Exam 2 Flashcards
Describe a lesion
General term that describes any pathological skin change or occurence
Describe an exanthem
Any cutaneous eruption or rash that accompanies a disease, more widespread skin involvement
Describe an enanthem
Lesions or rash found inside the body on mucosal membranes
Describe a macule
Flat, circumscribed area that is a change in color of surrounding skin.
Less than 2 cm. can be any color
Describe a papule
An elevated, firm, circumscribed area
Less than 1 cm in diameter
Describe a patch
A flat, non palpable, irregularly shaped macule
Greater than 1 cm in diameter
Describe a plaque
An elevated, firm and rough lesion with a flat top surface
Often a confluence of papules
Greater than 1 cm in diameter
Describe a wheal
Elevated, irregular-shaped area of cutaneous edema and swelling, also known as hives
Solid, transient, variable diameter
Describe dermatographism
Most common form of physical urticaria
Firmly stroking unaffected skin will produce a wheal along the shape of the stroke within seconds to minutes
Describe a nodule
Elevated, firm, circumscribed lesion that is deeper in the dermis than a papule
Greater than 1 cm in diameter
Describe a tumor
Elevated and solid lesion, deeper in dermis, greater than 2 cm
Describe a vesiccle
Elevated, circumscribed, superficial, not into dermis, filled with serous fluid
Less than 1 cm in diameter
Describe a bulla
Vesicle greater than 1 cm in diameter
Describe a pustule
Elevated, superficial lesion that is similar to a vesicle but filled with purulent fluid. May be white, yellow, or greenish yellow
Describe a cyst
Elevated, circumscribed, encapsulated lesion in dermis or subQ layer, filled with solid or semisolid material.
Spherical or oval shape
Describe telangiectasia
Fine, irregular red lines produced by persistent capillary dilation
Describe scale
Accumulation or abnormal shedding of strateum corneum, heaped up keratinized cells
Flaky, irregular, thick or thin, dry or oily, variation in size, adherent or loose
Describe lichenification
Rough, thickened epidermis (resembles tree bark)
Secondary to persistent rubbing, itching or skin irritation
Describe excoriation
Loss of the epidermis, linear, hollowed out crusted area, results from scratching
Describe fissure
Linear crack or break from the epidermis to the dermis
May be moist or dry
Describe erosion
Loss of part of the epidermis or mucosal epithelium
Depressed, moist, glistening
Often follows rupture of a vesicle or bulla, heals without scarring
Describe an ulcer
Loss of epidermis and dermis, concave, vary in size, heals with scar formation
Describe crust
Dried serum, blood, or purulent exudates. Slightly elevated, size varies
Describe atrophy
Thinning of skin surface and loss of skin markings
Skin translucent and paper like
Dermal melanosis, aka…
Mongolian spot
Describe dermal melanosis
Congenital macule/patch
Blue-grey, may be large, sacral/gluteal location
How long do Mongolian spots stay on the skin?
Usually fade in the first 1-2 years of life, common in Asian/black/Hispanic babies
Describe neous of Ota
Distribution on the 1st and 2nd branches of trigeminal nerve (CN V)
Can evolve to melanoma
A dermal melanocytose
Describe nevus of Ito
Congenital dermal melanocytosis
Posterior supraclavicular nerve
Describe blue nevi
Benign dermal proliferation of melanocytes, actively producing melanin
What is the Tyndall effect?
Blue color resulting in blue nevi from scattering of light by melanin
Blue nevi typical presentation?
Blue to blue-black domed papule that preserves skin markings.
Usually less than 1 cm.
Describe cafe au lait macules
Brown macule, 2 mm - larger than 15 cm. enlarge with growth, uniform color
How to CALM and neurofibromatosis relate?
> 6 CALMS that are greater than 1.5 cm are highly suggestive of NF-1
Describe congenital melanocytic nevi (CMN)
Present at birth or in first few months of life
Variable size, pebbly surface, extend deep into dermis and can track along neurovascular, adnexal structures
What is the main risk with CMN?
Melanoma
If large or evolving, removal is preferred
Describe ephelides
Irregular macules (freckles)
Increase with sun exposure
No risk of malignant change
Describe lentigines
Lentigo=sharply defined macule
Biopsy if growing!
Describe solar lentigines
Liver spots, benign and discrete hyper pigmented macules on sun exposed areas
Peutz-Jeghers syndrome
Autosomal dominant, pigmented macules on lips/oral mucosa/perinanal areas
Associated with GI polyps, lentigines syndrome
Describe xeroderma pigmentosum
Autosomal recessive, dark numerous freckles in dark-skinned individuals
Increase risk in skin CA, vision and hearing issues, and neuro disease
Dermatosis papulosa nigra
Papular lesions more akin to seborrheic keratosis
Common nevi can be three types…
Junctional - FLAT
Compound - PAPULAR
Intradermal - DERMIS ONLY
What is the ABCDE skin exam?
Asymmetry Border Color Diameter Evolving
Seborrheic keratosis
Warty, crusty, stuck on appearing papules, most common on trunk
Common in aging, watch for melanoma
SK treatment
Not essential, only a cosmetic issue, but an irritated one can use cryotherapy or curettage
Describe epidermoid cysts
Caused by lodging of epidermal tissue in dermis, cyst fills with macerated keratin (nasty, cheesy contents)
Can be anywhere
What is a pilar cyst?
