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Pathopharm I > Visual/Sensory Issues > Flashcards

Visual/Sensory Issues Flashcards

1
Q

Hordeolum (sty)

A

Infection of the oil-producing gland in the lid margin

Usually caused by bacteria Staph aureus

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2
Q

Hordeolum (sty) sympotms

A

Area of the eye is red, swollen, tender

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3
Q

Hordeolum (sty) treatment

A

Usually self-limiting; warm compresses 3-4 times a day; teach: do not squeeze or pop the sty bc that can spread the infection

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4
Q

Conjunctivitis (pink eye)

A

Infection or inflammation of the conjunctiva

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5
Q

Conjunctivitis etiology

A

Bacterial, viral, chlamydia, irritants (allergies)

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6
Q

Bacterial conjunctivitis treatment

A

Usually self-limiting; antibiotic drops can shorten the course

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7
Q

Viral conjunctivitis treatment

A

Topical steroids provide temporary relief for itching; antivirals are ineffective

BUT viral keratitis (herpes) treat with antiviral eye drops

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8
Q

Chlamydia conjunctivitis treatment

A

PO antibiotics; however, some infections are resistant

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9
Q

Allergic conjunctivitis treatment

A

Artificial tears, topical antihistamines, steroids

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10
Q

Keratitis

A

Inflammation/infection of the cornea — the clear, dome-shaped tissue on the front of your eye that covers the pupil and iris; may also involve the conjunctiva

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11
Q

Keratitis-bacteria

A

Contact lens wearers higher risk

Treat with antibiotics (topical, injection, IV)

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12
Q

Keratitis-amoeba

A

Caused by the contaminated contact lens

Treat with antifungal drops (often resistant)

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13
Q

Keratitis-viral

A

Caused by herpes virus

Treat with antiviral eye drops

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14
Q

Keratitis complication

A

Corneal ulcer

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15
Q

Corneal ulcer

A

Extremely painful
Constant feeling of something in your eye
Photophobia, discharge, redness
If untreated can lead to blindness

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16
Q

Keratoconjunctivitis sicca

A

Dry eye disorder

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17
Q

Dry eye disorder etiology

A

Aging, Sjogren’s syndrome (SLE), other systemic diseases

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18
Q

Sjogren’s syndrome (SLE)

A

Body’s immune system attacks its own healthy cells that produce saliva and tears

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19
Q

Dry eye disorder complaint

A

“Sand in my eye”

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20
Q

Dry eye disorder treatment

A

May need artificial tears

Cyclosporine eye drops can also be helpful

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21
Q

Cataracts

A

Cloudy lens
Gradual onset of PAINLESS blurry vision
If left untreated, may result in blindness

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22
Q

Cataracts treatment

A

Laser surgery

No medications

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23
Q

Cataract risk factors

A 
Older age
Eye trauma
Congenital risk 
Diabetes
Corticosteroid use
Smoking/ ETOH consumption
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24
Q

Cataract symptoms

A 
PAINLESS
Uni- OR bilateral vision changes
Blurry vision
Halo around lights
Altered color perceptions
Glare issues at night
Decreased accommodation
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25
Q

Cataract mechanism

A

Blocks some light from passing through the lens and scatters the light, preventing crisp focus on the retina

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26
Q

Nonproliferative DR

A

Capillary microaneurysms, retinal swelling, hard exudate
Macular edema: plasma leaks from macular blood vessels (common complication of DR)
Capillaries rupture, leading to “dot or blot” hemorrhaging

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27
Q

Proliferative DR

A

Advanced DR

All symptoms of NPDR + new blood vessels are fragile and leaky

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28
Q

Proliferative DR characteristics

A

Growth of abnormal blood vessels

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29
Q

Nonproliferative DR characteristics

A

Aneurysm, hard exudate, hemorrhage

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30
Q

NPDR-don’t memorize/for context

A

Hyperglycemia results in damage to retinal capillaries. This weakens the capillary walls and results in small outpouchings of the vessel lumens, known as microaneurysms. Microaneurysms eventually rupture to form hemorrhages deep within the retina, confined by the internal limiting membrane (ILM). Because of their dot-like appearance, they are called “dot-and-blot” hemorrhages. The weakened vessels also become leaky, causing fluid to seep into the retina. Fluid deposition under the macula, or macular edema, interferes with the macula’s normal function and is a common cause of vision loss in those with DR.

