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
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 long-acting release (LAR) preparations (Sandostatin LAR depot) are superior to shorter-acting 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) Paraseptal
b) Irregular c) Panlobulillar d) Centrolobulillar e) 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
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) Cultivo de exudado b) Pruebas de sensibilidad c) Microscopia de esputo d) Tele de tórax
e) 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 diagnóstico para la detección de tromboembolia pulmonar:
a) Broncografía contrastada b) Broncoscopía directa
c)
Gammagrafía de perfusión pulmonard)
Tele de tórax en posición supinae)
Espirometría computarizadaDe 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
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) Hemoptisis
b) Tos c) Síncope d) Disnea
e) 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
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) Fiebre
b) Flebitis c) Cianosis d) Taquipnea e) 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)
Prognatismoc)
Disminución del tamaño de los senos paranasales d) Hipotelorismoe) 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%
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) Hipermenorrea
b) Menorragia c) Oligomenorrea d) Metrorragia e) 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 hypothyroidism1008.- 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) Deficiencia de vitamina B 12 b) Rasgo de talasemia alfa c) Deficiencia de hierro
d) Esferocitosis hereditaria
e) 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:
a) Ferritina sérica b) Cuenta de reticulocitos c) Hierro sérico
d)
Porcentaje de saturación de transferrina e) Reservas de hierro de la medula óseaIron 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 iron-deficient 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
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) Talasemia alfa b) Rasgo trepanocitico c) Talasemia beta
d) Esferocitosis hereditaria
e) 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 F1011.- En un paciente alcohólico crónico se observa con frecuencia la presencia de macrocitosis que esta relacionada con:
a)
Reticulocitosis b) Consumo de alcohol c) Deficiencia de folato d) Deficiencia de vitamina B 12 e) Enfermedad hepáticaFolic 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
deficiency. Reduced folate absorption is rarely seen, since absorption occurs from the entire gastrointestinal tract. However, drugs such as phenytoin, trimethoprim-sulfamethoxazole, 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) Leucemia promielocítica
b) Linfoma de linfocitos pequeños c) Leucemia mieloide crónica d) Leucemia mieloblástica M2 e) 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) Artritis reumatoide b) Enfermedad de Raynaud c) Vasculitis
d) Lupus eritematosos sistémico e) 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 occur3.
Photosensitivity: Exposure to ultraviolet light causes rash4.
Oral ulcers: Includes oral and nasopharyngeal ulcers, observed by physician5.
Arthritis: Nonerosive arthritis of two or more peripheral joints, with tenderness, swelling, or effusion6.
Serositis: Pleuritis or pericarditis documented by ECG or rub or evidence of effusion7.
Renal disorder: Proteinuria >0.5 g/d or =3+, or cellular casts8.
Neurologic disorder: Seizures or psychosis without other causes9.
Hematologic disorder: Hemolytic anemia or leukopenia (<4000/uL) or lymphopenia (<1500/uL) or thrombocytopenia (<100,000/uL) in the absence of offending drugs10. Immunologic disorder: Anti-dsDNA, anti-Sm, and/or anti-phospholipid
11.
Antinuclear antibodies: An abnormal titer of ANA by immunofluorescence or an equivalent assay at any point in time in the absence of drugs known to induce ANAs1014.- Lesión más frecuente provocada por fiebre reumática: a) Insuficiencia mitral
b) Estenosis mitral c) Insuficiencia aórtica
d) Estenosis aórtica
e)
Estenosis tricúspideaNo single specific clinical manifestation or specific laboratory test unequivocally establishes the diagnosis of rheumatic fever.
Carditis: This important finding in acute rheumatic fever is a pancarditis that involves the pericardium, epicardium, myocardium, and endocardium. Carditis is the only residual of acute rheumatic fever that results in chronic changes. Common manifestations include evidence of valvular insufficiency, most frequently affecting the mitral valve, but the mitral and the aortic valve may be affected. Isolated involvement of the aortic valve is rare. Tricuspid valve or pulmonary valve involvement is unusual.
