ENARM 11a PARTE

ENARM 11ª PARTE by JD-MD ENARM by JD-MD 11a PARTE 1001.- un efecto adverso que puede ocurrir si se administra hormona del crecimiento antes de la pubertad es: Cierre prematuro de las metáfisis Hiperlipoproteinemia Aparición de diabetes Gigantismo Acromegalia Excessive GH causes tall stature and gigantism if it occurs before closure of epiphyses. Afterward, acromegaly develops. The term "acromegaly," meaning extremity enlargement, seriously understates the manifestations. The hands enlarge and a doughy, moist handshake is characteristic. The fingers widen, causing patients to enlarge their rings. Carpal tunnel syndrome is common. The feet also grow, particularly in width. Facial features coarsen since the bones and sinuses of the skull enlarge; hat size increases. The mandible becomes more prominent, causing prognathism and malocclusion. Tooth spacing widens. Macroglossia occurs, as does hypertrophy of pharyngeal and laryngeal tissue; this causes a deep, coarse voice and sometimes makes intubation difficult. Obstructive sleep apnea may occur. A goiter may be noted. Hypertension (50%) and cardiomegaly are common. At diagnosis, about 10% of acromegalic patients have overt heart failure, with a dilated left ventricle and a reduced ejection fraction. Weight gain is typical, particularly of muscle and bone. Insulin resistance is usually present and frequently causes diabetes mellitus (30%). Arthralgias and degenerative arthritis occur. Overgrowth of vertebral bone can cause spinal stenosis. Colon polyps are common, especially in patients with skin papillomas. The skin may also manifest hyperhidrosis, thickening, cystic acne, and areas of acanthosis nigricans. GH-secreting pituitary tumors usually cause some degree of hypogonadism, either by cosecretion of prolactin or by direct pressure upon normal pituitary tissue. Decreased libido and impotence are common, as are irregular menses or amenorrhea. Secondary hypothyroidism sometimes occurs; hypoadrenalism is unusual. Headaches are frequent. Temporal hemianopia may occur as a result of the optic chiasm being impinged by a suprasellar growth of the tumor. Endoscopic transnasal, transsphenoidal pituitary microsurgery removes the adenoma while preserving anterior pituitary function in most patients. Surgical remission is achieved in about 70% of patients followed over 3 years. GH levels fall immediately; diaphoresis and carpal tunnel syndrome often improve within a day after surgery. Transsphenoidal surgery is usually well tolerated, but complications occur in about 10% of patients, including infection, cerebrospinal fluid leak, and hypopituitarism. Hyponatremia can occur 4-13 days postoperatively and is manifested by nausea, vomiting, headache, malaise, or seizure. It is prudent to monitor serum sodium levels postoperatively. Dietary salt supplements for 2 weeks postoperatively may prevent this complication. Patients who fail to have a clinical or biochemical remission after surgery are treated with a dopamine agonist (eg, cabergoline), octreotide, pegvisomant, or a combination of these medications. Cabergoline may be used first, since it is an oral medication. Cabergoline therapy is most successful for tumors that secrete both prolactin (PRL) and GH, but can also be effective for patients with normal serum PRL levels. Therapy with cabergoline will shrink one-third of such tumors by more than 50%. Cabergoline is administered orally, starting with 0.25 mg twice weekly. If the patient tolerates cabergoline, the dosage may be increased gradually, based upon serum GH and IGF-I levels; the maximum dosage is 1 mg orally twice weekly. Side effects of cabergoline include nausea, fatigue, constipation, abdominal pain, and dizziness. Cabergoline is expensive. Somatostatin analogs may be used to treat patients who have persistent acromegaly despite pituitary surgery. Octreotide and lanreotide are somatostatin MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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ENARM 11ª PARTE by JD-MD analogs that are given by subcutaneous injection. Short-acting octreotide acetate in doses of 50 mcg is injected subcutaneously three times daily. Responders who tolerate the drug are switched to long-acting octreotide acetate injectable suspension in a dosage of 20 mg intragluteally per month. The dosage may be adjusted¾up to a maximum of 40 mg monthly¾to maintain the serum GH between 1 and 2.5 ng/mL, keeping IGF-I levels normal. Lanreotide SR (not available in the United States) is given by subcutaneous injection at a dosage of 30 mg every 7-14 days. Lanreotide Autogel (not available in the United States) is a newer formulation that is administered by deep subcutaneous injection in doses of 60-120 mg every 28 days; this preparation is better tolerated than lanreotide SR. All somatostatin analogs are expensive and must be continued indefinitely or until other treatment has been effective. Octreotide longacting release (LAR) preparations (Sandostatin LAR depot) are superior to shorteracting octreotide, ultimately achieving serum GH levels under 2 ng/mL in 79% of patients and normal serum IGF-I levels in 53% of patients. Headaches often improve, and tumor shrinkage of about 30% may be expected. Acromegalic patients with pretreatment serum GH levels exceeding 20 ng/mL are less likely to respond to octreotide therapy. Side effects are experienced by about one-third of patients and include injection site pain, loose acholic stools, abdominal discomfort, or cholelithiasis. Pegvisomant is a GH receptor antagonist that blocks the effects of GH. Pegvisomant therapy produces symptomatic relief and normalizes serum IGF-I levels in over 90% of acromegalic patients. The starting dosage is 10 mg subcutaneously daily. The maintenance dosage can be increased by 5-10 mg every 4-6 weeks, based upon serum IGF-I levels and liver transaminase levels; the maximum dosage is 30 mg subcutaneously daily. Pegvisomant does not shrink GH-secreting tumors. Patients need to be monitored carefully with visual field examinations, GH levels, and MRI scanning of the pituitary. Side effects of pegvisomant can include injection site reactions, hepatitis, edema, flu-like syndrome, nausea, and hypertension. In acromegalic diabetics, hypoglycemic drugs are reduced to avoid hypoglycemia during pegvisomant therapy. The effectiveness of pegvisomant is reduced by coadministration of opioids or propoxyphene. Pegvisomant is extraordinarily expensive. Acromegalic patients who have not had a complete remission with transsphenoidal surgery or medical therapy may be treated with stereotactic radiosurgery administered by gamma knife, heavy particle radiation, or adapted linear accelerator. Radiosurgery precisely radiates the pituitary tumor in a single session and reduces radiation to the normal brain. However, it cannot be used for pituitary tumors with suprasellar extension due to the risk of damaging the optic chiasm. Radiosurgery can be used for pituitary tumors invading the cavernous sinus, since cranial nerves III, IV, V, and VI are less susceptible to radiation damage. Compared to conventional radiation therapy, radiosurgery is more effective and carries a lower risk of hypopituitarism, cerebral necrosis, psychological impairment, and small vessel stroke. Radiosurgery can also be used for patients who have failed conventional radiation therapy. 1002.- Tipo de enfisema que se asocia al tabaquismo: a) b) c) d) e)

Paraseptal Irregular Panlobulillar Centrolobulillar Parahiliar

El enfisema es caracterizado por el aumento permanente y anómalo de los espacios aéreos distales al bronquiolo terminal, acompañado de destrucción de sus paredes, y sin signos de fibrosis. Existen 4 tipos principales: 1) centroacinar (centrolobulillar); 2) panacinar; 3) paraseptal, y 4) irregular. Solo los dos primeros causan una obstrucción del flujo de aire clínicamente significativa. El enfisema centroacinar es mucho más MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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ENARM 11ª PARTE by JD-MD frecuente que la forma panacinar y representa el 95% de los casos. Los productos del tabaco y el carbón tienen un papel predominante en la génesis de este tipo de enfisema. 1003.- El control mensual rutinario de la tuberculosis pulmonar se debe de hacer por medio de: a) b) c) d) e)

Cultivo de exudado Pruebas de sensibilidad Microscopia de esputo Tele de tórax Examen clínico

En el control del tratamiento antituberculosis, con una muestra mensual de expectoración con apoyo de los métodos convencionales (puño y palmo-percusión), toda muestra de control independientemente de la calidad y apariencia macroscópica debe ser procesada, principalmente al final del tratamiento. 1003.- Principal procedimiento tromboembolia pulmonar:

diagnóstico

para

la

detección

de

a) Broncografía contrastada b) Broncoscopía directa c) Gammagrafía de perfusión pulmonar d) Tele de tórax en posición supina e) Espirometría computarizada De las opciones presentadas la que parece “mas verdadera es la opción C”, enseguida se cita una breve referencia. Pulmonary arteriography remains the reference standard for the diagnosis of pulmonary thromboembolism. An intraluminal filling defect in more than one projection establishes a definitive diagnosis. Secondary findings highly suggestive of pulmonary thromboembolism include abrupt arterial cutoff, asymmetry of blood flow¾especially segmental oligemia¾or a prolonged arterial phase with slow filling. Pulmonary arteriography was performed in 755 patients in the PIOPED study. A definitive diagnosis was established in 97%; in 3% the studies were nondiagnostic. Four patients (0.8%) with negative arteriograms subsequently had pulmonary thromboemboli at autopsy. Serial arteriography has demonstrated minimal resolution of thrombus prior to day 7 following presentation. Thus, negative arteriography within 7 days of presentation excludes the diagnosis. Pulmonary arteriography is a safe but invasive procedure with well-defined morbidity and mortality data. Minor complications occur in approximately 5% of patients. Most are allergic contrast reactions, transient renal dysfunction, or related to percutaneous catheter insertion; cardiac perforation and arrhythmias are reported but rare. Among the PIOPED patients who underwent arteriography, there were five deaths (0.7%) directly related to the procedure. Pulmonary hypertension is thought to increase the risk of serious complications, though a study of patients with average pulmonary arterial pressures of 74/34 mm Hg developed no major complications or deaths associated with pulmonary arteriography. The appropriate role of pulmonary arteriography in the diagnosis of pulmonary thromboembolism remains a subject of active debate. There is wide agreement that arteriography is indicated in several specific situations: in patients with nondiagnostic V/Q scans, intermediate or high clinical pretest probability of pulmonary thromboembolism, and negative noninvasive leg studies; in any patient in whom the diagnosis is in doubt when there is a high clinical pretest probability of pulmonary thromboembolism; and when the diagnosis of pulmonary thromboembolism must be established with certainty, as when MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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ENARM 11ª PARTE by JD-MD anticoagulation is contraindicated or placement of an inferior vena cava filter is contemplated. A perfusion scan is performed by injecting radiolabeled microaggregated albumin into the venous system, allowing the particles to embolize to the pulmonary capillary bed. To perform a ventilation scan, the patient breathes a radioactive gas or aerosol while the distribution of radioactivity in the lungs is recorded. A defect on perfusion scanning represents diminished blood flow to that region of the lung. This finding is not specific for pulmonary embolism. Defects in the perfusion scan are interpreted in conjunction with the ventilation scan to give a high, low, or intermediate (indeterminate) probability that pulmonary thromboembolism is the cause of the abnormalities. Criteria for the combined interpretation of ventilation and perfusion scans (commonly referred to as a single test, the V/Q scan) are complex, confusing, and not completely standardized. A normal perfusion scan excludes the diagnosis of clinically significant pulmonary thromboembolism (negative predictive value of 91% in the PIOPED study). A high-probability V/Q scan is most often defined as having two or more segmental perfusion defects in the presence of normal ventilation and is sufficient to make the diagnosis of pulmonary thromboembolism in most instances (positive predictive value of 88% among PIOPED patients). In the presence of abnormal pulmonary vasculature, as commonly happens in prior pulmonary thromboembolism, or if the clinical pretest probability for embolism is low, angiography may be indicated even in the presence of a high-probability V/Q scan. Helical CT arteriography is rapidly supplanting V/Q scanning as the initial diagnostic study for suspected pulmonary thromboembolism. Helical CT arteriography requires administration of intravenous radiocontrast dye but is otherwise noninvasive. It is very sensitive for the detection of thrombus in the proximal pulmonary arteries but less so in the segmental and subsegmental arteries. Test results vary widely by study and facility. Factors influencing results include patient size and cooperation, the type and quality of the scanner, the imaging protocol, and the experience of the radiologist. One report comparing helical CT with standard arteriography reported sensitivity of 53-60% and specificity of 81-97%. Comparing helical CT to the V/Q scan as the initial test for pulmonary thromboembolism, detection of thrombi is comparable, but more nonthromboembolism pulmonary diagnoses are made with CT scanning. Independent of cost and availability, helical CT may offer advantages as a screening examination, especially in hospitalized patients and in patients with significant comorbidities. A contentious issue is whether a negative helical CT requires any further evaluation. False-negative results may occur in up to 20% of helical CTs. Advocates contend that these false-negatives represent small peripheral thromboemboli and that such patients can be monitored off anticoagulation without undue risk. One study reported a venous thromboembolism rate of 0.8% in 3-month follow-up of 376 patients with negative helical CT scans, but the mortality rate at 3 months was 10.1%. Further study is required to clarify the role of this diagnostic modality, especially in view of ongoing advances in CT technology and the increasing availability of multi-detector-row scanners. 1004.- Síntoma más frecuente de la tromboembolia pulmonar aguda: a) b) c) d) e)