Occurs in hair bearing areas
Epidermoid cysts exam
Freely mobile, fluctuant nodule, often with a visible pore and overlying skin smooth and shiny due to pressure
Vigorous inflammatory response with rupture
Describe keloid scars
Firm, irregularly shaped hypertrophic growth, often from skin damage (scar)
Hardened, brown, tender or itchy
Acrochordon aka…
Skin tags
Describe skin tags
Flesh colored, sessile (no stalk) and pedunculated papules
Neck, axilla, eyelids. Friction can precipitate
Describe infantile hemangioma
Strawberry hemangioma, most common benign tumor of childhood, present at birth or first 2 months of life
Proliferation of vascular endothelial cells
Describe cherry angioma
Oval/round, slightly elevated ruby red papules, mostly on trunk
Describe spider angioma
Central arteriole is the body, with small radiating vessels
Dilated vasculature, common in kids, pregnant females and liver disease
Describe venous lake
Small, dark blue blebs
Common on head, neck, forearms and hands due to chronic sun damage
WILL BLANCH
Describe erythrasma
Superficial bacterial infection of corynebacterium minutissimum
Often asymptomatic, invades stratum cornermen
Clinical findings of erythrasma
Often in toe web spaces or intertriginous areas
Scaly, macerated plaques, erythematous, appears brown over time
Often diagnosed as a fungal infection
Erythrasma diagnosis
Wood’s lamp, but often just a clinical diagnosis
Impetigo characteristics
Superficial intraepidermal infectin of the skin, spread by contact
Caused by staph or strep
What are the predisposing factors of impetigo?
Day care and contact sports
Clinical findings of impetigo
Painful or itchy lesions, frequently on the face
Tender, erythematous macules/papules, then vesicles or pustules, then HONEY CRUSTED LESIONS
Impetigo diagnosis
Usually clinical
Culture if diagnosis needs to be confirmed
Scarlet fever characteristics
Group A beta-hemolytic strep, exanthem associated with strep pharyngitis
Characteristic rash from GAS erythrogenic toxin
Scarlet fever clinical findings
High fever, sore throat, headache, malaise
Fine, maculopapular “sandpaper” rash that blanches to touch
What are pastia lines?
Red streaks in skin folds of scarlet fever that do NOT blanch
Scarlet fever physical exam
Red lips, flushed face, beefy tonsils, strawberry red tongue, fine, sandpaper rash
Scarlet fever diagnosis
Rapid strep test (RADT)
Throat culture is gold standard
Erysipelas characteristics
Infection of upper dermis of the skin
Most common in elderly, strep infection (GABHS or staph), usually in lower limbs unilaterally or on face
Erysipelas clinical findings/physical exam
Superficial rash with well demarcated borders, painful, shiny surface, peau d’orange, butterfly involvement, ear involvement, abrupt fever onset
Cellulitis characteristics
Acute infection of dermis and subQ tissue
GABHS or staph, MRSA more common
Cellulitis clinical findings
Break in skin barrier, fever/chills/malaise, pain/itching/burning, unilateral, indistinct margins
Cellulitis physical exam
Localized pain/tenderness, erythema, swelling, warmth, possible regional LAD
Facial or orbital are more serious
When does cellulitis need to be admitted?
Severe infection, systemic symptoms, suspicion if deeper infection/necrotizing fasciitis
Necrotizing fasciitis characteristics
Deep infection of muscle fascia that is rapidly spreading, surgical emergency!
Necrotizing fasciitis clinical findings
Will look like cellulitis, pain out of proportion to the skin appearance (exquisitely tender), swelling, appearance of toxicity (fever)
Lymphangitis characteristics
Acute or chronic inflammation of lymphatic channels, infectious or non, usually GAS, commonly associated with bacterial cellulitis, prior node dissection, lymphedema, etc.
Lymphangitis clinical findings
Malaise, loss of appetite, fever, chills, travel to tropical region
Lymphangitis physical exam
Erythematous, macular streaks from infection site toward regional lymph nodes
Warm, tender nodes on neighboring skin
Folliculitis characteristics
Superficial inflammation of a follicle, usually hair
Usually staph aureus
If pseudomonas aeruginosa, think water source (like hot tubs)
Folliculitis clinical findings
Pruritus, tender lesion, rash on hair bearing skin
Furuncle
Located in hair bearing site, especially friction areas, infection spreads from folliculitis
Usually staph aureus
Carbuncle
Larger and more extensive Furuncle, multiple drainage openings
Abscess
Localized collection of pus walled off by inflamed tissue
What are the two main reasons diabetics are predisposed to foot infections?
Decreased blood flow and decreased sensation
Vitiligo characteristics
Skin depigmentation disorder caused by autoimmune process (can be associated with other immune diseases), usually around 10-30
What are the three localized vitiligo classifications?
Focal
Segmental
Mucosal
Localized focal vitiligo
1 or more macules in one area
Localized segmental vitiligo
Unilateral, often in dermatomal distribution, white hair common
Localized mucosal vitiligo
Only involves mucous membranes
What are the three general vitiligo classifications?
Acrofacial
Vulgaris
Mixed
General acrofacial vitiligo
Distal fingers and periorificial areas, very symmetric
General vulgaris vitiligo
Scattered, symmetrical patches that are widely distributed
General, mixed vitiligo
Mixed combo of the types
Universal vitiligo
Complete or almost complete depigmentation of skin
What is the difference in vitiligo versus albinism?
Albinism still has melanocytes, just reduced melanin production. Vitiligo is an autoimmune process that kills melanocytes
OCA 1 description
Snow White hair, white/pink skin, blue eyes, significantly impaired visual acuity, photophobia, nystagmus, strabismus
OCA 2
Most common type in the world
Pink-cream skin, normal nevi or freckles possible, yellow-brown hair, blue to yellow-brown irides, may improve
OCA 3
Copper red skin and hair, diluted iris color
OCA 4
Rare, usually East Asian population
What are the pathognomonic findings of albinism?