Valvular insufficiency is present in the acute state of the disease. Later, in the chronic stage, scarring of the valve with either typical "fish-mouth" abnormality or even calcified valve tissue may lead to stenosis. A combination
of insufficiency and stenosis is often found. Carditis occurs in 40-80% of patients with rheumatic fever. In the recent outbreaks in the United States, more than 80% of patients in one of the large series had evidence of carditis. Other manifestations of carditis include pericarditis, pericardial effusion, and arrhythmias (usually first-degree heart block, but third-degree or complete heart block may occur). The carditis of rheumatic fever may be mild or very severe, leading to intractable heart failure; rarely, surgical intervention, even in the acute stage of the disease, may be necessary if medical management cannot control the heart failure. These patients usually have myocardial involvement and significant valvular insufficiency.
Polyarthritis: This is the most confusing of the major criteria and probably leads to more diagnostic errors than any of the other manifestations. The arthritis of acute rheumatic fever is exquisitely tender. It is not uncommon for children with this form of arthritis to refuse to allow even bed sheets or clothing to cover an affected joint. The joints are red, warm, and swollen. The arthritis is migratory and affects several different joints: the elbows, knees, ankles, and wrists. It rarely occurs in the fingers, toes, or spine. It need not be symmetric. Effusions may be present. If the joint is aspirated, a leukocytosis is usually found; polymorphonuclear leukocytes are the cells found most frequently. However, there are no specific laboratory findings in the synovial fluid. The arthritis does not result in chronic joint disease. After anti-inflammatory therapy is begun, the arthritis may disappear in 12-24 hr. Untreated, it may persist for a week or more. In many patients with early arthritis of rheumatic fever, because of treatment with anti-inflammatory drugs, the classic migratory polyarthritis does not develop, confusing the diagnosis.
Chorea: Sydenham chorea, a unique part of the rheumatic fever syndrome, occurs much later than other manifestations. These choreoathetoid movements may begin very subtly. The latent period following streptococcal pharyngitis may be as long as several months, and the movements are often very difficult to detect at the onset. However, careful questioning of parents and teachers usually reveals evidence of increased clumsiness. One of the best signs of this in school-aged children is a marked deterioration in their handwriting. Emotional lability is a frequent finding. Sydenham chorea may affect all four extremities or may be unilateral. Although at one time it could be seen in as many as one half of patients with acute rheumatic fever, more recent evidence suggests that it occurs, at least in the United States, in 10% or fewer cases. Sydenham chorea frequently is the only symptom of rheumatic fever. It usually disappears within weeks to months. It may return, but this has become a rare occurrence.
Erythema Marginatum: This unique rash seen in patients with rheumatic fever is another of the major manifestations that can be very difficult to diagnose. It occurs very infrequently, and therefore few clinicians have had extensive experience in recognizing it. Although early in the disease it may be manifested as nonspecific pink macules that are usually seen over the trunk, later in its fully developed form,
blanching occurs in the middle of the lesions, sometimes with fusing of the borders, resulting in a serpiginous-looking lesion. This rash can be made worse with application of heat, but characteristically it is evanescent. The rash does not itch. It often occurs in patients with chronic carditis. The rash of erythema marginatum can be mistaken for the rash seen with Lyme disease.
Subcutaneous Nodules: These lesions occur infrequently and are most commonly observed in patients with severe carditis. These pea-sized nodules are firm and nontender, and there is no inflammation. They are characteristically seen on the extensor surfaces of the joints, such as the knees and elbows, and over the spine. Minor Manifestations: The minor manifestations are much less specific but may be necessary to confirm a diagnosis of rheumatic fever. They include the clinical findings of fever and arthralgia. Arthralgia is present if a patient feels discomfort in a joint in the absence of objective findings (e.g., pain, redness, warmth) on physical examination. Fever, usually a temperature no higher than 101-102°F, may be present. High temperature of 103-104°F requires careful re-evaluation and consideration of other diagnoses.
The major complication of acute rheumatic fever is the development of rheumatic valvular heart disease. None of the other manifestations results in a
chronic disease. The mitral valve is most frequently involved, but the aortic and tricuspid valves also may be affected. The tricuspid valve usually becomes involved only in patients who have significant mitral or aortic disease resulting in pulmonary hypertension.