Hemoptisis Tos Síncope Disnea Dolor torácico pleurítico

The clinical diagnosis of pulmonary thromboembolism is notoriously difficult for two reasons. First, the clinical findings depend on both the size of the embolus and the patient's preexisting cardiopulmonary status. Second, common symptoms and signs of pulmonary emboli are not specific to this disorder. Indeed, no single symptom or sign MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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ENARM 11ª PARTE by JD-MD or combination of clinical findings is specific to pulmonary thromboembolism. Some findings are fairly sensitive: dyspnea and pain on inspiration occur in 75-85% and 65-75% of patients, respectively. Tachypnea is the only sign reliably found in more than half of patients. A common clinical strategy is to use combinations of clinical findings to identify patients at low risk for pulmonary thromboembolism. For example, 97% of patients in the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED) study with angiographically proved pulmonary emboli had one or more of three findings: dyspnea, chest pain with breathing, or tachypnea. Such a sensitive screen allows exclusion of the diagnosis on clinical grounds in a small number of patients. To establish the diagnosis or to exclude it definitively, further testing is required in the majority of patients. 1005.- Signo más frecuente en la tromboembolia pulmonar aguda: a) b) c) d) e)

Fiebre Flebitis Cianosis Taquipnea Taquicardia

The clinical diagnosis of pulmonary thromboembolism is notoriously difficult for two reasons. First, the clinical findings depend on both the size of the embolus and the patient's preexisting cardiopulmonary status. Second, common symptoms and signs of pulmonary emboli are not specific to this disorder. Indeed, no single symptom or sign or combination of clinical findings is specific to pulmonary thromboembolism. Some findings are fairly sensitive: dyspnea and pain on inspiration occur in 75-85% and 65-75% of patients, respectively. Tachypnea is the only sign reliably found in more than half of patients. A common clinical strategy is to use combinations of clinical findings to identify patients at low risk for pulmonary thromboembolism. For example, 97% of patients in the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED) study with angiographically proved pulmonary emboli had one or more of three findings: dyspnea, chest pain with breathing, or tachypnea. Such a sensitive screen allows exclusion of the diagnosis on clinical grounds in a small number of patients. To establish the diagnosis or to exclude it definitively, further testing is required in the majority of patients. 1006.- Característica física de la acromegalia: a) Micrognatia b) Prognatismo c) Disminución del tamaño de los senos paranasales d) Hipotelorismo e) Microglosia Excessive GH causes tall stature and gigantism if it occurs before closure of epiphyses. Afterward, acromegaly develops. The term "acromegaly," meaning extremity enlargement, seriously understates the manifestations. The hands enlarge and a doughy, moist handshake is characteristic. The fingers widen, causing patients to enlarge their rings. Carpal tunnel syndrome is common. The feet also grow, particularly in width. Facial features coarsen since the bones and sinuses of the skull enlarge; hat size increases. The mandible becomes more prominent, causing prognathism and malocclusion. Tooth spacing widens. Macroglossia occurs, as does hypertrophy of pharyngeal and laryngeal tissue; this causes a deep, coarse voice and sometimes makes intubation difficult. Obstructive sleep apnea may occur. A goiter may be noted. Hypertension (50%) and cardiomegaly are common. At diagnosis, about 10% MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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ENARM 11ª PARTE by JD-MD of acromegalic patients have overt heart failure, with a dilated left ventricle and a reduced ejection fraction. Weight gain is typical, particularly of muscle and bone. Insulin resistance is usually present and frequently causes diabetes mellitus (30%). Arthralgias and degenerative arthritis occur. Overgrowth of vertebral bone can cause spinal stenosis. Colon polyps are common, especially in patients with skin papillomas. The skin may also manifest hyperhidrosis, thickening, cystic acne, and areas of acanthosis nigricans. GH-secreting pituitary tumors usually cause some degree of hypogonadism, either by cosecretion of prolactin or by direct pressure upon normal pituitary tissue. Decreased libido and impotence are common, as are irregular menses or amenorrhea. Secondary hypothyroidism sometimes occurs; hypoadrenalism is unusual. Headaches are frequent. Temporal hemianopia may occur as a result of the optic chiasm being impinged by a suprasellar growth of the tumor. 1007.- Patrón menstrual más común en el hipotiroidismo: a) b) c) d) e)

Hipermenorrea Menorragia Oligomenorrea Metrorragia Amenorrea

ESSENTIALS OF DIAGNOSIS OF HYPOTHYROIDISM AND MIXEDEMA: • Weakness, fatigue, cold intolerance, constipation, weight change, depression, menorrhagia, hoarseness • Dry skin, bradycardia, delayed return of deep tendon reflexes • Anemia, hyponatremia • T4 and RAI uptake usually low • TSH elevated in primary hypothyroidism 1008.- Paciente femenino de 25 años de edad, diagnóstico de anemia establecido, hay antecedentes familiares de cálculos biliares a edad temprana en muchos miembros de su familia. Esta combinación sugiere el diagnóstico de: a) b) c) d) e)

Deficiencia de vitamina B 12 Rasgo de talasemia alfa Deficiencia de hierro Esferocitosis hereditaria Hemoglobinuria nocturna paroxística

Hereditary spherocytosis is an autosomal dominant disease of variable severity. It is often diagnosed during childhood, but milder cases may be discovered incidentally late in adult life. Anemia may or may not be present, since the bone marrow may be able to compensate for shortened red cell survival. Severe anemia (aplastic crisis) may occur in folic acid deficiency or when bone marrow compensation is temporarily impaired by infection. Chronic hemolysis causes jaundice and pigment (calcium bilirubinate) gallstones, leading to attacks of cholecystitis. Examination may reveal icterus and a palpable spleen. 1009.- Mejor prueba de detección para distinguir entre la anemia ferropénica y la anemia por enfermedad crónica en un paciente que acude a la consulta externa para valoración de un síntoma de fatiga y se detecta anemia microcítica: MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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ENARM 11ª PARTE by JD-MD a) Ferritina sérica b) Cuenta de reticulocitos c) Hierro sérico d) Porcentaje de saturación de transferrina e) Reservas de hierro de la medula ósea Iron deficiency is the most common cause of anemia worldwide. Iron is necessary for the formation of heme and other enzymes. Total body iron ranges between 2 and 4 g: approximately 50 mg/kg in men and 35 mg/kg in women. Most (70-95%) of the iron is present in hemoglobin in circulating red blood cells. One milliliter of packed red blood cells (not whole blood) contains approximately 1 mg of iron. In men, red blood cell volume is approximately 30 mL/kg. A 70-kg man will therefore have approximately 2100 mL of packed red blood cells and consequently 2100 mg of iron in his circulating blood. In women, the red cell volume is about 27 mL/kg; a 50-kg woman will thus have 1350 mg of iron circulating in her red blood cells. Only 200-400 mg of iron is present in myoglobin and nonheme enzymes. Aside from circulating red blood cells, the major location of iron in the body is the storage pool, as ferritin or as hemosiderin and in macrophages. The range for storage iron is wide (0.5-2 g); approximately 25% of women in the United States have none. The average American diet contains 10-15 mg of iron per day. About 10% of this amount is absorbed. Absorption occurs in the stomach, duodenum, and upper jejunum. Dietary iron present as heme is efficiently absorbed (10-20%) but nonheme iron less so (1-5%), largely because of interference by phosphates, tannins, and other food constituents. Small amounts of iron¾approximately 1 mg/d¾are normally lost though exfoliation of skin and mucosal cells. There is no physiologic mechanism for increasing normal body iron losses. Menstrual blood loss in women plays a major role in iron metabolism. The average monthly menstrual blood loss is approximately 50 mL, or about 0.7 mg/d. However, menstrual blood loss may be five times the average. To maintain adequate iron stores, women with heavy menstrual losses must absorb 3-4 mg of iron from the diet each day. This strains the upper limit of what may reasonably be absorbed, and women with menorrhagia of this degree will almost always become iron deficient without iron supplementation. In general, iron metabolism is balanced between absorption of 1 mg/d and loss of 1 mg/d. Pregnancy may also upset the iron balance, since requirements increase to 2-5 mg of iron per day during pregnancy and lactation. Normal dietary iron cannot supply these requirements, and medicinal iron is needed during pregnancy and lactation. Repeated pregnancy (especially with breast-feeding) may cause iron deficiency if increased requirements are not met with supplemental medicinal iron. Decreased iron absorption can on very rare occasions cause iron deficiency and usually occurs after gastric surgery, though concomitant bleeding is frequent. By far the most important cause of iron deficiency anemia is blood loss, especially gastrointestinal blood loss. Chronic aspirin use may cause it even without a documented structural lesion. Iron deficiency demands a search for a source of gastrointestinal bleeding if other sites of blood loss (menorrhagia, other uterine bleeding, and repeated blood donations) are excluded. Chronic hemoglobinuria may lead to iron deficiency since iron is lost in the urine; traumatic hemolysis due to a prosthetic cardiac valve and other causes of intravascular hemolysis (eg, paroxysmal nocturnal hemoglobinuria) should also be considered. As a rule, the only symptoms of iron deficiency anemia are those of the anemia itself (easy fatigability, tachycardia, palpitations and tachypnea on exertion). Severe deficiency causes skin and mucosal changes, including a smooth tongue, brittle nails, and cheilosis. Dysphagia because of the formation of esophageal webs (Plummer-Vinson syndrome) also occurs. Many irondeficient patients develop pica, craving for specific foods (ice chips, etc) often not rich in iron. Iron deficiency develops in stages. The first is depletion of iron stores. At this point, there is anemia and no change in red blood cell size. The serum ferritin will become abnormally low. A ferritin value less than 30 mcg/L is a highly reliable indicator MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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ENARM 11ª PARTE by JD-MD of iron deficiency. The serum total iron-binding capacity (TIBC) rises. Bone marrow biopsy for evaluation of iron stores is now rarely performed because of intraobserver variation in its interpretation. After iron stores have been depleted, red blood cell formation will continue with deficient supplies of iron. Serum iron values decline to less than 30 mcg/dL and transferrin saturation to less than 15%. In the early stages, the MCV remains normal. Subsequently, the MCV falls and the blood smear shows hypochromic microcytic cells. With further progression, anisocytosis (variations in red blood cell size) and poikilocytosis (variation in shape of red cells) develop. Severe iron deficiency will produce a bizarre peripheral blood smear, with severely hypochromic cells, target cells, hypochromic pencil-shaped cells, and occasionally small numbers of nucleated red blood cells. The platelet count is commonly increased. Other causes of microcytic anemia include anemia of chronic disease, thalassemia, and sideroblastic anemia. Anemia of chronic disease is characterized by normal or increased iron stores in the bone marrow and a normal or elevated ferritin level; the serum iron is low, often drastically so, and the TIBC is either normal or low. Thalassemia produces a greater degree of microcytosis for any given level of anemia than does iron deficiency. Red blood cell morphology on the peripheral smear is abnormal earlier in the course of thalassemia. 1010.- Paciente con anemia microcítica leve, el aumento en la concentración de la hemoglobina A2 sugiere el diagnóstico de: a) b) c) d) e)

Talasemia alfa Rasgo trepanocitico Talasemia beta Esferocitosis hereditaria Persistencia hereditaria de hemoglobina fetal

ESSENTIALS OF DIAGNOSIS OF THALASEMIAS: • Microcytosis out of proportion to the degree of anemia • Positive family history or lifelong personal history of microcytic anemia • Abnormal red blood cell morphology with microcytes, acanthocytes, and target cells • In b-thalassemia, elevated levels of hemoglobin A2 or F 1011.- En un paciente alcohólico crónico se observa con frecuencia la presencia de macrocitosis que esta relacionada con:

a) Reticulocitosis b) c) d) e)

Consumo de alcohol Deficiencia de folato Deficiencia de vitamina B 12 Enfermedad hepática

Folic acid is the term commonly used for pteroylmonoglutamic acid. In its reduced form of tetrahydrofolate, it serves as an important mediator of many reactions involving one-carbon transfers. Important reactions include the conversion of homocysteine to methionine and of deoxyuridylate to thymidylate, an important step in DNA synthesis. Folic acid is present in most fruits and vegetables (especially citrus fruits and green leafy vegetables) and daily requirements of 50-100 mcg/d are usually met in the diet. Total body stores of folate are approximately 5000 mcg, enough to supply requirements for 2-3 months. By far the most common cause of folate deficiency is inadequate dietary intake. Alcoholics, anorectic patients, persons who do not eat fresh fruits and vegetables, and those who overcook their food are candidates for folate MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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ENARM 11ª PARTE by JD-MD deficiency. Reduced folate absorption is rarely seen, since absorption occurs from the entire gastrointestinal tract. However, drugs such as phenytoin, trimethoprimsulfamethoxazole, or sulfasalazine may interfere with folate absorption. Folic acid requirements are increased in pregnancy, hemolytic anemia, and exfoliative skin disease, and in these cases the increased requirements (five to ten times normal) may not be met by a normal diet. Patients with increased folate requirements should receive supplementation with 1 mg/d of folic acid. 1012.- Variedad de hemopatía que presenta el cromosoma Philadelphia: a) b) c) d) e)

Leucemia promielocítica Linfoma de linfocitos pequeños Leucemia mieloide crónica Leucemia mieloblástica M2 Linfoma de Burkitt

El cromosoma Filadelfia es un cromosoma anormal originado por la translocación recíproca entre los brazos largos de los cromosomas 9 y 22, que aparece típicamente en la leucemia mieloide crónica. 1013.- Dolor articular, exantema malar, pleuritis, anticuerpos a DNA natural elevados y deficiencia del complemento C2: a) b) c) d) e)

Artritis reumatoide Enfermedad de Raynaud Vasculitis Lupus eritematosos sistémico Sífilis secundaria

