaction in retina receptors

• In photoreceptors of retina kvant of light
  connect with pigments. For example, rhodopsin has
  aldegid of vitamin A (retinals) and protein opsin
  (scotopsin). Action of light photon on vision
  pigment accompany by isomerization of retinal.
  That helps to connect retinal with opsin. It
  activate calcium ions. That increase to change of
  membrane penetration for sodium and rise of
  receptor potential (hyperpolarization of receptor
  cells). In dark case membrane make way for
  sodium, that is why it has very little level of
  polarization. When there is a big quantity of
  light increase amplitude of hyperpolarization.

21
(No Transcript)
22
Conductive and cortex part of analyzer

• Neural pathways of vision and processing of
  visual information. Impulses from the rods and
  cones pass through bipolar neurons to ganglion
  neurons. The 2 optic nerves converge at the optic
  chiasma. All the fibers arising from the medial
  half of each retina cross to the opposite side.
  The optic tract is a continuation of optic nerve
  fibers from the optic chiasma. It is composed of
  fibers arising from the retinas of both eyes.
• As the optic tract enters the brain, some of the
  fibers in the tracts terminate in the superior
  colliculi of the midbrain. These fibers and the
  motor pathways they activate constitute the
  tectal system, which is responsible for body-eye
  coordination. The tectal system is also insolved
  in the control of the intrinsic eye muscles.
• Approximately 70-80 of the fibers in the optic
  tracts pass to the lateral geniculate body of the
  thalamus. The fibers synapse with neurons whose
  axons constitute a pathway called the optic
  radiation. The optic radiation transmits impulses
  to the striate cortex area of the occipital
  cerebral lobe. This entire arrangement of visual
  fibers, known as the geniculostriate system, is
  responsible for perception of the visual field.

23
(No Transcript)
24
Recognize of coloring Theory of coloring
perception

• People must determine near 7 mln of colors touch.
  Each color has own wave of length (red 700 nm,
  green 546 nm, blue - 435 nm). Mixing of equal
  quantity of these colors is white color. Colors
  have 3 attributes hue, intensity and saturation.
• 3-component theory (Yung-Gelmgoltz) there are 3
  types of colors, which have different pigments
  (for red, green and violet color). Their
  combination process in all nervous centers of
  central nervous system and cortex. These process
  sensitive by our consciousness as corresponding
  color.
• Theory of oponent colors (Gering) said that
  there are 4 main colors which may connect one by
  one (green-red, yellow-blue).

25
(No Transcript)
26
Perception of spaceAcute of the central vision

• Determination acute of the central vision Put
  the table for the definition of the acute of the
  central vision on the well illuminate wall.
  Investigation has to sit in front of the table on
  the distance of 5 meters and close his one eye
  with the help of the shield. Show with the
  pointer letter, beginning from the upper line,
  find the lowest line, which letters investigating
  person can see clear. Acute of central vision
  define with the help of the formula
• V d D, where V acute of the vision d
  distance from the eye to the table D distance,
  on which healthy eye has to see clear this line.
  Than determine the acute of vision of another
  eye. In adult in norm is 1.0.

27
(No Transcript)
28

• b) Factors, which are determine acute of central
  vision
• c) Peripheral vision
• d) Binocular (stereoscopic) vision (Vision by
  both eyes)
• 4. Aged peculiarities of vision function
• a) Acute of vision, space vision
• b) Aged peculiarities of light sensitivity and
  color vision
• c) Prevent work in the case of breach vision in
  children and teenagers

29
Hearing
30
Anatomy of the Ear Region

• External ear collects sounds
• Middle ear cavity separated from external ear by
  eardrum and from internal ear by oval round
  window
• 3 ear ossicles connected by synovial joints
• Auditory tube leads to nasopharynx
• helps to equalize pressure on both sides of
  eardrum
• Membranous labyrinth contains organs of hearing
  and equilibrium

31
Inner Ear-Membranous Labyrinth

• Membranous labyrinth
• membranous tubes filled with endolymph
• contain sensory receptors for hearing and
  equilibrium

