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408 Cards in this Set

  • Front
  • Back
What kind of lesion is a cafe au lait spot?
A macule.
What kind of lesion is a lichen planus?
A papule.
What kind of lesion is a compound nevus?
A nodule or papule.
What kinds of lesions are classic for psoriasis?
Plaques.
Herpes simplex causes what kinds of lesions?
Vesicles/vesiculations.
What's the difference btw a vesicle and a bulla?
Bullas are larger, but both are raised and contain liquid.
The primary lesion of acne vulgaris falls under what categorization?
Pustule (pus-filled).
What is the difference btw a papule and a nodule?
A nodule is bigger than 5mm, less than 5cm. A papule is less than 5mm.
Urticaria is denoted by what lesions?
Wheals or hives (fluid filled lesions raising the normal epidermis above the dermis).
What lesions do scabies cause and where in the skin do they accumulate?
Burrows, linear rashes accumulating in the stratum corneum.
What secondary skin change is caused by excess scratching or rubbing (from say neurodermatitis) and leads to skin thickening and excess markings?
Lichenification.
What secondary skin changes can be caused by psoriasis, pityriasis rosea, or scabies leading to excess accumulation of loosely adherent keratin?
Scaling.
What secondary skin change occurs in children with strep or staph infections and is "honey-colored"?
Crusting characteristic of impetigo.
What secondary skin change is denoted by a loss of epidermis (w/o dermal scarring)?
Erosion.
What secondary skin change involves loss of epidermal and dermal layers and heals with scarring?
Ulcers/ulcerations.
What kind of secondary skin change is a linear abrasion is produced by scratching?
Excoriation, can be caused by scabies.
"Herpetiform" offers what descriptive configuration regarding lesions?
They're grouped together.
Wtf does "guttate" mean?
Drop-like, as if they were laying down and you dropped some liquid on their skin.
What disease characteristically causes target (iris) lesions?
ERYTHEMA MULTIFORME.
A "reticulated" pattern denotes what? What is its opposite?
Web-like, nearly uniform in distribution. Moribilliform is the opposite, irregularly distributed web-like rash.
What does "zosteriform" mean?
Like herpes a rash follows a dermatomal distribution.
"Confluent" lesions do what?
Meld together and act as a single lesion.
What disease often presents a rash that is mistaken for a ring worm/fungal infection because of the annular papular rash it causes?
Pityriasis rosea.
What are characteristic examples of diseases that cause extensoral or flexural distributions?
Extensor - psoriasis.
Flexural - atopic dermatitis, eczema, lichenification.
The Koebner phenomenon refers to lesions that form in response to what? What kinds of diseases proceed in this fashion?
Trauma. Psoriasis, lichen planus/nitidus, warts.
In children, what types of lesions are evident in atopic dermatitis?
Acute- Erythematous patches with overlying vesiculation or papules with crusting, often on the face/flexural surfaces. Chronic (lichenified)- dry, thickened patches and plaques due to scratching and rubbing.
What is the atopic triad?
Asthma, allergic rhinitis, atopic dermatitis.
What dz is assoc with a filaggrin mutation? What does filaggrin encode?
Atopic dermatitis and ichthyosis vulgaris, 70% heritable in nature. Component of terminal keratinocyte differentiation, absence leads to disruption of the skin barrier fxn.
What skin infection is common among children, typified by dome-shaped papules with central umbilication?
Molluscum contagiosum, poxvirus.
What are Dennie's lines?
Extra folds of lower eyelid in children with atopic dermatitis.
What dz is keratosis pilaris found in and where on the body?
Perifollicular hyperkeratoses seen primarily over extensor surfaces of arms and thighs in pts with atopic dermatitis.
What happens to IFN-gamma in pts with atopic dermatitis?
It like other Th1 cytokines goes down while Th2 cytokines like Il-4, IL-5, and IL-13 (allergic ones) go up, also IgE.
Children with atopic dermatitis are at inc risk for what?
Other atopic conditions like allergic rhinitis and asthma, but also skin infections.
What is the most important part of atopic dermatitis skin care?
Moisturizer. Others - UV light, immunosuppressants (tacrolimus, pimecrolimus, cyclosporine, mycophenolate). Acute attack tx w/ steroids.
T/F: Moisturizers should be applied to children with atopic dermatitis all over the body, not just in regions of involvement, even over areas that have already been topically treated with antimicrobials and even after the lesions disappear.
True True True.
Between infantile hemangiomas and vascular malformations, which ones are: a.) most common, b.) present at birth, and c.) marked by endothelial hyperplasia?
A.) Infantile hemangiomas
B.) Vascular malformations
C.) Infantile hemangiomas
What does PHACE syndrome stand for and for one childhood lesion does it apply?
Infantile hemangiomas, stands for Posterior fossa malformations, facial and segmental Hemangiomas, cerebrovascular Arterial anomalies, Coarctation of the aorta/Cardiac defects, Eye abnormalities, and Sternal defects/Supraumbilical raphe.
What is a segmental hemangioma often mistaken for?
Port-Wine stain.
What drugs can be administered for hemangiomas that threaten to affect vital functions?
Prednisone (or other oral steroids), propanolol, vincristine, interferon alpha-2a/b.
What kind of infantile lesion is a Port-Wine stain?
A capillary malformation (slow flow vascular malformation).
T/F: Vascular malformations generally regress on their own by the age of puberty.
False.
What vascular malformation does Sturge-Weber syndrome involve and in what distribution? What other malformations or diseases are associated?
Capillary malformation (Port-Wine stain) along V1. Ipsi leptomeningeal vascular malformations, seizures, glaucoma.
What vascular malformation is assoc with overgrowth of limbs?
Klippel-Trenaunay-Weber syndrome (complex malformations, usu venous or capillary).
T/F: All fungi have dimorphic growth phases.
False. Some not all fungi are dimorphic.
What two compounds are popular targets of anti-fungals? Where are they located?
Chitin (cell wall) and ergosterol (cell membrane).
What superficial fungal diseases may not be treated with topical therapies?
Tinea capitis (scalp) and onychomycosis (nails).
What are the main defense mechanisms of the body against superficial fungal infections? Deep fungal infections?
Keratinase inhibitors, epidermal desquamation. Complement activation, humoral response (particularly IgG), cell-mediated immunity (Th1), inc unsaturated transferrin production (depletes iron needs of fungus).
What are the physical findings of tinea capitis? What age group is usu affected?
Pediatric dz, alopecia +pruritis.
What types of fungus lead to what manifestations of tinea capitis?
Anthrophilic - "grey patch" scaly areas or "black dot" broken hairs
Zoophilic or geophilic - "kerion" highly inflammatory.
Where does tinea pedis usually first arise? Age group? Subtypes?
In the spaces btw the toes of feet of adults that wear shoes too long. Adults >> kids. Interdigital, dry scaly, vesicular.
In cases of tinea pedis, what other site must be examined to rule out a latent reservoir of fungi?
The NAILS.
Tinea manum and tinea cruris are associated with what preceding infection?
Tinea pedis.
How do you differentiate tinea cruris and erythasma corynebacterium infection?
Erythrasma does not display the annularity of tinea cruris. No border to it and centrifugal spread. Tinea cruris also spares scrotal skin.
What is the best way to confirm a fungal infection diagnosis at the bedside?
KOH prep of a tissue scrape.
Classic presentation: Pt comes to the clinic with scaly, itchy rashes on both the back and chest with colors varying from brown to white. Diagnosis? What do you confirm with?
Tinea versicolor. KOH prep showing spaghetti and meatballs.
What conditions predispose to Candida infections?
Diabetes, immunosuppression, immobility/sweating, long-term antibiotic tx.
What physical findings do Candida skin infections present with?
Satellite pustules.
