Physiology day 3

MAG SHARE NG TRANS KUNG AYAW NIYO BUMAGSAK KAYO, BWAHAHAHAH. sarap kaya pumasa nang nag shashare kaysa nagdadamot na bumagsak . bwahaha. chos lang =)
Special thanks to Cyril for the editing

The effects of lesion on in the optic pathway: if there is lesions or abnormality along the optic pathway. The fibers from the nasal half of each retina d ecussate in the optic chasm so that the fibers in the optic tract are those from the temporal half of 1 retin a and the nasal half of the other. If the optic nerve is damage : there will be blindness in the 1 eye, total blindness If the optic tract is where the place of the lesion : the damage there would be Homonymous Hemi ano psia blindness in the same side of both the visual fields If the damage in the optic chasm: there will be Heteronymous Hemi anopsia the opposite side of th e visual fields are blind. If the lesion is in the occipital area: there will be Discrete Quadratic Visual field Defects, either up or down quadrants of each half of the visual field will be blind.

Macular Sparing there is a loss of peripheral vision but intact central vision 4 types of Eye Movements 1. Smooth pursuit movement - tracking movement of the eye as they follow a moving object. 2. Saccades - sudden jerky movement as the gates shift from 1 object to another. 3. Vestibular movement - adjustment that occurs in response to stimuli that is initiated in the semicircular can al in the ear in order to maintain visual fixation as the head moves. 4. Convergence movement - brings visual axis towards its other as attention is focus in an object near the obs erver. Strabismus visual axis no longer maintain in a position that keeps the visual image in the corresponding reti na points, the eye is keeps on moving to focus but cant maintain it The visual image chronically fall on a none corresponding point in the 2 retinas specially in children under 6 yr, then there will be suppression of the adjustment of the visual field called Suppression Scotoma - the diploplia will disappear, this is a cortical phenomenon and ususallly does not develop in adults.

Amblypoia Ex Anopsia- a subsequent permanent loss of visual acuity can occur in children which the vision in 1 eye is blurred or distorted owing to a refractive error. HEARING and EQUILIBRIUM Receptors for these 2 sensory modalities are all house in the ear. Hearing - is in the external, inner, cochlea of inner ear. Equilibrium - is in semicircular canals, utricle, saccule of inner ear. Receptors in the semicircular canal - can detect rotational acceleration Receptors in the utricle - can detect linear acceleration in the horizontal direction (Forward or backward). Receptors in the saccules - can detect linear acceleration in the vertical direction (Upwards or downwards). The receptors of hearing and equilibrium are hair cells: There are 6 groups of hair cells in each inner ear. 1 on each of the 3 semicircular canals 1 in the utricle 1 in the saccule 1 in the cochlea Central auditory pathways: From the cochlear nucei - axons that carry auditory impulses will pass via a variety of pathways to the inferior colliculi which is the center for auditory reflexes and via the medial geniculate body in the thalamus going to th e auditory cortex. Other enters the reticular formation. Information from both ears converges on its superior oliv e of the brain and at all higher levels most of the neuron respond to inputs from both sides. The Primary Auditory Cortex is the Brodmanns area 41 it is in the superior portion of the temporal lobe, in human it is in the floor of the lateral cerebral fissure. There are several addition auditory receiving areas just as there are several receiving areas also of cutaneous sen sation. The olivocochlear Bundle is a prominent bundle of efferent fibers coming from each auditory nerve, and ari ses in both the ipsilateral and contralateral superior oligary complex end primarily in the base of the outer hairce lls of the organ of corti in the ear. A receptors structure called Crista Ampullaris is located in the expanded end of each of the membranous canal in the ear. Each crista consist of hair cell and sustentacular cell surrounded by a gelatinous partition called Cup ula - this is the one that closes the ampulla. The processes of the hair cells are embedded in the Cupula and the bases of the hair cells are in close contact w

