Pathology-Eye w:some Nose & Ear Flashcards

1
Q

What is the difference between lepromatous and tuberculoid leprosy?

A

Lepromatous: poor helper cell response. Schwann cell invasion causes demyelination in a “sock and glove” distribution. Tuberculoid: cell-mediated helper cell response forming granulomas. Asymmetric, dry, scaly lesions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

A patient presents to the clinic with deformities in both hands and loss of sensation in his feet. Biopsy of the foot lesion is shown below. What type of leprosy does this patient have?

A

Note the presence of many organisms packed in foamy macrophages (Lepra cells). This is indicative of lepromatous leprosy because the many cells indicate a weak Th1 immune response as opposed to the strong cell-mediated secretion of Il-2 and IF-gamma w/absence of lepra cells in tuberculoid leprosy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Most common peripheral nerve tumor. Common causes.

A

Schwannoma. Can be caused by nerve compression or mutation of NF2 gene on chromosome 22 that causes loss of merlin (cells will hyper proliferate w/loss of merlin).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

A 62 year old male presents with right-sided hearing loss, instability, vertigo and persistent ringing in his ears. Biopsy of his ear is shown below. What is your diagnosis?

A

Note the hypercellular (Antoni A in left image) and hypocellular (Antoni B in right image) areas. Also notice the Verocay bodies (palisading of spindle cells in the Antoni A area). This patient has an acoustic Schwannoma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

A 31 year old female presents with protruding eyeballs (protosis) and dry eye. She also has corneal clouding. Physical exam reveals edematous shins. What is your diagnosis?

A

She has Grave’s disease. In this disease muscle bodies accumulate extracellular matrix, proteins and fibrosis, causing them to swell up. Note that tendons are spared.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does the orbit get infected?

A

Ethmoidal sinusitis extends to the orbit and cause orbital cellulitis. Mucormycosis (rapidly progressing fungal infection in DKA or immunosuppression).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

A patient presents with enlarged eyelids from a blocked sebaceous gland. It got better with ward compress. What is your diagnosis?

A

Chalazion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Chronic inflammation at the eyelid margin

A

Blephatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are common neoplasms seen in the eyelid?

A

1) Basal cell carcinoma on the lower eye lid from UV exposure #2) Sebaceous carcinoma #3) Squamous cell carcinoma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the worst case scenario for this patient?

A

This patient has a uveal nevus on the iris. Atypical nevi can develop into melanomas, note that optic melanomas lack the radial growth phase that dermatologic melanomas have.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Common chronic diseases that present with uveitis.

A

Juvenile rheumatoid arthritis, pneumocystis jerivicii, sarcoid and sympathetic opthalmia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

A 22 year old male had a traumatic eye injury. Two weeks later he complains of bilateral floating spots, uveitis and photophobia. Biopsy of the uninjured eye is shown below. What is your diagnosis?

A

Sympathetic opthalmia. This is caused by retinal antigens in the injured eye initiating a delayed hypersensitivity reaction to both eyes. Note the granulomatous inflammation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the most common source of intra-ocular neoplasm?

A

Metastasis. The most common primary neoplasm is melanoma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

When do you decide if you want to biopsy and treat the lesion seen below?

A

If it’s diameter grows, NOT DEPTH. Benign nevi are common in 10% of the population and very few progress to melanoma. If the intra-ocular spot grows, it is likely melanoma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

A patient presents to the clinic complaining of weight gain. You exam his stomach and note that he has ascites. Labs reveal liver failure and imaging reveals a tumor in the liver. What eye lesion could have caused this?

A

Uveal melanomas spread hematogenously, not through the lymphatics like dermatologic melanomas do. The first place they usually spread to is the liver and can have very late metastasis decades later.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

A patient presents with difficulty seeing in one eye. Further exam reveals melanoma in the uvea. Biopsy reveals elongated neural-looking cells. What is your diagnosis?

A

Spindle cell melanoma. Epitheliod melanomas have cells with lots of cytoplasm, prominent cherry-red nucleoli and sheet-like congregation of cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Which patient with uveal melanoma has the better prognosis?

A

The bottom one. The top is spindle cell melanoma and the bottom is epitheliod melanoma. Epitheliod melanoma is worse.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Would you rather have a uveal melanoma on the iris or in the uvea?

A

Iris. Melanomas in the choroid or ciliary body tend to be more aggressive.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What conditions are associated with uveal melanoma?

A

Monosomy 3, Trisomy 8 and Vasculogenic Mimicry (PAS +, vascular channels surrounding the melanoma shown below)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How do you treat uveal melanoma?

A

Enucleation or radiation. You must treat quickly because hematogenous spread is fatal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

A patient presents to the clinic with vision problems. Physical exam findings are shown below. Histologically, where in the eye does this patient have problems?

A

In the nerve fiber layer. This is where arteriolosclerosis affects the retinal blood vessels. Note that the vessel is thinner, not as red and is compressing the vein in the fundoscopic exam.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What type of tissue damage can be caused in the retina from hypertension?

A

Cotton wool spots. Small infarcts and degeneration in the superficial nerve fiber layer.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What happens in the preproliferative phase of diabetic retinopathy?

A

1st, the basement membrane of retinal vessels thickens, causing decreased perfusion and macular edema. VEGF-induced angiogenesis of abnormal vessels in retina follows. The nerve fiber and ganglion layer will degenerate as seen below.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What happens in the proliferative phase of diabetic retinopathy?

A

Abundant new vessels sprout in the back of the retina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

A 77 year old woman presents with blurred central vision. What are risk factors for this condition?

