4 Flashcards
(351 cards)
1
Q
7–year–old with a swollen 3 x 4 cm tender, erythematous, anterior cervical neck node. Pet cat. What is the diagnosis?
A
Cat–scratch disease.
2
Q
What is the clinical presentation of cat–scratch disease?
A
3–5 mm red to white papules along a linear scratch plus chronic lymphadenitis. Fever, malaise, headache, anorexia. Abdominal pain, weight loss, hepatosplenomegaly, osteolytic lesion. Parinaud oculoglandular syndrome.
3
Q
What is parinaud oculoglandular syndrome?
A
Unilateral conjunctivitis, preauricular lymphadenopathy, cervical lymphadenopathy; caused by Bartonella; occurs after rubbing eye after touching a pet.
4
Q
How is cat–scratch disease diagnosed?
A
History of scratch from cat. Tissue: PCR and Warthin–Starry stain (shows gram–negative bacilli). Serology: variable immunoglobulin IgG and IgM response.
5
Q
What is the treatment for cat–scratch disease?
A
Azithromycin. Usually self–limiting and resolves in 2–4 months. Aspiration of large and painful lesions.
6
Q
9–year–old child with a positive tuberculin skin test. What is the diagnosis?
A
Latent tuberculosis.
7
Q
What are the high–risk reservoirs for Mycobacterium tuberculosis?
A
Recent immigrants, low socioeconomic status, HIV, elderly.
8
Q
What is primary complex tuberculosis?
A
Tuberculosis infection of the lung with hilar adenopathy. Latent infection: reactive TB skin test and absence of clinical or radiographic findings.
9
Q
How is latent tuberculosis diagnosed?
A
Delayed hypersensitivity skin testing: Mantoux (PPD) test. Positive 4–8 weeks after inhalation. Positive reaction is 5, 10, or 15 mm, depending on risk factors. Negative chest x–ray. No clinical disease.
10
Q
How is primary tuberculosis diagnosed?
A
Best test is to get sputum. If unable to obtain sputum, collect 3 consecutive early AM gastric aspirates (only 50% sensitive, even with PCR). A negative culture never excludes the diagnosis.
11
Q
What is the clinical presentation of primary tuberculosis?
A
Primary TB is asymptomatic in children. Low fever, mild cough, malaise that resolve in 1 week. Reactivation is rare and occurs during adolescence. Small number with extrapulmonary presentation; symptoms depend on location.
12
Q
What is the presentation of primary pulmonary tuberculosis?
A
Localized nonspecific infiltrate. Large adenopathy compared to infiltrate. Compression causes atelectasis and hyperinflation. Most resolve completely.
13
Q
What is the presentation of extrapulmonary tuberculosis?
A
Erosion into blood or lymph causes miliary tuberculosis. Lungs, spleen, liver, bone and joints: Pott disease (destruction of vertebral bodies leading to kyphosis).
14
Q
What are the signs of tuberculosis meningitis?
A
Mostly affects brainstem. Cranial nerve III, VI, VII palsies and communicating hydrocephalus.
15
Q
What is the treatment for latent tuberculosis?
A
INH x 9 months.
16
Q
What is the treatment of primary pulmonary tuberculosis?
A
Isoniazid, rifampin for 6 mth. Plus pyrazinamide in first 2 mth. If increased community resistance, add streptomycin, ethambutol or ethionamide. Corticosteroids in meningitis, severe miliary disease, pericardial/pleural effusions.
17
Q
What are the criteria for a positive Mantoux test reaction?
A
A reaction of >5 mm is positive in those who have been exposed to TB or are immunocompromised. >10 mm of induration is positive in high–risk populations. For low–risk persons, >15 mm is positive.
18
Q
What are the causes of a false–negative PPD reaction?
A
Immunocompromise, malnourishment, or received live–virus vaccines may cause a false–negative reaction.
19
Q
What is bacille Calmette–Guerin (BCG)?
A
BCG is not routinely used because of time–limited efficacy. Only used in high–risk with close or long–term exposures; continuous exposure to resistant strains. Contraindicated in primary or secondary immune deficiencies.
20
Q
What is the treatment of perinatal tuberculosis if the mother has a positive PPD and negative chest x–ray?
A
No separation, no evaluation of baby. Mother and baby are given INH for 9 months. If mother has suspected TB at delivery, then separate baby from mother until chest x–ray obtained. If positive, keep separate until sputum culture results.
21
Q
What is the treatment of perinatal tuberculosis if the mother has active tuberculosis?
A
If mother has disease, then treat infant with INH with no further separation from mother and treat mother with anti–TB therapy for 3 months. Then PPD skin–test infant: Negative, then stop INH. Positive, then continue for 9–12 months.
22
Q
What is the triad of Lyme disease?
A
Rash. Bell palsy or carditis. Arthritis.
23
Q
7–year–old child with a rash after camping in Connecticut with his family. Rash has a red raised border with central clearing. What is the diagnosis?
A
Lyme disease.
24
Q
What is Borrelia burgdorferi?
A
Most common vector–borne disease in the United States. Southern New England, eastern Middle Atlantic states, and upper Midwest, with small area along the Pacific coast. The vector is Ixodes scapularis, i.e., the deer tick.
25
What is the clinical presentation of early Lyme disease?
History of tick bite is usually absent. History of being in woods. Erythema migrans 3–32 days after bite at the site; target lesion (\>10 cm in diameter). Fever, headache, malaise. Without treatment, the lesion resolves in 1–2 weeks.
26
What are the signs of early disseminated Lyme disease?
Secondary lesions, which are smaller than the primary lesion, plus constitutional symptoms plus lymphadenopathy. Uveitis and Bell palsy (may be only finding); carditis (myocarditis, heart block). CNS findings (neuropathy, aseptic meningitis).
27
What are the signs of late Lyme disease?
Arthritis weeks to months later; affecting large joints, more likely to be chronic in adults.
28
How is Lyme disease diagnosed?
History plus rash. Serum antibodies for confirmation. Quantitative ELISA test and confirmatory Western blot if the ELISA is positive or equivocal.
29
What is the treatment of early Lyme disease?
Doxycycline 14–21 days (\>8 yr); amoxicillin (
30
10–year–old with fever, headache, and a rose–colored rash that began on his ankles and is spreading. Camping in North Carolina. What is the diagnosis?
Rocky Mountain spotted fever
31
What is the geography of Rocky Mountain spotted fever?
Seen in every state; most in Southeast, especially in North Carolina. Wooded areas, coastal grasses, and salt marshes. Most April–September; most patients
32
What is the clinical presentation of Rocky Mountain spotted fever?
Incubation period 2–14 days, then headache, fever, anorexia, myalgias, gastrointestinal symptoms. After third day: skin rash or extremities first (palms, soles). Spreads rapidly.
33
What are the physical signs of Rocky Mountain spotted fever?
Rash becomes petechial and hemorrhagic. Palpable purpura. Vascular obstruction because of vasculitis and thromboses. Hepatosplenomegaly. Delirium, coma. Myocarditis, acute renal failure, pneumonitis, shock.
34
How is Rocky Mountain spotted fever diagnosed?
Confirm with fourfold increase in antibody titer. Normal to decreased WBC with marked left shift. Low platelet count. Hyponatremia.
35
What is the treatment for Rocky Mountain spotted fever?
Doxycycline or tetracycline for all patients regardless of age.
36
Infant with white plaques on buccal mucosa that are difficult to scrape off. When removed, there is punctate bleeding. History of antibiotics for Streptococcus infection. What is the diagnosis?
Oral candidiasis.
37
What is Candida albicans?