What differentiates Candida skin infections from dermatophyte infections?
Satellite lesions in Candida versus continuous border dermatophyte rashes spreading centrifugally.
What is the level of serum urate above which crystals will begin to form?
6.8 mg/dL. Treat pts to get uric acid lvls below this.
Diuretics have what effect upon urate excretion?
Reduce it by reducing PCT secretion (or inc reabsorption).
Alcohol intoxication has what effect upon uric acid excretion?
Hypoxemia->lactic acidosis->inc urate reabsorption in the PCT->hyperuricemia->gout. Also inc breakdown of ATP leads to overproduction of uric acid.
What joints are most commonly affected in gout?
First metatarsophalangeal joint, knee and ankle, tarsus.
T/F: Progression of gout is a steady increase in severity until the chronic tophaceous phase.
False. It begins with acute intermittent episodes eventually leading to chronic tophaceous progression. The inter-critical periods are the asx times in btw acute episodes.
What is the best method of gout diagnosis? How does pseudogout differ?
Tophus/synovial fluid biopsy displaying negatively birefringent crystals intracellularly. Pseudogout will have rhomboid-shaped, weakly positive birefringent crystals.
X-ray findings of "rat bite" erosions on the big toe are an indication for what?
Gout diagnosis.
What is the difference between erosions of gout and rheumatoid arthritis?
Early RA shows periarticular osteopenia when gout doesn't.
What are the clinical manifestations of gout?
1. Recurrent arthritis attacks ("gouty") leading to chronic arthritis/inflammation.
2. Tophi (MSU soft tissue deposits)
3. Uric acid kidney stones
4. Gouty nephropathy (interstitial nephropathy+renal insufficiency)
Where do basic calcium phosphate deposition diseases tend to cause arthritis?
Large joints like the shoulder.
Which crystals are commonly found in osteoarthritic joints?
CPPD (pyrophosphate dihydrate) and BCP (like hydroxyapatite).
T/F: Hydroxyapatite crystal deposition in periarticular sites may be observed under light microscopy.
False.
What does PRPP synthetase do? HGPRT? How do disorders in each lead to hyperuricemia?
PRPP synthetase leads to de novo synthesis of purines, and HGPRT leads to salvage synthesis of purines from hypoxanthine. Overactivity of PRPP and deficiency of HGPRT (Lesch-Nyhan) lead to hyperuricemia.
How do myeloproliferative disorders inc risk of hyperuricemia?
They lead to excess nucleic acid production which inc degradation products eventually leading to inc xanthine and uric acid.
What lab test differentiates gout due to increased uric acid production vs decreased renal clearance?
Urine uric acid levels.
What can hyperparathyroidism, hypothyroidism, and respiratory acidosis cause in the kidneys?
Hyperuricemia due to dec uric acid clearance.
How can acute uric acid nephropathy occur? Where does the MSU collect?
When a massive inc in urate excretion occurs (as in tumor lysis or leukemia tx). Interstitium near the collecting tubules.
What are some drugs to treat acute attacks of gout? What drugs should be avoided.
NSAIDs, corticosteroids, less so colchicine. Avoid drugs that inc uric acid secretion and xanthine oxidase inhibitors.
What drugs prophylax against acute gout attacks during the intercritical and chronic tophaceous periods?
Colchicine, NSAIDs, uricosuric drugs like probenecid or sulfinpyrazone and xanthine oxidase inhibitors like allopurinol/febuxostat.
What is the mean age of presentation for pseudogout? Gender?
Mid-70's. Female > male (unlike gout).
What is the most popular joint involvement for pseudogout?
The knees.
What is the most common manifestation of pseudogout?
Asx chondrocalcinosis of the knees in elderly pts >90yo. Also acute episodes that mimic gout.
What kind of crystal deposition causes synovitis and tendinitis in a peak population of 30-60yrs age?
Basic calcium phosphate crystals.
Basic calcium phosphate crystals display what birefringence and are displayed on LM how?
No birefringence, displayed with alizarin red staining (nonspecific) or von Kossa's stain.
What is the best method of BCP crystal deposition diagnosis?
X-ray findings of periarticular deposits of apatite + clinical syndrome.
What is the pathogenesis behind dermatomyositis and polymyositis?
DM - immune complex deposition in blood vessels
PM - direct cell-mediated muscle injury
Which myositis is more assoc with cancer (implying they both are)?
Dermatomyositis more than polymyositis.
What viral etiologies can lead to limited myopathy?
Coxsackie, adenovirus, influenza/parainfluenza.
What is the most common marker for myositis?
Anti-Jo-1 Ab for histidyl-tRNA-synthetase, PM-ILD.
What are the cutaneous manifestations of myositis?
Erythematosus (light sensitive) of face, chest, extensors.
Nail bed telangiectasia, periorbital edema and Gottron's papules.
Periorbital edema and Gottron's papules?
Dermatomyositis.
What pulmonary manifestations are associated with myositis? Assoc symptoms to that?
ILD concurrent with arthritis, Raynaud's, and showing a positive Anti-Jo-1 Ab.
What are the most common EKG findings in myositis pts with cardiac involvement?
Left anterior hemiblock and RBBB.
What is a necessary finding to diagnose Raynaud's syndrome?
Red, white, and blue cyanotic phases of the finger tips.
What are the most specific lab tests to confirm myositis? Cardiac involvement? What other disorders would show this profile?
Creatine kinase levels, muscle-specific aldolase. Myocardial CK levels. AST/ALT/LDH also up. Hypokalemia or drug-induced muscle dmg shows the same thing.
What characteristics of muscle strength could rule out PM/DM in a pt with proximal muscle weakness?
Assymetric weakness and any weakness of the distal muscles.
What factors assist in predicting the outcome of pts with PM/DM?
Duration of disease prior to treatment, severity of weakness, presence of dysphagia (bad).
What organ systems are traditionally affected in scleroderma?
Skin, lungs, GI tract, kidneys, heart, muscles.
What is the difference in epidemiology btw DM/PM and scleroderma?
DM/PM: F:M = 2; scleroderma: M:F = 3; both higher in blacks.
What visceral manifestation of scleroderma is actually more common in the limited (CREST) disease than diffuse?
Pericardial effusions. Myocardial fibrosis is the diffuse dz equivalent.
What therapy for scleroderma is administered from day 1 in order to prevent what important GI symptom?
PPI tx to prevent acid aspiration into the lung - pneumonitis.
Pseudodiverticuli?
Scleroderma.
What is the first treatment for scleroderma that most prolongs survival?
BP control to obviate malignant hypertension.
T/F: Presence of anti-centromere Ab's denotes poorer prognosis for scleroderma.
False, it's better, denotes limited form of dz and less risk of pulmonary dz.
What antibody denotes diffuse scleroderma over limited?
Topoisomerase I (anti Scl-70). Others present: antinuclear antibodies, RNP and Smith Abs in overlap syndrome.
Pemphigus vulgaris vs bullous pemphigoid disorder?
PV - desmosomes (desmoglien)
BP - hemidesmosomes.
Crescent sign?
Avascular necrosis of the hip.
Mosaic/"pumice" bone pattern? How does this happen to the bone?
Paget's disease. Repeated episodes of osteoclastic resorption coupled with osteoblastic refill. New bone susceptible to fracture.
What are two bad systemic complications of Paget's disease?
High output cardiac failure and high grade sarcomas.
Joints affected by degenerative (osteoarthritis) and rheumatoid arthritis?
Degenerative - hips, knees, spine, DIP, PIP, CMC (thumb metacarpal), 1st metatarsal-phalangeal joint (big toe).
Rheumatoid - small joints, metacarpals PIP's and metatarsals symmetrically and universally, may also involve large joints.