the afferent of the vestibular division of the vestibulocochlear nerve. In the utricle and the saccule within each of this membranous labyrinth in the floor of the utricle, there is an Oto lithic Organ called Macula, another macula is located in the wall of the saccule in a semi vertical position. The macula contains sustentacular cells and hair cells surrounded by an otolithic membrane in which are embedded crystals of calcium carbonate called Otoliths otoconia or ear dust usually range from 3-19 nanometers and more dense that the endolymph. The processes of the hair cells are embedded by the membrane and the nerve fibers from the hair cells join those from the crystal in the vestibulocochlear nerve. The neural pathways is as follows: the cell bodies of the 19 000 neurons that supply the cristae, crista ampularis, and the macula in each side, the cell body of this neurons are located in the ipsilateral part of the vestibular nucl eus and in the folliculonodular lobe cerebellum. There are 2nd order neurons that synapse with these neurons and pass down the spinal cord form the vestibular nuclei in the vestibulospinal tract and ascend through the medial longitudinal fasciculi going to the motor nucl ei of the cranial nerves that are concerned with the control of eye movement. This Hair Cell has a common structure each is embedded in an epithelium made of supporting or sustentacular cells, the base end is in close contact with the afferent neurons and projecting to the apical end of each hair cell are 30 -150 rode shape processes or hairs, 1 of this is a true but non motile cilium, and there are 9 pairs of micro tubules around its circumference and a central part of a microtubule: Kinocillium the central parts of the rods that come from the hair cell Stereocilia has coarse composed of parallel filaments of actin. Electrical impulses of the hair cells: the membrane potential of each hair cells is about -60 microvolt. When the stereo cilia are pushed towards the kenocilium, membrane potential is decrease to -60 microvolt. When bundle o f processes is pushed in the opposite direction the cell is hyper polarized, displacing the processes in the directio n perpendicular to this axis will provide no chance in the membrane potential. Displacing the processes in the di rection that are intermediate or between these 2 directions will produce depolarization or hyper polarization that is proportionate to the degree which the direction is towards or away from the kenocilium thus the hair process es provide a mechanism for generating changes in the membrane potential proportional to the direction of displa cement. The stereocilia has mechanosensitive channels in there apices so potassium channel enter the hair cell when the y are open producing depolarization, then calcium also enters and a synaptic transmitter is released that depolar izes the afferent neurons that are in contact with the hair cells, that is the electrical response of the hair cells. Hearing

 sound is the sensation that is produce when longitudinal vibrations of the molecules in the external envir onment happens, there is an alternate of phases of condensation and rarefaction of the molecules that stri ke the tympanic membrane; This is the one that we perceive as sound waves. Sound waves travel to the air in speed of 344 m/sec or 770 miles/hour at sea level and at temperature of 20C. The speed of sound increases with temperature and also with altitude. Also differs in water and air so the speed of sound in fresh water is 1450 m/sec and greater in salt water *The loudness of a sound is correlated with the amplitude of the sound wave and each pitch is correlated with fr equency of the sound waves. The greater the amplitude the louder will be the sound, the greater the frequency the louder is the pitch We measure sound intensity or loudness using a Decibel Scale - measure of the amplitude of the sound. The po wer of the sound in decibels is the logarithm of the ration of the power of that sound and standard of sound. 1decibels is 0.01 bel. There is phenomenon in hearing called Masking presence of one sound will decrease an individual ability to hear the other sound due to the relativ e or absolute refractoriness of the previously stimulated auditory receptors and nerve fibers to the other stimuli. Sound transmission, the ear converts sound waves in the external environment into action potentials in the audit ory nerve, then the waves are transformed by the eardrum and the auditory ossicles into movements of the footp lates of the stapes. This movement will setup waves in the fluid in the inner ear. The action of the waves in the organ of corti will generate the action potential in the nerve fibers. The waves are transformed by the eardrum and the auditory ossicles into movements of the footplates and the stapes, and this movement will set up waves in the fluid inside the inner ear. The tympanic membrane - functions as a resonator that reproduces the vibration of the sound source. Auditory ossicles -function as a lever system that converts resonant vibration of the tympanic membrane into m ovement of the stapes and the perilymph( fluid that fills the scala vestibule of the cochlea) The middle ear muscle 1. Tensor tympani 2. Stapedius muscle *if these muscles contract they pull the manubrium of the maleus inward and the foot plates of the stapes outwa rd. This will tend to decrease sound transmission. Loud sound initiate a reflex contraction of these muscles of called the Tympanic Reflex. The function of this re flex is to prevent the strong sound from causing excessive stimulus of the auditory receptors.

