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August 2017 NHSPA CME Quiz

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August 2017 NHSPA CME Quiz
At the conclusion of this quiz PAs will be able to recognize DRESS Syndrome, know the treatment of rheumatoid arthritis, be able to differentiate benign vs. malignant moles, have more knowledge of bony anatomy of the foot, know the treatment of subungual hematomas, be able to identify patients who present with a spontaneous pneumothorax, be able to recognize and treat inverse psoriasis, and know likely laboratory findings in patients with sarcoidosis.

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  • You are required to complete the post-quiz evaluation to receive your CME credit and certificate. Please complete the post-quiz evaluation here. You will receive your CME certificate via email at the end of this CME calendar year. Please note that this CME activity was sponsored by the New Hampshire Society of Physician Assistants (NHSPA). When logging credit into your NCCPA account, the activity tittle will be “August 2017 NHSPA CME Quiz”.

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  1. Question 1 of 8
    1. Question

    A 41- year-old obese Caucasian female presents to the office with a red, dry rash under her breasts that began one week ago. She reports that the rash is very irritating, itches, and has been progressively getting worse. Patient denies pain, history of skin cancer, recent changes in medications, sick contacts, febrile illness, joint pains, or trauma. Punch biopsy confirms inverse psoriasis. Of the following choices, which is the best initial step in this patient’s management?

    Correct

    Answer is D. Triamcinolone acetonide 0.1% Cream. Inverse psoriasis is treated initially with a topical glucocorticoid which should only be applied for a short period of time to avoid atrophy of the skin. If the psoriasis is recurrent or fails to respond to treatment, systemic therapy should be considered. Watchful waiting would not be appropriate because psoriasis is a chronic disorder. Nystatin topical cream treats fungal infections such as Candidal Intertrigo. Topical 5-Fluorouracil has been FDA- approved for the treatment of basal cell carcinomas and actinic keratosis, however, it is not a recommended treatment for psoriasis.

    Discussion
    Psoriasis Vulgaris is a chronic disorder that affects 1.5-2% of the population in Western countries and has various clinical presentations.1 The types of psoriasis vulgaris include acute guttate, chronic stable plaque, palmoplantar, and inverse. Individuals may present with a few lesions in one location while other individuals may have widespread skin involvement. Most cases involve localized psoriasis, but out of the 3-5 million people in the United States diagnosed, 300,000 individuals have generalized lesions.1 The typical psoriatic lesions are scaly papules and plaques that are recurrent.1 Pustules as well as erythema at the base of the lesions are seen along with the plaques.1 Psoriasis affects men and women equally and is seen in all ages with a peak incidence at age 22.5.1 Patients who present at an earlier age tend to have more of an aggressive and longer course. Psoriasis also affects all races, but 3.6% of Caucasians have the condition compared to 1.9% of African Americans.2

    A positive family history is also strongly associated with psoriasis. Interestingly, if one parent has psoriasis the child has an 8% chance of developing the condition and a 41% chance if both parents have psoriasis.1 Triggers for psoriasis include stress, drugs such as glucocorticoids, lithium, interferon, β- adrenergic blockers, alcohol, and trauma such as rubbing or scratching the skin. 1 Guttate psoriasis is also associated with acute streptococcal infection.

    The pathophysiology of psoriasis is marked by the acceleration of the cell cycle of the keratinocytes. As a result there is an over proliferation of epidermal cells and CD8+ T cells (28 times the normal production).1 Psoriasis is treated as an autoimmune response and is considered a disease manifested by T cells.1

    A patient with psoriasis may present with the eruptive type, such as guttate psoriasis, which presents with multiple salmon-pink small plaques commonly on the trunk, and resolves spontaneously.1 However, most individuals diagnosed with psoriasis have the chronic plaque psoriasis type. These lesions present for long periods of time and minimally change. The red plaques have silvery white scales and are sharply demarcated.1 These plaques may coalesce and form larger lesions. Common sites for the chronic stable type include knees, elbows, scalp, palms, soles, and gluteal region.1 Psoriasis is usually symmetric and pruritus often times accompanies the visible plaques. Inverse psoriasis occurs in body folds such as the submammary region. The body folds create a moist and warm environment and often times scales are not seen in these regions. The inverse pattern involves a “brightly erythematous and glistening base”.1 On physical examination the clinician should examine the lesion’s appearance, size, and location. The clinician should determine if the psoriasis is mild, moderate, or severe by observing the total body surface area affected by the psoriasis. Mild is less than 3%, moderate is between 3 to 10% and severe is more than 10%.2 Well-demarcated “red plaques with silvery scales” found on extensor surfaces such as the elbows, knees, with thick scale on the scalp or nail pitting are diagnostic. 3 A skin biopsy or scraping of the body folds may be necessary and will differentiate psoriasis from other skin conditions such as candidal intertrigo.3

    There are various treatments for psoriasis and many factors need to be considered when managing this condition. Localized psoriasis may be effectively treated with topical glucocorticoids, Vitamin D analogues such as calcipotriene, or topical pimecrolimus 1%.1 Inverse psoriasis is treated with topical glucocorticoids for a short amount of time due to atrophy of the skin, and should be switched to topical Vitamin D derivatives, topical tacrolimus, or pimecrolimus.1 Systemic therapies such as oral Methotrexate or intravenous Adalimumab should be considered for psoriasis that recurs or does not respond to treatment. Psoriasis on the scalp typically involves thick scale and plaques which tar or ketoconazole shampoos are initially used and betamethasone valerate or clobestasol propionate may be applied after.1 Generalized psoriasis can also be managed with different therapies. Guttate psoriasis is treated with antibiotics and often times UVB phototherapy. Generalized chronic plaque type is managed with systemic medications such as biologics or phototherapy. They may be used in combination for greater efficacy.

    References

    1. Wolff K, Johnson R, Saavedra A, Roh E. Fitzpatrick’s Color Atlas And Synopsis Of Clinical Dermatology. 7th ed. The McGraw- Hill Companies, Inc.; :49-56.
    2. Learn about plaque psoriasis, guttate psoriasis, inverse psoriasis, and pustular psoriasis | National Psoriasis Foundation. Psoriasisorg. 2017. Available at: https://www.psoriasis.org/about-psoriasis. Accessed April 24, 2017.
    3. Papadakis M, McPhee S, Rabow M. 2015 Current Medical Diagnosis & Treatment. 1st ed. New York: McGraw-Hill Education/Medical; 2015:105-107.

    Incorrect

    Answer is D. Triamcinolone acetonide 0.1% Cream. Inverse psoriasis is treated initially with a topical glucocorticoid which should only be applied for a short period of time to avoid atrophy of the skin. If the psoriasis is recurrent or fails to respond to treatment, systemic therapy should be considered. Watchful waiting would not be appropriate because psoriasis is a chronic disorder. Nystatin topical cream treats fungal infections such as Candidal Intertrigo. Topical 5-Fluorouracil has been FDA- approved for the treatment of basal cell carcinomas and actinic keratosis, however, it is not a recommended treatment for psoriasis.

    Discussion
    Psoriasis Vulgaris is a chronic disorder that affects 1.5-2% of the population in Western countries and has various clinical presentations.1 The types of psoriasis vulgaris include acute guttate, chronic stable plaque, palmoplantar, and inverse. Individuals may present with a few lesions in one location while other individuals may have widespread skin involvement. Most cases involve localized psoriasis, but out of the 3-5 million people in the United States diagnosed, 300,000 individuals have generalized lesions.1 The typical psoriatic lesions are scaly papules and plaques that are recurrent.1 Pustules as well as erythema at the base of the lesions are seen along with the plaques.1 Psoriasis affects men and women equally and is seen in all ages with a peak incidence at age 22.5.1 Patients who present at an earlier age tend to have more of an aggressive and longer course. Psoriasis also affects all races, but 3.6% of Caucasians have the condition compared to 1.9% of African Americans.2

    A positive family history is also strongly associated with psoriasis. Interestingly, if one parent has psoriasis the child has an 8% chance of developing the condition and a 41% chance if both parents have psoriasis.1 Triggers for psoriasis include stress, drugs such as glucocorticoids, lithium, interferon, β- adrenergic blockers, alcohol, and trauma such as rubbing or scratching the skin. 1 Guttate psoriasis is also associated with acute streptococcal infection.

