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Instructional Tutorial Video
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Gynecomastia is hypertrophy of breast glandular tissue in males. It must be differentiated from pseudogynecomastia, which is increased breast fat, but no enlargement of breast glandular tissue.

During infancy and puberty, enlargement of the male breast is normal (physiologic gynecomastia). Enlargement is usually transient, bilateral, smooth, firm, and symmetrically distributed under the areola; breasts may be tender. Physiologic gynecomastia that develops during puberty usually resolves within about 6 mo to 2 yr. Similar changes may occur during old age and may be unilateral or bilateral. Most of the enlargement is due to proliferation of stroma, not of breast ducts. The mechanism is usually a decrease in androgen effect or an increase in estrogen effect (eg, decrease in androgen production, increase in estrogen production, androgen blockade, displacement of estrogen from sex-hormone binding globulin, androgen receptor defects).

If evaluation reveals no cause for gynecomastia, it is considered idiopathic. The cause may not be found because gynecomastia is physiologic or because there is no longer any evidence of the inciting event.

In infants and boys, the most common cause is:
• Physiologic gynecomastia
In men, the most common causes are:
• Persistent pubertal gynecomastia
• Idiopathic gynecomastia
• Drugs (particularly spironolactone, anabolic steroids, and antiandrogens)
Breast cancer, which is uncommon in males, may cause unilateral breast abnormalities but is rarely confused with gynecomastia.

History: History of present illness should help clarify the duration of breast enlargement, whether secondary sexual characteristics are fully developed, the relationship between onset of gynecomastia and puberty, and the presence of any genital symptoms (eg, decreased libido, erectile dysfunction) and breast symptoms (eg, pain, nipple discharge). 

Review of systems should seek symptoms that suggest possible causes, such as 

• Weight loss and fatigue (cirrhosis, undernutrition, chronic kidney disease, hyperthyroidism)
• Skin discoloration (chronic kidney disease, cirrhosis)
• Hair loss and frequent infections (undernutrition)
• Fragility fractures (undernutrition, hypogonadism)
• Mood and cognitive changes (hypogonadism)
• Tremor, heat intolerance, and diarrhea (hyperthyroidism)

Past medical history should address disorders that can cause gynecomastia and include a history of all prescribed and OTC drugs. 

Physical examination: Complete examination is done, including assessment of vital signs, skin, and general appearance. The neck is examined for goiter. The abdomen is examined for ascites, venous distention, and suspected adrenal masses. Development of secondary sexual characteristics (eg, the penis, pubic hair, and axillary hair) is assessed. The testes are examined for masses or atrophy. 

The breasts are examined while patients are recumbent with their hands behind the head. Examiners bring their thumb and forefinger together from opposite sides of the nipple until they meet. Any nipple discharge is noted. Lumps are assessed and characterized in terms of location, consistency, fixation to underlying tissues, and skin changes. The axilla is examined for lymph node involvement in men who have breast lumps. 

Red flags: The following findings are of particular concern: 

• Localized or eccentric breast swelling, particularly with nipple discharge, fixation to the skin, or hard consistency
• Symptoms or signs of hypogonadism (eg, delayed puberty, testicular atrophy, decreased libido, erectile dysfunction, decreased proportion of lean body mass, loss of visual-spatial abilities)
• Symptoms or signs of hyperthyroidism (eg, tremor, tachycardia, sweating, heat intolerance, weight loss)
• Testicular mass
• Recent onset of painful, tender gynecomastia in an adult

Interpretation of findings: With pseudogynecomastia, the examiner feels no resistance between the thumb and forefinger until they meet at the nipple. In contrast, with gynecomastia, a rim of tissue > 0.5 cm in diameter surrounds the nipple symmetrically and is similar in consistency to the nipple itself. Breast cancer is suggested by swelling with any of the following characteristics: 

• Eccentric unilateral location
• Firm or hard consistency
• Fixation to skin or fascia
• Nipple discharge
• Skin dimpling
• Nipple retraction
• Axillary lymph node involvement

Gynecomastia in an adult that is of recent onset and causes pain is more often caused by a hormonal abnormality (eg, tumor, hypogonadism) or drugs. Other examination findings may also be helpful.

Testing: If breast cancer is suspected, mammography should be done. If another disorder is suspected, appropriate testing should be done. Extensive testing is often unnecessary, especially for patients in whom the gynecomastia is chronic and detected only during physical examination. Because hypogonadism is somewhat common with aging, some authorities recommend measuring the serum testosterone level in older men, particularly if other findings suggest hypogonadism. However, in adults with recent onset of painful gynecomastia without a drug or evident pathologic cause, measurement of serum levels of LH, FSH, testosterone, estradiol, and human chorionic gonadotropin (hCG) are recommended. Patients with physiologic or idiopathic gynecomastia are evaluated again in 6 mo. 

In most cases, no specific treatment is needed because gynecomastia usually remits spontaneously or disappears after any causative drug (except perhaps anabolic steroids) is stopped or underlying disorder is treated. Some clinicians try tamoxifen 10 mg po bid if pain and tenderness are very troublesome in men or adolescents, but this treatment is not always effective. Tamoxifen may also help prevent gynecomastia in men being treated with high-dose antiandrogen (eg, bicalutamide) therapy for prostate cancer; breast radiation therapy is an alternative. Resolution of gynecomastia is unlikely after 12 mo. Thus, after 12 mo, if cosmetic appearance is unacceptable, surgical removal of excess breast tissue (eg, suction lipectomy alone or with cosmetic surgery) may be used.

Key Points
• Gynecomastia must be differentiated from increased fat tissue in the breast.
• Gynecomastia is often physiologic or idiopathic.
• A wide variety of drugs can cause gynecomastia.
• Patients should be evaluated for clinically suspected genital or systemic disorders.


A 15-year-old boy comes to the office for a physical examination before going to summer camp. He says that he has a tender "lump" in his right breast that he noticed a couple of months ago. He is very concerned because he is going to a new camp and he is worried that he is going to have to change clothes in front of other boys in his bunk. He thinks that the other boys are going to see it and make fun of his "breast". There are tears streaming down his face as he tells you this. Physical examination shows a 1.5-cm, tender, palpable mass symmetrically distributed beneath the right areola. There is no discharge from the right nipple. The left breast is unremarkable. The remainder of the physical examination shows a small amount of dark, curling pubic hair and open and closed comedones on his cheeks, forehead, and back. The most appropriate next step is to

A. order liver function tests
B. perform ultrasonography of the breast
C. prescribe testosterone to give him a more "masculine" body-type
D. reassure him that this is common and no further testing is indicated
E. refer him for a fine needle aspiration

The correct answer is D. Gynecomastia (puberal hypertrophy) is very common in adolescents during puberty and is frequently asymmetric and tender. It is important to reassure this patient that it affects approximately 50–60% of adolescent boys at around Tanner stage III. It usually regresses before age 20. Surgery is rarely indicated. The open and closed comedones (also known as "blackheads" and "whitehead") are part of acne vulgaris, which is another common problem that affects adolescents.

Evaluation for liver disease (choice A) is unnecessary at this point because gynecomastia is very common during adolescence. He has no other signs of liver disease.

An ultrasound (choice B) is often used to distinguish cystic from solid masses. It is not indicated at this time in this case because this patient most likely has puberal hypertrophy of the breast (gynecomastia).

It is completely inappropriate to prescribe testosterone to give him a more "masculine" body-type (choice C) because testosterone often causes gynecomastia. Testosterone is converted to estradiol in extraglandular tissues and leads to feminization.

Fine needle aspiration (choice E) and mammography are used to evaluate a dominant breast mass or possibly gynecomastia in a patient who is not going through puberty, has a negative drug history, or a rapidly growing, large (>4cm) mass. This patient's gynecomastia is most likely due to puberty, making further work-up too aggressive at this time.

The parents of a 7-year-old boy bring him to you for evaluation. They have noted bilateral breast development. There is no history of exogenous estrogen use. His vital signs are normal, including a regular heart rhythm at a rate of 88. He has otherwise been well and is on no mediations. There is no history of ambiguous genitalia at birth. On examination, the testes are approximately 1 cm each bilaterally. The penis is small. Breast tissue is palpable bilaterally with discernible areola development. There are no abdominal masses. The boy is 40th percentile for height and weight. Which of the following do you recommend?

A. Reassure parents that it is just benign gynecomastia and is probably transient
B. Begin treatment with testosterone enanthate 50 mg IU each month
C. Begin search for estrogen-secreting tumor
D. Obtain surgical consultation for excisional biopsy of breast masses
E. Review the family history for similar occurrences

The answer is C. Begin search for an estrogen-secreting tumor. In contrast to boys in puberty, in which over 30% have at least a transient gynecomastia, breast development in males before puberty causes concern about estrogen exposure, from either an estrogen-secreting tumor (adrenal, testicular, or bronchogenic) or exogenous estrogen exposure. Interesting is that fact that hyperthyroidism is sometimes associated with excess estrogen, but not hypothyroidism. Besides the obvious difference in setting between benign transient gynecomastia and an endocrinologically significant condition (pubertal vs. prepubertal), there may be the question of gynecomastia versus enlarged breast in an obese male. In case of obesity, there is neither palpable breast bud nor particular areola development. Thus, reassurance is inappropriate; treatment with testosterone is premature, as is surgical consultation for excisional biopsy. This condition is associated with no identifiable familiality. Thyroid function is not feasibly an issue in this case.

A 14-year-old boy comes to the office because his breasts have recently become tender and slightly swollen. He is worried that he is undergoing feminization and will grow up to become a “freak.” Upon examination a tender, 2-cm mass is found to be palpable in the subareolar region of both breasts. Which of the following describes the best course of action?

A. Excise the masses by performing a subcutaneous mastectomy.
B. Incise and drain the masses.
C. Treat the masses with topical steroids.
D. Aspirate the masses for culture and cytology.
E. Leave the masses alone.

