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HEENT 6- Flashcards

1
Q

Retinal detachment

A

Separation of the sensory retina from the pigment epithelium and underlying choroid

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2
Q

Traction or tear of retina allows what?

A

Fluid to accumulate between the two layers

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3
Q

Retinal detachment can result in what?

A

Ischemia and rapid progressive photoreceptor degeneration. Permanent blindness can occur if macula is detached

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4
Q

Photoreceptors are most highly concentrated in what?

A

Fovea, which is within the macula

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5
Q

Uncomplicated spontaneous retinal detachments can be cured how?

A

With one peration or proceudre

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6
Q

Spontaneous detachments are usually what?

A

Bilateral

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7
Q

Risk factors for retinal detachment

A

Myopia (near-sighted), Previous ocular surgery most common***
Fluoroquinolones, trauma, family history, Marfan disease

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8
Q

Causes of retinal detachment

A

Retinal tears or holes (spontaneous or traumatic), traction on the retina caused by systemic influences (diabetic retinopathy), tumors, exudative process (infection, malignancy)

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9
Q

Symptoms of retinal detachment

A

Increasing # of floaters, flashes of light in visual fields, shower of black spots in visual fields, curtain spreading over visual field, cloudy or smoky vision

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10
Q

Differential diagnosis of retinal detachment

A

Vitreous hemorrhage, vitreous inflammation, ocular lymphoma, intraocular foreign body

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11
Q

What will a retinal detachment look like on an ophthalmoscopic exam?

A

“billowing sail” or “ripple on a pond”

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12
Q

Treatment of retinal detachment

A

Consult ophthalmology ASAP! Drain the subretinal fluid, laster photocoagulation, cryotherapy to sclera, pneumoretinopexy, scleral buckely placement, vitrectomy surgery

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13
Q

What is photocoagulation

A

Numbing drops, retinal break is localized, 2-3 rows of 200 micron size laser burns (heat energy). Takes 2 weeks for body to form adhesions over burns

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14
Q

What is cryotherapy (cryoretinopexy)

A

Lidocaine injected first, cryoretinpexy probe is placed on conjunctiva under break, freezing ball is created at tip of probe, freezes through sclera, choroid and retina. Also take 2 weeks to form adhesions

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15
Q

What is pneumoretinoplexy?

A

For large retinal detachments, do the cryoretinoplexy and follow that with an injection of intravitreal gas bubble, the retinal detachment is pushed back by the gas, adhesion is then formed

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16
Q

What is scleral buckle placement?

A

Retrobulbar injection of lidocaine first, cryoretinpexy is preformed, an explant is sutured to the sclera, it indents the wall of the eye, closing the retinal breaks

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17
Q

What is vitrectomy surgery?

A

Removes tractional components and is only performed if the fovea is detached or appears imminently detached

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18
Q

Optic neuritis

A

Inflammatory disease of the optic nerve, characterized by a normal fundus exam initially

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19
Q

What is optic neuritis strongly associated with?

A

Demyelinating diseases like MS

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20
Q

Causes of optic neuritis

A

MS, sarcoidosis, neuromyelitis optica, herpes zoster, systemic lupus erythematosus

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21
Q

Symptoms of optic neuritis

A

Unilateral loss of vision* developing over few days, and pain exacerbated by movement*

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22
Q

Loss of vision characterization with optic neuritis

A

Usually central, loss of color vision. Visual acuity improves within 2-3 weeks

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23
Q

Management of optic neuritis

A

Brain MRI: assess for MS, consult neuro-ophthalmologist, systemic corticosteroids (controversial)

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24
Q

Multiple demyelinating plaques

A

Treatment with interferon Beta-1a can retard the development of more lesions, Interferon is a biologic that fights infection and is used to treat MS, injectable

