Week 5 EENT

Question 1

Describe the layers of the eye.

Answer 1

1. Sclera: thick fibrous opaque outer layer.

Composed of dense connective tissue, transparent at the cornea (allows light to enter the eye) .
Protects eye, provides shape, attachment point for ocular muscles.
Visible exterior surface of slcera and inner eyelids are lined with conjunctiva (mucous membrane).

2.Uvea: middle vascular layer, consists of iris+ ciliary body +choroid.
Choroid is deeply pigmented (melanin), highly vascular connective tissue layer. Prevents light from scattering inside the eye, and provides nutrients/O2.
Anterior part of choroid includes iris (controls pupil size) and ciliary body (produces aqueous humor, and controls lens shape for accommodation [near/far vision]).

3. Retina: innermost light-sensitive layer of nervous tissue.
   Millions special sensory cells, or photoreceptors called rods & cones.
   Rods: peripheral + dim light vision (black&white), densest @ periphery
   Cones: color + detail vision, densest @ center of retina.
   Rods and cones transmit impulses to nerve cells in retina–> optical nerve–> visual cortex

Huether p. 349

Question 2

Describe the formation and flow of aqueous humour.
What is the fx of the aqueous humor?
What happens if flow is blocked?

Answer 2

Secreted by the ciliary processes

Fills the aqueous chamber and helps keep pressure inside the eye, as well as supply nutrients to the lens and cornea.

Reabsorbed into the scleral venous sinus.

Intraocular pressure increases if a blockage occurs (causing glaucoma)

Question 3

In which structure of the eye are rods and cones found? What do they do?

Answer 3

Found at the back of the retina in the photosensitive region.

Rods: More sensitive to light and the receptors for low-light conditions.

Cones: Less sensitive to light but highly sensitive to red, green, and blue regions of the visual spectrum.

Question 4

What is the “blind spot” in our eye, and why?

Answer 4

The optic disc, in the retina, has no rods or cones.

Question 5

Describe the structure of the retina and their function.

Answer 5

The Retina is the inner layer of the eye.

Consists of:

-Neural (Optic) Retina (Sensitive to light) (at the back of the eye). This is composed of the outer retinal pigmented epithelium (lying adjacent to the vascular choroid) and the photosensitive region of rods (more sensitive to light and the receptors for low-light conditions) and cones (less sensitive to light but highly sensitive to red, green, and blue regions of the visual spectrum).

-Optic Disc: no rods or cones (therefore, our blind spot).

-Fovea centralis, which is the central focusing area. It is the most sensitive portion because it is thin and most layers of the retina are absent. It consists only of cones, specialized for colour vision and acute discrimination.

-Nonvisual Retina: Lines the internal surface of the ciliary body and iris at the front of the eye .

Question 6

How do images transfer from eye to brain?

Answer 6

The Retina has interspersed layers of conducting and association neurons .

Axons of ganglion cells convey the photosensory info to the Optic disc. This information is then transmitted to the optic nerve and relayed centrally.

Question 7

What is a detached retina?

Answer 7

A retinal detachment is a tear or break in the retina with build-up of fluid and separation from underlying tissue.

Question 8

What are risk factors associated with increased risk of retinal detachment?

Answer 8

Extreme myopia (nearsightedness), previous cataract surgery, ocular trauma, diabetic retinopathy, sick cell disease, family history of retinal detachment.

Question 9

What are the signs and symptoms of retinal detachment?

Answer 9

Painless vision disturbance/ loss

Early: floaters, flashes of light, blurred vision

Progresses to: curtain/ greyness over visual field, decreased peripheral or central vision

Question 10

Describe the 5 common origins of epistaxis(etiology and location).