Ocular findings:
Nystagmus, iris translucency, reduced visual acuity, decreased retinal pigment, strabismus, foveal hypoplasia
Acanthosis nigrans characteristics
Acquired/inherited skin condition
Hyperinsulinemia plays a role
Causes velvety, hyper pigmented plaques in intertriginous areas
Type 1 AN
Hereditary benign, no associated endocrine disorder
Type 2 AN
Benign, endocrine disorders with insulin resistance
Type 3 AN
Pseudo-AN
With obesity
Type 4 AN
Drug induced: growth hormone, high dose nicotinic acid, steroid therapy, OCP
Type 5 AN
Malignant, usually adenocarcinoma of GI or GU tract, or lymphoma
AN clinical manifestations
Dark and velvety, can also involve mucous membranes, delicate furrows
AN diagnosis
Clinical, skin biopsy, can look at chemistry panels to look at underlying disease
Pityriasis versicolor characteristics
Aka tinea versicolor, superficial fungal infection from overgrowth of malassezia furfur
PV clinical manifestations
Hypo or hyper pigmented macules, round or oval, sharp margins
Commonly on trunk, usually asymptomatic
PV diagnosis
Scraping of scales from lesion and adding KOH, find spaghetti and meatballs yeast forms
Urticaria characteristics
Aka hives/welts
Very pruritic due to edema of the papillary body
May or may not be accompanied by angioedema
Acute versus chronic urticaria
Acute=
Clinical manifestations of urticaria
Blanchable, raised, erythematous plaques, central pallor, variable in size
Intense pruritus
Pemphigus characteristics
Rare group of life threatening blistering skin disorders
What is the histological hallmark of pemphigus?
Acantholysis: loss of cell to cell adhesion mediated by auto antibodies to epidermal cell surface proteins
Pemphigus vulgaris
Most common, classic Bullae, always involves mucous membranes
Pemphigus foliaceous
Less severe, never involves mucous membranes
Paraneoplastic pemphigus
Associated with numerous types of benign and malignant neoplasms
Pemphigus clinically
Painful lesions, nikolsky sign (press on their skin, causes a crinkle in the skin because there is no support to stabilize)
General psoriasis characteristics
Autoimmune inflammatory disease, genetically susceptible, plaques with overlying silvery-white scales
Triggers for psoriasis
Medication, stress, alcohol, trauma, cold weather, etc.
Clinical manifestations of psoriasis
Sharply marginated erythematous papule/plaque with a silvery white scale, typically symmetric
Pruritis is intense, auspitz sign, nail pitting
What is auspitz sign?
Remove a psoriasis scale and see droplets of blood
What is Blepharitis?
The most common ocular finding in psoriasis
What is psoriatic arthritis?
Occurs in a varying number of patients with psoriasis, inflammation at joints
Describe inverse psoriasis
In body folds, smooth and inflamed lesions without scaling
**similar presentation to candidiasis
Describe guttate psoriasis
Abrupt appearance of multiple psoriatic lesions, usually small plaques on trunk or extremities
No previous history of psoriasis generally
Pustular psoriasis
Acute onset of widespread erythema, scaling, superficial pustules
Can have life threatening complications as the skin is coming off in sheets
Erythrodermic psoriasis
Generalized erythema and scaling from head to toe, acute or chronic
Keratosis pilaris
Form of dominant ichthyosis vulgaris
Perifollicular hyperkeratosis usuallly on arms or legs
KP clinical manifestations
Dry skin may cause pruritis
Spiny papules on normal skin
Cheeks, upper arms and legs
What layers of skin does dermatitis involve?
Epidermis and dermis
General characteristics of atopic dermatitis
Eczema, chronic inflammatory skin condition, genetic defect in the proteins supporting the epidermal barrier
Describe the pathogenesis of AD
IgE mediated hypersensitivity reaction from Ag- release of vasoactive substances
Clinical manifestation of AD
“The itch that rashes”
Poorly defined, often in patches, red papules/plaques/maybe scales
Could be moist, crusted, oozing
Where in the body is AD commonly found?
Flexures, front and sides of neck, eyelids, forehead, face, wrists, hand and feet
Complications of AD
Can cause secondary infection, commonly staph aureus or HSV
Describe dyshidrotic eczema
Vesicular type of hand and foot dermatitis
Tapioca-like vesicles
Describe nummular eczema
Chronic and pruritic dermatitis
Coin shaped plaques
Winter months and extremities
UNRELATED to atopy (normal IgE levels)
Nummular eczema clinical manifestations
Pruritus is intense, plaques with distinct borders, most often on trunk and extremities
General info on seborrheic dermatitis
Chronic dermatitis that occurs in regions with most active sebaceous glands
SD pathogenesis
Malassezia furfur (like PV) Immune status Nutritional deficiency
Describe the common timing of SD flare ups
Fall/winter, sun may improve or cause flare up, lots of recurrences/remission
SD clinical manifestations
Pruritus is variable
Can be all different colored lesions, fissures, sharply demarcated, dandruff or cradle cap
Management of SD
Removal of crusts, medicated shampoos, steroids/antifungals
Contact dermatitis
Inflammatory reaction to substance that comes in contact with the skin
2 categories- irritant and allergic
Irritant contact dermatitis
Acute cytotoxic cell damage, most commonly affects hands (occupational), focal
ICD clinical manifestations
Burning, stinging (immediate or delayed)
Minutes-hours later erythematous, vesicular, fissured, crusted, necrotic, edema
Lesions do NOT spread beyond the site of contact, configuration may be bizarre
ICD prevention and treatment
Prevent with avoidance of irritant, barrier creams, and rinsing after exposure
Treat with gauze soaked in burow’s solution, glucocorticoids, protective creams
Allergic contact dermatitis
Inflammatory rash that develops after contact with a particular substance
Delayed type IV hypersensitivity reaction
Sensitization of cells and re exposure releases cytokines
Clinical manifestations of ACD
Itching, pain, 12-72 hours after exposure, confined to area of contact initially then spreads, linear often
Acute skin lesions of ACD
Closely spaced, well demarcated erythematous papules and or vesicles
Chronic skin lesions of ACD
Plaques, scaling with satellite papules, hyper pigmentation
Lichen simplex chronicus
Localized form of lichenification from repetitive rubbing no scratching
Pruritus is pleasurable and habitual
Skin lesions of LSC
Confluence of small papules forms solid plaque of lichenification
Thickened skin with accentuated markings
Dull red, brown, or black hyperpigmentation
Actinic keratosis general characteristics
Pre malignant, evolve to SCC at a slow rate, better felt than seen
Caused by UV damage in sun exposed areas
What are all of the clinical presentations of actinic keratosis?
