exam 1 - chapter 11 - pain and sensory regulation + eyes and ears

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Last updated 10:00 PM on 9/11/26
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84 Terms

1
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what is the definition of pain?

an uncomfortable phenomenon where stimuli send signals from inside or outside the body along neural pathways from the PNS to the CNS

2
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what is nociception?

the processes of receiving messages from noxious stimuli

3
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what are the four processes of pain perception?

transduction, transmission, perception, and modulation

4
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what are the most notable sites of pain perception?

thalamus and cortex

5
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what is transduction?

stimuli damages the tissue which activates nerve endings, facilitated by nociceptors

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what is neurogenic inflammation?

mast cells degenerate, releasing inflammatory chemical mediators, increasing the induction of the action potential from nociceptors inducing chemical changes

7
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the ______ the AP, the ______ the pain

greater

8
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what is transmission?

relaying the message from the stimuli to the brain

9
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what are the fibers in transmission and what are they responsible for?

  • myelinated A-delta fibers are fast causing sharp sensation at time of injury

  • unmyelinated C fibers are slow causing dull, burning, or aching pain


10
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what is first order transmission?

transduction nociceptors → dorsal horn of the spine

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what is second order transmission?

spinal cord → brain stem; axons of some second-order cells cross over to the opposite side of the spinal cord and project for long distances into the brainstem

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what is third order transmission?

brainstem → thalamus, somatosensory cortex, and limbic system

13
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what is perception?

complex integration of several processes resulting in interpretation of pain; takes place in the cortex, limbic system, and reticular system

14
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what happens when blood is seen during perception?

pain might be interpreted as worse

15
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what is modulation?

modification of neurotransmission activity to decrease the intensity; endogenous opioids released to inhibit pain sensation, gate control theory

16
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how is the electrical signal for pain created?

transfer of sodium and potassium ions between extracellular and intracellular fluid

17
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what is gate theory?

“gates” are built into the normal pain pathway that can modify the pain impulse’s movement to the brain

18
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what is the neuromatrix theory?

our perception of pain is the result of a broad network of impulses that trigger somatic, limbic, thalamic, and cortical areas of the brain, and with stimulation, pain perception utilizes cognitive, affective, and sensory components influenced by a persons genetics and past; helps explain phantom limb pain and pain tolerance

19
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what is referred pain?

sensation of pain that is not where the noxious stimuli is located

20
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where are half of our sensory receptors?

in the eyes, responsible for visual input based on detecting visible light

21
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where is visual input processed?

cerebral cortex

22
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what are the parts and functions of the eye?

  • palpebrae: protection, lubrication

  • lacrimal caruncle: small, pink, ball shaped structure in inner corner; contains oil and sweat glands

  • conjunctiva: thin, protective mucous membrane that covers the sclera

  • lacrimal apparatus: produces and drains tears

  • lacrimal glands: secrete tears to the excretory ducts

  • lacrimal punctum: two small openings in which tears enter to drain into the lacrimal canals

  • lacrimal canals: lead fluid to lacrimal sac and then to the nasolacrimal duct


23
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what muscles coordinate eye movements?

superior rectus, superior oblique, medial rectus, lateral rectus, inferior rectus, and inferior oblique

24
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what are the three layers (tunics) of the eye?

fibrous tunic (sclera and cornea), vascular tunic (choroid, ciliary body, and iris), and inner retina

25
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what is the macula?

responsible for central vision, color vision, and fine detail; contains fovea centralis

26
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what is the pain pathway?

nociceptors stimulated → afferent fibers (a delta, C) → synapse → cross over spinal cord → ascending tract to brain → RAS → somatic sensory areas

27
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what is the OPQRSTU pain assessment?

onset, provocation/palliation, quality, region/radiation, severity, timing, and understanding

28
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what is stevens-johnson syndrome & toxic epidermal necrolysis? how do you treat it?

a violent immune response that is a severe adverse reaction to a drug that causes acute destruction of epithelium of skin and mucous membranes; identify and stop offending drug

29
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what is myopia?

inability to see far away objects clearly; nearsightedness

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what is hyperopia?

inability to see nearby objects clearly; farsightedness

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what is presbyopia?

gradual decrease in the ability to see nearby; affected by age

32
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what is conjunctivitis?

inflammation of the conjunctiva

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what is conjunctivitis pathophysiology?

exposure to virus, bacteria, fungi, allergen, or other irritant causes inflammation → blood vessel dilation and migration of immune cells to combat infection or remove irritants

34
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what are conjunctivitis clinical manifestations?

bacterial → purulent discharge

viral → watery discharge/cold-like symptoms

allergic → itching, tearing, clear discharge

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conjunctivitis management

if mild, no treatment or topical antibiotic eye drops; may need systemic antibiotics if caused by STD

36
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conjunctivitis nursing considerations

transmitted via direct contact, so wash hands and don’t share towels

37
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cataracts definition

lens becomes cloudy and interferes with light transmission

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cataracts epidemiology

affects more than 24.4 million americans over 40

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cataracts pathophysiology

proteins in the lens break down and clump together, which blocks or scatters light passing through the lens, causing blurry vision

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cataracts etiology

aging, genetics, nutrition, smoking, diabetes, medications, UV radiation

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cataracts clinical manifestations

halos around lights, reading difficulty, and progressive blurred vision that darkens over time