The patient has gynecomastia, the development of breast tissue in males, which is normal in the neonate, pubertal boy, and elderly male. Increased estrogen stimulation (hyperestrinism) of breast tissue is the common factor in all cases of gynecomastia.

Adolescent gynecomastia is usually bilateral, and the tissue averages 2 to 3 cm in diameter. The breast enlargement is transient and most often subsides within 1 year; as a consequence the gynecomastic breast usually should be left alone (choice E). The boy should be reassured that he is normal and does not have to worry about developing breasts.

However, if the mass is greater than 5 cm or does not regress by 16 to 17 years of age, a subcutaneous mastectomy should be performed (choice A). Incision (choice B), aspiration (choice D), and topical steroids (choice C) are not indicated under any circumstances. Gynecomastia in a postpubertal, adult male younger than 70 to 80 years is not normal and hyperestrinism should be suspected. Hyperestrinism in an adult male is most commonly due to decreased catabolism of estrogen due to liver cirrhosis, most often induced by alcoholism. However, hyperestrinism also can be due to increased synthesis secondary to an adrenal or testicular tumor; increased human chorionic gonadotropin (HCG) from a testicular tumor; the hyperplastic Leydig’s cells in Klinefelter syndrome; decreased androgen activity, which leaves estrogen unopposed (e.g., caused by hypothalamic or pituitary disorders); and by several drugs.
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Asthma Diagnosis
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Asthma is a disease of diffuse airway inflammation caused by a variety of triggering stimuli resulting in partially or completely reversible bronchoconstriction. Symptoms and signs include dyspnea, chest tightness, cough, and wheezing. The diagnosis is based on history, physical examination, and pulmonary function tests. Treatment involves controlling triggering factors and drug therapy, most commonly with inhaled β2-agonists and inhaled corticosteroids. Prognosis is good with treatment.

Development of asthma is multifactorial and depends on the interactions among multiple susceptibility genes and environmental factors. Environmental factors may include the following:

• Allergen exposure
• Diet
• Perinatal factors (eg. prematurity, low birthweight)

Asthma involves:
• Bronchoconstriction
• Airway edema and inflammation

Triggers: Common triggers of an asthma exacerbation include:

• Environmental and occupational allergens (numerous)
• Infections
• Exercise
• Inhaled irritants (eg. air pollution, cigarette smoke)
• Emotion (eg. anxiety, anger)

Response: In the presence of triggers, there is reversible airway narrowing and uneven lung ventilation. Relative perfusion exceeds relative ventilation in lung regions distal to narrowed airways; thus, alveolar O2 tensions fall and alveolar CO2 tensions rise. Most patients can compensate by hyperventilating.

Severity is the intrinsic intensity of the disease process. Severity can usually be assessed directly only before treatment is started, because patients who have responded well to treatment by definition have few symptoms. Asthma severity is categorized as

• Intermittent
• Mild persistent
• Moderate persistent
• Severe persistent

Control is the degree to which symptoms, impairments, and risks are minimized by treatment. Control is the parameter assessed in patients receiving treatment. The goal is for all patients to have well controlled asthma regardless of disease severity. Control is classified as

• Well controlled
• Not well controlled
• Very poorly controlled

Symptoms and Signs
Patients with mild asthma are typically asymptomatic between exacerbations. Patients with more severe disease and those with exacerbations experience dyspnea, chest tightness, audible wheezing, and coughing. Coughing may be the only symptom in some patients (cough-variant asthma). Symptoms can follow a circadian rhythm and worsen during sleep, often around 4 am. Many patients with more severe disease waken during the night (nocturnal asthma).

Signs include wheezing, pulsus paradoxus (ie, a fall of systolic BP > 10 mm Hg during inspiration), tachypnea, tachycardia, and visible efforts to breathe (use of neck and suprasternal [accessory] muscles, upright posture, pursed lips, inability to speak). The expiratory phase of respiration is prolonged, with an inspiratory:expiratory ratio of at least 1:3. Wheezes can be present through both phases or just on expiration, but patients with severe bronchoconstriction may have no audible wheezing because of markedly limited airflow.

• Clinical evaluation
• Pulmonary function testing
Diagnosis is based on history and physical examination and is confirmed with pulmonary function tests.

Pulmonary function tests: Patients suspected of having asthma should undergo pulmonary function testing to confirm and quantify the severity and reversibility of airway obstruction.

Impairment is assessed by spirometry, mainly forced expiratory volume in 1 sec (FEV1), and the ratio of FEV1 to forced vital capacity (FVC).

Spirometry should be done before and after inhalation of a short-acting bronchodilator. 
Signs of airflow limitation before bronchodilator inhalation include a reduced FEV1. 
The FVC may also be decreased because of gas trapping, such that lung volume measurements may show an increase in the residual volume (RV). 
An improvement in FEV1 of > 12% in response to bronchodilator treatment confirms reversible airway obstruction.

Peak expiratory flow (PEF) measurements with inexpensive handheld flow meters are recommended for home monitoring of disease severity and for guiding therapy. 

Evaluation of exacerbations: Patients with asthma with an acute exacerbation should have certain tests: 

• Pulse oximetry
PEF or FEV1 measurement

All 3 measures help establish the severity of an exacerbation and document treatment response. PEF values are interpreted in light of the patient's personal best, which may vary widely among patients who are equally well controlled. A 15 to 20% reduction from this baseline indicates a significant exacerbation. When baseline values are not known, the percent predicted FEV1 value gives a general idea of airflow limitation but not the individual patient's degree of worsening. When measuring FEV1 is impractical (eg, in an emergency department) and baseline PEF is unknown, percent of predicted PEF based on age, height and sex may be used.

ABG (arterial blood gas) measurements should be done in patients with marked respiratory distress or symptoms and signs of impending respiratory failure. 


An 18-year-old girl complains of symptoms of an upper respiratory tract infection for 1–2 days, followed by an increase in shortness of breath and greater use of inhaled bronchodilators for treatment of her chronic stable asthma. She presents to the emergency room with increased use of accessory muscles of ventilation, tachypnea, and wheezing. Shortly after the symptoms of her asthmatic attack have resolved, pulmonary function testing is most likely to show which of the following?

A. Normal values for peak expiratory flow
B. Decreased lung compliance
C. Increased residual volume (RV)
D. No change in peak expiratory flow after inhalation of bronchodilator
E. Elevated FEV1/FVC ratio

The answer is C. In asthma, a person cannot exhale maximally, so the residual volume (RV) will be increased. In addition, in asthma, air is trapped inside the lungs, adding to the residual volume.

Patients who have had a recent asthmatic attack, even though asymptomatic, still have residual airflow obstruction that may take a couple of months to disappear. During this time, patients still respond to bronchodilators but show abnormal peak expiratory flow, increased lung compliance, and continued maldistribution of ventilation. The FEV1/FVC ratio is either normal or decreased (due to obstruction) in asthma. It is often increased in restrictive lung diseases.

A 23-year-old woman comes to the emergency department because of a "severe asthma flare." She reports that over the past hour, she has had progressively more difficulty breathing and that her medications at home have not helped her. She has a 7-year history of asthma with multiple hospitalizations. She was last hospitalized 3 years ago for a severe flare that required inpatient therapy with corticosteroids. Her current medications include albuterol 4 times daily, oral leukotriene inhibitors, cromolyn sodium, and theophylline. Her temperature is 37.0 C (98.6 F), blood pressure is 160/80 mm Hg, pulse is 90/min, and respirations are 32/min. Her breath sounds are scant with a prolonged expiratory phase. She appears to be moving minimal air. Albuterol and ipratropium nebulizers are initiated. An arterial blood gas is drawn and is most likely to show

A. PaCO2 14 mm Hg, pH 7.22, PaO2 90 mm Hg
B. PaCO2 14 mm Hg, pH 7.56, PaO2 86 mm Hg
C. PaCO2 35 mm Hg, pH 7.22, PaO2 60 mm Hg
D. PaCO2 35 mm Hg, pH 7.39, PaO2 98 mm Hg
E. PaCO2 65 mm Hg, pH 7.24, PaO22 60 mm Hg

The correct answer is B. This patient has a severe asthma flare which caused her to hyperventilate to relieve her dyspnea. When looking at arterial blood gases, examine the pH to identify the acid-base disturbance, and then determine whether the acid-base disturbance is respiratory (change in CO2) or metabolic. The relationship between PaCO2 and pH determines whether the condition is acute or chronic. Chronic conditions have a pH closer to 7.4 than would be predicted based upon PCO2 because of compensation. For this patient, she is hyperventilating, but with no current inability to oxygenate. She should be alkalotic with a low PCO2 and her oxygenation should be nearly normal: PaCO2 14 mmHg, pH 7.56, PaO2 86 mm Hg.

A PaCO2 of 14 mm Hg, pH 7.22, PaO2 90 mm Hg (choice A) represents an acidosis that is likely metabolic since the PaCO2 is low. Oxygenation is normal. This is typical for a diabetic in ketoacidosis where they hyperventilate (Kussmaul breathing) to compensate for their systemic acidosis.

A PaCO2 of 35 mm Hg, pH 7.22, PaO2 60 mm Hg (choice C) reflects acidosis, likely metabolic since PCO2 is normal, with profound hypoxemia. This is typical for lactic acidosis of sepsis.

A PaCO2 of 35 mm Hg, pH 7.39, PaO2 98 mm Hg (choice D) represents a completely normal blood gas.