Classic, hypertrophic, atrophic, cutaneous horn, pigmented, and actinic chelitis
Classic actinic keratosis
Erythematous, scale macule/papule/plaque
Hypertrophic actinic keratosis clinical presentation
Thick, adherent scale on an erythematous base
Atrophic actinic keratosis
No scale, smooth, red macule
Cutaneous horn actinic keratosis
Mound of keratin
DDX- SCC, verruca
Pigmented actinic keratosis
Rule out melanoma, perhaps using dermoscopy
Actinic chelitis actinic keratosis
Rough, scaly area on *usually lower lip, constantly dry and flaking
Describe topical chemotherapy
5-fluorouracil, tough treatments to tolerate, must avoid sun exposure and treating only parts of the field at a time
Photodynamic therapy
Topically apply pophyrin analogue, incubate for a few hours, place patient under specific light wavelength and porphyrin enters pre/malignant cells and causes apoptosis
Describe basal cell carcinoma
Most common type of skin cancer, least aggressive
Pearly papule/plaque, may bleed/ulcerate, telangiectasias common
Basal cell carcinoma treatments
Excision preferred
Can used Mohs and ED&C
When is radiation needed in BCC?
If the BCC is extensive or unable to be excised
Describe squamous cell carcinoma
More aggressive than basal cell carcinoma, can metastasize to nodes and elsewhere
Erythematous, scaly plaque. Will feel thick and rough on palpation
Describe bowen’s disease
SCC in situ, the most superficial cancer that can be called a cancer
Describe keratoacanthoma
Subtype of SCC, rapidly growing then eventually involutes and can go away
Nodular lesion with central necrotic core, needs to be excised because it is locally destructive and can spread
Malignant melanoma general characteristics
Least common but most deadly skin cancer
Be aware of patients with many nevi
Dysplastic nevus
If severely dysplasia, basically a melanoma
Watch for evolution
Melignant melanoma screening
A- asymmetry B- irregular border C- multiple colors D- diameter > 6 mm E- evolution (most important!)
Lentigo maligna MM
MM in situ, slow to invade deeply
Superficial spreading MM
Most common
Actual lentiginous MM
Bad prognosis, nail involvement
Nodular MM
Another type of MM
Amelanotic melanoma
Don’t do cryosurgery on pigmented lesions, can destroy melanocytes and lesions can evolve into melanoma still
Punch biopsy versus shave biopsy
Punch- useful when you need to asses depth and deep dermis/full thickness
Shave- easy, quick, superficial
Describe sentinel lymph node biopsy
Inject tracer into site around lesions, see which lymph nodes update it, surgically visualize/excise nodes to rule out malignant cells
What is the role of propionibacterium acnes in acne?
Metabolizes sebum to free fatty acids, which are then pro-inflammatory
Comedone
Occlusion of follicle
Accumulation of sebum
Papule/pustule
What are some hormones that can cause acne?
Cushing’s (elevated cortisol)
Polycystic ovarian syndrome (hyperandrogenism)
Describe neonatal acne
Maternal hormones, no treatment needed
Under age 8-9 acne
Rule out endocrine causes
Cushing’s, hyperandrogenism, precocious puberty
Describe acne conglobata
Suppurations cystic lesions with sinus formation, very inflammatory
Acne fulminans
Rapidly progressive inflammatory nodules/plaques
Acne venenata
Acnegenic chemicals
Acne mechanica
Mechanical forces trigger eruption (chinstrap acne)
Describe pseudofolliculitis barbae
Curly facial hair being shaven and causing ingrown hairs
**acne imposter
Describe hidradenitis suppurativa
Recurrent sterile abscesses in axilla, groin, butt, breast
Not to be I&D’d, causes scarring and fibrotic tissue
Common in obesity and smoking
Describe keratosis pilaris
Hyperkeratotic follicular papules, usually on arms and legs, **acne imposter
No treatment needed
Describe rosacea
More common in adults, telangiectasias, flushing, rosy hue, can be acneiform
Glandular rosacea
Hyperplasia of soft tissue of nose, “rhinophyma” is a severe deformity in later disease
Ocular rosacea
Dryness, gritty, stinging or burning, Blepharitis, conjunctivitis, keratitis, iritis
Perioral dermatitis
Fairly common, symmetric around the mouth but sparing the vermillion border, seen in people that try to manage lesions or eruptions on their face
Describe erythema multiforme
Inflammatory, immune mediated
EM major- mucosal involvement
EM minor- NO mucosal involvement
Can be caused by HSV
Erythema multiforme clinically
Distinct target lesions, hands and feet and sometimes mucosal surfaces, can have central bullae
Erythema multiforme treatments
With severe disease, means that there is severe mucosal involvement, so nutrition is a big concern
Steroids
Stevens-Johnson syndrome and toxic epidermal necrolysis
Medication is the most common cause
Epidermal detachment is the hallmark
Difference: SJS 30% of total body surface
What is nikolsky sign?