Classification Criteria for the Diagnosis of SLE: 1. Fixed erythema, flat or raised, over the malar eminences 2. Discoid rash: Erythematous circular raised patches with adherent keratotic scaling and follicular plugging; atrophic scarring may occur 3. Photosensitivity: Exposure to ultraviolet light causes rash 4. Oral ulcers: Includes oral and nasopharyngeal ulcers, observed by physician 5. Arthritis: Nonerosive arthritis of two or more peripheral joints, with tenderness, swelling, or effusion 6. Serositis: Pleuritis or pericarditis documented by ECG or rub or evidence of effusion 7. Renal disorder: Proteinuria >0.5 g/d or =3+, or cellular casts 8. Neurologic disorder: Seizures or psychosis without other causes 9. Hematologic disorder: Hemolytic anemia or leukopenia (4 mg/d intravenously. The intravenous dose for acute gouty arthritis is 1 to 2 mg given slowly through an established venous line over 10 min in a soluset, and two additional doses of 1 mg each may be given at 6-h intervals, but the total dose should never exceed 4 mg. NSAIDs are affective in ~90% of patients, and the resolution of signs and symptoms usually occurs in 5 to 7 days. The most effective drugs are those with a short half-life and include indomethacin, 25 to 50 mg tid, ibuprofen, 800 mg tid, or diclofenac, 50 mg tid. Cyclooxigenase-2 highly selective inhibitors are probably equally effective but with less short-term gastrointestinal toxicity. Oral glucocorticoids such as prednisone, 30 to 50 mg/d as the initial dose and tapered over 5 to 7 days, a single intravenous dose of methylprednisolone, 7 mg of betametasone, or 20 to 40 mg of intraarticular triamcinolone acetonide have been equally effective. ACTH2 as an intramuscular injection of 40 to 80 IU in a single dose or every 12 h for 1 to 2 days is effective in patients with acute polyarticular refractory gout or with a contraindication for using colchicine or NSAIDs. Attempts to normalize serum uric acid to 800 mg per 24 hours, presence of uric acid stones, and risk for acute uric acid nephropathy during chemotherapy for myeloproliferative disorders. Uricosuric agents, such as probenecid, can be used in patients with good renal function who underexcrete uric acid, with 140 mg/kg, or 7 g in an average adult), hepatocellular glutathione is rapidly depleted and the reactive intermediate attacks other cell proteins, causing necrosis. Patients with enhanced P450 activity, such as chronic alcoholics and patients taking anticonvulsants, are at increased risk of developing hepatotoxicity. Hepatic toxicity may also occur after chronic accidental overuse of acetaminophen - eg, as a result of taking two or three acetaminophen-containing products concurrently or intentionally exceeding the recommended maximum dose of 4 g/d. Shortly after ingestion, patients may have nausea or vomiting, but there are usually no other signs of toxicity until 24-48 hours after ingestion, when hepatic aminotransferase levels begin to increase. With severe poisoning, fulminant hepatic necrosis may occur, resulting in jaundice, hepatic encephalopathy, renal failure, and death. Rarely, massive ingestion (eg, serum levels over 400-500 mg/L) can cause acute coma, hypotension, and metabolic acidosis unrelated to hepatic injury. The diagnosis of severe poisoning after acute overdose is based on measurement of the serum acetaminophen level. Ingestion of sustained-release products or coingestion of an anticholinergic agent, salicylate, or opioid drug may cause delayed elevation of serum levels and may render the nomogram useless. The nomogram is not useful after chronic overdose. Administer activated charcoal if it can be given within 1-2 hours of the ingestion. Although charcoal may interfere with absorption of the oral antidote acetylcysteine, this is not considered clinically significant. If the serum acetaminophen level is above the toxic line on the nomogram, begin treatment with a loading dose of N-acetylcysteine, 140 mg/kg orally, followed by 70 mg/kg every 4 hours. Dilute the solution to 5% with water, juice, or soda. If vomiting interferes with oral N-acetylcysteine administration, consider giving the antidote intravenously. The most widely used oral N-acetylcysteine protocol in the United States calls for 72 hours of treatment. However, other regimens have demonstrated equivalent success with 20-48 hours of treatment. The San Francisco Bay Area Poison Center recommends treatment until 36 hours after ingestion, at which time N-acetylcysteine can be discontinued if liver transaminases are normal. Treatment with N-acetylcysteine is most effective if started within 8-10 hours after ingestion. If the precise time of ingestion is unknown or if the patient is at higher risk of hepatotoxicity (eg, alcoholic, liver disease, chronic use of P450-inducing drugs), then use a lower threshold for initiation of N-acetylcysteine (ie, the lower nomogram line; in some case reports, a level of 100 mg/L at 4 hours was suggested in very high-risk patients). Nacetylcysteine may also be given intravenously; this is the preferred method in Europe and Canada, and a parenteral formulation (Acetadote) was recently approved by the Food and Drug Administration (FDA) for use in the United States. The conventional oral formulation may also be given intravenously using a micropore filter and a slow rate of infusion. Call a regional poison control center or medical toxicologist for assistance. MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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1064.- El azul de metileno esta indicado en el tratamiento de la intoxicación por: a) b) c) d) e)

Anilina Morfina Dextrometorfan Cianuro Fenotiazidas

El azul de metileno es una sustancia cristalina verde-azulada que se utiliza como tinte histológico e indicador de laboratorio. También se emplea en el tratamiento de la intoxicación por cianuro y en la metahemoglobinemia. 1065.- El tratamiento de la enfermedad celiaca consiste en: a) b) c) d) e)

Suprimir el gluten de la dieta Proporcionar una dieta libre de lactosa Administrar colestiramina Indicar una dieta rica en trigliceridos Administrar enzimas pancreaticas

La enfermedad celiaca es un error congénito del metabolismo caracterizado por la incapacidad para hidrolizar los péptidos del gluten. La enfermedad afecta a adultos y niños pequeños, y sus síntomas son distensión abdominal, vómitos, diarrea, pérdida de masa muscular y letargia extrema. La mayoría de los pacientes responde bien a una dieta sin gluten rica en proteínas y calorías. 1066.- Caso clinico seriado: Una paciente de 22 años, gesta 1, que cursa con embarazo de 37 semanas de evolución, presenta perdida del conocimiento posterior a crisis convulsivas tonicoclonicas, presion arterial de 170/120 mmHg, frecuencia cardiaca de 100 por minuto, reflejos osteoteninosos aumentads, frecuencia cardiaca fetal de 130 por minuto y edema importante en los miembros inferiores, no se aprecian signos de trabajo de parto ni modificaciones cervicales. Primer enunciado: El diagnostico más probable es: a) b) c) d) e)

Eclampsia Preeclampsia severa Crisis epilepticas tipo gran mal Crisis hipertensiva Hipertension inducida por el embarazo

1067.- Segundo enunciado: Una posible complicación en esta paciente es el síndrome de Hellp que consiste en: a) b) c) d) e)

Edema, hipertensión y albuminuria de mas de 3 grs Elevación de las enzimas hepaticas y hemolisis Hemolisis, plaquetopenia y elevación de las enzimas hepaticas Anemia, plaquetopenia y hemolisis Hemolisis, plaquetopenia e hipertension arterial

Eclampsia occurs in 0.2–0.5% of all deliveries, with occurrence being influenced by the same factors as in preeclampsia. In rare instances, eclampsia develops before 20 weeks' gestation. About 75% of eclamptic seizures occur before delivery. About 50% of postpartum eclamptic seizures occur in the first 48 hours after delivery, but they may MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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ENARM 11ª PARTE by JD-MD occur as late as 6 weeks postpartum. The pathogenesis of eclamptic seizures is poorly understood. Seizures have been attributed to platelet thrombi, hypoxia due to localized vasoconstriction, and foci of hemorrhage in the cortex. There is also a mistaken tendency to equate eclampsia with hypertensive encephalopathy. There is a poor correlation between occurrence of seizures and severity of hypertension. Seizures may occur with insignificant blood pressure elevations that are only slightly higher than readings recorded 24 hours previously. The hallmarks of hypertensive encephalopathy (retinal hemorrhages, exudates, and papilledema) are very infrequent in eclampsia, where funduscopic changes are minimal. There is usually no aura preceding the seizure, and the patient may have one, two, or many seizures. Unconsciousness lasts for a variable period of time. The patient hyperventilates after the tonic-clonic seizure to compensate for the respiratory and lactic acidosis that develops during the apneic phase. Fever is rare but is a poor prognostic sign. Seizure-induced complications may include tongue biting, broken bones, head trauma, or aspiration. Pulmonary edema and retinal detachment have also been noted following seizures. 1068.- El uso de corticoides esta indicado en los niños que padecen: a) b) c) d) e)

Síndrome nefritico Asma Hepatitis B Artritis séptica Meningitis viral

Management of status asthmaticus includes early supplemental oxygen, a frequently or continuously administered b2-adrenergic agent (albuterol, terbutaline), a nebulized anticholinergic agent (ipratropium), and a corticosteroid. Delivery of b2adrenergic agents may be achieved by either nebulization or metered-dose inhaler (MDI) with spacer or face masks. Subcutaneous epinephrine may be indicated in children with severe bronchospasm who are unable to tolerate nebulization treatment. Intravenous (IV) terbutaline should be considered in children unresponsive to nebulized b2-adrenergic treatment. A corticosteroid should be administered early, orally or parenterally. Incremental benefit from the addition of methylxanthine (aminophylline) appears to be offset by the increased incidence of adverse effects. Intravenous fluid should be administered in limited quantity and monitored carefully to prevent overhydration and pulmonary edema. Antibiotics are not routinely indicated but may be considered in cases of suspected bacterial, mycoplasma, or Chlamydia pneumoniae pneumonia. Adjunctive therapy for patients refractory to b-agonists and corticosteroids includes IV magnesium sulfate, helium-oxygen (heliox), and ketamine. Although there is insufficient evidence to recommend the routine use of magnesium sulfate, it may be considered in severe airway obstruction with impending respiratory failure. Heliox is a mixture of 60–80% helium and 20–40% oxygen. Because of its low density (one third that of room air), it reduces airway resistance by converting turbulent to laminar flow, thereby reducing work of breathing. The exact role of heliox in status asthmaticus is unknown. Limited data suggest it may be a temporizing measure that may avert the need for intubation and mechanical ventilation. 1069.- A que nivel actua la aldosterona: a) b) c) d) e)

Tubulo proximal Membrana glomerular Asa de Henle Tubulo contorneado distal Tubulo colector MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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ENARM 11ª PARTE by JD-MD Los principales sitios de acción de la aldosterona son el túbulo distal y la región cortical de los colectores, donde promueve la reabsorción de sodio. La aldosterona se elabora en la zona glomerulosa de la corteza suprarrenal. Es el mineralocorticoide más potente producido en esta glandula. La tasa de secreción de aldosterona es cien veces inferior a la del cortisol y su aclaramiento plasmático mucho más rápido. 1070.- A que nivel se lleva la mayor reabsorción de sodio y agua: a) b) c) d) e)

Túbulo contorneado proximal Porción ascendente del asa de Henle Túbulo colector Túbulo contorneado distal Arteriola aferente

El túbulo contorneado proximal resorbe alrededor del 70% del agua filtrada utilizando como impulsor la fuerza osmótica transtubular, generada por la absorción de solutos. Cuando el equilibrio de sodio corporal es el adecuado, la reabsorción de sodio y agua aumenta en paralelo. 1071.- El antiparasitario cuya acción consiste en inhibir a la colinesterasa y ocasionar la despolarización de la placa neuromuscular por medio de su actividad nicotinica es: a) b) c) d) e)

Metronidazol Ornidazol Pamoato de pirantel Piperacina Pirimetamina

Pyrantel pamoate (Antiminth, Combantrin): depolarizing neuromuscular blocker, wich causes parálisis of nematodos. Pyrymethamine: inhibits dehydrofolate reductase. Uses (plus sulfadoxine) vs primarily active against erythocytic forms of malaria, some activity vs primary Plasmodium infection in the liver, pyrimethamine is used with sulfadiazine for treatment of toxoplasmosis. Metronidazole (Flagyl): Forms cytotoxic producs via reductive bioactivation of its nitro group, causes oxidative damage to DNA of trophozoite. Most effective drug against invasive form of Entamoeba histolytica, drug of choice for giardiasis, trichomoniasis, Gardnerella vaginalis infections, and infections caused by anaerobic bacteria 1072.- La estimulación de los receptores beta-1 por acción de la dopamina produce: a) b) c) d) e)

Inotropismo y cronotropismo negativos Inotropismo positivo y cronotropismo negativo Inotropismo y cronotropismo positivos Disminución de la resistencia vascular periferica Activación de la respuesta vagal

Dopamine uses: short-term use in cardiac decompensation secondary to decreased contractility; increases organ perfusion (at low dose). Positive inotropic agent with dose dose-related response. 2-10 mcg/kg/min B-effects (increases cardiac output and renal perfusion). 10-20 mcg/kg/min B-effects (periferal vasocontriction, pressor). > 20 mcg/kg/min peripheral and renal vasoconstriction. MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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ENARM 11ª PARTE by JD-MD 1073.- La digoxina es util para el tratamiento de insuficiencia cardíaca cuando se acompaña de: a) b) c) d) e)

Arritmia sinusal Extrasistoles ventriculares Bloqueo auriculoventricular Fibrilación auricular Taquicardia sinusal