A PaCO2 of 65 mm Hg, pH 7.24, PaO2 60 mm Hg (choice E) reflects very late asthma. At this stage, PaCO2 has risen secondary to the inability to ventilate from severe bronchoconstriction, pH has fallen because of a respiratory induced acidosis, and oxygenation fails. When PaCO2 normalizes or becomes high in asthmatics, they have an impending respiratory failure in their near future.
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Instructional Tutorial Video
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Epiglottitis is a rapidly progressive bacterial infection of the epiglottis and surrounding tissues that may lead to sudden respiratory obstruction and death. Symptoms include severe sore throat, dysphagia, high fever, drooling, and inspiratory stridor. Diagnosis requires direct visualization of the supraglottic structures, which is not to be done until full respiratory support is available. Treatment includes airway protection and antibiotics.

The epiglottis is a flap that is made of elastic cartilage tissue covered with a mucous membrane, attached to the entrance of the larynx. During swallowing, it prevents food from going into the trachea and instead directs it to the esophagus.

Epiglottitis used to primarily affect children and usually was caused by Haemophilus influenzae type B. Now, because of widespread vaccination, it has been almost eradicated in children (more cases occur in adults). Causal organisms in children and adults include Streptococcus pneumoniae,Staphylococcus aureus, nontypeable H. influenzae, Haemophilus parainfluenzae,β-hemolytic streptococci, Branhamella catarrhalis, and Klebsiella pneumoniae. H. influenzae type B is still a cause in adults and unvaccinated children.

Bacteria that have colonized the nasopharynx spread locally to cause supraglottic cellulitis with marked inflammation of the epiglottis, vallecula, aryepiglottic folds, arytenoids, and laryngeal ventricles. With H. influenzae type B, infection may spread hematogenously.

The inflamed supraglottic structures mechanically obstruct the airway, increasing the work of breathing, ultimately causing respiratory failure. Clearance of inflammatory secretions is also impaired.

Symptoms and Signs
In children, sore throat, odynophagia, and dysphagia develop abruptly. Fatal asphyxia may occur within a few hours of onset. Drooling is very common. Additionally, the child has signs of toxicity (poor or absent eye contact, failure to recognize parents, cyanosis, irritability, inability to be consoled or distracted) and is febrile and anxious. Dyspnea, tachypnea, and inspiratory stridor may be present, often causing the child to sit upright, lean forward, and hyperextend the neck with the jaw thrust forward and mouth open in an effort to enhance air exchange (tripod position). Relinquishing this position may herald respiratory failure. Suprasternal, supraclavicular, and subcostal inspiratory retractions may be present.

In adults, symptoms are similar to those of children, including sore throat, fever, dysphagia, and drooling, but peak symptoms usually take > 24 h to develop. Because of the larger diameter of the adult airway, obstruction is less common and less fulminant. Often, there is no visible oropharyngeal inflammation. However, severe throat pain with a normal-appearing pharynx raises suspicion of epiglottitis. A delay in diagnosis and treatment increases the risk of airway obstruction and death.

• Direct inspection (typically in operating room)
• X-ray in milder cases with low suspicion

Epiglottitis is suspected in patients with severe sore throat and no pharyngitis and also in patients with sore throat and inspiratory stridor. Stridor in children may also result from croup, bacterial tracheitis, and airway foreign body. The tripod position may also occur with peritonsillar or retropharyngeal abscess.

The patient is hospitalized if epiglottitis is suspected. Diagnosis requires direct examination, usually with flexible fiberoptic laryngoscopy. (Caution: Examination of the pharynx and larynx may precipitate complete respiratory obstruction in children, and the pharynx and larynx should not be directly examined except in the operating room, where the most advanced airway intervention is available.) 

Although plain x-rays may be helpful, a child with stridor should not be transported to the x-ray suite. Direct laryngoscopy that reveals a beefy-red, stiff, edematous epiglottis is diagnostic. Cultures from the supraglottic tissues and blood can then be taken to search for the causative organism. Adults may, in some cases, safely undergo flexible fiberoptic laryngoscopy.

• Adequate airway ensured
• Antibiotics (eg, ceftriaxone)

In children with stridor, any intervention that could be upsetting (and thus could trigger airway obstruction) should be avoided until an airway is established. In children with epiglottitis, the airway must be secured immediately, preferably by nasotracheal intubation. Securing the airway can be quite difficult and should, if possible, be done by experienced personnel in the operating room. An endotracheal tube is usually required until the patient has been stabilized for 24 to 48 h (usual total intubation time is < 60 h). Alternatively, a tracheotomy is done. If respiratory arrest occurs before an airway is established, bag-mask ventilation may be a life-saving temporary measure. For emergency care of children with epiglottitis, each institution should have a protocol that involves critical care, otolaryngology, anesthesia, and pediatrics.

Adults whose airway is severely obstructed can be endotracheally intubated during flexible fiberoptic laryngoscopy. Other adults may not require immediate intubation but should be observed for airway compromise in an ICU with an intubation set and cricothyrotomy tray at the bedside.

A β-lactamase–resistant antibiotic, such as ceftriaxone 50 to 75 mg/kg IV once/day (maximum 2 g), should be used empirically, pending culture and sensitivity test results.

Epiglottitis caused by H. influenzae type B can be effectively prevented with the H. influenzae type B (HiB) conjugate vaccine.

Key Points
• The incidence of epiglottitis has decreased significantly, particularly in children, because of widespread vaccination against the most common cause, Haemophilus influenzae type B.
• Stridor, as well as sore throat with a normal-appearing pharynx, are important clues.
• Examination of the pharynx or larynx in children with epiglottitis and stridor may precipitate complete airway obstruction.
• If the diagnosis is suspected, do flexible fiberoptic laryngoscopy in the operating room; reserve imaging studies for cases with very low suspicion.
• Children typically should have their airway secured by tracheal intubation; adults often can be observed for signs of airway compromise.
• Give a β-lactamase–resistant antibiotic, such as ceftriaxone.


Sample Clinical Decision Making (CDM) Case for the MCCQE Part 1:

A 2-year-old girl is brought to the emergency department by her mother. The mother reports that the child went to bed with mild upper respiratory symptoms and then woke up in the middle of the night with sudden respiratory distress. On entering the examination room, you notice that the child is in respiratory distress and is sitting on the examination table, drooling saliva from her mouth. Due to the urgent nature of the patients presentation, you do a direct laryngoscopy that reveals a beefy-red, stiff, edematous epiglottis.

Question 1
In an unvaccinated child, which of the following is the most likely causative organism for this condition (Select only one):

A. Haemophilus influenzae
B. Streptococcus viridans
C. Staphylococcus aureus
D. Candida albicans
E. Escherichia coli
F. Clostridium botulinum
G. Campylobacter jejuni
H. Pseudomonas aeruginosa

Question 2
The appropriate management of this child may include which of the following (select up to 3 only):

A. Oral antibiotics
B. Humidified Air
C. Anticholinergic medication
D. IV Ceftriaxone
E. Epinephrine
F. Antiemetic medication
G. Nasotracheal intubation
H. Enemas
I.  Interferon
K. Antihistaminic medication
L. Anti-viral medications
M. Cricothyrotomy
N. IV Ipratropium
O. Systemic steroids

Question 1: A
Question 2: D, G, M

Question 1:
The correct answer is A. 
Epiglottitis is the most common disease of the upper respiratory tract produced by Haemophilus influenzae type b, a gram-negative encapsulated rod. It is also a common cause of otitis media in children and may cause bronchitis, bronchiolitis, and pneumonia in adults. The incidence of serious disease caused by Haemophilus influenzae type b has decreased greatly with the introduction of an effective vaccine. The vaccine is composed of the H. influenzae type b capsular polysaccharides coupled to a carrier molecule, given to children between 2 and 15 months of age. The patient had not received the Hib conjugate vaccine and therefore was susceptible to this organism.

Question 2:
The correct answers are: D, G, M. 
This child has a classical appearance of acute epiglottitis, which is a life-threatening illness. Epiglottitis in children is usually associated with sudden difficulty in breathing, sore throat, and dysphagia. Acute epiglottitis in children is usually because of Haemophilus influenza. The child classically appears in severe acute respiratory distress of sudden onset, leaning forward in a sitting position with drooling of saliva from the mouth.

A β-lactamase–resistant antibiotic, such as ceftriaxone 50 to 75 mg/kg IV once/day (maximum 2 g), should be used empirically, pending culture and sensitivity test results.

In children with stridor, any intervention that could be upsetting (and thus could trigger airway obstruction) should be avoided until an airway is established. In children with epiglottitis, the airway must be secured immediately, preferably by nasotracheal intubation. Securing the airway can be quite difficult and should, if possible, be done by experienced personnel in the operating room.

This emergency should be diagnosed immediately and help must be obtained by calling an anesthesiologist and a senior pediatrician. The operating room must be alerted for an emergency cricothyrotomy (also called a cricothyroidotomy), if emergency intubation fails. An oxygen mask should be held close to the child's face and one should wait by the child's side until senior help arrives.
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Thrombotic Thrombocytopenic Purpura (TTP)
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Thrombotic thrombocytopenic purpura (TTP) is a rare blood disorder characterized by clotting in small blood vessels of the body (thromboses), resulting in a low platelet count. In its full-blown form, the disease consists of the pentad of microangiopathic hemolytic anemia, thrombocytopenic purpura, neurologic abnormalities, fever, and renal disease. To make an accurate diagnosis, the clinician must recognize the similarity between thrombotic thrombocytopenic purpura (TTP) and hemolytic-uremic syndrome (HUS).

TTP can affect any organ system, but involvement of the peripheral blood, the central nervous system, and the kidneys causes the clinical manifestations. The classic histologic lesion is one of bland thrombi in the microvasculature of affected organs. These thrombi consist predominantly of platelets with little fibrin and red cells compared with thrombi that occur secondary to intravascular coagulation.

Signs and symptoms
Patients with TTP typically report an acute or subacute onset of symptoms related to neurologic dysfunction, anemia, or thrombocytopenia.