C. albicans is part of normal gastrointestinal tract and vaginal flora. Oral infection is thrush; white plaques; seen with antibiotic treatment and immunodeficiency; punctate bleeding with scraping.
38
What is the treatment for thrush?
Oral nystatin gargles; if recalcitrant or recurrent, single–dose fluconazole.
39
What is diaper dermatitis?
Confluent, papular erythema with satellite lesions of intertriginous areas of perineum.
40
How is diaper dermatitis diagnosed?
Skin scrapings; see yeast with KOH prep.
41
What is the treatment for candida diaper dermatitis?
Topical nystatin; if significant inflammation, add 1% hydrocortisone for 1–2 days.
42
How is catheter–related fungemia diagnosed?
Buffy coat of catheter tips, urine shows yeast; culture.
43
What is the treatment for catheter–related fungemia?
Remove all catheters; amphotericin B is drug of choice.
44
What is chronic mucocutaneous candidiasis?
Chronic mucocutaneous candidiasis is a primary defect of T lymphocytes in response to Candida; often with diabetes mellitus or autoimmune disease.
45
What is the triad of Rocky Mountain spotted fever?
Headache; fever; pale, rose–colored, maculopapular rash.
46
What is the source of Cryptococcus neoformans infection?
Soil contaminated with bird droppings, or in fruits, vegetables. Predominant fungal infection in HIV; rare in immunocompetents. Inhalation spores; disseminate to brain, meninges, skin, eyes, and skeletal system; forms granulomas.
47
What is the presentation of Cryptococcus neoformans infection?
Pneumonia is most common presentation; often asymptomatic, progressive pulmonary disease.
48
How is Cryptococcus neoformans infection diagnosed?
Latex agglutination for cryptococcal antigen in serum; most useful for CSF infections. India ink preparation for CSF is less useful than culture and antigen detection.
49
What is the treatment for Cryptococcus neoformans infection?
Oral fluconazole for 3–6 months if immunocompetent and only mild disease. Amphotericin B and flucytosine if immunocompromised. In HIV: lifelong prophylaxis with fluconazole.
50
12–year–old with flu–like symptoms for 6 days, fever, cough, and malaise. Exposure to mountain caves. What is the diagnosis?
Histoplasmosis.
51
What is the source of infection for Histoplasma capsulatum?
Soil contaminated with bird droppings or decayed wood; throughout Midwest, especially Ohio and Mississippi River valleys. Bat droppings in caves. Inhalation of micronidia causes proliferate as yeast.
52
What is the pathophysiology of Histoplasma capsulatum infection?
Bronchopneumonia (granuloma and central necrosis) that disseminates through reticuloendothelial system; resolves over 2–4 months; may calcify and appear similar to tuberculosis.
53
What is the clinical presentation of acute pulmonary histoplasmosis?
Most asymptomatic. Symptomatic in young children causing flu–like symptoms, hepatosplenomegaly, respiratory distress. Most have normal chest x–ray or patchy bronchopneumonia and hilar adenopathy.
54
What is the presentation of chronic pulmonary histoplasmosis?
Seen in adults (rarely in children) as a centrilobular emphysema.
55
What is the presentation of progressive disseminated histoplasmosis?
Infants, immunosuppressed. Fever, HSM, anemia, thrombocytopenia. Weight loss, interstitial pulmonary disease, oropharyngeal ulcers, meningitis. AIDS–defining: presents with fever, weight loss, lymphadenopathy, rashes.
56
How is histoplasmosis diagnosed?
Radioimmunoassay of serum or urine for the antigen. Blood culture is sterile; sputum may be positive or negative. Seroconversion.
57
What is the treatment for histoplasmosis?
None for mild acute disease or oral itraconazole. Progressive pulmonary disease or disseminated infection should be treated with amphotericin B.
58
16–year–old in Arizona with fever, headache, malaise, chest pain, and dry cough. Maculopapular rash and tibial erythema nodosum. What is the diagnosis?
Coccidiomycosis.
59
What is the presentation of coccidiomycosis?
Flu symptoms, chest pain, dry, cough, maculopapular rash, tibial erythema nodosum. Dissemination can be fatal; more common in males, Filipino/Asians, blood group B. Inhaled arthroconidia from dust; no person–to–person spread.
60
How is coccidiomycosis diagnosed?
Sputum obtained via bronchoalveolar lavage or gastric aspirates.
61
What is the triad of Coccidiomycosis?
Flu–like symptoms sometimes chest pain, maculopapular rash, erythema nodosum.
62
How is coccidiomycosis diagnosed?
Confirmed by culture, PCR.
63
What is the treatment for coccidiomycosis?
For those at high risk of severe disease, treatment with itraconazole or amphotericin B.
64
Unimmunized child with coryza, cough, conjunctivitis, fever. Morbilliform rash that began on head and spread caudad, including palms. Grayish white dots on buccal mucosa next to third molar. What is the diagnosis?
Measles
65
What is measles?
Rubeola. RNA Paramyxovirus, very contagious. Incubation–10–12 days before prodrome of cough, coryza, conjunctivitis. Koplik spots (grayish–white spots on buccal mucosa); cervical lymphadenitis. Rash and fever.
66
What are the characteristics of the measles rash?
Macular rash; starts at head and spreads downward.
67
How is measles diagnosed?
Rarely may need titers or demonstration of multi–nucleated giant cells in nasal mucosal smears for confirmation.
68
What are the complications of measles?
Otitis media (most common), pneumonia, encephalitis.
69
5–year–old unimmunized child with low–grade fever, pinpoint rash, post–occipital and retroauricular lymphadenopathy, and rose spots on the soft palate. What is the diagnosis?
Rubella
70
What is Rubella?
German measles. Incubation 14–21 days; contagious 2 days before rash and 5–7 days after rash.
71
What is the triad of rubella?
Maculopapular rash. Posterior cervical lymphadenopathy. Polyarthritis.
72
What is the clinical presentation of rubella?
Rash similar to measles, begins on face and spreads to body, lasts 3 days. Rash, fever concurrent. Retroauricular, posterior, occipital lymphadenitis. Forchheimer spots on soft palate appear before rash. Polyarthritis.
73
How is rubella diagnosed?
Confirm with serology or culture. Prevention: immunization with MMR vaccine.
74
What is the triad of roseola?
High fever preceding rash. Rose–colored papules on trunk. Occipital lymphadenopathy.
75
12–month–old infant with rash. Fever of 40 C. Fever resolved, then pink, slightly raised lesions on the trunk, upper extremities, face, and neck. What is the diagnosis?
Roseola
76
What is the cause of roseola?
Febrile illness caused by infection with human herpes virus: HHV–6; usually 6–15 months old; incubation period 5–15 days.
77
What is the clinical presentation of roseola?
High fever (up to 41 C) lasting a few days with symptoms of URI. Occipital lymphadenopathy. By the 3rd or 4th day, fever resolves and a maculopapular rash appears on the trunk, arms, neck, and face.
78
What are the characteristics of the rash of roseola?
Rose–colored rash begins as papules; treatment is supportive.
79
4–year–old child with swelling in his face and fever. Incomplete immunizations, tender facial swelling around the masseter muscle. What is the diagnosis?
Mumps
80
What is mumps?
Viral infection caused by Paramyxovirus transmitted by airborne droplets and respiratory and oral secretions in winter/spring. Incubation period 14–24 days. History of lacking immunizations.
81
What is the clinical presentation of mumps?
Fever, headache, and malaise. Salivary gland swelling, predominantly parotids. Arthritis; orchitis is rare before puberty; may result in sterility if bilateral.
82
How is mumps diagnosed?
Enzyme immunoassays for IgG and IgM for confirmation. Elevated serum amylase.
83
What is the treatment of mumps?
