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OPT 533-Ocular Disease > Midterm 2 > Flashcards

Midterm 2 Flashcards

1
Q

Macule

A

Circumscribed, FLAT discoration less then 1 cm.

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2
Q

Patch

A

Circumscribed, Flat discoloration greater then 1 cm

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3
Q

Papule

A

Circumscribed, ELEVATED, superficial solid lesion less then 1 cm

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4
Q

Plaque

A

Circumscribed, ELEVATED superficial solid lesson greater then 1 cm

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5
Q

Nodule

A

Solid lesion with depth above, level or below surface less then 1 cm

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6
Q

Tumor

A

Solid lesion with depth above or below greater then 1 cm

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7
Q

Vesicle

A

Circumscribed elevation containing serous fluid less then 1 cm

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8
Q

Bulla

A

Circumscribed elvation containing serous fluid greater then 1 cm

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9
Q

Petechia

A

Circumscribed deposits of blood or blood products less then 1 cm

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10
Q

Purpura

A

Circumscribed deposits of blood or blood products greater then 1 cm

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11
Q

Sessile

A

A lesion fixed to the skin on a broad base

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12
Q

Pedunculated

A

A lesion on a stalk

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13
Q

Papillomatous

A

A lesion with a surface like a cauliflower or artichoke

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14
Q

Scales

A

Shedding, dead epidermal cells, dry or greasy

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15
Q

Umbilicated

A

The lesion exhibits a center crater like an umbicilicus or belly button

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16
Q

Crusts

A

Dried masses of skin exudates

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17
Q

Ulcer

A

Irregularly sized shaped excavations extending into the dermis

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18
Q

Hyperplasia

A

Increase in the number of cells

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19
Q

Metaplasia

A

Change in type of an adult cell which is abnormal for that tissue

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20
Q

Dysplasia

A

Alternation in size, shape, organization of adult cells

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21
Q

Neoplasia

A

Mass of NEW cells which proliferate without control and serve no useful function

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22
Q

Anaplasia

A

Loses resemblance to cell of origin AKA tumor or cancer

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23
Q

Malignant vs. benign

A

Malignant grows faster, metasstasizes, infiltrates the surrounding tissue, and can recur when excised. Benign tumor usually is separated from the tissue by a capsule.

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24
Q

Carcinoma

A

Epithelial tissue

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25
Q

Sarcoma

A

Tissue of CT which develops into cartilage and bone, fat, and muslce.

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26
Q

Hemangioma

A

Tumor comprised of blood vessels

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27
Q

Lymphoma

A

Tumor of lymphatic tissue

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28
Q

Melanoma

A

Tumor of pigmented cells

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29
Q

Hamartoma

A

Tumor made of tissue normally present there

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30
Q

Blastoma

A

Tumor derived from embryonic cells

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31
Q

Tumor treatment

A

Chemotherapy, cryotherapy, radiotherapy, surgery

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32
Q

Neoplastic consideration (subjective)

A

Lesion does not act like anticipated, history of other neoplasm’s or disease, excessive UV exposure, not common for patient’, older patient, rapid or irregular growth patter, pain.

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33
Q

Rule of thumb with neoplastic considerations.

A

Asymmetry, Borders (irregular), Color(irregular), Diameter (larger then 6 mm), Evolving. Also if there is bleeding, Neovascularization, recurrent infections at site.

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34
Q

Ephilis (ephilides)

A

Freckle. Larger sized melanocyte (normal in #). Autosomal dominant inheritance.

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35
Q

Solar lentigines (AKA liver spots, age spots)

A

Result of long term sun exposure, Persists without sunlight. Middle age to older patients. Expanding macules. Normal number of melanocytes. Can treat with lasers. Will turn gray and slough off.

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36
Q

Simple lentigines

A

Can occur at any age. Not due to sun. Don’t darken with sunlight exposure. Can treat with lasers. Will turn grey and slough off.

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37
Q

Nevus

A

Mole. Common begin neoplasm or melanocyte. Congenital or early onset with occasional change in shape and size. Can be dermal, junctional, or compound.