Neurologic manifestations include alteration in mental status, seizures, hemiplegia, paresthesias, visual disturbance, and aphasia. Fatigue may accompany the anemia. Severe bleeding from thrombocytopenia is unusual, although petechiae are common. TTP can affect any organ system, but involvement of the peripheral blood, the central nervous system, and the kidneys causes the clinical manifestations.

In its full-blown form, the disease consists of the following pentad (FAT RN):

Fever | Anemia | Thrombocytopenia | Renal disease | Neurologic abnormalities

A closely related disorder, hemolytic-uremic syndrome (HUS), shares many clinical characteristics of TTP but is more common in children. Renal abnormalities tend to be more severe in HUS. Although once considered variants of a single syndrome, recent evidence suggests differing pathogenic mechanisms of TTP and HUS. The mortality of TTP is greatly reduced with the routine use of aggressive high-volume total plasma exchange (TPE). The effect of TPE on the outcome of patients with HUS is more controversial.

Patients with thrombotic thrombocytopenic purpura (TTP) typically report an acute or subacute onset of the following symptoms related to neurologic dysfunction, anemia, or thrombocytopenia:

Neurologic manifestations include alteration in mental status, seizures, hemiplegia, paresthesias, visual disturbance, and aphasia
Fatigue may accompany the anemia
Severe bleeding from thrombocytopenia is unusual, although petechiae are common
Clinical manifestations may also include the following:

Fever occurs in approximately 50% of patients
Patients may notice dark urine from hemoglobinuria.
Clinical differentiation of hemolytic-uremic syndrome (HUS) and TTP can be problematic. Differentiation is often based on the presence of central nervous system involvement in TTP and the more severe renal involvement in HUS. In HUS, an antecedent history of diarrheal illness is more often present. In fact, some investigators suggest a clinical classification of HUS based on the presence or absence of diarrhea.

In children, the distinction between HUS and TTP may be of more importance, as general supportive measures (with dialysis as needed) are the standard therapy for HUS, versus plasma exchange for TTP.

Patients with TTP or HUS have no characteristic physical findings. Findings upon examination depend on the severity of involvement of the target organ systems.

Hemolytic anemia and thrombocytopenia cause pallor, jaundice, and petechiae. Abnormal findings upon neurologic examination consist of mental status changes and/or focal neurologic deficits. These defects can be evanescent and, thus, present as transient ischemic attacks. Organomegaly is not typical.

The exact etiology of HUS and TTP is not clear, although much recent data are available on the role of bacterial Shiga toxin in HUS and of a deficiency in a protease designated ADAMTS13 in TTP. HUS, and to some extent TTP, commonly occur following a diarrheal illness with enterohemorrhagic Escherichia coli O157:H7 and Shigella dysenteriae serotype I. These bacteria, besides causing bloody diarrhea, are able to secrete an exotoxin called Shiga toxin (in the case of Shigella) or Shigalike toxin (in the case of E coli).

Laboratory Studies
Complete blood count (CBC) findings in patients with thrombotic thrombocytopenic purpura (TTP) are usually as follows:

• Total white blood cell count is normal or slightly elevated
• Hemoglobin concentration is moderately depressed at 8-9 g/dL
• Platelet count generally ranges from 20,000-50,000/μL
• Peripheral blood smears reveal moderate-to-severe schistocytosis.

Early in the course of illness, schistocytes may not be seen, but, eventually, they will be present. Some consider schistocytosis the sine qua non for diagnosis.

Prothrombin time (International Normalized Ratio) and activated partial thromboplastin time results typically are normal in both TTP and in hemolytic-uremic syndrome HUS), although some series report patients with slight elevations on both tests.

D-dimer and fibrinogen assay findings are as follows:

D-dimers are indicative of fibrinolysis and thus, thrombin activation, which usually is normal or mildly elevated in patients with TTP
Fibrinogen typically is in the high to high-normal range
These tests are useful in differentiating TTP/HUS from disseminated intravascular coagulation (DIC), in which most of these coagulation parameters are abnormal
Evaluation of renal function with a blood urea nitrogen (BUN) and creatinine level is necessary to establish the presence and severity of renal impairment. This also aids in differentiating HUS from TTP, but patients who are classified as TTP in some studies have an elevated creatinine level and those with HUS have had neurologic abnormalities, again emphasizing that these are clinical diagnoses.

Lactate dehydrogenase (LDH) and bilirubin (direct and total) levels are indirect measures of the degree of hemolysis. An LDH level in the 1000 IU/L range (normal, < 200 IU/L) is not unusual. Generally, a moderate degree of hyperbilirubinemia (2.5-4 mg/dL) is present, with the indirect form predominating.

Therapy should be initiated if the diagnosis of thrombotic thrombocytopenic purpura (TTP) is seriously considered.  Only the minority of patients (20-30%) present with the classic pentad. The presence of microangiopathic hemolytic anemia (schistocytes, elevated lactate dehydrogenase [LDH] level, and indirect hyperbilirubinemia) and thrombocytopenia in the absence of other obvious causes (eg, disseminated intravascular coagulation, malignant hypertension) is justification to begin total plasma exchange.

Plasma exchange with fresh frozen plasma is the therapy of choice for TTP. Replacement with normal saline and albumin is not adequate. When immediate plasma exchange is not available, simple plasma infusion can be performed until the patient can be transferred to a facility that performs plasma exchange.

Patients with hemolytic-uremic syndrome (HUS), usually children, often require dialysis. Plasma exchange is reserved for refractory cases. Some large series have reported resolution of HUS with dialysis alone or with steroid therapy.

Complete response criteria differ depending on the investigator, but they generally include the following:

Resolution of neurologic symptoms
Normalization of hemoglobin, platelet count, LDH, and bilirubin
Normalization of creatinine
Adequate initial response is fulfilled if neurologic signs and symptoms disappear, the platelet count climbs to greater than 50,000/μL, and the LDH level declines. In patients who respond to plasma exchange, the mean time to resolution of neurologic changes is approximately 3 days, to a normal LDH is 5 days, to a normal platelet count is 10 days, and to normal renal function is 15 days.

The overall response rate to plasma exchange is 75-90%. The early mortality rate is 10-20%.


A 35-year-old woman presents to her physician with blood in her urine. She has also felt malaise and had a fever for the past day. She has inconsistent answers to further questioning. Her past medical history is unremarkable. She does not take any medications and does not drink alcohol or smoke. On physical examination, blood pressure is 122/71 mm Hg and pulse is 89 beats/min. She is oxygenating 97% on room air. She is slightly somnolent but easily arousable. Head and neck exam reveals mild scleral icterus. There is no jugular venous distension. The lungs are clear to auscultation, and there are no murmurs, rubs, or gallops. Abdominal exam reveals no ascites or hepatosplenomegaly. Her peripheral exam reveals a petechial rash but no clubbing, cyanosis, or edema. Laboratory values are:

Hematocrit 29% (low)
Platelets 75,000/mm3 (low)
BUN 28 (elevated)
Creatinine 1.5 (elevated)
PTT 23 sec (normal)
PT 15 sec (normal)

On peripheral blood smear, schistocytes are noted. Which of the following is the most likely etiology for the patient's symptoms.

A. Disseminated intravascular coagulation (DIC)
B. Hemolytic uremic syndrome
C. Idiopathic thrombocytopenic purpura
D. Thrombotic thrombocytopenic purpura

Correct answer D. This patient has either thrombotic thrombocytopenic purpura (TTP) or hemolytic uremic syndrome (HUS) (choice B). These two diseases are often considered one and the same except for presenting symptomatology. Both syndromes present with the classic pentad of a microangiopathic hemolytic anemia (schistocytes on smear), renal failure, fever, altered mental status, and thrombocytopenia. PT and PTT are normal. Although TTP and HUS are clinically very similar, the way to differentiate them on a test question is by the predominance of renal failure and altered mental status. In TTP, the predominant symptom is altered mental status; whereas in HUS, the predominant symptom is acute anuric renal failure. This patient is somnolent and confused, and 90% of TTP cases have this type of altered mental status. Further, although there is renal impairment, she does not have acute anuric renal failure, which is seen in only 2% of people with TTP. Acute anuric renal failure is seen in 98% of patients with HUS. Further, on history, a patient with HUS will likely have exposure to E. coli 0157:H7.

Disseminated intravascular coagulation (DIC) (choice A) is seen in the setting of infection, sepsis, trauma, or obstetric procedures. It is characterized by massive recruitment of the coagulation system that leads to thrombosis and exhaustion of the coagulation factors. Because of consumption of coagulation factors, the PT and PTT are usually prolonged. TTP and DIC are clinically differentiated on the basis of coagulation studies.

Idiopathic thrombocytopenic purpura (choice D) results only in thrombocytopenia, and is usually seen in a female patient with a previous viral infection or drug exposure.

A 33-year-old woman is brought to the emergency department accompanied by her husband. Her husband reports that she has periodic episodes of confusion that quickly resolve. He also reports that she has been extremely weak and fatigued over the last 4 or 5 days. Her temperature is 39.0 C (102.2 F), blood pressure is 140/70 mm Hg, pulse is 103/min, and respirations are 18/min. Physical examination shows jaundiced skin and mild scleral icterus. She has a III/VI systolic ejection murmur that does not radiate and 1+ edema in her lower extremities. Laboratory studies show anemia, thrombocytopenia, elevated BUN and creatinine. A peripheral smear shows hemolysis with few platelets. The most appropriate next step is

A. conservative management with supportive care as needed
B. begin high-dose prednisone therapy
C. begin large-volume plasmapheresis
D. give platelet and red cell transfusion
E. obtain a surgical consult for urgent splenectomy

The correct answer is C. This patient has thrombotic thrombocytopenic purpura (TTP). She has the classic pentad of anemia, thrombocytopenia, neurological abnormalities (which are often waxing and waning), fevers, and renal abnormalities. The treatment is large-volume plasmapheresis daily until the patient is in complete remission. This condition needs to be differentiated from ITP, which typically has isolated thrombocytopenia and hemolytic uremic syndrome (HUS), which is similar to TTP except that renal abnormalities predominate over neurological findings.