Treat orchitis with bedrest and testicular support. NSAIDs on steroids for severe arthritis.
84
What are the complications of mumps?
Meningoencephalomyelitis is the most common complication; pancreatitis, thyroiditis, myocarditis, deafness, and dacryoadenitis.
85
5–year–old with a fever of 38.8 C, pruritic rash in various stages of papules, vesicles, crusts. Began on trunk and spread to his extremities. What is the diagnosis?
Varicella
86
What is the cause of chicken pox?
Caused by varicella–zoster virus, a herpes virus. Incubation 10–21 days. Transmitted through respiratory secretions. Remains latent in sensory ganglia after recovery; reactivation in immunosuppressed.
87
What is the clinical presentation of varicella?
Mild abdominal pain and fever preceding pruritic rash in various stages. Macules then papules then vesicle and pustules. Lesions can turn hemorrhagic. Crops. Tzanck prep of lesion may reveal multinucleated giant cells.
88
What is the triad of varicella?
Rash in various stages. Crops. Pruritus.
89
What is the treatment for varicella?
Treat secondary infections. Consider acyclovir and VZIG in immunocompromised or if at risk for severe disease.
90
What are the complications of varicella?
Worse in adolescence and may cause scarring. Chickenpox pneumonia seen in 15–20%. Other sequelae include Guillain–Barre syndrome, encephalitis, cerebellar ataxia, post–herpetic neuralgia, and Ramsay–Hunt syndrome.
91
5–year–old with red slapped cheek appearance and a lacy rash on upper extremities and trunk. What is the diagnosis?
Erythema infectiosum (Fifth disease).
92
What is the cause of fifth disease?
Parvovirus B19, a DNA virus; seen most commonly in spring.
93
What is the clinical presentation of erythema infectiosum?
Mild systemic symptoms, arthritis, intensely red, slapped cheek" appearance. Lacy reticular rash over trunk and extremities; sparing of palms and soles; rash remains up to 40 days."
94
How is fifth disease diagnosed?
Viral DNA in fetal blood is often helpful for diagnosing hydrops.
95
What are the complications of erythema infectiosum?
Aplastic crisis in patients with hemolytic anemia, such as sickle cell; erythroblastosis fetalis in neonates during maternal infection.
96
What is the triad of fifth disease?
Slapped cheeks". Aplastic crisis. Fetal hydrops."
97
What are the characteristics of the rash of fifth disease?
Slapped cheek, then to trunk, then central clearing to a lacy appearance.
98
What are the characteristics of the rash of varicella?
Crops of papules vesicles, crusts at same time; spreads centrally to peripherally.
99
What are the complications of scarlet fever?
Acute renal failure, glomerulonephritis.
100
What are the complications of varicella?
Superinfection of rash, zoster, pneumonia, hepatitis, encephalitis, congenital varicella.
101
What are the complications of measles?
Pneumonia, encephalitis, subacute sclerosing panencephalitis.
102
What are the complications of rubella?
Congenital rubella is teratogenic.
103
What is the complication of mumps?
Encephalitis, orchitis, pregnancy aqueductal stenosis; pancreatitis.
104
What is the complication of fifth disease?
Aplastic anemia.
105
What are the characteristics of the rubella rash?
Macules of face, neck, then trunk and extremities; posterior cervical and auricular lymphadenopathy. German measles.
106
What are the characteristics of the roseola rash?
Fever falls rapidly, then fine macular rash on trunk, which spreads to extremities.
107
What is the prodrome of scarlet fever?
Sore throat.
108
What is the enanthem of scarlet fever?
Exudative pharyngitis, strawberry tongue.
109
What are the characteristics of the rash in scarlet fever?
Fine maculopapular rash that feels like sandpaper, especially in antecubitus and inguinal areas; Pastia lines.
110
What is the exanthem of mumps?
Swollen parotid and submandibular glands.
111
23–year–old with fever, fatigue, sore throat. Generalized adenopathy most prominent in the anterior and posterior cervical nodes. What is the diagnosis?
Epstein–Barr virus.
112
What disease is caused by Epstein–Bar virus?
Infectious mononucleosis (90%)
113
What malignancies are associated with Epstein–Bar virus?
Nasopharyngeal carcinoma, Burkitt lymphoma; Hodgkin disease, lymphoproliferative disorders, and leiomyosarcoma in immunodeficiency states.
114
What is the mode of transmission for Epstein–Bar virus?
Transmitted in oral secretions by close contact (kissing disease); intermittent shedding for life. Incubation period 30–50 days; most cases in infants and young children are asymptomatic.
115
What is the clinical presentation of infectious mononucleosis?
Older child with insidious prodrome for 1–2 weeks with fever, fatigue, headache, myalgia, sore throat, abdominal pain.
116
What is the presentation of infections mononucleosis?
Lymphadenopathy (cervical submandibular; less often axillary, inguinal, epitrochlear nodes), splenomegaly. Pharyngitis with tonsillar enlargement, maculopapular rash occurs if treated with ampicillin or amoxicillin.
117
How is Epstein–Barr virus infection diagnosed?
Atypical lymphocytosis. Mild elevation in hepatic transaminases. Heterophile antibodies (Monospot test). IgM to viral capsid antigen is the most specific test.
118
What is the treatment for infectious mononucleosis?
No contact sports or strenuous activity with splenomegaly. Short course of steroids for airway obstruction, thrombocytopenia with hemorrhage, autoimmune hemolytic anemia, seizures, or meningitis.
119
What are the complications of Epstein–Barr virus infection?
Splenic hemorrhage or rupture (very rare) after trauma. Swelling of tonsils, causing airway obstruction. Guillain–Barre syndrome or Reye syndrome is rare, aplastic anemia, interstitial pneumonia, myocarditis.
120
What is the disease course in infectious mononucleosis?
Most cases resolve in 2–4 weeks; some disability that comes and goes for a few months is common; and there may be fatigue for a few years, but there is no evidence that EBV is related to chronic fatigue syndrome.
121
What is the triad of infectious mononucleosis?
Fatigue. Pharyngitis. Generalized adenopathy.
122
What infection is associated with a rash after taking ampicillin or amoxicillin for URI symptoms?
Infectious mononucleosis.
123
12–year–old girl with fever of 39 C, headache, sore throat, myalgia, chills and non–productive cough. What is the diagnosis?
Influenza
124
What are the causes of influenza?
Types: A, B, and C; A and B are the primary pathogens. Migratory avian hosts spread disease. Annual spread between Northern and Southern hemispheres; origin in Asia. 1 or 2 strains spread annually. Colder months. Transmission by aerosol.
125
What is the clinical presentation of influenza?
Predominantly respiratory illness. Abrupt onset with coryza, conjunctivitis, pharyngitis, and dry cough. Prominent systemic signs of fever, myalgia, malaise, headache.
126
How is influenza diagnosed?
Rapid diagnostic test with ELISA. Can be confirmed serologically with acute and convalescent titers. Virus can be isolated from nasopharynx early in course.
127
What is the treatment for influenza?
Antiviral drugs decrease severity and duration if administered within first 48 hours of symptoms. Oseltamivir, zanamivir.
128
What are the complications of influenza?
Otitis media, pneumonia; secondary bacterial infection, myocarditis.
129
What is the clinical presentation of AIDS in infants?
Rapid onset of symptoms and AIDS in first few months of life, lymphadenopathy, hepatosplenomegaly, failure to thrive, chronic diarrhea, interstitial pneumonia, oral thrush.
130
What manifestations of AIDS are more common in children than adults?
Recurrent bacterial infections, chronic parotid swelling, lymphocytic interstitial pneumonitis, early progressive neurological deterioration.
