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41 Cards in this Set

  • Front
  • Back

What are the common skin diseases?

Psoriasis, seborrehic dermatitis, eczema/dermatitis, acne vulgaris, cutaneous drug reations

What are the types of secondary skin lesions?

Scale - flakes of compated stratum corneum.


Crust - dried exudate on skin.


Artophy - thinning of skin/subcuntaneous fat.


Lichenification - thickening of epidermis due to rubbing.


Erosion - depressed area of skin with epidermis loss.


Exoriation - skin abrasion by rubbing.


Fissure - linear leavage into dermis.


Scar - permanent fibrosis due to dermal damage.


Eschar - overlying dark hard cover on ulcer indicating necrosis/gangrene.


Keloids - exaggerated connective tissue response beyond edge of injury

What is the prevalence and risk of psoriasis?

~3% of the population (1 million Canadians).


High rate in Caucasians.


Even gender split.


Common onset young adults.


Inherited susceptibility (1 in 3 people have affected relative)

How is psoriasis autoimmune mediated?

Skin is 'non-self'.


Dendritic cells & T-cells.


Migrate from dermis to epidermis.


Cytokine release - inflammatory reponse, keratinocytes proliferate.

What are the precipitating factors for psoriasis?

Skin injury, discontinuation of systemic corticosteroids, cold water, streptococcal throat infections, emotional stress, alcohol, smoking, HIV, medications - beta blockers, ACE inhibitors, lithium, antimalarial drugs

What are complications of psoriasis?

Increased risk for myocardial infarction (7x increase).


Depression.


Psoriatic arthritis - 30% of patients.

What are the classifications of psoriasis?

Pustular - raised noninfectious pustules; surrounding skin is red, tender, inflammed; localized or generalized.



Nonpustular - most common; papules -> plaques; well defined, raised, red plaques, scales are silver/white

What are the diagnostics of psoriasis?

Auspitz sign - punctate bleeding spots when scale is scratched off.



Candle sign - scratched edges of scales should be 'greasy'.



Sign of last hautchen - lesion is dry to final layer

Where are the lesions found?
Scalp, elbows, legs, knees, nails, lower back, palms/soles, buttocks
What are the three classifications of psoriasis?

Mild - only a few patches, less than 3% of the skin surface.



Moderate - 3% - 10% of the skin surface.



Severe - more than 10% of the skin surface.

What is the pathology of psoriasis?

Keratinocyte proliferation.


Hyperkeratosis - thickening of the epidermis.


Dilated blood vessels.


Elongation of rete pegs - epithelial extensions into connective tissue under skin.

What are the types of psoriasis?

Psoriasis vulgaris - annular/limpet like.


Guttate psoriasis - small scaly papules.


Erythrodermic psoriasis - generalized form.


Pustular psoriasis - noninfectious pustules.

What is the prevalence and risk of seborrheoic dermatitis?

Common, chronic inflammatory dermatitis, 1-5% of the population.


Affects all ages, affects more males than females.


In regions with many sebaceous (oil) glands - face, scalp, behind ears, upper trunk, skin folds.


Hereditary - positive family history.

What is seborrheoic dermatitis linked to?

Linked to yeast infection - sp Malassezia.


Believed to release lipid metabolites that inflame/irritate the skin, particularly on the scalp.


Some individuals have increased oil production.

What are the risk factors?
Illness, stress, fatigue, reduced general health, low humidity, cold temperatures.
What are drug triggers of SD?
Cimetidine, lithium, methyldopa, buspirone, ethionamide, haloperidol, phenothiazines.
Describe SD.

Lesions - pink to red, superficial, itchy patches/plaques, yellow-red-brown, flaky, occasionally greasy scale.


Can attach to hair shaft.


Dandruff is common on scalp.

What is eczema/dermatitis?
Eczema = dermatitis. Involves both the epidermis and dermis.
What are the two classes of eczema?

Acute eczema - itchy, red, papulovesicular, crusted.


Chronic eczema - itchy, leathery hypertrophied dry scales.


Dry skin.


Lichenification.

What are the two classes of dermatitis?
Atopic and Contact
What is atopic dermatitis?

React abnormally and easily to irritants.


Begins in childhood <5.


Common - places of flexion.