Answer 10

1. Hereditary hemorrhagic telangiectasia (HHT), also known as Osler Weber Rendu syndrome, is a genetically inherited condition. People with HHT have small blood vessel malformations, known as telangiectasias, which affect the skin and mucosal membranes. Nosebleeds are the most common symptom; between 50 percent and 80 percent have recurrent bleeds.
2. Spontaneous epistaxis usually occurs in the fifth decade of life and may be associated with hypertension or liver insufficiency. This type of nosebleed resolves without medical treatment; however, in some patients, the intensity or repetition of hemorrhages in a short period of time may require more invasive nosebleed treatment such as embolization.
3. Trauma
4. Tumors. Occasionally bleeding from the nasal or oral cavities may be related to the presence of a tumor. If there is concern for this, further imaging such as computer tomography scan or magnetic resonance imaging to evaluate what is happening.

5.Vascular Malformations

Question 11

What are the treatment options for persistent epistaxis?

Answer 11

1st step - “packing” the nose, which should be performed by an appropriately trained physician. If this does not stop the bleeding

2nd step - embolization is performed by which the blood vessel supplying the inner lining of the nose is blocked.
Embolization can be used to treat severe, recurring nosebleeds that cannot be controlled by traditional means.

• Can investigate the source of the bleeding via angiography. After we identify the vessels responsible for the bleeding, we can go back in through a catheter and block the vessels to stop the bleeding (embolization). In some cases, this technique can be lifesaving.

Question 12

What are some adverse outcomes from prolonged persistent/recurrent epistaxis?

Answer 12

If you experience severe blood loss from a nosebleed, it can cause serious anemia or cardiac dysfunction and reduced quality of life.

Question 13

What condition are we referring to below?

-One of the most commonly seen eye conditions.

-More common in adults than children; prevalence increases with age.

-Risk factors: diabetes, candida, seborrheic dermatitis, acne rosacea, contact lens use, retinoids, chemo agents

-Inflammation of eyelid, can be acute or chronic.

Answer 13

Blepharitis

Question 14

What are the 3 main causes of’; blepharitis?

Answer 14

1. Staphylococcus -most common colonizing bacteria, responsible for bacterial infection of lid margin
2. Inflammatory skin conditions:
   -seborrheic dermatitis: excessive shedding of skin cells and blockage of glands
   -rosacea, eczema, psoriasis
   -contact dermatitis (i.e., due to irritant such as cosmetics)
3. Meibomian gland dysfunction -modified sebaceous gland, responsible for secretion of oily layer of tear film (critical for eye lubrication); altered gland function provides and environment that promotes bacterial growth

Question 15

What are the signs and symptoms you might see with blepharitis?

Answer 15

-bilateral condition, but may have asymmetric findings

-erythema, edema, flaking/ scales of eyelid

-burning, itching, dryness and flaking of eyelid margin

-tearing, dry eyes, crusting/matting of eyelashes in morning

-photophobia

-recurrent eye infections, styes, or chalazions

-rarely causes problems with vision, however, can occur with conjunctival irritation

Staphylococcus: erythema/ edema, scaling, burning, tearing, itching, recurrent styes

Seborrheic: lid margin swelling and erythema, flaking, nasolabial erythema, scaling

Question 16

How is blepharitis diagnosed?

What are some differential diagnoses to consider?

Answer 16

Diagnosis is based on clinical picture (erythema, irritation, crusting/ flakes on eyelid)

-differentiate between bacterial infection or inflammatory skin condition/ disease

Ddx: conjunctivitis, eyelid malignancy, stye or chalazion, URTI, sinusitis

Question 17

Discuss treatment and management considerations for a patient diagnosed with blepharitis.

Answer 17

-assess for vision changes

-f/u with ophthalmology for recurrent episodes, impaired vision or corneal abnormalities

-all patients should follow up with primary provider in 1-2 weeks

Eyelid hygiene:

-wash eye with antibacterial soap and water (or gentle baby shampoo)

-apply warm compress to eye (comfort and liquifies secretions)

-lid massage in circular motion towards eye

-use clean washcloth or gauze to clean along lash line

-stop use of contacts until healed

Pharmacological:

-usually if mild/ mod, good eyelid hygiene is all that is needed

-for severe/ chronic, consider antibiotics

Topical bacitracin or erythromycin ophthalmic ointment to margin of eye at bedtime

Oral antibiotics: tetracycline (not for peds under 8, pregnant or lactating women) or doxycycline (alternative: erythromycin or azithromycin)

Question 18

What age group is tonsillitis most seen in, and why?