Glycosides of digitalis, which have been used in the treatment of heart failure for more than 200 years, are the most frequently used inotropic agents and the only oral positive inotropic preparation approved for treatment of heart failure. Digitalis glycosides, of which digoxin if the agent most commonly used, relieve symptoms by improving cardiac performance through increased myocardial contractility, improved LV function, and increased cardiac output and renal perfusion. Neurohumoral modulating actions have also been reported. Several studies suggest that treatment with digitalis decreases plasma renin activity, attenuates sympathetic drive, reduces plasma norepinephrine levels, and improves baroreceptor sensitivity. These effects are seen as playing an important role in treating heart failure. The beneficial effect of digitalis glycosides in patients with heart failure complicated by the occurrence of atrial fibrillation has been well documented and is generally well accepted by most clinicians. The results of several studies indicate that in patients with heart failure, digitalis does exert sustained beneficial hemodynamic effects accompanied by improvement in both clinical status and exercise tolerance. (Those who did not benefit from treatment with digitalis had milder degrees of heart failure or evidence of primarily diastolic dysfunction.) Because some evidence suggests that use of digitalis in suspected or confirmed MI may be associated with adverse outcome, it is appropriate to consider alternatives to treatment with digoxin for patients with MI and heart failure. 1074.- En los casos de incompatibilidad por sistema ABO, es común observar la prueba de Coombs: a) b) c) d) e)

Directa negativa Directa positiva Indirecta positiva Indirecta negativa Directa e indirecta positivas

La enfermedad hemolítica del recién nacido, o eritroblastosis fetal, es una enfermedad del feto y del recién nacido, debida a la incompatibilidad sanguínea entre la madre y el feto. La sensibilización por embarazo se produce cuando el feto hereda un antígeno paterno ausente en la madre, que atraviesa la placenta durante el parto, estimulando la producción de aloanticuerpos maternos. Otras veces, la sensibilización se produce con anterioridad al embarazo, por la inyección o transfusión de sangre portadora de antígenos ausentes en la madre. En ambos casos, los anticuerpos IgG de sensibilización atraviesan la placenta, se unen a los antígenos de los eritrocitos fetales y provocan su hemólisis. La sensibilización puede deberse a antígenos de los sistemas ABO, Rhesus u otros sistemas de grupos sanguíneos. En la actualidad la EHRN por incompatibilidad Rh es mucho menos frecuente que por ABO u otros. La madre Rh (D) negativa se sensibiliza al antígeno D y forma anti-D por transfusión con sangre Rh positiva o por un embarazo previo con un feto que ha heredado el antígeno D paterno. Si, una vez sensibilizada, vuelve a embarazarse con un feto Rh positivo, los hematíes fetales pueden entrar en la circulación materna, originando una respuesta inmune secundaria en la madre, que formará anticuerpos anti-D, IgG. El anticuerpo IgG MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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ENARM 11ª PARTE by JD-MD sintetizado por la madre atraviesa la placenta, se une a los hematíes fetales e induce su hemólisis. Clínicamente el feto puede estar ligera o gravemente afecto, según la cantidad de anticuerpo y la capacidad de la eritropoyesis fetal para compensar la hemólisis. Si la hemólisis puede ser compensada por el feto, este llegará a término sin grandes problemas, dado que el exceso de bilirrubina es metabolizado por la madre. Si la hemólisis es muy grave, el feto sufrirá anemia severa, insuficiencia cardiaca y puede morir intraútero con grandes edemas; es el denominado hydrops fetalis. El diagnóstico anteparto puede establecerse mediante la prueba de Coombs, indirecta en la madre, y con espectofotometría del líquido amniótico, que proporciona información sobre el grado de afectación fetal. El tratamiento consistirá en transfusiones intraútero, exanguinotransfusión o fototerapia, según la afectación fetal. Recientemente se han empleado con éxito las inmunoglobulinas intravenosas. 1075.- Cantidad máxima de aire que puede expulsarse después de una inspiración máxima: a) b) c) d) e)

Volumen corriente Volumen residual Capacidad residual funcional Capacidad vital Capacidad pulmonar total

1076.- Para el tratamiento de la encefalopatia hepatica crónica esta indicado: a) b) c) d) e)

Furosemida Diazepam Espironolactona Lactulosa Eritromicina

Hepatic encephalopathy is a state of disordered central nervous system function resulting from failure of the liver to detoxify noxious agents of gut origin because of hepatocellular dysfunction and portosystemic shunting. The clinical spectrum ranges from day-night reversal and mild intellectual impairment to coma. Patients with minimal hepatic encephalopathy have no recognizable clinical symptoms but MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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ENARM 11ª PARTE by JD-MD demonstrate mild cognitive and psychomotor deficits on standardized tests. Ammonia is the most readily identified and measurable toxin but is not solely responsible for the disturbed mental status. Pathogenic factors may include production of false neurotransmitters, increased sensitivity of central nervous system neurons to the inhibitory neurotransmitter g-aminobutyric acid (GABA), an increase in circulating levels of endogenous benzodiazepines, decreased activity of urea-cycle enzymes due to zinc deficiency, decreased brain levels of myoinositol, deposition of manganese in the basal ganglia, and swelling of astrocytes in the brain. Bleeding into the intestinal tract may significantly increase the amount of protein in the bowel and precipitate rapid development of encephalopathy. Other precipitants include constipation, alkalosis, and potassium deficiency induced by diuretics, opioids, hypnotics, and sedatives; medications containing ammonium or amino compounds; paracentesis with attendant hypovolemia; hepatic or systemic infection; and portosystemic shunts (including TIPS). Dietary protein should be withheld during acute episodes if the patient cannot eat. When the patient resumes oral intake, protein intake should be 60-80 g/d as tolerated; vegetable protein is better tolerated than meat protein. Gastrointestinal bleeding should be controlled and blood purged from the gastrointestinal tract. This can be accomplished with 120 mL of magnesium citrate by mouth or nasogastric tube every 3-4 hours until the stool is free of gross blood, or by administration of lactulose. The value of treating patients with minimal hepatic encephalopathy is uncertain. Lactulose, a nonabsorbable synthetic disaccharide syrup, is digested by bacteria in the colon to short-chain fatty acids, resulting in acidification of colon contents. Lactulose also leads to a change in bowel flora so that fewer ammonia-forming organisms are present. When given orally, the initial dose of lactulose for acute hepatic encephalopathy is 30 mL three or four times daily. The dose should then be titrated so that two or three soft stools per day are produced. When rectal use is indicated because of the patient's inability to take medicines orally, the dose is 300 mL of lactulose in 700 mL of saline or sorbitol as a retention enema for 3060 minutes; it may be repeated every 4-6 hours. Lactilol is a less sweet disaccharide alternative available as a powder in some countries. The ammonia-producing intestinal flora may also be controlled with neomycin sulfate, 0.5-1 g orally every 6 or 12 hours for 7 days. Side effects of neomycin include diarrhea, malabsorption, superinfection, ototoxicity, and nephrotoxicity, usually only after prolonged use. Alternative antibiotics are vancomycin, 1 g orally twice daily, or metronidazole, 250 mg orally three times daily. Patients who do not respond to lactulose alone may improve with a 1-week course of an antibiotic in addition to lactulose. Opioids and sedatives metabolized or excreted by the liver are avoided. If agitation is marked, oxazepam, 10-30 mg, which is not metabolized by the liver, may be given cautiously by mouth or by nasogastric tube. Zinc deficiency should be corrected, if present, with oral zinc sulfate, 600 mg/d in divided doses. There is limited evidence that eradication of Helicobacter pylori, which generates ammonia in the stomach, may improve encephalopathy. Sodium benzoate, 10 g daily, and ornithine aspartate, 9 g three times daily, may lower blood ammonia levels, but there is less experience with these drugs than with lactulose. The benzodiazepine competitive antagonist flumazenil is effective in about 30% of patients with severe hepatic encephalopathy, but the drug is short-acting and intravenous administration is required. Use of special dietary supplements enriched with branchedchain amino acids is usually unnecessary except in occasional patients who are intolerant of standard protein supplements. Treatment by modulating the gut flora with prebiotic and probiotic agents is under study. 1077.- Una lactante de ocho meses presenta un cuadro de 24 horas de evolucion con fiebre de 39.2 °c, vomito y rechazo al alimento. Se encuentra somnolienta e irritable con desviacion de la mirada hacia arriba y movimientos anormales de las manos y los pies; rigidez de la nuca e MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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ENARM 11ª PARTE by JD-MD hiperreflexia practicar:

osteotendinosa.

Para

confirmar

el

diagnostico

se

debe

a) Biometría hematica completa, examen general de orina y ultrasonido transfontanelar b) Biometría hemática completa, punción lumbar y cultivo c) Biometría hemática completa, examen de orina y radiografia de tórax d) Radiografia de craneo, hemocultivo y tomografia craneal e) Biometría hemática, tomografia del craneo y radiografia de tórax Bacterial infections of the CNS may present acutely (symptoms evolving rapidly over 1– 24 hours), subacutely (symptoms evolving over 1–7 days), or chronically (symptoms evolving over more than 1 week). Diffuse bacterial infections involve the leptomeninges, superficial cortical structures, and blood vessels. Although the term “meningitis” is used to describe these infections, it should not be forgotten that the brain parenchyma is also inflamed and that blood vessel walls may be infiltrated by inflammatory cells that result in endothelial cell injury, vessel stenosis, and secondary ischemia and infarction. While awaiting the results of diagnostic tests, the physician should start broad-spectrum antibiotic coverage as noted below. After specific organisms are identified, antibiotic therapy can be tailored based on antibiotic sensitivity patterns. Bacterial meningitis in children under age 3 months is treated initially with cefotaxime (or ceftriaxone if the child is over age 1 month) and ampicillin; the latter agent is used to treat Listeria and enterococci infections, which rarely affect older children. Children over age 3 months are given ceftriaxone, cefotaxime, or ampicillin plus chloramphenicol. If Streptococcus pneumoniae cannot be ruled out by the initial Gram stain, vancomycin or rifampin are added until cultures are reported, because penicillin-resistant pneumococci are common in the United States. Therapy may be narrowed when organism sensitivity allows. Duration of therapy is 7 days for meningococcal infections, 10 days for H influenzae or pneumococcal infection, and 14– 21 days for other organisms. Slow clinical response or the occurrence of complications may prolong the need for therapy. Although therapy for 7 days has proved successful in many children with H influenzae infection, it cannot be recommended without further study if steroids are also used. Neuroimaging with CT and MRI scans may be helpful in demonstrating the presence of brain abscess, meningeal inflammation, or secondary problems such as venous and arterial infarctions, hemorrhages, and subdural effusions when these are expected. In addition, these procedures may identify sinus or other focal infections in the head or neck region that are related to the CNS infection. CT scanning may demonstrate bony abnormalities, such as basilar fractures. EEGs may be helpful in the assessment of patients who have had seizures at the time of presentation. The changes are often nonspecific and characterized by generalized slowing. In some instances, such as herpes simplex virus infection, focal electronegative activity may be seen early in the course and may be one of the earliest laboratory abnormalities to suggest the diagnosis. EEGs may also show focal slowing over regions of abscesses. Unusual but characteristic electroencephalographic patterns are seen in some patients with subacute sclerosing panencephalitis. 1078.- El mecanismo principal por el que las bacterias parenquima renal y producen pielonefritis en el niño es: a) b) c) d) e)