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25
Optic Neuritis summary
Painful, monocular vision loss, fundoscopic exam is intially normal, MRI is indicated of brain, consult specialist!
26
What is papilledema?
PE finding during a fundoscopic exam, loss of definition of the optic disc (edema of the head of the optic nerve) Vessels are pushed forwad, veins dilated
27
Where does pipilledema occur initially?
Superiorly and inferiorly and then nasally and temporally
28
Causes of papilledema
ICP transmitted along the optic nerve (only true cause), Hypertensive Retinopathy (often described as papilledema)
29
Causes of increased ICP
Intracranial mass lesions, cerebral edema, hydrocephalus (increased CSF production or decreased absorption), obstruction of venous flow, intracranial HTN (pseudotumor cerebri)
30
Symptoms of increased ICP
Headache thats worse lying down and upon awakening in morning, N/V, binocular horizontal diplopia, pulsatile machinery-like sound in ear, brief transient visual blurring
31
What are the 3 stages of papilledema?
1. Early 2. Fully developed 3. Chronic
32
Early papilledema
Loss of spontaneous venous pulsations, optic cup is retained early on
33
Fully developed papilledema
Optic disc elevated, cup is obliterated, disc margins are obscured, blood vessels buried, engorged veins, flame hemorrhages, cotton wool spots
34
What are the cotton wool spots a result from (papilledema)
Nerve fiber infarction
35
Late chronic papilledema
Cup remains obliterated, hemorrhagic and exudative components resolve, nerve appears flat with irregular margins, disc pallor
36
Diagnostic testing for papilledema
MRI or CT, lumbar puncture (to check opening pressure >180), visual field testing (to detect subclinical abnormalities and monitor changes over time)
37
Management of papilledema
Reducing intracranial pressure (for intracranial HTN)
38
Management of elevated ICP
Continuous ICP monitoring, osmotic therapy and diuresis (reduce brain volume), hypertonic saline (reduces ICP early), Glucocorticoids (reducing swelling for tumors and infections)
39
Other ways to manage elevated ICP
Hyperventilation, barbiturates (reduces brain metabolism and cerebral blood flow), removal of CSF with a shunt, decompressive craniectomy
40
Clinical features of idopathic intracranial HTN
N/V, HA, blurred vision, CN VI paresis/horizontal diplopia, bilateral papilledema, spontaneous venous pulsations are absent, visual field defects
41
Management of IIHTN
Weight loss, serial lumbar punctures, Acetazolamide, high dose corticosteroids if rapid vision loss, surgery for severe refractory cases
42
Retinal vein occlusions
HTN, diabetes, sickle cell anemia, conditions that slow venous blood flow. Reduction in flow results in neovascularization between retinal and vitreous humor, new vessels prone to hemorrhage
43
Retinal artery occlusion
Acute, painless loss of monocular vision, considered a form of stroke
44
What are the two types of retinal artery occlusion?
1. Central retinal artery occlusion | 2. Branch retinal artery occlusion
45
Risk factors for retinal artery occlusion
Carotid artery atherosclerosis, cardiogenic embolism, giant cell arteritis, sickle cell disease, hypercoagulable states, carotid artery dissection
46
CRAO symptoms
Sudden, profound vision loss in one eye, usually painless. Occasionally preceded by transient monocular blindness, stuttering, or fluctuating course. Rarely "flashing lights" in visual field
47
BRAO symptoms
Monocular vision loss, which may be restricted to just part of the visual field
48
Associated symptoms with retinal artery occlusions
HA if from GSA or carotid dissection, possible unilateral numbness, weakness, slurred speech if related to carotid disease
49
Physical exam findings of retinal artery occlusion
Visual acuity reduced, severley ranges from part of visual field (BRAO) to nearly complete visual loss, afferent pupillary defect (Marcus Gunn pupil)
50
Fundoscopic exam findings for retinal artery occlusion
Ischemic retinal whitening, cherry red spot in macula
51
Management of acute retinal artery occlusion
Check ESR rate and CRP to rule out giant cell arteritis, immediate administration of steroids can preserve vision! Consult ophtho ASAP, irreversible damage occurs within hours
52
Retinal vein occlusion
Occluded retinal vein from thrombus formation of compression of the vein by retinal arterioles at the arterivenous crossing point
53
Classifications of retinal vein occlusions
1. BRVO: brach retinal vein 2. CRVO: central retinal vein occlusion 3. HRVO: Hemiretinal vein occlusion
54
BRVO
Distal vein is occluded leading to hemorrhage along the distribution of a small vessel
55
CRVO
Occurs due to thrombus within central retinal vein leading to involvement of the entire retina
56
HRVO
Occurs when blockage is in a vein that drains the superior or inferior hemiretina
57
Associated conditins of retinal vein occluison
DM, HTN, Leukemia, Sick cell disease, Multiple myeloma
58
Clinical presentation of retinal vein occlusion
Sudden painless loss of vision
59
Fundoscopic exam findings of retinal vein occlusion
Few scattered retinal hemorrhages and cotton wool spots to a marked hemorrhagic appearance
60
Management of acute retinal vein occlusion
No treatment in acute stage-consult ophto ASAP!
61
What can the ophthalmologist do for retinal vein occlusion?
Infections of VEGF inhibitors or Triamcinoone, Retinal laser photocoagulation, various surgical techniques, vitrectomy with injection of tPA, incision of sclera and edge of optic disc
62
What types of cancer are typically head and neck lesions?
Squamous cell carcinoma
63
SCC of head and neck include tumors of
Paranasal sinuses, naropharynx, oropharynx. larynx
64
Oropharynx