131
What is the category A classification of HIV infection?
Mild symptoms; at least two: lymphadenopathy, parotitis, hepatomegaly, splenomegaly, dermatitis, recurrent or persistent otitis media/sinusitis.
132
What is the category B classification of HIV virus infection?
Moderate symptoms: lymphocytic interstitial pneumonitis, thrush \>2 m, chronic diarrhea, persistent fever \>1 m, hepatitis, recurrent HSV stomatitis, esophagitis or pneumonitis, disseminated varicella, cardiomegaly, nephropathy.
133
What is the category C classification of HIV virus infection?
Severe symptoms: 2 serious bacterial infections in 2 y, esophageal/respiratory candidiasis, cryptococcosis, cryptosporidiosis, encephalopathy, malignancies, disseminated mycobacterial, PJP, cerebral toxoplasmosis, weight loss.
134
What infections occur in HIV–infected children?
Recurrent bacterial infections with encapsulated organisms and other gram–positive, gram–negatives. PJP, Mycobacterium avian complex: disseminated disease in severely compromised. Candidiasis, invasive fungal. Viral, herpes.
135
What are the non–infectious complications of HIV infection?
CNS disease, cardiomyopathy, enteropathy, wasting syndrome, nephropathy, cutaneous, manifestations, hematologic manifestations, malignancies.
136
How is HIV infection diagnosed in newborn children?
HIV–DNA by PCR. Maternal HIV IgG antibodies cross the placenta. Antibody screen will be positive in all newborns of HIV mothers up to 18 months of age. In any child \>18 months of age: test for infection through IgG Ab by ELISA, confirm with Western blot.
137
What is the treatment of HIV in infants born to HIV–infected mothers?
Mother: perinatal triple antiretroviral therapy. Infant should be started on ZDV at birth until neonatal disease is excluded. Also start PCP prophylaxis (TMP–SMZ) at 1 month until disease excluded. CBC, platelets, CD4, CD8 counts.
138
What is ascariasis?
Ascaris lumbricoides; nematode (roundworm). Most prevalent human helminth in the world. High prevalence in poor countries with use of human waste as fertilizer and with geophagia.
139
What is the life cycle of Ascaris?
Travels to the small intestines then releases larvae then migrates through the venous circulation to the lungs and causes pulmonary ascariasis; enter through alveoli and bronchi to trachea and are swallowed to intestine to adult worms.
140
What is the clinical presentation of ascariasis?
Most are asymptomatic or mild. Most common symptom is cough and blood–stained sputum. Obstructive intestinal or biliary tract disease causing colicky abdominal pain or bile–stained emesis.
141
What are the laboratory abnormalities in ascariasis?
Eosinophilia. Worms can be identified on fecal smear.
142
What is the treatment of ascariasis?
Albendazole, mebendazole, or pyrantel pamoate.
143
6–year–old girl with lack of appetite, abdominal pain, and diarrhea. Yellow–green pallor. What is the diagnosis?
Hookworm
144
What is hookworm?
Ancylostoma and Necator americanus are nematodes transmitted in warm, moist soil in rural areas where human waste is fertilizer. Penetrate skin causing pruritus or ingested. Migration to lungs and swallowed; teeth attach mucosa, eggs.
145
What is the clinical presentation of hookworm?
Blood loss, iron deficiency anemia. Hypoalbuminemia, edema, anasarca. Cough, colicky abdominal pain, anorexia, diarrhea. Growth retardation, cognitive, intellectual deficits. Green–yellow skin (chlorosis).
146
What is the laboratory abnormality in hookworm?
Blood eosinophilia. Eggs on fecal smear.
147
What is the treatment of hookworm?
Mebendazole or albendazole; pyrantel pamoate is an alternative. Ferrous sulfate if iron deficient.
148
4–year–old with anal pruritus attends daycare. What is the diagnosis?
Enterobiasis
149
What is enterobiasis?
Most common helminth; 5–14 years. Eggs ingested from fingernails, clothing, bedding, dust; after ingestion, adult worms within 1 month. Inhabits cecum, appendix, ileus, and ascending colon; female migration at night to deposit eggs on perianus, perineum.
150
What is the clinical presentation of enterobiasis?
Itching and restless sleep and no eosinophilia.
151
How is enterobiasis diagnosed?
Adhesive cellophane tape (tape test) at night when child is asleep.
152
What is the treatment for enterobiasis?
Infected person and entire family receive single oral dose of mebendazole and repeat in 2 weeks.
153
What is trichinosis?
Caused by Trichinella spiralis infection; worldwide nematode; contracted through ingestion of meat containing larvae.
154
What is the life cycle of trichinella?
Ingestion raw or poorly cooked meat, then larva enters small intestine and develops into adult larvae; seed striated muscle fibers, become encysted, and may be viable for years. Common in Asia, Latin America, and Central Europe.
155
What is the clinical presentation of trichinosis?
Ssymptomatic or mild diarrhea with vomiting and abdominal pain. Periorbital edema, fever and myalgia; peak 2–3 weeks after ingestion as larvae encyst in muscle; headache, cough, dyspnea, dysphagia, rash. Serology or muscle biopsy.
156
What is the treatment of trichinosis?
Mebendazole or albendazole.
157
What is Enterobius vermicularis?
Enterobius vermicularis is the parasite that causes infection. Small, white, threadlike nematodes on stool examination.
158
What is the treatment for Enterobius vermicularis infection?
Mebendazole or albendazole.
159
What is trichuriasis?
Also called whipworm (nematode). Rural communities with soil contaminated with feces. Southeastern United States. Resides in cecum and ascending colon after ingestion of eggs. Larvae penetrate villi and lay eggs in cecum.
160
What is the clinical presentation of trichuriasis?
Asymptomatic or mild. Right lower quadrant pain or periumbilical pain. Chronic dysentery, rectal prolapse.
161
How is trichuriasis diagnosed?
Fecal smear; no eosinophilia.
162
What is the treatment for trichuriasis?
Mebendazole or albendazole
163
3–year–old with vesicular rash in his mouth, palms and soles. Rash on buttocks. What is the diagnosis?
Coxsackievirus
164
What is the presentation of Coxsackievirus infection?
Characteristic lesions occur anywhere, but usually on the oral mucosa, hands and feet; hand–foot–mouth disease. Rash on the buttocks. Coxsackievirus B may cause viral myocarditis.
165
11–year–old with fever, sore throat, and follicular conjunctivitis. What is the diagnosis?
Adenovirus
166
What is adenovirus?
DNA virus responsible for URIs in infants and children, causing fever, pharyngitis, conjunctivitis, and diarrhea. Less common features include pharyngoconjunctival fever, myocarditis, and intussusception.
167
What is poliovirus?
Lives in gastrointestinal tract. Can cause URI symptoms. Paralytic polio is an asymmetric flaccid paralysis. Prevent with vaccination.
168
Child with a pruritic rash for the past 3 weeks in the webs of the fingers and spread to the wrists, elbows, and axilla. What is the diagnosis?
Scabies
169
What is the cause of scabies?
Sarcoptes scabiei mite; burrows into skin and releases toxic substances (female).
170
What is the clinical presentation of scabies?
Intense pruritus at site of infection especially at night. 1– to 2–mm red papules with excoriation, crusting, scaling. Threadlike; burrow under the skin. Interdigital, wrist flexors, anterior axillary folds, ankles, areola, buttocks, genital.
171
How is scabies diagnosed?
Microscopic examination of scraping.
172
What is the treatment for scabies?
\>2 months of age: permethrin 5% or lindane 1% (neurotoxic) on entire body from neck down. Infants
173
What is the causes of pediculosis (body louse)?
