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ATOPIC DERMATITIS aka: Eczema -Pruritic erythematous, oozing rash with vesicles and edema -Involves the face and flexor surfaces. -Type I HSR, associated with asthma and allergic rhinitis
Rx: Topical steroids, if needed. |
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CONTACT DERMATITIS -pruruitic erythematous, oozing rash with vesicles and edema (looks like eczema) -arrises upon exposure to allergens.
Irritants: -poison ivy and nickel jewelery (type IV HSR) -irritant chemicals (e.g. detergernts) -drugs (e.g. PCN)
Rx: -removal of offending agent -topical steroids, if needed |
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ACNE VULGARIS -Comedones (whiteheads and blackheads) -Pustules (pimples) -Nodules
**due to chronic inflammation of hair follicles and sebaceous glands -hormone related increase in sebum and excess keratin block follicles (comedones) -Proponium bacterium acnes infection leads to inflammation (pustules and nodules)
Rx: -benzoyl peroxide (antimicrobial) -vitamin A derivatives (isotretinoin)-reduces keratin production |
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PSORIASIS -well-circumscribed salmon-colored plaques with silvery scale. -usually on extensor surfaces and scalp -pitting of nails may also be present
**due to excessive keratinocyte proliferation -possible autoimmne etiology -associated with HLA-C -lesions often arise in areas of trauma (environmental trigger)
On Micro: -acanthosis -parakaratosis (w/retention of nuclei) -elongation of dermal papilla -thin epidermis (leeds to pinpoint bleeding Osbitz sign)
Rx: corticosteroids -UVA light with Psoralen (PUVA): damages proliferating keratin -immune modulating therapy |
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LICHEN PLANUS -pruritic, planar, polygonal, purple, papules -often with reticular white lines on surface (wickham striae) -commonly involves wrists, elbows, oral mucosa
Histology: inflammation @ dermal-epidermal junction (saw-tooth appearance at the junction)
Etiology is unknown **associated with chronic Hepatitus C-virus infection. |
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PEMPHIGUS VULGARIS -autoimmune destruction of desmosomes -due to IgG antibody against desmoglein -IF highlights surrounding keratinocytes ("fish net") -involves the skin and oral mucosa
Histology -blister in the spinosum, with basal layer intact -thin epidermis (rptures easily, allowing for shallow crusts on the skin) -the basal layers are attached via hemidesmosomes, allowing for the "tomb-stone" appearance |
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BULLOUS PEMPHIGOID -autoimmune destruction of hemidesmosomes -IgG antibody against basement membrane (linear IF) -presents as subepidermal blisters of skin; oral mucosa spared -tense bullae do not rupture easily (due to thick dermis)
HISTOLOGY: entire epidermis is lifted off the basement membrane. |
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DERMATITUS HERPETIFORMIS -autoimmune deposition of IgA at tips of dermal papillae -presents as pruritic vesicles and bullae that are grouped. -strong association with celiac disease Rx: treat celiac disease with gluten free diet. |
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ERYTHEMA MULTIFORME -HSR with targetoid rash and bullae -most commonly associated with HSV infection
*EM w/oral mucosa involvement and fever is termed SJS -TEN is a severe form of SJS -diffuse sloughing of skin resembling a large burn -most often arises due to an adverse drug reaction |
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SEBORRHEIC KERATOSIS -benign squamous proliferation, commonly in the elderly -"stuck on", coin like appearance
Histology -raised lesion with hallmark "pseudocysts" |
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LESER-TRELAT SIGN -sudden onset of multiple seborrheic keratosis -suggests underlying carcinoma of GI tract |
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ACANTHOSIS NIGRICANS -epidermal hyperplasia with darkening of skin (velvet-like skin) -often involves groid or axilla -associated with insulin resistance (T2 DM) or malignancy (gastric carcinoma) |
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BASAL CELL CARCINOMA -malignant proliferation of basal cells of the epidermis -risk factors include prolonged exposure to sunlight, albinism, xeroderma pigmentosum (defect in nucleotide excision repair)--ALL THESE HAVE TO DO WITH UVB! ***arises on upper lip
Histology: nodules of basal cells peripherial pallisading
Rx: surgical excision, rarely mets. Excellent prognosis :) |
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-malignant proliferation of squamous cells -risk factors: exposure to UVB sunlight, albinism, xeroderma pigmentosum **pyrimidine dimers -additional risk factors: immunosuppressive therapy, arsenic poisoning, chronic inflammation (scar from burn, draining sinus tract) -presents as an ulcerated, nodular mass -usually on the face, classically involving the lower lip. Rx: excision, mets are uncommon, excellent prognosis |
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ACTINIC KERATOSIS -precursor to squamous cell carcinoma -presents as a hyperkeratotic scaly plaque on face, back, neck (dysplasia of squamous cells) |
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KERATOACANTHOMA -well differentiated SCC -develops rapidly and regresses spontaneously -presents as a cup shaped tumor filled with keratin debris |
