1. Review the anatomy of the throat – from exam 2…
• Hard and soft palate, anterior pillar, posterior pillar, palatine tonsils
2. What is trismus?
• Spasm of facial and jaw muscles - unable to open mouth fully - similar to lockjaw
• Child - drooling, unable to swallow, muffled voice
• MBDT peritonsillar abscess or damage to trigeminal nerve
3. How is peritonsillar abscess (Quinsy) diagnosed?
• Trismus – although not specific for PTA
• Unilaterally enlarged tonsil with displaced uvula
• Tender cervical nodes on same side
• Less severe form - peritonsillar cellulitis - can treat with oral antibiotics
• Ultrasound and CT scanning are useful in confirming diagnosis
• Needle aspiration is the gold standard for diagnosis and treatment
4. What are the suppurative complications of poorly or untreated pharyngitis?
5. What is Ludwig’s Angina? – (angina means strangling) – fatal if untreated
• Infection in submental (submandibular) space
• Rapidly spreading, bilateral, indurated cellulitis occurring in both the submandibular and submaxillary spaces – no abscess formation or lymphatic involvement
• Not a true abscess but clinically resembles one and is treated the same
• Usu develops from dental or periodontal infxn – esp 2nd 3rd mandibular molars
• Px: Severe trismus, drooling, and airway compromise, fever, chills, tachycardia
• Collar of brawny edema (neck), elevation of tongue, possible airway obstruction
• Complications – asphyxiation, aspiration pneumonia, lung abscess, metastatic sepsis
• Can lead to chest pain, the more classic “angina” if infection spreads to sub-sternal space
6. Be familiar with the DDX of chronic sore throat.
• Infectious – can become chronic
Reflux pharyngitis – (heartburn)
Toxins - sick house syndrome; smoking; solvent use
Improper vocal cord hygiene, vocal abuse
Chronic cough - constant clearing irritation
o Nasal and oral pharyngeal carcinoma
o Laryngeal carcinoma
o Upper esophageal carcinoma
o Tumor under the sternum
7. What is globus, what are the common causes? * Globus means “lump”
o Thyroglossal cyst
o Mucosal edema – dt reflux – 50% of cases
o Barrett’s metaplasia – can cause strictures or webs
o Cervical osteophytes
o Neck masses - NOS
o Globus hystericus – subjective sensation of a lump in the throat - rare
8. Know how to work up hoarseness, when is referral needed and why?
• Don’t have to know this for final – if you want this article – or a similar one, go to http://www.aafp.org/afp/980600ap/rosen.html
9. Know diagnostic criteria for croup and epiglottitis.
• Most common in 2-5 year old - tends to run a very fulminant course
• Adults rarely get- runs a much more benign course
• Infectious agents - Haemophilus Influenzae type B is most common.
o Sore throat
o High fever (over 102)
o Weak or hot potato voice
o Marked drooling
o Sit very upright with head forward and neck extended
o Stridor (harsh high-pitched sounds – 2° to obstruction) a late and ominous sign.
o Physical Exam
Trismus - painful/difficulty to open mouth and swallow, excess drooling
Inspect uvula for swelling
Visualization of the supraglottic area is contraindicated in children
Thumb print sign - a broadening and flattening of the epiglottis
• 90% of time viral; RSV
• Most prevalent in infant to 5 year old age group
• More common in fall and spring
Viral Croup - most cases of viral croup can safely be managed at home
Signs and Symptoms
• Inspiratory stridor
• Barking cough; paroxysmal cough
• Starts as URI with low grade fever
o Coryza --> cough that goes into barking cough on 2nd or 3rd day
• Worst at night; can be absolutely fine during day
o Also called tracheitis
o First 3-5 days - picture very similar to viral croup
o After that period - patient gets really sick, really fast
o Respiratory distress – hypoxia – signs for hospitalization
o Treatment - IV antibiotics and intubation
10. How do you treat croup?
Depends on etiology – viral croup – can be treated at home
o Homeopathy - Acon, Spong, Hepar, Drosera
o Warm showers
o Humidifiers – cool
o Echatin Plus
o Compound liniment with Stillingia
Bacterial croup is treated in the hospital with IV abx and intubation
From the Article on Sleep apnea
11. What is the typical history in a patient who presents with sleep apnea?
• Obese - male
• Loud snoring, gasping
• Restless sleep
• Daytime somnolence
• Paroxysmal nocturnal dypsnea
• Morning headache or disorientation
• Severe disease can → impaired cognitive function, behavorial and personality changes
• Increased risk for MVA’s
12. What is the morbidity of sleep apnea?
Obesity is MC risk factor
• Obesity (usu dt insulin resistance) - is mc risk factor for OSA – share common patholgies
o Airway patency affected by narrowing dt hypertrophy and fat deposits surrounding the collapsible region of pharynx
o Central obesity - characterized by ↑ brown adipose tissue - an important source of leptin – too much leptin production → leptin resistance → metabolic and respiratory derangements, including OSA.