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38
Q

Dermal Nevus

A

Most common. Located in the dermis. Raised or flat.

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39
Q

Junctional Nevus

A

Dermoepidermal junction, superficial. usually flat. May convert to melanoma.

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40
Q

Compound Nevus

A

Both in dermoepidermal tissue and dermis. Transistional

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41
Q

Dysplastic (odd appearance) Nevus

A

Fried egg appearance. Increased melanoma risk if multiple and with FHx of melanoma. Pigmented or a melanotic. Found at lid margins. Less then 8-10 mm. May increase in size with aging. Occasional shows hairs growing on the surface (know layers below are healthy). Uneven borders.

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42
Q

Nevus Plan

A

photodocument or measure for observation. Monitor q3-6 months if suspicious. Monitor q1 year if normal. Refer for biopsy if changes occur

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43
Q

Malignant Melanoma

A

Tumor of the melanocytes. may not directly relate to sun exposure. Fair skin type. Asymmetrical, pigmented lesion with irregular border. Var in size and color. Can by superficially spreading or nodular.

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44
Q

Superficial Spreading Melanoma

A

Rapid increase in size. Less metastases (moves nor)

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45
Q

Nodular Melanoma

A

Vertical growth into other tissues. Early metastasize.

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46
Q

Clark’s Levels of malignant melanoma

A

Less accurate.
Level 1: epidermis (called in situ melanoma) 100% cure
Level 2: invasion of the papillae upper dermis
Level 3: filling papillary dermis
Level 4: filling reticular dermis (50% dead in 10 years)
Level: invasion of the deep subcutaneous tissue

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47
Q

Breslow Depth of malignant melanoma

A

More accurate
.75mm deep–>0% mest.
.85mm–>97% survival in ten years
3.6mm–>50% survival in ten years

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48
Q

Malignant melanoma Plan

A

Rule out other pigmented lesions. Refer for biopsy

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49
Q

Punch Biopsy

A

Take a little punch out of the skin to see if it is malignant

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50
Q

Mohs Surgery

A

Remove all the suspect tissue. It is a specialized skill.

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51
Q

Basal Cell carcinoma

A

Most common lid malignant tumor. More common with sun exposure, elderly, and fair skinned. Like to form inferior nasal. Early forms look like vascularized nodules. Varying degrees of central umbilicated. “pearly” borders (big clue) pigmentation (skin colored or pigmented), surface can become inflamed, infected, or both. Types: sclerosing and noduloulcerative. Rarely metastasize. Inner can thus require more rapid attention.

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52
Q

Basal cell carcinoma Plan

A

If infected AB, derm consult, surgical excision and repair, radiation, cryotherapy, curettage, electrodessication, imiquimod cream (aldara), 5-Fu (fluorourocil) PDT (photodynamic therapy), pt. edu.

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53
Q

squamous cell carcinoma

A

3rd most common ocular tumor. Keratinizing epidermal cells. 2nd most common skin cancer. A red scab that doesn’t heal. Treat with excision, radiation, and PDT.

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54
Q

Meiobomian Gland Carcinoma

A

Confused with recurrent meiobomian chalazion. Sebacious gland carcinoma. Can mimic chronic eyelid/conj. infection. Treat with radiation and excision.

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55
Q

Actinic Keratosis

A

Precursor to cancer. Squamous cell dysplasia. Caused by UV skin exposure. Dry scaly lesion 2-5 mm, flat.

56
Q

Actinic Keratosis Treatment

A

Refer, cryo, cutterage, topical anti-cancer cream, PDT

57
Q

Keratoacanthoma

A

Precursor to cancer. Papular lesion originating from sebaceous gland. Benign prolif. of squamous epidermal cell. Etiology unknown. Fast growing. Starts as erythmatous papule. Grows into a firm, raised indurated nodule up to 2 cm, keratin filled crater, spontaneously regresses, must R/O SCC. Plan-derm. consult, excision.

