EXAM 2 - Week 5 (pain, ear, eye) Flashcards
What are the two tracts of the spinothalamic bundle in the spinal cord? What does it connect to?
Neospinothalamic tract
Paleospinothalamic tract
Connects with reticular formation of brain
Neospinothalamic tract
Fast impulses; actue pain
Paleospinothalamic tract
Slow impulses; chronic/dull pain
Pain Control - Gate Open
Painful stimulus - substance P - pain stimulus to brain - RAS alert - pain received
Pain Control - Gate Closed
Painful stimulus - interneuron activated by efferent impulses from brain or affront impulses from touch stimulus - interneuron releases Enkephalin - Enkephalin blocks opiate receptors - thus Substance P is NOT released - Gate closed/transmission blocked on affarent tract
Nociceptive pain
Caused by stimulation of peripheral nerve fibers; respond only to stimuli approaching or exceeding harmful intensity
Neuropathic pain
Caused by damage/disease affecting nervous system - involves “imbodily” findings
Psychogenic
AKA psychoalgia, somatoform pain
Pain caused by increased or prolonged mental, emotional, or behavioral factors - sufferers are often stigmatized b/c medical professionals and public thinks these pains are not real
Pain Characteristics - Somatic Pain
From skin (cutaneous) or bone muscle and conducted by sensory fibers
- Fades once injury heals
- Respond well to NSAIDs
- Nocicpetors pick up sensations r/t temperature, vibration, and swelling
Pain Characteristics - Visceral Pain
Pain resulted from activation of nociceptors of thoracic, pelvic, or abdominal viscera, conducted by sympathetic fibers
- Sickening, deep, dull, squeezing feeling
- Symptoms often include nausea, vomit, change in vitals, emotional manifestation
- Highly sensitive to dissension, ischemia, and inflammation
- Diffuse - difficult to localize
What is Referred Pain?
Pain may be perceived at site distant from source
- Characteristic of visceral damage in the abdominal organs , heart attack, or ischemia in the heart
- Multiple sensory fibers from different sources connecting to single level of spinal cord make it difficult for brain to discern actual origin of pain
What can increase Pain Tolerance?
Endorphin release
What can decrease Pain Tolerance?
Fatigue, or stress
COLDSPA
character onset location duration symptoms precipitating events alleviating factors
Pain Management - Opiate-like Chemicals (Opioids)
Secreted by interneurons of the CNS (endogenous)
- Block conduction of pain impulses to the CNS
- Resemble morphine
Ex: Enkephalins, dynorphins, beta-lipoproteins
Analgesic Drugs - Mild Pain
ASA, NSAIDs, Acetominophen
- Decreases pain at peripheral site
- Antipyretic
- ASA and NSAIDs are anti-inflammatory
- ASA and NSAIDs have many adverse effects (nausea, gastric ulcers, bleeding, allergies)
Analgesic Drugs - Moderate Pain
Codeine, Oxycodone
- Acts on central nervous system and effect perception
- Adverse effects: Narcotic (opium) - often combined with ASA/acetominophen
- High dose may depress respiration
Analgesic Drugs - Severe Pain
Morphine, Meperidine
- Acts on central nervous system; euphoria and sedation
- Adverse effects: Narcotic - tolerance and addiction
- High dose depresses respiration, nausea, constipation common
Pain mangement - PCA?
PCA = patient controlled analgesia
- Patient administers medication as needed
- Lessen overall consumption of narcotics
Structure of the Ear - external ear
Captures and amplifies sound
Structure of the Ear - middle ear
Transmit sound waves from tympanic membrane to nerve center of the ear
-May be stimulated by head movement position
Structure of the Ear - inner ear
Ventilation of middle ear and equalizing middle ear in pressure change
-Drainage: secretion will drain to the nasopharynx from the inner ear
Otitis Externa
Inflammation of the external ear (can be due to infection)
Swimmer’s Ear
Often seen with otitis external
Water sits in the ear and doesn’t drain out. This creates an optimal environment for bacterial growth.