Obese pts have high serum leptin levels (assumed to be tissue deficiency)
Leptin modulates respiratory physiology
Leptin deficiency and resistance → deficits in nocturnal respiratory control
o Sympathetic activation - increased in obese pts – mb associated ć leptin resistance
Morbidities associated with sleep apnea: HTN, Heart Failure, Pulmonary HTN, CAD, CVA
• Hypertension – OSA → 3 x risk of HTN
o 50 % of OSA pts have HTN, and 50% of HTN pts have OSA!
o Acute elevations in BP occur during apnic episodes – may extend into waking hours
• Heart Failure
o OSA → ↑ muscle sympathetic nerve activity and ↑ plasma noradrenaline levels.
o Death caused by heart failure relates directly to increased sympathetic drive
• Pulmonary HTN
o Apnea → vasoconstriction of the pulmonary arterial bed.
o When severe, these changes extend into the waking hours
o OSA may trigger acute ischemia → predisposition to more chronic conditions, such as atherosclerotic vascular disease.
o Risk factors include inflammation, hyperleptinemia, chronic sympathetic activation, and endothelial dysfunction.
o Acute derangements in cerebral perfusion, coagulation proteins and blood pressure occurring during obstructive apneas may contribute to neurologic events, even though most of these events occur during the daytime in patients with OSA
13. How does one make the diagnosis of sleep apnea?
• Polysomnography is the gold standard for diagnosing OSA
14. What are a patient’s treatment options for sleep apnea?
Mechanical devices such as nasal CPAP
Surgery for craniofacial abnormalities
Bariatric surgery – nearly always cures OSA
15. How is Bordatella pertussis spread?
16. What are the 3 phases of the condition (pertussis)? Can last 1 – 5 months
Catarrhal – resembles viral URI – lasts 1-2 weeks
Parosysmal – whooping cough, emesis, cyanosis – lasts 1-6 weeks
Convalescent – paroxysms gradually improve over 2-12 weeks
17. How effective are vaccines? How long is immunity conferred?
o Immunity from vaccinations is short-lived and incomplete.
o Immunity declines after 4-12 years causing adolescent and adult susceptibility
18. What complications are associated with bad cases of pertussis?
• Asphyxia and or/ convulsions - infants
• Bronchiectasis – esp in debilitated children
• Bronchopneumonia and residual emphysema in elderly
• Atelectasis – if mucus plug occludes a bronchiole
• Severe paroxysms can → OM, cerebral hemorrhage, umbilical hernia and rectal prolapse.
o Pneumonia is 1°
o Acute dehydration and malnutrition, weight loss
o Sleep disturbance,
o Cerebral hypoxia → seizures, and, rarely, encephalopathy or death.
19. What age group is most at risk for these complications?
Children and elderly
Young infants at greatest risk for 2° bacterial pneumonia – MCC death from pertussis
20. Which diagnostic test has the greatest sensitivity for detecting pertussis infection?
PCR - Sensitivity of 94% and Specificity of 97%
21. How are specimens for testing collected?
A polyester swab of the nasopharynx - should be inserted into the base of a nostril and left in the posterior pharynx for 10 seconds before withdrawing.
Nasopharyngeal aspirates yield better sample, but equipment required for aspirates is not widely available.
22. Is pertussis reportable to County Health Departments? Yes
23. Be familiar with The CDC Case definition for Pertussis
a. Cough lasting more than 2 weeks that develops a paroxysmal quality
b. Inspiratory whooping, or post-tussive emesis
c. Infants with severe cough, apnea, or bradycardia for any length of time.