Answer 18

Tonsillitis most often affects children, and tonsillitis caused by bacteria is most common in children ages 5 to 15.

Frequent exposure to germs. School-age children are in close contact with their peers and frequently exposed to viruses or bacteria that can cause tonsillitis.

The tonsils are the immune system’s first line of defense against bacteria and viruses that enter your mouth. This function may make the tonsils particularly vulnerable to infection and inflammation. However, the tonsil’s immune system function declines after puberty — a factor that may account for the rare cases of tonsillitis in adults.

Question 19

What it the time course for tonsillitis?

What are the common causes of tonsillitis?

Answer 19

The time course is 7-10 days.

Tonsillitis is most often caused by common viruses, but bacterial infections also can be the cause. The most common bacterium causing tonsillitis is Streptococcus pyogenes (group A streptococcus), the bacterium that causes strep throat. Other strains of strep and other bacteria also may cause tonsillitis.

Question 20

Common s/s of tonsillitis include:

Answer 20

Red, swollen tonsils

White or yellow coating or patches on the tonsils

Sore throat and painful swallowing

Fever

Enlarged, tender glands (lymph nodes) in the neck

A scratchy, muffled or throaty voice

Neck pain or stiff neck

Headache

Question 21

What s/s might you see with tonsillitis in young children unable to describe how they are feeling?

Answer 21

Drooling due to difficult or painful swallowing

Refusal to eat

Unusual fussiness

Question 22

What are tonsillitis s/s that are of increasing concern?

Answer 22

A sore throat with fever

A sore throat that doesn’t go away within 24 to 48 hours

Painful or difficult swallowing

Extreme weakness, fatigue or fussiness

Difficulty breathing

Extreme difficulty swallowing

Excessive drooling

Question 23

What are some possible advanced tonsillitis complications?

Answer 23

Disrupted breathing during sleep (obstructive sleep apnea)

Infection that spreads deep into surrounding tissue (tonsillar cellulitis)

Infection that results in a collection of pus behind a tonsil (peritonsillar abscess)

Gayle’s note - I took this from an ILO illness script that stated these are ‘chronic’ complications, but I disagree so I labelled them ‘advanced’ complications. Then I checked UTD and they are called ‘suppurative’ complications.
They also list Otitis media.

Question 24

Tonsillitis due to streptococcus that is not properly treated has an increased chance of manifesting into these rare disorders.

Answer 24

1. Rheumatic fever, a serious inflammatory condition that can affect the heart, joints, nervous system and skin
2. Complications of scarlet fever, a streptococcal infection characterized by a prominent rash
3. Inflammation of the kidney (poststreptococcal glomerulonephritis)
4. Poststreptococcal reactive arthritis, a condition that causes inflammation of the joints

Question 25

How is strep throat diagnosed?

Answer 25

- Diagnosis is based on physical exam (pt history, symptoms), swollen lymph nodes, characteristics of tonsils. (Gayle's addition: sore throat score) - Throat swab - Complete blood cell count (CBC): can indicate whether an infection is more caused by a bacterial or viral agent. A CBC is not often needed to diagnose strep throat. However, if the strep throat lab test is negative, the CBC may be needed to help determine the cause of tonsillitis.

Question 26

What are the treatment recommendations for someone you've diagnosed with strep throat?

Answer 26

Antibiotics if warranted. Teachings re: importance of finishing course. Encourage rest Adequate fluids Comforting foods and beverage. Warm liquids and cold treats can soothe a sore throat. Saltwater gargles TID Humidify the air Offer lozenges. Avoid irritants Treat pain and fever Surgery to remove tonsils, once a common procedure to treat tonsillitis, is usually performed only when tonsillitis occurs frequently, doesn't respond to other treatments or causes serious complication

Question 27

What is the time course of hordeolum vs. chalazion?