    The pathophysiology of psoriasis is marked by the acceleration of the cell cycle of the keratinocytes. As a result there is an over proliferation of epidermal cells and CD8+ T cells (28 times the normal production).1 Psoriasis is treated as an autoimmune response and is considered a disease manifested by T cells.1

    A patient with psoriasis may present with the eruptive type, such as guttate psoriasis, which presents with multiple salmon-pink small plaques commonly on the trunk, and resolves spontaneously.1 However, most individuals diagnosed with psoriasis have the chronic plaque psoriasis type. These lesions present for long periods of time and minimally change. The red plaques have silvery white scales and are sharply demarcated.1 These plaques may coalesce and form larger lesions. Common sites for the chronic stable type include knees, elbows, scalp, palms, soles, and gluteal region.1 Psoriasis is usually symmetric and pruritus often times accompanies the visible plaques. Inverse psoriasis occurs in body folds such as the submammary region. The body folds create a moist and warm environment and often times scales are not seen in these regions. The inverse pattern involves a “brightly erythematous and glistening base”.1 On physical examination the clinician should examine the lesion’s appearance, size, and location. The clinician should determine if the psoriasis is mild, moderate, or severe by observing the total body surface area affected by the psoriasis. Mild is less than 3%, moderate is between 3 to 10% and severe is more than 10%.2 Well-demarcated “red plaques with silvery scales” found on extensor surfaces such as the elbows, knees, with thick scale on the scalp or nail pitting are diagnostic. 3 A skin biopsy or scraping of the body folds may be necessary and will differentiate psoriasis from other skin conditions such as candidal intertrigo.3

    There are various treatments for psoriasis and many factors need to be considered when managing this condition. Localized psoriasis may be effectively treated with topical glucocorticoids, Vitamin D analogues such as calcipotriene, or topical pimecrolimus 1%.1 Inverse psoriasis is treated with topical glucocorticoids for a short amount of time due to atrophy of the skin, and should be switched to topical Vitamin D derivatives, topical tacrolimus, or pimecrolimus.1 Systemic therapies such as oral Methotrexate or intravenous Adalimumab should be considered for psoriasis that recurs or does not respond to treatment. Psoriasis on the scalp typically involves thick scale and plaques which tar or ketoconazole shampoos are initially used and betamethasone valerate or clobestasol propionate may be applied after.1 Generalized psoriasis can also be managed with different therapies. Guttate psoriasis is treated with antibiotics and often times UVB phototherapy. Generalized chronic plaque type is managed with systemic medications such as biologics or phototherapy. They may be used in combination for greater efficacy.

    References

    1. Wolff K, Johnson R, Saavedra A, Roh E. Fitzpatrick’s Color Atlas And Synopsis Of Clinical Dermatology. 7th ed. The McGraw- Hill Companies, Inc.; :49-56.
    2. Learn about plaque psoriasis, guttate psoriasis, inverse psoriasis, and pustular psoriasis | National Psoriasis Foundation. Psoriasisorg. 2017. Available at: https://www.psoriasis.org/about-psoriasis. Accessed April 24, 2017.
    3. Papadakis M, McPhee S, Rabow M. 2015 Current Medical Diagnosis & Treatment. 1st ed. New York: McGraw-Hill Education/Medical; 2015:105-107.

  2. Question 2 of 8
    2. Question

    A 72 year-old African American man hospitalized due to worsening shortness of breath, cough and chest pain is found incidentally to have an elevated calcium level of 15mg/dL. He reports a 1 year history of mild dyspnea, fatigue, and weight loss. Chest x ray with follow up CT shows bilateral hilar adenopathy and reticular opacities distributed within the upper lung lobes. Laboratory evaluation of this patient may show which of the following?

    Correct

    The answer is D. The patient’s presentation above is suggestive for sarcoidosis, a granulomatous disease that causes an increase in intestinal absorption of calcium. This is due to enhanced secretion of 1 alpha hydroxylase which leads to an increased production of the vitamin D metabolite called calcitriol (1,25 dihydroxyvitamin D) 2. In sarcoidosis, elevated serum calcium concentrations are independent of PTH, therefore intact PTH levels are low. Option A is suggestive of primary hyperparathyroidism, a PTH mediated disease leading to elevated serum and urine calcium levels. Option B is suggestive of familial hypercalciuric hypercalcemia, a genetic disorder affecting the gene that codes for the calcium sensing receptor (CaSR) of the body3. These patients present with normal to mildly elevated PTH levels with increased urinary calcium levels. Option C is suggestive of hypercalcemia of malignancy. Intact PTH levels and vitamin D metabolites are decreased while PTH-rP levels are increased due to secretion by the underlying tumor.

    References:
    1. Agraharkar M. Hypercalcemia. Medscape. http://emedicine.medscape.com/article/240681-overview#a6. Published August 2, 2016. Accessed June 1, 2017.
    2. Agus ZS. Hypercalcemia in Granulomatous Disease. UpToDate. https://www.uptodate.com/contents/hypercalcemia-in-granulomatous-diseases?source=search_result&search=pth-rp%20in%20granulomatous%20disease&selectedTitle=1~150. Published October 29, 2015. Accessed June 1, 2017.
    3. Brown EM. Disorders of the calcium-sensing receptor: Familial hypocalciuric hypercalcemia and autosomal dominant hypocalcemia. UpToDate. https://www.uptodate.com/contents/disorders-of-the-calcium-sensing-receptor-familial-hypocalciuric-hypercalcemia-and-autosomal-dominant-hypocalcemia?source=search_result&search=familial%20hypocalciuric%20hypercalcemia&selectedTitle=1~15. Published April 18, 2017. Accessed June 6, 2017.
    4. Horwitz MJ. Hypercalcemia of Malignancy: Mechanisms. UpToDate. https://www.uptodate.com/contents/hypercalcemia-of-malignancy-mechanisms?source=search_result&search=hypercalcemia%20of%20malignancy&selectedTitle=1~150. Published August 22, 2016. Accessed June 1, 2017.
    5. Shane E. Clinical Manifestations of Hypercalcemia. UpToDate. https://www.uptodate.com/contents/clinical-manifestations-of-hypercalcemia?source=see_link#H12. Published April 24, 2017. Accessed June 6, 2017.
    6. Shane E. Diagnostic Approach to Hypercalcemia. UpToDate. https://www.uptodate.com/contents/diagnostic-approach-to-hypercalcemia?source=search_result&search=hypercalcemia&selectedTitle=1~150#H10. Published November 1, 2016. Accessed June 6, 2017.

    Incorrect

    The answer is D. The patient’s presentation above is suggestive for sarcoidosis, a granulomatous disease that causes an increase in intestinal absorption of calcium. This is due to enhanced secretion of 1 alpha hydroxylase which leads to an increased production of the vitamin D metabolite called calcitriol (1,25 dihydroxyvitamin D) 2. In sarcoidosis, elevated serum calcium concentrations are independent of PTH, therefore intact PTH levels are low. Option A is suggestive of primary hyperparathyroidism, a PTH mediated disease leading to elevated serum and urine calcium levels. Option B is suggestive of familial hypercalciuric hypercalcemia, a genetic disorder affecting the gene that codes for the calcium sensing receptor (CaSR) of the body3. These patients present with normal to mildly elevated PTH levels with increased urinary calcium levels. Option C is suggestive of hypercalcemia of malignancy. Intact PTH levels and vitamin D metabolites are decreased while PTH-rP levels are increased due to secretion by the underlying tumor.

    References:
    1. Agraharkar M. Hypercalcemia. Medscape. http://emedicine.medscape.com/article/240681-overview#a6. Published August 2, 2016. Accessed June 1, 2017.
    2. Agus ZS. Hypercalcemia in Granulomatous Disease. UpToDate. https://www.uptodate.com/contents/hypercalcemia-in-granulomatous-diseases?source=search_result&search=pth-rp%20in%20granulomatous%20disease&selectedTitle=1~150. Published October 29, 2015. Accessed June 1, 2017.
    3. Brown EM. Disorders of the calcium-sensing receptor: Familial hypocalciuric hypercalcemia and autosomal dominant hypocalcemia. UpToDate. https://www.uptodate.com/contents/disorders-of-the-calcium-sensing-receptor-familial-hypocalciuric-hypercalcemia-and-autosomal-dominant-hypocalcemia?source=search_result&search=familial%20hypocalciuric%20hypercalcemia&selectedTitle=1~15. Published April 18, 2017. Accessed June 6, 2017.
    4. Horwitz MJ. Hypercalcemia of Malignancy: Mechanisms. UpToDate. https://www.uptodate.com/contents/hypercalcemia-of-malignancy-mechanisms?source=search_result&search=hypercalcemia%20of%20malignancy&selectedTitle=1~150. Published August 22, 2016. Accessed June 1, 2017.
    5. Shane E. Clinical Manifestations of Hypercalcemia. UpToDate. https://www.uptodate.com/contents/clinical-manifestations-of-hypercalcemia?source=see_link#H12. Published April 24, 2017. Accessed June 6, 2017.
    6. Shane E. Diagnostic Approach to Hypercalcemia. UpToDate. https://www.uptodate.com/contents/diagnostic-approach-to-hypercalcemia?source=search_result&search=hypercalcemia&selectedTitle=1~150#H10. Published November 1, 2016. Accessed June 6, 2017.