32
Physiology of Hearing

• Auricle collects sound waves
• Eardrum vibrates
• Ossicles vibrate and push on oval window
• Amplify signal
• produces pressure waves in scala vestibuli and
  scala tympani
• Causes pressure fluctuations inside cochlear duct
  which move hair cells against tectorial membrane
• Microvilli are bent producing receptor potentials

33
Hair Cell Physiology

• Hair cells convert mechanical deformation into
  electrical signals
• As microvilli bend mechanically-gated channels
  open in membrane
• Causes depolarisation
• Depolarisation opens voltage-gated Ca2 channels
  at base of the cell
• Triggers release of neurotransmitter onto the
  first order neuron

34
Pitch and volume

• Sounds at different frequencies vibrate different
  portions of the basilar membrane
• high pitched sounds vibrate the stiffer more
  basal portion of the cochlea
• low pitched sounds vibrate the upper cochlea
  which is wider and more flexible
• Loud sounds vibrate cause a greater vibration of
  the basilar membrane stimulate more hair cells
  which our brain interprets as louder

35
Auditory Pathway

• Auditory signals propagate to nuclei within
  medulla oblongata
• differences in the arrival of impulses from both
  ears, allows us to locate the source of a sound
• Fibres ascend to
• thalamus
• primary auditory cortex

36
Equilibrium

• Two types of equilibrium
• Static
• maintenance of position of body (mainly head)
  relative to gravity
• Dynamic
• maintenance of body position (mainly head) during
  movement
• Vestibular apparatus located in inner ear

37
Equilibrium

• Sense organs of static equilibrium are Otolithic
  organs
• Saccule and utricle
• Both contain maculae
• Perpendicular to each other
• Gravity moves otolithic membrane which bends hair
  bundles
• opens and closes ion channels
• Depolarises and repolarises hair cells which
  release neurotransmitter
• Neurotransmitter depolarises first order sensory
  neuron
• Saccule and utricle also involved in detecting
  linear acceleration in dynamic equilibrium

38
Equilibrium

• Sense organs of dynamic equilibrium
• cristae of semicircular canals
• Located on 3 axes

39
Equilibrium

• Bending of hairs of cristae as endolymph flows
  generates receptor potentials

40
Equilibrium pathways

• Most fibres in vestibular nerve enter brain stem
  and terminate in vestibular nuclei in Medulla
  Oblongata and Pons
• Axons from vestibular nuclei synapse with nuclei
  of cranial nerves controlling
• eye movement
• head and neck movement
• Rest synapse with cerebellum
• Cerebellum co-ordinates sensory and motor
  information (i.e. via motor cortex) to ensure
  appropriate activation of skeletal muscles to
  maintain balance

41

PAIN -definition of pain an unpleasant sensory
or emotional experience -perception of pain is a
product of brains abstraction and elaboration of
sensory input. -perception of pain varies with
individuals and circumstances (soldier
injured) -activation of nociceptors does not
necessarily lead to experience of pain (asymbolia
for pain patient under morphine) -pain can be
perceived without activation of nociceptors
(phantom limb pain, thalamic pain
syndrome) -important for survival, protect from
damage congenital and acquired insensitivity
(diabetic neuropathy, neurosyphilis) to pain can
lead to permanent damage -pain reflexes can be
stopped if not appropriate (step on nail near
precipice, burn hands while holding a baby. Pain
can be suppressed if not needed for survival
(soldier). In general 2 clinical states of
pain Physiological (nociceptive) pain ? direct
stimulation of nociceptors. Neuropathic
(intractable) pain ? result from injury to the
peripheral or central nervous system that causes
permanent changes in circuit sensitivity and CNS
connections.
42
Nociceptors (Free nerve ending) Mechanical
nociceptors activated by strong stimuli such as
pinch, and sharp objects that penetrate,
squeeze, pinch the skin. ? sharp or pricking
pain, via A-delta fibers. Thermal nociceptors
activated by noxious heat (temp. above 45C),
noxious cold (temp. below 5C), and strong
mechanical stimuli. ? via A-delta
fibers. Polymodal nociceptors activated by
noxious mechanical stimuli, noxious heat,
noxious cold, irritant chemicals. ? slow dull
burning pain or aching pain, via
non- myelinated C fibers. Persists long after
the stimulus is removed. Research for a
transduction protein capsaicin (from chili
peppers) bind to capsaicin receptor on nociceptor
endings?transducer for noxious thermal and
chemical stimuli?burning sensation associated
with spicy food. Knockout mouse lacking capsaicin
receptor drinks solution of capsaicin, has
reduced thermal hyperalgesia
43
(No Transcript)
44
(No Transcript)
45
Mechanisms associated with peripheral
sensitization to pain
46
Agents that Activate or Sensitize
Nociceptors Cell injury ? arachidonic acid ?
prostaglandins ? ? vasc. permeability

