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denniskwinn's version from 2015-04-25 16:11


Question Answer
CellulitisAcute, painful spreading infectin of dermis and subcutaneous tissues - usually from S.pyogenes or S. Aureus
Necrotizing fasiitisDeeper tissue injury usually from anaerobic bacteria and S. Pyogenes - results in crepitus from methane and CO2 production - flesh eating bacteria
Staphy scalded skin syndrome (SSSS)Exotoxin destroys keratinocyte attachments in the stratum granulosum only- Characterized by fever and generalized erythematous rash with sloughIng of the upper layers of the epidermIS. Seen in newboms and children.
HairyleukoplakiaWhite, painless plaques on the tongue that cannot be scraped off. EBV mediated. Occur in HIV-positive patients
Pemphigus vulgarisPotentIally fatal autoImmune skin dIsorder WIth IgG anlobody against desmosomes (anti-epithelIal cell antibody); Immunofluorescence reveals antibodies around cells of epIdermis in a retIcular or netlike pattern. Acantholysis - intraepldermal bullae involving the skin and oral mucosa. Positive Nikolsky’s sign (separation of epidermis upon manual stroking of skin)
Bullous pemphigoidAutoimmune dIsorder with IgG antibody against hemidesmosomes (epldermal basement membrane; antibodies are "bullow" the epidermis); shows Iinear immunofluorescence. Eosinophil WIthin blisters. Similar to but less severe than pemphigus vulgaris- affects skin but spares oral mucosa. Negative Nikolsky's sign.
Dermatitis herpetiformisPruritic papules and vesicles. Deposits of lgA at the tips of dermal papillae. Associated with celiac disease
Erythema multiformeAssociated with infections (e.g., Mycoplasma pneumoniae, I-lSV), drugs (e .g. , sulfa drugs, - B lactams, phenytoin ), cancers, and autoimmune disease. Presents with multiple types of lesions-macules, papules, vesicles, and target lesIons (red papules with a pale central area).
Steven’s Johnson syndrome Characterized by fever, bulla formation and necrosis, sloughing of skin, and a high mortality rate. Usually associated with adverse drug reaction. A more severe form of Stevens-Johnson syndrome is known as toxic epidermal necrolysis
Lichen planusPruritic, Purple, Polygonal Papules. Sawtooth infiltrate of lymphocytes at dermal-epidermal junction . Associated with hepatitis C.
Actinic keratosisPremalignant lesions caused by sun exposure. Small, rough, erythematous or brownish papules. "Cutaneou shorn." Risk of carcinoma is proportional to epithelial dysplasia. (precursor of squamous cell)
Acanthosis nigricansHyperplasia of stratum spinosum. Associated with hyperinsulinemia (e.g., from Cushing's disease, diabetes) and visceral malignancy.
Erythema nodosumInflammatory lesions of subcutaneous fat, usually on anterior shins. Associated with coccidioidomycosis, histoplasmosis, TB, leprosy, streptococcal infections , sarcoidosis.
Pityriasis rosea“Herald patch" followed days later by "Christmas tree" distribution. Multiple papular eruptions; remits spontaneously
Strawberry hemangiomaFirst few weeks of life (1/200 births); grows rapidly and regresses spontaneously at 5-8 years of age - most on head or neck.
Cherry HemangiomaAppears in 30-40s, does not regress
Necrolytic migratory erythemared, blistering rash that spreads across the skin, particularly the lower abdomen, buttocks, perineum, and groin - strongly associated with glucagonoma
Squamous cell carcinomaVery common. Associated with excessive exposure to sunlight and arsenic exposure. Commonly appear on hands and face. Locally ivasive, but rarely metastasizes. Ulcerative red lesion . Associated with chronic draining sinuses. Histopathology: keratin "pearls"
Keratoacanthoma variant of squamous cell carcinoma that grows rapldl) (4-6 weeks) and regresses spontaneously (4-8 weeks)
Basal cell carcinomaMost common in sun-exposed areas of body. Locally invasive, but almost never metastasizes. Rolled edge with central ulceration,gross: pearly papules, commonly with telangiectasias - pallisading nuclei.
