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Clin med 1 > HEENT 6- > Flashcards

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
Q

Optic Neuritis summary

A

Painful, monocular vision loss, fundoscopic exam is intially normal, MRI is indicated of brain, consult specialist!

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26
Q

What is papilledema?

A

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

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27
Q

Where does pipilledema occur initially?

A

Superiorly and inferiorly and then nasally and temporally

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28
Q

Causes of papilledema

A

ICP transmitted along the optic nerve (only true cause), Hypertensive Retinopathy (often described as papilledema)

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29
Q

Causes of increased ICP

A

Intracranial mass lesions, cerebral edema, hydrocephalus (increased CSF production or decreased absorption), obstruction of venous flow, intracranial HTN (pseudotumor cerebri)

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30
Q

Symptoms of increased ICP

A

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

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31
Q

What are the 3 stages of papilledema?

A
  1. Early
  2. Fully developed
  3. Chronic
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32
Q

Early papilledema

A

Loss of spontaneous venous pulsations, optic cup is retained early on

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33
Q

Fully developed papilledema

A

Optic disc elevated, cup is obliterated, disc margins are obscured, blood vessels buried, engorged veins, flame hemorrhages, cotton wool spots

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34
Q

What are the cotton wool spots a result from (papilledema)

A

Nerve fiber infarction

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35
Q

Late chronic papilledema

A

Cup remains obliterated, hemorrhagic and exudative components resolve, nerve appears flat with irregular margins, disc pallor

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36
Q

Diagnostic testing for papilledema

A

MRI or CT, lumbar puncture (to check opening pressure >180), visual field testing (to detect subclinical abnormalities and monitor changes over time)

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37
Q

Management of papilledema

A

Reducing intracranial pressure (for intracranial HTN)

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38
Q

Management of elevated ICP

A

Continuous ICP monitoring, osmotic therapy and diuresis (reduce brain volume), hypertonic saline (reduces ICP early), Glucocorticoids (reducing swelling for tumors and infections)

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39
Q

Other ways to manage elevated ICP

A

Hyperventilation, barbiturates (reduces brain metabolism and cerebral blood flow), removal of CSF with a shunt, decompressive craniectomy

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40
Q

Clinical features of idopathic intracranial HTN

A

N/V, HA, blurred vision, CN VI paresis/horizontal diplopia, bilateral papilledema, spontaneous venous pulsations are absent, visual field defects

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41
Q

Management of IIHTN

A

Weight loss, serial lumbar punctures, Acetazolamide, high dose corticosteroids if rapid vision loss, surgery for severe refractory cases

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42
Q

Retinal vein occlusions

A

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

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43
Q

Retinal artery occlusion

A

Acute, painless loss of monocular vision, considered a form of stroke

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44
Q

What are the two types of retinal artery occlusion?

A
  1. Central retinal artery occlusion

2. Branch retinal artery occlusion

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45
Q

Risk factors for retinal artery occlusion

A

Carotid artery atherosclerosis, cardiogenic embolism, giant cell arteritis, sickle cell disease, hypercoagulable states, carotid artery dissection

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46
Q

CRAO symptoms

A

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
Q

BRAO symptoms

A

Monocular vision loss, which may be restricted to just part of the visual field

48
Q

Associated symptoms with retinal artery occlusions

A

HA if from GSA or carotid dissection, possible unilateral numbness, weakness, slurred speech if related to carotid disease

49
Q

Physical exam findings of retinal artery occlusion

A

Visual acuity reduced, severley ranges from part of visual field (BRAO) to nearly complete visual loss, afferent pupillary defect (Marcus Gunn pupil)

50
Q

Fundoscopic exam findings for retinal artery occlusion

A

Ischemic retinal whitening, cherry red spot in macula

51
Q

Management of acute retinal artery occlusion

A

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
Q

Retinal vein occlusion

A

Occluded retinal vein from thrombus formation of compression of the vein by retinal arterioles at the arterivenous crossing point

53
Q

Classifications of retinal vein occlusions

A
  1. BRVO: brach retinal vein
  2. CRVO: central retinal vein occlusion
  3. HRVO: Hemiretinal vein occlusion
54
Q

BRVO

A

Distal vein is occluded leading to hemorrhage along the distribution of a small vessel

55
Q

CRVO

A

Occurs due to thrombus within central retinal vein leading to involvement of the entire retina

56
Q

HRVO

A

Occurs when blockage is in a vein that drains the superior or inferior hemiretina

57
Q

Associated conditins of retinal vein occluison

A

DM, HTN, Leukemia, Sick cell disease, Multiple myeloma

58
Q

Clinical presentation of retinal vein occlusion

A

Sudden painless loss of vision

59
Q

Fundoscopic exam findings of retinal vein occlusion

A

Few scattered retinal hemorrhages and cotton wool spots to a marked hemorrhagic appearance

60
Q

Management of acute retinal vein occlusion

A

No treatment in acute stage-consult ophto ASAP!

61
Q

What can the ophthalmologist do for retinal vein occlusion?

A

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
Q

What types of cancer are typically head and neck lesions?

A

Squamous cell carcinoma

63
Q

SCC of head and neck include tumors of

A

Paranasal sinuses, naropharynx, oropharynx. larynx

64
Q

Oropharynx

A

Posterier 1/3rd of tongue, soft palate. Laterl and posterior walls of thoart.

65
Q

Pharynx is aproximately how long?

A

5 inches that start behind the nose and ends at trachea and esophagus

66
Q

Tumors and precancerous lesions include what of head and neck?