Inherited predisposition - increased risk of allergic reactions, asthma.


Increase in IgE production.


*Itching leads to rashing.*


Increased risk of infection.

What is contact dermatitis?

Allergic/irritant contact dermatitis - inflammation due to contact with substance; large, burning rashes, itchy.


Chemical irritants - lead to necrosis in area of exposure - phenols, organic solvents, alkali hydroxides.


Allergic stimulus via Hypersensitivity IV - CD4+ T cell activation, spread to surrounding tissue, includes drug-induced reactions.


-Poison oak.


-Poison ivy.

What is acne vulgaris?

Chronic inflammation


- Pilosebaceous unit - hair follicle, sebaceous gland, arrector pili muscle.



Common - with puberty (70-90%), diminishes by 25, more males affected, genetic component, face, shoulders, back, chest.

What are the precipitating/risk factors for acne vulgaris?

Hormones - androgens increase during puberty in both genders, anabolic steroids, steroids, progestins.


Family history.


Stress.


Tropical climate.


Cosmetics.


Environment - diet & exposure.


Drugs - phenytoin, phenobarbital, lithium.

What are the types of follicle blockages?

Comedones - blackhead.


Papules.


Pustules.


Nodules/cysts.


Scars.

What does the pathophysiology of AV involve?

Hyperkeratosis - follicular epidermal hyperproliferation (leads to clumping of keratinocytes plugging hair follicle).


Excess sebum production - oil glands increase size and production; sebum - oily/waxy matter lubricate and waterproof the skin, becomes trapped, solidifies behind keratin plug.


Bacterial growth and colonization - Propionibacterium acnes proliferation and activity, P. acnes oil metabolism to fatty acids, fatty acids induce inflammation.

Describe non-inflammatory acne vulgaris.

Closed and open comedones.



Closed comedones (1-2mm) - whiteheads, first clinical sigh, high tendency to rupture.



Open comedones (2-5mm) - blackheads, visible keratin plug, oxidized melanin and oil = black colour, stable.

Describe inflammatory acne vulgaris.

Papulopustular/nodular lesions.


Deep pimples.


PRISH.

What are the types of cutaneous drug reactions?

Maculopapular rash.


Urticaria/andioedema.


Fixed drug eruption.


Steven-Johnson's syndrome (SJS) - toxic epidermal necrolysis (TEN)

What is a maculopapular rash?

95% of cutaneous drug reactions.


Flat, red area on the skin that is covered with small confluent bumps.


Papules/macules - red, symmetric, occationally itchy.


Begin on body truck - peripheral spread to extremitites.

What is the time course for Maculopapular Rash?
~1 week of starting therapy, 7-14 day duration.
What are the common drug reactions causing MR?

Penicillins/cephalosporins, sulfonamides, allopurinol, anticonvulsants

What is the morphology of urticaria?
Hives, itchy, red wheals of varying size, can lead to cardiorespiratoy failure.
What is the morphology of angioedema?

Swelling, dermal and subcutaneous fluid retention.


Impact respiratory and GI mucous membranes.


Can cause anaphylactic shock.

How does does urticaria/angioedema last?

<24 hours

What are the common drug reactions causing U/A?
ACE inhibitors, penicillins, aspirin, ibuprofen
What are fixed drug eruptions?

Systemic and intermittent exposure to a drug.



Macule - one or more well defined, can develop plaque, burning sensation.



Acute inflammatory response - can lead to hyperpigmentation.



Localized - to fixed (same) location.

What are the common drugs causing fixed drug reactions?
Penicillins, tetracycline, sulfonamides, barbituates, phenolphthalein, gold salts.
What is SJS/TEN?

SJS is a milder form of TEN.



Delayed hypersenstivity reaction - T lymphocyte mediated.



Rare life-threatening ~30% mortality.

What is the disease progression for SJS/TEN?

~1 week after medication onset. 1-2 week fever.



Symptoms of upper resp tract infection (pain, sore throat, conjunctivitis).



Macules/bullae/ulcers and desquamation on mucosal membranes and skin.



T-cell mediated death and release of keratinocytes

What are the drugs causing SJS/TEN?

Sulfonamides, carbamazepine, ethosuximide, ethosuximide, lamotringe, phenobarbital, phenytoin