DERM ROTATION Flashcards

Question

WHY CAN'T ISOTRETINOIN AND DOXYCYCLINE BE GIVEN TOGETHER

Answer 1

INCREASED INTRACRANIAL PRESSURE | PSEUDOTUMOR CEREBRI

Answer 2

- velvety thickening + hyperpigmentation of skin ``` - associated with ⦁ endocrine disorders - diabetes*** - insulin resistant syndrome - PCOS - Acromegaly - Cushing's Syndrome - Addison's - Hypothyroidism ``` ⦁ obesity*** ⦁ Paraneoplastic Syndrome - internal malignancy (most commonly GI, GU or lung) or lymphoma Most of the cases of acanthosis nigricans are associated with obesity. Patients with new-onset acanthosis nigricans should be screened for the presence of DM , as it is a common underlying cause. Diabetes causes acanthosis nigricans due to stimulation of insulin-like growth factor receptor-1. Obesity and diabetes mellitus are among the most frequently associated disorders. Rarely, acanthosis nigricans develops as a sign of internal malignancy (most commonly GI) Abdominal adenocarcinomas, particularly gastric adenocarcinomas, represent the majority of acanthosis nigricans-associated tumors Rarely, certain medications can cause AN = steroids, insulin, OCP, Niacin, testosterone, Aripiprazole (SGA) ⦁ Acanthosis nigricans is a potential cutaneous adverse effect of niacin (cholesterol med + vitamin B3) use due to the hyperglycemia it causes. The familial cases of acanthosis nigricans are inherited in an autosomal DOMINANT manner HX = insidious onset; first visible change = darkening of pigmentation - skin changes occur slowly - skin may also have an odor or an itch PE = hyperpigmentation, velvety looking, skin line accentuation, surface becomes wrinkled or creased MOST COMMON SITES = axilla, neck (back + sides), groin, antecubital fossa, knuckles if < 40 = usually diabetes or endocrinopathy if > 40 = should rule out adenocarcinomas of the colon if dark thickening in the mouth = think malignancy DIAGNOSIS ⦁ usually made clinically ⦁ biopsy = will show hyperkeratosis with melanocytes TREATMENT - 1) rule out diabetes - 2) treat underlying cause - usually acanthosis nigricans will then resolve - 3) usually no tx required for pigmentation itself ⦁ topical retinoids can be tried in patients with persistent acanthosis nigricans despite treatment of the underlying cause