A

Risk factors for macular degeneration are: old age, female, obesity, smoking & CFH (complement factor H)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is pathological progression of macular degeneration?

A

Blood vessels in the choroid proliferate and go through the Bruch membrane, affecting the retinal pigment epithelium (RPE). Disturbance of the macula causes atrophy of overlying photoreceptors in retina and blindness.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the prognosis for the two types of macular degeneration?

A

Wet: injection of anti-VEGF. Dry: no treatment (not from vascular growth, from atrophy of RPE is from calcification)

28
Q

Most common primary intra-ocular tumor in kids (age 5 or younger)? What is its origin?

A

Retinoblastoma (note leukokoria in left eye). 40% of these are caused by mutation of one RB allele. Mutation prevents RB from regulating the G1-S phase stop and cells replicate very rapidly.

29
Q

Tumors associated with retinoblastomas

A

Pinealblastomas, osteosarcoma, breast, lung and colon cancer.

30
Q

A mother brings her 3 year old boy in because of an abnormal appearance to his left eye. They eye is taken out and shown below. What would you expect the histology of this tumor to look like?

A

Retinoblastoma is a small round blue cell tumor. Retinoblastoma tends to grow around blood vessels, however, the tumor proliferates so quickly that cells further from blood vessels are necrotic. Cells also form Flexner-Wintersteiner rosettes (blue cells around a cleared space).

31
Q

How do we treat retinoblastoma? What makes the prognosis worse for retinoblastoma?

A

Chemotherapy and laser therapy. If there is extra-ocular spread, prognosis is worse.

32
Q

Where do retinoblastomas like to metastasize to?

A

Brain and bone

33
Q

Atopy in patients with nasal polyps

A

Rare

34
Q

Peripheral eosinophil activation

A

Late phase cytokine release in type I hypersensitivity

35
Q

Nose biopsy: pink proteinaceous fluid

A

Nasal polyp

36
Q

Normally straight lines now seem curved

A

Metamorphopsia (elevation of retina)

37
Q

Most common type of macular degeneration

A

Dry. Characterized by drusen deposits in RPE basement membrane (Bruch membrane)

38
Q

Most vision loss in macular degeneration

A

Wet. Leaky choroidal neovasculature penentrates RPE or situates beneath retina.

39
Q

Treatment for wet macular degeneration

A

VEGF antagonist

40
Q

Angiogenesis beneath the internal limiting membrane and macular edema

A

Common presentations in the background (preproliferative) phase of diabetic retinopathy.

41
Q

New vessels on optic nerve head or retinal surface

A

Common presentations in proliferative phase of diabetic retinopathy.

42
Q

Copper vessels compressing veins, cytoid bodies and cotton-wall spots

A

Common presentations of hypertensive retinopathy. Cytoid body = mitochondrial swellings that accumulate at axon terminals to form cotton-wool spots.

43
Q

Location of exudate in diabetic and hypertensive retinopathy

A

Plexiform layer

44
Q

Early stage sign of macular degeneration

A

Drusen

45
Q

Most common primary intraocular tumor in adults? Kids?

A

Adults = melanoma. Kids = retinoblastoma

46
Q

Enlarged liver

A

Metastatic ocular melanoma

47
Q

Most common type of ocular tumor

A

Metastatic

48
Q

Adverse prognosis in ocular melanoma

A

Epitheliod, vasculogenic mimicry, Monosomy 3, Trisomy 8, extra-ocular extension.

49
Q

Type IV eye hypersensitivity

A

Sympathetic opthalmia

50
Q

Mutton fat & candle wax drippings

A

Sarcoid

51
Q

Blindness in ocular melanoma

A

Retinal detachment

52
Q

Knudson hypothesis

A

2 hits before RB causes malignancy

53
Q

Why treat retinoblastoma w/chemo?

A

Hematogenous spread, intracranial spread

54
Q

Leukocoria, Flexner Wintersteiner rosettes, mitotic figures

A

Retinoblastoma

55
Q

Palisaded nuclei surrounding nuclear free zones

A

Verocay bodies found in the Antoni A area in patients with Schwannoma

56
Q

S-100 positive, loss of expression of NF2 gene product, Merlin. Hearing loss and tinnitus.

A

Acoustic (vestibular) schwannoma.

57
Q

Cafe au lait spots, chromosome 22q12

A

NF1 gene, also a tumor suppressor gene like NF2 and found on same chromosome

58
Q

Cerebro-pontine angle tumor

A

Schwannoma

59
Q

Bacteria in acute otitis media

A

Strep pneumo, H. influenzae, Moraxella

60
Q

Bacteria in chronic otitis media

A

Pseudomonas, staph aureus

61
Q

Proptosis of left eye in young male

A

Nasopharyngeal angiofibroma

62
Q

Fibrocollagenous stroma

A

Nasopharyngeal angiofibroma

63
Q

Scaly, hypopigmented, asymmetric lesions w/o sensation

A

Tuberculoid leprosy

64
Q

Symmetrical skin infiltration in cool extremities (sock and glove), thickened facial skin (Leonine facies), impaired sweating and cracking of skin.

A

Lepromatous leprosy.

65
Q

Granulomatous leprosy

A

Tuberculoid, few bacilli.

66
Q

Lepra cells

A

Lepromatous leprosy (foamy macrophages filled with acid fast bacilli)

67
Q

Leprosy treatment and prevention

A

Treat: dapsone & rifampin. Prevent: BCG vaccine