Lobular arrangement of neoplastic tissue with arc and ring mineralization circumferentially around bone?
Endochondroma.
What is the most common presenting symptom in patients with chondrosarcoma?
Pain.
What are the most common primary tumors of bone? Overall tumor of bone?
Osteosarcoma and multiple myeloma. Metastases overall.
Ground glass appearance of radiographically lucent or dense bone formation which may include cartilage/de novo osteoid?
Fibrous dysplasia.
What do corticosteroids bind to?
Intracellular hormone responsivee elements (HRE's), DNA targets involved in the regulation of promoters.
When is cortisol use indicated?
In hormone replacement therapy along with fludrocortisone (synth mineralocorticoid) for tx of Addison's disease.
What are the sx of Cushing's syndrome?
Muscle weakness (dec muscle mass), central obesity, moon face, abd stria, glucose intolerance, neuropsychiatric disorders.
Administration of corticosteroids in pts with infectious diseases has what benefits/drawbacks?
Benefits - fever and symptomatic suppression.
Drawbacks - inc susceptibility to severe infxn.
Long term steroid administration has what effect on metabolism?
Can lead to glucose intolerance and hyperglycemia, plus sodium and water retention (hypervolemic states).
Why must steroid administration be tapered off?
Most common: Flare-up of disease.
Most severe: Adrenal insufficiency.
What does cyclosporin bind to? What signal production does it inhibit? Dose-limiting toxicity?
Cyclophilin which then dimerizes with calcineurin inhibiting it. IL-2. Nephrotoxicity.
What does tacrolimus bind to?
FKBP which then binds to calcineurin -> same mechanism as cyclosporin, even more nephrotoxic.
What does sirolimus bind to, and what is the pathway by which it immunosuppresses? Clinical significance?
Binds to FKBP-12 but acts differently than tacrolimus - mTOR kinase inhibition arresting cell cycle. None of the dose-crippling nephrotoxicity hurrah.
Mycophenolate mofetil inhibits what? Indications? Adverse effect(s)?
Purine synthesis in lymphocytes, blocks the secondary antibody response mediated by B cells. Renal grafts, SLE, RA in conjunction with other immunosuppressants. Dose-limiting leukopenia.
What are the indications for methotrexate use in skin and soft tissue diseases?
RA, psoriasis, and psoriatic arthritis.
Cyclophosphamide can be used for what autoimmune disease?
SLE and other severe systemic AI dzes, administered along with corticosteroids, NOT alone and NOT for allograft rejection like other immunosuppressants.
Difference between eczema and urticaria histologically?
Both involve interstitial dermatitis, but eczema's is more superior than urticaria's and induces spongiosis + eosinophils.
What organisms produce impetigo and what kind of lesions?
Staphylococcus - bullous impetigo/pustule
Streptococcus - nonbullous
What kind of lesions does impetigo cause and where on the body?
Golden-crusted erosions, superficial bullae or vesicles. Face, hands, genitalia, scalp.
Where do superficial folliculitis lesions tend to appear? Organism?
Scalp, face, buttocks, extremities. Staph aureus.
What causes gram-negative folliculitis? Coincident with what condition?
Klebsiella, Enterobacter, Proteus, Pseudomonas. Superinfection in acne.
Hot tub folliculitis?
Pseudomonas aeruginosa.
Folliculitis barbae?
Staph aureus. Beards.
What's the difference between furuncles and carbuncles?
Carbuncles are comprised of interconnected furuncles. Both are painful, circumscribed, staph abscesses.
What is the common setting for cellulitis formation? Etiology?
Complication of a wound or trauma. Group A strep or Staph aureus.
How is erysipelas different than cellulitis?
More superficial form, border more defined, strep A but not staph, more commonly on the face.
What causes erythrasma and where? What pts get it?
Corynebacterium minitussimum, axilla and groin, toe webs. Diabetics, obese, debilitated pts.
Wood lamp examination yielding coral red fluorescence?
Erythrasma, Corynebacterium minitussimum.
Warts are caused by what organism?
Papillomavirus.
Which wart types are not elevated? Which are slightly elevated papules up to several hundred in number?
Plantar warts flat. Flat warts slightly elevated papules.
Where are characteristic locations for the morphologies of warts?
Verruca vulgaris- extremities (fingers), filiform/digitate- face, neck, plantar- sole/palm, condyloma accuminata- genital.
Gingivostomatitis and whitlow and generalized eczema are potential sequelae of what dz?
Primary herpes simplex infection.
Tzanck smear?
Stain to show multinucleated giant cells in fresh herpes simplex lesions.
What is the gold standard of herpes diagnosis?
Viral culture.
Which antivirals treat the various HSV's?
Acyclovir and valacyclovir for HSV1/2, famciclovir for herpes zoster HSV3. Ganciclovir for CMV.
Where does primary VZV infection (chicken pox) cause lesions? Lesion progression?
Erythematous macules->vesicles->pustules->rupture->crusts. Trunk, face, proximal extremities.
How are the herpes viruses spread?
Simplex - physical contact. VZV - respiratory droplets.
Which epidermal sweat glands empty onto hair follicles?
Apocrine and pilosebaceous glands.
How does each type of sweat gland empty?
Pilosebaceous - holocrine sloughing off of whole cells; Apocrine - decapitation with apical cytoplasmic sloughing off; Eccrine - exocytosis of vesicles (Check this).
In which skin layer does hyperkeratosis occur and what are its clinical manifestations? Acanthosis? Acantholysis? Spongiosis?
Corneum - scaling. Spinosum - lichenification, papules, plaques, tumors. Spinosum - blister (Herpes, pemphigus). Spinosum - vesicles.
What are some general pathologic changes that can occur in the stratum basalis?
Basilar vacuolation, hydropic degeneration, interface dermatitis.
Orthokeratosis v Parakeratosis?
Ortho - anucleate thickening of the stratum corneum; Para - nucleate thickening, hyperplasia too fast for nuclei expulsion.
What disorders can lead to spongiosis of the stratum spinosum?
Eczema (incl contact dermatitis), very common finding of edema in the spinosum.
What is the disorder in which keratinocytes lose their desmosomal connections in the stratum spinosum? Usu cause?
Acantholysis producing blistering disorders w eosinophilia due to contracting IF's. Antibodies to desmosomes as exists in pemphigus vulgaris.
What disease is at an increased risk in atrophic skin?
Malignant melanoma.
What dermal inflammatory changes are due to type I hypersensitivity reactions? III? IV?
I - Urticaria (hives); III - allergic angiitis; IV - allergic contact dermatitis;
What disease classically demonstrates interstitial dermatitis with eosinophilia that is not perivascular or periadnexal?
Urticaria (hives).
Vacuolar alteration along the dermal/epidermal interface?
Basilar vacuolation or hydropic degeneration.
How can one differentiate SLE from discoid LE by direct immunofluorescence?
Both will show granular deposits of Ig/C3 along the basement membrane zone in lesioned areas, but SLE shows deposits in uninvolved sun-exposed areas too.
Perivascular inflammation of the dermis with epidermal atrophy and keratin/follicular plugs in the dermis?
Discoid lupus erythematosus.
What is the most common vasculitis of any size vessels? What kind of cellular inflammatory infiltrate is notable here?
Leukocytoclastic vasculitis (microscopic polyangiitis). Eosinophils+neutrophils on biopsy.
What kind of hyperkeratosis is present in psoriasis?
Parakeratosis due to hastened desquamation.
Papulosquamous dermatitis with erythematous plaques and silvery white scales, extensor preferential?
Psoriasis duh. Don't forget parakeratosis and superficial epithelial neutrophils.
Pemphigus vulgaris vs bullous pemphigoid in terms of classic pt presentations?