Melanomacommon tumor with significant risk of metastasis - S-100 tumor marker. Associated with sunlight exposure; fslr-skinned persons are at i risk. Depth of tumor correlates with risk of metastasis. - Dark with irregular borders
Dysplastic nevus (atypical mole)precursor to melanoma
Superficial spreading melanomaMost common types, lower extremities, arms, upper back
Lentigo malignant melanomacommon in elderly, least likely to have vertical phase - on face
Nodular melanomaNo radial growth, sun exposed trunk, poor prognosis
Acral lentigious melanomaNot related to sun exposue - palm, sole, beneath the nail - Asians and blacks - poor prognosis
Criteria for malignancy in melanomaABCD - Asymmetry, Border irregularity, Color variation, Diameter>6mm
Lipoxygenase pathway yieldsLeukotrienes
LTB4 is a neutrophil chemotactic agent (nphils arrive B4 others)
LTC4,D4,E4 function inbronchoconstriction, vasoconstriction, contraction of smooth muscle and ↑ vascular permeability
PGI2 inhibitsplatelet aggregation and promotes vasodilation
Aspirin mechanismIrreversibly inhibits cycloxygenase by covalent binding, which ↓ synthesis of both thromboxane and prostaglandins
Aspirin clinical useLow dose(<300 mg/day): ↓ platelet aggregatIon. Intermediate dose (300-2400 mg/day): antipyretIc and analgesic. High dose (2400-4000 mg/day): anti-inflammatory
Aspirin ToxicityGastrIc upset. Chronic use can lead to acute renal failure, interstitIal nephritis, and upper Gl bleeding. Reye's syndrome in children with vIral infectIon
NSAIDSIbu, Naproxen, Indomethacin, Ketocorolac
NSAIDs mechanismReversibly inhibit cycloxygenase (both COX- I and COX-2J. Block prostaglandin Synthesis
NSAIDs clinical useAntipyretic, analgesic, anti-inflammatory, indomethacin is used to close PDA
NSAIDs toxicityRenal damage, fluid retention, aplastic anemia, GI distress, ulcers
Celcoxib mechanismReversibly inhibit specifically the cycloxygenase (COX) isoform 2, which is found in inflammatory cells and vascular endothelium and mediate lnflammation and pain; spares COX-l, which helps maintain the gastric mucosa. Thus, should not have the corrosive effects of other NSAIDs on the Gl lining.
Celecoxib clinical useRheumatoid and osteoarthritis
Celecoxib toxicity↑ risk of thrombosis, sulfa allergy, less toxicity to GI mucosa (lower incidence of ulcers, bleeding than NSAIDs
Acetaminophen mechanismReversibly inhibits cyclooxygenase, mostly in CNS. Inactivated peripherally.
Acetaminophen clinical useAntipyretic, analgesic, but lacking anti-inflammatory properties. Used instead of aspirin to prevent Reye's syndrome in children with viral infection
Acetaminophen toxicityOverdose produces hepatic necrosis; acetaminophen metabolite depletes glutathione and forms toxic tissue adducts in liver. N-acetylcysteine is antidote-regenerates glutathione
BisphosphonatesEtidronate, pamidronate, alendronate, risedronate
Bisphosphonates mechanismInhibit osteoclastic activity; reduce both formation and resorption of hydroxyapetite
Bisphosphonates clinical useMalignancy associated hypercalcemia, Paget’s disease of bone, postmenopausal osteoperosis
Bisphosphonates toxicityCorrosive esophagitis, nausea, diarrhea
ColchicineAcute gout treatment. Binds and stabilizes tubulin to inhibit polymerization, impairing leukocyte chemotaxis and degranulation. GI side effects, especially if given orally
Probenecidtx for chronic gout for underexcreters - inhibits reabsorption of uric acid in PCT (also inhibits secretion of penicillin)
AllopurinolChronic gout treatment for all - inhibits xanthine oxidase, ↓ conversion to uric acid - also used in lymphoma and leukemia to prvent tumor lysis (associated with urate nephropathy). ↑ concentrations of azathiprine and 6MP
Do not treat gout withsalicylates (they depress uric acid clearance) - and don’t treat acute episodes with treatment for chronic


TNF alpha inhibitors
DrugMechanismClinical useToxicityNotes
EtanerceptRecombinant form of human TNF receptor that binds TNFRheumatoid arthritis, psoriasis, ankylosing spondylitis EtanerCEPT is a TNF decoy reCEPTor
InfliximabAnti-TNFCrohn’s disease, rheumatoid arthritis, ankylosing spondylitisPredisposes to infections (reactivation of latent TB
AdalimumabDirectly binds TNF alphaRheumatoid arthritis, psoriasis, ankylosing spondylitis