Conservation management with supportive care (choice A) is a reasonable option in HUS in children. In the pediatric population, this is typically self limited and only supportive care for acute renal failure is required.

High-dose prednisone therapy (choice B) is a treatment option in ITP. It is thought to work by both decreasing antibody production and by reducing binding of antibodies to platelets. In TTP it is often an adjuvant therapy based on theoretical principles, but it's true role has not been studied.

Platelet and red cell transfusions (choice D) are typically reserved for life-threatening bleeds since it is likely that exogenous platelets and red cells will quickly be destroyed.

Splenectomy (choice E) in combination with steroids is reserved for patients who do not respond to plasmapheresis and would not be the appropriate step at this time.
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Nasolacrimal Duct Obstruction
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Dacryostenosis is obstruction or stenosis of the nasolacrimal duct, causing excess tearing.

Nasolacrimal obstruction may be congenital or acquired. One cause of congenital obstruction is inadequate development of any part of the nasolacrimal ducts. Typically, a membrane at the distal end of the nasolacrimal duct persists. There is tearing and purulent discharge; the condition may manifest as chronic conjunctivitis, usually beginning after the age of 2 wk (most often at age 3 to 12 wk).

There are many causes of acquired nasolacrimal duct obstruction. The cause is most often age-related stenosis of the nasolacrimal duct. Other causes include past nasal or facial bone fractures and sinus surgery, which disrupt the nasolacrimal duct; inflammatory diseases (eg, sarcoidosis, granulomatosis with polyangiitis [formerly Wegener granulomatosis]); and dacryocystitis.

Causes of punctal or canalicular stenosis include chronic conjunctivitis (especially herpes simplex), certain types of chemotherapy, adverse reactions to eye drops (especially topical echothiophate iodide), and radiation.

Diagnosis is usually based on clinical criteria. Sometimes ophthalmologists probe and irrigate the lacrimal drainage system with saline, with or without fluorescein dye. Reflux indicates stenosis.


The primary treatment is nasolacrimal duct massage. Approximately 90% of nasolacrimal duct obstructions spontaneously resolve in the first year of life. Until age 1 year, this condition is treated with simple massage of the nasolacrimal area and cleansing of the eyelid 2 to 3 times daily. Most cases are unilateral and resolve by age 1 year. If the condition remains unresolved at that time, the nasolacrimal duct should be surgically probed by a pediatric ophthalmologist.

Congenital nasolacrimal duct obstruction often resolves spontaneously by about age 6 to 9 mo; before 1 yr, manual compression of the lacrimal sac 4 or 5 times/day may relieve the obstruction. After age 1 yr, the nasolacrimal duct may need probing, usually under general anesthesia; if obstruction is recurrent, a temporary silastic tube may be inserted.

In acquired nasolacrimal duct obstruction, the underlying disorder is treated when possible. If treatment is not possible or is ineffective, a passage between the lacrimal sac and the nasal cavity can be created surgically (dacryocystorhinostomy).

In cases of punctal or canalicular stenosis, dilation is usually curative. If canalicular stenosis is severe and bothersome, a surgical procedure that places a tube made of low thermal-expansion borosilicate glass leading from the caruncle into the nasal cavity can be considered.


An 8-week-old infant is found to have excessive tearing of the left eye on his well-child visit. During the examination, he is found to have overflow of tears onto the lower eyelid and cheek and frequent appearance of mucoid material that the mother continuously cleans away with wet gauze. The infant was born at home to a 28-year-old gravida 2, para 1, healthy mother. There were no complications during the bathtub birth. The mother denied any recent vaginal infections or discharge before the delivery. The child is otherwise growing and developing well and feeding on breast milk. What is the next best step in management?

A. Administration of ophthalmologic erythromycin ointment
B. Fluorescein staining of the cornea
C. Instillation of ophthalmic corticosteroid drops
D. Nasolacrimal massage and cleansing of the lids
E. Probing of the nasolacrimal duct

The correct answer is D. The child described has a blocked tear duct, also known as dacryostenosis. Until age 1 year, this condition is treated with simple massage of the nasolacrimal area and cleansing of the eyelid 2 to 3 times daily. Most cases are unilateral and resolve by age 1 year. If the condition remains unresolved at that time, the nasolacrimal duct should be surgically probed (choice E) by a pediatric ophthalmologist.

The infant is not described as having bacterial conjunctivitis, because there is no injection of the conjunctiva mentioned. With no obvious infection, administration of erythromycin would not be appropriate treatment (choice A). Administration of fluorescein (choice B) is done to diagnose corneal abrasions by way of a blue lamp. There is no injection of the eye and the infant is not showing any signs of pain, both of which would be seen with a corneal abrasion. Instillation of ophthalmic corticosteroid drops (choice C) is not recommended for children and may in fact carry serious risks if administered.

A 3-month-old boy is brought to the clinic by his mother because "ever since the child was born he has had constant tearing from both eyes." She tells you that when the baby wakes up in the morning there is a small amount of watery discharge at the medial corner of his eyelids and that she must wipe the child's eyes multiple times throughout the day. The child is developmentally normal and is reaching his normal milestones. On physical examination the baby is able to fix and follow you with either eye. Extraocular movements are full. The pupils are round and reactive and there is no relative afferent papillary defect. The conjunctiva, sclera, and cornea are normal. There is a bit of dry crust on the medial side of the left lower lid. The most appropriate next step in management is to

A. admit the patient for intravenous antibiotics
B. instruct the mother to apply warm compresses to both eyes 4 times a day
C. instruct the mother to perform nasolacrimal duct massage 2-3 times a day
D. refer the patient to an ophthalmologist for nasolacrimal duct probing
E. take cultures and prescribe topical antibiotics

The correct answer is C. Nasolacrimal duct obstruction is a very common condition in pediatrics. The nasolacrimal ducts are usually patent at 3-4 weeks. Tearing and crusting are the typical features of an obstruction. The primary treatment is nasolacrimal duct massage. Approximately 90% of nasolacrimal duct obstructions spontaneously resolve in the first year of life.

IV antibiotics (choice A) are appropriate for preseptal or postseptal orbital cellulites but the patient does not present with red, swollen, and tender lids. Warm compresses (choice B) are the appropriate treatment for a chalazion. This patient did not present with a nodular, non-infectious swelling in the eyelids.

Since most obstructions spontaneously resolve, surgical intervention and probing are usually not recommended until age 6 months (choice D). When a patient has a nasolacrimal duct obstruction and there are signs of a localized infection (mucoid discharge with matting of the eyelashes) then topical antibiotics have a role. However, if the patient is just experiencing tearing, antibiotics are not indicated (choice E).
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Primary Aldosteronism (Conn’s Syndrome)
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Primary aldosteronism is aldosteronism caused by autonomous production of aldosterone by the adrenal cortex (due to hyperplasia, adenoma, or carcinoma). Symptoms and signs include episodic weakness, elevated BP, and hypokalemia. Diagnosis includes measurement of plasma aldosterone levels and plasma renin activity. Treatment depends on cause. A tumor is removed if possible; in hyperplasia, spironolactone or related drugs may normalize BP and eliminate other clinical features.

Aldosterone is the most potent mineralocorticoid produced by the adrenals. It causes Na retention and K loss. In the kidneys, aldosterone causes transfer of Na from the lumen of the distal tubule into the tubular cells in exchange for K and hydrogen. The same effect occurs in salivary glands, sweat glands, cells of the intestinal mucosa, and in exchanges between ICFs and ECFs.

Aldosterone secretion is regulated by the renin-angiotensin system and, to a lesser extent, by ACTH. Renin, a proteolytic enzyme, is stored in the juxtaglomerular cells of the kidneys. Reduction in blood volume and flow in the afferent renal arterioles induces secretion of renin. Renin transforms angiotensinogen from the liver to angiotensin I, which is transformed by ACE to angiotensin II. Angiotensin II causes secretion of aldosterone and, to a much lesser extent, secretion of cortisol and deoxycorticosterone; it also has pressor activity. Na and water retention resulting from increased aldosterone secretion increases the blood volume and reduces renin secretion.

Primary aldosteronism is caused by an adenoma, usually unilateral, of the glomerulosa cells of the adrenal cortex or, more rarely, by adrenal carcinoma or hyperplasia. Adenomas are extremely rare in children, but the syndrome sometimes occurs in childhood adrenal carcinoma or hyperplasia. In adrenal hyperplasia, which is more common among older men, both adrenals are overactive, and no adenoma is present. The clinical picture can also occur with congenital adrenal hyperplasia from deficiency of 11 β-hydroxylase and the dominantly inherited dexamethasone-suppressible hyperaldosteronism. Hyperplasia as a cause of hyperaldosteronism may be more common than previously recognized but remains an infrequent cause in the presence of hypokalemia.

Symptoms and Signs
Hypernatremia, hypervolemia, and a hypokalemic alkalosis may occur, causing episodic weakness, paresthesias, transient paralysis, and tetany. Diastolic hypertension and hypokalemic nephropathy with polyuria and polydipsia are common. In many cases, the only manifestation is mild to moderate hypertension. Edema is uncommon.

• Electrolytes
• Plasma aldosterone
• Plasma renin activity (PRA)
• Adrenal imaging

Diagnosis is suspected in patients with hypertension and hypokalemia. Initial laboratory testing consists of plasma aldosterone levels and PRA. Ideally, the patient should not take any drugs that affect the renin-angiotensin system (eg, thiazide diuretics, ACE inhibitors, angiotensin antagonists, β-blockers) for 4 to 6 wk before tests are done. PRA is usually measured in the morning with the patient recumbent. Patients with primary aldosteronism typically have plasma aldosterone > 15 ng/dL (> 0.42 nmol/L) and low levels of PRA, with a ratio of plasma aldosterone (in ng/dL) to PRA (in ng/mL/h) > 20.