Answer 27

Most hordeola resolve spontaneously over one to two weeks and do not require specific intervention. Untreated, chalazia may take several weeks to months to resolve

Question 28

How do the s/s of hordeola differ from those of chalazia?

Answer 28

A hordeolum (stye) is an acute inflammation of the sebaceous glad of eyelid (near eyelash) that presents as a localized painful and erythematous swelling or nodule. A chalazion is red, swollen, typically painless localized swelling/nodule in eye.

Question 29

What is the pathophysiology behind external and internal hordeola?

Answer 29

External hordeola arise from glands in the eyelash follicle or lid-margin. Internal hordeola are caused by inflammation of the meibomian gland, resulting in swelling just under the conjunctival side of the eyelid. Staphylococcus aureus is the pathogen implicated in most cases, but hordeola can also be sterile. Hordeola sometimes transform into chalazia after the inflammation resolves.

Question 30

What are chalazia?

Answer 30

Non-infectious lipogranuloma of the Meibomian (oil-secreting gland) that often appears with hordeolum and appears as a deep nodule in eyelid. Chalazia and hordeola can have a similar appearance; however, chalazia tend to be painless and are less erythematous and angry-appearing. Hordeola sometimes transform into chalazia after the inflammation resolves.

Question 31

What is the management of hordiola?

Answer 31

Hordeola can be managed with warm, moist compresses placed on the affected areas frequently (eg, for 5 to 10 minutes at least twice a day) in order to facilitate drainage. Massage and gentle wiping of the affected eyelid after the warm compress can also aid in drainage. Patients should discontinue eye makeup to support healing. If, despite management with warm compresses, the lesion does not reduce in size within one to two weeks, the patient should be referred to an ophthalmologist for consideration of incision and drainage.

Question 32

What is the management of chalazia?

Answer 32

Draining can be facilitated by placing warm compresses on the eyelid for 5 to 10 minutes at least twice a day. Patients with lesions that do not resolve over one to two months should be referred to an ophthalmologist for consideration of incision and curettage or glucocorticoid injection.

Question 33

What structure provides blood supply to the retina?

Answer 33

The central retinal artery supplies blood to the inner retinal surface

Question 34

What are 3 possible causes for retinal ischemia?

Answer 34

1. Occlusion of the retinal artery, resulting in retinal hypo-perfusion. The blockage usually comes from a blood clot or cholesterol in the vessels. 2. Diabetes and glaucoma. 3. High blood pressure, aging.

Question 35

List the 3 structures of the external ear and briefly describe their function.

Answer 35

1. PINNA (auricle): Visible portion of the ear 2. EXTERNAL AUDITORY CANAL: -A tube that leads to the middle ear -Mastoid air cells are air filled sinuses in the mastoid process that promote conductivity of sound between the external and middle ear . 3. TYMPANIC MEMBRANE (ear drum): -Separates the external ear from the middle ear -Vibrates in response to sound waves entering the auditory canal -Causes vibration of the malleus in the middle ear

Question 36

The tympanic cavity, a small chamber in the temporal bone, is the area known as the middle ear. What 3 bones are found in this cavity, and what is their function?

Answer 36

Malleus (hammer), incus (anvil) and stapes (stirrup). The 3 small bones in the tympanic cavity transmit vibration of the tympanic membrane to the inner ear (malleus-->incus-->stapes). The stapes presses against the oval window, which is a small membrane of the inner ear. The oval window sets the fluid of the inner ear in motion.

Question 37

The oval window is a structure in the inner ear. What does it do?

Answer 37

The oval window is a small membrane that has contact with the stapes (stirrup). Vibrations from this membrane sets the fluid (perilymph) of the inner ear in motion.

Question 38

The bony labyrinth of the inner ear has 3 parts. What are they? Briefly describe their function.