58
Q

Lentigo maligna (Hutchinson’s Freckle)

A

Precursor to cancer. A sub type of melanoma in situ. Associated with sun exposure and fair skin. Above age 40. mean at 65. Dark lesions with irregular pigment and margins. 15% malignancy risk. Plan-refer for biopsy or surgical removal.

59
Q

Acrochordon

A

Skin tags. Soft benign usually pedunculated neoplasm found in the obese. In the elastic tissue. Fix with snipping it, zapping it, freezing it, or chromium picolinate 200 mcg bid.

60
Q

Papilloma

A

Benign epithelial tumor (overgrowth of epithelial). Lobulated. Pigmented or non. Can get anywhere. Avascular. Can be sessile or pedunculated.

61
Q

Papilloma treatment

A

Pt. ed, remove (if uncomfortable), RTC 3-6 months if suspicious, RTC 1 year if normal, deem consult

62
Q

Seborrheic Keratosis

A

Barncles of old age. Basal cell hyperplasia. Hyperkeratinized plaque. Most common benign epidermal tissue in elderly. Flat or slightly elevated 1-6mm. Round to oval. Waxy, greasy, scaly.

63
Q

Seborrheic Keratosis Treatment

A

Derm consult, cryo, excision, cuterage. RTC 6-12 months

64
Q

Lichen Planus

A

Common prussic eruptions affecting patient 30-60. Flat toped and 2-4 mm. Cell mediated response of unknown cause. Also commonly affects mouth.

65
Q

Lichen Planus Treatment

A

Biopsy, steroids, vitamin A, Retinoids

66
Q

Verrucae

A

Viral warts. Caused by virus (HPV common). Type of plantar wart. Benign skin tumor. Single or multiple non-secreating warts. Skin colored. Various shapes: plans, vulgarism, digitalis.

67
Q

Verrucae Treatment

A

Resolution, patient education, excision, Keratolytic agents (dicholroacetic acids), laser, cryo, duct tape. Colored or non-colored.

68
Q

Molluscum Contagiosum

A

Benign skin tumor. Caused by virus (pox), STD, or HIV. Contagious. Children pass it between them frequently. Umbilicated nodule with central core. Elevated, round, waxy, pearly. Multiple. Keratitis can occur with it. Non-pigmented. Follicular conjunctivitis can occur.

69
Q

Molluscum contagiosum

A

If quiet leave alone. If central discharge express. Excision, cryo, Topical salicylic acid. Pt. ed.

70
Q

Herpetic eyelid lesions

A

Can be zoster or simplex. Can cause many ocular disease. Will be discussed later

71
Q

Hypothryoid causes

A
  1. Inflammation (Most common is Hashimoto’s disease)

2. Medical treatments

72
Q

Grave’s Disease

A

Characterized by three entities 1. thyrotoxicosis 2. infiltrative dermopathy 3. infiltrative opthalmopathy

73
Q

Thyroid eye disease major risk

A

Smoking. Women. Radioiodine treatment!

74
Q

Opthalmic Grave’s Disease

A

Aka euthyroid condition. When the eye signs of grave’s disease occurs in a patient who is not clinically hyperthyroid.

75
Q

Why does graves have orbital changes?

A

Muscle and fat expansion results in proptosis, restricted eye muscle movement, and in some patients optic neuropathy.

76
Q

Lid signs in Graves

A
  1. Puffy lids (enroth’s sign)
  2. lid retraction (dalrymple’s sign)
  3. Delay of upper lid in following globe movement in downward gaze*(von Graefe’s sign) (MOST IMPORTANT)
  4. Jerky downward movement of eyelid (boston)
  5. Delay of lowering lid in following globe movement in upward gaze (griffith’s sign)
  6. Globe lagging behind upper lid on upward gaze (Kocher’s sign)
77
Q

Treatment for lid signs

A
  1. lube 2. topical alpha adrenergic blockers (relaxes muscles) 3. Topical beta adrenergic blockers (providers rapid releif of thrytoxicosis symptoms) 3. Botox 4. Levatory surgery 5. MMuller’s muscle recession
78
Q