Both disorders are blistering, but pemphigus = young pts, flaccid bullae+erosions, yes mucosa, bullous pemphigoid = old pts, tense bullae, no mucosa.
Fishnet pattern of epithelium when stained with anti-IgG/C3? What protein do they attach to?
Pemphigus vulgaris, attaching to desmoglien.
Blister locations in the skin of pemphigus/pemphigoid?
Pemphigus- suprabasilar; pemphigoid - subepidermal.
T/F: Freckles (ephelid) involve hyperactivity of melanocytes with melanocytic hyperplasia.
False. No hyperplasia involved.
Elongation of epidermal rete and hyperplasia of melanocytes along the basal aspect of the epidermis?
Lentigos, benign tan to brown macules.
T/F: A junctional nevus straddles the dermis and epidermis.
False, it sits in the epidermis alone. Compound is defined here.
Which lesion involves bridging of the reeny ridges with melanocytic hyperplasia?
Dysplastic nevus.
T/F: Nevus removal therapy is an option for patients with familial atypical mole/malignant melanoma syndrome.
False, since the majority of malignancies do not arise from preexisting dysplastic nevi but rather de novo.
What are the most important prognostic features of malignant melanoma?
Invasive vs in situ dz (Clark's level 1-5: epidermis, papillary dermis, papillary-reticular jxn, reticular dermis, subQ fat), and tumor thickness (Breslow thickness) - the MOST important factor of the three.
Melanoma on the hands and feet, darker and thicker than others?
Acral lentiginous melanoma.
Which melanoma is difficult to diagnose due to the absence of pigmentation?
Desmoplastic melanoma, presents as a scarred plaque, undifferentiated w inflammation, diagnose w IHC.
Which melanoma does not metastasize along lymph nodes but rather via nerves?
Desmoplastic (aka neurotropic) melanoma.
Which melanoma is slow growing in situ by definition? The opposite (invasive w little epidermal involvement)?
Lentigo maligna. Nodular.
What is the malignant melanoma description system denoting a potential malignant lesion?
ABCDE - assymetrical, regular borders, multiple colors, diameter>6mm, evolution.
T/F: Seborrheic keratosis is not malignant or premalignant.
True.
Benign pigmented epithelial neoplasm, "stuck on"?
Seborrheic keratosis.
Benign scaly superficial lesion showing epidermal atypia (but not of full thickness of epidermis) and parakeratosis w potential squamous cell carcinoma transformation?
Actinic keratosis.
What causes actinic keratosis and related squamous cell carcinomas? Metastasis?
Sun-exposure, radiation, hydrocarbons, arsenicals. Metastasis to LN's possible but unusual. SCC's arising from actinic keratosis less metastatic than spontaneous SCC's.
Most common type of skin cancer? Cause? Metastasis?
Basal cell carcinoma, chronic sun exposure. Almost never met but can be locally aggressive.
What layer of the skin is mostly affected by basal cell carcinoma?
Dermis.
Which skin cancer metastasizes often and histologically looks like small cell carcinoma of the lung?
Merkel cell carcinoma.
Classic presentation: 34-yo female presents with a nodular dimple on her left lower leg. Biopsy shows nonspecific dermal fibrosis. Inc melanin pigmentation on overlying epidermis. Excise?
Dermatofibrosis, usu benign, excision results in reoccurrence, don't do it.
Classic presentation: 34-yo female presents with a nodular dimple on her left lower leg. Biopsy shows dermal fibrosis with "cartwheel" or storiform patterns and extension into subQ fat. Excise?
Dermatofibrosarcoma protuberans. Yes excise, they are malignant and aggressive although non-metastasizing.
Hemangioma vs Kaposi's sarcoma?
Hemangioma - benign; KS - malignant, M>F, assoc w AIDS, affects skin, mucosa, LN, other organ systems.
IHC stain to diagnose Kaposi's sarcoma? Other histologic giveaway?
HHBA+ stain. Slit-like spaces running through dermis.
Mycosis fungoides is a product of what malignancy?
CD4+ T cell lymphoma.
Difference btw skin nodules of B cell and T cell lymphomas?
B cell lymphomas spare the epidermis. T cell = mycosis fungoides.
Swan-neck deformity?
Rheumatoid arthritis. DIP hyperflexion and PIP hyperextension.
What joints are commonly involved in osteoarthritis between men and women?
Men - hips.
Women - knees and hands.
Early stage osteoarthritis demonstrates what chondrocyte action?
Cloning and clumping in an attempt to reproduce the lost cartilage being worn off due to a dec in proteoglycan content of the synovium.
What happens to the bone and cartilage in osteoarthritis?
Cartilage is sloughed off, subchondral bone is eburnated by friction, cancellous bone beneath is sclerosed. Joint mice and cysts form in the synovium/subchondral space.
Osteophytes are characteristic of what arthritis?
Osteoarthritis.
What are some common causes of avascular necrosis of the large joints (hip>shoulder>knee)?
Fracture, corticosteroids (high dose), thromboembolism (incl the bends), vasculitis, radiation therapy, venous hypertension.
Wedge-shaped necrosis?
Avascular necrosis of the femoral head. Followed by collapse and distortion of articular cartilage.
Shawl sign?
Rash on the upper thorax and neck, pathognomonic for dermatomyositis.
Female pt with SLE for a prolonged period of time suddenly develops hip pain?
Avascular necrosis due to corticosteroid use.
ILD can be caused by what dermatologic diseases?
Dermatomyositis, polymyositis, systemic lupus erythematosus, rheumatoid arthritis, all vasculitides.
What two dermatologic diseases can cause pulmonary hemorrhage?
SLE and the vasculitides (like Wegener's).
What does CREST stand for in the case of localized scleroderma?
Calcinosis, Raynaud phenomenon, esophageal dysmotility, sclerodactyly, telangiecatasias.
Scleroderma involves fibrosis of what with disappearance of what histologically?
Fibrosis of dermis and vessels. Adnexal structures like sweat glands and hair follicles disappearded.
What cell types mediate the immune reactions for scleroderma and inflammatory myopathies (myosites)?
Scleroderma - CD4 cells -> mast cells, macrophages, fibroblasts.
Myopathies - CD8 cells -> macrophages, others.
What MHC class II genes are known to be associated with rheumatoid arthritis? Lupus? Ankylosing spondylitis? Myositis?
HLA-DRB1. HLA-DR3. HLA-B27. HLA-DR3.
Which disease coincides with synovial cell hyperplasia? What inflammatory cells proliferate?
Rheumatoid arthritis. Lymphocytes and plasma cells.
Where do rheumatoid nodules tend to arise in RA pts? Histologically what is in the middle?
Elbow or ulnar aspect of forearm. Central pink acellular amorphous region with central fibrinoid necrosis lined by epithelioid histiocytes.
Which arthritis is accompanied by ulnar deviation of the fingers?
Rheumatoid arthritis, but also lupus arthritis potentially.
Lesch-Nyhan syndrome?
Deficiency of HGPRT leading to hyperuricemia and potentially gout.
Thiazides+joint pain?
Hyperuricemia leading to gout.
What two diseases are impossible to distinguish on a radiograph showing PIP arthritis with proximal periarticular tissue accumulation?
Rheumatoid arthritis and gout.
Erosive changes within the sacroiliac joints, sclerotic changes on either side of the joint?
Ankylosing spondylitis aka spondyloarthritis.
What are the inflammatory and non-inflammatory forms of arthritis?
Inflammatory - Rheumatoid arthritis, psoriatic arthritis, polymyositis, scleroderma, SLE.
Non-inflammatory - Osteoarthritis, avascular necrosis, fibromyalgia.
Inflammatory but categorized otherwise- gout, pseudogout, and the vasculitides.
Btw inflammatory and non-inflammatory arthritis, which presents in the morning? Stiffness? Swelling?