Answer 38

1. Cochlea: transmits impulses along the cochlear nerve to the auditory cortex of temporal lobe in the brain where sound is interpreted. 2. Semicircular canals: contain equilibrium receptors that respond to changes in direction and movement. Impulses are sent via the vestibular nerve to the cerebellum 3. Vestibule: contains maculae which are receptors essential to the body’s static equilibrium – as the head moves, small pieces of calcium salts (otoliths) move in a gel-like material in response to changes in pull of gravity, which pulls on the gel, which pulls on the hair cells in the maculae. The hair cells then transmit signals to the brain. ***Semicircular canals and vestibule are important in the body’s ability to maintain balance through equilibrium receptors***

Question 39

Describe the functions of the eustachian tube.

Answer 39

Eustachian tube connects to the middle ear and the nasopharynx and acts as a valve. The tube is flat when closed, and opens briefly during swallowing, chewing and yawning to equalize the pressure in the middle ear. -equalizing allows the tympanic membrane (TM) to vibrate freely -tube has a mucosal lining filled with tiny cilia to clear out middle ear mucous secretions 3 functions: 1) equalizes pressure across eardrum 2) protects middle ear from nasopharynx fluid 3) clears out middle ear secretions

Question 40

What are some possible dysfunctions of the eustachian tube?

Answer 40

1) Functional issues: tube does not open because the tube is swollen or filled with secretions and block passage way. Cause: cold, allergies 2) Anatomical issues: tumors, scarring 3) Chemicals & Bacterial can enter the middle ear via the nasopharynx because: -The eustachian tube doesn’t close or stays open at all times. Congenital defect in which the tube is not structurally built with valve. -Short and Floppy Eustachian tube – provide little resistance against middle ear reflux during increased positive pressure on nasopharyngeal end of tube. When infant or child is crying or blowing nose – access point. 4) Cilia dyskinesia/dysfunction – cilia unable to clear middle ear mucous secretions. -Toxins like cigarette smoke can damage cilia – the cilia flick back and forth mvmt is impaired. -Cystic fibrosis cause for thicker secretions. If secretions are not cleared and are stagnant, infection can occur. S&S: pain, plugged-fullness sensation, muffled sounds, autophony (hearing ones own voice)

Question 41

How does eustachian tube defect contribute to acute otitis media?

Answer 41

Reflux or aspiration of secretions into the middle ear can occur, normally sterile environment may become infected with bacteria that contaminate through nasopharynx to middle ear.

Question 42

What is otitis media with effusion (OME)? How does eustachian tube defect contribute to OME?

Answer 42

OME is a presence of fluid in middle ear without symptoms of acute infection. Most common pediatric hearing loss cause. OME can occur in all ages. The eustachian tube may not be equalizing pressure effectively due to dysfunction, which leads to a build-up of fluid in the middle ear.

Question 43

What is this condition: -also known as iritis -inflammation of the uveal tract (iris, ciliary body, and choroid) and is usually accompanied by a dull ache and photophobia resulting from the irritative spasm of the pupillary sphincter. -specific cause is unknown, underlying causes include infections, viruses, and arthritis

Answer 43

Uveitis.

Question 44

What are some s/s of uveitis?

Answer 44

Eye pain: Painless to deep-seated ache Photophobia. Blurred vision with decreased visual acuity. Black spots. Eye redness. Unilateral or bilateral symptoms: (Unilateral: The pupil is smaller than that of the other eye because of spasm of the circular muscles of the iris. ) Ciliary flush. Nausea and vomiting with vagal stimulation Halos around lights Hypopyon (pus in anterior chamber) Limbal flush with small pupil

Question 45

How is uveitis diagnosed?

Answer 45

These will be done by an ophthalmologist, as the client needs immediate referral: A. Slit-lamp test: Slit-lamp examination reveals cells in the anterior chamber and “flare,” representing increased aqueous humour protein. Inflammatory cells, called keratic precipitates, can collect in clusters on the posterior cornea. B. Penlight examination: Flashlight examination shows a slightly cloudy anterior chamber in the uveitic eye.