alcanzan

el

Vaciamiento vesical frecuente Peristalsis ureteral Recurrencia de infecciones Diseminación hematogena Reflujo vesiculouretral MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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ENARM 11ª PARTE by JD-MD Pediatric urinary tract infection (UTI) may involve the urethra, bladder, or kidney. Outside the clinical setting of systemic perinatal infection or prematurity, UTIs in infants raise the possibility of urinary tract abnormalities. Boys less than 3 months of age are more susceptible than girls. During the first year of life, circumcised males are more likely to experience UTI due to a urinary tract abnormality than are females and uncircumcised males. Older boys with a first infection should also be examined for urinary tract abnormalities. A more conservative, watchful approach may be taken with older girls, especially if they are sexually active or have poor personal hygiene and no clinical features that arouse suspicion of significant urinary tract disease (eg, enuresis or short stature). At least 8% of girls and 2% of boys will have a UTI in childhood. It is particularly important to detect these infections in young children, since many children less than 5 years of age with febrile UTIs have pyelonephritis. In this age group, the infection commonly leads to renal scarring, especially in those less than a year of age. Focal renal scarring may be a risk factor for hypertension and renal disease later in life. The most common organisms causing UTI are E coli (> 80%), Klebsiella, Proteus (increaed in males), enterococcus, all normal fecal flora, and, infrequently, Staphylococcus. In the absence of bacteremia, enteric organisms are presumed to gain access to the urinary tract via the urethra. The likelihood of infection is increased with abnormalities of the urinary tract, poor perineal hygiene or infection, sexual activity, instrumentation, or dysfunctional voiding. Normal voiding serves to safeguard against bacterial contamination of the urethra developing into infection. Newborns may exhibit fever or hypothermia, poor feeding, jaundice, failure to thrive, or sepsis. Infants may have unexplained fever, irritability, or foul-smelling urine. Preschool children may have abdominal pain, vomiting, strong-smelling urine, fever, enuresis, or frequency, dysuria, or urgency. School-age children are often afebrile, but usually have the classic signs of UTI, such as enuresis, frequency, dysuria, and urgency. Costovertebral angle tenderness may be elicited in cases of pyelonephritis. It is very rare for children with bacterial UTI to present with hemorrhagic cystitis, which is more common with viral infections. Urinary tract infection is the most common occult bacterial cause of unexplained fever in infants less than 2 years of age. Sick children should be treated presumptively when the laboratory findings are suggestive. Initial therapy should be based on prior antibiotic use, location of the infection (eg, kidney, bladder), and the organism and its drug sensitivities. Uncomplicated urethritis or cystitis can be treated with a single oral antibiotic that the patient has not used recently. Amoxacillin, trimethoprimsulfamethoxazole (TMP-SMX), or a later generation cephalosporin can be used as initial therapy. Choice of antibiotic should also take into account community bacterial resistance patterns. TMP-SMX has generally yielded higher cure rates when compared with amoxacillin. TMP-SMX and cephalosporins are not active against enterococcus. Enterococcus might be suspected when a Gram stain is performed. Duration of therapy should be 7 to 10 days. Short course, high dose therapy should not be used in children. The choice of antibiotic should be reviewed when culture and sensitivity results are available. In toxic, dehydrated children who cannot receive oral therapy, especially if there is suspected pyelonephritis, hospitalization should be considered. Many of these children will be bacteremic (~5% of children less than 2 years of age). A non-toxic, older child with suspected pyelonephritis need not be admitted to the hospital (as long as compliance is not in question), but antibiotic coverage should be broad (ampicillin or cephalosporin plus gentamicin) until the bacteria's sensitivity to antibiotics is known. Antibiotic dosage must be adjusted for patients with associated acute or chronic renal failure. If the organism is sensitive to the antibiotic chosen and the child improves within 2 days, no test of cure is needed. If symptoms persist, bacterial sensitivity should be checked, the child reexamined, and a repeat urine culture obtained. Persistent symptoms and bacteriuria indicate one of the following: 1) wrong choice of antibiotic; 2) development of bacterial resistance; 3) superinfection with a different organism; or 4) a significant anatomic abnormality in the urinary tract. MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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1079.- La complicación hematologíca que más frecuentemente presentan los hijos de madres diabeticas es la: a) b) c) d) e)

Policitemia Plaquetopenia Leucopenia Hiperleucocitosis Enfermedad hemorragica del recién nacido

Los lactantes con un riesgo especial de padecer policitemia son los lactantes PEG a término y postérmino, los niños de madres diabéticas, los lactantes con pinzamiento tardío del cordón y los que presentan hipertiroidismo neonatal, síndrome adrenogenital, trisomía 21, síndrome de transfusión gemelar (receptor) y síndrome de Beckwith-Wiedemann. En algunos lactantes, la policitemia puede reflejar una compensación por pedíodos prolongados de hipoxia feral debida a insuficiencia placentaria; estos lactantes tienen niveles de eritropoyetina más altos en el nacimiento. 1080.- Caso clinico seriado: Hombre de 32 años, desde hace tres meses presenta debilidad muscular; se fatiga facilmente y hace algunos días noto la aparicion de manchas hiperpigmentadas en las rodillas, el cuello y en las areas expuestas al sol. Sus examenes de laboratorio muestran: sodio 123 mEq/l y potasio 5.3 mEq/l. Primer enunciado: el diagnostico probable es: a) b) c) d) e)

Hipercortisolismo Feocromocitoma Insuficiencia suprarrenal Aldosteronismo primario Hipotiroidismo

Addison's disease is an uncommon disorder caused by destruction or dysfunction of the adrenal cortices. It is characterized by chronic deficiency of cortisol, aldosterone, and adrenal androgens and causes skin pigmentation that can be subtle or strikingly dark. Volume and sodium depletion and potassium excess eventually occur in primary adrenal failure. In contrast, if chronic adrenal insufficiency is secondary to pituitary failure (atrophy, necrosis, tumor), mineralocorticoid production (controlled by the reninangiotensin system) persists and hyperkalemia is not present. Furthermore, if ACTH is not elevated, skin pigmentary changes are not encountered. Autoimmune destruction of the adrenals is the most common cause of Addison's disease in the United States (accounting for about 80% of spontaneous cases). Tuberculosis was formerly a leading cause of Addison's disease. The association is now relatively rare in the United States but common where tuberculosis is more prevalent. The symptoms may include weakness and fatigability, weight loss, myalgias, arthralgias, fever, anorexia, nausea and vomiting, anxiety, and mental irritability. Some of these symptoms may be due to high serum levels of IL-6. Pigmentary changes consist of diffuse tanning over nonexposed as well as exposed parts or multiple freckles; hyperpigmentation is especially prominent over the knuckles, elbows, knees, and posterior neck and in palmar creases and nail beds. Nipples and areolas tend to darken. The skin in pressure areas such as the belt or brassiere lines and the buttocks also darkens. New scars are pigmented. Some patients have associated vitiligo (10%). Emotional changes are common. Hypoglycemia, when present, may worsen the patient's weakness and mental functioning, rarely leading to coma. Manifestations of other autoimmune disease (see above) may be present. Patients tend to be hypotensive and orthostatic; about 90% have systolic blood pressures under 110 mm Hg; blood pressure over 130 MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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ENARM 11ª PARTE by JD-MD mm Hg is rare. Other findings may include a small heart, hyperplasia of lymphoid tissues, and scant axillary and pubic hair (especially in women). The white count usually shows moderate neutropenia, lymphocytosis, and a total eosinophil count over 300/mcL. Among patients with chronic Addison's disease, the serum sodium is usually low (90%) while the potassium is elevated (65%). Patients with diarrhea may not be hyperkalemic. Fasting blood glucose may be low. Hypercalcemia may be present. Young men with idiopathic Addison's disease are screened for adrenoleukodystrophy by determining plasma very long-chain fatty acid levels; affected patients have high levels. Replacement therapy should include a combination of glucocorticoids and mineralocorticoids. In mild cases, hydrocortisone alone may be adequate. Hydrocortisone is the drug of choice. Most addisonian patients are well maintained on 15-25 mg of hydrocortisone orally daily in two divided doses, two-thirds in the morning and one-third in the late afternoon or early evening. Some patients respond better to prednisone in a dosage of about 2-3 mg in the morning and 1-2 mg in the evening. Adjustments in dosage are made according to the clinical response. A proper dose usually results in a normal differential white count. Many patients, however, do not obtain sufficient salt-retaining effect and require fludrocortisone supplementation or extra dietary salt. Fludrocortisone acetate has a potent sodium-retaining effect. The dosage is 0.05-0.3 mg orally daily or every other day. In the presence of postural hypotension, hyponatremia, or hyperkalemia, the dosage is increased. Similarly, in patients with fatigue, elevated plasma renin activity indicates the need for a higher replacement dose of fludrocortisone. If edema, hypokalemia, or hypertension ensues, the dose is decreased. DHEA is given to some women with adrenal insufficiency. Women taking DHEA 50 mg orally each morning have experienced an improvement in their overall sense of well-being, mood, and sexuality. Because over-the-counter preparations of DHEA have variable potencies, it is best to have the pharmacy formulate this with pharmaceutical-grade DHEA. 1081.- Segundo enunciado: estudio para apoyar el diagnóstico: a) b) c) d) e)

Determinación de TSH Determinación de ácido vanilmandelico Determinación de cortisol en el plasma Determinación de renina Prueba de dexametasona

Low plasma cortisol (< 3 mcg/dL) at 8 AM is diagnostic, especially if accompanied by simultaneous elevation of the plasma ACTH level (usually > 200 pg/mL). The diagnosis is made by a simplified cosyntropin stimulation test, which is performed as follows: (1) Synthetic ACTH1-24 (cosyntropin), 0.25 mg, is given parenterally. (2) Serum is obtained for cortisol between 30 and 60 minutes after cosyntropin is administered. Normally, serum cortisol rises to at least 20 mcg/dL. For patients receiving glucocorticoid treatment, hydrocortisone must not be given for at least 8 hours before the test. Other glucocorticoids (eg, prednisone, dexamethasone) do not interfere with specific assays for cortisol. Serum DHEA levels are under 1000 ng/mL in 100% of patients with Addison's disease and a serum DHEA above 1000 ng/mL excludes the diagnosis However, serum DHEA levels below 1000 ng/mL are not helpful, since about 15% of the general population have such low DHEA levels, particularly children and elderly individuals. Antiadrenal antibodies are found in the serum in about 50% of cases of autoimmune Addison's disease. Antibodies to thyroid (45%) and other tissues may be present. Elevated plasma renin activity indicates the presence of depleted intravascular volume and the need for higher doses of fludrocortisone replacement. 1082.- Tratamiento urgente de la crisis corticosuprarrenal: MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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ENARM 11ª PARTE by JD-MD

a) b) c) d) e)

Reposición de líquidos y ACTH Glucanato de calcio y aldosterona Reposición de líquidos y vasopresina Solución mixta y somatostatina Solución salina e hidrocortisona

Acute adrenal insufficiency is an emergency caused by insufficient cortisol. Crisis may occur in the course of chronic treated insufficiency, or it may be the presenting manifestation of adrenal insufficiency. Acute adrenal crisis is more commonly seen in primary adrenal insufficiency (Addison's disease) than in disorders of the pituitary gland causing secondary adrenocortical hypofunction. Adrenal crisis may occur in the following situations: (1) following stress, eg, trauma, surgery, infection, or prolonged fasting in a patient with latent insufficiency; (2) following sudden withdrawal of adrenocortical hormone in a patient with chronic insufficiency or in a patient with temporary insufficiency due to suppression by exogenous glucocorticoids or megestrol; (3) following bilateral adrenalectomy or removal of a functioning adrenal tumor that had suppressed the other adrenal; (4) following sudden destruction of the pituitary gland (pituitary necrosis), or when thyroid is given to a patient with hypoadrenalism; and (5) following injury to both adrenals by trauma, hemorrhage, anticoagulant therapy, thrombosis, infection, or, rarely, metastatic carcinoma. The patient complains of headache, lassitude, nausea and vomiting, abdominal pain, and often diarrhea. Confusion or coma may be present. Fever may be 40.6°C or more. The blood pressure is low. Patients with preexisting type 1 diabetes may present with recurrent hypoglycemia and reduced insulin requirements. Other signs may include cyanosis, dehydration, skin hyperpigmentation, and sparse axillary hair (if hypogonadism is also present). Meningococcemia may be associated with purpura and adrenal insufficiency secondary to adrenal infarction (Waterhouse-Friderichsen syndrome). The eosinophil count may be high. Hyponatremia or hyperkalemia (or both) are usually present. Hypoglycemia is frequent. Hypercalcemia may be present. Blood, sputum, or urine culture may be positive if bacterial infection is the precipitating cause of the crisis. The diagnosis is made by a simplified cosyntropin stimulation test, which is performed as follows: (1) Synthetic ACTH1-24 (cosyntropin), 0.25 mg, is given parenterally. (2) Serum is obtained for cortisol between 30 and 60 minutes after cosyntropin is administered. Normally, serum cortisol rises to at least 20 mcg/dL. For patients receiving glucocorticoid treatment, hydrocortisone must not be given for at least 8 hours before the test. Other glucocorticoids (eg, prednisone, dexamethasone) do not interfere with specific assays for cortisol. Plasma ACTH is markedly elevated if the patient has primary adrenal disease (generally > 200 pg/mL). If the diagnosis is suspected, draw a blood sample for cortisol determination and treat with hydrocortisone, 100-300 mg intravenously, and saline immediately, without waiting for the results. Thereafter, give hydrocortisone phosphate or hydrocortisone sodium succinate, 100 mg intravenously immediately, and continue intravenous infusions of 50-100 mg every 6 hours for the first day. Give the same amount every 8 hours on the second day and then adjust the dosage in view of the clinical picture. Since bacterial infection frequently precipitates acute adrenal crisis, broad-spectrum antibiotics should be administered empirically while waiting for the results of initial cultures. Hypoglycemia should be vigorously treated while serum electrolytes, BUN, and creatinine are monitored. When the patient is able to take food by mouth, give oral hydrocortisone, 10-20 mg every 6 hours, and reduce dosage to maintenance levels as needed. Most patients ultimately require hydrocortisone twice daily (AM, 10-20 mg; PM, 5-10 mg). Mineralocorticoid therapy is not needed when large amounts of hydrocortisone are being given, but as the dose is reduced it is usually necessary to add fludrocortisone acetate, 0.05-0.2 mg daily. Some patients never require fludrocortisone or become edematous at doses of more than 0.05 mg once or twice MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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ENARM 11ª PARTE by JD-MD weekly. Once the crisis has passed, the patient must be investigated to assess the degree of permanent adrenal insufficiency and to establish the cause if possible. 1083.- Caso clínico seriado: Un recien nacido primogenito de 3 semanas de vida extrauterina, presenta vómitos de contenido gástrico posprandial inmediato. Primer enunciado: El diagnóstico más probable es: a) b) c) d) e)

Enfermedad por reflujo Atresia intestinal Malrotación intestinal Hipertrofia congenita del piloro Membrana duodenal