Inflammatory - morning, stiffness that subsides over the day, more swelling than non-.
STAT4 is a gene involved in downstream signaling and inflammation predisposing to what diseases?
SLE and rheumatoid arthritis.
What are the cardiac and pulmonary manifestations of rheumatoid arthritis?
Cardiac - pericardial effusions, 3x inc in MI risk;
Pulmonary - pleural effusions, UIP/ILD.
Felty's syndrome?
Splenomegaly, neutropenia, and thrombocytopenia in the context of severe RA.
Uveitis or aortitis with back pain?
Ankylosing spondylitis.
What is the Reiter's syndrome triad?
Arthritis of small peripheral joints (over ankylosing spondylitis), urethritis, and conjunctivitis. "Can't see, pee, bend knee."
Classic presentation: Nurse develops redness, scaling, fissuring, cracks in the skin after a long day of work.
Irritant contact dermatitis due to excess hand-washing. (Type IV hypersensitivity.)
What kind of allergic disease does latex exposure lead to?
Contact urticaria, a type I hypersensitivity (immediate).
What side effects can heavy dose topical steroids cause?
Topically - skin atrophy and stria;
Diffusion to the systemic - Addisonian crisis (adrenal insufficiency) and other systemic SE - Cushing's, avascular hip necrosis etc.
How long do invidual wheals last in urticaria? The total outbreak?
<24hr. Outbreaks last for less than 6wks when acute, >6wks when chronic.
Most common causes of acute urticaria? Chronic?
Medications- Anbs, NSAIDs, contrast dyes.
Infections- URIs, strep, viral gastroenteritis.
Foods- Shellfish, nuts, berries.
Chronic- assortment, H. pylori/hepatitis /parasites/pressure/cold/heat /exercise/sun
Mainstay of urticarial treatment?
Antihistamines to stop the allergic response (type I). Systemic steroids if uncontrollable.
How long after a drug exposure does it take for a morbiliform rash to develop? Character? Hypersensitivity?
7-10d post-exposure, diffuse blanching erythematous maculopapular rash, confluent. Undefined immunologic reaction.
Top causes of morbilliform drug eruption?
Antibiotics, NSAIDs, anticonvulsants, anti-hypertensives.
How does Stevens-Johnson syndrome differentiate itself from a morbilliform rash?
Both involve erythematous macules and papules, but SJS demonstrates necrosis, erosions, blisters, targetoid regions with dusky centers, vesicles and bullae. MUCOUS MEMBRANE INVOLVEMENT. Ocular genital and rectal. SJS involves a worse fever too.
Top causes of Stevens-Johnson syndrome or Toxic Epidermal Necrolysis?
Antibiotics: 1. Penicillin, 2. Sulfa drugs
3. Anticonvulsants: Phenytoin, carbamazepine, barbiturates;
4. NSAIDs, 5. Allopurinol.
What three pathophysiologic events happen in acne?
1. Follicular hyperkeratosis leading to follicular occlusion and formation of comedones.
2. Inc sebum production.
3. Propionibacterium breakdown of sebum to free fatty acids which irritate skin.
Colloquial term of occluded comedone? Open comedone?
Whitehead, blackhead. Leads to acne.
What therapies are available for acne?
Tretinoin (Retin-A), isoretinoin (Accutane), benzoyl peroxide, topical antibiotics like erythromycin/clindamycin, systemic antibiotics like minocycline, doxycycline, tetracycline.
Rosacea differs from acne how?
Different age group (>30yo), due to repeated flushing, NO COMEDONES evident.
Rhinophyma?
Thickening and hypertrophy of oil glands in skin esp nose, occurs in the setting of rosacea.
T/F: Treat rosacea with corticosteroids?
False. May work transiently but induce a rebound effect later. Topical antibiotics more indicated.
Dry skin, scaling near the eyebrows and nasolabial fold? It resembles dandrum in the scalp.
Seborrheic dermatitis.
Estradiol has what effect upon the immune system. Impacts rheumatic disease how?
Estradiol is anti-apoptotic for B cells, induces formation of self-reactive B cells in SLE.
ANA (anti-nuclear) antibodies are present in which diseases? What can precipitate their formation?
SLE, Sjogren's, scleroderma, dermato/polymyositis. Chronic ingestion of drugs, perhaps EBV infxn.
Lupus rash vs rosacea?
The malar rash does not cross the nasolabial folds, rosacea does.
Erythematous scaly eruption on the extensor surfaces of the fingers? Differential?
MCP/PIP dorsal surfaces -> Gottron's papules of myositis;
Dorsal surface btw MCP and PIP -> Discoid lupus erythematosus.
Classic presentation: Pt with rash, anti-Ro antibody positive. Dx?
Acute cutaneous (discoid) lupus.
What antibody correlates with the progression of disease in SLE?
Anti-dsDNA. C3 levels can also be useful to chart, but not C4 since many lupus pts have a congenital deficiency.
Class I to IV lupus nephritis induces deposits where?
Subendothelial space. Subepithelial (membranous and sclerosis lupus nephropathy) occur at class V and beyond.
A pt with lupus presents with pleuritic chest pain, DDx?
1. Infection!
2. Pleural effusion
3. Diffuse Alveolar Hemorrhage (+effusion).
What are the most common cardiac manifestations related to SLE?
Pericarditis and pericardial effusion, also myocarditis and endocarditis (Libman-Sachs lesions.)
What are the most common nervous system manifestations in pts with SLE?
Headaches, peripheral neuropathy more common than mononeuritis. Seizures and psychosis uncommon but suspect if pt has no other comorbidities.
What is the most specific antibody to detect in pts with non-drug-induced SLE? Drug-induced SLE?
Anti-dsDNA and anti-Smith Ab but anti-dsDNA is more sensitive. Drug-induced is anti-histone Ab.
Pts with SLE get what kind of anemia? Platelet disorder?
Anemia or chronic inflammation -> dec EPO, no steroids needed. Acute attacks of AIHA -> treat w steroids, check Coombs test. Thrombocytopenia due to anti-phospholipid Ab syndrome (cardiolipin) -> thrombophilia, clotting.
Which antibodies in SLE complicate pregnancy for women of childbearing age?
Anti-Ro Ab - congenital heart block, fetal emergency;
Anti-phospholipid Ab - recurrent abortion;
ANA Ab - neonatal lupus rash;
What antibodies denote drug-induced lupus when present?
Anti-histone Abs.
T/F: SLE and rheumatoid arthritis diagnoses can be made based on serologies alone.
FALSE. Each disease is a CLINICAL diagnosis! Many pts in the population are positive for certain Ab's like ANA but asx and have no disease or diff dz.
Which rheumatologic disease is characteristically exacerbated by sunlight exposure?
Lupus erythematosus.
What diagnostic use do ANA Ab's have?
Good negative predictive value. 99% of pts with lupus have it +.
Treat lupus patients with a positive anti-phospholipid antibody with:
Anticoagulation therapy (especially if they are pregnant!), starting at aspirin.
Treat lupus patients w/o involvement of the kidneys or nervous system with a baseline of what? What about pts with more severe disease?
NSAIDs, hydroxychloroquine (dec cholesterol also, dec cardiac risk), and low dose glucocorticoids. High dose steroids, methotrexate, cyclophosphamide, and mAbs like rituximab(CD20)/belimumab (BAFF).
T/F: Arthritis is a disease.
False. It means inflammation of a joint.
Hereditary osteoarthritis is caused by what genetic defect?
Type II procollagen mutations.
Which arthritis involves synovial membrane proliferation with perivascular inflammation?
Rheumatoid arthritis.
In rheumatoid arthritis, effusion into the joint space occurs as a result of what? Chronic rheumatoid arthritis hypertrophy of the synovial membrane induces a permanent what?
