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Pathophysiology > Vision and Hearing Disorders > Flashcards

Vision and Hearing Disorders Flashcards

1
Q

Describe the characteristics of conjunctivitis?

A
  • Known as pink eye
  • transmitted through contaminated fingers
  • redness and irritation of eye
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2
Q

Compare and contrast viral and bacterial conjunctivitis.

A
  • Viral: less exudate, lasts day or weeks

- Bacterial: less common, caused by staph or strep or the flu; inflamed and produces yellow drainage

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3
Q

What other things can cause conjunctivitis?

A

chemicals or allergic reactions

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4
Q

How is conjunctivitis transmitted from person to person?

A

contaminated finger, swimming pools, and personal items

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5
Q

How long does viral and bacterial conjunctivitis last?

A

Viral: several days to two weeks
Bacterial: 10-14 days without antibiotics; 1-3 days with antibiotics

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6
Q

What is ophthalmia neonatorum (ON)?

A
  • baby’s eyes become contaminated with Neisseria or chlamydia while exiting vagina.
  • Erythromycin ointment put on eyes to prevent this
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7
Q

Layers of retina

A
  1. Neural

2. Pigmented: absorb scattered light which helps with clear images and prevents buildup of light

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8
Q

Name the 3 layers of neurons that make up the neural layer of the retina

A

-ganglion cell, bipolar neurons and the photoreceptors

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9
Q

How light passes through the eye

A

light-> retina-> blood vessels-> ganglia cells-> bipolar cells-> photoreceptors-> pigmented cells

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10
Q

What is a fundoscopic examination?

A

optic disc is located closer to the nose compared to the macula so you can tell which is the right and left eye

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11
Q

What are the two sources for the blood supply that feed the retina?

A

choreocapillaries and the central retinal artery

-fovea only receives blood from choreocapillaries

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12
Q

Do most diseases of the retina cause pain? Why is this significant?

A

Most retinopathy conditions don’t cause pain. Most people don’t go to the hospital until vision problems are so bad.

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13
Q

What are pericytes and what is their function on the retinal vasculature?

A

contractile cells just outside the endothelium that give the capillaries extra structure

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14
Q

Describe microaneurysms, neovascularization, and opacities

A
  • microaneurysms: caused by weakness in the walls of the vessels because of pericyte loss
  • neovascularization: occurs when the retina cells are not getting enough oxygen
  • opacities: dark or cloudy areas on the retina that can be caused by bleeding, tissue proliferation, exudates, edema and something called “cotton wool spots”
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15
Q

Describe non-proliferative (background) and the proliferative type of diabetic retinopathy

A
  • Nonproliferative: blood sugars are high which leads to a dysregulation of ocular blood flow
  • Proliferative: follows the non-proliferative stage and is characterized by an expansion of newly formed blood vessels that are fragile and leak easily
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16
Q

Explain the three types of retinal detachment and describe what type is common in diabetic retinopathy

A
  1. Exudative: accumulation of fluid occurs under the neurosensory retina
  2. Traction: mechanical forces on the retina
  3. Rhegmatogenous: tear in the retina (rhegma means tear)-> vitrous seeps underneath
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17
Q

Explain how high blood sugar contributes to diabetic retinopathy that progresses from nonproliferative to proliferative

A

Glucose will get into the basement membranes making them super thick. This thickness will disrupt the intimate association of pericytes. Pericytes will die.

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18
Q

Treatments for retinopathy

A

laser photocoagulation, intravitreal injections of anti VEGF agents and vitrectomy to remove vitreous hemorrhage and vitreoretinal membranes

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19
Q

How often should diabetics have eye examinations? What is the best approach to prevent the progression of diabetic retinopathy and to preserve vision?

A
  • Annually

- control blood glucose levels, hypertension, and hyperlipidemia

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20
Q

Recall what area of vision (central or peripheral) is affected by AMD

A

central

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21
Q

Risk factors for AMD

A

advancing age, family history of the disease, history of smoking, being a woman, being Caucasian, obesity, and hypertension

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22
Q

What form forms first in macular degeneration

A

dry forms first with no symptoms early on.

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23
Q

Explain what Drusen is, how it is formed and where it is found.