Found in SJS/TEN, rubbing of the skin causes separation of dermis and epidermis
Rule of nines for adult
Head- 9 Front of trunk- 9 Back of trunk- 9 Each arm- 9 Genitals/hands- each 1 Front leg- 9 Back leg- 9
What is the general treatment for SJS and TEN?
Admit to hospital, usually treated as burn victims/wound care
Type A adverse drug reactions
Extensions of pharmacology of drug, not allergy or hypersensitivity
Type B adverse drug reactions
Genetic predispositions, allergy
Type II type B adverse drug reaction
Antibody dependent, days to weeks after starting drug, antibodies form and causes lysis of target cells (usually blood cells)
Type III type B adverse drug reaction
Immune complex deposition, Ag and Ab complexes deposited in small vessels and create an arthus reaction (local inflammation)
Can lead to serum sickness
Type IV type B adverse drug reaction
Cell mediated, T cells activated with exposure to offending substance
Morbilliform rash, fixed drug reaction, focal tissue damage
DRESS sydrome
What is DRESS syndrome?
Drug rash with eosinophilia and systemic symptoms
Type IV drug allergy
Superficial burn
Erythema, small epidermal/dermal blisters
Scarring rare
Partial thickness burn
Blistering, scarring
Full thickness burn
All layers of dermis, may extend into sub dermal structure
Eschar forms (scab-like, can’t expand to accomodate blood flow if circumferential)
Chilblains
Pernio, inflammatory lesions without freezing of tissue, cold injury
Trench foot
Prolonged immersion in cold water/mud, cold injury
Frost bite
Ice crystals in tissue, treatment is gradual rewarming
Do not use friction to warm!
Lichen plants
4 p’s
Pruritic purple polygonal papule
White lines atop the lesion “wickham striae”
Erythema nodosum
Hypersensitivity reaction, looks like erythema but feels like nodules
Inflammation of subq tissue
High predominance for females
Clinically erythema nodosum
Tender, red/purple nodules commonly on the skin
Scabies
Severe pruritis, vesicles, pustules and burrows. Commonly in interdigital webs, wrist, elbow, groin, axilla and breast
Usually spares head and neck
Scabies diagnosis and treatment
Scrape tissue and use mineral oil under a microscope
Topical permethrin
Pediculosis
Aka lice, can often be found in seams of clothing, can have severe pruritis
Nits attached to hair shafts and even live bugs
Bed bugs
Live in crevices of beds and furniture
Papular with or without urticarial appearance, LINEAR AND CLUSTERED
When you hear spider bite, think…
MRSA infected abcess
Brown recluse spider bite typically causes…
Tissue necrosis, outer ring of redness around the bite
Black widow spider bite
Often mild and local symptoms, could cause systemic symptoms
Local pain and target lesion are suggestive
What to do for a snake bite?
Don’t manipulate the area, get to a hospital for anti venom
Tinea corporis
Aka ringworm, variety of fungal infections
Erythema with advancing scaly border and central clearing
Tinea cruris
Aka jock itch, pruritic rash, leading edge
Tinea manuum
Scaly eruption, often chronic and unilateral from scratching itchy feet, in combo with tinea pedis
Tinea pedis
Often chronic, increases with sweating, scaling is common, in between toes often
Tinea ungum
Onychomycosis, yellowish/brown discoloration and nail thickening, can be a setup for a bacterial infection
Tinea capitis
Scalp/hair infection, can manifest with scale, alopecia, pustules, or a kerion (boggy plaque with pustules)
Pityriasis rosea
Acute, self-limited exanthem, usually clears in 4-6 weeks
Pityriasis rosea clinical features
HA, malaise, pharyngitis, then a herald or mother patch (scaly with central clearing, sharply demarcated on chest, neck or back)
What is the distribution of pityriasis rosea?
Christmas tree distribution, eruption spreads centrifugal lay
Meibomian glands
Sebaceous gland, located at the inner eyelid margins
Glands of zies
Sebaceous glands in eyelid, located at the outer lid margin
Glands of moll
Large sweat glands at the outer eyelid margin
General Hordeolum characteristics
Acute purulent inflammation of eyelid, involving either sebaceous glands of Zies or meibomian glands
External Hordeolum
Eyelash follicle or lid, point away from conjunctival surface
Internal Hordeolum
Meibomian gland abscess, points toward the conjunctival surface of the lid
Clinical manifestations of Hordeolum
Red, localized swelling, painful and or itchy, bump that resembles a pimple
General Chalazion characteristics
Chronic granulomatous inflammation of a meibomian gland, may follow internal Hordeolum (obstruction of gland)
Chalazion clinical manifestations
Eyelid swelling and erythema, painless, rubbery, nodular lesion
Entropion General characteristics and symptoms
Inward turning of the eyelid
Symptoms: excessive tearing, eye discomfort, redness, possible cornea damage
Entropion & symptoms
Outward turning of the eyelid, common in elderly
Symptoms: scleral and conjunctival erythema, excessive tearing, dryness/pain, keratitis, conjunctivitis
Blepharitis characteristics, anterior vs. posterior
Chronic inflammatory condition of the lid margins
Anterior: eyelid skin, eyelashes, associated glands. Can be ulcerative or seborrheic