Answer 3

a small, rough growth resembling a cauliflower or a solid blister A hard, rough, skin-colored growth on the skin It typically occurs on humans' hands or feet but often in other locations. Warts are caused by a VIRAL INFECTION of keratinocytes, specifically by one of the many types of human papillomavirus (HPV). ⦁ HPV 1, 2, 4 cause common warts on skin ⦁ HPV 6, 11 cause 90% of genital warts that rarely develop into cancer ⦁ HPV 16, 18 = dangerous ones - cause about 70% of cervical cancer There are as many as 10 varieties of warts, the most common considered to be mostly harmless. HPV infects keratinized skin, causing excessive proliferation and retention of the stratum corneum, which leads to papule formation Infection occurs in the superficial layers of the epidermis, causing proliferation of the keratinocytes (skin cells) and hyperkeratosis — the wart HPV is spread by direct skin-to-skin contact or autoinoculation. This means if a wart is scratched or picked, the viral particles may be spread to another area of skin. The incubation period can be as long as twelve months. CUTANEOUS HPV ⦁ verruca vulgaris (common warts), verruca plantaris (plantar warts), verruca plana (flat warts) MUCOSAL HPV ⦁ condyloma acuminate (genital warts) ⦁ cervical dysplasia / cancer ⦁ anogenital carcinoma (intraepithelial) HPV has the ability to cause malignant transformation It is possible to get warts from others; they are contagious and usually enter the body in an area of broken skin. CLINICAL MANIFESTATIONS / PHYSICAL EXAM ⦁ firm, hyperkeratotic papules between 1-10mm with red-brown punctations (thrombosed capillaries) = food source ⦁ borders = can either be rounded or irregular ⦁ common on hands and feet PLANTAR WARTS - can be painful/uncomfortable if located in areas of pressure - have black dots that are blood vessels SUBUNGUAL / PERIUNGUAL WARTS - a subclassification of palmar/plantar warts - found around + under nail apparatus - can cause nail dystrophy / pain on grasping objects - long-standing periungual/subungual warts that have a changing morphology should be biopsied to rule out malignant transformation into SCC FILIFORM WARTS = Filiform warts are on a long stalk like a thread. They commonly appear on the face. They are also described as digitate (like a finger). FLAT WARTS (VERRUCA PLANA) = numerous, small, discrete, flesh-colored papules measuring 1-5mm in diameter and 1-2mm in height. Plane warts have a flat surface. The most common sites are the face, hands and shins. They are often numerous. They may be inoculated by shaving or scratching, so that they appear in a linear distribution (pseudo-Koebner response). Plane warts are mostly caused by HPV types 3 and 10. ``` GENITAL WARTS (CONDYLOMA ACUMINATA) ⦁ tiny, PAINLESS, papules that evolve into soft, fleshy, cauliflower-like lesions that range from skin-colored to pink/red ⦁ occur in clusters in genital regions + oropharynx ⦁ lesions persist for months, and may spontaneously resolve or may remain unchanged / grow if not treated ``` DIAGNOSIS - clinical diagnosis based on appearance - biopsy - mucosal HPV = *** whitening of lesion with acetic acid application *** ``` Plantar warts (HPV 1/2/4) vs callus ⦁ plantar warts interrupt skin lines ⦁ calluses - skin lines are retained ``` TREATMENT - most warts resolve spontaneously within a few years, 50% will resolve within 2 years if immunocompetent To get rid of them, we have to stimulate the body's own immune system to attack the wart virus. Persistence with the treatment and patience is essential ⦁ cryotherapy - ring warts commonly seen after cryotherapy - ring or donut shaped wart with central clearing ⦁ topical retinoids (adapalene, tretinoin) ⦁ Efudex ⦁ Salicylic acid - works by removing the dead surface skin cells ⦁ Trichloroacetic acid = particularly helpful for vaginal warts ⦁ electrocautery ⦁ podophyllin - a resin extracted from the root of the plant Podophyllum sp. Berberidaceae (mandrake), which contains podophyllotoxin; a cytotoxic agent that has been used topically in the treatment of genital warts. It arrests mitosis in metaphase. a cytotoxic agent - must not be used in pregnancy or in women considering pregnancy ⦁ Imiquimod (Aldara) = Topical immunomodulator - works by increasing the activity of the body's immune system - used to treat warts (specifically works well for genital/perianal warts****), also used for AKs / superficial BCCs ⦁ Cantharidin - secreted by many species of blister beetles. It is a burn agent or a poison in large doses. It's cutaneous effect is the separation (acantholysis) and death of epidermal cells ⦁ Bleomycin - intralesional injection - antibiotic derived from the fungus Streptomyces verticillus but is mainly used as a chemotherapy drug. It causes DNA strand scission (breakages in the DNA strand), preventing cell replication. ⦁ Candida Albicans injection - stimulates an immune response