There are different ways wherein sound will be conducted through the ear. 1. Ossicular Conduction - via the tympanic membrane and the auditory ossicles. 2. Air conduction- through the vibration of the secondary membrane that closes the round window. 3. Bone conduction- transmission of vibration through the bone of the skull to the fluids in the inner ear. The movement of the foot plates of the stapes will set a series of waves in the perilymp of the scala vestibule. A s the waves move up in the cochlea the height of the wave increases to a maximum and it drops very rapidly. Th is movement of waves in the scala vestribuli called Travelling Waves. 2 types of hair cells 1. Inner hair cells primary sensory cells that generate action potential in the auditory nerve. 2. Outer hair cells innervated by cholinergic efferent fibers from the superior olivary complexes. They are t he ones improving the hearing by influencing the by vibration patterns of the basilar membrane. The frequency of the action potential in a single auditory nerve is proportionate to the loudness of the so und stimuli. The major determinate of the pitch that we perceive is the place in the organ of corti that is maximally st imulated. Low tones will produce maximal stimulation in the apex of the cochlea, while high tones prod uce stimulation at the base of the cochlea. The pathways from the various part of the cochlea to the brain are also distinct.

In the auditory cortex: a. low tones - are represented anterolaterally b. high tones - are represented posteromedially The auditory cortex= is concern with recognition of tonal process, with analysis of properties of sound and soun d localization. This sound localization depends upon detecting of differences in time between the arrival of stimulus in the 2 ea rs and the consequent difference in the phase of the sound waves in the 2 sides. Different types of deafness 1. Conduction deafness - impaired sound transmission in the external or middle ear. 2. Nerve deafness - impaired or damage hair cells or the neural pathways are damage. Test for deafness to distinguish between nerve or conduction deafness using tuning fork 1. Weber test this method is done by striking the fork and put the base of the vibrating tuning fork in t he vertex of the skull Results:

a. Normal - hears the sound equally in both ears. b. Conduction deafness in 1 Ear - the sound is louder in the disease ear because of the masking effect of the e nvironmental noise is absent in the diseased ear. c). Nerve deafness - the sound is louder in the normal ear. 2. Rinne Test strike the fork and you place the base of the vibrating tuning fork in the mastoid process until your patient to longer hears it and hold it in air next to the ear. Results: a. Normal - will hear the vibration in air even the bone conduction is over. b. Conduction deafness - the vibration in air is not heard after bone conduction is over. c. nerve deafness - the vibration is heard in air after bone conduction is over. 3. Schwaback Test compare the bone conduction of the patient with that of a normal subject. You can use yourself as the normal subject Results: a. Conduction deafness - the bone conduction will be better than normal because the conduction defect will ex clude the masking noise b. Nerve deafness - bone conduction will be less heard than normal. Auditometry use to test auditory acuity. It will present the patient with pure tone with varying frequency thr ough an earphone. At each frequency the threshold intensity is determined and it is plotted in the graph as a perc entage of normal hearing. Provides objective measurement of the degree of deafness and picture of the tonal zon e of that deafness that is most affected. Otosclerosis development causes the attachment of the footplates of the stapes to the oval window, the attac hment becomes abnormally rigid. Fenestration procedures surgical procedure for otosclerosis. An outlet is created by drilling a small hole in the horizontal semicircular canal and covering it with skin. Vestibular function is it responds to rotational acceleration in a plane of a given semicircular canal will sti mulate the crista of that semicircular canal. The endolymph because of its inertia is displace in an direction that is opposite to the direction opposite to the rotation, so the fluid is pushes into the cupula, deforming it, and this bends the processes of the hai r cells here. When the constant speed of rotation is reach, then the fluid spins at the same rate as the body and the cu pula swings back into the upright position.

When the rotation stops or there is a deceleration, this will produce displacement again of the endolymp h in the direction of the rotation; the cupula will be again be deformed in a direction opposite to that duri ng acceleration. This will result into a midpoint position which will last for 25-30 seconds. The movement of the cupula in 1 direction commonly causes increase impulse traffic in a single nerve fi ber while movement in the opposite direction commonly inhibits neural activity. Rotating will cause maximal stimulation of the semicircular canal most nearly in the plane of rotation. Si nce the canal in 1 side of the head is a mirror image of those on the other side, the endolymph is diplace d towards the ampulla on one side and away from the ampulla in the other side. So the pattern of stimula tion reaching the brain varies with the direction as well as the plane of rotation. Linear acceleration fails to displace the cupula and therefore in wont stimulate the crista ampularis. When 1 part of the labyrinth is destroyed, other parts takes place its function. The nerve tracts that descent from the vestibular nuclei into the spinal cord are concern with postural adj ustments, while the ascending connection going to the cranial nerve nuclei are largely concerned with ey e movement.