(cyclo-oxygenase) ? sensitizes
nociceptor Cell injury ? arachidonic acid ?
leukotrienes ? ? vasc. permeability

(lipoxygenase) ?
sensitizes nociceptor Cell injury ? ? tissue
acidity ? ? kallikrein ? ? bradykinin ? ? vasc.
permeability ? activates nociceptors
? ? synthesis release of prostaglandins Substanc
e P (released by free nerve endings) ? sensitize
nociceptors ? ? vasc. perm., plasma
extravasation (neurogenic
inflammation) ? releases histamine (from
mast cells) Calcitonin gene related peptide (free
nerve endings) ? dilation of peripheral
capillaries Serotonin (released from platelets
damaged endothelial cells) ? activates
nociceptors Cell injury ? potassium ? activates
nociceptors
47
Peripheral sensitization to pain
Some definitions Hyperalgesia? increased
sensitivity to an already painful
stimulus Allodynia? normally non painful stimuli
are felt as painful (i.e .light touch of a
sun-burned skin)
48
Peripheral sensitization to pain
CGRP
CGRP
49
To summarize peripheral sensitization to pain
-Sensitization results from the release of
various chemicals by the damaged cells and
tissues (bradykinin, prostaglandins,
leukotrienes). These chemicals alter the type
and number of membrane receptors on free nerve
endings, lowering the threshold for nociceptive
stimuli. -The depolarized nociceptive sensory
endings release substance P and CGRP along their
branches (axon reflex), thus contributing to the
spread of edema by producing vasodilation,
increase in vascular permeability and plasma
transvasation, and the spread of hyperalgesia by
leading to the release of histamine from mast
cells. -Aspirin and NSAID block the formation of
prostaglandins by inhibiting the enzyme
cyclooxygenase. -Local anesthetic preferentially
blocks C fiber conduction, cold decreases firing
of C fibers, ischemia blocks first the large
myelinated fibers.
50
Pain input to the spinal cord -Projecting
neurons in lamina I receive A-delta and C fibers
info. -Neurons in lamina II receive input from C
fibers and relay it to other laminae. -Projecting
neurons in lamina V (wide-dynamic range neurons)
receive A-delta, C and A-beta (low threshold
mechanoceptors) fibers information.
How is pain info sent to the brain hypotheses ?
pain is signaled by lamina I and V neurons acting
together. If lamina I cells are not active, the
info about type and location of a stimulus
provided by lamina V neurons is interpreted as
innocuous. If lamina I cells are active then it
is pain.
Thus lamina V cells? details about the stimulus,
and lamina I cells? whether it is painful or
not -A-delta and C fibers release glutamate and
peptides on dorsal horn neurons. -Substance P
(SP) is co-released with glutamate and enhances
and prolongs the actions of glutamate.
-Glutamate action is confined to nearby neurons
but SP can diffuse and affect other populations
of neurons because there is no specific reuptake.
51
Mechanisms of early-onset central
sensitization Windup?homosynaptic
activity-dependent plasticity characterized by a
progressive increase in firing from dorsal horn
neurons during a train of repeated low-frequency
C-fiber or nociceptor stimulation. During
stimulation, glutamate substance P CGRP
elicit slow synaptic potentials lasting
several-hundred milliseconds. Windup results from
the summation of these slow synaptic potentials.
This produces a cumulative depolarization that
leads to removal of the voltage-dependent Mg2
channel blockade in NMDA receptors and entry of
Ca2. Increasing glutamate action progressively
increases the firing-response to each individual
stimulus (behavioral correlate repeated
mechanical or noxious heat are perceived as more
and more painful even if the stimulus intensity
does not change.
52
Centrally mediated hyperalgesia ?Under
conditions of persistent injury, C fibers fire
repetitively and the response of dorsal horn
neurons increase progressively (wind-up
phenomenon). This is due to activation of the
N-methyl-D-aspartate (NMDA)-type glutamate
receptor and diffusion of substance P that
sensitizes adjacent neurons. Blocking NMDA
receptors can block the wind-up. ?Noxious
stimulation can produce these long-term changes
in dorsal neurons excitability (central
sensitization) which constitute a memory of the C
fiber input. Can lead to spontaneous pain and
decreases in the threshold for the production of
pain. ?Carpal tunnel syndrome median nerve
frequently injured at the flexor retinaculum.
Pain ends up affecting the entire arm. (rat model
? partial ligature of sciatic nerve or nerve
wrapped with irritant solution)
53
Gate Control Theory of Pain
54