Answer 4

Tinea versicolor (pityriasis versicolor) is a common superficial fungal infection. ``` Tinea = fungus pityriasis = rash that causes scale/flake lesions ``` Patients often present with hypopigmented, hyperpigmented, or erythematous macules on the trunk and proximal upper extremities. Tinea versicolor is a skin condition displaying hyperpigmentation as well as hypopigmentation due to infection with Malassezia species. Unlike other disorders utilizing the term tinea, it is NOT A DERMATOPHYTE infection (trichophyton, epidermophyton, microsporum). The causative organisms are saprophytic, lipid-dependent yeasts in the genus MALASEZZIA FURFUR. CAUSE - The Malassezia fungus causing tinea versicolor degrades FATTY ACIDS leading to destruction of melanocytes - which is why areas of the body that typically produce more sebum are typically affected (back / chest / shoulders) - The degradation of lipids produces azelaic acid which damages melanocytes --> pigment changes The yeasts produce chemicals: Azeleic Acid (used to treat acne and rosacea) that reduces the pigment in the skin The Malassezia fungus causing tinea versicolor degrades fatty acids leading to destruction of melanocytes. ⦁ Tinea versicolor thrives in a hot + humid environment DIAGNOSIS ⦁ clinical diagnosis ⦁ *** KOH Prep *** - The microscopic pathognomonic ** SPAGHETTI + MEATBALL ** appearance of tinea versicolor represents hyphae and spores (fungus) ⦁ Wood's Lamp - ** yellow/green fluorescence ** The involved skin fails to tan with sun exposure TREATMENT - The treatment for tinea versicolor are selenium sulfide, topical and/or oral antifungal medications. ``` ⦁ Ketoconazole (Xolegel)*** / Miconazole ⦁ Selenium Sulfide (Selsun blue) ⦁ Pyrithione Zinc (Head + Shoulders) ⦁ Nizoral shampoo ⦁ Fluconazole (Diflucan) or Itraconazole if widespread or failed topical therapy ``` Anti-dandruff shampoos work for tinea versicolor because same yeast is present in both conditions (Malassezia Furfur) Azoles are delivered to the skin via sweat, so best not to shower for 8-12 hrs after oral azole therapy

Answer 5

Caused by HHV-3 - Varicella Zoster Virus Chicken Pox = Primary varicella infection Transmission = respiratory droplets, direct contact The virus spreads mainly by touching or breathing in the virus particles that come from chickenpox blisters, and possibly through tiny droplets from infected people that get into the air after they breathe or talk 10-20 day incubation period It takes about 2 weeks (from 10 to 21 days) after exposure to a person with chickenpox or shingles for someone to develop chickenpox Usually lasts 5-7 days - highly contagious! ⦁ is highly contagious from 2 days before onset of rash until all lesions have crusted A person with chickenpox can spread the disease from 1 to 2 days before they get the rash until all their chickenpox blisters have formed scabs (usually 5-7 days). RASH - appears on face + trunk (chest / back), then spreads to extremities - CENTRIPETAL RASH = lesions mostly distributed on face / trunk, less so on extremities (smallpox = centrifugal - mostly face + extremities) ⦁ vesicles - "dew drops on a rose petal" = clusters of vesicles on erythematous base ⦁ pruritic ⦁ become pustules + crust over vesicles are in *** DIFFERENT STAGES *** - have macules, papules, vesicles, pustules, and crusted lesions ``` SYMPTOMS - may begin to show 1-2 days prior to rash ⦁ fever ⦁ malaise ⦁ headache ⦁ decreased appetite ``` - more severe presentation may occur in adults Some people who have been vaccinated against chickenpox can still get the disease. However, the symptoms are usually milder with fewer red spots or blisters and mild or no fever. Though uncommon, some vaccinated people who get chickenpox will develop illness as serious as chickenpox in unvaccinated persons. Chickenpox can be spread from people with shingles to others who have never had chickenpox or received the chickenpox vaccine. This can happen if a person touches or breathes in virus from shingles blisters If a person vaccinated for chickenpox gets the disease, they can still spread it to others. For most people, getting chickenpox once provides immunity for life. However, for a few people, they can get chickenpox more than once, although this is not common. The best way to prevent chickenpox is to get the chickenpox vaccine. Children, adolescents, and adults should get two doses of chickenpox vaccine. Chickenpox vaccine is very safe and effective at preventing the disease. Most people who get the vaccine will not get chickenpox. If a vaccinated person does get chickenpox, it is usually mild—with fewer red spots or blisters and mild or no fever. The chickenpox vaccine prevents almost all cases of severe disease. TREATMENT - usually self-limiting - Calamine lotion and colloidal oatmeal baths may help relieve some of the itching - Keeping fingernails trimmed short may help prevent skin infections caused by scratching blisters - if symptomatic ⦁ benadryl for pruritus ⦁ tylenol for fever Do not use aspirin or aspirin-containing products to relieve fever from chickenpox. The use of aspirin in children with chickenpox has been associated with Reye’s syndrome, a severe disease that affects the liver and brain and can cause death Encourage kids/adults not to scratch chickenpox lesions, as this can lead to scarring - Systemic ⦁ Acyclovir (Zovirax) = 800mg 5x/day x 7 days ⦁ Valacyclovir (Valtrex) = 1g TID x 7 days ⦁ Famciclovir = 500mg TID x 7 days Acyclovir, an antiviral medication, is licensed for treatment of chickenpox. The medication works best if it is given within the first 24 hours after the rash starts. Other antiviral medications that may also work against chickenpox include valacyclovir and famciclovir CDC recommends two doses of chickenpox vaccine for children, adolescents, and adults. Children should receive two doses of the vaccine—the first dose at 12 through 15 months old and a second dose at 4 through 6 years old