Question 46

Touch on treatment and management of uveitis.

Answer 46

General interventions: -Treat underlying cause as indicated. -Provide immediate referral to an ophthalmologist due to possible complications of cataracts and blindness. Client teaching: -Inform the client that recurrent attacks are common and also require immediate attention Pharmacological therapy: -Medications are given per ophthalmologist. -Uveitis and colitis often flare simultaneously; oral steroids are effective for both.

Question 47

What pharmacological therapies are available to treat tinnitus?

Answer 47

1. No medication “cures” tinnitus. 2. Vasodilators, tranquilizers, antidepressants, and seizure medications have been shown to reduce symptoms. 3. Placebos are also of therapeutic value.

Question 48

What is the condition? Pathology is poorly understood. It is best described as a nonspecific manifestation of pathology of the inner ear, eighth cranial nerve, or the central auditory mechanism. an be unilateral or bilateral and can be triggered anywhere along the auditory pathway. If generated by the central nervous system: can be unilateral or bilateral, and the side of the presentation may not always correspond with the side of initial injury. Positron-emission tomography (PET) scanning and functional magnetic resonance imaging (MRI) studies indicate that the loss of cochlear input to neurons in the central auditory pathways

Answer 48

Tinnitus.

Question 49

What is the difference between ulcerative and nonulcerative keratitis?

Answer 49

Keratitis is inflammation of the cornea. Nonulcerative keratitis is usually limited to the epithelial layer; a superficial infection of the corneal that doesn’t lead to corneal ulcers. It affects just the epithelium of the cornea. Etiology, S/S, causes and epidemiology are similar to ulcerative keratitis.

Question 50

How does ulcerative keratitis (inflammation of the cornea) occur and develop?

Answer 50

Infection of the cornea caused by bacteria, fungi or viruses. Bacterial infection is the most common cause. Herpes simplex virus can cause a viral infection. Acanthamoeba can cause a parasitic infection and is common with contact lenses wearers related to poor hygiene. Contact lens, abrasion or minor trauma can lead to a tear in the corneal layer allowing bacteria to enter. Bacteria enters through the abrasion where they proliferate and cause open sores or ulceration in the stroma. Infection extends beyond the epithelial layer to the stroma and beyond. Inflammatory cells surround the beginning ulcer and cause necrosis. This leads to diffusion of inflammatory cells causing further corneal damage. This can lead to corneal scarring, corneal thinning and perforation and infection extending to the whole eye or surrounding tissues. Ulcerative keratitis is vision threatening and requires quick diagnosis and intervention.

Question 51

What are the s/s of keratitis?

Answer 51

Eye redness, pain, excessive tearing, foreign body sensation, photophobia, decreased vision. Fluorescein eye stain shows damage to the corneal abrasion or ulcerations.

Question 52

What are some treatment options for keratitis?

Answer 52

Antibiotics, corticosteroids, UV irradiation of corneal ulcer and corneal transplant if scarring is severe or corneal perforation.

Question 53

What contributes most to poorer outcomes in diabetic retinopathy?

Answer 53

Poorly controlled diabetes. A1C >7.5% patient is at increased risk.

Question 54

What are the s/s of diabetic retinopathy vs hypertensive retinopathy?

Answer 54

Diabetic retinopathy is usually asymptomatic. Later stages may have decreased vision, possibly floaters. Routine eye exams are recommended for all patients with diabetes because of the slow progression (10-20 years) and lack of symptoms until advanced stages. Hypertensive retinopathy is mostly asymptomatic but patients may c/o headaches, decreased/blurry vision. Vision loss is rare but may can follow optic atrophy or retinal detachment, which is possible with severe HTN.

Question 55

Diabetic retinopathy results from microvascular end-organ damage as a result of diabetes mellitus. What are the two types of diabetic retinopathy?