  3. Question 3 of 8
    3. Question

    A 65 year-old patient presents to your office with a painful erythematous macular rash all over her body for the past 2 weeks. Patient states she has been recently hospitalized for the flu, fever of 102.4, dehydration, UTI, and diminished kidney function. The patient states she is currently prescribed Allopurinol for her Gout that she began 4 weeks ago. Blood work was ordered which revealed a decrease in lymphocytes, increased creatinine, and lowered GFR. Patient denies use of new lotions, soaps, or detergents. What is the most likely diagnosis?

    Correct

    The correct answer is C (Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS) Syndrome). Allopurinol is a common drug that causes DRESS syndrome.

    DRESS Syndrome:

    DRESS Syndrome is an acronym for Drug Reaction with Eosinophilia and Systemic Symptoms. It is a drug-induced condition, which is characterized by a widespread rash, lymphadenopathy, fever, hematologic abnormalities, involvement of the kidneys, lungs, pancreas, or heart, and hepatitis. It is an idiosyncratic adverse effect from particular drugs and could be fatal. Medications including anticonvulsants, antibiotics (particularly beta-lactams), and allopurinol are a cause of DRESS. Other medications, but less commonly cause DRESS syndrome include non-steroidal anti-inflammatory drugs, captopril, mood stabilizers, and antiretroviral. This syndrome arises from 1 in 1,000 to 1 in 10,000 drug exposures and generally occurs with initial exposure to a drug. The risk of DRESS induced by allopurinol is increased in patients who have renal impairment and use of thiazide diuretics. The mortality rate for DRESS is 10-20% with most deaths resulting from liver failure. Genetics can also be a factor in this syndrome. Patients have a risk as high as 25% if they have a first degree relative who has experienced this syndrome.

    The pathogenesis of DRESS syndrome is thought to be multifactorial and include both nonimmunologic and immunologic factors, but not fully understood yet. It is considered an idiosyncratic reaction with three potential factors that are identified as a factor: 1. reactivation of human herpesvirus 6 (HHV-6), human herpesvirus 7 (HHV-7), Epstein-Barr virus (EBV), or cytomegalovirus (CMV), 2. a genetic susceptibility that alters the immune response, 3. a defect in drug metabolism causing the failure to eliminate toxic reactive intermediates.

    The hallmarks of DRESS syndrome include a long latency period between initiation of the provoking medication and onset of the reaction (2-3 weeks), which consists of fever, rash and at least one involvement of internal organ system. Rash and Fever are the most common clinical manifestations and occur in 75% and 85% of cases respectively. Central facial erythema and edema are common, which can serve as an important clue when it comes to the diagnosis. Other common findings include leukocytosis, abnormal liver function tests, generalized lymphadenopathy, and peripheral eosinophilia. The most common organ involved is the liver, and fulminant hepatitis is major cause of deaths due to DRESS. Cutaneous and visceral inflammation may remain for weeks to months after the drug is discontinued.

    DRESS syndrome can be difficult to diagnose because of the variable presentations of the syndrome. The European Registry of Severe Cutaneous Adverse Reaction to Drugs and Collection of Biological Samples (RegiSCAR) has produced diagnostic criteria to aid in the diagnosis of DRESS. The diagnostic criteria include three requirements (acute rash, hospitalization, and suspicion of a drug related reaction) PLUS at least three of the four systemic features: 1. Fever > 38C, 2. lymphadenopathy involving at least two sites, 3. involvement of at least one internal organ (heart, liver, kidney, etc.) and 4. Hematologic abnormalities, including lymphocyte count above or below the normal limits and eosinophil count higher than normal limits or platelet count below normal limits.

    Treatment of DRESS syndrome includes immediate discontinuation of the drug that is prompting the reaction. Supportive care is recommended for patients. Systemic corticosteroids are used to treat DRESS as first line therapy. Patients are tapered over a prolonged period of time. Systemic steroids are continued for several months to avoid flare. Intravenous immunoglobulin has also been used and reported being effected, but there is no data to support this claim.

    References:

    Buck ML. DRESS Syndrome. Medscape. http://www.medscape.com/viewarticle/776164_1. Published 2012. Accessed June 1, 2017.

    DRESS Syndrome: remember to look under the skin. Medsafe. http://www.medsafe.govt.nz/profs/PUArticles/DRESSsyndromeJune2011.htm. Published June 2011. Accessed June 1, 2017.

    Khetarpal S, Fernandez A. Dermatological Emergencies. Disease Management. http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/dermatology/dermatological-emergencies/. Published August 2014. Accessed June 1, 2017.

    Incorrect

    The correct answer is C (Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS) Syndrome). Allopurinol is a common drug that causes DRESS syndrome.

    DRESS Syndrome:

    DRESS Syndrome is an acronym for Drug Reaction with Eosinophilia and Systemic Symptoms. It is a drug-induced condition, which is characterized by a widespread rash, lymphadenopathy, fever, hematologic abnormalities, involvement of the kidneys, lungs, pancreas, or heart, and hepatitis. It is an idiosyncratic adverse effect from particular drugs and could be fatal. Medications including anticonvulsants, antibiotics (particularly beta-lactams), and allopurinol are a cause of DRESS. Other medications, but less commonly cause DRESS syndrome include non-steroidal anti-inflammatory drugs, captopril, mood stabilizers, and antiretroviral. This syndrome arises from 1 in 1,000 to 1 in 10,000 drug exposures and generally occurs with initial exposure to a drug. The risk of DRESS induced by allopurinol is increased in patients who have renal impairment and use of thiazide diuretics. The mortality rate for DRESS is 10-20% with most deaths resulting from liver failure. Genetics can also be a factor in this syndrome. Patients have a risk as high as 25% if they have a first degree relative who has experienced this syndrome.

    The pathogenesis of DRESS syndrome is thought to be multifactorial and include both nonimmunologic and immunologic factors, but not fully understood yet. It is considered an idiosyncratic reaction with three potential factors that are identified as a factor: 1. reactivation of human herpesvirus 6 (HHV-6), human herpesvirus 7 (HHV-7), Epstein-Barr virus (EBV), or cytomegalovirus (CMV), 2. a genetic susceptibility that alters the immune response, 3. a defect in drug metabolism causing the failure to eliminate toxic reactive intermediates.

    The hallmarks of DRESS syndrome include a long latency period between initiation of the provoking medication and onset of the reaction (2-3 weeks), which consists of fever, rash and at least one involvement of internal organ system. Rash and Fever are the most common clinical manifestations and occur in 75% and 85% of cases respectively. Central facial erythema and edema are common, which can serve as an important clue when it comes to the diagnosis. Other common findings include leukocytosis, abnormal liver function tests, generalized lymphadenopathy, and peripheral eosinophilia. The most common organ involved is the liver, and fulminant hepatitis is major cause of deaths due to DRESS. Cutaneous and visceral inflammation may remain for weeks to months after the drug is discontinued.

    DRESS syndrome can be difficult to diagnose because of the variable presentations of the syndrome. The European Registry of Severe Cutaneous Adverse Reaction to Drugs and Collection of Biological Samples (RegiSCAR) has produced diagnostic criteria to aid in the diagnosis of DRESS. The diagnostic criteria include three requirements (acute rash, hospitalization, and suspicion of a drug related reaction) PLUS at least three of the four systemic features: 1. Fever > 38C, 2. lymphadenopathy involving at least two sites, 3. involvement of at least one internal organ (heart, liver, kidney, etc.) and 4. Hematologic abnormalities, including lymphocyte count above or below the normal limits and eosinophil count higher than normal limits or platelet count below normal limits.

    Treatment of DRESS syndrome includes immediate discontinuation of the drug that is prompting the reaction. Supportive care is recommended for patients. Systemic corticosteroids are used to treat DRESS as first line therapy. Patients are tapered over a prolonged period of time. Systemic steroids are continued for several months to avoid flare. Intravenous immunoglobulin has also been used and reported being effected, but there is no data to support this claim.

    References:

    Buck ML. DRESS Syndrome. Medscape. http://www.medscape.com/viewarticle/776164_1. Published 2012. Accessed June 1, 2017.

    DRESS Syndrome: remember to look under the skin. Medsafe. http://www.medsafe.govt.nz/profs/PUArticles/DRESSsyndromeJune2011.htm. Published June 2011. Accessed June 1, 2017.