Hair follicles get infected, and can lead to ischemia
Barotrauma
Changes in the tympanic membrane due to blood/fluid buildup behind the membrane
-Extremely painful!
Otitis Media
Inflammation of the middle ear
AOM = acute otitis media
OME = otitis media with effusion
Mastoiditis
Ear infection spread to the mastoid bone causing
- Ear pain
- Otorrhea
- Fever
- Headache
- Swelling and redness behind the ear
Otosclerosis
New spongy bone formation around stapes and ova window in the inner ear
- Now these bones cannot properly transfer sounds into the inner ear, leading to progressive deafness
- Ringing in the ears (Tinnitus)
- Hearing loss on innervation of ear (Vertigo)
Conductive Hearing loss
Sounds are not produced through tympanic membrane, stapes, and ova window
AOM
Acute Otitis Media - infection in the middle ear, associated with upper respiratory infections
-Infected fluid in the middle ear creates an optimal environment for pathogen growth
Recurrent: more than 3 episodes in 6 months, or more than 4 episodes in a year
Clinical Manifestations: enlarged periacular lymph nodes, rinorrhea (runny nose), fever, impaired hearing
Treatment: antibiotics if unresponsive to observation
OME
Otitis Media with Effusion
- No infection, just fluid build up
- Trapping of fluid by obstruction in the Eustachian tube
- Not an infection thus not associated with inflammation
- Acute pain from pressure on the tympanic membrane; this pressure can also lead to impaired hearing
Neural dysfunction of the inner ear (3)
Sensorineural Hearing loss
Tinnitus
Equilibrium disruption
Sensorineural Hearing Loss
Occurs due to permanent damage to the cochlea of the inner ear (due to disease, trauma, genetic defect)
Tinnitus
Ringing in ears
Equilibrium disruption
Could be from vertigo
Objective Vertigo
Person is still but feels that everything around is moving
Subjective Vertigo
Person is in motion but the room is still
Physiologic Vertigo
Motion sickness from repeated rhythmic stimulation
Meniere disease
Occurs due to fluid build up in the inner ear, creating pressure build up in the cochlea and vestibule. The increased pressure creates a feeling that the ear is full.
Caused by trauma, infection, or endocrine disorders
-Equilibrium disruption
Labyrinthitis
Inflammation of the inner ear
Hyperopia
Farsightedness
-Anterior:posterior dimension of eyeball is too short causing the focal point to fall behind the retina
-Convex lenses needed
Myopia
Nearsightedness
-Anterior:posterior dimension of eyeball is too long causing the focal point to fall in front
Presbyopia
Loss of nearsightedness commonly associated with aging
Strabismus
Any abnormality of eye coordination and alignment that results in loss of binocular vision
R/t paralysis of eye muscles or weak eye muscles, or other issues that lead eye to pull inward
-Eye pulls toward the stronger muscle and away from the weaker muscle
Can lead to amblyopia if left untreated
Amblyopia
Lazy eye = diminished vision when there is no detectable lesion in the eye
Brain processes input from normal in view, but over time, brain will block any input from the affected eye, causing permanent blindness in that eye
Diplopia
Double vision that occurs when binocular vision isn’t quite lined up
_more permanent damage occurs if r/t muscle tissue
Nystagmus
Involuntary rhythmic occultation of eye movement that happens when trying to focus on an object in the extremities of our peripheral vision
R/t semilunar ducts and vestubuler apparatus of ears
Ptosis
Weakness of the lavender muscle (the muscle that holds up the eyelid)
Entropion
Lower lid turns IN, causing eye irritation and tearing
Ectropion
Lower lid turns OUT, causing eye irritation, tearing, and dryness
Hordeolum
Infection of the sebaceous glands of eyelid
“sty”
Can be internal or external
Chalazion
Chronic inflammation of myobomium gland inside the eyelid that leads to constant sty
Conjunctivitis
Inflammation of conjunctiva
Viral vs Bacterial
Bacterial Conjunctivitis
Caused by Chlamydia trachomatis and Neisseria gonorrhea
Creates lots of crusting, yellow-green drainage
Can be seen in babies at birth
Viral Conjunctivitis
Viral infection, AKA pink eye
Causes profuse watery discharge, redness/pink of the eye
VERY contagious
Typically starts in one eye then spreads to the other from wiping that eye and touching the other
Keratitis
Herpes Simplex infection of the cornea that causes severe pain and photophobia
-Can be from Herpes lesions around the mouth, or transferred by fingers, dental visits sprays of contaminated saliva
Increases risk of ulceration/eroding of the cornea. The scar tissue formation and trauma to cornea interferes with vision and can lead to permanent damage to the vision.