Conj and cornea in Graves

A

Can have injected, chemotic conj. Signs of corneal exposure

79
Q

Conj and cornea in graves treatment

A
  1. lub 2. Elevate head during sleep 3. Tinted cosmetic lenses 4. Steroids* (systemic and periocular) Number one treatment

If exposure ketatopathy present treat with lube, AB, steroids, orbital decompression

80
Q

Globe in Grave’s Disease

A
  1. Exophthalmos (measured with exophthalmos) 2. Ocular Bruit (can hear increased blood flow through arteries)
81
Q

EOM in Graves

A

Fibrosis of IR is most common (diplopia in up gaze) MR is second most. Elevated IOP with up gaze.

82
Q

Treatment for globe in graves

A

May be permanent and have no TX. Lub, lid taping, steroids, tarsorrhaphy.

83
Q

EOM in grave TX

A

lubrication, eye patching or prisms, steroids, botox, surgery.

84
Q

ON in graves

A

Optic disc edema. Painless gradual loss of vision. 70% improve with steroids.

85
Q

On in graves TX

A

Steroids, cytotoxic or immunosupresent, orbital radiation, orbital decompression.

86
Q

NOSPECS

A

Classify severity of grave’s involvement.
class o: No physical signs or symptoms
Class 1: only signs, no symptoms (upper eyelid retraction-Dalrymple sign, stare, and lid lag-Van Graefe sign)
Class 2: Soft tissue involvement (symptoms and signs)–>first sign of infiltrative opthalmopathy.
Class 3: Proptosis
Class 4: EOM invo.
Class 5: Corneal inv.
Class 6: Sight loss. Painless gradual vision loss.

87
Q

Clinical activity score

A

Used to assess disease activity in thyroid eye disease. One point is given for each symptom present. The total is the sum of all of the points. it has a higher predictive value for therapy outcomes.

88
Q

VISA classification

A

Vision loss, Inflamation/congestion and activity in TED Strabisumus/motility, Appearance/expsoure.. Reflects the order in which problems should be treated.

89
Q

Diagnosing thyroid eye disease

A

Blood test (usually abnormal but can be normal)

90
Q

Treatment for thyroid eye disease

A

Correct thyroid disfunction (meds, thyroectomy) ocular lub, systemic steroids for severe corneal damage due to exophthalmos and lid retraction, surgery to narrow palpebral fissure, surgical decompression (hole in one or two of the orbit bones to relieve pressure) Local radiation, Surgical tx of EOM when stable.

91
Q

Demodex infestation/Demodicosis (aka mites)

A

Eyelid (also facial hair and eyebrow) mite infestation. More prevalent with age. Topical agents and compromised immune system make more likely. Patient will experience itching (especially in the morning), burning, crusting, swelling of lid, lash loss. Dr. will see lid margin erythema, conj. infection, bleph, cuffing around lashes, plugged meiobomian. Can form chalazion and hordeolum.

92
Q

Demodex Folliculorum

A

Cigar shaped. Colonial. Upper section of hair follicle. Form collarettes

93
Q

Demodex brevis

A

Shorter, stubbier species. Solitary. like sebaceous gland. Damage/plugging gland causes dry eye and chalazion formation.

94
Q

Demodex Treatment

A

In office do aggressive lid scrub, use lid hygiene (Tea tree oil products may work. Cliradex has only 4-terpineol) Anti-microbial Tx for any super infections. Ung 10-14 days. Mites can live 3-4 weeks so patients must be treated 6-8 weeks. Immunocompromised patients may retain more mites and for a longer time period. It is impossible to remove all of them.

95
Q

Phthirus Pubis

A

Crab louse

96
Q

Pediculus corporis

A

Body louse

97
Q

Pediculus capitus

A

Head louse. Can only live from body for 6 hours. Many people don’t scratch their head.

98
Q

Lice

A

Vector of serious disease. Free moving (pedicures) vs localized (phthirasis) Nits. Patient will have itchy, red eye, insomnia, occasional preaurticalar lymphadenopathy. Dr. will see nit cases, crusty lid margin, madarosis, conj. injections, lid edema, adults.