Nystagmus jerky movement of the eye observe at the start and at the end of the period of rotation. It is actually a refl ex that maintains visual fixation of stationary objects while the body rotates although it is not initiated b y visual impulses because they found out the even blind subjects has nystagmus. It frequently horizontal but can also be vertical when the head is tipped sidewise during rotation or when they rotate you with the head tilt forward.

Vestibulo-Ocular Reflex or VOR When the rotation start, the eyes move slowly to a direction opposite to the direction of the rotation and t his will maintain your visual fixation. When the limit of this movement is reach, the eye quickly snaps back to a new fixation point and again moves slowly in the other direction. Slow component of the VOR - is initiated by impulse from the labyrinth Quick competent of the VOR= is triggered by a center in the brainstem.

* The direction of eye movement in nystagmus is identified by the direction of the quick component. The directi on of the quick component during the rotations is the same direction as the rotation, while the pause rotatory ny stagmus (nystagmus after rotation) occurs owing to the displacement of the cupula when the rotation stop is at t he opposite direction. Responses to linear acceleration: in general: a. The utricle respond to horizontal acceleration.

b. The saccule to vertical acceleration. If there is acceleration to any direction, this will cause the otoliths to be displaced to the opposite direction so it will distort the hair cell processes and generate activity in the nerve fibers. The impulse generated from this rece ptors are partly responsible for the reflex righting of the head and other important postural adjustment during ac celeration. Although most of the responses to stimulation of the macula are reflex in nature, vestibular impulses also reach the cerebral cortex and this impulses are responsible for conscious perception of motion and supply part of the i nformation necessary for orientation and space. If there is an excessive vestibular stimulation, the subject will feel: Nauseated BP changes Sweating Pallor

vomiting This is due to a reflex mediated via the vestibular connections in the brain stem. Vertigo - this is sensation of rotation in the absence of actual rotation. There is a way of stimulating the semicircular canals either clinically or accidentally: 1. By instilling water with hotter or colder than the body temperature, instill it in the external auditory meatus. The temperature difference will set up a convection current in the endolymh with consequent motion of the cup ula called Caloric Stimualtion and it causes nystagmus, vertigo and nausea. The temperature of water must be the same as the body temperature, not colder or hotter to avoid caloric stimul ation. Orientation in Space - depend in large part upon inputs coming from the vestibular receptors but visual clues are also important. - Pertinent information is also supplied by impulses from proprioceptors in the join capsule which supply data about the relative position of the various parts of the body and also impulses coming from the cutaneous extra re ceptors specially touch and pressure receptors. So orientation in space depends in so many receptors. These 4 in puts are synthesized in the cortical level into continues picture in our orientation in space. The effect of labyrinthectomy - postural changes due to the unbalance discharge from the remaining normal side will be effected. Defects in or ientation, there will be nausea, vomiting, and diarrhea. - Compensation for the loss will occur immediately after the removal of the labyrinth but in 1-2 months the sym

ptoms will disappear completely. - The symptoms are absent after bilateral destruction of the labyrinth but the defects in the orientation will be pr esent, so person with defective labyrinth should not engaged in diving

Smell and Taste - classified as visceral senses, because of their close association with GI function. - Physiologically they are related to each other, actually the flavor of various foods are inlarge part in com bination of both taste and smell. - Both taste and smell receptors are chemoreceptor. They are stimulated by molecules in solution in the m ucous in the case of the noise and in the saliva in case of the oral cavity. The smell receptors called Distance Receptors or Teleceptors. The smell pathway has no relay in the thalamus and there is no neocortical projection area also for smell. The taste pathways pass up the brain stem, goes to the thalamus, and project in the post central gyrus along with touch and pressure sensibility from the mouth. SMELL: - The olfactory receptors are located in a specialize portion of the nasal mucosa called the olfactory muco us membrane. Olfactory mucous membrane - In humans it is a small covering, an area about only 5 square centimeters loca ted at the roof of the nasal cavity near the septum. It contains supporting cells and nueroblast like progenitors ce lls that form the olfactory receptor neurons. Interspaced between this cells are about 10-20million receptor cells. Each olfactory receptor is a neuron, and the neuron have short thick dendrite with expanded ends called Olfacto ry Rods from this rods, cilia projects in the surface of the mucus then cilia are unmyelinated process. There are 10-20 cilia per receptor neurons. The axons of these olfactory receptor neurons will pears the cribiform plate in the ethmoid bone and enter the ol factory bulbs. This olfactory is mucus membrane is constantly covered with mucus; the mucus here is produces by specialized gland called Bowmans Glands which are just under the basal lamina of the membrane. The olfa ctory bulbs, the axon of the receptors terminate along the dendrite of a special cells called the Mitral Cells to fo rm a complex globular synapses called Olfactory Glomeruli. There is an average of 26,000 receptors cells axo n that converges in each glomerulus. In the next layer of the olfactory membrane, the dendrites of the mitral and granule cells will form extensive rec iprocal synapses, the axon of these mitral cells pass posteriorly to the intermediate olfactory straea and lateral ol factory staea going to the olfactory cortex.