Glaucoma Pathophysiology
Vision loss due to increased intraocular pressure buildup from aqueous production issue
Congenital or acquired lesions mechanically obstruct aqueous outflow (not flushed out properly). This increases the intraocular pressure causing atrophy of optic nerve axons. Changes in the axons causes pallor of optic cup and increase in the size and depth of the optic cup. This change in the cup precedes vision loss. If the optic disk breaks away from the nerve, it can cause blindness.
Glaucoma categorizations
Angle closure (emergency) vs open angle (slow damage)
Congential vs acquired
Primary (no evidence of pre-existing conditions) vs secondary (result of other inflammatory process in the eye)
Primary Open Angle Glaucoma
Chronic
Clogged trabecular network at the point where the iris and cornea meets causes impaired aqueous human drainage, leading to increased intraocular pressure (IOP).
IOP causes blind spots in the field of vision, initially limited to the periphery but then progresses centrally
Gradual, irreversible vision loss
Acute Angle Closure Glaucoma
Acute
Rapid IOP from blocked aqueous humor drainage, induced by increased pupil dilation.
The eye pain can lead to headache, nausea, blurred vision, and rainbows around lights at night.
The damage to the optic nerve leads to vision loss.
Medications can help alleviate the pressure, but surgery is needed to unclog routes
Cataracts
Progressive opacity or clouding of the lens leading to blurry vision
Rate of impairment varies per individual; one eye can develop faster than the other
Changes can be r/t age, metabolic abnormalities (smoking, DM), excessive exposure to sunlight, congenital, or traumatic.
Makes night driving difficult
Outpatient surgery involves lens replacement where they implant intraocular lenses.
Macular Degeneration
Loss of central vision due to degeneration of the retinal macular (and fovea)
Fovea
Central portion of the retinal macula where all vision signals come to and sent from
Dry (atrophic) Macular Degeneration
Atrophy and degeneration of the outer retina
Drusen deposition: fatty lipid deposits (drusen) develop in the macula, affecting blood flow, leading to damage to the fovea and thus scar tissue formation in the fovea. Damaged fovea leads to damage to central retinal macula
Slow progression of symptoms
No cure- need regular screening and monitoring
Wet (exudative) Macular Degeneration
Mini ‘hemorrhaging’ in the back of the eye leads to rapid and severe vision loss and eventually blindness
Formation of a choroidal neovascular membrane, which are weaker than normal vessels, thus are prone to leakage. Leakage and hemorrhage of serous fluid causes damage to the retinal macula and separates the optic disk from back of the eye.
Starts with a dark central spot with vision loss in the central field first. As damage increases, vision loss spreads center outward.
Decreases ability to read, recognize faces, colors, etc.
Not reversible or treatable.
Retinal Detachment
Emergency eye condition that typically results from trauma
There is no pain, but bright flashes of light in the peripheral vision, blurred vision, floaters, and shadow blindness in part of the visual field occur.
Acute/Closed Angle Glaucoma
Emergency eye condition that bring on sudden onset of severe pain (due to IOP), blurred vision with halos around lights, loss of vision
Herpes Zoster Keratitis
Emergency eye conditions that is like shingles but in the eye
Painful, red eye, tearing, blurred vision, photophobia
Occlusion to the artery that provides eye with blood causes the eye to become ischemic and thus stops working, causing sudden vision loss.
Important to get history to see if its related to herpes zoster
Central Retinal Artery Occlusion
Sudden vision loss, painless