A

yellowish in color and builds up between Bruch’s membrane (the innermost layer of the choroid) and the pigmented epithelium.

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24
Q

Explain what wet AMD is and why it is more serious

A

new vessels are leaky, and these leaky vessels greatly contribute to the macular edema in wet AMD

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25
Q

Describe the visual changes with AMD and what an Amsler grid is

A
  • blurred vision or scotomata

- Amsler grid: straight line grid but if it appears wavy, might have AMD

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26
Q

Tx for wet AMD

A

laser photocoagulation, photodynamic laser therapy, and intravitreal injection of VEGF inhibitors.

27
Q

What can be done to help reduce a person’s risk for developing AMD?

A
  • high doses of antioxidants such as vitamins E and C and zinc and beta-carotene
  • spinach and kale
28
Q

Recall where aqueous humor is made and how it is circulated and drained

A
  1. Ciliary body (where aqueous humor is made)
  2. Posterior chamber
  3. Iris
  4. Anterior chamber
  5. Trabecular network
  6. Canal of Schlemm
  7. Venous blood
29
Q

Explain open angle and angle closure glaucoma.

A
  • open angle: more common and caused by abnormalities in the trabecular meshwork that drains AH
  • angle closure: caused by an obstruction of outflow of AH from the anterior chamber due to a narrow angle (more onset)(high IOP)
30
Q

Describe the optic disc: optic cup ratio and how this suggests the possibility of increased IOP

A

-compares the diameter of the cup
portion with the diameter of the entire disc
-normal level is 1/3=.3
-glaucoma is 2/3=.6

31
Q

Explain the mechanism of action for each of the treatment options listed for glaucoma

A
  • beta 1 blockers: on ciliary body and increase aqueous humor
  • cholinergic agonists: constrict pupil
  • prostaglandin analogs: cause remodeling and widens space for aqueous humor to flow
  • alpha agonists: inhibit aqueous humor production and constrict blood vessels to reduce AH productions
  • Carbonic anhydrase inhibitors: reduces Cl- and associated water in the aqueous humor
32
Q

clinical manifestations of an acute attack due to angle-closure glaucoma?

A

episodes of unilateral eye pain and headache, conjunctival redness, and blurred vision with halos around lights

33
Q

Laser peripheral iridotomy

A

laser blasting away some of the trabecular network in order to widen the angle and relieve pressure

34
Q

Explain how the ANS and lens and suspensory ligaments work to enable us to see far and near

A
  • Tension on the suspensory ligaments by relaxed ciliary bodies put force on the lens to make more flat for distant vision
  • Contracted ciliary bodies making suspensory ligaments slackened making the lens see more near sighted things
  • ANS: sympathetic is more active for distance and parasympathetic is more active for near sighted vision
35
Q

Understand the terms Myopia, Hyperopia and Presbyopia

A
  • Myopia: “near sighted”, far is blurry
  • Hyperopia: “far sighted”, close is blurry
  • Presbyopia: loss of elasticity in the lens, hard to see things up close
36
Q

Which lens is used to treat myopia and hyperopia?

A
  • Myopia: concave, diverging lens (minus)

- Hyperopia: convex, converging lens (plus)

37
Q

Explain what an astigmatism is

A
  • blurry vision because of irregular shaped cornea or even lens
  • bend light differently
  • hard to correct vision
38
Q

Explain what a cataract is

A

clouding of lens

39
Q

What causes cataracts?

A
  • due to aging as the lens protein fibers become damaged over time
  • trauma, radiation, genetics, smoking, low vitamin C, diabetes
40
Q

How are cataracts treated?

A

Surgery, artificial lens replaces old one

41
Q

Pathway traveled for visual information

A

Beginning with visual fields

  1. Optic nerve
  2. Optic chiasm
  3. Optic tract
  4. Lateral geniculate nucleus (LGN)
  5. Optic radiations
  6. Visual cortex
42
Q

Information from what portion of the visual field crosses over at the optic chiasm?