Low levels of both PRA and aldosterone suggest nonaldosterone mineralocorticoid excess (eg, due to licorice ingestion, Cushing syndrome, or Liddle syndrome). High levels of both PRA and aldosterone suggest secondary hyperaldosteronism. In children, Bartter syndrome (see Bartter Syndrome and Gitelman Syndrome) is distinguished from primary hyperaldosteronism by the absence of hypertension and marked elevation of PRA.

Patients with findings suggesting primary hyperaldosteronism should undergo CT or MRI to determine whether the cause is a tumor or hyperplasia. Aldosterone levels measured on awakening and 2 to 4 h later while standing also may help make this distinction; in adenoma, levels decline and in hyperplasia, levels increase. However, imaging tests and postural changes on standing are relatively insensitive, and most patients require bilateral catheterization of the adrenal veins to measure cortisol and aldosterone levels to confirm whether the aldosterone excess is unilateral (tumor) or bilateral (hyperplasia).

• Surgical removal of tumors
• Spironolactone or eplerenone for hyperplasia
Tumors should be removed laparoscopically. After removal of an adenoma, serum K normalizes and BP decreases in all patients; complete normalization of the BP without the need for hypotensive therapy occurs in 50 to 70% of patients.

Among patients with adrenal hyperplasia, 70% remain hypertensive after bilateral adrenalectomy; thus, surgery is not recommended. Hyperaldosteronism in these patients can usually be controlled by a selective aldosterone blocker such as spironolactone, starting with 50 mg po once/day and increasing over 1 to 3 mo to a maintenance dose, usually around 100 mg once/day; or by amiloride 5 to 10 mg po once/day or another K-sparing diuretic. The more specific drug eplerenone 50 mg po once/day to 200 mg po bid may be used because, unlike spironolactone, it does not block the androgen receptor; it is the drug of choice for long-term treatment in men. About half of patients with hyperplasia need additional antihypertensive treatment (see General Treatment).

Key Points
• Diagnosis should be suspected in hypertensive patients with hypokalemia in the absence of Cushing syndrome.
• Initial testing includes measurement of plasma aldosterone levels and plasma renin activity.
• Adrenal imaging tests are done, but usually bilateral adrenal vein catheterization is needed to distinguish tumor from hyperplasia.
• Tumors are removed and patients with adrenal hyperplasia are treated with aldosterone blockers such as spironolactone.


A 35-year-old woman presents to you with BP readings of 150/100, 145/98, and 160/95 on three successive days. A routine metabolic profile shows normal BUN, creatinine, blood sugar, sodium, chloride, and bicarbonate, but a potassium level of 2.8 mEq/L. She denies diarrhea, vomiting, past or present fistulae or enterostomy, or taking any prescription medications. Which of the following types of hypertension is most likely present?

Essential hypertension of the vasoconstrictive type 
Essential hypertension of the salt-retentive type 
Primary aldosteronism
Renovascular hypertension

The answer is D. Hypertension in the face of hypokalemia and in the absence of diuretic medication or gastrointestinal or other pathologic loss of potassium is primary aldosteronism until proven otherwise.

A 48-year-old female presents as a new patient to your office. She has not seen a physician for several years and her medical history is unknown. Her BMI is 24.4 kg/m2 and she is not taking any medication. Her blood pressure is 172/110 mm Hg in the left arm sitting and 176/114 mm Hg in the right arm sitting; her cardiovascular examination is otherwise unremarkable. A baseline metabolic panel reveals a creatinine level of 0.68 mg/dL (N 0.6–1.1) and a potassium level of 3.3 mEq/L (N 3.5–5.5). If the patient’s hypertension should prove refractory to treatment, which one of the following tests is most likely to reveal the cause of her secondary hypertension?

A. A 24-hour urine catecholamine level
B. A plasma aldosterone/renin ratio
C. MRA of the renal arteries
D. Echocardiography
E. A sleep study (polysomnography)

Answer: B. Primary hyperaldosteronism is the most common cause of secondary hypertension in the middle-aged population, and can be diagnosed from a renin/aldosterone ratio. This diagnosis is further suggested by the finding of hypokalemia, which suggests hyperaldosteronism even though it is not present in the majority of cases.

An echocardiogram would help make a diagnosis of coarctation of the aorta, but this is more common in younger patients. Renal MRA may demonstrate renal artery stenosis, but this condition is more common in older patients. Sleep apnea is increasing in prevalence along with the rise in obesity, but it is not suggested by this case. A 24-hour urine catecholamine test is used to diagnose pheochromocytoma, which is not suggested by this patient’s findings. Pheochromocytoma is also less common than aldosteronism (SOR C).

A 36-year-old man is admitted to the hospital for severe hypertension. He has had high blood pressure for the past 3 years that has been very difficult to control. There is no history of hypertension in his family and he has no other medical problems. His current medications include hydralazine, amlodipine, and atenolol. His blood pressure log-book that he keeps at home shows that his daily pressures have been on average 180/90 mm Hg. Today he was admitted for a blood pressure of 220/120 mm Hg with pulse of 82/min. On physical examination, he is appropriately anxious but in no distress. He fundi are clear with no evidence of papilledema. His heart exam is benign. An electrocardiogram shows left ventricular hypertrophy at 80 beats per minute with no strain pattern. Laboratory studies show:

Sodium 151 mEq/L
Potassium 2.6 mEq/L
Bicarbonate 28 mEq/L
BUN 10 mg/dL
Creatinine 0.8 mg/dL

The most appropriate diagnostic test at this time is
A. an abdominal CT scan
B. a head CT scan
C. a renal scan
D. a renal vein renin level
E. urine catecholamine and VMA levels

The correct answer is A. It is generally true that greater than 90% of patients with hypertension have essential hypertension. The remainder have a variety of secondary causes, all of which are in general rare. For this patient, hypernatremia and hypokalemia imply excess aldosterone. The electrolyte imbalance coupled with the hypertension strongly suggests Conn's disease or primary hyperaldosteronism. The imaging modality of choice would be the one that looks for an adrenal mass.

A head CT scan (choice B) is not indicated as there is no evidence for any intracranial pathology.

A renal scan (choice C) is used to assess for renal artery stenosis and possible renovascular hypertension. In this case, the electrolyte disturbance is so characteristic of elevated aldosterone, that RAS is not a diagnosis to pursue.

Renal vein renin levels (choice D) are used to assess for possible secondary aldosteronism. This is a useful diagnostic test but cumbersome to perform and should not be done prior to the potentially high yield and simple abdominal CT scan.

Urine catecholamine and VMA levels (choice E) are useful in the diagnosis of pheochromocytoma. This is also a rare cause of hypertension but is less likely than aldosteronism because excess catechols are not associated with salt retention and potassium wasting.
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Asthma Treatment
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Asthma is a disease of diffuse airway inflammation caused by a variety of triggering stimuli resulting in partially or completely reversible bronchoconstriction. Symptoms and signs include dyspnea, chest tightness, cough, and wheezing. The diagnosis is based on history, physical examination, and pulmonary function tests. Treatment involves controlling triggering factors and drug therapy, most commonly with inhaled β2-agonists and inhaled corticosteroids. Prognosis is good with treatment.

Major drug classes commonly used in the treatment of chronic asthma and asthma exacerbations include 

• Bronchodilators (β2-agonists)
• Corticosteroids
• Leukotriene modifiers

β2-Agonists relax bronchial smooth muscle, decrease mast cell degranulation and histamine release, inhibit microvascular leakage into the airways, and increase mucociliary clearance. β2-Agonists come in short- and long-acting preparations. Short-acting β2-agonists (eg, albuterol) 2 puffs q 4 h inhaled prn are the drug of choice for relieving acute bronchoconstriction and preventing exercise-induced asthma. They should not be used alone for long-term maintenance of persistent asthma. They take effect within minutes and are active for up to 6 to 8 h, depending on the drug. Tachycardia and tremor are the most common acute adverse effects of inhaled β2-agonists and are dose-related. Mild hypokalemia occurs uncommonly. Use of levalbuterol (a solution containing the R-isomer of albuterol) theoretically minimizes adverse effects, but its long-term efficacy and safety are unproved. Oral β2-agonists have more systemic effects and generally should be avoided. 

Long-acting β2-agonists (eg, salmeterol) are active for up to 12 h and are used for moderate and severe asthma but should never be used as monotherapy. They interact synergistically with inhaled corticosteroids and permit lower dosing of corticosteroids. The safety of regular long-term use of β2-agonists is controversial. Long-acting β2-agonists may increase the risk of asthma-related death when used as monotherapy. Therefore, when treating patients with asthma, these drugs (salmeterol and formoterol) should be used only in combination with an inhaled corticosteroid for patients whose condition is not adequately controlled with other asthma controllers (eg, low- to medium-dose inhaled corticosteroids) or whose disease severity clearly warrants additional maintenance therapies. Daily use or diminishing effects of short-acting β2-agonists or use of ≥ 1 canister per month suggests inadequate control and the need to begin or intensify other therapies. 

Corticosteroids inhibit airway inflammation, reverse β-receptor down-regulation, and inhibit cytokine production and adhesion protein activation. They block the late response (but not the early response) to inhaled allergens. Routes of administration include oral, IV, and inhaled. In acute asthma exacerbations, early use of systemic corticosteroids often aborts the exacerbation, decreases the need for hospitalization, prevents relapse, and speeds recovery. Oral and IV routes are equally effective. Inhaled corticosteroids have no role in acute exacerbations but are indicated for long-term suppression, control, and reversal of inflammation and symptoms. They substantially reduce the need for maintenance oral corticosteroid therapy. Adverse local effects of inhaled corticosteroids include dysphonia and oral candidiasis, which can be prevented or minimized by having the patient use a spacer, gargle with water after corticosteroid inhalation, or both.