    Khetarpal S, Fernandez A. Dermatological Emergencies. Disease Management. http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/dermatology/dermatological-emergencies/. Published August 2014. Accessed June 1, 2017.

  4. Question 4 of 8
    4. Question

    A 48 year-old female presents to the office with a gradual, progressive increase of joint pain and swelling of the PIP joints bilaterally as well as bilateral wrists. She states she has morning stiffness lasting greater than 1 hour as well as low grade fevers, fatigue, and 10lb weight loss without dieting over the last month. Labs were completed prior to the office visit and she had a positive rheumatoid factor, positive anti CCP antibody, negative ANA and negative SS-A and SS-B antibodies. A physical exam was performed and ulnar deviation was present bilaterally as well as bilateral subluxation of the MCP joints. She denies any recent infections, nausea, vomiting, dry eyes, dry mouth and rashes or change in skin. What would the next appropriate step in treatment be with her assumed diagnosis?

    Correct

    The correct answer is A methotrexate. The patient described above should be diagnosed with rheumatoid arthritis. She has a positive RF and CCP antibody which would indicate seropositive RA. She also has morning stiffness lasting greater than one hour which is a hallmark sign. She also has systemic symptoms such as low grade fevers, weight loss and fatigue. It is also symmetric swelling affecting the PIP joints and wrists which are common areas that RA targets. She also has ulnar deviation indicating the RA is aggressive and has started damaging her joints. The first line treatment for moderate to severe rheumatoid arthritis is methotrexate. Hydroxychloroquine is first line treatment for systemic lupus erythematous and mild treatment for rheumatoid arthritis. Since her ANA was negative lupus can be ruled out. Pilocarpine can be used to help treat the symptoms of Sjogrens. This patient doesn’t have sjogrens because her SS-A and SS-B were negative and she didn’t have symptoms such as dry eyes or dry mouth. NSAIDS can be used to treat the pain and inflammation in osteoarthritis. You wouldn’t use NSAIDS to treat rheumatoid arthritis since it’s an autoimmune disorder. She doesn’t have osteoarthritis because it usually spares the wrists and MCP joints .Also joint pain is relieved with rest and morning stiffness lasting more than one hour is usually not characteristic of osteoarthritis. Also osteoarthritis is usually not associated with systemic symptoms such as fever, weight loss and fatigue.

    Discussion
    Rheumatoid arthritis is an autoimmune disorder that precipitates systemic inflammation within the body. This disease targets joints in a progressive and symmetrical fashion and causes significant destruction and damage to cartilage and bone that leads to detrimental and lasting joint effects.
    Although RA affects both males and females it tends to affect females at a significantly greater rate. Females are 2.5 times more likely to develop RA than males. The peak incidence usually occurs between the fourth and fifth decades of life. The average annual incidence in the US is 0.5 per 1000 persons per year.1

    Genetics significantly contribute to the development of RA and are roughly 50% the risk. 3 Chances of developing RA grossly increase with family history. The risk of developing the disease in first degree relatives of RA patients is 1.5 times higher than the general population. The PTPN22 gene is thought to play a significant role in developing RA. There is a fourfold higher risk in homozygotes that carry the polymorphism and a twofold higher chance in heterozygotes to develop RA. This polymorphism is also thought to be involved with type I diabetes and SLE. Sex and hormones are also thought to contribute to RA. Women are 2-3 times more likely to develop RA than men1. Hormones more specifically estrogen is thought to play a significant and detrimental role in the development of RA. For example, many times during pregnancy RA flares will dramatically decrease and the mother will go into remission while pregnant. Shortly after giving birth usually a few weeks the mother will have a flare. Also women on oral contraceptives have a decreased incidence of RA which is why hormones are thought to contribute in some aspect to RA3. Many other factors are also thought to contribute to RA including environmental .Tobacco can increase the risk of developing RA. Cigarette smoke can lead to a low positive CCP and also activate the innate immune system as well as cause inflammation within the body. Bacteria and viruses also play a role in the etiology of RA. They stimulate the innate immune system which eventually leads to stimulation of the adaptive immune system. Two of the main culprits are thought to be EBV and parvovirus B-19.EBV stimulates B lymphocytes and increases production of RF and Parvovirus B-19 is commonly found in RA joints and leads to infected fibroblast-like synoviocytes1.

    The pathophysiology of RA is very complicated and is thought to be a combination of cellular and molecular pathways. This combination inherently precipitates joint degeneration and destruction especially effecting joint space. Innate and adaptive immunity are hypothesized to play a significant role in RA1. Many different types of immune factors play a significant role in RA. These include CD4 Tells, mononuclear phagocytes, fibroblasts, osteoclasts, and neutrophils .There is also abnormal proliferation of cytokines, chemokines such as TNF-a, IL-1, IL-6, IL-8, transforming growth factor beta, fibroblast growth factor and platelet derived growth factor in the development of rheumatoid arthritis3. Many medications used in rheumatoid arthritis work by targeting and inhibiting these various agents1.

    In order to make an accurate diagnosis of rheumatoid arthritis it is important to gather a pertinent history and perform a focused physical exam. It is important to focus on articular symptoms, gradual or rapid onset of symptoms and perform a careful examination of which joints are affected. It’s also important to determine if the patient has morning stiffness lasting greater than one hour since this is a classic sign of rheumatoid arthritis. Since RA is a systemic disease patients may have fever, weight loss and fatigue. Joint pain and swelling is gradual and usually happens over weeks to months. The most frequent joints affected are the wrists, metacarpophalangeal joints, proximal interphalangeal joints and metatarsal phalangeal joints. As rheumatoid arthritis evolves the ankles, knees elbows and shoulders become involved. However, DIP joints and the thoracolumbar spine are usually not affected. Rheumatoid arthritis usually affects Joints symmetrically and morning stiffness lasting greater than one hour is a hallmark sign to be aware of and screen for in the patient. More often than not articular manifestations are present on physical exam. Joint swelling usually stays within the joint capsule and fusiform swelling of the PIP joint is one of the earliest findings. Hand deformities occur as the disease progresses, becomes more aggressive or is left untreated or treated incorrectly. Joint deformities can include ulnar deviation of the fingers, dorsal subluxation of the MCP joints, swan neck deformity and boutonniere deformity at the PIP. There may be also swelling of the elbows and wrists. Rheumatoid nodules may also be present and can occur over the elbows, achilles tendons, fingers, scalp and ischial tuberosities1. Extra articular manifestations can also occur and need to be monitored and checked during a physical exam. These can include rheumatoid nodules, interstitial lung disease, pleural effusion, pericarditis, splenomegaly with leukopenia, vasculitis and sjogrens syndrome. Sjogrens syndrome will manifest as dry eyes, mouth and other mucous membranes2.

    Diagnostic imaging and labs can be very helpful in diagnosing and determining the severity of rheumatoid arthritis. Laboratory findings can be useful in determining the amount of systemic inflammation going on within the body. Laboratory tests that may come back as being elevated or abnormal are inflammatory joint fluid, anemia of chronic disease, rheumatoid factor and anti CCP. Roughly about 75-80% of patients with RA will test positive for anti CCP and RF factor. This is known as seropositive RA .Elevations in CRP and ESR, which are inflammatory markers can correlate with disease activity and be an indication that active inflammation is present within the body. Imaging can also be helpful in determining joint destruction and progression of the disease. Plain film radiography will show progressive changes in the joints such as joint space narrowing, osteopenia and bone erosions. An MRI can be used to detect joint erosions and changes in joints and is more sensitive than radiography and can detect changes earlier than plain radiography. Finally, ultrasonography may also be used to detect inflammation in the joint but other methods will usually be utilized before using this method. 4

    Once diagnosed with rheumatoid arthritis, treatment should be initiated as quickly as possible to decrease the risk of developing lasting and devastating destruction of the joints. Rheumatoid arthritis should be categorized as mild, moderate or severe depending on patient presentation and lab values. Treatment should then be tailored to the degree of the disease. NSAIDS and COX-2 inhibitors are used to help relieve joint pain. Inflammation present within the body can try to be lowered by corticosteroids such as prednisone in 5mg-10mg doses. Corticosteroids can decrease systemic inflammation and slow the rate of joint destruction2. Sulfasalazine and hydroxychloroquine can be used for mild forms of RA. However, the backbone of treatment is the use of DMARDS. They are used to decrease the signs and symptoms of RA and to stop the progression of joint damage. Methotrexate is the first line treatment due to its proven benefits in slowing the progression of RA damage. Methotrexate can also be combined with other biologics such as humira or Enbrel if flares, systemic inflammation and other symptoms are present. Methotrexate has been shown to have a greater effect on reducing systemic inflammation when combined with two or three other biologics and is more effective than methotrexate alone in preventing joint damage1.