Answer 6

- one of the most common benign skin growths - due to fibrous tissue proliferation - exact etiology = unknown - usually occur on the extremities - predilection for the legs DF = seen almost exclusively in adults, and tend to occur slightly more often in females than in males - no race predilection CLINICAL MANIFESTATIONS ⦁ DFs can range from 2mm to 2cm ⦁ round or oval in shape ⦁ usually solitary, but may have multiple in various locations ⦁ usually small (4-5mm), firm, red or slightly purple papules that DIMPLE with lateralized pressure The "dimple" sign is often used clinically to differentiate DFs from other growths CAUSE - history of possibly inciting local trauma at the site, such as from an insect bite or superficial puncture wound from thorns or wood splinters. Dermatofibromas occur in people of all ages, although more commonly during the ages of the 20s to 40s, and develop more frequently in females than males They are a benign tumor, although there have been cases of local recurrence, and even more rarely, distant metastases have been reported. When considering the differential diagnosis of these lesions, it is vitally important to distinguish dermatofibromas from dermatofibrosarcoma protuberans, a similar appearing but more aggressive cutaneous neoplasm. DIAGNOSIS ⦁ Clinical diagnosis - dimple sign ⦁ Dermoscopic evaluation of these lesions will most commonly exhibit a central white patch with a peripheral pigmented network ("starburst appearance") TREATMENT ⦁ NONE - benign ⦁ can excise

Answer 7

- Cause = unknown - Vesicular eruption on the skin of hands + feet - marked by intense itching*** - vesicles are deep - scaling, fissures and lichenification may follow ``` TRIGGERS ⦁ sweating ⦁ emotional stress ⦁ warm / humid weather ⦁ pollen ⦁ metals (nickel / cobalt / chromium salts in objects and/or food) ``` - Association with seasonal allergies dyshidrotic eczema blisters are known to erupt more frequently during the spring allergy season. The blisters may last up to three weeks before they begin to dry and can sometimes be large and painful. As the blisters dry, they may turn into skin cracks or cause the skin to feel thick and spongy, especially if you’ve been scratching the area Dyshidrotic eczema usually appears in adults ages 20 through 40 but it can also affect children People with contact dermatitis, atopic dermatitis or hay fever, are at higher risk of developing dyshidrotic eczema Dyshidrotic eczema seems to run in families, so if you have a close relative with this form of eczema, your chance of also developing it is increased. CLINICAL MANIFESTATION ⦁ pruritic "tapioca like" tense vesicles on soles, palms and fingers (common on lateral digits) Characterized by a pruritic vesicular eruption comprised of clear, deep-seated vesicles without erythema erupting on the lateral aspects of fingers, the central palm, and plantar surfaces. The eruption has been described as resembling tapioca pudding. The onset may be acute, recurrent, or chronic. TREATMENT ⦁ High potency topical steroids - ointments preferred; may need to be given with occlusion ⦁ hydration of skin with emollient cream ⦁ cold compresses, Burrow's solution, Tar soaks