Answer 55

Non-proliferative: More common form. Walls of blood vessels are weakened over time, leaking fluid and blood into the retina. Proliferative: Damaged blood vessels become non-functioning, leading to proliferation of new blood vessels (angiogenesis), that are weak and can leak into the vitreous. Scar tissue from angiogenesis can eventually lead to retinal detachment. Retinal angiogenesis is due to upregulation of vascular endothelial growth factor, or VEGF.

Question 56

What are the 3 phases of hypertensive retinopathy? Briefly describe them.

Answer 56

VASOCONSTRICTIVE PHASE: Microvascular retinal changes occur in response to acute or chronic HTN. Acute: autoregulation -> arteriolar narrowing. SCLEROTIC PHASE: Chronic: structural changes consistent with arteriosclerosis. Endothelial wall damage is seen. EXUDATIVE PHASE: (May occur acutely without sclerotic activity.) The blood-retina barrier is disrupted and can lead to smooth muscle necrosis. Leaking blood and plasma can obliterate the vascular lumen. **Poor perfusion can lead to atrophy, ischemia and even retinal detachments. **Phases are not necessarily sequential.

Question 57

Through which examination are both diabetic and hypertensive retinopathy diagnosed?

Answer 57

Dilated fundoscopy by an optometrist.

Question 58

What are some of the things that might be seen via dilated fundoscopy if a person has diabetic retinopathy?

Answer 58

Non-proliferative: -Flame hemorrhages (bleeding into superficial nerve fibres) -Retinal microaneurysms -Cotton -wool spots (nerve fibre microinfarctions) -Hard exudates (Lipo-proteins, common feature) -Macular edema (Fluid and proteins collect on or under the macula. An ominous finding.) Proliferative: Can include same findings as non-proliferative, as well as one or more of: -Presence of retinal or optic disc neovascularization. Retinal angiogenesis is hallmark. -Vitreous hemorrhage -Retinal detachment -Glaucoma due to buildup of pressure in eye damaging the optic nerve

Question 59

What are some of the things that might be seen via dilated fundoscopy if a person has diabetic retinopathy?

Answer 59

-Flame hemorrhages (bleeding into superficial nerve fibres) -Arteriovenous nicking – atherosclerotic arteries compress adjacent veins at nearly perpendicular angles -Retinal microaneurysms -Cotton-wool spots (nerve fibre microinfarctions) -Macular star – white/yellow lipid deposit -Bleeding into inner retinal layer (dot-blot hemorrhages) -Papilledema – swelling of the optic disc (in severe cases of uncontrolled HTN

Question 60

What are the treatment options to consider if your patient is diagnosed with diabetic retinopathy?

Answer 60

Treating diabetes slows disease progression Glycemic control Diabetes medication Interventions specific to retinopathy may include: -Photocoagulation – high powered pulse laser to reduce retinal angiogenesis -VEGF (vascular endothelial growth factor) inhibitors -Surgeries such as iridotomy, vitrectomy or retinal repair, may be options to treat proliferative retinopathy

Question 61

What are the treatment options to consider if your patient is diagnosed with hypertensive retinopathy?

Answer 61

Control HTN. Increased risk for CAD and stroke if retinopathy has already developed. Antihypertensives Smoking cessation.

Question 62

What follow-up recommendations and patient teachings should you include if your patient has been diagnosed with diabetic retinopathy?

Answer 62

Routine fundoscopic eye exams Routine BW to monitor A1C Diabetes teachings – nutrition, exercise. Regular eye exams.

Question 63

What follow-up recommendations and patient teachings should you include if your patient has been diagnosed with hypertensive retinopathy?

Answer 63

Monitor HTN Reassess fundus until resolution, then routine follow up exams HTN teachings: decreased sodium, weight loss, exercise.

Question 64

What are the 3 types of conjunctivitis?