    References:
    1.Klippel JH. Primer on the rheumatic diseases. New York, NY: Springer; 2008.
    2.Papadakis MA, McPhee SJ, Rabow MW. Current medical diagnosis & treatment 2015. New York: McGraw-Hill Education; 2015.
    3.Rheumatoid Arthritis. Practice Essentials, Background, Pathophysiology. http://emedicine.medscape.com/article/331715-overview#a2. Published May 5, 2017. Accessed May 17, 2017.
    4. Venables PJW, Maini R. Clinical manifestations of rheumatoid arthritis. Clinical manifestations of rheumatoid arthritis. https://www.uptodate.com/contents/clinical-manifestations-of-rheumatoid-arthritis?source=search_result&search=rheumatoid arthritis&selectedTitle=2~150. Accessed May 17, 2017.

    Incorrect

    The correct answer is A methotrexate. The patient described above should be diagnosed with rheumatoid arthritis. She has a positive RF and CCP antibody which would indicate seropositive RA. She also has morning stiffness lasting greater than one hour which is a hallmark sign. She also has systemic symptoms such as low grade fevers, weight loss and fatigue. It is also symmetric swelling affecting the PIP joints and wrists which are common areas that RA targets. She also has ulnar deviation indicating the RA is aggressive and has started damaging her joints. The first line treatment for moderate to severe rheumatoid arthritis is methotrexate. Hydroxychloroquine is first line treatment for systemic lupus erythematous and mild treatment for rheumatoid arthritis. Since her ANA was negative lupus can be ruled out. Pilocarpine can be used to help treat the symptoms of Sjogrens. This patient doesn’t have sjogrens because her SS-A and SS-B were negative and she didn’t have symptoms such as dry eyes or dry mouth. NSAIDS can be used to treat the pain and inflammation in osteoarthritis. You wouldn’t use NSAIDS to treat rheumatoid arthritis since it’s an autoimmune disorder. She doesn’t have osteoarthritis because it usually spares the wrists and MCP joints .Also joint pain is relieved with rest and morning stiffness lasting more than one hour is usually not characteristic of osteoarthritis. Also osteoarthritis is usually not associated with systemic symptoms such as fever, weight loss and fatigue.

    Discussion
    Rheumatoid arthritis is an autoimmune disorder that precipitates systemic inflammation within the body. This disease targets joints in a progressive and symmetrical fashion and causes significant destruction and damage to cartilage and bone that leads to detrimental and lasting joint effects.
    Although RA affects both males and females it tends to affect females at a significantly greater rate. Females are 2.5 times more likely to develop RA than males. The peak incidence usually occurs between the fourth and fifth decades of life. The average annual incidence in the US is 0.5 per 1000 persons per year.1

    Genetics significantly contribute to the development of RA and are roughly 50% the risk. 3 Chances of developing RA grossly increase with family history. The risk of developing the disease in first degree relatives of RA patients is 1.5 times higher than the general population. The PTPN22 gene is thought to play a significant role in developing RA. There is a fourfold higher risk in homozygotes that carry the polymorphism and a twofold higher chance in heterozygotes to develop RA. This polymorphism is also thought to be involved with type I diabetes and SLE. Sex and hormones are also thought to contribute to RA. Women are 2-3 times more likely to develop RA than men1. Hormones more specifically estrogen is thought to play a significant and detrimental role in the development of RA. For example, many times during pregnancy RA flares will dramatically decrease and the mother will go into remission while pregnant. Shortly after giving birth usually a few weeks the mother will have a flare. Also women on oral contraceptives have a decreased incidence of RA which is why hormones are thought to contribute in some aspect to RA3. Many other factors are also thought to contribute to RA including environmental .Tobacco can increase the risk of developing RA. Cigarette smoke can lead to a low positive CCP and also activate the innate immune system as well as cause inflammation within the body. Bacteria and viruses also play a role in the etiology of RA. They stimulate the innate immune system which eventually leads to stimulation of the adaptive immune system. Two of the main culprits are thought to be EBV and parvovirus B-19.EBV stimulates B lymphocytes and increases production of RF and Parvovirus B-19 is commonly found in RA joints and leads to infected fibroblast-like synoviocytes1.

    The pathophysiology of RA is very complicated and is thought to be a combination of cellular and molecular pathways. This combination inherently precipitates joint degeneration and destruction especially effecting joint space. Innate and adaptive immunity are hypothesized to play a significant role in RA1. Many different types of immune factors play a significant role in RA. These include CD4 Tells, mononuclear phagocytes, fibroblasts, osteoclasts, and neutrophils .There is also abnormal proliferation of cytokines, chemokines such as TNF-a, IL-1, IL-6, IL-8, transforming growth factor beta, fibroblast growth factor and platelet derived growth factor in the development of rheumatoid arthritis3. Many medications used in rheumatoid arthritis work by targeting and inhibiting these various agents1.

    In order to make an accurate diagnosis of rheumatoid arthritis it is important to gather a pertinent history and perform a focused physical exam. It is important to focus on articular symptoms, gradual or rapid onset of symptoms and perform a careful examination of which joints are affected. It’s also important to determine if the patient has morning stiffness lasting greater than one hour since this is a classic sign of rheumatoid arthritis. Since RA is a systemic disease patients may have fever, weight loss and fatigue. Joint pain and swelling is gradual and usually happens over weeks to months. The most frequent joints affected are the wrists, metacarpophalangeal joints, proximal interphalangeal joints and metatarsal phalangeal joints. As rheumatoid arthritis evolves the ankles, knees elbows and shoulders become involved. However, DIP joints and the thoracolumbar spine are usually not affected. Rheumatoid arthritis usually affects Joints symmetrically and morning stiffness lasting greater than one hour is a hallmark sign to be aware of and screen for in the patient. More often than not articular manifestations are present on physical exam. Joint swelling usually stays within the joint capsule and fusiform swelling of the PIP joint is one of the earliest findings. Hand deformities occur as the disease progresses, becomes more aggressive or is left untreated or treated incorrectly. Joint deformities can include ulnar deviation of the fingers, dorsal subluxation of the MCP joints, swan neck deformity and boutonniere deformity at the PIP. There may be also swelling of the elbows and wrists. Rheumatoid nodules may also be present and can occur over the elbows, achilles tendons, fingers, scalp and ischial tuberosities1. Extra articular manifestations can also occur and need to be monitored and checked during a physical exam. These can include rheumatoid nodules, interstitial lung disease, pleural effusion, pericarditis, splenomegaly with leukopenia, vasculitis and sjogrens syndrome. Sjogrens syndrome will manifest as dry eyes, mouth and other mucous membranes2.

    Diagnostic imaging and labs can be very helpful in diagnosing and determining the severity of rheumatoid arthritis. Laboratory findings can be useful in determining the amount of systemic inflammation going on within the body. Laboratory tests that may come back as being elevated or abnormal are inflammatory joint fluid, anemia of chronic disease, rheumatoid factor and anti CCP. Roughly about 75-80% of patients with RA will test positive for anti CCP and RF factor. This is known as seropositive RA .Elevations in CRP and ESR, which are inflammatory markers can correlate with disease activity and be an indication that active inflammation is present within the body. Imaging can also be helpful in determining joint destruction and progression of the disease. Plain film radiography will show progressive changes in the joints such as joint space narrowing, osteopenia and bone erosions. An MRI can be used to detect joint erosions and changes in joints and is more sensitive than radiography and can detect changes earlier than plain radiography. Finally, ultrasonography may also be used to detect inflammation in the joint but other methods will usually be utilized before using this method. 4

    Once diagnosed with rheumatoid arthritis, treatment should be initiated as quickly as possible to decrease the risk of developing lasting and devastating destruction of the joints. Rheumatoid arthritis should be categorized as mild, moderate or severe depending on patient presentation and lab values. Treatment should then be tailored to the degree of the disease. NSAIDS and COX-2 inhibitors are used to help relieve joint pain. Inflammation present within the body can try to be lowered by corticosteroids such as prednisone in 5mg-10mg doses. Corticosteroids can decrease systemic inflammation and slow the rate of joint destruction2. Sulfasalazine and hydroxychloroquine can be used for mild forms of RA. However, the backbone of treatment is the use of DMARDS. They are used to decrease the signs and symptoms of RA and to stop the progression of joint damage. Methotrexate is the first line treatment due to its proven benefits in slowing the progression of RA damage. Methotrexate can also be combined with other biologics such as humira or Enbrel if flares, systemic inflammation and other symptoms are present. Methotrexate has been shown to have a greater effect on reducing systemic inflammation when combined with two or three other biologics and is more effective than methotrexate alone in preventing joint damage1.