Pediculosis humanus corporis, which is body, clothing louse and is the only one that serves as a vector for human disease (typhus, trench fever, relapsing fever). Caused by poor hygiene (homeless).
174
What is the clinical presentation of pediculosis?
Lesion is small red macule or papule; intensely pruritic.
175
What is the treatment for body louse?
Hot–water launder all clothing. Lindane or permethrin to eradicate eggs and lice on body hair.
176
What are the causes of head louse?
Pediculosis humanus capitis. Eggs deposited on the proximal hair shaft.
177
What is the treatment for pediculosis capitis?
0.5% Malathion or permethrin cream rinse or pyrethrum shampoos or lindane (Kwell).
178
What are the complications of head louse?
Secondary pyoderma from scratching.
179
What are the causes of pubic louse?
Pediculosis pubis; skin–to–skin or sexual contact (100% transmission); most in adolescents.
180
What is the clinical presentation of pediculosis pubis?
Genital and groin pruritus with excoriation. Nits are visible with hand lens.
181
What is the treatment for pediculosis pubis?
0.5% Malathion or permethrin cream rinse or pyrethrum shampoos or lindane (Kwell). Launder all clothes and bedding; test for other venereal diseases.
182
What is the most common cause of poisoning in children less than 5 years of age?
Most likely accidental ingestion. In adolescents poisonings are usually intentional (suicide) or experimental (drugs) ingestion. Any poisoning in a child older than 5 years of age should be considered intentional.
183
What is the treatment of choice in emergency departments to prevent absorption?
Activated charcoal. Not effective in preventing cyanide, heavy metal, Na, K, Cl, acid and base absorption.
184
What is the pathophysiology of acetaminophen toxicity?
Acetaminophen undergoes liver metabolism and results in liver damage after glutathione stores are depleted.
185
What is the toxic dose for acetaminophen?
In children
186
What is the disease course in acetaminophen overdose?
Stage 1: 24 h, nausea, vomiting, diaphoresis. Stage 2 (24–28 hours): improvement, rising LFTs, RUQ pain. Stage 3 (72 hours): peak LFTs, more GI symptoms. Stage 4 (4 days–weeks): resolution, or
187
What are the laboratory abnormalities in acetaminophen overdose?
Acetaminophen level at 4 or more hours post ingestion. Use Rumack–Matthew nomogram to plot plasma level against hours post–ingestion. Increased ALT, AST, PT, bilirubin.
188
What is the treatment for acetaminophen overdose?
N–acetylcysteine (NAC, Mucomyst) if patient took toxic dose of acetaminophen (\>150 mg/kg). Best if started within 8 hours post–ingestion.
189
What are the laboratory abnormalities in alcohol intoxication?
Blood alcohol level, hypoglycemia. Dialysis for blood alcohol \>400 mg/dL.
190
What is the presentation of acute amphetamine toxicity?
Diarrhea, palpitations, arrhythmias, syncope, convulsions, coma. Urine drug screen.
191
What is the treatment of amphetamine toxicity?
Cooling blankets for hyperthermia. Haloperidol for delusions or hallucinations. Sedation with lorazepam or diazepam.
192
What is the most common drug poisoning in the United States?
Aspirin
193
What is the pathophysiology of aspirin overdose?
Uncouple oxidative phosphorylation and increase metabolic rate causes a hypermetabolic state. Inhibits Krebs cycle, causing metabolic acidosis. Direct damage to hepatocytes results in increased liver function tests.
194
What is the presentation of mild aspirin toxicity?
Vomiting, hyperpnea, fever, lethargy, confusion.
195
What is the presentation of severe aspirin toxicity?
Seizures, coma, dehydration, respiratory/cardiac collapse.
196
What is the presentation of chronic aspirin toxicity?
Hyperventilation, tinnitus, dehydration, bleeding, hepatotoxicity, seizures, coma.
197
What is the acute toxic dose for aspirin?
More than 150 mg/kg.
198
What are the characteristics of the first 12 hours after aspirin overdose (stage 1)?
Respiratory alkalosis from direct stimulation of respiratory drive; loss of sodium and bicarbonate in the urine; simulates diabetic ketoacidosis.
199
What are the clinical findings 12–24 hours after aspirin overdose (stage 2)?
Paradoxical aciduria, which may lead to hypokalemia.
200
What are the clinical findings more than 24 hours after aspirin overdose (stage 3)?
Metabolic acidosis (lactic acidosis, dehydration, hypokalemia) appears 4–6 hours after ingestion in an infant but after 24 hours in an adolescent or adult. Hyperpnea is caused by acidosis.
201
What are the laboratory abnormalities associated with aspirin overdose?
Elevated WBC count, platelets, and hematocrit. Electrolytes variable. BUN and creatinine are increased. Children have metabolic acidosis and respiratory compensation. Adolescents have respiratory alkalosis.
202
What is the treatment of aspirin overdose?
Alkalinize the urine to pH of 7.0–7.5 with IV bicarbonate. Dialysis in severe cases.
203
What are the clinical signs of carbon monoxide toxicity?
Headache, lethargy, nausea, vomiting, confusion, syncope, tachycardia, tachypnea, syncope, coma, seizures, coma, hypertension, respiratory failure, death. Cherry red color of blood.
204
How is carbon monoxide toxicity diagnosed?
Carbon monoxide level is the best test. Arterial blood gases. Urinalysis for myoglobin if rhabdomyolysis is suspected.
205
What is the treatment for carbon monoxide toxicity?
100% supplemental oxygen. In severe cases, hyperbaric oxygen. Maintain urine output \>1 mL/kg/h.
206
What are the complications of carbon monoxide toxicity?
Behavioral changes, memory loss, blindness.
207
What are the common sources of acid and alkali ingestions?
Heavy–duty household cleaners and batteries. Most cleaners are strong bases, such as bleach, lye, Drano, detergents.
208
What is the pathogenesis of acid and base ingestions?
Bases cause liquefactive necrosis of the stomach (high risk of perforation). Acids result in coagulation of proteins. Serious injuries occur when the pH is 12.
209
What is the presentation of caustic ingestion?
Mucosal membrane burns. Drooling. Refusal to swallow because of pain.
210
What are the laboratory abnormalities in acid and alkali ingestions?
CBC shows hemorrhage; abdominal x–ray shows perforation and free air.
211
What is the treatment for caustic ingestions?
Copious fluids. Wash area thoroughly if on skin. Emesis and lavage are contraindicated. Endoscopy after first 24 hours if patient is symptomatic or gastric burns are suspected.
212
What is the clinical presentation of cocaine intoxication?
Restlessness, excitation, agitation, hypertension. HTN, hemorrhagic infarction or acute myocardial ischemia. Hypotension, seizures, coma. Perforated nasal septum seen in insufflation. Chronic users may develop cardiomyopathy.
213
What are the laboratory abnormalities in cocaine intoxication?
Urine drug screen. Abdominal film for suspected packers" (smuggling within body cavities."
214
What is the treatment for cocaine intoxication?
Drug half–life is only 1 hour, usually good prognosis unless cerebral hemorrhage or myocardial infarction. GI decontamination with activated charcoal if packing" leads to acute intoxication through leakage."
215
What are the common sources of hydrocarbon poisoning?
Fuels, solvents, household cleaners, polishes.
216
What is the clinical presentation of hydrocarbon poisoning?
Aspiration is more likely than ingestion. Aspiration pneumonia is suggested by cough, emesis, fever, shortness of breath, wheezing, rales, dullness to percussion.
217
What is the role of lavage in hydrocarbon ingestion?
Lavage is contraindicated for hydrocarbon ingestion.
218
Child exposed to fertilizers with drooling, tearing, and emesis. Areflexive and lethargic. What is the diagnosis?