The cause of postnatal pyloric circular muscle hypertrophy leading to gastric outlet obstruction is not known. The incidence is 1–8:1000 births, with a 4:1 male predominance and a positive family history present in 13% of patients. Recent studies suggest that erythromycin therapy may be associated with development of pyloric stenosis in infants under 30 days. Vomiting usually begins between ages 2 and 4 weeks and rapidly becomes projectile after every feeding; it starts at birth in about 10% of cases. Onset of symptoms may be delayed in premature infants. The vomitus is rarely bilious but may be blood-streaked. The infant is hungry and nurses avidly. Constipation, dehydration, weight loss, fretfulness, and finally apathy occur. The upper abdomen may be distended after feeding, and prominent gastric peristaltic waves from left to right may be seen. An olive-sized mass can be felt on deep palpation in the right upper abdomen, especially after the child has vomited. Hypochloremic alkalosis with potassium depletion occurs. Hemoconcentration is reflected by elevated hemoglobin and hematocrit values. Elevated unconjugated bilirubin occurs in 2–5% of cases. 1084.- Segundo enunciado: Para confirmar el diagnóstico se debe practicar: a) b) c) d) e)

Endoscopia Serie esofagogastroduodenal Radiografía simple de abdomen Colon por enema Ultrasonido

An upper gastrointestinal series reveals delay in gastric emptying and an elongated narrowed pyloric channel with a double tract of barium. Many infants have some delay in gastric emptying due to pylorospasm. This by itself is insufficient to make a diagnosis of pyloric stenosis. The enlarged pyloric muscle causes characteristic semilunar impressions on the gastric antrum. Ultrasonography shows a hypoechoic ring with a hyperdense center. Thickness of circular muscle is greater than 4 mm in pyloric stenosis. 1085.- Tercer enunciado: El tratamiento quirugico más adecuado para este paciente es: a) b) c) d) e)

Funduplicatura de Nissen Piloromiotomia Resección intestinal Colostomia Gastrostomia

Pyloromyotomy is the treatment of choice and consists of incision down to the mucosa along the pyloric length. The procedure can be performed laparoscopically. Prior to MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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ENARM 11ª PARTE by JD-MD surgery, it is imperative to repair hydration and electrolyte abnormalities even if it takes 24–48 hours. The outlook is excellent following surgery. Patients often vomit postoperatively as a consequence of gastritis, esophagitis, or associated gastroesophageal reflux. The postoperative barium x-ray remains abnormal despite relief of symptoms. 1086.- Cual es el mejor tratamiento en la brucelosis humana: a) b) c) d) e)

Ciprofloxacino Rifampicina Tetraciclina Tetraciclina + estreptomicina TMP-SMX

Brucellosis (also called undulant fever, Mediterranean fever, Malta fever) is an infection that causes abortion in domestic animals. It is caused by one of six species of Brucella coccobacilli. It may occasionally be transmitted to humans, in whom the disease could be acute or chronic with ongoing fever and constitutional symptoms without localized findings. After a 2- to 8-week incubation period, affected patients present with a spectrum of disease that varies from an asymptomatic form to a severe illness with bacteremia. Affected patients typically present with fever, sweats, headaches, malaise, and weight loss. If undiagnosed, these symptoms may persist for months to a year. When symptoms last for more than 12 months without any localization, the disease is classified as chronic. Physical examination, though normal in most cases, may reveal bilateral diffuse lymphadenopathy, splenomegaly, and hepatomegaly in 20%-30% of patients. In the localized form, the infection may affect virtually any organ system. The osteoarticular, gastrointestinal, genitourinary, and cardiovascular are among the more common affected systems. These forms have signs and symptoms related to the affected organ system. An infectious discitis with adjacent vertebral bony osteomyelitis typically in the lumbar area, is the most common manifestation of localized osteoarticular disease. Sacroilitis is also characteristic of the musculoskeletal form of the infection. Infective endocarditis occurs in < 2% of brucellosis cases. Patients with chronic brucellosis may have long periods of no symptoms followed by the intermittent recurrence of fever, chills, myalgias, and nonspecific symptoms. This form of relapsing brucellosis may persist for decades and is often refractory to antimicrobial therapy and is frequently associated with multiple or large calcific lesions in the liver and spleen. Many other common illnesses can mimic the most common clinical presentation of brucellosis. Treatment of acute brucellosis first choice: Adults: Doxycycline, 100 mg orally twice daily, PLUS rifampin, 600-900 mg orally daily for 4-6 weeks Children: Doxycycline,2 2 mg/kg orally twice daily, PLUS rifampin, 15 mg/kg orally daily for 4-6 weeks Treatment of acute brucellosis second choice: Adults: Doxycycline, 100 mg orally twice daily for 4-6 weeks, PLUS streptomycin, 1 g IM daily for the first 15 days Children: TMP/SMX,3 2.5 mg/kg orally of TMP component 4 times daily, PLUS rifampin, 15 mg/kg orally daily for 4-6 weeks Treatment of Endocarditis-Meningitis-Spondylitis-Localized Forms first choice Adults: Doxycycline, 100 mg orally twice daily, PLUS rifampin, 600-900 mg orally daily for 6 mo, PLUS streptomycin, 1 g IM daily for the first 2-3 weeks Children: Doxycycline,2 2 mg/kg orally twice daily, PLUS rifampin, 15 mg/kg orally daily for 6 mo, PLUS streptomycin, 10 mg/kg IM twice daily for the first 7-14 days Treatment of Endocarditis-Meningitis-Spondylitis-Localized Forms second choice MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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ENARM 11ª PARTE by JD-MD TMP/SMX,3 2.5 mg/kg orally of TMP component 4 times daily, PLUS rifampin, 15 mg/kg orally daily for 6 mo, PLUS gentamicin, 1.5-2 mg/kg (IV or IM) in three daily doses for the the first 7-14 days 1087.- Lugar donde actua la paratohormona: a) b) c) d) e)

Medula ósea, eritrocitos y plaquetas Sistema nervioso central, tejido musclar y plaquetas Tejido renal, tejido óseo y mucosa intestinal Músculo cardíaco, cerebro y músculo estriado Eritrocito, tejido hepatico y estomago

1088.- En la actualidad se ha abandonado la monoterapia en el tratamiento de la brucelosis, indique el tratamiento deprimera linea combinado: a) b) c) d) e)

Ampicilina + amikacina por 2 semanas TMP-SMX por 2 semanas Doxiciclina + estreptomicina por 2 semanas Doxiciclina + rifampicina durante 4 semanas a 8 semanas Rifampicina + ampicilina por 3 semanas

Treatment of acute brucellosis first choice: Adults: Doxycycline, 100 mg orally twice daily, PLUS rifampin, 600-900 mg orally daily for 4-6 weeks Children: Doxycycline,2 2 mg/kg orally twice daily, PLUS rifampin, 15 mg/kg orally daily for 4-6 weeks Treatment of acute brucellosis second choice: Adults: Doxycycline, 100 mg orally twice daily for 4-6 weeks, PLUS streptomycin, 1 g IM daily for the first 15 days Children: TMP/SMX,3 2.5 mg/kg orally of TMP component 4 times daily, PLUS rifampin, 15 mg/kg orally daily for 4-6 weeks 1089.- El antimicrobiano más útil para el tratamiento de la disenteria por Shigella es: a) b) c) d) e)

Amikacina Trimetoprim-sulfametoxazol Gentamicina Eritromicina Cefutoxima

Enteritis caused by Shigella species may be watery (Shigella sonnei, Shigella boydii) or dysenteric (Shigella dysenteriae, Shigella flexneri). Risks include ingestion of fecally contaminated food or water and contact with infected individuals. Definitive diagnosis requires microbiologic isolation and identification of Shigella species or molecular evidence of infection. Early in the course of disease, when bacteria are present in the small intestine, patients develop acute, watery diarrhea; fever; and abdominal pain. Patients may become toxemic and fever may reach as high as 104 °F. Later in the course of disease, the primary site of infection is the colon. In this phase, fever continues, but is usually less pronounced. The pain that is present is usually in the lower abdominal quadrants. Stools become dysenteric, consisting of a mixture of neutrophils, blood, mucus, and debris. Frequent, small-volume or fractionated stools may occur, and tenesmus is often present. Patients experience pain upon rectal examination. Colonoscopy discloses hyperemic and friable-to-ulcerated colonic mucosa. Patients with acute diarrhea, which may be watery to dysenteric; fever; MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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ENARM 11ª PARTE by JD-MD abdominal pain; and systemic symptomatology/toxemia may have shigellosis. A history of exposure to individuals with shigellosis, travel to endemic areas, and exposure to a high-risk population, such as persons in a custodial-care facility, should raise the index of suspicion. The presence of leukocytes in the stool, although supportive, is by no means definitive for shigellosis. Fecal leukocytes may be present in the stools of patients with other bacterial enteritides, amoebic dysentery, pseudomembranous colitis, and noninfectious disease, such as inflammatory-bowel disease. The definitive diagnosis requires the microbiologic identification of a Shigella species. Shigellae are particularly susceptible to some environmental changes, and they die rapidly in transport. Therefore, it is imperative to rapidly transport the stool of patients suspected of having shigellosis to the laboratory. This is especially important for patients in the latter stages of disease, in whom the number of shigellae in the stool are relatively few. Fluid and electrolyte replacements are necessary for patients with dehydration. In most instances, this is readily accomplished by oral rehydration. Unlike in many other bacterial enteritides, antibiotic therapy is important in the treatment of shigellosis. Antibiotic therapy limits the clinical course of the disease, may decrease the likelihood of intestinal complications, and decreases the fecal excretion of viable pathogenic organisms, which in turn diminishes transmission. Fluoroquinolones are the treatment of choice for adults. TMP/SMX is the treatment of choice for children. Alternatives are ampicillin, chloramphenicol, and nalidixic acid. In areas of known resistance to TMP/SMX, such as parts of Southeast Asia, Africa, and South America, quinolones should be used for adults, and one of the above mentioned alternatives for children with shigellosis. When available, the antimicrobialsusceptibility profile should guide therapy. Antimotility agents, such as diphenoxylate, should not be used. The inhibition of diarrhea increases the contact between the intestinal mucosa and the pathogenic organisms and their toxins and may cause more fulminant disease. 1090.- Pneumocystis carinii es un patogeno oportunista colocado dentro del reino de los hongos, se considera que el fármaco más adecuado para atacar todas las formas de esta micosis es: a) b) c) d) e)

Miconazol TMP-SMX Praziquantel Amikacina Anfotericina B

Pneumocystis carinii, when examined using molecular techniques, most closely resembles a fungus. Stains of either bronchoalveolar-lavage (BAL) or transbronchialbiopsy samples yield a diagnosis in > 90% of patients and should be considered the gold standard in diagnosis. BAL with transbronchial biopsy increases diagnostic yield to ~ 100%. P. carinii has not yet been cultured in vitro. Polymerase chain reaction (PCR) (especially on sputum) increases sensitivity but reduces specificity. The prophylactic use of aerosolized pentamidine reduces the sensitivity of sputum and bronchoscopic samples. The primary treatment of moderate to severe pulmonary or extrapulmonary infection caused by P carinii remains the combination of trimethoprim (TMP) and sulfamethoxazole (SMX), either orally or intravenously (IV). Several medications (atovaquone, trimetrexate, and pentamidine) and combination regimens (dapsone + TMP and clindamycin + primaquine) probably afford nearly equal efficacy to TMP-SMX in mild to moderate PCP and may be better tolerated in specific populations of patients.

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ENARM 11ª PARTE by JD-MD 1091.- En la enfermedad de Anisen debida a Micobacterium leprae, un bacilo intracelular obligado acidorresistente, se recomienda como tratamiento antimicrobiano: a) b) c) d) e)

Dapsona + rifampicina Isoniazida + etambutol Ciprofloxacina + etambutol Isonicida + ciprofloxacina Ceftrixona + amikacina

The manifestations of leprosy involve the skin, upper respiratory system, peripheral nerves, and, in men, testes. The peripheral neuropathy that is seen in leprosy results in impaired sensation of fine touch, temperature, and pain, whereas proprioception and vibratory sensation are intact. Such loss of sensation leads to recurrent trauma and ulceration in the extremities. For example, loss of sensation in the feet can lead to chronic nonhealing ulcers, especially at the metatarsal heads. Large nerve trunks may also be affected. A common nerve trunk that is affected in leprosy is the ulnar nerve at the elbow, which results in clawing of the fourth and fifth digits of the hand, dorsal interosseus muscle atrophy, and loss of sensation in the hand along the ulnar nerve distribution. The lepromatous or multibacillary form of leprosy is characterized by symmetric skin nodules, plaques, and thickened dermis. Usually, the ear lobes and extremities are affected. Diffuse lepromatosis is seen usually in patients from Mexico, who show areas of diffuse dermal infiltration and no focal lesions. Untreated, lepromatous leprosy results in a high level of continuous bacteremia. Peripheral neuropathy is symmetric and generalized. There is a characteristic deformity associated with this type of leprosy, "saddle-nose deformity," which occurs because of infiltration of the upper respiratory system and nasal cartilage. Other upper respiratory system effects include chronic nasal congestion and epistaxis. The tuberculoid, or paucibacillary, form of leprosy is characterized by one or few hypopigmented macules, which are anesthetic and variable in size. These macules have distinct and elevated borders. Peripheral neuropathy in this form of leprosy is usually asymmetric and affects large nerves. Neural leprosy is characterized by functional impairment of large nerve trunks without skin lesions. The upper respiratory system is not involved. M leprae Infection. Leprosy generally requires a long duration of treatment, and compliance is a major problem. Lepromatous leprosy requires a longer treatment time course than tuberculoid leprosy because of the greater number of organisms involved. Currently, the recommended treatment is dapsone and rifampin for 6 months for tuberculoid leprosy. Dapsone alone is not recommended because of reports of emerging resistance. For lepromatous leprosy, dapsone with rifampin or clofazimine for 24 months is recommended. Nonetheless, there have been reports of relapses even after such long courses of treatment. Other agents such as ethionamide, prothionamide, the aminoglycosides, minocycline, clarithromycin, and the fluoroquinolones may also prove to be beneficial. 1092.- El tratamiento de elección para la infección gonococcica no complicada del cervix y la uretra es: a) b) c) d) e)