Posterier 1/3rd of tongue, soft palate. Laterl and posterior walls of thoart.
65
Pharynx is aproximately how long?
5 inches that start behind the nose and ends at trachea and esophagus
66
Tumors and precancerous lesions include what of head and neck?
SCC, Leukoplakia, Melanoma
67
Most common oral cavity lesion
SCC!!
68
SCC of oral cavity associated with what?
Non-healing ulcers or masses, dental changes or poorly fitting dentures
69
Tongue and lip cancers present as what?
Exophytic or ulcerative lesions often associated with pain
70
Often __ of patients with primary tongue lesions have nodal disease
2/3
71
What are major risk factors for tongue lesions?
Tobacco, ETOH
72
SCC of the oropharynx
HPV major risk factor
73
Majority of HPV-related head and neck SCC arise where?
Particularly int he palatine and lingual tonsils
74
HPV 16 does not produce what?
Visible lesions/discolorations (early warning sings)
75
Oropharynx 3 spots of SCC
1. Carcinomas of oral cavity proper 2. Carcinomas arising in oropharynx 3. Carcinomas of the lip vermilion
76
Oral CA can be divided into 3 categories
1. Well differentiated 2. Moderately well differnentiated 3. Poorly differentiated categories (worse prognosis)
77
Malignant Oropharyngeal lesion etiology
Alcohol (3-9x more risk), Tobacco (5-9x greater), HPV, EBV, Diet
78
HPV 16 accounts for what?
90% HPV-positive oropharyngeal SCCs
79
Oral-cavity SCCs often preceded by
Leukoplakia (white patch cannot be removed), Erythroplakia (red patch similar to leukoplakia except that is has erythematous component), Speckled erythroplakia (combination of red and white features)
80
BUT, most head and neck CA patients do not present with what?
History of premalignant lesions
81
"potentially malignant disorder"
Leukoplakia, most will not progress to OC-SCC
82
Leukoplakis
Classified as: hyperplasia, dysplasia, carcinoma in situ, carcinoma
83
Clinical presentation of speckled erythroplakia
Fiery red patch, cannot be identified as any other definable disease* will show evidence of high-grade dysplasia, carcinoma in situ, or invasive SCC
84
What does the lesion look like in speckled erythroplakia?
Red, velvety patch, often well-demarcated. Some may have rough granular surface
85
Oral cavity SCC
Can appear as ulcer without mucosal change, continued growth can result in mass with raised border. Pain/tenderness often develops later. Most common site tongue
86
Vast majority of tongue lesions occur where?
Lateral and ventrolateral aspects
87
Oropharyngeal SCC
Develops most frequently in tonsillar region and base of tongue.
88
What does OP-SCC appear as?
Ulcerated mass, fullness, or irregular erythematous mucosal change
89
Most common chief complaint with OP-SCC
Presence of neck mass, sore throat, dysphagia
90
SCC with leukoplakia
Rough, papillary patch of leukoplakia seen in retromolar trigone and soft palate
91
As the cancer develops (head and neck) patient may notice what?
The presence of a nonhealing ulcer
92
Symptoms of malignant lesions to head and neck
Pain, otalgia, dysphagia, odynphagia, airway obstruciton
93
Signs of malignant lesions to head and neck
Cervical LAD, cranial neuropathies, decreased tongue mobility, fistulas, skin involvement
94
Oral cavity lesion common locations
Tips, tongue, floor of mouth, maxillary alveolar ridge/hard palate, mandibular alveolar ridge, buccal vestibules
95
Pharynx lesion common locations
Nasopharynx
96
Oropharynx lesion common locations
Tongue base, soft palate, palatine tonsils, posterior wall of pharynx
97
Hypopharnyx lesion common location
Piriform sinuses and postcricoid area leading into esophagus below
98
Larynx lesion common location
Supraglottis (epiglottis, false vocal cords), cancers here spread early to LNs
99
Glottis lesions common location
True vocal cords, most common site of laryngeal cancer. present with hoarseness
100
Late-stage symptoms of head and neck malignancies
Bleeding, loosening of teeth, difficulty wearing dentures, dysphagia, dysarthria, hoarseness, development of a neck mass
101
Granular Leukoplakia
Small leukoplakic lesions with rough, granular surface on posterior lateral border of tongue.
102
Stage 1 head and neck malignancy
<2cm, do not involve eep extrinsic tongue muscles or the mandible
103
T2 cancers
2-4 cm and may involve adjacent structures (higher incidence of occult lymph node metastasis)
104
Diagnosis/Imaging for head and neck malignancies
MRI and or CT/PET for assessment and staging, full-body often required
105
Distant metastases found in <10% of patients at initial diagnosis, more common in what?
patients with advanced lymph node stage
106
Prognosis for head and neck malignancies
Those with localized disease, those with locally or regionally advanced disease, those with recurrent and or metastatic disease
107
How to treat localized disease?
Curative intent by surgery or radiation therapy. 5 year overall survival of 60-90% Surgery is preferred to avoid complications like xerostomia and dental decay
108
Localized Disease
Have T1 or T2 lesions without detectable lymph node involvement or distant metastases
109
How to treat advanced disease?
Curative intent, but with combine -modality therapy using: surgery, radiation, and chemotherapy
110
How to treat recurrent and/or metastatic disease?
Treated with palliative intent, local or regional radiation therapy for pain control, most given chemo. Response rate to chemo is 30-50%
111
HPV 16 cancers have the advantage why?
They have a better 3-year rate of overall survival than those with HPV negative cancers
112
What is the major determinant for overall survival?
HPV status of tumor
113
HPV vaccines
Proved nearly 100% protection against persistent cervical infections with HPV 16 and 18

Clin med 1 (9 decks)

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