The mitral cell cortex terminates to the apical dendrites of the pyramidal cells in the olfactory cortex. The Olfac tory Cortex includes the anterior nucleus, the olfactory tubercle, the corticomedial amygdala, and the transition al entorinal cortex. Olfactory receptors respond only in substances that are in contact with the olfactory epitheli um and are dissolved in the thin layer of mucus that covers it. There is a remarkable sensitivity of the olfactory receptor to some substances, but discrimination of differences in the intensity of any given odor is very poor. The concentration of the odor producing substance must be chan ge in 30 percent or more for us to perceive a difference in the intensity of the odor. Odoriferous molecules bind to receptors of the cilia of the olfactory receptor neurons. The activated receptor act ivate Adenylate Cyclase via Golf, a G protein closely related to G5 but it is unique protein present only in the o lfactory system. This activation will produce a increase a Intracellular cyclic AMP. The cyclic AMP will bind to an open sodiu m channel, and the resultant influx of sodium will produce receptor potential then it depolarized the initial seg ment of the axon up to the firing level, and opening of the voltage gate channels in the area and it in initiate a tra nsmitted impulse. Odor producing molecules are generally small. They contain from 3-4 up to 18-20 carbon atoms and the molec ules with the same number of carbon atoms but different structural configuration have different odors. Relatively high water and lipid solubility are characteristics of substances with strong odors. There is a pronounce degree inhibitory control within the olfactory pathways. The reciprocal synaptic connectio ns between the mitral and granule cell dendrites mediate inhibitory control of the output. So in the olfactory cort ex, the responds to an odor is excitation of pyramidal cell s followed by inhibition. The pyramidal cells are then subjected to self reexcitation via long axon collaterals. The olfactory mucus contains 1 or more type of protein called the Odorant Binding Proteins or OBP. These a re contained in the olfactory mucus. There are 1 or more odorant binding proteins that concentrate the odorants and transfer them in the receptors. There has been an isolated type of odorant binding protein that they are able to see in the nasal cavity and these are unique protein just in the nasal cavity called 18k OBP How can human know different odor? - human can differentiate between 2000 to 4000 different odors. Different odors are produce by different spacial patterns of increase metabolic activity in the olfactory bulb, and

each particular odor depends on the special pattern of stimulation of the receptors on the olfactory mucus mem brane. Different odors produce also different patterns of increase metabolic acuity in the olfactory cortex. The s ense of smell is more acute in female than in male. The sense of smell in women is even more acute in the time of ovulation. Sniffing the amount of air is greatly increase by sniffing, an action including a contraction of the lower part of the nares to deflect the air stream upward. This sniffing is a semi reflex response that usually occur when a ne w odor attracts your attention. The role of pain fibers in the nose: - There are many trigeminal pain fibers found in the olfactory mucus membrane in a form of naked nerve ending of the trigeminal nerve, and they are stimulated by irritating substances and irritative trigeminally mediated component is part of the characteristic odor of such substances as peppermint, mentol, chlorin e. These ending are also responsible for initiating sneezing, lacrimation, respiratory inhibition and other ref lex response to nasal stimulation.