Altered permeability of blood vessels. Swelling of the joints.
Anti-CCP and elevated RF can be used as a serology to confirm diagnosis of?
Rheumatoid arthritis. RF elevation is more sensitive, less specific, assoc w aggressive dz, takes time to rise. Anti-CCP is more specific, less sensitive.
Celecoxib in dermatology?
CELEBREX - Newer NSAID, selective COX-2 inhibitor, less gastritis, no anti-platelet, inc risk MI. Can be used as first-line therapy for rheumatoid arthritis.
Bamboo spine?
Fused together vertebral ligaments in ankylosing spondylitis.
Reactive arthritis correlates with what haplotype of MHC class II? What differentiates it from other rheumatic dz? What is the most common cause.
HLA-B27 although not as rigorous as ankylosing spondylitis. Rheumatoid factor negative. Caused by infection, of which Chlamydia trachomatis (STD) is most common.
What rheumatic diseases are NSAID's prescribed for?
Rheumatoid arthritis, osteoarthritis, acute gouty arthritis, spondyloarthropathies, SLE (ALL OF THEM).
Which COX is constitutive? Which COX is inducible and inflammatory?
COX-1 constitutive, COX-2 inducible/inflammatory.
Inhibition of which COX pathway leads to side effects like gastric ulcers? Due to loss of what prostaglandins?
COX-1. PGE2 and PGI2 (loss of cytoprotection).
Inhibition of which COX pathway via what compound reduction inhibits platelet activity?
COX-1, TXA2.
NSAIDs have what effect upon pregnancy?
Prolongs gestation by inhibiting the contractile effects of prostaglandins.
NSAIDs have what effect upon the kidneys?
Fluid retention and reduced Na excretion by inhibiting prostaglandin dilation of afferent arteriole to inc GFR, potential induction of aTIN, acute papillary necrosis.
NSAIDs have what rheumatologic complications?
Bronchospasm, urticaria, and rhinitis.
T/F: Aspirin is an irreversible COX 1 and 2 inhibitor.
False. Reversible.
Most common indication for use of aspirin (and the only indication we should be giving it out for)?
Inhibition of platelet fxn.
Aspirin overdose has what metabolic imbalance effects?
AG metabolic acidosis (AMUDPILES), but ALSO respiratory alkalosis due to stimulation of the resp system. Salicylate depressant effect leads to resp acidosis.
Children with influenza B>A should not take what medicine and why?
Aspirin, Reye's syndrome, edema of liver and brain.
Acetaminophen toxicity occurs how? Treatment? Latent period? Death period?
Hepatic and renal failure by depletion of glutathione. Mucomyst (N-acetyl-cysteine) (replaces glutathione stores). 24hrs before bad sx occur. 5d before death.
T/F: Activated charcoal should be given with Mucomyst (N-acetyl-cysteine) orally for treatment of acetaminophen poisoning.
False. Act charcoal will deplete Mucomyst concs, so give Mucomyst IV if given with charcoal.
What's the best drug indicated for general analgesia?
Tylenol.
What is the best NSAID indicated for acute gouty arthritis and ankylosing spondylitis?
Indomethacin (Indocin).
What is the best NSAID indicated for use in rheumatoid arthritis and degenerative joint disease?
Ibuprofen/naproxen. Better SE profile than indomethacin.
What is unique about fenamates (ketorolac)?
Only NSAID approved for parenteral administration - post-op pain or when pt cannot swallow.
Aspirin has what effect on warfarin?
Increases levels of warfarin by displacing it from plasma protein stores. Inc PT INR.
What selective COXIB is indicated to treat rheumatoid arthritis and osteoarthritis?
Celebrex, very effective for these pts. Less gastropathy and risk of GI bleed, but more severe GI adverse events.
Celecoxib drug interactions?
Fluconazole causes it to rise.
Celecoxib causes lithium levels to rise.
Also inc warfarin conc, in PT INR.
Leukocytoclasic vasculitis demonstrates what kind of microvascular changes?
Fibrinoid necrosis due to immune-complex deposition (p-ANCA) with acute (polys) perivascular inflammatory infiltrates w nuclear debris (karyorrhexis).
Penicillin treatment can cause what kind of vasculitis?
Leukocytoclastic (aka hypersensitivity) vasculitis, aka microscopic polyangiitis.
Which types of basal cell carcinoma are more invasive locally?
Sclerosing forms. Multifocal superficial or nodular types are less likely to be invasive.
Basal cell carcinoma appearance vs that of squamous cell carcinoma?
BCC exists in the dermis, SCC in the epidermis with dermal invasion. BCC grossly shows a pearly appearance with rolled borders. SCC shows invading nests of atypical cells with intercellular bridges, where BCC shows palisading rows of outer cells and corresponding CT stroma proliferation to match the tumor.
Sunlight exposure can lead to which cancers? Other dermatologic conditions exacerbated/brought about by sunlight?
Squamous cell carcinoma (+actinic keratosis), basal cell carcinoma (most common), melanoma. Freckles (ephilides), solar lentigo, SLE, chronic urticaria.
Btw pemphigus and pemphigoid which one involves acantholysis?
Pemphigus vulgaris. Bullous pemphigoid involves a subepidermal non-acantholytic blister.
Histology: Biopsy of bony lesion shows malignant spindle cell stroma with acellular pink eosinophilic material. Nuclear pleomorphism and hyperchromasia also evident. Diagnosis?
Osteosarcoma and osteoid production.
What are the three borders of Codman's triangle and what disease does it denote?
Periosteum, cortical bone, and tumor, a lesion seen in bone tumors (most commonly osteosarcoma).
Classic presentation: 70yo man presents with a round, regular, soft, nonulcerating mass that has been slow growing w/o other signs of aggressiveness. DDx if painful/not?
Painless: lipoma, benign fibrous histiocytoma.
Painful: angiolipoma.
Most common soft tissue tumor of adulthood? Locations usually? Treatment?
Lipoma, upper back, neck, shoulders, abdomen, proximal extremities, butt. Nothing or simple excision.
Oil red O stains can help detect tissue with what etiology?
Adipose tissue or lipoblastic tissue in poorly differentiated liposarcomas.
Chicken wire vessels?
Myxoid liposarcomas indicating delicately branching arborizing vascular networks.
What genetic mutation in myxoid liposarcomas denotes a good prognosis?
t(12,16).
Clinical and pathologic features distinguishing liposarcoma from lipoma are:
A. Deep location
B. Inc cellularity and pleomorphism
C. Elderly age of patients
A and B only.
APAP?
N-acetyl-para-amino-phenol = Acetaminophen = Tylenol.
Which NSAID should be administered with a PPI?
Naproxen (Aleve)
T/F: Benign lesions are generally more superficial in soft tissue tumors.
True.
Most common sarcoma in children and adolescents? Adults?
Rhabdomyosarcoma. Histiocytoma and liposarcoma.
What is the age of presentation of synovial sarcomas?
20-40yo.
Where do liposarcomas typically present?
Deep tissues of thigh and retroperitoneum.
Most common (benign) soft tissue neoplasm in females?
Leiomyoma (fibroids).
What histologic finding in any tumor immediately indicates a malignant process?
Any sign of atypical mitoses. Also presence of necrosis (this means the tissue is outstripping its vascularization).
What six tissues do soft tissue cancer arise from?
Fat, fibroblasts, skeletal muscle, smooth muscle, endothelial cells, neural tissue.
Cancer: tissue culture-like myofibroblasts with occasional mucin production?
Nodular fasciitis.
What "reactive pseudosarcoma" can grow quickly yet have sharply demarcated borders? Where does it occur?
Nodular fasciitis, forearms, chest, back.