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VITILIGO -localized loss of skin pigmentation -due to autoimmune destruction of melanocyte
(easily seen on dark skin, but with those who have light skin, they will not be able to tan in a certain area). |
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ALBINISM -congenital lack of pigmentation -due to enzyme defect (usually tyrosinase) that impairs melanin production -may involve eyes (ocular form) or both the eyes and skin (oculocutaneous form) -increased risk of skin cancer: squamous, basal, melanoma |
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MELASMA -mask-like hyperpigmentation of cheecks -associated with pregnancy and OCPs |
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What is the most common cause of death from skin cancer? |
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What are the risks for melanoma? |
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prolonged exposure to sunlight, albinism, xeroderma pigmentosum
DYSPLASTIC NEVUS SYNDROME: autosomal dominant disorder characterized by dysplastic nevi-->melanoma |
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What are the ABCDs of Melanoma? |
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A: Asymmetry B: Borders are irregular C: color is not uniform D: diameter is > 6mm |
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What are the two growth phases of Melanoma? What is the key feature for mets? |
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1. radial growth horizonally along the epidermis and superficial dermis 2. vertical growth into deep dermis **key feature for mets |
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-lentigous proligeration (radial growth) - good prognosis |
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Superficial Spreading Melanoma |
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-Most Common Subtype -Dominant Early Radial Phase -Good Prognosis |
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-early vertical phase -poor prognosis :( |
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Acral Lentigenous Melanoma |
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-arises on palms or soles, often in dark-skinned individuals -not related to UV light exposure |
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IMPETIGO -superficial bacterial skin infection -most often due to S.aureus, S.pyogenes -commonly affects children (extremely contagious)
Presents as an erythematous macules (flat lesions) that progress to pustules -usually on face -results in erosions and dry, crusted, honey-colored serum |
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CELLULITIS
-deeper (dermal) infection -usually due to S aureus or S pyogenes -presents as a red, tender, swollen rash with fever -risk factors: recent surgery, trauma, insect bite (all of which introduce bacteria)
can progress to NECROTISING FASCITIS -necrosis of subcutaneous tissue due to infection with anaerobic "flesh eating" bacteria -production of CO2 leads to crepitus -surgical emergency |
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STAPHLOCOCCAL SCALDED SKIN SYNDROME -sloughing of the skin with erythematous rash and fever -leads to significant skin loss -A +B toxins are exfoliative toxins that separate stratum granulosum from rest of skin
**distinguished from TEN @ level of skin separation (separation in TEN occurs in dermal/epidermal junction). |
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VERRUCA aka: wart -flesh colored papule with rough surface -due to HPV infection of keratinocytes -usually on hands and feet |
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MOLLESCUM CONTAGIOSUM -firm, pink, umbilicated papules due to poxvirus -most often arise in children; also occur in sexually active adults and immunocompromised individual
**mollescum bodies with viral inclusions |
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Clinical Manifestiation: abrupt onset characterized by fever, chills, prostration, myalgia, HA followed by respiratory sympx of rhiniis and dry cough. Recovery slow, cough last 2-4 weeks.
People: CHRONIC cardiac or pulmonary disease; the elderly
Type: Orthomyxovirus
Description: Enveloped, -SS RNA, 8-segment genome
Virulence Factors: Hemagglutinin (promotes viral entry), Neuraminidase (promotes progeny viron release) PATHOGENESIS: infects respiratory epithelial cells, resulting in cell death.
Risks: fatal bacterial superinfection, RAPID GENETIC CHANGES
Protection: Killed viral vaccine (reformed each FALL); Neruoamidase inhibitors- Zanamivir and Oseltamivir; Amandaine, rimantadine
Other: there are 3 types of influenza: A,B,C. A infects humans and other animals and causes EPIDEMIC disease. B is only humans (milder epidemic dz). C doesn't really do much. Spread by RESPIRATORY DROPS
SHIFT-Just A DRIFT- A and B REYE'S SYNDROME-associated with Influenza B |
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Causes TYPHOID FEVER
Description: Gram negative, rod
Etiology- FOUND ONLY IN HUMANS
Clinical Manifestations: characterized by rose spots on the abdomen, fever, headache, diarrhea.
**Can remain in gallbladder and cause a carrier state (TYPHOID MARY)
Rx: Ampicillin, Chloramphenicol, trimethoprim, ceftriaxone, criprofloxacin. Prevention involves PROPER SANITATION, Carriers NOT handling food, and vaccine against the vi polysaccharide |
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Causes Cutaneous Antrax.