Adaptation - when one is expose to even the most disagreeable odor, perception of the decreases and eventually seize s. This is due to the fairly rapid adaptation that occurs in the olfactory system, and it is primarily central in origin. It is specific for a particular odors that is being smelled, and the threshold for other odors still r emain unchanged, only in that particular odor that adaption occurs. Abnormalities in the smell sense: 1. Anosmis - absence in sense of smell 2. Hyposmia - decrease in the sense of smell 3. Dysosmia - distorted sense of smell Olfactory threshold increase in advancing age. Taste Taste buds sense organ for taste. They are ovoid bodies measuring about 50-70 nanometers, Each taste bud is made of 4 types of cell. 1. Base cell 2. Type 1 and 2 which are sustentacular cells 3. Type 3 which are gustatory receptor cells that make synaptic connections to the sensory nerve fibers. Type 1,2,3 cell have microvilli which project to the taste pores of the taste buds Each taste buds is innervated by about 50 nerve fibers, each nerve fibers receives input from an average of about 5 taste buds.

The basal cells arise from the epithelial cells surrounding the taste buds, they differentiate to a new recep tors cell and the old receptors cells are continuously replace. The half time of a taste bud is 10 days, meaning half of the taste buds replace every 10 days. In humans taste buds are located in the mucosa of the epiglottis, palate, pharynx, and in the walls of the fungi form and valiate papilla of the tongue.

Fungiform Papilla rounded structures and most numerous in the tip of the tongue. There are about 5 taste b uds located to each fungi form papillae usually located at the top of the papillae. Valiate Papilla prominent structures that are arrange in V shape in the back of the tongue. Each papilla cont ain about 100 taste buds usually located in the side of the papilla. Filiform Papillae Covers the whole dorsum of the tongue usually do not contain taste buds. About 10,000 taste buds in each person. The sensory nerve fibers from the taste buds, on the anterior 2/3 of the tongue will travel in the Corda t ympani branch of the facial nerve. Those from the posterior 1/3 of the tongue reaches the brain stem via the glossoparyhngeal nerve. The fibers from the areas other than the tongue reach will reach the brainstem via the vagus nerve.

On each side the myelinated taste fiber in this 3 nerve will unite in the medulla oblongata to enter the nucleus of the ductus solitatious of the brain, there they will synapse with the 2nd order neuron. And the axons of this will cross the midline and join the medial lemniscus ending with the fibers of touch, pain, temperature sensibility in the specific of sensory relay nuclei of the thalamus. The impulses are relayed from there to the taste projection area in the cerberal cortex at the foot of the posterior central gyrus. Taste sensations dont have a separate cortical projection area, but it is represented in the portion of the post cen tral gyrus that sub serves cutaneous sensation from the face. In human there are 4 basic taste - sweet, sour, bitter, salt a. Bitter- tasted at the back of the tongue b. Sour-along the edges c. Sweet-at the tip d. Salty-at the dorsum anteriorly Sour and bitter are also tasted in the palate along with some sensitivity to sweat and salt.All the 4 modalities of t aste can be sense in the pharynx and the epiglottis.

The Gustatory receptors cells are chemoreceptors. They respond to substances that are dissolved in the oral flu ids. These substances act on the exposed microvilli in the taste pore to evoke a generator potential in the recepto r cell which will generate the action potential in the sensory neurons. The way this molecules in the solution produce a generator potential varies from one gustatory modality to anot her. Salt stimuli depolarizes salt receptor cells by influx of sodium through the passive ungated apical channels. While acids which taste sour depolarizes receptors cell by hydrogen blocking of the apical potassium channels. Substance that taste sweet appears to bind to the membrane potential and via the G5 they activate adenyl cyclas e with a resulting increase in the intracellular cyclic AMP. The substances that taste bitter dont increase current flow, but act via receptors and phospholipase C to trigger t he release of calcium ions from the endoplasmic reticulum. A protein that binds taste producing molecule is produce by a specific gland called Ebners gland, they produc e mucus into the cleft around the valiate papillae and has a concentrating and transport similar to that of the odo r binding protein in the olfactory. Taste threshold and intensity discrimination this intensity discrimination of taste is relatively crude in hu mans. We need 30% of change in the concentration of substance being tasted before an intensity differences can be detected. The threshold concentration of substances to which the taste buds respond varies with the particular substance. So the substance that evoke this primary taste sensations are acid taste sour because of the sodium ion rather tha t the associated anion that stimulates the receptors. Salty taste - produce by sodium ion Bitter taste - is due to the cation Sweet Flavor: There are infinite varieties of taste that are sensitized from the 4 basic taste components and this will produce th e flavor. Smell, consistency, temperature will also contribute to the food we eat. Abnormalities in sensation of taste 1. Ageusia - absence of the sense of taste. 2. Hypogeusia - decrease of sense of taste. 3. Dysgeusia - distortion of sense of taste.