99
Q

Treating lice

A

In office procedure is removal. Ung tie X 10-14 days for ocular tx. Only Ovide will kill lice. Use erythromycin, bacitracin, physostigimine. Can also use alcohol coated swab lid margins with epithelial debridement. Can also give oral ivermectin (off label but effective). Also repeat treatment one week later to kill eggs hatching.

100
Q

Poliosis

A

Loss of pigmentation of the lashes. Caused by immune response to melanin. Can occur with staph. bleph, albinoism, VKH. Plan-treat the blepharitis and consult if albinism or VKH present.

101
Q

Vitiligo

A

Hypopigmentation of the skin. Usually bilateral present on the lids. . usually a +FHx. Usually present before age 20, progressive, asymptomatic, more prominent in darker races. Cause is unknown.

102
Q

Vitiligo Treatment

A

Determine if Fhx. R/o other syndromes (refer), cosmetic camouflage, skin protection, melanocyte stim. and skin color blending with aa. Topical steroids, Derm will do PUVA, grafting, depig.

103
Q

Vogt-Koyanagi-Harada syndrome

A

Rare multi-system disorder. Possible autoimmune disease against pigmented tissue. Afters darker pigmented. Common 20-50. Has 4 phases.

104
Q

Prodromal Phase

A

1 phase. Lasts only a few days. Patient can have meningitis, encephalophay (brain diseases), auditory disturbances.

105
Q

Acute Uveitic Phase

A

2nd phase. Can have anterior uveitis, posterior uveitis, RD. Patient will have pain, red eye, and be photophobic.

106
Q

Convalescent phase

A

3rd phase. Follows several weeks after acute uveitis. Will have alopecia, poliosis, vitilgo, funds lesion, depigmented gimbal lesions.

107
Q

Chronic-Recurrent phase

A

4th phase. Smoldering ant. uveitis with exacerbation. Can have posterior synechie.

108
Q

VKH diagnosis

A

At least 3 of the following groups need to be present for diagnosis. Bilateral chronic anterior uveitis, posterior uveitis, neurological features, cutaneous lesions. Note: acute serous RD is a hallmark of VKH.

109
Q

VKH vs Harada

A

VKH has worse visual prognosis. Sometimes they are divided.

110
Q

VKH TX

A

Oral steroids, periorcular injections of steroids, topical steroids for anterior uveitis. If steroids don’t work immunosuppresents may be necessary.

111
Q

Ocular Cicatrical Pemphigoid (OCP)

A

An eye scaring blister. Chronic. Slowly progressive. Bilateral but asymmetrical with onset, severity, rate of progression. Potentially blinding. Systemic. Autoimmune. A skin and mucus membrane disorder. primarily a type II hypersensitivity. Very rare but can have big vision loss. Have recurrent sub epithelial blisters or bullae with a tendency to scar. Idiopathic. F>M. No racial preference. Typically diagnosed in 60-70s. There are 4 stages.

112
Q

Stage 1 of OCP

A

Conjunctivitis. Red eye, tearing, burning, irritation, mucous discharge. Most common initial sign is conj. associated with subconj. fibrosis

113
Q

Stage 2 of OCP

A

Conj. scarring and shrinkage. Worsens within the next 3-4 years. Conj. in the other eye. Conj. scarring and shrinkage.

114
Q

Stage 3 of OCP

A

Disease progression leads to symblepheron formation.

115
Q

Stage 4 of OCP

A

End stage with corneal scarring and ankyloblepheron. Get severe dry eye. Vision loss.

116
Q

OCP objective

A

Bleph and keratinization of lid margin, entropion, trichiasis, cicatrices closure of puncta, shortening of the fornices, ankyloblepharon. In more advanced cases cornea will show persistent epithelial defects, infiltration and peripheral vasculerization. Limbal inflammation with stem cell destruction leading to keratinization. Stromal thinning and ulceration.

117
Q

OCP diagnosis

A

Take history, conj biopsy to confirm.