Organophosphate toxicity.
219
What are the causes of organophosphate toxicity?
Direct acetylcholinesterase inhibitors can be ingested, inhaled, or absorbed through skin. Insecticides are the most common source of organophosphate poisoning.
220
What is the clinical presentation of organophosphate toxicity?
Cholinergic muscarinic effects in acute poisoning. Diarrhea, urination, miosis, bradycardia. Emesis, pulmonary edema. Lacrimation, salivation.
221
What are the signs of severe organophosphate poisoning?
Nicotinic effects: Cramps, fasciculations, twitching, weakness, areflexia, paralysis.
222
What are the CNS effects of organophosphate toxicity?
Anxiety, ataxia, dizziness, headache, convulsions, and coma.
223
How is organophosphate toxicity diagnosed?
Decreased RBC cholinesterase is best test for confirmation (do not delay treatment while waiting for results).
224
What is the treatment of organophosphate toxicity?
Atropine for muscarinic symptoms. Pralidoxime for nicotinic symptoms. Wash skin and give gastric lavage.
225
3–year–old child with ingestion of bottle of multivitamins. Abdominal pain and vomiting profusely. What is the diagnosis?
Iron overdose
226
What are the causes of iron overdose?
Children's preparations do not contain sufficient iron for overdose; usually overdose is caused by adult vitamins or iron supplements. \>60 mg/kg is a toxic dose. Iron is the most common cause of childhood death because of poisoning.
227
What are the signs of iron overdose?
Stage 1: 30 min after ingestion: nausea, vomiting, abdominal pain, hemorrhagic gastroenteritis. Stage 2: after 6 h: clinical improvement. Stage 3: 24 h: shock, hepatorenal failure, bleed, metabolic acidosis. Stage 4: 1–2 m later GI obstruction, stenosis.
228
What are the laboratory abnormalities in iron overdose?
Serum iron level (4 hours after ingestion), 500 microgram/dL is severe poisoning. Abdominal x–ray may show radiopaque, iron–laden tablets.
229
What is the treatment for iron overdose?
Deferoxamine IV is indicated in: any symptomatic patient regardless of lab values; or if serum iron is \> TIBC. Serum iron \>350 micrograms/dL.
230
2–year–old with overdose of allergy medication with tremors and hyperactivity. Fever, flushed skin, tachycardia, and fixed dilated pupils. What is the diagnosis?
Antihistamine overdose
231
What are the causes of antihistamine toxicity?
Over–the–counter medications for allergies (Benadryl, Claritin), cough/cold (decongestants), antiemetics (motion sickness tablets). May also contain alcohol.
232
What is the clinical presentation of antihistamine toxicity?
Variable stimulation or suppression of CNS, causing drowsiness, insomnia, nervousness, restless. Hyperactivity, hallucinations, seizures. No lab tests are needed.
233
What is the treatment of antihistamine overdose?
Gastric lavage if not sustained–release. Whole bowel irrigation if sustained–release. Seizure control.
234
What is the mechanism of barbiturates?
Enhanced effects of GABA on tissues, resulting in depressive effects on muscles and nerves.
235
What is the clinical presentation of barbiturate toxicity?
Lethargy, hypotension to coma. Mild to moderate toxicity mimics alcohol intoxication. Severe toxicity results in coma.
236
2–year–old ingested imipramine capsules. Drowsy; QRS widening, QT, and QTc prolongation. What is the diagnosis?
Tricyclic overdose.
237
What is the mechanism of tricyclic antidepressant toxicity?
Alpha–blocking, anticholinergic, quinidine–like effects; blocks norepinephrine, 5–hydroxytryptamine, dopamine in CNS. Sedation. Affects CNS and heart. Seizures, arrhythmias. ECG: wide QRS, long QTc.
238
What is the treatment for tricyclic antidepressant overdose?
Initial treatment of arrhythmias with bicarbonate, then lidocaine if no response.
239
What are the physical signs of anticholinergic toxicity?
Pupils are dilated and nonreactive. Confusion, tachycardia, dry skin. Decreased bowel sounds.
240
What are the physical signs of sympathomimetic toxicity?
Pupil is dilated and reactive, hyperactivity, tachycardia, wet skin, increased bowel sounds.
241
What are the physical signs of cholinergic toxicity?
Small pupils, lethargy, bradycardia, wet skin, increased bowel sounds.
242
What are the physical signs of opiate toxicity?
Pupil is pinpoint, depressed CNS, bradycardia, decreased bowel sounds.
243
What is the antidote for acetaminophen toxicity?
N–acetylcysteine
244
What is the antidote for anticholinergic toxicity?
Physostigmine sulfate.
245
What is the antidote for anticholinesterases poisoning?
Atropine sulfate, pralidoxime (2–PAM) chloride.
246
What is the antidote for cyanide poisoning?
Amyl nitrite. Followed by sodium nitrite. Followed by sodium thiosulfate.
247
That is the treatment of extrapyramidal signs from neuroleptics (haloperidol)?
Diphenhydramine, benztropine.
248
What is the treatment of heavy metal poisoning (eg, arsenic, copper, gold, lead, mercury)?
Chelators: calcium disodium edetate (EDTA), dimercaprol (BAL), penicillamine, 2,3–dimercaptosuccinic acid (DMSA, Succimer).
249
What is the antidote for heparin overdose?
Protamine sulfate
250
What is the antidote for iron overdose?
Deferoxamine mesylate
251
What is the antidote for isoniazid (INH) poisoning?
Pyridoxine
252
What is the antidote for nitrite toxicity?
Methylene blue
253
What is the antidote for opioid poisoning?
Naloxone hydrochloride
254
What is the antidote for tricyclic antidepressant toxicity?
Sodium bicarbonate
255
What is the antidote for salicylate toxicity?
Sodium bicarbonate
256
What is the antidote for warfarin overdose?
Vitamin K1 (phytonadione) or fresh–frozen plasma.
257
What are the physical examination signs of head trauma?
Linear or depressed skill fracture, basilar skill fracture, battle sign, raccoon eyes, hemotympanum, CSF rhinorrhea, otorrhea.
258
What are the clinical signs of an epidural hematoma?
Loss of consciousness, lucid interval, then loss of consciousness occurs again. Lens–shaped hemorrhage on CT scan. Intubation is indicated if the Glasgow coma scale is
259
What is the appearance of a subdural hematoma on CT scan?
Crescent shaped hematoma.
260
What is the most common cause of burns in children?
Scalding burns from hot liquids account for \>85% of clinical burns in children
261
What are the types of burns?
1st degree: epidermis (sunburn). 2nd degree: blisters and painful. 3rd degree: full thickness, resulting in tissue that is numb and painless.
262
What is the Parkland formula for fluid resuscitation of burn patients?
4 mL/kg x % BSA burn = fluid resuscitation for 2nd and 3rd degree burns. Give one half of fluids in first 8 h and second half of fluids in next 16 h. The rule of nines does not apply to children because of proportionally larger head; Lund–Browder used.
263
What is the tetanus prophylaxis for burn patients who have had less than 3 doses of DTaP?
Tetanus prophylaxis with Tdap and tetanus immune globulin are administered in patients who have had
264
What is the criteria for delayed puberty in girls?
Delayed puberty is diagnosed if no breast development occurs by age 13, if no pubic hair appears by age 14, if \> 5 yr elapse between the beginning of breast growth and menarche, or if menstruation does not occur by age 16.
265
What is the criteria for delayed puberty in boys?
Delayed puberty is diagnosed if no testicular enlargement occurs by age 14, if no pubic hair appears by age 15, or if \> 5 yr elapse between initial and complete growth of the genitals. Short stature.