    References:
    1.Klippel JH. Primer on the rheumatic diseases. New York, NY: Springer; 2008.
    2.Papadakis MA, McPhee SJ, Rabow MW. Current medical diagnosis & treatment 2015. New York: McGraw-Hill Education; 2015.
    3.Rheumatoid Arthritis. Practice Essentials, Background, Pathophysiology. http://emedicine.medscape.com/article/331715-overview#a2. Published May 5, 2017. Accessed May 17, 2017.
    4. Venables PJW, Maini R. Clinical manifestations of rheumatoid arthritis. Clinical manifestations of rheumatoid arthritis. https://www.uptodate.com/contents/clinical-manifestations-of-rheumatoid-arthritis?source=search_result&search=rheumatoid arthritis&selectedTitle=2~150. Accessed May 17, 2017.

  5. Question 5 of 8
    5. Question

    A 67 year-old female with no personal or family history of skin cancer presents for her annual full body skin exam. On exam you notice a solitary well circumscribed 3 mm dark brown circular lesion on her left shoulder. During palpation you note that the lesion has raised borders equally throughout the lesion. When you ask her about it she states that it has been there since she was little and has never changed. She denies any fevers, chills or recent unexplained weight loss. What would the next step in the management of this lesion?

    Correct

    A: This lesion is consistent with a typical benign nevus and does not need to be biopsied at this time. B: This is the correct answer. This lesion is consistent with a typical nevus due to its symmetric shape, even border, small size, no variation in color and no evolution over time. This lesion should be observed for any changes or signs of melanoma. C: This lesion is not consistent with melanoma due to its symmetry.

    Discussion:
    Atypical or dysplastic nevi are moles that look unusual and can sometimes look like melanoma. They are benign lesions, but people who have dysplastic nevi are at an increased risk of developing melanoma. This risk of melanoma can be in the dysplastic mole itself or in another area on the body. The greater number of dysplastic moles someone has, the higher their risk of developing melanoma. A person who has more than ten dysplastic moles has a twelve times greater risk of developing melanoma.

    Dysplastic moles tend to have a genetic component and can be seen in multiple family members. These types of moles are most commonly found in Caucasians. Individuals who have dysplastic moles and a family history of melanoma are at a very high risk.

    If a physician identifies a mole as atypical or if there is a patient who develops a new mole after age 40, the lesion should be biopsied. Those with atypical moles should monitor them and seek medical attention with any changes or signs of melanoma. When looking for signs of melanoma we can use the ABCs. A is for asymmetry, B is for irregular border, C is for multi-colored, D is for diameter greater than 6mm and E is for evolution or a spot that is changing.

    The pathophysiology behind dysplastic nevi is either inherited or sporadic. UV light can play a role in the development of dysplastic nevi and can be both an initiator and promotor in the transformation of the melanocytes into atypical melanocytes or melanoma.

    A person presenting with a dysplastic nevus may have a personal and/or family history of skin cancer, particularly melanoma. They may have a personal history of increased sun exposure, a recent or rapid change of an existing nevus or the development of a new nevus.

    On physical exam the patient may have a large pigmented lesion 5-15 mm in diameter. The lesion may be asymmetric and contain an irregular, notched or ill-defined border. There may be macular and papular areas within a single lesion. The color may be highly inconstant and range from tan to dark brown to pink. These lesions are most commonly found in the back, chest, buttocks, breasts and scalp. They can be found in sun exposed areas as well as sun protected areas, so it is important to check all areas including in the mouth and between the toes.

    In the initial evaluation a dermatoscope can be used to evaluate atypical pigmentation. If a lesion is said to be atypical or dysplastic a biopsy needs to be performed for histologic confirmation. A shallow scoop saucerization with at least 2 mm margin or normal appearing skin can be performed if lesion is removed entirely.

    The management of dysplastic nevus is somewhat controversial. The Skin Cancer Foundation examined outcomes of surgical excision of dysplastic nevi and their association with melanoma in order to help find a better idea of this relationship. The results of the study lead to their clinical recommendations for the management of dysplastic nevi. DN that contain severely atypical components (moderately-to-severely and severely dysplastic nevi) showed an increased association with melanoma and increased rate of melanoma diagnosis and supports the management with excision. When looking at moderately dysplastic nevi the data suggests a generally benign behavior similar to mild dysplastic nevi. This supports management with periodic observation for both moderate and mild DN with a positive margin. Histologic classification of atypia provides some guidance to melanoma risk, but an improved classification may allow better risk stratification in the management of dysplastic nevi. Since further evidence is needed the management of each lesion should be individualized and excision should be considered if judged appropriate by both the patient and provider.

    References

    1) Goldberg L, Lebwohl M. Atypical mole (dysplastic nevi). Skin Cancer Foundation. http://www.skincancer.org/skin-cancer-information/atypical-moles. Accessed May 24, 2017.

    2) Reddy K, Rogers G. Management of dysplastic nevi: the role of complete surgical excision. The Skin Cancer Foundation. http://www.skincancer.org/publications/the-melanoma-letter/summer-2014-vol-32-no-2/management. Published 2014. Accessed May 16, 2017.

    3) Valdebran, M. Atypical mole (clark nevus or dysplastic nevus). Medscape. http://emedicine.medscape.com/article/1056283-overview#a4. Updated April 4, 2017. Accessed May 24, 2017.

    Incorrect

    A: This lesion is consistent with a typical benign nevus and does not need to be biopsied at this time. B: This is the correct answer. This lesion is consistent with a typical nevus due to its symmetric shape, even border, small size, no variation in color and no evolution over time. This lesion should be observed for any changes or signs of melanoma. C: This lesion is not consistent with melanoma due to its symmetry.

    Discussion:
    Atypical or dysplastic nevi are moles that look unusual and can sometimes look like melanoma. They are benign lesions, but people who have dysplastic nevi are at an increased risk of developing melanoma. This risk of melanoma can be in the dysplastic mole itself or in another area on the body. The greater number of dysplastic moles someone has, the higher their risk of developing melanoma. A person who has more than ten dysplastic moles has a twelve times greater risk of developing melanoma.

    Dysplastic moles tend to have a genetic component and can be seen in multiple family members. These types of moles are most commonly found in Caucasians. Individuals who have dysplastic moles and a family history of melanoma are at a very high risk.

    If a physician identifies a mole as atypical or if there is a patient who develops a new mole after age 40, the lesion should be biopsied. Those with atypical moles should monitor them and seek medical attention with any changes or signs of melanoma. When looking for signs of melanoma we can use the ABCs. A is for asymmetry, B is for irregular border, C is for multi-colored, D is for diameter greater than 6mm and E is for evolution or a spot that is changing.

    The pathophysiology behind dysplastic nevi is either inherited or sporadic. UV light can play a role in the development of dysplastic nevi and can be both an initiator and promotor in the transformation of the melanocytes into atypical melanocytes or melanoma.

    A person presenting with a dysplastic nevus may have a personal and/or family history of skin cancer, particularly melanoma. They may have a personal history of increased sun exposure, a recent or rapid change of an existing nevus or the development of a new nevus.

    On physical exam the patient may have a large pigmented lesion 5-15 mm in diameter. The lesion may be asymmetric and contain an irregular, notched or ill-defined border. There may be macular and papular areas within a single lesion. The color may be highly inconstant and range from tan to dark brown to pink. These lesions are most commonly found in the back, chest, buttocks, breasts and scalp. They can be found in sun exposed areas as well as sun protected areas, so it is important to check all areas including in the mouth and between the toes.

    In the initial evaluation a dermatoscope can be used to evaluate atypical pigmentation. If a lesion is said to be atypical or dysplastic a biopsy needs to be performed for histologic confirmation. A shallow scoop saucerization with at least 2 mm margin or normal appearing skin can be performed if lesion is removed entirely.

    The management of dysplastic nevus is somewhat controversial. The Skin Cancer Foundation examined outcomes of surgical excision of dysplastic nevi and their association with melanoma in order to help find a better idea of this relationship. The results of the study lead to their clinical recommendations for the management of dysplastic nevi. DN that contain severely atypical components (moderately-to-severely and severely dysplastic nevi) showed an increased association with melanoma and increased rate of melanoma diagnosis and supports the management with excision. When looking at moderately dysplastic nevi the data suggests a generally benign behavior similar to mild dysplastic nevi. This supports management with periodic observation for both moderate and mild DN with a positive margin. Histologic classification of atypia provides some guidance to melanoma risk, but an improved classification may allow better risk stratification in the management of dysplastic nevi. Since further evidence is needed the management of each lesion should be individualized and excision should be considered if judged appropriate by both the patient and provider.

