what are 5 senses?
touch, smell, hearing, vision, taste
where does touch + proprioception info travel?
dorsal column up to somatic sensory area of cerebral cortex
what is touch acuity? what is it proportional to?
ability to know where touch is
# of receptors
what are 4 touch mechanoreceptors?
superficial slowly adapting - markets receptors - pressure
superficial rapidly adapting - meissner receptors - feather
deep slowly adapting - Ruffini's corpuscles - skin stretch
deep rapidly adapting - vibrations
what are 2 areas that help with proprioception?
semi circular ear canals - balance
muscle spindles - position in space
how do semi circular canals help with proprioception?
has 1 for each dimensional plane
When your head moves around, the liquid inside the semicircular canals sloshes around and moves the tiny hairs that line each canal.
how do muscle spindles help with proprioception?
They run parallel to the extrafusal muscle fibers and act as receptors that provide information on muscle length and the rate of change in muscle length.
what is signal transduction?
sensory cells translating chemical electromagnetic and mechanical stimuli into action potentials that our nervous system can make sense of
what are types of receptors?
chemoreceptors
what is link between olfactory nerve and limbic system?
mitral cell picks up info from olfactory neuron -> olfactory tract -> olfactory cortex -> limbic system
emotional pathway triggers memories if smell is associated w/things:
danger -> triggers fight or flight
what is link between taste and smell?
taste is 80 percent smell
as u chew food air is forced up nose so olfactory receptor cells are processing info at the same time as taste receptors
what are 5 different tastes? how are they sensed?
salty
sweet
sour
bitter
umami
all taste registers in all parts
taste receptors on tongue (epithelial cells)
gustatory or basal cells
what is sound frequency?
sometimes referred to as pitch, is the number of times per second that a sound pressure wave repeats itself.
what is sound amplitude?
the relative strength of sound waves (transmitted vibrations), which we perceive as loudness or volume
how do sound waves produce action potentials?
SOUND WAVES enter the ear canal and cause the eardrum to vibrate. VIBRATIONS pass through 3 connected bones in the middle ear. This motion SETS FLUID MOVING in the inner ear. Moving fluid bends thousands of delicate hair-like cells which convert the vibrations into NERVE IMPULSES.
how is head movement/acceleration sensed?
The otolith organs allow us to sense the direction and speed of linear acceleration and the position (tilt) of the head. The semicircular canals allow us to sense the direction and speed of angular acceleration.
what causes motion sickness?
when the body, the inner ear, and the eyes send conflicting signals to the brain -> doesn't know if you are stationary or moving
what is light frequency?
The number of waves which pass through a given point in one second
what is light amplitude?
associated with our experience of brightness or intensity of color,with larger amplitudes appearing brighter.
what are rods? what are cones?
the receptors in the retina responsible for your sense of sight
rods: vision at low light, low spatial acuity
cones: vision at higher light, color vision, high spatial acuity
what is the sequence of signal transduction for vision?
1- photon of light hits photoreceptors on cones and/or rods
2- photoreceptors activate cellular mechanism causing opening/closure of Na+ channels
3- changes in voltage travels through bipolar cells and converge on ganglion cells
4- ganglion cells translate voltage changes into AP
5- AP relayed to cortex via CN II
what is the sequence of signal transduction for hearing?
1. sound waves amplified by auditory canal produce tympanic membrane vibrations
2. tympanic vibrations are mechanically amplified by malleus + incus + stapes
3. vibrations pushing oval window produce inner ear fluid motion
4. fluid motion pulls ion channels open on hair cells
5. ion influx produces action potentials relayed via CN VIII
what are structures of external eye + their role?
eyelids: control light + anti particles protection
lacrimal glands: lubrication + wash out pathogens
conjunctivae: protective lining
what are 3 main layers of the eye?
fibrous: sclera + cornea
vascular: choroid + iris + pupil
inner: retina
what are 3 cones types?
red green blue
what are some visual dysfunctions?
scotoma
strabismus
cataract
glaucoma
AMD
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what are the primary pathogens found in Otitis Media (OM)?
haemophilus influenzae
what is OM management?
all kids receive analgesic
antibiotics not always necessary but amoxicillin best option
< 6 months: always antibacterial therapy
6 - 12 months: observe if illness not severe
> 2 years: antibacterial if severe, observe rest
what is OM prevention?
breastfeed for first 6 months
decrease tobacco smoke exposure + pacifier use after 6 months
vaccination vs S pneumoniae + influenza
what is recurrent OM?
3+ cases/6months or 4+ cases/year
how to treat recurrent OM?
tympanostomy tubes -> good
influenza prevention + Tx -> benefits only in flu season
prophylactic antibacterial -> not recommended, small benefits
what are acute otitis external treatments?
pain -> analgesic
PO antibiotics -> only severe + immunocompromised/diabetic
Topical antibiotics -> best efficacy:toxic
what are acute otitis external prevention?
optimal ear hygiene
drying external auditory canal
avoiding earplugs
avoid removing ear wax
avoid inserting things
what are major structures of eye part 1?
Iris: regulates the amount of light that enters your eye (controls pupil)
Pupil: the circular opening in the centre of the iris through which light passes into the lens of the eye.
Cornea: the transparent circular part of the front of the eyeball. It refracts the light entering the eye onto the lens.
Lens: a transparent structure situated behind your pupil, helps to refract incoming light and focus it onto the retina.
Choroid: the middle layer of the eye between the retina and the sclera, absorbs excess light so preventing blurring of vision.
Ciliary body: the part of the eye that connects the choroid to the iris.
what are major structures of the eye part 2?
Retina: a light sensitive layer that lines the interior of the eye (rods + cones)
Macula: a yellow spot on the retina at the back of the eye which surrounds the fovea.