A

SCC, Leukoplakia, Melanoma

67
Q

Most common oral cavity lesion

A

SCC!!

68
Q

SCC of oral cavity associated with what?

A

Non-healing ulcers or masses, dental changes or poorly fitting dentures

69
Q

Tongue and lip cancers present as what?

A

Exophytic or ulcerative lesions often associated with pain

70
Q

Often __ of patients with primary tongue lesions have nodal disease

A

2/3

71
Q

What are major risk factors for tongue lesions?

A

Tobacco, ETOH

72
Q

SCC of the oropharynx

A

HPV major risk factor

73
Q

Majority of HPV-related head and neck SCC arise where?

A

Particularly int he palatine and lingual tonsils

74
Q

HPV 16 does not produce what?

A

Visible lesions/discolorations (early warning sings)

75
Q

Oropharynx 3 spots of SCC

A
  1. Carcinomas of oral cavity proper
  2. Carcinomas arising in oropharynx
  3. Carcinomas of the lip vermilion
76
Q

Oral CA can be divided into 3 categories

A
  1. Well differentiated
  2. Moderately well differnentiated
  3. Poorly differentiated categories (worse prognosis)
77
Q

Malignant Oropharyngeal lesion etiology

A

Alcohol (3-9x more risk), Tobacco (5-9x greater), HPV, EBV, Diet

78
Q

HPV 16 accounts for what?

A

90% HPV-positive oropharyngeal SCCs

79
Q

Oral-cavity SCCs often preceded by

A

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
Q

BUT, most head and neck CA patients do not present with what?

A

History of premalignant lesions

81
Q

“potentially malignant disorder”

A

Leukoplakia, most will not progress to OC-SCC

82
Q

Leukoplakis

A

Classified as: hyperplasia, dysplasia, carcinoma in situ, carcinoma

83
Q

Clinical presentation of speckled erythroplakia

A

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
Q

What does the lesion look like in speckled erythroplakia?

A

Red, velvety patch, often well-demarcated. Some may have rough granular surface

85
Q

Oral cavity SCC

A

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
Q

Vast majority of tongue lesions occur where?

A

Lateral and ventrolateral aspects

87
Q

Oropharyngeal SCC

A

Develops most frequently in tonsillar region and base of tongue.

88
Q

What does OP-SCC appear as?

A

Ulcerated mass, fullness, or irregular erythematous mucosal change

89
Q

Most common chief complaint with OP-SCC

A

Presence of neck mass, sore throat, dysphagia

90
Q

SCC with leukoplakia

A

Rough, papillary patch of leukoplakia seen in retromolar trigone and soft palate

91
Q

As the cancer develops (head and neck) patient may notice what?

A

The presence of a nonhealing ulcer

92
Q

Symptoms of malignant lesions to head and neck

A

Pain, otalgia, dysphagia, odynphagia, airway obstruciton

93
Q

Signs of malignant lesions to head and neck

A

Cervical LAD, cranial neuropathies, decreased tongue mobility, fistulas, skin involvement

94
Q

Oral cavity lesion common locations

A

Tips, tongue, floor of mouth, maxillary alveolar ridge/hard palate, mandibular alveolar ridge, buccal vestibules

95
Q

Pharynx lesion common locations

A

Nasopharynx

96
Q

Oropharynx lesion common locations

A

Tongue base, soft palate, palatine tonsils, posterior wall of pharynx

97
Q

Hypopharnyx lesion common location

A

Piriform sinuses and postcricoid area leading into esophagus below

98
Q

Larynx lesion common location

A

Supraglottis (epiglottis, false vocal cords), cancers here spread early to LNs

99
Q

Glottis lesions common location

A

True vocal cords, most common site of laryngeal cancer. present with hoarseness

100
Q

Late-stage symptoms of head and neck malignancies

A

Bleeding, loosening of teeth, difficulty wearing dentures, dysphagia, dysarthria, hoarseness, development of a neck mass

101
Q

Granular Leukoplakia

A

Small leukoplakic lesions with rough, granular surface on posterior lateral border of tongue.

102
Q

Stage 1 head and neck malignancy

A

<2cm, do not involve eep extrinsic tongue muscles or the mandible

103
Q

T2 cancers

A

2-4 cm and may involve adjacent structures (higher incidence of occult lymph node metastasis)

104
Q

Diagnosis/Imaging for head and neck malignancies

A

MRI and or CT/PET for assessment and staging, full-body often required

105
Q

Distant metastases found in <10% of patients at initial diagnosis, more common in what?

A

patients with advanced lymph node stage

106
Q

Prognosis for head and neck malignancies

A

Those with localized disease, those with locally or regionally advanced disease, those with recurrent and or metastatic disease

107
Q

How to treat localized disease?

A

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
Q

Localized Disease

A

Have T1 or T2 lesions without detectable lymph node involvement or distant metastases

109
Q

How to treat advanced disease?

A

Curative intent, but with combine -modality therapy using: surgery, radiation, and chemotherapy

110
Q

How to treat recurrent and/or metastatic disease?

A

Treated with palliative intent, local or regional radiation therapy for pain control, most given chemo. Response rate to chemo is 30-50%

111
Q

HPV 16 cancers have the advantage why?

A

They have a better 3-year rate of overall survival than those with HPV negative cancers

112
Q

What is the major determinant for overall survival?

A

HPV status of tumor

113
Q

HPV vaccines

A

Proved nearly 100% protection against persistent cervical infections with HPV 16 and 18

Clin med 1 (9 decks)

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