Ciprofloxacina TMP-SMX Ceftriaxona Amoxicilina Neomicina

Transmission associated with unprotected sex. Purulent urethral discharge, dysuria in men. Vaginal discharge, dysuria, intermenstrual bleeding in women. Dermatitis-arthritis MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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ENARM 11ª PARTE by JD-MD syndrome with disseminated infection. Gram-negative diplococci inside neutrophils on stained smears of urethral, cervical, skin, or joint material. Fastidious organism requires special media and growth conditions. DNA amplification methods (PCR, LCR) offer improved sensitivity and specificity. Genital infection with N gonorrhoeae most often presents as urethritis in men and cervicitis in women. Ceftriaxone in a single dose is the treatment of choice for uncomplicated gonorrhea at all sites. Ciprofloxacin has the advantages of a single oral dose, less expense than ceftriaxone, and effectiveness in patients who are intolerant of cephalosporins; however, resistance has been observed with ciprofloxacin, and it is not active against Treponema pallidum. Complicated infections or disseminated gonococcal infections, such as arthritis, perihepatitis, or bacteremia resulting in petecchial or pustular skin lesions, require a higher dose of antibiotics than uncomplicated gonorrhea infections and a longer duration of therapy. These regimens should be continued for 24-48 h after clinical improvement is noted (ie, they become afebrile, or joint erythema or skin lesions improve) and then switched to an oral regimen for a total of 7 d. Patients with gonococcal meningitis or endocarditis require higher doses and longer duration of therapy. Meningitis is treated with ceftriaxone for 14 d. Endocarditis should be treated for = 4 wk. Concurrent infection with C trachomatis is estimated to occur in 40% of those infected with N gonorrhoeae. Therefore doxycycline or azithromycin must be added to the antigonococcal regimen. In pregnant women, for whom doxycycline is contraindicated, an erythromycin base can be used. If erythromycin cannot be tolerated, amoxicillin for 7-10 d is indicated. Antibiotic resistance has been a major concern, as penicillin resistance has spread and, more recently, fluoroquinolone resistance has been increasingly reported. Beta-lactams remain the drugs of choice in most instances. Antibiotic resistance occurs by one or more mechanisms, including chromosomal mutations leading to decreased penicillin-binding-protein affinity, decreased outer membrane permeability, or beta-lactamase production. 1093.- Paciente de 35 años, 12 horas después de la ingesta de alimentos mal preparados presenta nausea, vomitos y dolor abdominal. Al examen físico se encuentra ptosis bilateral, midriasis con reacción lenta y paralisis flacida aguda. Entre las medidas urgentes que se deben efectuar para tratar a este paciente, la primordial consiste en: a) b) c) d) e)

Antitoxina botulinica por vía intravenosa Intubación orotraqueal y oxigeno al 100% Traqueostomia electiva temprana Antiespasmodicos y antihelminticos Dosis altas de penicilina sodica por via intravenosa

This clinical syndrome is caused by the neurotoxin of C botulinum. There are seven types (A-G) of neurotoxin, all of which inhibit the release of acetylcholine at the level of peripheral neuromuscular junctions. In the majority of cases, the disease is acquired by ingestion of preformed toxin in home-canned vegetables, fruits, and fish. In Japan, the former Soviet Union, Scandinavia, and the Great Lakes region of the United States, type E toxin causes disease in people who consume raw or lightly smoked fish. There are four categories of botulism: Food borne (most common), Wound botulism caused by the absorption of toxin from a wound contaminated by C botulinum (the rarest form), Infant botulism resulting from in vivo elaboration of toxin by colonizing organisms in the bowel, Undetermined, which refers to cases that occur in individuals > 1 year old in whom no food or wound source is identified. Symptoms and signs arise 12-36 h after food ingestion and consist of acute onset and progressive flaccid paralysis involving the facial musculature and the cranial nerves bilaterally, then descending symmetrically to the pharynx, thoracic region, and the upper and lower extremities. This evolves into respiratory failure without impairment of consciousness. MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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ENARM 11ª PARTE by JD-MD Fever is classically absent. In cases of infant botulism, which is found in children 6 days to 11 months old, constipation is the initial symptom, followed by lethargy, feeding difficulties, altered cry, floppiness, ophthalmoplegia, and respiratory failure. Treatment is mainly supportive; antitoxin made from equine serum can be used. In the United States, it is obtained through state health departments or the Centers for Disease Control. The standard dose is one vial intravenously and one vial intermittently. It may be repeated every 4 h in severe progressive cases. Clinical trials evaluating its efficacy are lacking. Full recovery takes from 3 months to 1 year. Risk of death ranges from 4 to 25%, depending on the promptness with which the diagnosis is made. 1094.- Germen causal frecuente de la otitis media aguda: a) b) c) d) e)

Pseudomona sp. Streptococcus pneumoniae Streptococcus pyogenes Klebsiella sp. Haemophylis influenzae

Acute otitis media is a bacterial infection of the mucosally lined air-containing spaces of the temporal bone. Purulent material forms not only within the middle ear cleft but also within the mastoid air cells and petrous apex when they are pneumatized. Acute otitis media is usually precipitated by a viral upper respiratory tract infection that causes auditory tube edema. This results in accumulation of fluid and mucus, which becomes secondarily infected by bacteria. The most common pathogens both in adults and in children are Streptococcus pneumoniae, Haemophilus influenzae, and Streptococcus pyogenes. Acute otitis media is most common in infants and children, although it may occur at any age. Presenting symptoms and signs include otalgia, aural pressure, decreased hearing, and often fever. The typical physical findings are erythema and decreased mobility of the tympanic membrane. Occasionally, bullae will be seen on the tympanic membrane. Although it is taught that this represents infection with Mycoplasma pneumoniae, most cases involve more common pathogens. Rarely, when middle ear empyema is severe, the tympanic membrane can be seen to bulge outward. In such cases, tympanic membrane rupture is imminent. Rupture is accompanied by a sudden decrease in pain, followed by the onset of otorrhea. With appropriate therapy, spontaneous healing of the tympanic membrane occurs in most cases. When perforation persists, chronic otitis media frequently evolves. Mastoid tenderness often accompanies acute otitis media and is due to the presence of pus within the mastoid air cells. This alone does not indicate suppurative (surgical) mastoiditis. The treatment of acute otitis media is specific antibiotic therapy, often combined with nasal decongestants. The first-choice antibiotic treatment is either amoxicillin (20-40 mg/kg/d) or erythromycin (50 mg/kg/d) plus sulfonamide (150 mg/kg/d) for 10 days. Alternatives useful in resistant cases are cefaclor (20-40 mg/kg/d) or amoxicillin-clavulanate (20-40 mg/kg/d) combinations. Tympanocentesis for bacterial (aerobic and anaerobic) and fungal culture may be performed by any experienced physician. A 20-gauge spinal needle bent 90 degrees to the hub attached to a 3-mL syringe is inserted through the inferior portion of the tympanic membrane. Interposition of a pliable connecting tube between the needle and syringe permits an assistant to aspirate without inducing movement of the needle. Tympanocentesis is useful for otitis media in immunocompromised patients and when infection persists or recurs despite multiple courses of antibiotics. Surgical drainage of the middle ear (myringotomy) is reserved for patients with severe otalgia or when complications of otitis (eg, mastoiditis, meningitis) have occurred. Recurrent acute otitis media may be managed with long-term antibiotic prophylaxis. Single daily doses of sulfamethoxazole (500 mg) or amoxicillin (250 or 500 mg) are given over a period of 1-3 months. Failure of this regimen to control infection is an indication for insertion of ventilating tubes. MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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ENARM 11ª PARTE by JD-MD

1095.- Para precisar la presencia de diverticulitis se debe realizar: a) b) c) d) e)

Ultrasonografia Rectosigmoidoscopia Tomografia computarizada Colonoscopia Colon por enema

Colonic diverticulosis increases with age, ranging from 5% in those under age 40, to 30% at age 60, to more than 50% over age 80 years in Western societies. In contrast, it is very uncommon in developing countries with much lower life expectancies. Most are asymptomatic, discovered incidentally at endoscopy or on barium enema. Complications in one-third include lower gastrointestinal bleeding and diverticulitis. Colonic diverticula may vary in size from a few millimeters to several centimeters and in number from one to several dozen. Almost all patients with diverticulosis have involvement in the sigmoid colon; however, only 15% have proximal colonic disease. In most patients, diverticulosis is believed to arise after many years of a diet deficient in fiber. The undistended, contracted segments of colon have higher intraluminal pressures. Over time, the contracted colonic musculature, working against greater pressures to move small, hard stools, develops hypertrophy, thickening, rigidity, and fibrosis. Diverticula may develop more commonly in the sigmoid because intraluminal pressures are highest in this region. The extent to which abnormal motility and hereditary factors contribute to diverticular disease is unknown. Patients with diffuse diverticulosis may have an inherent weakness in the colonic wall. Patients with abnormal connective tissue are also disposed to development of diverticulosis, including Ehlers-Danlos syndrome, Marfan's syndrome, and scleroderma. Perforation of a colonic diverticulum results in an intra-abdominal infection that may vary from microperforation (most common) with localized paracolic inflammation to macroperforation with either abscess or generalized peritonitis. Thus, there is a range from mild to severe disease. Most patients with localized inflammation or infection report mild to moderate aching abdominal pain, usually in the left lower quadrant. Constipation or loose stools may be present. Nausea and vomiting are frequent. In many cases, symptoms are so mild that the patient may not seek medical attention until several days after onset. Physical findings include a low-grade fever, left lower quadrant tenderness, and a palpable mass. Stool occult blood is common, but hematochezia is rare. Leukocytosis is mild to moderate. Patients with free perforation present with a more dramatic picture of generalized abdominal pain and peritoneal signs. Plain abdominal films are obtained in all patients to look for evidence of free abdominal air (signifying free perforation), ileus, and small or large bowel obstruction. In patients with mild symptoms and a presumptive diagnosis of diverticulitis, empiric medical therapy is started without further imaging in the acute phase. Patients who respond to acute medical management should undergo complete colonic evaluation with colonoscopy or barium enema after resolution of clinical symptoms to corroborate the diagnosis or exclude other disorders such as colonic neoplasms. In patients who do not improve rapidly after 2-4 days of empiric therapy and in those with severe disease, CT scan of the abdomen is obtained to look for evidence of diverticulitis, including colonic diverticula and wall thickening, pericolic fat infiltration, abscess formation, or extraluminal air or contrast. Endoscopy and barium enema are contraindicated during the initial stages of an acute attack because of the risk of free perforation, though sigmoidoscopy with minimal air insufflation is sometimes required to exclude other diagnoses. Most patients can be managed with conservative measures. Patients with mild symptoms and no peritoneal signs may be managed initially as outpatients on a clear liquid diet and broad-spectrum oral antibiotics with anaerobic activity. Reasonable regimens include amoxicillin and clavulanate potassium MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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ENARM 11ª PARTE by JD-MD (875 mg/125 mg) twice daily; or metronidazole, 500 mg three times daily; plus either ciprofloxacin, 500 mg twice daily, or trimethoprim-sulfamethoxazole, 160/800 mg twice daily orally, for 7-10 days or until the patient is afebrile for 3-5 days. Symptomatic improvement usually occurs within 3 days, at which time the diet may be advanced. Patients with increasing pain, fever, or inability to tolerate oral fluids require hospitalization. Patients with severe diverticulitis (high fevers, leukocytosis, or peritoneal signs) and patients who are elderly or immunosuppressed or who have serious comorbid disease require hospitalization acutely. Patients should be given nothing by mouth and should receive intravenous fluids. If ileus is present, a nasogastric tube should be placed. Intravenous antibiotics should be given to cover anaerobic and gram-negative bacteria. Single-agent therapy with either a secondgeneration cephalosporin (eg, cefoxitin), piperacillin-tazobactam, or ticarcillin clavulanate appears to be as effective as combination therapy (eg, metronidazole or clindamycin plus an aminoglycoside or third-generation cephalosporin [eg, ceftazidime, cefotaxime]). Symptomatic improvement should be evident within 2-3 days. The antibiotics should be continued for 7-10 days, after which time elective evaluation with colonoscopy or barium enema should be performed. Approximately 20-30% of patients with diverticulitis will require surgical management. Surgical consultation should be obtained on all patients with severe disease or those who fail to improve after 72 hours of medical management. Indications for emergent surgical management include free peritonitis and large abscesses. Patients with fistulas or colonic obstruction due to chronic disease will require elective surgery. Patients with a localized abdominal abscess can be treated acutely with a percutaneous catheter drain placed by an interventional radiologist. This permits control of the infection and resolution of the immediate infectious inflammatory process. In this manner, a subsequent single-stage elective surgical operation can be performed in which the diseased segment of colon is removed and primary colonic anastomosis performed. In patients in whom catheter drainage is not possible or helpful or in cases requiring emergency surgery, it is necessary to perform surgery in two stages. In the first stage, the diseased colon is resected and the proximal colon brought out to form a temporary colostomy. The distal colonic stump is either closed (forming a Hartmann pouch) or exteriorized as a mucous fistula. Weeks later, after inflammation and infection have completely subsided, the colon can be reconnected electively. 1096.- El tratamiento farmacologico complementario en caso de cólera en el adulto es: a) b) c) d) e)