Which tumor looks like a scar on histology? Where does it occur? What is a particular danger?
Fibromatosis. Superficial - plantar, palmar. Deep - extra/intra-abdominal, shoulder, chest wall, back, extremities. Spontaneous recurrence which inc with each instance.
Which tumors exist in the dermis and induce fibrosis in a storiform pattern?
Benign/malignant fibrous histiocytomas and dermatofibromas/dermatofibrosarcomas.
What differentiates malignant from benign fibroblastic histiocytomas?
Atypical mitotic figures, pleomorphism, multinucleated tumor giant cells.
T/F: Skeletal muscle tumors are benign.
False, they are almost all malignant. Rhabdomyomas very rare.
Where do rhabdomyosarcomas occur?
Head and neck, GU system, retroperitoneum.
Most common location of leiomyomas?
Uterine wall.
Most common locations of hemangiomas? Most common age group? Subtype?
Head and neck, liver. Infants and children. Capillary group.
What cancer is defined histologically by nodules of capillary sized vessels with flattened endothelia and connection by a feeder vessel, like a glomerulus?
Capillary hemangiomas.
What is the most common cause of angiosarcomas? Where do they occur?
Radiation therapy for some other cancer. They can occur ANYWHERE, likely fatal.
List the three types of common fibroblastic soft tissue tumors.
Nodular fasciitis, fibromatosis, fibrous histiocytoma.
In soft tissue tumors are most tumors malignant or benign?
Benign, 100:1.
Antoni A vs. B, which on involves more cellular proliferation with Verocay bodies? What tumors do they refer to?
Antoni A. Schwannomas.
Is a Schwannoma benign or malignant? What is its counterpart?
Benign although it obstructs the neural exit eventually obliterating CN8. Malignant peripheral nerve sheath tumor.
What are the two important glucocorticoid analogs and fluorinated steroid analogs we should know?
Prednisone, prednisolone.
Dexamethasone, triamcinolone.
Mineralocorticoids have what primary physiologic function? Prototype?
Salt-retention, aldosterone.
What are lipocortins? What signals their synthesis, and what is their effect?
They are inhibitors of phospholipase A2 activation. Glucocorticoids stimulate their production. In effect lipocortins shut down the inflammatory response.
What signals increase the activity of phospholipase A2 (in opposition to steroids)?
Bradykinin and angiotensin.
Which prostaglandin regulates gastric mucosal and acid secretion?
PGE2. PGI2 also has protective attributes by vasodilation moderation.
T/F: Corticosteroids inhibit the normal physiologic repair mechanisms in connective tissue regeneration.
False, they promote repair, but the new tissue is not as hardy or robust as normal tissue.
Corticosteroids increase risk for what duodenal condition?
Peptic ulcers (loss of protective prostaglandin effects, just like NSAIDs).
Chronic high dose steroid use can have what effects on bone?
Osteoporosis and osteonecrosis (recall SLE steroid use-induced avascular necrosis of hip).
Rheumatoid arthritis patients on long term steroid therapy risk what complication?
Cataract formation.
What are the primary indications for use of immunosuppressive drugs today?
1. Autoimmune diseases like RA and myasthenia gravis. 2. Prevention of organ transplant rejection.
What is the most important step in the immune response to organ transplantation that must be suppressed by drugs to prevent rejection?
Formation of secondary memory lymphocytes, since the secondary immune system is much harder to suppress than the primary.
What immunosuppressive effect do corticosteroid analogs have?
They suppress IL-2 synthesis, proliferative responses of T cells and early B cell activation steps.
Which immunosuppressant increases the risk for developing lymphomas in renal transplants, as well as hepatic artery thrombosis?
Sirolimus (just think, it's the non-nephrotoxic one).
What does methotrexate bind to, inhibiting what?
Dihydrofolate reductase (DHFR), inhibiting nucleic acid synthesis by acting as a folic acid analog.
Which immunosuppressant crosslinks DNA?
Cyclophosphamide.
What does azathioprine inhibit and what are its indications?
Anti-purine (precursor of 6-MP) inhibiting DNA synthesis, used for kidney and liver graft prophylaxis.
Monoclonal antibodies are used in organ transplantation to prevent what part of the immune response?
Acute phase rejection of organ transplants. Can be used with cyclosporin to reduce the pharmacologic dose.
What are the monoclonal antibodies Basiliximab, Daclizumab, Muromonab, and Rituximab directed against?
B/D - CD25 (the IL-2 receptor);
M - CD3 (acute phase rejection prevention)
R - CD20 (B-cell NHL)
The principle of apoptosis states that reversible vs irreversible cell death is determined by what event (and applicable to bone deposition)?
Mitochondrial bursting releasing intracellular stores of calcium, occurring in chondrocytes during endochondrial ossification.
Which bones form via intramembranous ossification?
Flat bones of skull, sternum, pelvis (no prior cartilage skeleton that was built upon).
Which bone cell produces alkaline phosphatase? Acid phosphatase? Osteocalcin? Bone sialoprotein?
Osteoblasts. Osteoclasts. Osteoblasts. Osteoblasts.
What enzymes do osteoclasts contain to cause acidification and mineral dissolution in their Howship's lacunae?
Carbonic anhydrase II.
What are the two forms of lamellar bone?
Trabecular (cancellous, medullary) and cortical bone.
T/F: Achondroplasia pts have defects in intramembranous ossification.
False, the bones formed in this manner are normal. Endochondrial ossification is the defective process (long bones).
T/F: Achondroplasia and osteogenesis imperfecta are autosomal dominant mutations.
True.
Match the congenital bone disorders with the defective cell type!
Achondroplasia, osteogenesis imperfecta, osteopetrosis.
Chondroblast, osteoblast, osteoclast.
Which congenital bone disorder has symptoms of anemia and infection?
Osteopetrosis due to filling of the marrow cavity and inadequate hematopoiesis.
Which congenital bone disorder has symptoms of blindness and deafness?
Osteopetrosis due to constriction of the optic and vestibulocochlear nerves in the cranial foramina. Cranial nerve palsy and hydrocephalus also part of this.
What are the three phases of bone fracture healing?
Circulatory -> cellular -> vascular -> metabolic.
Wtf is a blastema? What can it be confused with?
Primitive callus, forms during the circulatory phase of fracture healing, proliferates in the cellular phase, reinforced and converted to callus in the metabolic phase. Since it is a rapidly enlarging mass, it was once mistaken for an osteosarcoma.
How can neutrophils mimic osteoclasts? What enzymes do they share?
Both can resorb bone, and neutrophils due during osteomyelitis. Elastase, collagenase, protease.
Increasing grade for chondrosarcomas corresponds with what histopath?
Less cartilaginous (chondroid) matrix, the matrix that is present tends to be more myxoid, and more cellularity and nuclear pleomorphism.
"Punched out" lesions of bone w/o surrounding sclerosis, usu in vertebrae, pelvis, ribs, skull?
Multiple myeloma.
"Herald patch" - a plaque as the first of two stages of a skin lesion appearing on the trunk due to what disease? What is the second stage of this lesion?
Pityriasis rosea. "Christmas tree" pattern.
How long does pityriasis rosea last? Treatment?
3-6 weeks, no treatment necessary.
What is the seasonal occurrence of pityriasis rosea? This suggests what viral etiology? What is the seasonal occurrence for psoriasis?
In the spring. HHV6 or HHV7. Winter months.
How is pityriasis rosea differentiated from tinea corporis, viral exanthem, morobilliform drug eruptions, and secondary syphilis?
KOH stain for tinea, viral exanthem has a more prominent malaise+fever, drug eruptions usu occur 7-14d post-exposure w/o herald patches, and secondary syphilis involves palms and soles (run VDRL FTA-ABS to be sure).