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31
Q

PDR-don’t memorize/for context

A

As mentioned earlier, the retina has a high metabolic requirement, so with continued ischemia, retinal cells respond by releasing angiogenic signals such as vascular endothelial growth factor (VEGF). Angiogenic factors, like VEGF, stimulate growth of new retinal blood vessels to bypass the damaged vessels. This is referred to as neovascularization. In PDR, the fibrovascular proliferation extends beyond the ILM. This may sound like a good idea, but the new vessels are leaky, fragile, and often misdirected. They may even grow off the retina and into the vitreous.

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32
Q

Hypertensive retinopathy etiology

A

Untreated high blood pressure creates BLOCKAGES in retinal blood vessels

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33
Q

Hypertensive retinopathy symptoms

A

Initially: no vision changes
Sustained: severe HTN can cause sudden visual loss related to swelling of the optic disc/ nerve
Normal vision is restored with the treatment of the HTN

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34
Q

Detached retina

A

Retina has a tear or leak –> vitreous humor flows behind the retina –> rapid, progressive detachment from the choroid

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35
Q

Detached retina

A

Usually spontaneous

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36
Q

Detached retina risks

A

Myopia (nearsightedness; close clear/far blurry)
Age >40
Traumas to the head
Eye tumors
Complication or history of cataract surgery

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37
Q

Detached retina symptoms

A 
SUDDEN, unilateral vision loss
Painless
Floaters
Flashes of light
“Scene coming in”
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38
Q

Macular degeneration

A

Most common cause of irreversible vision loss in people > 60 in the US

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39
Q

Macular degeneration etiology

A

Retinal aging

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40
Q

Macula

A

Area near the center of the retina where cones are; cones: color vision, visual acuity

41
Q

Dry macular degeneration

A 
Yellow deposits (drusen) in the retinal pigment epithelium
Most common (90% of cases)

DRy DRusen

42
Q

Dry macular degeneration

A

Non-exudative

43
Q

Wet macular degeneration

A

Growth of new, leaky blood vessels in an abnormal location of the retina
New hemorrhages
Less common (10%)

44
Q

Wet macular degeneration

A

Exudative

45
Q

Macular degeneration risk factors

A

Family history, genetics, UV light, hyperopia (farsightedness), smoking, light-colored eyes

46
Q

Macular degeneration prevention

A

Dark green, leafy vegetables have protective properties

47
Q

Macular degeneration symptoms

A 
Asymptomatic in early stages
Blurred, darkened vision
Blind spots (scotomas) 
Distorted vision (metamorphopsia)
Vision does not improve
48
Q

Macular degeneration treatment

A

Treatment is limited

One option: medications injected into the eye

49
Q

Glaucoma

A

Elevated intraocular pressure (IOP) with vision changes OR optic nerve damage

50
Q

Glaucoma

A

Chronic condition

51
Q

Glaucoma

A

Usually involves bilateral eyes

52
Q

Open-angle glaucoma patho

A

Outflow obstruction of aqueous humor at the trabecular meshwork or canal of Schlemm even with adequate space for drainage
Reduced drainage of aqueous humor into canal of Schlemm
Imbalance between inflow and outflow
Results in increased IOP –> damage to optic nerve –> vision problems

53
Q

Open-angle glaucoma patho

A

Blockage of the trabecular meshwork slows drainage of the aqueous humor, which increases IOP

54
Q

Open-angle glaucoma risk factors

A 
Elevated IOP
Older age
Race: African-Americans 3-4x higher risk 
Family history 
Myopia
Diabetes 
HTN 
Migraines
55
Q

Open-angle glaucoma symptoms

A 
Initially asymptomatic
Progressive loss of sight
Vague eye pain
Halos around lights
Tunnel vision
56
Q

Closed-angle glaucoma patho

A

Displacement of the iris toward the cornea with obstruction of the trabecular meshwork and obstruction of outflow of aqueous humor from the anterior chamber

57
Q

Closed-angle glaucoma patho

A

Abnormal angle between the iris and later cornea

Outflow is blocked when the pupil is DILATED

58
Q

Closed-angle glaucoma AKA

A

Acute angle-closure glaucoma (AACG)

Narrow-angle glaucoma

59
Q

Closed-angle vs. open-angle glaucoma

A

Closed-angle is much less common

60
Q

Closed-angle glaucoma risk factors

A 
Asian American ethnicity 
Females 
Hyperopia 
Family history 
Older age
61
Q

Acute angle-closure glaucoma

A

Medical emergency; outcome based on onset time to treatment

62
Q

Acute angle-closure glaucoma

A

Triggered by anticholinergic drugs

63
Q

Anticholinergics

A

Drugs that block the action of acetylcholine

Acetylcholine stimulates the PNS (rest/digest)

64
Q

Acute closed-angle glaucoma: clinical manifestations

A 
Typically UNILATERAL (but other eye is at risk)
SEVERE eye pain 
Nausea and vomiting 
Blurry vision
Halos
Reddened eyes
Dilated pupil– non-reactive to light
Cloudy cornea
65
Q