    References

    1) Goldberg L, Lebwohl M. Atypical mole (dysplastic nevi). Skin Cancer Foundation. http://www.skincancer.org/skin-cancer-information/atypical-moles. Accessed May 24, 2017.

    2) Reddy K, Rogers G. Management of dysplastic nevi: the role of complete surgical excision. The Skin Cancer Foundation. http://www.skincancer.org/publications/the-melanoma-letter/summer-2014-vol-32-no-2/management. Published 2014. Accessed May 16, 2017.

    3) Valdebran, M. Atypical mole (clark nevus or dysplastic nevus). Medscape. http://emedicine.medscape.com/article/1056283-overview#a4. Updated April 4, 2017. Accessed May 24, 2017.

  6. Question 6 of 8
    6. Question

    A 15-year-old boy presents to the emergency room after experiencing a sudden onset of sharp, unilateral chest pain while playing basketball. His vital signs are stable with the exception of mild tachycardia and tachypnea. On exam, he has diminished breath sounds on the right, hyperresonance on percussion on the right, and decreased tactile fremitus. He has a normal S1 and S2, and no murmurs are noted. Of note, he recently went through a growth spurt and has no underlying medical conditions. Based on this information, what is the suspected diagnosis?

    Correct

    The correct answer is spontaneous pneumothorax (A). This patient demonstrates the classic presentation of an individual with this condition. A spontaneous pneumothorax is most commonly diagnosed in individuals between the ages of 10 and 40. Additionally, this patient recently went through a growth spurt, demonstrating that he is most likely tall and thin. His physical exam findings of diminished breath sounds, hyperresonance on percussion, and decreased tactile fremitus are typical of patients with this condition.1 Hypertrophic cardiomyopathy (B) is incorrect. Although this patient developed symptoms during exercise, most patients with HCM develop other symptoms such as dyspnea, presyncope, syncope, heart palpitations, and/or dizziness. The absence of a fourth heart sound (S4) or a heart murmur combined with his abnormal lung exam do not support the diagnosis of HCM.7 Pleural effusion (C) is also incorrect. While this patient’s physical exam findings of diminished breath sounds, hyperresonance on percussion, and decreased tactile fremitus support the diagnosis of a pleural effusion, the background information makes this diagnosis inaccurate. Most patients diagnosed with a pleural effusion suffer from an underlying cardiac or pulmonary disease.8 Pulmonary embolism (D) is incorrect. Although this patient experienced a sudden onset of chest pain, the remainder of his presentation does not support the diagnosis of a PE. This diagnosis is more common in overweight women rather than thin men. Most patients with a PE have an antecedent deep vein thrombosis (DVT) and experience lower extremity pain or swelling. Additionally, patients are at an increased risk of developing a PE if they meet the criteria for Virchow’s triad: venous stasis, vessel wall injury, and hypercoagulability. This patient does not meet these criteria. This patient’s history, physical exam findings, and chest x-ray findings do not support the diagnosis of a PE.9

    References
    1 Daley BJ. Pneumothorax. Medscape. http://emedicine.medscape.com/article/424547-overview. Updated July 20, 2016. Accessed April 19, 2017.
    2 Chesnutt MS, Prendergast TJ. Chapter 9: Pulmonary disorders. In: Papadakis MA, McPhee SJ, ed. Current Medical Diagnosis and Treatment. 54th ed. New York, NY: McGraw-Hill Education. 2015: 312-313.
    3 Gonzales, CA. Spontaneous pneumothorax in children. In: DynaMed [database online]. Ipswich, MA: EBSCO Information Services. http://web.b.ebscohost.com.ezproxymcp.flo.org/dynamed/detail?vid=2&sid=c01dbb52-d28a-438f-b577-5c4bc2c6c9c9%40sessionmgr101&hid=118&bdata=JnNpdGU9ZHluYW1lZC1saXZlJnNjb3BlPXNpdGU%3d#AN=306335&db=dme. Updated January 11, 2016. Accessed April 19, 2017.
    4 Patel A. Spontaneous pneumothorax in adults. In: DynaMed [database online]. Ipswich, MA: EBSCO Information Services. http://web.b.ebscohost.com.ezproxymcp.flo.org/dynamed/detail?sid=c01dbb52-d28a-438f-b577-5c4bc2c6c9c9%40sessionmgr101&vid=3&hid=118&bdata=JnNpdGU9ZHluYW1lZC1saXZlJnNjb3BlPXNpdGU%3d#AN=114714&db=dme. Updated January 9, 2017. Accessed April 19, 2017.
    5 Mayo Clinic Staff. Pneumothorax. Mayo Clinic. http://www.mayoclinic.org/diseases-conditions/pneumothorax/home/ovc-20179880. Updated January 28, 2016. Accessed April 19 2017.
    6 Gluckman W. Pediatric Pneumothorax. Medscape. http://emedicine.medscape.com/article/1003552-overview. Updated October 26, 2015. Accessed April 19, 2017.
    7 Shah SN. Hypertrophic Cardiomyopathy. Medscape. http://emedicine.medscape.com/article/152913-overview. Updated January 5, 2016. Accessed April 19, 2017.
    8 Rubins J. Pleural Effusion. Medscape. http://emedicine.medscape.com/article/299959-overview. Updated March 30, 2017. Accessed April 19, 2017.
    9 Ouellette DR. Pulmonary Embolism. Medscape. http://emedicine.medscape.com/article/300901-overview. Updated June 22, 2016. Accessed April 19, 2017.

    Incorrect

    The correct answer is spontaneous pneumothorax (A). This patient demonstrates the classic presentation of an individual with this condition. A spontaneous pneumothorax is most commonly diagnosed in individuals between the ages of 10 and 40. Additionally, this patient recently went through a growth spurt, demonstrating that he is most likely tall and thin. His physical exam findings of diminished breath sounds, hyperresonance on percussion, and decreased tactile fremitus are typical of patients with this condition.1 Hypertrophic cardiomyopathy (B) is incorrect. Although this patient developed symptoms during exercise, most patients with HCM develop other symptoms such as dyspnea, presyncope, syncope, heart palpitations, and/or dizziness. The absence of a fourth heart sound (S4) or a heart murmur combined with his abnormal lung exam do not support the diagnosis of HCM.7 Pleural effusion (C) is also incorrect. While this patient’s physical exam findings of diminished breath sounds, hyperresonance on percussion, and decreased tactile fremitus support the diagnosis of a pleural effusion, the background information makes this diagnosis inaccurate. Most patients diagnosed with a pleural effusion suffer from an underlying cardiac or pulmonary disease.8 Pulmonary embolism (D) is incorrect. Although this patient experienced a sudden onset of chest pain, the remainder of his presentation does not support the diagnosis of a PE. This diagnosis is more common in overweight women rather than thin men. Most patients with a PE have an antecedent deep vein thrombosis (DVT) and experience lower extremity pain or swelling. Additionally, patients are at an increased risk of developing a PE if they meet the criteria for Virchow’s triad: venous stasis, vessel wall injury, and hypercoagulability. This patient does not meet these criteria. This patient’s history, physical exam findings, and chest x-ray findings do not support the diagnosis of a PE.9

    References
    1 Daley BJ. Pneumothorax. Medscape. http://emedicine.medscape.com/article/424547-overview. Updated July 20, 2016. Accessed April 19, 2017.
    2 Chesnutt MS, Prendergast TJ. Chapter 9: Pulmonary disorders. In: Papadakis MA, McPhee SJ, ed. Current Medical Diagnosis and Treatment. 54th ed. New York, NY: McGraw-Hill Education. 2015: 312-313.
    3 Gonzales, CA. Spontaneous pneumothorax in children. In: DynaMed [database online]. Ipswich, MA: EBSCO Information Services. http://web.b.ebscohost.com.ezproxymcp.flo.org/dynamed/detail?vid=2&sid=c01dbb52-d28a-438f-b577-5c4bc2c6c9c9%40sessionmgr101&hid=118&bdata=JnNpdGU9ZHluYW1lZC1saXZlJnNjb3BlPXNpdGU%3d#AN=306335&db=dme. Updated January 11, 2016. Accessed April 19, 2017.
    4 Patel A. Spontaneous pneumothorax in adults. In: DynaMed [database online]. Ipswich, MA: EBSCO Information Services. http://web.b.ebscohost.com.ezproxymcp.flo.org/dynamed/detail?sid=c01dbb52-d28a-438f-b577-5c4bc2c6c9c9%40sessionmgr101&vid=3&hid=118&bdata=JnNpdGU9ZHluYW1lZC1saXZlJnNjb3BlPXNpdGU%3d#AN=114714&db=dme. Updated January 9, 2017. Accessed April 19, 2017.
    5 Mayo Clinic Staff. Pneumothorax. Mayo Clinic. http://www.mayoclinic.org/diseases-conditions/pneumothorax/home/ovc-20179880. Updated January 28, 2016. Accessed April 19 2017.
    6 Gluckman W. Pediatric Pneumothorax. Medscape. http://emedicine.medscape.com/article/1003552-overview. Updated October 26, 2015. Accessed April 19, 2017.
    7 Shah SN. Hypertrophic Cardiomyopathy. Medscape. http://emedicine.medscape.com/article/152913-overview. Updated January 5, 2016. Accessed April 19, 2017.
    8 Rubins J. Pleural Effusion. Medscape. http://emedicine.medscape.com/article/299959-overview. Updated March 30, 2017. Accessed April 19, 2017.
    9 Ouellette DR. Pulmonary Embolism. Medscape. http://emedicine.medscape.com/article/300901-overview. Updated June 22, 2016. Accessed April 19, 2017.