Trimetoprim con sulfametoxazol Ciproxina Ceftrixona Rifampicina Doxiciclina

Cholera is a fulminant diarrheal disease caused by V cholerae. Patients with cholera develop frequent, watery stools, which may reach volumes =1 L/h. If these patients are untreated, they will develop rapid dehydration and electrolyte abnormalities, which may result in death within hours from the onset of disease. Therefore cholera is a medical emergency. V cholerae is noninvasive and produces diarrhea by the elaboration of a potent enterotoxin. This enterotoxin consists of two subunits that have been well characterized. The circular, pentameric B-subunit binds monosialosyl ganglioside residues on the surface of the intestinal epithelial cell and introduces the enzymatic A-subunit into the cytoplasm. The A-subunit functions as an adenosine diphosphate (ADP) ribosylase and transfers an ADP-ribose moiety from cytoplasmic nicotinamide adenine dinucleotide (NAD) to the cell-membrane-associated adenylate cyclase. ADP-ribosylation renders adenylate cyclase unresponsive to feedback MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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ENARM 11ª PARTE by JD-MD inhibition. The result is dramatically increased intracellular cyclic adenosine monophosphate (cAMP) levels. Elevated cytoplasmic cAMP levels cause massive fluid and electrolyte transit into the bowel lumen, resulting in the characteristic "rice water" stool of cholera. Patients with cholera initially develop increased peristalsis, a feeling of fullness, and occasionally vomiting. Diarrhea develops rapidly and soon becomes watery. Abdominal pain and high fever are usually minimal or absent and distinctly disproportionate to the amount of diarrhea. Fever, when present, is usually caused by dehydration. Electrolyte abnormalities, from voluminous diarrhea, may manifest as muscle weakness, intestinal ileus, or even cardiac dysrhythmia. The clinical manifestations of infection and the possibility of severe complications correlate with the patient's hydration and electrolyte abnormalities. Mental status changes secondary to hypoglycemia may also occur. Without urgent fluid and electrolyte replacement therapy, hypovolemic shock and death may occur rapidly. Primary therapy of cholera consists of fluid and electrolyte replacement. Published guidelines for fluid and electrolyte replacement in cholera are available. Either a citrate (10 mmol/L)- or bicarbonate (30 mmol/L)-based solution may be used for oral rehydration. These should contain sodium (90 mmol/L), potassium (20 mmol/L), chloride (80 mmol/L), and glucose (111 mmol/L). The glucose is actively transported into enterocytes. This osmotically drives water from the lumen and into the body. In developing countries, the water residua from boiled rice may be used for rehydration. This is an inexpensive and excellent source of oligosaccharides, which like glucose, aid in the osmotic shifting of water from the lumen to the body. Intravenous fluid replacement therapy is necessary for patients with severe dehydration (=10% of their body weight) and acidosis (pH 2 months old); TMP, 3-6 mg, + SMX, 15-30 mg/kg every 12 h for 5 d Adults:Ampicillin, 250 mg orally or IV every 6 h for 5 d Penicillin Allergic Children: TMP/SMX OR Furazolidone (liquid = 3.33 mg/ml): >5 years old, 7.5-15 ml; 1-4 years old, 5.0-7.5 ml; 1 month-1 year old, 2.5-5.0 ml orally every 6 h for 5 d Adults:Tetracycline OR TMP/SMX2 orally or IV: TMP, 160 mg, + SMX, 800 mg orally or IV every 12 h for 5 d OR Furazolidone, 100 mg orally every 6 h for 5 d 1097.- Paciente masculino de 17 años de edad que se presenta con sudoración, palidez, hipertensión arterial, nausea y vomito. El diagnóstico más probable es: a) b) c) d) e)

Glomerulonefritis Feocromocitoma Síndrome nefrótico Insuficiencia suprarrenal Tumor renal MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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ENARM 11ª PARTE by JD-MD Pheochromocytomas are rare, being found in less than 0.3% of hypertensive individuals. The incidence is higher in patients with moderate to severe hypertension. Pheochromocytomas can be lethal unless they are diagnosed and treated appropriately. They typically cause attacks of severe headache (80% of patients), perspiration (70% of patients), and palpitations (60% of patients); other symptoms may include anxiety (50% of patients), a sense of impending doom, or tremor (40% of patients). Vasomotor changes during an attack cause mottled cyanosis and facial pallor; as the attack subsides, facial flushing may occur as a result of reflex vasodilation. Other findings may include tachycardia, precordial or abdominal pain, vomiting, increasing nervousness and irritability, increased appetite, and loss of weight. Anginal attacks may occur. Physical findings usually include hypertension (90% of patients), which may be sustained (20% of patients), sustained with paroxysms (50% of patients), or paroxysmal only (25% of patients). There may be cardiac enlargement and cardiomyopathy, postural tachycardia (change of more than 20 beats/min) and postural hypotension, and mild elevation of basal body temperature. Retinal hemorrhage or cerebrovascular hemorrhage occurs occasionally. Catastrophic hypertensive crisis and fatal cardiac arrhythmias can occur spontaneously or may be triggered by intravenous contrast dye or glucagon injection, needle biopsy of the mass, anesthesia, and surgical procedures. The manifestations of pheochromocytoma are quite varied and mimic other conditions. Some patients are normotensive and asymptomatic. In addition to the above symptoms, some patients can present with psychosis or confusion, seizures, hyperglycemia, bradycardia, hypotension, constipation, paresthesias, or Raynaud's phenomenon. Other patients may have pulmonary edema and heart failure due to cardiomyopathy. Epinephrine secretion may cause episodic tachyarrhythmias, hypotension, or syncope. Some patients may be entirely asymptomatic despite high serum levels of catecholamines. Others may present with abdominal discomfort from a large hemorrhagic pheochromocytoma, or with pain from metastatic disease. In addition to catecholamines and their metabolites, pheochromocytomas secrete a wide range of other peptides that can sometimes cause symptoms of Cushing's syndrome (ACTH), erythrocytosis (erythropoietin), or hypercalcemia (PTHrP). Hypermetabolism is present; thyroid function tests are normal, including serum T4, FT4, T3, and TSH. Hyperglycemia is present in about 35% of patients but is usually mild. Leukocytosis is common. The ESR is sometimes elevated. Plasma renin activity may be increased by catecholamines. Assay of urinary catecholamines and metanephrines (total and fractionated) and creatinine detects most pheochromocytomas, especially when samples are obtained during or immediately following an episodic attack. A 24-hour urine specimen is usually obtained, although an overnight or shorter collection may be used; patients with pheochromocytomas generally have more that 2.2 mcg of total metanephrine per milligram of creatinine, and more than 135 mcg total catecholamines per gram creatinine. Urinary assay for total metanephrines is about 97% sensitive for detecting functioning pheochromocytomas. Urinary assay for vanillylmandelic acid (VMA) is about 89% sensitive and is not usually required. 1098.- El agente coqueluchoide es: a) b) c) d) e)

que

con

mayor

frecuencia

produce

el

síndrome

Streptococo beta-hemolítico Diplococo Pneumoniae Haemophylus influenzae Mycoplasma pneumoniae Bordetella pertussis

Classical pertussis occurs in three clinical stages: catarrhal, paroxysmal, and convalescent. The catarrhal stage is characterized by nonspecific upper respiratory MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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ENARM 11ª PARTE by JD-MD symptoms, including rhinorrhea, mild cough, and low-grade fever. During this stage, which typically lasts 1-2 weeks, the disease is highly communicable. The paroxysmal stage is marked by sudden attacks or paroxysms of severe, repetitive coughing, often culminating with the characteristic whoop (tos coqueluchoide-whooping coughTos espasmódica en la que la primera inspiración ocurre con la glotis semicerrada, produciendo un ruido característico) and frequently followed by vomiting. A marked lymphocytosis usually accompanies this stage of the disease, with lymphocyte counts sometimes exceeding 50,000/mm3 and usually representing 70% or more of total circulating leukocytes. The paroxysmal stage typically lasts 1-4 weeks and can be associated with a variety of complications, including secondary bacterial infections such as pneumonia and otitis media, toxic central nervous system manifestations such as seizures and encephalopathy, and effects of increased intrathoracic and intra-abdominal pressure such as pneumothorax, hernia, and rectal prolapse. The beginning of the convalescent (recovery) stage is marked by a reduction in frequency and intensity of coughing spells. After clinical pertussis, immunity to disease is lifelong. Although most cases of pertussis follow a characteristic course, exceptions exist. In infants < 3 months, the catarrhal stage is usually no longer than a few days, and the paroxysmal and convalescent stages are extremely protracted, with coughing spells that continue throughout the first year of life. In infants < 6 months, apnea is a common manifestation, and the whoop is often absent. Paradoxically, in infants, cough and whoop may become louder and more classic during convalescence, reflecting growth in body mass and increased strength. In immunized children, all three stages are shortened, and in adults, only a protracted cough may be present. Posttussive vomiting is common in pertussis at all ages and is a major clue to the diagnosis in adolescents and adults. With subsequent respiratory illnesses over the next several months, paroxysmal coughing may recur, though not because of recurrence of active Bordetella infection. 1099.- La medida más adecuada para iniciar el tratamiento de la diverticulitis consiste en usar: a) b) c) d) e)

Dieta blanda con bajo residuo Dieta blanda con alto residuo Metronidazol y cefalexina Ciprofloxacino y clindamicina Cefotaxima y metronidazol

Most patients can be managed with conservative measures. Patients with mild symptoms and no peritoneal signs may be managed initially as outpatients on a clear liquid diet and broad-spectrum oral antibiotics with anaerobic activity. Reasonable regimens include amoxicillin and clavulanate potassium (875 mg/125 mg) twice daily; or metronidazole, 500 mg three times daily; plus either ciprofloxacin, 500 mg twice daily, or trimethoprim-sulfamethoxazole, 160/800 mg twice daily orally, for 7-10 days or until the patient is afebrile for 3-5 days. Symptomatic improvement usually occurs within 3 days, at which time the diet may be advanced. Patients with increasing pain, fever, or inability to tolerate oral fluids require hospitalization. Patients with severe diverticulitis (high fevers, leukocytosis, or peritoneal signs) and patients who are elderly or immunosuppressed or who have serious comorbid disease require hospitalization acutely. Patients should be given nothing by mouth and should receive intravenous fluids. If ileus is present, a nasogastric tube should be placed. Intravenous antibiotics should be given to cover anaerobic and gram-negative bacteria. Singleagent therapy with either a second-generation cephalosporin (eg, cefoxitin), piperacillin-tazobactam, or ticarcillin clavulanate appears to be as effective as combination therapy (eg, metronidazole or clindamycin plus an aminoglycoside or third-generation cephalosporin [eg, ceftazidime, cefotaxime]). Symptomatic MX-Biomedical Research Group / JD-MD Bioinformatics Labs JD-MD Medicine and Technology

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ENARM 11ª PARTE by JD-MD improvement should be evident within 2-3 days. The antibiotics should be continued for 7-10 days, after which time elective evaluation with colonoscopy or barium enema should be performed. Approximately 20-30% of patients with diverticulitis will require surgical management. Surgical consultation should be obtained on all patients with severe disease or those who fail to improve after 72 hours of medical management. Indications for emergent surgical management include free peritonitis and large abscesses. Patients with fistulas or colonic obstruction due to chronic disease will require elective surgery. Patients with a localized abdominal abscess can be treated acutely with a percutaneous catheter drain placed by an interventional radiologist. This permits control of the infection and resolution of the immediate infectious inflammatory process. In this manner, a subsequent single-stage elective surgical operation can be performed in which the diseased segment of colon is removed and primary colonic anastomosis performed. In patients in whom catheter drainage is not possible or helpful or in cases requiring emergency surgery, it is necessary to perform surgery in two stages. In the first stage, the diseased colon is resected and the proximal colon brought out to form a temporary colostomy. The distal colonic stump is either closed (forming a Hartmann pouch) or exteriorized as a mucous fistula. Weeks later, after inflammation and infection have completely subsided, the colon can be reconnected electively. 1100.- El cuadro característico que comprende ataque agudo bilateral de pares craneales, debilidad con parálisis de vías descendentes, transtornos de la visión, disfagia, boca seca, parálisis flácida simétrica, sin fiebre, relacionada al consumo de alimentos contaminados corresponde a: a) Cólera b) Shigelosis c) Giardiasis d) Botulismo e) Tétanos Symptoms and signs fo botilusm arise 12-36 h after food ingestion and consist of acute onset and progressive flaccid paralysis involving the facial musculature and the cranial nerves bilaterally, then descending symmetrically to the pharynx, thoracic region, and the upper and lower extremities. This evolves into respiratory failure without impairment of consciousness. Fever is classically absent. In cases of infant botulism, which is found in children 6 days to 11 months old, constipation is the initial symptom, followed by lethargy, feeding difficulties, altered cry, floppiness, ophthalmoplegia, and respiratory failure.

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