Study Questions - Eye
24. Review the anatomy of the eye
Bulbar conjunctiva - corner of eye
Palpebral conjunctiva - under surface of lids
Touches fibrous tissue making up the white of the eye
Preserves the shape and protects the delicate inner layers
Cornea - transparent anterior segment of outer coat
• Allows passage of light through outer coat
• Covering over pupil; protects pupil
• Very highly innervated (CN V - corneal reflex) – by ophthalmic branch of trigeminal nerve
Pupil - circular opening in iris; entry point for light
Iris - colored muscular ring surrounding the pupil
Connects with ciliary body
Controls the pupil
• Responsible for mydriasis (dilation) and myosis (constriction) of pupil
Ciliary body - connective tissue and smooth muscle
Function - produces aqueous humour - fills anterior chambers
Acts as media for light refraction
Vitreous body – transparent jelly-like substance filling interior eyeball behind the lens
A delicate network (vitreous stroma) enclosing a watery fluid (vitreous humor)
Lens - directly behind pupil
Function - bring light rays to focus on retina through refraction
Choroid - vascular coats of sclera; highly pigmented; major blood supply to eye
Retina - lining in back of the eye
Receptors - rods and cones which transfer light into neuronal impulses
Rods - very sensitive to light; insensitive to color; night vision, dim light
Cones - highly sensitive to color with increased visual acuity
Macula Lutea -a yellow spot in the center of the retina located 2 cm lateral to optic disk
Fovea centralis - pit in middle of macula lutea;
Optical pathway of direct light – has highest concentration of cones
Optic disk - where fibers from rods and cone stream into the optic nerve, CN II
Physiological cup - source of blind spot
25. What is amblyopia? How and when is it best detected?
Amblyopia occurs when a child does not use one eye.
Neurones from retina of unused eye to the brain fail to develop → suppression of images.
3 main causes
o Congenital cataracts
o Refractive errors
Detection of amblyopia:
o Screening = Hirschberg corneal reflection testing
o Cover/Uncover test - child will often cry when "good" eye is covered
26. How do you manage trauma to the eye? What are some common remedies?
o Ice the first day, alterating ice and heat 2nd and 3rd
o Bromelain, plant enzymes
• Aconite- Trauma and abrasions to the cornea of the eye
• Symphytum - specific for blunt trauma to the eye and orbit
• Arnica - for injuries to the orbit, with typical arnica picture
27. What is a subconjunctival hemorrhage?
o Spontaneous appearing patch of hemorrhage over the sclera, painless; normal vision
28. Be very familiar with the DDX of the red eye.
DDX for red eye which is painful:
• Corneal abrasions (usually easy to get from history) - foreign bodies
• Ulcer or infection
• Keratitis (inflammation of cornea)
• Acute angle closure glaucoma
• Iritis - involves more superficial structures
• Uveitis - involves more of middle and posterior eye structures
o Inflammation of iris, ciliary body and choroid, or the entire uvea
DDX for red eye which is not painful
• Subconjunctival hemorrhage - vision is fine; treat to help resolve
• Conjunctivitis - allergic, viral, bacterial and toxic
• MH mild discomfort usually described as scratchiness or sand in eye; not significant pain
• Significant pain - implies involvement of cornea or iris
DDX for red eye with impaired vision
Always ask patients with a red eye if they have impaired vision.
• Acute glaucoma - refer immediately
• Corneal disease
DDX if eye is painful, but not red - consider referred pain from sinuses, orbit and nose, may be neuropathic--from trigeminal neuralgia, herpes zoster, CNS disorders
29. Know how to differentiate by history and physical exam conjunctivitis from iritis.
o Exposure to infections or irritants
o Recent URI
o Systemic inflammatory disease
o Ocular trauma or surgery
o Acute to sub-acute onset – although cb chronic in some cases
o Peripheral injection – spares iris
o Hyperacute dt neisseria – px ć very edematous eyelids ć copious thick, purulent d/c
o Viral – comes on after URI – eyelid mildly edematous ć morning crusting
o Bacterial – eyelid mb edematous ć mild to moderate thick yellow d/c and crusting
o Ciliary injection
o Refraction error not improved with pinhole test
o Pupil small, irregular, poorly reactive
o The sine qua non of anterior uveitis is the presence of cells and flare in the anterior chamber (like lights in fog) with a slit lamp exam
30. What is ciliary injection, versus peripheral injection?
Ciliary injection (iritis) Peripheral injection (conjunctivitis)
31. What is hyperacute conjunctivitis?
• Presentation – acute red swollen eye, swollen eyelids and copious thick purulent discharge
• Onset – comes on extremely fast
• Secondary to Neisseria gonococcal infection
32. What technique will help you visualize corneal abrasions?
o Fluorescein dye and cobalt blue light
o Abrasions will take up fluorescein and appear apple-green under cobalt light
33. Know the treatments for bacterial conjunctivitis.
o Eye irrigation: using botanical formulas or normal saline
o Wash medial to lateral, to avoid infection of the lachrymal apparatus.