• Gate Control Hypothesis
• Wall Melzack 1965
• Hypothesized interneurons activated by A-beta
  fibers act as a gate, controlling primarily the
  transmission of pain stimuli conveyed by C
  fibers to higher centers.
• i.e. rubbing the skin near the site of injury to
  feel better.
• i.e. Transcutaneous electrical nerve stimulation
  (TENS).
• i.e. dorsal column stim.
• i.e. Acupuncture

55
Referred Pain
56
Ascending Pathways
-gtarousal, emotion involves limbic
system, amygdala, insula, cingulate cortex,
hypothalamus. Mediate descending control of pain
(feedback loop)
-gtlocalization, intensity, type of pain stimulus
57
New pathway for visceral pain ?selective lesion
of fibers in the ventral part of the fasciculus
gracilis reduces dramatically the perception of
pain from the viscera. General problems with
surgery ?Rhizotomy (cutting dorsal
root) ?Anterolateral cordotomy (cutting ALS) In
both cases, pain come back, excruciating. Thalamus
lesion VPL, VPM ? thalamic syndrome.
Intralaminar nuclei ? (arousal limbic) Cortex
S1 cortex ? localization, quality and intensity
of pain stimuli. Lesion of cingulate gyrus and
insular cortex ? asymbolia for pain
58
Descending pathways regulating the transmission
of pain information ?intensity of pain varies
among individuals and depends on circumstances
(i.e. soldier wounded, athlete injured, during
stress). ?Stimulation of PAG causes analgesia so
profound that surgery can be performed. ?PAG
stimulation can ameliorate intractable pain. PAG
receives pain information via the
spinomesencephalic tract and inputs from cortex
and hypothalamus related to behavioral states and
to whether to activate the pain control system.
PAG acts on raphe locus ceruleus to inhibit
dorsal horn neurons via interneurons and morphine
receptors. ?Application Intrathecal morphine
pumps
59

• Analgesics
• May act at the site of injury and decrease the
  pain associated with an inflammatory reaction
  (e.g. non-steroidal anti-inflammatory drugs
  (NSAID) such as aspirin, ibuprofen, diclofenac).
  Believed to act through inhibition of
  cyclo-oxygenase (COX). COX-2 is induced at sites
  of inflammation. Inhibition of COX-1 causes the
  unwanted effects of NSAID, i.e. gastrointestinal
  bleeding and nephrotoxicity. Selective COX-2
  inhibitor are now used.
• May alter nerve conduction (e.g. local
  anesthetics) block action potentials by blocking
  Na channels. Used for surface anesthesia,
  infiltration, spinal or epidural anesthesia. Used
  in combination to steroid to reduce local
  swelling (injection near nerve root). Local
  anesthetic preferentially blocks C fiber
  conduction, cold decreases firing of C fibers,
  ischemia blocks first the large myelinated
  fibers.
• May modify transmission in the dorsal horn (e.g.
  opioids endorphin, enkephalin, dynorphin).
  Opioids act on G-protein coupled receptors Mu,
  Delta and Kappa. Opioid agonists reduce neuronal
  excitability (by increasing potassium
  conductance) and inhibit neurotransmitter release
  (by decreasing presynaptic calcium influx)
• May affect the central component and the
  emotional aspects of pain (e.g. opioids,
  antidepressant). Problems of tolerance and
  dependence