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cataracts management

surgical replacement of lens

43
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diabetic retinopathy definition

damage to the retina due to hyperglycemia

44
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diabetic retinopathy epidemiology

global prevalence predicted to be 700 million by 2045

45
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diabetic retinopathy pathophysiology

hyperglycemia → chronic activation of inflammatory pathways → release of cytokines, fluid, and blood into retinal tissue → ischemia/hypoxia of the retina

46
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diabetic retinopathy clinical manifestations

initially asymptomatic → floaters, distortions, blurred vision

ophthalmic exam: microaneurysms

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diabetic retinopathy management

control blood glucose, BP, and lipid levels; regular eye exams; laser therapy, surgery; injection of steroids into the eye or use of immunosuppressants

48
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age-related macular degeneration definition

progressive eye condition usually affecting older adults

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age-related macular degeneration epidemiology

200 million people globally, leading cause of vision loss globally

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age-related macular degeneration risk factors

age, smoking, high BMI, high HDL levels, history of cataract surgery, vascular disease, exposure to blue light

51
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age-related macular degeneration pathophysiology

nonneovascular AMD: “early stage”, deposits build up under retina and retinal cells gradually thin nd atrophy

neovascular AMD: less common, abnormal “leaky” blood vessels damage retinal tissue

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age-related macular degeneration clinical manifestations

nonneovascular: asymptomatic, loss in visual acuity and function, decreased reading speed

neovascular: abrupt vision loss, can be severe and irreversible

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age-related macular degeneration management

annual visual exams, avoid smoking/sun/blue light exposure, prevent CV disease

for neovascular AMD, intravitreal injections of anti-VGEF meds to lower risk, as well as corticosteroids and NSAIDs to reduce angiogenesis and inflammation

54
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glaucoma types

primary open-angle glaucoma**, secondary open-angle glaucoma, and primary angle-closure glaucoma

55
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primary open-angle glaucoma (POAG) definition

90% of cases, exact cause unknown

56
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POAG risk factors

increased IOP, family history, female sex, race, age over 40, myopia

57
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glaucoma epidemiology

2nd leading cause of blindness globally

58
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glaucoma pathophysiology

  • complex with various factors leading to optic nerve damage

  • vascular dysfunction → ischemia to the optic nerve

  • compression of the axons → dysfunction of the optic nerve


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glaucoma clinical manifestations

asymptomatic in early stages; eventually develop patchy loss of peripheral vision then loss of central vision later

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glaucoma management

  • prevention: avoid eye injury, manage chronic conditions, healthy lifestyle

  • early detection: regular eye exams

  • treatment: lower IOP through meds (latanoprost, timolol maleate), laser therapy, and surgery


61
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what is conduction hearing loss?

sound cannot get in to make the vibrations to transmit sound waves to cochlear nerve

62
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how do you treat conduction hearing loss?

remove/fix obstruction

63
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what is sensorineural hearing loss?

a disconnect within the inner ear prohibits sounds from being transmitted to the brain

64
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what are ototoxic drugs?

drugs that can cause temporary or permanent hearing loss; antibiotics, analgesics, diuretics

65
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what is tinnitus?

ringing in the ears; early sign of toxicity

66
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what are some interventions for all kinds of hearing loss?

hearing aids, lip reading, ASL, cochlear implants, therapy with SLP

67
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definition of otitis externa

inflammatory condition of external ear canal

68
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otitis externa pathophysiology

usually bacterial, can be fungal infection → inflammatory response

69
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otitis externa clinical manifestations

erythema and edema of ear canal, ear pain, purulent discharge, increased pain with movement of pinna

70
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otitis externa management

acetaminophen or NSAIDs, topical antibiotic

71
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otitis media definition

inflammation of middle ear (behind tympanic membrane)

72
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otitis media epidemiology

most common childhood PCP visit

73
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otitis media pathophysiology

dysfunction of the eustachian tube → edema, accumulation of pathogens from nasopharynx

74
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otitis media clinical manifestations

otalgia, fever, irritability, anorexia, rubbing of the ears, crying, otorrhea

75
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otitis media treatment

antibiotics are questioned because resistance may occur, so insertion of drainage tubes through TM are used to facilitate drainage

76
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when do you use antibiotics for otitis media?

bilateral, unilateral with severe symptoms, or take oral amoxicillin

77
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otosclerosis definition

excess bone in middle ear → stapes becomes fixed and blocks sound conduction to the cochlea; genetic, primarily in young females

78
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otosclerosis clinical manifestation

hearing loss

79
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otosclerosis treatment

hearing aids, surgical removal of the stapes with prosthetic replacement

80
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ménière disease definition

cyclical attacks with period of relief in between, exact cause is unknown

81
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ménière disease pathophysiology

excessive endolymph stretches membrane and interferes with hair cells in cochlea and vestibule; perilymph and endolymph may mix

82
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ménière disease clinical manifestations

vertigo, fluctuating hearing loss, tinnitus, ear fullness

83
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ménière disease management

prevention: avoid triggers (chocolate, caffeine, smoking); manage symptoms (N/V, inflammation); take vestibuulosuppresants

84
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how to install ear drops

  • patient upright, tilt head toward unaffected side

  • pull down and back for kids, up and out for adults

  • drops should be aimed at the side of the ear: avoid dropping directly on TM

  • avoid instilling medications that are cold