Fovea: forms a small indentation at the centre of the macula and is the area with the greatest concentration of cone cells. When the eye is directed at an object, the part of the image that is focused on the fovea is the image most accurately registered by the brain.
Optic disc: the visible portion of the optic nerve, also found on the retina, also known as the 'blind spot’.
Optic nerve: leaves the eye at the optic disc and transfers all the visual information to the brain.
Sclera: the white part of the eye, a tough covering with which the cornea forms the external protective coat of the eye.
what is necrotizing otitis external? who is at risk? what is management?
infection spreads to skull base, risk of meningitis and CN damage, rare fatal complication
elderly diabetic, immunocompromised
immediate referral to specialist
proper ear cleaning + drugs (ear drops + antibiotics)
what is fungal otitis external? what is management?
10% of otitis externa
proper ear cleaning + acetic solution, if severe oral antifungals
what is the pathophysiology of primary open angle glaucoma (POAG)?
most common/leading cause of blindness
characterized by increased resistance to drainage in the trabecular meshwork, even though the drainage angle between the cornea and iris remains open.
intraocular pressure (IOP) not always elevated
no Sx until significant optic nerve damage
TX: decreased IOP can stop progression/no cure
what is the pathophysiology of angle-closure glaucoma (ACG)?
very rare/emergency situation
occurs when the iris bulges. The bulging iris partially or completely blocks the drainage angle. As a result, fluid can't circulate through the eye and pressure increases.
loss of vision within 48h
IOP rises rapidly
Tx: decreases IOP + corrective surgery
what are glaucoma drugs available?
beta-blockers: decreased aqueous humor formation -> good for closed angle
prostaglandin analogs: increased aqueous humor formation -> less efficient for closed angle
alpha-adrenergic agonists: decreased aqueous humor formation
what is management for glaucoma?
topical administration for all drugs
beta-blockers + prostaglandin analogs = most effective for acute decreased IOP
prostaglandin analogs = preferred -> less toxicity
alpha2-agonist brimonidine: best for long term decreases IOP -> can delay optic nerve damage
what is management for age-related macular degeneration (ARMD) ?
initiate therapy when diseases progresses from dry to wet ARMD -> decreases risk of advanced ARMD development, possible to partially restore lost vision
where does pain and temperature info travel?
both travel via the anterolateral column
what is pain? what is influenced by?
complex somatic + emotional experienced -> associated w/actual or perceived tissue damage
cognition, history, motivations...
what is best theory of pain?
gate control theory (GCT):
A-delta + C fibres (nociceptors) -> open the gate (substantia gelatinosa)
descending CNS pathways + non-nociceptor A-beta fibers -> partial or complete closing (ex: rubbing site of injury decreases pain sensation)
what are 3 processes required for pain sensation + perception?
1- afferent pathways: PNS pain neurons -> spinal gate -> anterolateral tract -> CNS
2- interceptive centers: brainstem + cerebral cortex
3- descending efferent pathways: CNS neurons -> spinal gate (dorsal horn)
what are 4 phases of nociception?
1- pain transduction
2- pain transmission
3- pain perception
4- descending pain modulation
how does pain transduction work?
harmful stimuli activates nociceptors (free nerve endings) -> increases AP
A-fibers -> rapid severe mechanical pain (high myelination)
C-fibers -> slow dull mechanothermal pain
what are the 3 neurons needed for pain transmission?
1- PNS -> spinal cord interneuron: 1st order neuronal = A + C fibers
2- interneuron -> thalamus via anterolateral tract: 2nd order neurons = stimulatory or inhibitory
3- thalamus -> pain interpretation centers: 3rd order neurons
what are the 3 interpretive systems of pain perception?
1- sensory-discriminative
location: somatosensory cortex
purpose: character, location, intensity...
2- affective-motivational
location: reticular formation + limbic system + prefrontal
purpose: conditioning/avoidance + emotional response to pain
3- cognitive-evaluative
location: cerebral cortex
purpose: modulation and analysis, compare pains, decrease it
what are 2 possibilities of pain modulation?
open gate: feeling of pain increases
closed gate: feeling of pain decreases
what are neurotransmitters of pain modulation?
excitatory (open gate): glutamate on AMPA + NMDA receptors
inhibitory (closed): GABA, glycine, serotonin, opioids, endorphins
what is allodynia? what is hyperalgesia?
excessive glu stimulation -> feels pain when it is not painful (no injury)
inflammatory mediators -> decrease pain threshold = pain sensation increases with actual injury
what are things that affect pain modulation?
descending modulation from cortex: powerful inhibition of afferent pain signals
diffuse noxious inhibitory controls (DNICs): non noxious stimuli elsewhere decreases attention to major pain (ex: acupuncture)
expectancy related activation: placebo + nocebo effect
pain threshold: usually constant
pain tolerance: variable (past exposure, motivations, drugs...)
what is referred pain?
pain is felt somewhere that is not site of nociception origin
organs borrow nociceptors
what is neuropathic pain?
direct injury to CNS or PNS nociceptive neurons
CNS: brain or SC trauma -> think strokes, hemiagnosia = hyperalgesia/allodynia of one half of body
PNS: peripheral nerve trauma, phantom limb pain, possibly due to scar tissue + absence of inhibitory signals
what is the body's cold adaptation?
heat production + conservation via activation of HPT axis:
T4 -> increase metabolism + adrenal glands -> increase cellular work (shivering) + vasoconstriction
what is the body's hot adaptation?
heat loss via shut down of HPT axis:
decreased T4 -> decrease metabolism + vasodilation + sweat
what is a fever?
temporary reset to higher temp in response to pathogens