Answer 8

Chronic acneiform disorder of facial pilosebaceous units an inflammatory facial skin disorder characterized by erythematous papules and pustules, but no comedones. - increased reactivity of capillaries to heat PATHOPHYSIOLOGY - *** dermal matrix degeneration *** - This leads to the pathologic pooling of blood and concentration of reactive oxygen species and inflammatory mediators in the dermis. The exact etiology for rosacea is unknown. Some believe that it may be a T-cell mediated immune response to the presence of microbial agents (particularly the Demodex species, which are mites that typically infect human hair follicles). However, the evidence is conflicting - onset: 30-50 years old - predominantly affects females ``` EXACERBATING ROSACEA FACTORS ⦁ hot liquids ⦁ spicy foods ⦁ alcohol ⦁ exposure to sun + heat ⦁ exercise ⦁ stress ``` CLINICAL PRESENTATION OF ROSACEA ⦁ redness to cheeks, nose and chin ⦁ burning or stinging with episodes ⦁ skin dryness, edema The nose, cheeks, forehead, chin, and glabella are the most commonly affected areas. Clinical features include flushing, telangiectasias, erythema, papules and pustules, and rhinophyma. More than 50% of patients with rosacea have ocular manifestations, and ocular findings may be the first manifestation of rosacea in some patients. Variable erythema and telangiectasia are seen over the cheeks and the forehead. Inflammatory papules and pustules may be predominantly observed over the nose, the forehead, and the cheeks. Prominence of sebaceous glands may be noted, with the development of thickened and disfigured noses (rhinophyma) in extreme cases. Unlike acne, patients generally do not report greasiness of the skin; instead, they may experience drying and peeling. The absence of comedones is another helpful distinguishing feature. Rhinophyma may occur as an isolated entity, without other symptoms or signs of rosacea. Rhinophyma can be disfiguring Manifestations of ocular rosacea range from minor irritation, foreign body sensation, dryness, and blurry vision to severe ocular surface disruption and inflammatory keratitis. Patients frequently describe a gritty feeling, and they commonly experience Blepharitis and conjunctivitis. Other ocular findings include lid margin and conjunctival telangiectasias, eyelid thickening, eyelid crusts and scales, chalazia and hordeolum, punctate epithelial erosions, corneal infiltrates, corneal ulcers, corneal scars, and vascularization Ocular rosacea is most frequently diagnosed when patients also suffer from cutaneous disease. However, ocular signs and symptoms may occur prior to cutaneous manifestations in 20% of patients with rosacea ``` 4 SUBTYPES OF ROSACEA ⦁ erythematotelangiectatic rosacea ⦁ papulopustular rosacea ⦁ phymatous rosacea (large nose - rhinophyma) ⦁ ocular rosacea ``` TREATMENT FOR ROSACEA - to minimize precipitating factors - TOPICAL ANTIBIOTICS = 1st line therapy for mild to moderate patient use gel or creams ⦁ Azelaic acid ⦁ Metronidazole - most common ⦁ Erythromycin ⦁ Clindamycin ⦁ Brimonidine (Mirvaso) = alpha -2 agonist = vasoconstrictor; best for facial flushing / persistent redness) - brimonidine can also be used for acute angle closure glaucoma ⦁ Topical Ivermectin cream (Soolantra) = for ppl who get papulopustular acneiform rosacea due to being immunologically sensitive to mites ⦁ Laser SYSTEMIC ANTIBIOTICS = for mod/severe rosacea ⦁ Tetracycline ⦁ Doxycycline (Oracea) / Minocycline ⦁ Erythromycin FACIAL REDNESS/FLUSHING TX = BRIMONIDINE (MIRVASO) PAPULOPUSTULAR DISEASE TX = metronidazole, azelaic acid, ivermectin (soolantra) = 1st line; can try sodium sulfacetamide can do oral antibiotics for mod/severe = tetracyclines (doxy/tetra), oral metronidazole, oral ivermectin, sodium sulfacetamide