o Infants – drop breast milk into eyes
o Antibiotics: Erythromycin ophthalmic ointment
o Cochrane Review: abx hasten remission of bacterial conjunctivitis
o Cool compresses, using any of the eyewashes noted below
34. Know how to diagnose Hordeolum, Chalazion, Blepharitis, Dacryocystitis.
Localized infection or inflammation of the eyelid margin involving hair follicles of the eyelashes (ie, external hordeolum) or meibomian glands (ie, internal hordeolum)
Chalazion – a painless granuloma of the meibomian glands.
Blepharitis - inflammation of the eyelids.
Dx: Foreign body or burning sensation, excessive tearing, itching, photophobia, red and swollen eyelids, red dry eye, blurred vision, frothy tears, or crusting of the eyelashes on awakening.
• Anterior blepharitis affects the outside front of the eyelid, where the eyelashes are attached. The two most common causes of anterior blepharitis are Staphylococcus and scalp dandruff.
• Posterior blepharitis affects the inner eyelid (the moist part that makes contact with the eye) and is caused by problems with the oil (meibomian) glands in this part of the eyelid.
o Two skin disorders can cause this form of blepharitis:
Rosacea and seborrheic dermatitis of the scalp (scalp dandruff).
Dacrocystitis/dacrocystenosis – obstruction of naso-lacrimal duct
Symptoms of tearing and bacterial super infection.
To assess patency apply fluorescein to the effected eye and insert a cotton swab in the ipsilateral nares
The dye should be appreciated on the swab within a minute if the canal is patent.
35. Know History, PE and risk factors for cataracts. Be able to suggest treatments.
History - Patients' will complain of gradual loss of vision, hard to drive at night
Ophthalmoscopic exam to help rule out other intraocular disease (macular degeneration)
1) Red reflex decreased or absent
2) If you can see in, then the patient can see out - so probably not cataracts
Risk Factors for cataracts
1) Ocular disease, injury, surgery
2) Diabetes mellitus
4) UV light
7) Slow acetylators are at higher risk of developing age-related cataracts than fast
acetylators. N-acetylation metabolizes xenobiotics such as UVB, smoking, and alcohol,
which may induce cataract formation.
Treatment of cataracts
o Avoid UV exposure – wear lenses with 100% UV block
o Increase antioxidants, especially quercetin and other flavanoids
o Supplement with NAC, ALA, gingko
36. Know history, risk factors, diagnostic criteria, pathophysiology and treatments for glaucoma
• Epidemiology: Major cause of irreversible blindness.
• Prevalence- profoundly affected by age and ethnicity
• Age, ethnicity
• ↑ intraocular pressure, myopia
• Diabetes, HTN,
• High EtOH intake in Caucasians
• Family history of glaucoma
o Loss of peripheral vision initially → loss of central visual acuity.
o PE reveals loss of peripheral fields on confrontation.
o Increased cup to disc ratio on ophthalmoscopic exam [Glaucomatous cupping]
o Increased intra-ocular pressure (IOP)
• Pathogenesis: 3 primary theories:
o Mechanical (IOP related)
o Vascular mechanism.
o Glutamate toxicity
Allopathic treatment of POAG
o Aimed at treating high intraocular pressure (IOP)
o Primarily use beta blockers (timolol, betaxololol), cholinergic agents (pilocarpine)
o Drugs to decrease aqueous secretion
o Surgery to enlarge the canal of Schlemm (trabeculectomy)
Naturopathic Treatment of POAG:
• Treat underlying disorder: diabetes, hypertension, and hypothyroidism
• Avoid vasoconstrictors, i.e. caffeine, nicotine...
• Avoid excess fluid intake
• Stress management.
• Autogenic training can decrease IOP – note that pts ć glaucoma are more emotionally unstable and have a heightened response to stressful situations.