Posterior: meibomian glands
Clinical manifestations of Blepharitis (anterior and posterior)
Irritation, burning, itching,
Anterior: red-rimmed, scales or granulations may cling to the lashes
Posterior: hyperemic lid margins, inflamed glands, dilated and plugged, frothy or greasy tears
Dacryocystitis characteristics
Infection of lacrimal sac due to partial obstruction of nasolacrimal system
Commonly in infants
Dacryocystitis clinical manifestations
Pain, redness, swelling in tear sac area, tearing and eye discharge, may be able to express purulent material
Dacryocystocele characteristics
Develops when BOTH proximal and distal portions of nasolacrimal system are obstructed
Usually noted shortly after birth, bluish swelling of the skin overlying the lacrimal sac, up-slanting of medial canthal tendon
Viral conjunctivitis
- adenovirus
- bilateral eyes from the beginning, copious watery discharge, cobblestoning (follicular conjunctivitis)
Bacterial conjunctivitis
-copious purulent discharge, mild discomfort, pruritic, matted eyelids
Usually self limited
Allergic conjunctivitis
Bending inflammation of the conjunctiva due to type 1 mediated IgE hypersensitivity to an allergen trigger
Allergic conjunctivitis clinical presentation
Almost always bilateral, hyperemia and chemosis, pruritus/burning, tearing, photophobia, eyelid edema, cobblestone papillae
Keratoconjunctivitis Sicca (aka dry eyes)
Tear deficient or evaporative, dryness, redness, FB sensation, could have marked discomfort with photophobia
Rose-Bengal stain
Uptake will happen with keratoconjunctivitis Sicca because of the dryness
Pinguecula characteristics
Non cancerous growth of the conjunctiva that lies over the sclera
Yellow, elevated, nodular, commonly on the nasal side
Pterygium characteristics
Fleshy, triangular encroachment of the conjunctiva onto the nasal side of the cornea
Starts medial, extends lateral
Associated with wind, sun, sand and dust exposure
Periorbital or preseptal cellulitis
Bacterial infection of the anterior portion of the eyelid, usually from local spread of sinusitis or dacryocystitis, external ocular infection, or trauma
Preseptal cellulitis clinical presentation
Ocular pain, erythema, eyelid swelling
Orbital cellulitis
Medical emergency, infection involving the contents of the orbit
Fever, proptosis, swelling and redness, systemically sick
Confirm orbital cellulitis with…
CT scan
Vestibular system is most. Sensitive to…
The onset of motions
What bone is the vestibular system encased in?
Temporal bone
What kind of motion to semicircular canals detect?
Angular or rotational motion of the head
What kind of motion do the utricle and saccule detect?
Linear motion (have otoliths)
Nystagmus
Eye movement in response to rotation of head
Eye moves opposite the direction of rotation, then jump to fixate on a new start point
Post rotary nystagmus
After rotation is abruptly stopped, eyes move in opposite direction of original rotation, people fall in direction of original rotation
Oculocephalic reflex
“Dolls eye reflex”
Turn head and see if eyes remain fixed on visual point or stay in same position through rotation (if they follow rotation, bad sign)
Caloric reflex
Thermal stimulation of inner ear, induces endolymph flow
Warm water- nystagmus towards treated side
Cold water- nystagmus toward opposite side
Vertigo
Sensation of motion when there is no motion
Exaggerated sense of motion in response to movement
Peripheral vestibular disease
Sudden vertigo onset, tinnitus and hearing loss may be associated, other neurological signs are absent
Central vestibular disease
Develops gradually, becomes progressively severe
Nystagmus is not always present, but can occur in any direction
No hearing loss or tinnitus
Peripheral vertigo causes
Meniere syndrome, labyrinthitis, benign paroxysmal positioning vertigo
Central vertigo causes
Migraine, brainstem ischemia, mass/hemorrhage/Cerebellar infarct, MS
Meniere syndrome
“Endolymphatic hydrops”, increased volume in vestibular system
Episodic vertigo, discrete spells lasting minutes/hours, fluctuating hearing loss, tinnitus, sensation of unilateral aural pressure
Labyrinthitis
Infection of vestibular apparatus, acute onset of continuous usually severe vertigo lasting days to a week, accompanied by hearing loss and tinnitus
Benign paroxysmal positioning vertigo
Recurrent spells of vertigo, seconds to minutes per spell, occurs with changes in head position
Dix hallpike maneuver
Putting head down and off the table a bit and turning it 45 degrees
Tinnitus
Perception of abnormal ear or head noises, persistent tinnitus often indicates the presence of sensory hearing loss
Pulsatile tinnitus
Often described by the patient as listening to one’s own heartbeat
Ascribed often to conductive hearing loss, but could indicated vascular abnormality
Frequency dictates…
Tone
Amplitude dictates…
Volume
Traumatic hematoma of the ear description
Common in contact sports, collection of blood between cartilage and perichodrum (leads to ischemia and necrosis of cartilage)
Cauliflower ear
Necrosis of cartilage from untrained hematoma, leads to disorganized fibrosis and neocartilagenesis