266
What is adolescence?
Period bridging childhood and adulthood. Begins at 11–12 yrs, ends at 18–21. Pubertal and somatic growth become complete. Develops socially, cognitively, emotionally. Moves from concrete to abstract thinking. Independence. Prepares for career.
267
What are the most common causes of mortality in adolescents?
Accidents, especially motor vehicle accidents. Suicide: boys are more successful. Cancer: Hodgkin lymphoma, bone, CNS.
268
What are the most common causes of morbidity in adolescents?
Unintended pregnancy, sexually transmitted diseases, smoking, depression, crime.
269
What changes occur in the early stage of adolescence (10–14 years)?
Physical changes (puberty) including rapid growth, puberty including development of secondary sexual characteristics. Compare themselves to peers (develop body image and self–esteem). Concrete thinkers and awkward.
270
What changes occur in the middle stage of adolescence (15–16 years)?
More independent and have a sense of identity. Mood swings are common. Abstract thinking. Relationships are one–sided and narcissistic.
271
What changes occur in the late stage of adolescence (\>17 years)?
Less self–centered. Relationships with individuals rather than groups. Contemplate future goals, plans, and careers. Idealistic and have a sense of right and wrong.
272
17–year–old girl with fever, chills, pain, and swelling in the small joints of her hands, and a maculopapular rash on her upper and lower extremities. What is the diagnosis?
Disseminated gonococcal infection
273
What is the pathophysiology of Neisseria gonorrhoeae infection?
Neisseria gonorrhoeae usually infects mucosal membranes of the genitourinary tract and less commonly the oropharynx, rectum, and conjunctiva.
274
What is the clinical presentation of Neisseria gonorrhoeae infection?
Urethritis, cervicitis, and dysuria. Asymptomatic patients are at higher risk for dissemination, including fever, chills, and arthritis.
275
What are the physical examination findings in Neisseria gonorrhoeae infection?
Males present with dysuria and purulent penile discharge. Females present with purulent vaginal discharge, cervicitis, abdominal pain, dysuria. Rectal gonorrhea causes proctitis, rectal bleeding, anal discharge, and constipation.
276
What tests are used to diagnose gonorrhea?
Culture of discharge on Thayer Martin media. Blood cultures if dissemination is suspected. Gram strain may show intracellular diplococci. Test for syphilis and HIV.
277
What is the treatment of gonorrhea?
Treat with single–dose ceftriaxone or single–dose azithromycin; treat partners. Alternatives include doxycycline for 7 days (not in children
278
What is Chlamydia?
Cause of nongonococcal urethritis. Intracellular obligate parasite. Most common STD. Mucoid discharge in females or lymphogranuloma venereum (tender inguinal lymphadenopathy).
279
What tests are used to diagnose Chlamydia?
Nucleic acid amplification by PCR. Culture of infected tissue.
280
What is the treatment for Chlamydia?
Single–dose azithromycin or doxycycline for 7 days. Erythromycin if pregnant.
281
16–year–old with yellow, foul–smelling vaginal discharge, strawberry cervix." What is the diagnosis?"
Trichomonas vaginalis
282
What is Trichomonas vaginalis?
Trichomonas vaginalis is a protozoa which causes vaginitis. Girls with multiple sexual partners are at high risk.
283
What is the presentation of trichomoniasis?
Frothy, foul–smelling vaginal discharge; males asymptomatic. Strawberry cervix" because of hemorrhages in the mucosa. Wet prep shows motile protozoans in females. In males examine urine sediment after prostatic massage."
284
What is the treatment of Trichomonas?
Treat with metronidazole
285
16–year–old, boy with painful ulcerations on his glans penis and on the shaft of his penis. Fever and inguinal adenopathy. What is the diagnosis?
Herpes
286
What disease is caused by herpes simplex virus type 1?
Nongenital infections of mouth, eye, and lips most common.
287
What diseases are caused by herpes simplex virus type 2?
Genital, neonatal, oral infection. Cervix is primary site in girls; penis in boys. Tzanck prep shows multinuclear giant cells. ELISA testing. Culture is definitive test.
288
What is the treatment of herpes simplex virus infections?
Treat with acyclovir, valacyclovir, famciclovir.
289
What are the distinguishing features of bacterial vaginosis?
Profuse, discharge with a fishy" odor. Clue cells "whiff test" with KOH pH \>4.5. Not sexually transmitted."
290
What are the distinguishing features of trichomoniasis?
Gray–green, frothy discharge. Wet prep shows motile Trichomonads, pH \>5. Sexually transmitted.
291
What are the distinguishing features of Candida?
Cottage cheese discharge, Hyphae seen with KOH prep, pH
292
What are the distinguishing features of Chlamydia and gonorrhea?
Purulent discharge. Wet prep: WBCs. Sexually transmitted.
293
What is the pathogenesis of acne?
Propionibacterium acnes, forms free fatty acids within follicle. Abnormal keratinization of follicular epithelium and impaction of keratinized cells in sebaceous follicles. Increased sebum production. Inflammation.
294
What is the treatment of acne?
Benzoyl peroxide. Tretinoin (Retin–A) is the single most effective agent for comedonal acne. Adapalene (Differen gel). Topical erythromycin or clindamycin.
295
What is the systemic treatment of severe acne?
Tetracycline, minocycline, doxycycline, erythromycin, clindamycin. Isotretinoin for nodulocystic disease; very teratogenic, increased triglycerides, cholesterol. Hormonal therapy. Corticosteroid injections. Dermabrasion.
296
What is impetigo?
Infection of the dermis; contagious; autoinoculable. Two subtypes are nonbullous and bullous.
297
What is nonbullous impetigo?
Nonbullous impetigo is honey–colored, crust, which may spread. S. aureus is predominant organism, followed by group A beta–hemolytic strep (nephritogenic strains may result in glomerulonephritis).
298
What is bullous impetigo?
Infection of infants and young children; always caused by coagulase positive S. aureus.
299
What is the treatment for impetigo?
Topical mupirocin for local disease. Widespread disease or disease not responding to topical therapy should be treated with an oral beta–lactamase drug (dicloxacillin, cephalexin)
300
What is cellulitis?
Bacterial infection and inflammation of subcutaneous tissue, with limited involvement of the dermis (and sparing of epidermis); predisposed by a break in the skin.
301
What are the causes of cellulitis?
S. pyogenes and S. aureus are the most common bacteria.
302
What are the signs of cellulitis?
Local edema, erythema, warmth, and tenderness with indistinct lateral margins. Blood culture or culture from site of inflammation is positive in only 25%.
303
What is the treatment for cellulitis?
Obtain blood cultures if sepsis is suspected. If patient is not toxic–appearing, then oral therapy with dicloxacillin or cloxacillin or first–generation cephalosporin (cephalexin).
304
What is the treatment of cellulitis?
If the patient appears septic, then parenteral treatment with oxacillin or nafcillin is required.
305
What is erysipelas?
Bacterial infection of epidermis and underlying connective tissue (dermis), but not subcutaneous tissue.
306
What is the cause of erysipelas?
Streptococcus pyogenes.
307
What is the presentation of erysipelas?
Very tender, superficial skin blebs; sharply defined erythema with slightly elevated border. May have reddish streaks of lymphangitis. Fever, chills, and bacteremia.
308
What is the treatment for erysipelas?
Culture locally infected area and blood. Parenteral antibiotics are required.
309
What is staphylococcal scalded skin syndrome?
310
What is Nikolsky sign?
Areas of epidermis separate from dermis in response to gentle shearing force; large areas peel away, resulting in denuded areas in staphylococcal scalded skin syndrome.