• Vit C, high dose, IV best but IM is OK
• Bilberry extract and bioflavonoids
• Botanical eye drops
• Ginkgo biloba
• Alpha Lipoic acid - 150 mg/day
• Vitamin B12
• Cannabis and cannabinoids will lower IOP. The mechanism is not clear but it is thought to decrease aqueous formation in the ciliary body
37. Know signs and symptoms of acute angle closure glaucoma and keratitis (read Merck).
Acute Angle Closure Glaucoma characteristically presents with:
• Red eye, nausea, vomiting, and diminished vision.
• Symptom may begin after exposure to a dark environment.
• Perilimbal injection
o Cornea is cloudy and the anterior angle is narrow
o Pupil is fixed and dilated
o *Tactile tonometry is firm (only manifests if pressure is over 30 mm Hg)
*Assessment of IOP by palpation – success not validated
o This is an ocular emergency that requires emergency ophthalmologic assessment to prevent blindness.
Interstititial Keratitis – refer to opthamologist (Merck)
• Chronic, non-ulcerative infiltration of deep layers of cornea
• Often associated with uveitis
Peripheral Ulcerative Keratitis – refer to opthamologist (Merck)
• Peripheral corneal inflammation and ulceration
• Often associated with active collagen vascular diseases
o RA, Wegeners granulomatosis, relapsing polychondritis
Keratitis Sicca (Merck)
• Chronic, B/L dessication of conjunctiva and cornea
• MBDT inadequate tear volume
• MBDT xs loss of tears dt accelerated evaporation because of poor tear quality.
• Tx = frequent use of artificial tears
Herpes simplex keratitis – (keratoconjunctivitis) (Merck and Eileen H)
• HSV infection of the cornea
• Commonly → recurring corneal inflammation, ulceration, scarring and loss of vision
• Initial lesion usu simple conjunctivitis accompanied by vesicular blepharitis
• Recurrences usu in form of epithelial keratitis, characterized by dendritic lesions (branched lesion of corneal epithelium resembling the veins of a leaf)
• Multiple recurrences of dendritic lesions can lead to disciform keratitis involving the corneal stroma
This is a deeper, disc shaped, localized area of corneal edema and haze ć iritis
MBDT to immunologic response to the virus
Superficial Punctate Keratitis (aka SPK)
Scattered, fine, punctate damage to epithelium of the corneal surface of the eye
• Viral conjunctivitis - resolves spontaneously in about 3 weeks.
• Over-wearing contact lenses
• Staph blepharitis
• Keratitis sicca
• UV light exposure, welding arcs, sunlamps
Symptoms: photophobia, foreign-body sensation, lacrimation, conjunctival hyperemia, and decreased visual acuity.
• Slit Lamp Exam: Numerous superficial lesions that will stain with fluorescein dye.
o Epithelium may be eroded.
• SPK resolves spontaneously in about 3 weeks if dt viral conjunctivitis
o If dt contact lenses, tx ć abx ointment or drops – DO NOT PATCH
• Blepharitis, trachoma, and keratitis sicca require specific therapy.
• Ultraviolet light exposure is treated with short-acting cycloplegic drugs, an antibiotic ointment, and patching for 24 h.
38. Know treatments for macular degeneration. Know the difference between Dry and Wet ARMD.
AGE RELATED MACULAR DEGENERATION (ARMD)
o Progressive visual loss due to degeneration of the macula lutea
o Macula is the area of greatest visual acuity. 8% of 75 year olds have some degree of ARMD
o 2 types - WET and DRY
Dry Macular Degeneration 80-95% of cases
Signs and Symptoms:
o Straight objects appear distorted or bent
o Dark spot around center of visual field
o Parts of words are missing while reading - often must use magnifying glass to read.
o Onset is slow and peripheral vision remains intact.
o Drusen bodies are evident before the onset of central vision loss,
Presence of Drusen increase likelihood of developing ARMD by 23%.
Risk Factors: Age, Smoking, family history, hypertension, obesity, hyperlipidemia, oxidative stress, Caucasian race, sun exposure. There is a very high association between cardiovascular risk factors and ARMD.
Treatment: Control atherosclerosis, patients with confirmed atherosclerosis (carotid bruits, retinal AV changes) have a 4.7 times increased prevalence of ARMD. Smoking cessation is essential because oxidative damage contributes significantly to the progression of the disease.
Wet Macular Degeneration
• Characterized by growth of abnormal blood vessels
• Intra-vitreous injection of anti-VEGF (Vascular endothelial growth factor) monoclonal antibodies is a very promising treatment.
• Lutein – Zeaxanthin
• IV Therapy