Auricular cellulitis characteristics
Must be treated promptly to avoid perichondritis
**involves lobule!!
Relapsing polychondritis
Immunological problem affecting cartilaginous structures
Auricular inflammation
Saddle nose deformity
Other signs of cartilage destruction
Otitis externa
Otalgia, pruritus, purulent discharge
Gram negative rods (fungi if chronic)
Otitis externa clinical findings
Erythema and edema of ear canal skin, often with purulent exudate, auricle manipulation elicits pain
Malignant otitis externa
Diabetic or immunocompromised patient, may evolve into osteomyelitis of the skull base, usually pseudomonas
Pruritus
Usually self induced wither from excoriation or overzealous ear cleaning, could be excessively dry
Osteoma
Benign, slow growing unilateral bone tumor
Can cause discomfort, otorrhea, conductive hearing disturbance
Exostosis
Reactive growth of periosteum
Usually due to chronic cold water/wind exposure (surfer’s ear)
Conductive hearing loss
Results from dysfunction of external or middle ear
Obstruction, mass loading, stiffness effect of ossicles, discontinuity
Sensory hearing loss
Results from deterioration of the cochlea usually due to loss of hair cells from the organ of corti
Neural hearing loss
Lesions involving eighth nerve, auditory nuclei, ascending tracts, auditory cortex
Vestibular schwannoma
Intercranial tumor, unilateral, associated with neurofibromatosis type 2
Acute otitis media
Results in accumulation of fluid and mucus which becomes infected by bacteria
Acute otitis media clinical findings
Otalgia, aural pressure, decreased hearing, fever
Erythema, decreased mobility of the tympanic membrane
TM can rupture, otorrhea follows
Mastoid tenderness, presence of pus within the mastoid air cells
Chronic otitis media
Pseudomonas
Purulent aural discharge, with perforation common
Pain is uncommon except during acute exacerbations
Complications of otitis media
Petrous apicictis, sigmoid sinus thrombosis
Cholesteatoma
Special variet of chronic otitis media, caused by prolonged Eustachian tube dysfunction
Squamous epithelium lined sac, fills with desquamated keratin and becomes chronically infected
Eustachian tube dysfunction
Examination may reveal retraction of tympanic membrane and decreased mobility on pneumatic otoscope
Serous otitis media
Prolonged Eustachian tube dysfunction and negative middle ear pressure may cause a transudate on of fluid
Usually accompanied by air bubbles in the middle ear and conductive hearing loss
Myringotomy
Small eardrum perforation, provides immediate relief and is appropriate in the setting of severe otalgia and hearing loss
Central retinal vein occlusion is at the level of…
The optic nerve
Branch retinal vein occlusion is at the level of…
Any distal branch of the central vein
Clinical findings of CRVO
Acute, painless vision loss, unilateral
Can be more subtle and incomplete, which suggests nonischemic type
clinical findings of BRVO
May be asymptomatic with complaint of blurred vision, worsening over hours to days
Vein occlusion physical signs and symptoms
Decreased visual acuity Dilated tortuous veins Retinal hemorrhages (blood and thunder appearance) Disk edema Cotton wool spots
Retinal artery occlusion
Painless loss of monocular vision, central or branch
Embolism of retinal artery, aka ocular stroke
**opthalmologic emergency!!
What causes a cherry red spot at the macula?
Obstruction of blood flow to the retinal artery, but continued blood flow to the choroid from the ciliary artery
Would also cause a pale retina
Complete vs. sectional vision loss for artery occlusions?
Complete vision loss suggests CRAO
Sectional vision loss suggests BRAO
Physical exam and signs of artery occlusions
Ischemic edema, cherry red spot, boxcarring, pale fundus
Describe amaurosis fugax
Transient loss of vision in one or both eyes, sudden onset that lasts a few seconds to a few minutes
Painless, precursor to artery occlusion
Amaurosis fugax clinical findings
Usually monocular, “curtain or shade pulling down over the eye”, painless, transient vision loss, vision restored to normal after each episode
Optic neuritis
Inflammation of the optic nerve, strongly associated with demyelinating disease (MS)
Optic neuritis clinical findings
Hx of previous viral illness, unilateral loss of vision, usually over a few days, ocular pain, loss of color vision, vision loss exacerbated by heat or exercise
Optic neuritis physical exam
Relative afferent pupillary defect (Marcus gunn pupil)
Central scotomata (can’t see center of vision)
What is the Marcus gunn pupil?
Pupil dilates with direct light into the eye instead of constricting
What are well tolerated FB on the cornea?
Inert objects, like paint, glass, plastic, or fiberglass
Diagnosis for corneal foreign body
Fluorescein stain, slit lamp test, topical anesthetics
Clinical findings and exam for corneal abrasion
Severe pain, FB sensation, tearing, photophobia
Fluorescein stain
Subconjunctival hemorrhage
Bleeding from small vessels under the conjunctiva
Occurs spontaneously and resolves spontaneously
Ocular chemical burns
EMERGENCY
Alkali burns- more severe
Copious irrigation!!
Hyphema
Pooling of blood in the anterior chamber, usually from blunt trauma
Indicated significant ocular injury!!
Seidel’s sign
Fluorescein streams like a waterfall from the iris, found in Hyphema/globe rupture
Orbital floor fracture
Blowout fracture, significant consequence is entrapment of inferior reclusive muscle and/or orbital fat
Globe rupture
Opthalmologic emergency
Full thickness corneal or scleral injury from trauma
Pain, severely decreased acuity, Hyphema, corneal laceration, irregular pupil, seidel’s sign
Keratitis
Inflammation of the cornea, from direct exposure to UV light
Clinical findings and treatment of keratitis
Bilateral eye pain, photophobia, tearing, FB sensation, acuity may be mildly diminished, may have diffuse corneal haze if severe
Herpes keratitis
Dendritic lesion!
Rhinitis is the presence of 1 or more of the following symptoms…
Sneezing
Rhinorrhea (anterior and or posterior)
Nasal congestion
Nasal itching
Rhinosinusitus definition
Encompasses disorders affecting both the nasal passages and paranasal sinuses
Allergic rhinitis general and pathophysiology
Can be seasonal or perennial, often seen with eczema or asthma patients
Airborn allergen, humoral and cytotoxic immune responses are activated
Symptoms of allergic rhinitis
Nasal itching, watery rhinorrhea, congestion, sneezing
Fatigue, snoring, poor sleep
Ocular irritation, Pruritus, conjunctival erythema, excessive tearing
Physical exam in allergic rhinitis
Nasal mucosa: pale, edematous, normal, nasal polyps
Allergic conjunctivitis
Allergic shiners
Allergic salute
Non allergic rhinitis
Diagnosis of exclusion, perennial symptoms, examination is normal
Acute viral rhinitis general
“Common cold”, self limited viral illness
Acute viral rhinitis symptoms
Sore throat, cough, malaise, HA, fever, sneezing, rhinitis, nasal congestion and watery discharge
Minimal findings, may have erythematous and edematous nasal mucosa
Rhinitis medicamentosa
Inflammatory rhinitis that leads to rebound nasal congestion, leading to dependence on causative agent
(Like OTC nasal decongestant sprays)
Swollen, beefy red nasal mucosa
Acute rhinosinusitis General
Inflammation of nasal cavity and paranasal sinuses lasting
Acute rhinosinusitis clinically
Nasal congestion and obstruction, purulent nasal discharge, maxillary tooth discomfort, facial pain and pressure, maybe fever, fatigue, cough, HA, etc.