Leukotriene modifiers are taken orally and can be used for long-term control and prevention of symptoms in patients with mild persistent to severe persistent asthma. The main adverse effect is liver enzyme elevation (which occurs with zileuton). Although rare, patients have developed a clinical syndrome resembling eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome). 

Monitoring response to treatment: Guidelines recommend office use of spirometry (FEV1, FEV1/FVC, FVC) to measure airflow limitation and assess impairment and risk. Outside the office, home PEF monitoring, in conjunction with patient symptom diaries and the use of an asthma action plan, is especially useful for charting disease progression and response to treatment in patients with moderate to severe persistent asthma. When asthma is quiescent, one PEF measurement in the morning suffices. Should PEF measurements fall to < 80% of the patient's personal best, then twice/day monitoring to assess circadian variation is useful. Circadian variation of > 20% indicates airway instability and the need to re-evaluate the therapeutic regimen. 

Patient education: The importance of patient education cannot be overemphasized. Patients do better when they know more about asthma—what triggers an exacerbation, what drug to use when, proper inhaler technique, how to use a spacer with a metered-dose inhaler (MDI), and the importance of early use of corticosteroids in exacerbations. Every patient should have a written action plan for day-to-day management, especially for management of acute exacerbations, that is based on the patient's best personal peak flow rather than on a predicted normal value. Such a plan leads to much better asthma control, largely attributable to improved adherence to therapies. 


For each patient with asthma, select the most appropriate therapy for asthma management in adults and children older than 5 years of age.

A. Symptomatic use of albuterol by metered- dose inhaler
B. Daily inhaled fluticasone and symptomatic use of albuterol by metered-dose inhaler
C. Daily inhaled fluticasone, daily inhaled salmeterol, and symptomatic use of albuterol by metered-dose inhaler
D. Daily inhaled fluticasone; oral prednisone; and daily inhaled salmeterol, with symptomatic use of albuterol by metered-dose inhaler

[1] A 21-year-old female college student complains of occasional, brief episodes of shortness of breath, wheezing, and cough. These episodes occur twice a month on average, never more than once a week. Office pulmonary function tests are within normal limits.

[2] An 18-year-old woman with a history of severe eczema complains of continued wheezing, short- ness of breath, and cough. Her symptoms are continuous in nature. During the past 2 weeks, she has visited the ED with these complaints 3 times. Last year, she was admitted to a hospital on four occasions with severe shortness of breath and wheezing. She has never been intubated. Office pulmonary function testing reveals a peak flow that is 40% of predicted.

[3] A 25-year-old man is referred to you secondary to worsening complaints of wheezing and dyspnea. He says that he has symptoms every day despite using an albuterol inhaler 7 to 10 times a day. He reports that, perhaps once a week, the symptoms become so severe that he has to limit his activity. Office pulmonary function testing reveals a peak flow that is 65% of predicted.

[4] A 30-year-old man complains of episodic wheezing and dyspnea, which occur 3 or 4 times per week. They rarely force him to limit his activity. Once a month, perhaps, he suffers from nighttime wheezing. Office pulmonary function testing re- veals a peak flow that is 90% of predicted.

In Question 1, answer is A. The patient has symptoms consistent with step 1 asthma. Symptomatic treatment with albuterol is indicated.

In Question 2, answer is D. The patient has severe, persistent symptoms. Aggressive treatment with oral steroids, inhaled steroids, and a long-acting bronchodilator is warranted at this time.

In Question 3, answer is C. the patient has step 3 asthma. He should receive an inhaled steroid with a long-acting bronchodilator.

In Question 4, answer is B. The patient has step 2 asthma. He should receive inhaled steroids.

A 22-year-old man with a history of asthma controlled with albuterol metered dose inhaler (MDI) alone complains of worsening symptoms of shortness of breath. Over the last 10 years he rarely needed his inhaler more than 2 times a month. However, over the last 4 months he reports requiring rescue inhaler treatment 4-5 times a week. A canister of albuterol, which used to last 2-3 months, is now being replaced every 3 weeks. He denies any other symptoms. The most appropriate pharmacotherapy at this time is

A. cromolyn MDI
B. ipratropium bromide MDI
C. montelukast
D. salmeterol MDI
E. fluticasone MDI

The correct answer is E. This patient has worsening of his asthma. Patients should not need albuterol rescue treatments more than 2 times each week. Patients should not wake up at night more than 2 times each month with asthma symptoms, and patients should not need 2 canisters of albuterol in any given month. If your patient fits any of the above criteria, his asthma is poorly controlled. The next treatment is steroid MDI such as fluticasone. Remember: Asthma is inflammation and steroids decrease inflammation.

Cromolyn (choice A) is a mast-cell stabilizer. It is commonly used in children, but its role in adult asthma is not as well studied as steroids. It is not typically a first- or second-line treatment in asthma of the adult.

Ipratropium bromide (choice B) is an anticholinergic agent which is used for acute treatment of asthma and is helpful in bronchospasm associated with COPD. It is an effective agent in the acute setting of asthma but it takes about 45 minutes to have any effect. It is not the proper drug to be added if rescue inhalers are not providing adequate control of symptoms.

Montelukast (choice C) is a relatively new therapy for asthma. It is a leukotriene inhibitor and is useful in selective patients with asthma such as those with aspirin sensitivity or those that are unable to use MDI properly. Its use should be initiated in select patients on inhaled steroids who continue to have poor control of their asthma symptoms.

Salmeterol (choice D) is a long-acting beta agonist. It is a useful medication to be added to patients who are already on inhaled steroids but continue to have symptoms of asthma.
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Kaposi Sarcoma
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Kaposi sarcoma (KS) is a multicentric vascular tumor caused by herpesvirus type 8. It can occur in classic, AIDS-associated, endemic (in Africa), and iatrogenic (eg, after organ transplantation) forms. Diagnosis is by biopsy. Treatment for indolent superficial lesions involves cryotherapy, electrocoagulation, excision, or electron beam radiation therapy. Radiation therapy is used for more extensive disease. In the AIDS-associated form, antiretrovirals provide the most improvement.

KS originates from endothelial cells in response to infection by human herpesvirus 8 (HHV-8). Immunosuppression (particularly by AIDS and drugs for organ transplant recipients) markedly increases the likelihood of KS in HHV-8–infected patients. The tumor cells have a spindle shape, resembling smooth muscle cells, fibroblasts, and myofibroblasts.

Classic KS: This form occurs most often in older (> 60 yr) men of Italian, Jewish, or Eastern European ancestry. The course is indolent, and the disease is usually confined to a small number of lesions on the skin of the lower extremities; visceral involvement occurs in < 10%. This form is usually not fatal. 

AIDS-associated (epidemic) KS: This form is the most common AIDS-associated cancer and is more aggressive than classic KS. Multiple cutaneous lesions are typically present, often involving the face and trunk. Mucosal, lymph node, and GI involvement is common. Sometimes KS is the first manifestation of AIDS. 

Endemic KS: This form occurs in Africa independent of HIV infection. There are 2 main types: 

Prepubertal lymphadenopathic form: It predominantly affects children; primary tumors involve lymph nodes, with or without skin lesions. The course is usually fulminant and fatal.
Adult form: This form resembles classic KS.
Iatrogenic (immunosuppressive) KS: This form typically develops several years after organ transplantation. The course is more or less fulminant, depending on the degree of immunosuppression.

Symptoms and Signs
Cutaneous lesions are asymptomatic purple, pink, or red macules that may coalesce into blue-violet to black plaques and nodules. Some edema may be present. Occasionally, nodules fungate or penetrate soft tissue and invade bone. Mucosal lesions appear as bluish to violaceous macules, plaques, and tumors. GI lesions can bleed, sometimes extensively, but usually are asymptomatic.

• Biopsy
Diagnosis is confirmed by punch biopsy. Patients with AIDS or immunosuppression require evaluation for visceral spread by CT of the chest and abdomen. If CT is negative but pulmonary or GI symptoms are present, bronchoscopy or GI endoscopy should be considered.

• Surgical excision, cryotherapy, or electrocoagulation for superficial lesions
• Local radiation therapy for multiple lesions or lymph node disease
• Antiretroviral therapy or sometimes IV interferon alfa for AIDS-associated KS
Reduction of immunosuppressants for iatrogenic KS
Indolent lesions often require no treatment. One or a few superficial lesions can be removed by excision, cryotherapy, or electrocoagulation. Intralesional vinblastine or interferon alfa is also useful. Multiple lesions and lymph node disease are treated locally with 10 to 20 Gy of radiation therapy.

AIDS-associated KS responds markedly to highly active antiretroviral therapy (HAART), probably because CD4+ count improves and HIV viral load decreases; however, there is some evidence that protease inhibitors in this regimen may block angiogenesis. AIDS patients with indolent disease and CD4+ counts > 150/μL and HIV RNA < 500 copies/mL can be treated with IV interferon alfa. Patients with more extensive or visceral disease can be given liposomal doxorubicin 20 mg/m2 IV q 2 to 3 wk. If this regimen fails, patients may receive paclitaxel. Other agents being investigated as adjuncts include IL-12, desferrioxamine, and oral retinoids. Treatment of KS does not prolong life in most AIDS patients because infections dominate the clinical course.

Iatrogenic KS responds best to stopping immunosuppressants. In organ transplant patients, reduction of immunosuppressant dosage often results in reduction of KS lesions. If dosage reduction is not possible, conventional local and systemic therapies used in other forms of KS should be instituted. Sirolimus may also improve iatrogenic KS.

Key Points
• Consider KS in older men, Africans, and patients with organ transplants or AIDS.
• Test patients with immunosuppression (including AIDS) for metastases.
• Treat superficial lesions with locally ablative methods.