Glaucoma and blindness

A

Open-angle glaucoma long-term leads to blindness

Untreated acute angle-closure can lead to blindness

66
Q

Glaucoma and blindness

A

Due to the increased IOP –> more pressure on inner eye structures –> decreased blood flow to optic nerve –> nerve fiber death –> blindness

67
Q

Open-angle glaucoma pharm

A

Drugs that DECREASE aqueous humor production AND/OR INCREASE aqueous humor drainage

68
Q

Acute angle-closure glaucoma pharm

A

Surgery

69
Q

timolol (non-selective beta blocker)

A

DECREASES aqueuous humor production

70
Q

betaxolol (selective beta blocker)

A

DECREASES aqueuous humor production

71
Q

brimonidine (alpha-2 adrenergic agonist)

A

DECREASES aqueous humor production

MAYBE INCREASES aqueous humor drainage

72
Q

latanoprost (prostaglandin analogs)

A

INCREASES aqueous humor drainage

73
Q

Aqueous humor

A

Clear fluid filling the space in the front of the eyeball between the lens and the cornea.

74
Q

Administering optical topical agents

A

Use nasolacrimal pressure with instillation
Helps prevent systemic effects/ensures localization
Hold pressure for 2 minutes

75
Q

timolol

A

non-selective beta blocker

76
Q

betaxolol

A

beta-1 selective blocker

77
Q

timolol, betaxolol MOA (beta-blockers)

A

Block SNS stimulation of beta receptors

DECREASES aqueuous humor production

78
Q

timolol, betaxolol indications

A

Open-angle glaucoma maintenance treatment

If acute-angle closure– need drops ASAP and other interventions

79
Q

timolol, betaxolol (beta-blockers) SE

A

Transient burning & discomfort

If allowed to go systemic- can have systemic effects

80
Q

timolol, betaxolol (beta-blockers) contraindications

A

timolol, bc nonselective, contraindicated for patients with asthma, COPD, bradycardia, etc.

81
Q

timolol, betaxolol (beta-blockers) patient teaching

A

Must take– otherwise will progress to blindness

Apply nasolacrimal pressure with instillation

82
Q

latanoprost (Xalatan) class

A

Prostaglandin analogs

83
Q

latanoprost (Xalatan) MOA

A

INCREASES outflow drainage of aqueous humor

INCREASES aqueous humor drainage

84
Q

latanoprost (Xalatan) indications

A

Open-angle glaucoma

Ocular hypertension

85
Q

latanoprost (Xalatan) SE

A

Well-tolerated

86
Q

brimonidine (Alphagan) class

A

Alpha-adrenergic agonist

87
Q

brimonidine (Alphagan) MOA

A

DECREASES aqueous humor production

MAYBE INCREASES aqueous humor drainage/outflow

88
Q

brimonidine (Alphagan) indication

A

Open-angle glaucoma

Increased intraocular pressure

89
Q

brimonidine (Alphagan) SE

A 
Burning/stinging
Dry mouth 
Fatigue
H/A
Blurred vision
Hypotension
90
Q

dorzolamide (Trusopt) class

A

Carbonic anhydrase inhibitor

91
Q

dorzolamide + timolol

A

Cosopt

92
Q

dorzolamide (Trusopt) indication

A

Second-line treatment
Open-angle glaucoma
Increased IOP

93
Q

dorzolamide (Trusopt) MOA

A

DECREASES production of aqueous humor

94
Q

dorzolamide (Trusopt) SE

A

Stinging
Bitter taste
Allergic reactions (conjunctiva or lid reactions)

95
Q

Meniere’s Disease

A

Endolymphatic hydrops
Episodic disorder of the middle ear
Can occur at any age; more common between 20-40
Can be unilateral or bilateral
Endolymph: fluid that fills the hearing/balance structures of inner ear
Fluctuation in endolymph –> distension –> disruption of hearing and balance
Excessive endolymph and pressures in the membranes disrupt vestibular (balance) and hearing function

96
Q

Meniere’s Disease symptoms

A

Recurring episodes of vertigo [usually with nausea & vomiting], hearing loss, ringing in the ears (tinnitus), and feeling of fullness

97
Q

Meniere’s Disease treatment

A

Symptomatic treatment

Some pharm treatment but none widely available; no meds affecting the endolymph-just helps the vertigo

98
Q

Meniere’s Disease diet changes

A

Disease can be triggered by high salt, caffeine, alcohol, MSG, stress, allergies
Most patients require sodium restriction

Pathopharm I (10 decks)

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