Diffuse edema of nasal mucosa, narrowing of middle meat us, purulent discharge
Chronic rhinosinusitis
Inflammatory condition involving paranasal sinuses and nasal mucosa lasting 12 WEEKS OR MORE
Must have at least 2 of the signs and symptoms, mucosal inflammation required
Nasal polyps
Benign nasal tumors, usually from long standing inflammation of nasal and sinus cavities
Pale, edematous, mucosally covered masses
What should you suspect in kids with nasal polyps?
cystic fibrosis
What is samter’s triad?
Asthma
Nasal polyps
Aspirin, NSAID sensitivity
Apthous ulcers
Aka canker sores, ulcerative stomatitis
Self limited, painful ulcerations
Small, round ulcerations with yellow gray centers with red halo surrounding
Bacterial findings in pharyngitis
Tonsillar exudate, fever, lack of URI symptoms, anterior cervical lymphadenopathy
Findings most suggestive of EBV (mono)
Classic triad: fever, pharyngitis, and marked lymphadenopathy
Fatigue, malaise, splenomegaly
Peritonsillar abcess clinical findings
Sore throat, odynophagia, fever, deviation of uvula, hot potato voice, lock jaw
Retro pharyngeal abscess
Spread of infection from sinuses, ear or Nasopharynx
Needs aggressive treatment
Dysphagia, drooling, strider, muffled voice, fever
Ludwig’s angina - tooth source
Sialadenitis
Inflammation/infection of any salivary gland
Commonly from Sialolithiasis
Sialadenitis clinical findings
Acute swelling of gland, increased with meals
Tenderness and erythema of duct opening, pus can be massaged out
Dysphonia
Any disorder of phonation affecting the voice quality or ability to produce voice
Stridor
High pitched, noisy respiration
Usually from respiration obstruction of trachea or larynx
Laryngitis general
Inflammation, erythema, edema of larynx/vocal chords
Acute: usually viral, or voice overuse
Chronic: GERD, inhaled irritants
Epiglottitis
Severe acute bacterial infection of epiglottis and supra glottis structures
LIFE THREATENING EMERGENCY
Epiglottitis clinical findings
Abrupt onset of high fever, sore throat, dysphagia
Hot potato voice, drooling, sniffing or tripod position
Rapid progression of toxicity or respiratory distress
Supraclavicular lymph nodes that are enlarged are…
Always abnormal
Bronchial cleft cyst
Congenital lesion
Soft, cystic mass on anterior portion of sternocleidomastoid
Thyroglossal duct cyst
Congenital abnormality
Midline neck mass, residual from thyroid
Episcleritis
Inflammation of episclera
Abrupt onset, usually self limited
Episcleritis clinical manifestations
Acute onset of ocular redness, irritation, watering
Pain is rare, vision is normal
*refer to ophthalmology
Scleritis
Painful, destructive, and potentially blinding
Highly symptomatic- severe boring pain, tender to palpation, painful EOMs, diplopia, violaceous redness of eye
Ciliary flush
Ciliary flush
Erythema goes right up to the iris, seen in scleritis
Uveitis
Intra ocular inflammation, leukocytes
Hypopyon may be present (pus in anterior chamber)
Anterior chamber uveitis
Iritis, presents with pain, ciliary flush, constricted pupil
Iris can adhere to cornea (posterior synechiae)
Posterior chamber uveitis
Painless, with floaters and decreased visual acuity
Cataracts
Opacification of the lens, usually protein clumping
Often bilateral, painless progressive decline in vision
Cataracts treatment
Surgery if unable to perform ADLs or inability to monitor retinal/optic nerve or glaucoma
Retinoblastoma
***be aware of this
Classically presents as leukocoria in a child less than two
Leukocoria
White pupillary reflex
Glaucoma
Optic neuropathy, usually increased intra ocular pressure
Cupping of optic disk, ocular hypertension
Acute angle closure glaucoma
Narrowing or closure of anterior chamber angle
Risk factors: shallow angle, could be increased pupil dilation
Acute angle closure glaucoma presentation
Severe pain, blurry/decreased vision, halos around lights, headache, nausea
Conjunctival injection, steamy cornea, sluggish response to light
Iridotomy
Allows for decompression of anterior chamber, acute angle closure glaucoma
Chronic glaucoma
Insidious onset, peripheral vision loss
Open angle or closed angle
Need two of three: cupping, visual field defects, increased intra ocular pressure
Retinal detachment
Usually spontaneous, cloud like retina,
Typically starts inferior then spreads upward
Urgent ophthalmology referral, keep head tilted backwards
Vitreous hemorrhage
Sudden vision loss with floaters
May see blood and hemorrhage in the eye
Age related macular degeneration
Loss of central vision, progressive and usually bilateral
Can have hard or soft drusen and lipid deposits beneath the retina
Atrophic “dry” age related macular degeneration
Hard drusen (Small, bright yellow), depigmentation of retina suggests atrophy
Neovascular “wet” age related macular degeneration
Soft drusen, proliferation of new vessels, more rapidly progressive and severe
Amsler grid
Useful in age related macular degeneration