A 35-year-old homosexual man with HIV infection presents with recent painless purple skin plaques on his lower legs and generalized lymphadenopathy. He has similar skin lesions on his trunk and a purple-colored mass on his hard palate. Infection with which of the following viruses would most likely be directly related to the development of this tumor?

A. Epstein-Barr virus (EBV)
B. Hepatitis B virus (HBV)
C. Human herpesvirus type 8 (HHV 8)
D. Human papillomavirus (HPV)
E. Human T-lymphocyte virus (HTLV-1)

Correct Answer is C. HHV 8 (a member of the herpes family, choice C) is associated with Kaposi's sarcoma.

Hepatocellular carcinoma is associated with hepatitis B virus (HBV) infection, alcohol use, and hemochromatosis.

EBV (choice A) is associated with Burkitt's lymphoma and nasopharyngeal carcinoma.

HPV (human papillomavirus, choice D) is associated with cervical, penile, and anal carcinoma.

HTLV-1 (human T-lymphocyte virus, choice E) is associated with adult T-cell leukemia.

A 32-year-old gardener comes to the office because of a lesion on his nose that has been increasing in size over the past few weeks. He says that he rarely sees a doctor and is reluctant to discuss his medical history. He works outside for 9 to 10 hours a day, smokes two packs of cigarettes a day, and drinks approximately a case of beer a night. He states that he sometimes "shoots up" heroin with a few guys that "hang out on a stoop around the block." Physical examination shows a 1.5-cm, purple nodule on the tip of his nose, a 0.6-cm, reddish-purple raised macule on the tragus of his left ear, a 1-cm, purplish-blue area of discoloration on the roof of his mouth, and a 4-cm, confluent lesion made up of purplish-brown plaques, patches, nodules, and tumors on the anterior surface of his right leg. The results of the punch biopsy, which return in one week, show spindle cells, endothelial cells, and the extravasation of red blood cells. The factor in this patient's history most closely correlated with these lesions is

A. alcohol intake
B. cigarette smoking
C. intravenous drug use
D. pesticide exposure
E. sun-exposure

The correct answer is C. This patient most likely has Kaposi's sarcoma, which is one of the most common malignancies affecting HIV-infected individuals. It is a vascular tumor characterized by purplish lesions (macules, plaques, nodules, and tumors) that occur most commonly on the face, oral mucosa, lymph nodes, lungs, and gastrointestinal tract. Biopsies of the lesions show spindle cells, endothelial cells, and the extravasation of red blood cells. Management of Kaposi's sarcoma is dependent on the size, location, and the severity of other diseases, and includes observation, surgery, radiation, biological therapy, and chemotherapy. This patient was most likely infected with HIV from intravenous drug use.

Alcohol (choice A) and cigarette smoking (choice B) are not associated with Kaposi's sarcoma.

Pesticide exposure (choice D) may be associated with contact dermatitis, which is a cutaneous response to an irritant. The typical characteristics are pruritus, erythema, edema, and vesicles. Kaposi's sarcoma is not associated with pesticide exposure.

Sun-exposure (choice E) is associated with basal-cell carcinoma, squamous cell carcinoma, and malignant melanoma. Basal-cell carcinoma typically occurs on the face and is characterized by a papule with central ulceration and a "pearly" border. Histological evaluation shows nests and clusters of deeply basophilic epithelial cells with "palisading" nuclei on the periphery. Squamous-cell carcinoma typically occurs on the face, especially the ears and lower lip, and is characterized by an indurated and hyperkeratotic plaque with crusting and ulceration. Histological evaluation shows sheets and nests of neoplastic epidermal cells. Malignant melanoma, which has many clinical variants, is typically associated with sun exposure in childhood. It can occur almost anywhere on the skin or on the body and can be melanotic or amelanotic. The typical lesions occur on the trunk, and extremities, are irregularly pigmented, and have asymmetric borders. Microscopic evaluation shows neoplastic melanocytes. Kaposi's sarcoma is not associated with any of these malignancies.
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Candida Vaginitis
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Candidal vaginitis is vaginal infection with Candida sp, usually C. albicans.

Most fungal vaginitis is caused by C. albicans, which colonizes 15 to 20% of nonpregnant and 20 to 40% of pregnant women. Risk factors for candidal vaginitis include the following:

• Diabetes
• Use of a broad-spectrum antibiotic or corticosteroids
• Pregnancy
• Constrictive nonporous undergarments
• Immunocompromise
• Use of an intrauterine device
• Candidal vaginitis is uncommon among postmenopausal women except among those taking systemic hormone therapy.

Symptoms and Signs
Vaginal vulvar pruritus, burning, or irritation (which may be worse during intercourse) and dyspareunia are common, as is a thick, white, cottage cheese–like vaginal discharge that adheres to the vaginal walls. Symptoms and signs increase the week before menses. Erythema, edema, and excoriation are common. Infection in male sex partners is rare. Recurrences after treatment are uncommon.

Vaginal pH and wet mount
Vaginal pH is < 4.5; budding yeast, pseudohyphae, or mycelia are visible on a wet mount, especially with KOH. If symptoms suggest candidal vaginitis but signs (including vulvar irritation) are absent and microscopy does not detect fungal elements, fungal culture is done. Women with frequent recurrences require culture to confirm the diagnosis and to rule out non-albicans Candida.

• Antifungal drugs (oral fluconazole in a single dose preferred)
• Avoidance of excess moisture accumulation

Keeping the vulva clean and wearing loose, absorbent cotton clothing that allows air to circulate can reduce vulvar moisture and fungal growth. Topical or oral drugs are highly effective. Adherence to treatment is better when a one-dose oral regimen of fluconazole 150 mg is used. Topical butoconazole, clotrimazole, miconazole, and tioconazole are available OTC. However, patients should be warned that topical creams and ointments containing mineral oil or vegetable oil weaken latex-based condoms. If symptoms persist or worsen during topical therapy, hypersensitivity to topical antifungals should be considered.

Frequent recurrences require long-term suppression with oral drugs (fluconazole 150 mg weekly to monthly or ketoconazole 100 mg once/day for 6 mo). Suppression is effective only while the drugs are being taken. These drugs may be contraindicated in patients with liver disorders. Patients taking ketoconazole should be monitored periodically with liver function tests.


A 19-year-old college student comes to the physician because of vaginal irritation and pain with urination for 5 days. Two weeks ago, she had streptococcal pharyngitis treated with amoxicillin. She has been sexually active with two partners over the past year; she uses condoms for contraception. Her last menstrual period was 1 week ago. Her temperature is 37.2°C (99°F), and blood pressure is 90/60 mm Hg. Pelvic examination shows erythema of the vulva and vagina and a thick white vaginal discharge. The pH of the discharge is 4. Which of the following is the most likely cause of these findings?

A. Bacterial vaginosis
B. Candidiasis
C. Chlamydia trachomatis infection
D. Escherichia coli infection
E. Neisseria gonorrhoeae infection

Answer: B. Recent antibiotic use is a risk factor for developing candida vaginitis. This patient also has the classic white vaginal discharge. The pH is also < 4.5, which is consistent with Candida.

BV (choice A) would have a pH > 4.5. Chlamydia (choice C) and Neisseria (choide E) are sexually transmitted diseases and this patient is using condoms, which greatly reduces her risk of acquiring such STDs. E. Coli (Choice D) is more commonly associated with urinary tract infections with dysuria rather than vaginitis with discharge.

A 25-year-old exercise instructor comes to the office because of "another episode of white vaginal discharge." She has had 4 episodes of vaginal candidiasis in the past 6 months and it is beginning to "drive her crazy." She is so uncomfortable all day long that she "cannot take it anymore." She has not been sexually active in 2 months, does not take medications, only wears sanitary napkins during her menstrual period, wears cotton underwear, and changes her clothing immediately after exercising. She has never had a sexually transmitted disease and has never used illegal drugs. Physical examination shows a thick, white vaginal discharge, and an erythematous and edematous vulva. A urinalysis is normal, a urine pregnancy test is negative, and a potassium hydroxide preparation of the vaginal discharge shows hyphae and buds. Culture grows Candida albicans. You prescribe oral ketoconazole for 14 days. She returns 1 month later and says that the symptoms resolved for 2 weeks, but have returned. Her social history is unchanged. Physical and microscopic examinations are the same as the last visit. At this time you should

A. advise her to stop exercising for a month and then return for reexamination
B. ask her to consent to HIV testing
C. have her contact past sexual partners for evaluation
D. determine blood glucose level
E. prescribe one 500 mg vaginal tablet of clotrimazole for prophylaxis, and ask her to return for reexamination in 1 month

The correct answer is D. Patients with recurrent episodes of candidiasis should be evaluated for predisposing factors such as diabetes mellitus and immunosuppression. Since she has no other obvious risk factors for HIV or any other immune defects, it is best to first rule out diabetes before testing for immunodeficiency (choice B). Other risk factors for recurrences were ruled out in the history (habitual use of panty liners, wearing warm moist clothing for prolonged periods of time, antibiotic usage, and reinfection from an infected sexual partner).

Advising her to stop exercising for a month and then return for reexamination (choice A) is inappropriate. While wearing warm, moist clothing for prolonged periods of time can increase the risk of Candida infection, as long as she changes after exercising, she should be fine. She should be tested for diabetes at this time.

Since she has not been sexually active in months, it is inappropriate to have her contact past sexual partners for an evaluation (choice C). She has recurrences despite sexual activity.

It is incorrect to prescribe one 500 mg vaginal tablet of clotrimazole for prophylaxis, and ask her to return for reexamination in 1 month (choice E), because she has a current infection and requires evaluation and treatment, not prophylaxis.
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Instructional Tutorial Video
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hey i am a medical student in my first year has ended and will be going to second year after exams .....i just wanted to request you that as i will be preparing for usmle could you help me out and post weekly mcq question over here and thanks your videos have been informative ....
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