  7. Question 7 of 8
    7. Question

    Figure 1
    The yellow arrow in figure 1 (lateral x-ray of the foot) points to which structure?

    Correct

    Knowing the complex anatomy of the foot is crucial in differentiating potential pain generators. Over 26 bones make up three regions of the foot including the hindfoot, midfoot, and forefoot. The hindfoot contains the talus and calcaneus, the midfoot contains the navicular, cuboid, and three cuneiform bones, and the forefoot contains the metatarsals and phalanges. The hindfoot and midfoot are separated by the transverse tarsal joint (Chopart joint) and the midfoot and the forefoot by the tarsometatarsal joint. 1

    The tarsal tunnel is a fibro-osseus canal formed on one side by the medial calcaneus and on the other by the flexor retinaculum. Structures that course through the tunnel include flexor tendons and the neurovascular bundle. The posterior tibial nerve can become entrapped in the tarsal tunnel causing pain and numbness, a condition called tarsal tunnel syndrome. 1

    The sinus tarsi is a bony canal between the under surface of the talus and the superior surface of the calcaneus, often referred to as the “eye of the foot”. The sinus tarsi can be a source of painful pathology, or a condition known as sinus tarsi syndrome, where the soft tissue within the sinus tarsi can become inflamed. This can occur after an ankle sprain that causes scar tissue and inflammation to develop within the sinus tarsi. 2

    The sustentaculum tali is a horizontal shelf of the anterior medial calcaneus that helps support the talus superiorly, provides an attachment site for the plantar calcaneonavicular ligament anteriorly, provides an attachment site for the deltoid ligament medially, and forms the roof of the tarsal tunnel and flexor hallucis longus tendon posterior and inferiorly. The sustentaculum tali can become painful with such conditions as tarsal coalition and fracture. 1

    References
    1. Netter, FH. Netter’s Concise Atlas of Orthopaedic Anatomy. Elsevier, Inc. 2002. Philadelphia, PA. Pages 244-279.
    2. Sinus tarsi syndrome. http://www.radiopaedia.org. Accessed 6/13/17.

    Incorrect

    Knowing the complex anatomy of the foot is crucial in differentiating potential pain generators. Over 26 bones make up three regions of the foot including the hindfoot, midfoot, and forefoot. The hindfoot contains the talus and calcaneus, the midfoot contains the navicular, cuboid, and three cuneiform bones, and the forefoot contains the metatarsals and phalanges. The hindfoot and midfoot are separated by the transverse tarsal joint (Chopart joint) and the midfoot and the forefoot by the tarsometatarsal joint. 1

    The tarsal tunnel is a fibro-osseus canal formed on one side by the medial calcaneus and on the other by the flexor retinaculum. Structures that course through the tunnel include flexor tendons and the neurovascular bundle. The posterior tibial nerve can become entrapped in the tarsal tunnel causing pain and numbness, a condition called tarsal tunnel syndrome. 1

    The sinus tarsi is a bony canal between the under surface of the talus and the superior surface of the calcaneus, often referred to as the “eye of the foot”. The sinus tarsi can be a source of painful pathology, or a condition known as sinus tarsi syndrome, where the soft tissue within the sinus tarsi can become inflamed. This can occur after an ankle sprain that causes scar tissue and inflammation to develop within the sinus tarsi. 2

    The sustentaculum tali is a horizontal shelf of the anterior medial calcaneus that helps support the talus superiorly, provides an attachment site for the plantar calcaneonavicular ligament anteriorly, provides an attachment site for the deltoid ligament medially, and forms the roof of the tarsal tunnel and flexor hallucis longus tendon posterior and inferiorly. The sustentaculum tali can become painful with such conditions as tarsal coalition and fracture. 1

    References
    1. Netter, FH. Netter’s Concise Atlas of Orthopaedic Anatomy. Elsevier, Inc. 2002. Philadelphia, PA. Pages 244-279.
    2. Sinus tarsi syndrome. http://www.radiopaedia.org. Accessed 6/13/17.

  8. Question 8 of 8
    8. Question

    Figure 3
    A 50 year-old female presents to your office with a fingertip injury after getting her right index finger caught between a board and a cement block. X-rays taken in the ED 4 days ago show a distal phalanx fracture (tuft fracture) to the index finger. She also has a subungual hematoma involving over 50% of her nail (figure 1). She rates her pain as a 5/10 which is somewhat improved over the last few days. What is the best treatment option?

    Correct

    A subungual hematoma, or bleeding under the nail, commonly occurs after crush injuries of the fingertip. The affected nail may become swollen and significantly painful. Treatment of these injuries is controversial with conflicting recommendations among authors. Subungual hematomas involving over 50% of the nail will generally have a nail bed injury. Patients with tuft fractures (distal phalanx fractures) have nail bed injuries in 90% of cases. Several authors recommend removing the nail in these cases in order to repair the nail bed directly. However, more commonly in clinical practice the nail is left in place regardless of the size of the subungual hematoma. Removing the nail can be a traumatic experience for patients and requires a lengthy period of wound care as the nail heals back down. Leaving the nail intact helps keep the nail bed approximated and is much easier for patients to care for. Patients with severe pain with a subungual hematoma may require decompression of the hematoma. Decompression can be achieved by making 2-3 small holes in the nail (nail trephination) above the hematoma with electro cautery or a heated paper clip. Distal phalanx fractures should be treated with a splint to immobilize and protect against contact for 6 weeks. Patients can be advised that these fractures can heal slowly, especially if there is displacement or comminution, and sensitivity over the finger tip for 3-4 months is not uncommon. 1,2

    References
    1. Steven E. Roser, MD, Harris Gellman, MD. Comparison of nail bed repair versus nail trephination for subungual hematomas in children. The Journal of Hand Surgery 1999. (24) 6. 1166–1170.
    2. Wang QC, Johnson BA. Fingertip Injuries. Am Fam Physician. 2001 May 15;63(10):1961-1966.

    Incorrect

    A subungual hematoma, or bleeding under the nail, commonly occurs after crush injuries of the fingertip. The affected nail may become swollen and significantly painful. Treatment of these injuries is controversial with conflicting recommendations among authors. Subungual hematomas involving over 50% of the nail will generally have a nail bed injury. Patients with tuft fractures (distal phalanx fractures) have nail bed injuries in 90% of cases. Several authors recommend removing the nail in these cases in order to repair the nail bed directly. However, more commonly in clinical practice the nail is left in place regardless of the size of the subungual hematoma. Removing the nail can be a traumatic experience for patients and requires a lengthy period of wound care as the nail heals back down. Leaving the nail intact helps keep the nail bed approximated and is much easier for patients to care for. Patients with severe pain with a subungual hematoma may require decompression of the hematoma. Decompression can be achieved by making 2-3 small holes in the nail (nail trephination) above the hematoma with electro cautery or a heated paper clip. Distal phalanx fractures should be treated with a splint to immobilize and protect against contact for 6 weeks. Patients can be advised that these fractures can heal slowly, especially if there is displacement or comminution, and sensitivity over the finger tip for 3-4 months is not uncommon. 1,2

    References
    1. Steven E. Roser, MD, Harris Gellman, MD. Comparison of nail bed repair versus nail trephination for subungual hematomas in children. The Journal of Hand Surgery 1999. (24) 6. 1166–1170.
    2. Wang QC, Johnson BA. Fingertip Injuries. Am Fam Physician. 2001 May 15;63(10):1961-1966.

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