Answer 9

also known as barber's itch, folliculitis barbae traumatica, razor bumps, scarring pseudofolliculitis of the beard, and shave bumps - "razor bumps" - very common in african americans - occurs when free ends of tightly coiled hairs re-enter skin and cause foreign body inflammatory response - firm papules with embedded hair ⦁ extrafollicular penetration = curly hair coming out and coming back into the hair = more common ⦁ intrafollicular penetration = hair grows out of a different spot - out of the follicle DIAGNOSIS = made based on clinical appearance TREATMENT ⦁ Most effective and safe is stop shaving (first line) ⦁ Laser hair removal ⦁ Adjunctive medical therapy - Topical retinoids (Tretinoin) - Low potency topical corticosteroids (treat only for 3-4 weeks) - Topical antimicrobials (benzoyl peroxide 5% or clindamycin 1%) is a medical term for persistent irritation caused by shaving

Answer 10

= Antimicrobial antibiotics that inhibit bacterial ribosomes- which make proteins ⦁ transcription = DNA --> mRNA ⦁ translation = mRNA --> protein (via ribosomes) Prokaryotic Cells (Bacteria) have smaller ribosomes than Eukaryotic Cells (Humans) Bacterial Ribosomes are made up of a 50S subunit and a 30S subunit, which combine to form a 70S ribosome Eukaryotic Ribosomes are made up of a 60S subunit and a 40S subunit, which combine to form a 80S ribosome Can therefore create antibiotics that selectively interfere with the bacterial ribosomes and not our own In both Prokaryotic and Eukaryotic Cells, protein formation occurs in 3 stages of 1) Initiation 2) Elongation 3) Termination In Prokaryotic Cells, Initiation consists of the 50S and 30S subunit combining and attaching to mRNA to form ribosome-mRNA complex - the mRNA serves as a blueprint for the protein that is going to be synthesized Tetracyclines were initially derived from soil-dwelling Streptomyces bacteria - get their name from their structure of 4 rings bound together (tetra) (cyclines) Tetracyclines bind to the A-SITE of the 30S SUBUNIT - this inhibits tRNA from binding to the mRNA-ribosome complex, which therefore shuts down protein synthesis of the prokaryotic bacteria TETRACYLINE ANTIBIOTICS are divided based on DURATION OF ACTION ⦁ Tetracycline = short half life (about 8 hrs) ⦁ Doxycycline/ Minocycline = longer half life (16+ hrs) Some bacteria have developed enzymes that can break down Tetracyclines, or they have proteins on their membrane that can pump the medication out ---> developed TIGECYCLINE TIGECYCLINE = Glycylcycline drug class = modified tetracyclines with an additional Dimethylglycocylamido side chain that prevents the medication from directly binding to the bacterial proteins so that they can overcome bacterial defense mechanisms - was created in response to increasing resistance TETRACYCLINE ADMINISTRATION - topical - oral - Tigecycline = IV only ORAL TETRACYCLINES should NOT be taken with food, as it can readily bind with magnesium, iron, aluminum and calcium, which makes it unable to be absorbed - which is why Tetracyclines are NOT given to patients on iron + calcium supplements, or antacids, which can contain aluminum salts TETRACYCLINES = BROAD SPECTRUM - meaning they can target a wide variety of both gram + and gram - bacteria INDICATIONS FOR TETRACYLINES ⦁ Acne ⦁ Community acquired Pneumonia ⦁

Answer 11

an inherited connective tissue disease that causes blistering of the skin and mucosal membranes This disease is most often diagnosed in newborns and young children. Epidermolysis bullosa encompasses a clinically and genetically heterogeneous group of rare inherited disorders characterized by marked mechanical fragility of epithelial tissues with blistering and erosions following minor trauma.

DERM ROTATION Flashcards

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