A
  • right optic nerve leads to right eye blindness
  • a lesion in the optic chiasm leads to bitemporal hemianopia
  • a lesion in the left optic tract leads to bilateral right hemianopia
43
Q

Explain how damage to the optic nerve causes anopsia

A

caused by infections, immune conditions that attack nerve tissue (like multiple sclerosis), trauma, glaucoma, and any diseases that affect the brain and central nervous system

44
Q

Explain what tunnel vision is

and how it occurs and the other names for this condition

A
  • vision is missing from the inner half of both right and left visual fields
  • caused by: tumor that presses on the optic chiasma
45
Q

Explain what homonymous

hemianopsia is and how it occurs

A
  • a person can only see one side (right or left) of the visual field in each eye
  • most common cause: stroke
46
Q

What are the parts that make up the external, middle, and internal subdivisions of the ear?

A
  • external ear: auricle, ear lobe, external acoustic meatus
  • middle ear: tympanic membrane, ossicles
  • inner ear: semicircular canals, cranial nerve VIII, cochlea, and Eustachian tube
47
Q

What can cause otitis externa

A

infectious agents like Pseudomonas, E. coli and S. aureus

48
Q

What are risk factors for development of otitis externa?

A

prolonged exposure to moisture

49
Q

What are some manifestations of otitis externa?

A

inflammation and pruritus (itching) with tenderness and pain with earlobe retraction

50
Q

What are common treatments for otitis externa?

A

eardrops that contain acidifying agents (acetic acid 5%), antimicrobials, and local anesthetics (benzocaine)

51
Q

Give a description for acute otitis media. Describe the similarities and differences for AOM and OME

A
  • Acute otitis media(AOM): rapid onset of signs and symptoms of a middle ear infection
  • Otitis media with effusion(OME): inflammation of the middle ear and the presence of fluid but no signs or symptoms of an acute infection
52
Q

In what age group does OM most commonly occur. List some risk factors for the development of OM

A
  • Young children

- allergies or colds that can affect upper respiratory tract and increase congestion

53
Q

What are some nonspecific signs and symptoms often observed in younger children with AOM

A
  • otalgia (ear pain), fever and hearing loss

- create exudate behind the tympanic membrane, so it cannot vibrate well

54
Q

What are tympanostomy tubes and what is their purpose?

A
  • ventilation tubes or pressure equalization tubes

- put holes in tympanic membrane and placing small plastic tubes to allow for drainage of the fluid

55
Q

Why might chronic otitis media cause speech and language delays?

A

conductive hearing loss, choleastomas, chronic mastoiditis and rare intracranial complications

56
Q

Why might a tonsil and adenoidectomy help relieve otitis media?

A

Because tonsillitis can block eustachian tube

57
Q

What is a cholesteatoma?

A

sloughed off epithelial cells that accumulate around the ear bones so they are unable to vibrate. leads to hearing loss

58
Q

Symptoms for OME

A

hinting that brain structures are involved include persistent headaches, stiff neck, tinnitus, or cranial nerve disturbances (e.g., visual disturbances, facial paralysis)

59
Q

What is Otosclerosis?

A

formation of new spongy bone around the stapes and oval window and results in progressive deafness due to immobilization of the middle ear bones

60
Q

What is objective and subjective tinnitus? What are some causes for these two types of tinnitus?

A
  • Objective: potentially detectable by another observer like turbulent blood flow due to vascular disorders
  • Subjective: mechanism like cerumen, medications, noise induced hearing loss, HTN, atherosclerosis or a head injury
61
Q

Describe the difference between conductive and sensorineural hearing loss

A
  • Conductive: stimuli not conducted to the inner ear

- Sensorineural: stimuli failure to stimulate the inner ear or pathways that go to the brain

62
Q

Describe how an infant might be tested for hearing using OAE and ABR.

A
  • otoacoustic emission (OAE): sound that is generated by the cochlea. The outer hairs of the cochlea are tested with sound clicks.
  • auditory brainstem evoked response(ABR): measuring EEG waves generated by the brain after applying a stimulus like tones or clicks to the hearing apparatus. They assess the neurons firing and the speed of transmission.
63
Q

Describe what a cochlear implant is and how it works.

A
  • small electronic device that has an external component and an internal component
  • external: microphone
  • internal: electrical current to the cochlea

Pathophysiology (10 decks)

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