What are the differences between scales of pityriasis rosea and psoriasis?
PR - fine scales
Psoriasis - very thick scales, bleed if scraped, symmetric btw parts of the body.
Onycholysis with nail bed pitting (+/- arthritis) and thickening/discoloration of nails occurs in what disease?
Psoriasis.
Guttate psoriasis may be precipitated in children by an infection with what?
Strep pneumo URI.
Systemic withdrawal from steroids may induce what kind of life-threatening skin rash with widespread lesions and assoc fever/arthralgias?
Pustular psoriasis. Never treat these patients with systemic steroids, only topical.
Localized pustular psoriasis affects what parts of the body?
Palms and soles (pustules so impossible to mistake for syphilis).
Psoriasis is mediated by what cells of the immune system? Cytokines?
T cells, epidermal = CD8+, dermal = CD4+. Th1 mediated, so IFN-gamma, IL-2. In the skin, IL1, IL6, and TNF-alpha inc.
What are all the autoimmune diseases that share an association with HLA-B27 positivity?
IBD - Crohn's, CUC; Ankylosing spondylitis; Psoriasis.
Is eczema mediated by a Th1 or Th2 immune reaction?
Th2 - allergic reaction.
What is the general practice of pharmacologic cutaneous lesion-based psoriasis therapy?
Topical corticosteroids + vitamin D3 analogues (calcipotriene) in intertriginous areas. +/-: topical retinoids, salicylic acid, phototherapy.
T/F: Systemic corticosteroids are indicated for psoriasis only after topicals fail.
False, NEVER use systemic steroids for psoriasis! When the dose is tapered off the dz comes back nastier than before, inc pustular incidence.
Alefacept (Amevive)?
Immunosuppressant, fusion protein of extracellular CD2 linked to Fc of human IgG1. Attacks T cells, monitor CD4 counts to make sure it's not too strong. Treats psoriasis.
Etanrecept (Enbrel)?
TNF-inhibitor, treats psoriasis, inc risk of acquiring TB/reactivation dz, lymphoma.
What are the TNF inhibitors used to treat psoriasis?
Etanrecept (Enbrel), Adalimumab (Humira), Infilximab (Remicade).
Wickham's striae? Locations?
Lichen planus. Mucosal surfaces of mouth and genitalia as well as dorsal aspects of hands/feet/genitals and flexural aspects of wrist/forearm.
What skin lesions produce purple polygonal lesions, severe pruritis, symmetrically on the dorsal aspects of the hands/feet/genitalia and flexural aspects of wrists/forearms?
Lichen planus.
What is lichen planus of the hair follicles called?
Lichen planopilaris.
Angel wing deformity of nails?
Longitudinal ridging during onycholysis, indicative of lichen planus.
Silvery scales?
Either psoriasis or lichen planus depending on severity, hard to tell based on buzz word alone.
T-cell mediated skin disorders where basal keratinocytes express altered self-antigens?
Lichen planus.
Where does lichen nitidus tend to occur?
Flexural aspects of upper extremities, genitalia, anterior trunk, head.
Papular lesions traveling along lines of Blaschko, usu on extremities?
Lichen striatus.
What broader type of disease does dermatosis papulosa nigra belong to? Benign or malignant? What pt population does it occur in? Distribution on body?
Seborrheic keratosis. Benign. Darker-skinned people. Malar distribution on face/cheeks.
Sudden onset of pruritic seborrheic keratosis, usually in older adults, indicating cancer of what origin? What is this sign called? (Near mythic status due to rarity of finding.)
Sign of Leser-Trelat. Early gastric adenocarcinoma.
"Skin tags"? Popular locations on the body? Benign or malignant?
Acrochordons. Neck, axilla, groin, inframammary (intertriginous areas). Benign.
"Dimple sign" on compression of a papule on the legs of a middle-aged woman? Benign or malignant? What is the theory for why they pop up?
Dermatofibroma. Benign. Trauma like an insect bite.
What is Von Recklinghausen's disease also known as? Associated skin lesions? Benign or malignant?
Neurofibromatosis I (peripheral nerve tumor with defect in gene Neurofibromin on chr. 17, which can also be defective in schwannomas). Cutaneous neurofibromas - rubbery nodules, also cafe au lait spots. Benign.
What pt population do keloids tend to present in, and where on the body?
Darker-skinned peoples, sternum, neck, ears, back, legs.
Hypertrophic scar in African Americans as a fibroblastic response to injury? Benign or malignant?
Keloids. Benign.
Red bump, well circumscribed, onset usu in 30's, acquired, tends to run in familes, easy to treat with a pulse-dye laser? Benign or malignant?
Cherry hemangioma. Benign.
Lesion looking like a balloon with epidermal lining and a central puncta through which cheesy material can flow forth? Other names? Benign or malignant? Assoc with what systemic syndrome if there are multiple?
Epidermal inclusion cyst. Sebaceous cyst. Benign. Gardner's syndrome where you get osteomas, fibromas, lipomas, polyps which can yield cancer.
Benign brown patch, occurring in men more than women, commonly on the shoulders, thickening and growing hair during puberty?
Becker's nevus.
Freckles also know as?
Ephelides.
Brown macules on sun-exposed areas that come with inc age? (Smooth regular borders, no crazy colors.) Due to what cellular process?
Solar lentigo. Localized melanocyte proliferation.
Between congenital, compound, junctional, and intradermal nevi, order them from superficial to deep.
Superficial->junctional, compound (both dermis and epidermis), intradermal, congenital->deep.
Which nevus is most associated with vitiligo and malignant melanoma?
Halo nevus. Immune system is fighting transformation to malignancy already.
Nevus spilus? Benign or malignant?
"Freckle party" - dark brown macules w darker pigmented papules within, benign but may degenerate to melanoma.
Is a dysplastic nevus benign or malignant? Associated with melanoma?
Benign. NOT assoc with melanoma unless family hx+ (dysplastic nevus syndrome) with many dysplastic nevi on the body.
Arsenic exposure can lead to which skin cancers?
Basal cell carcinoma, squamous cell carcinoma and Bowen's disease (in situ SCC).
Which type of basal cell carcinoma is the most common?
Nodulo-ulcerative - pearly, telangiectasial papules wihch frequently ulcerate.
Bowen's disease involves what kind of cancer? Frequent cause?
In situ squamous cell carcinoma (not invasive), arsenic exposure.
T/F: Skin cancers that arise out of burned or injured areas are more likely to metastasize.
True for SCC and BCC at least.
Squamous cell cancer metastasis is commonly where?
LN's (85%), also liver, lung, bone, brain.
Kaposi's sarcoma is assoc with which viral infection/reactivation? Lesion looks like?
HHV8 (KSV). Mediterranean form has purple-red violaceous lower extremity plaques. HIV lesions more widespread, not seen much anymore due to HAART.
Stage I melanoma ten-year survival rate? Stage IV?
99%, 6%.
What is the most common early symptom of malignant melanoma?
Pruritis, although not all lesions need to be pruritic.
Hutchison's freckle?
Lentigo maligna. Macular melanoma in situ.
What is the most common type of malignant melanoma? Second most common type? Epidemiology?
Superficial spreading melanoma (age 30-50's). Nodular melanoma (age in 60's).
Which type of malignant melanoma are darker-skinned peoples more likely to present with?
Acral lentiginous melanoma.
Where are the most common sites of superficial spreading melanoma?
White individuals, back of males and posterior thighs of women.
"Sawtooth" infiltrate of lymphocytes at the dermal-epidermal junction with an overlying papular lesion?
Lichen planus
What body part serves as the usual reservoir for tinea pedis?
The toenails.
Overuse of topical steroids leads to what skin defects in situ?
Dermal atrophy and striae. Also subcutaneous fat atrophy.