118
Q

OCP Treatment

A

Systemic Therpy: topical steroids (not alone though), Oral/systemic steroids, Dapasone has been shown to be effective in treating acute inflammatory stages of OCP. In advanced stages cyclophasphamide and azathioprine are used. Chronic ocular pub for dry eye, Eyelash depilation, soft Cls (bandage but caution so don’t cause infections) lid scrubs. Prognosis is variable.

119
Q

Erythema Multiforme (EM)

A

An acute but generally self limiting disorder of skin and mucous membrane. Divided into major and minor forms. EM can last 1-4 weeks.

120
Q

EM minor

A

Typically targets or raised, edematous papules in the extremities.

121
Q

EM Major

A

Typically targets or raised edematous papules distributed to the extremities with involvement of one or more mucus membrane. Epidermal detachment involves less then 10% of total body SA.

122
Q

Diagnosing EM

A

Target or bull’s eye lesion which has an erythemous center surrounded by a pale zone, and encircled by an erthematous ring. Usually on the extremities.

123
Q

Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysing (TEN)

A

One division of EM. Has Widespread blisters predominant on the trunk and face, presenting with erythematous or pruritic macules and one or more mucus membrane erosions. Overlapping SJS/TEN is detachment of 10-30 BSA. Acute onset. Occurs in all ages. M>W. No race. No specific etiology.

124
Q

SJS

A

A minor form of TEN with less then 10% Body surface area detachment. Acute inflame skin and mucus membrane. Rare. Ocular complications in 50%. Systemic toxicity. Moratlity rate of 5%. Can last up to 6 weeks.

125
Q

TEN

A

Detachment of more than 30% of body surface area. Acute inflammatory skin and mucous membrane disorder. Rare. Massive erosion of epidermis. Systemic toxicity. Mortality of 25-35. ocular in 50

126
Q

SJS/TEN causes

A

Drugs (Sulfonamides*), Microbial infections (particularly Mycoplasma pneumonia, bac., viruses (HSV), fungi.

127
Q

Systemic involvment in SJS and TEN

A

Fever, Malaise, HA, loss of appetite, NV, cough, Sore throat, URTI

128
Q

Diagnosing SJS and TEN

A

Skin involvement on trunk of the body. Crops of lesion may develop every 2 weeks for 6 weeks. If extensive necrosis and sloughing of the epidermis it is called TEN. Mucuous membrane affects mouth, eye, geneital.

129
Q

Ocular involvement in SJS and TEN

A

Swollen lids, conj. invovlement (can involve both palpbral and bulbar), pseudomembranous conj. feqencly associated with discharge. Has a rapid onset. Bullae formation with rapid rupture and scaring. Vascular changes of the conj. with fibrosis, necrosis, keratinization. Triachiasis, entropian. Corneal opacification. Lacrimal disfunction. Keratopathy.

130
Q

SJS and TEN Treatment

A

No specific treatment exists. Systemic steroids, treat associated infections, oral AB, systemic Antivirals, pain control, Ocular–>Braod AB, topical steroids, soft cls, surgery, lid scribes, epilation, cool compresses, treat dry eye.

131
Q

Chemical Cautery

A

Employs dicholoracetic acid to remove lesions. Must swab with alcohol first and then petroleum jelly on outside. Will turn white, then black, and then scab and fall off in 10 days.

132
Q

Stab incision

A

Cuts and separates but does not remove tissue. Used to release pus or relieve pressure.

133
Q

Lineate Incision

A

Started from a stab incision and continue in a straight line using deliberate strokes. Should always be parallel to the rhytids (folds) of the skin.

134
Q

Incision and Curettage

A

Place champ after anesthetized and make a linear incision parallel to lid margins and apply pressure on either side of the incision.

135
Q

Excision and Curettage

A

Place clamp after anesthetized , evert lid and make lineate incision then make a cruciate incision by making a second linear incision and bisection the first inspections. and excisize each of the flaps.

136
Q

Shave excision

A

Cut off excess skin

OPT 533-Ocular Disease (2 decks)

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