Answer 64

Bacterial -caused by bacteria, often types of staphylococcus or streptococcus. Spread through poor hygiene or contact with other people or insects, results in a thick, sticky discharge from the eye Viral - Most viruses that cause conjunctivitis spread through hand-to-eye contact by hands or objects that are contaminated with the infectious virus Allergic - The pathogenesis of allergic conjunctivitis is predominantly an IgE-mediated hypersensitivity reaction. Activation of mast cells induces enhanced tear levels of histamine, tryptase, prostaglandins and leukotrienes

Question 65

"Dizziness caused from crystals moving into semicircular canals that obstruct the normal flow of endolymph." Is this BPPV, Meniere's Disease, or Labyrinthitis?

Answer 65

BPPV

Question 66

"Dizziness, hearing loss, tinnitus caused by build up of fluid – endolymph in inner ear." Is this BPPV, Meniere's Disease, or Labyrinthitis?

Answer 66

Meniere's Disease

Question 67

"Viral or post-viral inflammatory disorder affecting the inner ear. Inflammation causes vertigo AKA Vestibular Neuritis." Is this BPPV, Meniere's Disease, or Labyrinthitis?

Answer 67

Labyrinthitis

Question 68

There are a few s/s that can help you to differentiate Meniere's Disease from BPPV. What are they?

Answer 68

Vertigo – feeling that you or your surroundings are spinning that can minutes to hours often accompanied by severe nausea and vomiting. This occurs in BPPV but is often less than 1 minute in duration. Tinnitus – can be constant or fluctuate. Pitch and intensity vary Hearing loss – can be temporary or permanent. Usually fluctuates and often initially affects only the lower frequencies. Typically progresses and often results in permanent hearing loss at all frequencies Some patients have a feeling of pressure or fullness in the ear. Some with Meniere’s disease experience “drop attacks” or sudden fall that occurs without warning while standing or walking.

Question 69

Otitis externa is an infection that usually follows prolonged exposure to moisture ( AKA swimmer's ear). It may be associated with swimming, irritation or the introduction of organisms when cleaning the ear, or frequent use of earphones or earplugs. If the presentation becomes recurrent or chronic, what are the likely causes to consider?

Answer 69

Allergies and/or skin disorders.

Question 70

What condition are we talking about here? -Result of allergies or infection in the mucosa of the nasopharynx and respiratory structures. -Most common pathogens are S. pneumoniae, Haemophilus influenzae, and M. catarrhalis. -Increasing incidence of penicillin-resistant microorganisms. -May also be caused by viral infection and secondary bacterial infection. -Scar tissue due to rupture/damage/ adhesions to the tympanic membrane may cause hearing damage

Answer 70

Acute otitis media (AOM) with effusion.

Question 71

Briefly describe the differences between conductive hearing loss and sensorineural hearing loss.

Answer 71

Conductive hearing loss is a result of an obstruction of some sort - impacted cerumen, foreign bodies, benign tumors of middle ear, carcinoma external auditory canal or middle ear, eustachian tube disfunction, Otis media, cholesteatoma, otosclerosis . Sensorineural hearing loss is the impairment of organ of corti or its central connections causing hearing loss . Can be due to: -Impairment of hair cells function of organ of corti (Recap: outer hair cells = making soft sounds louder, inner hair cells = convert movement of fluid into electrical signals). -Damaged or missing Hair cells causing impaired transmission of sound to hearing nerve.

Question 72

What is presbycusis and what are the most common causes?

Answer 72

Presbycusis is age-related hearing loss. Possible contributing factors are atrophy of basal end of the organ corti, loss of auditory receptors, vascular changes or stiffness of basilar membrane.

Question 73

What are some risk factors for acute bacterial rhinosinusitis?

Answer 73

-recent urti -allergens -nicotine/ smoke exposure -air pollutants -deviated septum -adenoidal hypertrophy -dental abscess -diving and swimming -neoplasms -cystic fibrosis -trauma -medical disorders -flying or rapid altitude changes

Question 74

What are some risk factors for chronic bacterial rhinosinusitis?

Answer 74

-smoking -lower income -hx allergies -asthma -COPD -allergic rhinitis -gerd -F>M