311
How is staphylococcal scalded skin syndrome diagnosed?
Intact bullae are sterile (compared with bullous impetigo, which is contagious at site of bullae). Obtain local cultures from site of infection, plus blood cultures.
312
What is the treatment for staphylococcal scalded skin syndrome?
If localized, oral antistaphylococcal antibiotics. Parenteral penicillinase–resistant penicillin for systemic illness.
313
What is folliculitis?
Superficial infection of hair follicle caused by S. aureus. Small, dome–shaped pustules with an erythematous base (scalp, buttocks, extremities). Caused by poor hygiene. Gram stain and culture from purulent material.
314
What is the treatment for folliculitis?
Warm compresses. Topical antibiotic cleanser (chlorhexidine) and topical mupirocin.
315
What are furuncles and carbuncles?
Furuncles originate from folliculitis, which becomes a deep, perifollicular nodule on hair–bearing areas of face, neck, axillae, buttocks, groin. Carbuncles are extensive furuncles and may be associated with fever, bacteremia, leukocytosis.
316
What is the cause of furuncles and carbuncles?
Staphylococcus aureus; predisposing conditions include obesity, hyperhidrosis, friction, preexisting dermatitis, diabetes, malnutrition, and immunodeficiency.
317
What is the treatment for furuncles and carbuncles?
Antimicrobial soaps. Loose–fitting clothing. Large lesions require drainage. Hot, moist compresses; systemic penicillinase–resistant antibiotics (dicloxacillin or cephalexin). Carbuncles are treated with IV nafcillin. If MRSA, clindamycin.
318
What is tinea versicolor?
Chronic fungal infection of stratum corneum; Malassezia furfur. Predisposing factors are warmth, humidity, excessive sweating, occlusion, high plasma cortisol, immunosuppression, malnutrition, genetics; adolescents and young adults.
319
What is the clinical presentation of tinea versicolor?
In whites: reddish–brown lesions. In blacks: hypo– or hyperpigmented lesions. Macules covered with a fine scale. Enlarge to form patches, most often on neck, upper chest, back, and upper arms.
320
How is tinea versicolor diagnosed?
Wood lamp examination shows yellowish–gold fluorescence. KOH scraping of lesions reveals fungal hyphae. Culture is rarely needed.
321
What is the treatment for tinea versicolor?
M furfur is not eradicated and recurs. Selenium–sulfide suspension topically every 2–3 weeks. Oral antifungals, such as itraconazole and fluconazole.
322
What are the causes of dermatophytoses?
Trichophyton, Microsporum, Epidermophyton.
323
What are the predisposing factors for dermatophytoses?
Skin trauma, elevated temperature, hydration of skin with maceration, immunodeficiency, diabetes, and increased cortisol levels.
324
How are dermatophytoses diagnosed?
KOH preparation of lesion scrapings. Culture is the most accurate test.
325
What is the clinical presentation of tinea capitis?
Trichophyton tonsurans. Erythematous and scaly circular plaque; alopecia and severe pruritus. Black dot ringworm is areas of alopecia with hairs broken off. Kerion. Fever, pain; adenopathy, scarring, and alopecia.
326
What is the treatment for tinea capitis in children?
Oral griseofulvin therapy is treatment of choice.
327
What is a kerion?
Severe inflammatory skin response to tinea, which is an elevated, boggy, granulomatous mass. Incision and drainage is not effective.
328
What is the cause of tinea corporis?
Most from T rubrum and T mentagrophytes.
329
What are the physical characteristics of tinea corporis?
Dry, mildly erythematous, elevated, scaly papule with central clearing (ringworm).
330
What is the treatment of tinea corporis?
Topical miconazole, clotrimazole, or ketoconazole for 4–8 weeks
331
What is the cause of tinea cruris?
E. floccosum or T rubrum infection. Infection of groin and inner thighs seen mostly in adolescent males.
332
What are the characteristics of tinea cruris?
Bilateral, irregular, sharply bordered patches with hyperpigmented, scaly centers. Severe pruritus initially.
333
What is the treatment of tinea cruris?
Topical treatment with imidazole or tolnaftate creams.
334
What is tinea pedis (Athlete's foot)?
Most often seen in adolescent males. Caused by T rubrum, T mentagrophytes, and E. floccosum. Lateral toe webs and subdigital crevice and fissures with maceration and peeling of skin. Itching and foul odor.
335
What is the treatment for tinea pedis?
Avoid occlusive footwear. Keep feet dry. Absorbent antifungal powder (zinc undecylenate) or miconazole nitrate spray for mild cases.
336
What is the cause of common warts (verruca vulgaris)?
HPV types 2 and 4; seen on hands, knees, and elbows.
337
What is the cause of plantar warts?
Human papilloma virus type 1; flush with surface of sole.
338
What are the causes of genital warts?
HPV types 6 and 11; condyloma acuminata are mucous membrane warts.
339
What is the treatment for verruca vulgaris?
Half of common warts disappear spontaneously after 2 years. Keratosis is removed with scalpel. Liquid nitrogen, cantharidin, curettage. Daily 5–fluorouracil. Plantar warts: 40% salicylate or urea plasters.
340
What is molluscum contagiosum?
Poxvirus. Transmitted through contact or fomites, autoinoculation. Discrete, pearly, skin–colored, cone–shaped papules 1 to 5 mm, umbilicated; face, eyelids, neck, axillae, thighs; groin genital; with other STDs; lesions grouped.
341
How is molluscum contagiosum diagnosed?
Express central plug with comedo–extractor and examine with KOH prep, Wright or Giemsa stain; rounded, cup–shaped mass of homogeneous cells with lobules is diagnostic.
342
What is the treatment for molluscum contagiosum?
Infection is usually self–limited, lasting 6–9 months. Liquid nitrogen cryotherapy. Curettage.
343
What is pityriasis rosea?
Benign eruption in children, young adults; cause unknown. Herald patch looks like ringworm. Large, solitary lesion with raised borders and fine, adherent scales. Rash appears as widespread macules with fine scale, occasionally pruritus.
344
How is pityriasis rosea diagnosed?
Long axis is aligned with cutaneous cleavage lines, creating a Christmas tree" pattern on the back. Lesions may be hyper– or hypopigmented."
345
What is the treatment of pityriasis rosea?
None; self–limiting disease lasting 2–12 weeks. Emollient with menthol, camphor, or oral antihistamines for pruritus
346
What is erythema multiforme?
10–30 years old. Target–like papules with an erythematous border. An inner pale ring, and a purple to necrotic center. Extensor surfaces of upper extremities is the most common site of lesions. Resolve 2 wks. No Stevens–Johnson.
347
What is the cause of erythema multiforme?
Infection with herpes simplex virus.
348
What is the treatment for erythema multiforme?
Emollients, antihistamines, prednisone, and NSAIDs. Prophylactic acyclovir for 6 months in cases of recurrent erythema multiforme caused by HSV infection.
349
What is Stevens–Johnson syndrome?
Also called erythema multiforme major. Erythematous macules that rapidly develop central necrosis, resembling a morbilliform rash. Vesicles, bullae, and areas of denudation on face, trunk, and extremities.
350
What is the presentation of Stevens–Johnson syndrome?
More widespread than erythema multiforme and involve two mucous membranes (eyes, oral cavity, upper airway or esophagus, GI tract, anogenital mucosa). Burning, edema, erythema of lips and buccal mucosa. Nikolsky's sign. Fluid losses. Secondary bacterial.
351
What is the cause of Stevens–Johnson syndrome?
Mycoplasma pneumoniae infection has been implicated, but most cases are drug–related effects of sulfonamides, NSAIDs, anticonvulsants (phenytoin, phenobarbital).