Bacillus Anthracis
Description: Gram positive rod, end-to-end chains. Capsule made from B-lactamases(polypeptide capsule)
Virulence Factors: Edema factor (mimics the adenylate cyclase enzyme:increase cAMP-->likely responsible for characteristic edematous borders of black eschar in cutaneous antrhax); SPORE FORMING IN SOIL;anthrax toxin
Other forms: INHALATIONAL ANTHRAX-fatal and characterized by rapid and massive edema in the chest followed by cardiovascular shock. GASTROINTESTINAL ANTHRAX-injestions of spores (rare, but highly fatal)
Treatment/Prevention: ciprofloxacin, doxycycline, and rifampin |
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Clostridium tetani
Cause of Tetanus
Description: gram positive anaerobic rod; tennis racket appearance because of terminal spore
Transmission: associated with deep puncture wound which spores in the soil are inoculated
Virulence Factors: tetanospasmin (muscle rigidity and "lock jaw,"; toxin prevents release of inhibitory (GABA, gly) neruotransmitters in spinal cord)
Treatment: antitoxin +vaccine booster +diazepam |
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Causes Acute Enterocolitis
Description: gram negative rode, lactose non-fermenter, faculative intracellular, encapsulated, oxidase negative, have flagella, produce hyprogen sulfide
Transmission: can disseminate hematogenously; invades intestinal mucosa and causes a monocytic response
Reservoirs: have many animal reservoirs (chicken)
Diarrhea type: can cause bloody diarrhea
Rx:fluid replacement due to diarrhea |
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Causes Food Poisoning
Description: Gram-positive anaerobic rod Characteristics: Spore formation
Associations: reheated meat dishes
Etiology-spores are in the soil and colon of many animals and humans. Transmission is thru wound contamination and by ingestion of contaminated food
Clinical manifestiations-gas gangrene, food poisoning
Pathogenesis-gas gangrene: alpha toxin (lecithinase that causes damage to membranes and tissues, bleeding, and increased vascular permiability that can lead to systemic spread of |
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Found in water contaminated with animal urine, causes leptospirosis: flu-like symptoms, jaundice, photophobia with conjunctivitis.
People: prevalent among surfers and in tropics (e.g. Hawaii)
Weil's disease (icterohemorrhagic leptospirosis)-severe form with jaundice and azotemia from liver and kidney dysfunction; fever, hemorrhage and anemia. |
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**Reheated rice syndrome
Causes food poisoning. Spores survive cooking rice. Keeping rice warm results in germination of spores and enterotoxin formation
Emetic type- rice and posta. N/V seen within 1-5 hours. Caused by cereulide, a preformed toxin
Diarrheal type causes watery, nonbloody diarrhea in 8-18 hours. |
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Corynebacterium diptheriae
Description: Gram positive rod, pleomorphic
Virulence: Toxin-Diptheria toxin (A-B toxin) inactivates elongation factor (EF-2): pharyngitis with pseudomembranes in throat and severe lymphadenopathy (bull neck)
Causes diptheria via exotoxin encoded by B-prophage. Potent exotoxin inhibits protein synthesis via ADP-ribosylation of EF-2.
Symptoms: pseudomembranous pharyngitis (grayish-white membrane) with lymphadenopathy, myocarditis, and arrythmias.
Lab diagnosis based on gram-positive rods with metachomic (blue and red) granules and Elek's test for toxin.
Toxoid vaccine prevents diptheria
Corne=club shaped Black colonies on cystine-tellurite agar ABCDEFG: A-ADPribosylation, B-Beta prophage, C-Corynebacterium, D-Diptheria, E-EF2, G-granules. |
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Presentation: Invasive;dysentery
Microbe invades intestinal mucosa and causes necrosis and inflammation. No toxins produced. Clinical manifestations similar to Shigella
Disease is self limiting
Rare in the US, most often associated with disease in developing countries |
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Traveller's diarrhea (watery)
Labil toxin/stable toxin. No inflammation |
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UNDERCOOKED MEAT
O157:H7 most common serotype. Produces Shiga-like toxin (Inactivate 60S ribosome by removing adenine from rRNA-->enhances cytokine release, causing HUS; does not invade host cells) and Hemolytic-uremic syndrome (triad of anemia, thrombocytopenia, acute renal failure).
Endothelium swells and narrows lumen, leading to mechanical hemolysis and reduced renal blood flow; damaged endothelium consumes platelets.
Dysentery (toxin alone causes necrosis and inflammation)
Does not ferment sorbital (distinguishes it from other E.Coli |
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Rubella
A togavirus (+SS, linear, icosahedral). Causes rubella (aka German (3-day) measles). Fever, postauricular adenopathy, lymphadenopathy, arthalgias, fine truncal rash that starts at head and moves down. Causes mild disease in children, but serious congenital disease
Rash of childhood: rash begins at head and moves down-->fine truncal rash; post auricular lymphadenopathy.
CONGENTIAL Mode of Transmission: respiratory droplets Maternal Manifestations: Rash, lymphadenopathy, arthritis Neonatal Manifestatons: Classic triad-PDA-giving continuous machine-like murmur; loudest at S2 (L infraclavicular area) (or pulmonary artery hypoplasia), cataracts, and deafness +/- 'blueberry muffin' rash
MMR VACCINE |
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