1015.- Carditis, poliartritis y corea son criterios de: a) Thompson
b) Ranson c) Reiter d) Jones e) Child
Criterios diagnósticos de Jones: Conjunto de criterios mayores (carditis,
poliartritis, corea minor, nódulos subcutáneos, eritema anular de Leiner-Lehndorff) y
menores (fiebre; artralgias; prolongación PR en el electrocardiograma; aumento de la velocidad de sedimentación globular, proteína C reactiva o leucocitosis; signos de infección previa por estreptococo -hemolítico; fiebre reumática previa, cardiopatía reumática inactiva), que sirven para diagnosticar la fiebre reumática. La presencia de dos criterios mayores o un criterio mayor y dos menores, hace altamente probable el diagnóstico.
1016.- La fiebre reumática es una enfermedad infecciosa de tipo: a) Degenerativa
b) Proliferativa
c)
Congénita d) Inmunológica e) TóxicaDespite remarkable increases in our knowledge of the biology of the group A streptococci and of the human host and despite important observations about the epidemiologic association between group A streptococci and the human host, the pathogenetic mechanism responsible for the development of acute rheumatic fever remains unknown. Two basic theories are postulated to explain the development of this sequel to group A streptococcal pharyngitis: a toxic effect produced by an extracellular toxin of group A streptococci on target organs such as myocardium, valves, synovium,
and brain; and an abnormal immune response by the human host. The search for the correct hypothesis has been severely hampered by the fact that there is no adequate animal model. The most popular hypotheses are those that postulate an abnormal immune response by the human host to some still undefined component of group A streptococci. The resulting antibodies might then cause the immunologic damage leading to clinical manifestations. The latent period, usually 1-3 wk between the onset of the actual group A streptococcal infection and the onset of symptoms of acute rheumatic fever, lends support to an immunologic mechanism of tissue damage. Although the specific antigen or antigens responsible for inciting such an immune response have still to be identified, several possibilities exist. Group A Streptococcus is a complex microorganism producing a large number of somatic and extracellular antigens that evoke brisk immune responses. This theory is further supported by the observation that different humans appear to respond quantitatively differently to streptococcal antigens. For example, in vitro studies with human lymphocytes show that individuals can be divided into high and low responders to streptococcal blastogen A, an extracellular product of the organism. This finding is compatible with the clinical and epidemiologic observations that not all people appear to be susceptible to developing rheumatic fever. The possibility of an abnormal immune response is also based on cross reactivity between group A streptococci M protein and human tissue. The M protein is the virulence factor that is responsible for the organism's ability to resist phagocytosis. In addition, after infections with group A streptococci, type-specific immunity is conferred against the specific M protein type. The group A streptococcal M protein shares certain amino acid sequences with some human tissues, and this has been proposed as a possible source of cross reactivity between the organism and its human host, leading to the abnormal immune response. One of the two classes of M protein correlates with serotypes of group A streptococci that are frequently isolated from patients with acute rheumatic fever. In patients with Sydenham chorea, common antibodies to antigens are found in the group A streptococcal cell membrane and the caudate nucleus of the brain. This observation further supports the concept of an abnormal autoimmune mechanism for the central nervous system manifestations of rheumatic fever and Sydenham chorea. An understanding of the pathogenesis of rheumatic fever must encompass the differences in human susceptibility to the development of acute rheumatic fever, including an unusual incidence of rheumatic fever and rheumatic heart disease among members of certain family groups. In regard to this genetic influence, a specific alloantigen is present on the surface of non-T lymphocytes in 70-90% of rheumatic individuals, but fewer than 30% of "control" nonrheumatic individuals have the marker. The marker is more common in families in which there is an index case of rheumatic fever than in nonaffected members of "control" families. Although humans may have genetic differences in rheumatic susceptibility, the exact mechanism remains unknown. It is unlikely that the recent outbreaks of acute rheumatic fever in the United States are caused by an increasingly susceptible population based only on genetics. It is most likely that the pathogenetic mechanism for the development of rheumatic fever after upper respiratory tract infection with group A beta-hemolytic streptococci involves a combination of specific characteristics of the organism and some yet incompletely defined genetic predisposition in the human host.
1017.- Bloqueador beta no cardioselectivo: a) Atenolol
b) Metoprolol c) Betaxolol d) Propanolol e) Acebutolol
El propanolol es un beta-bloqueador no selectivo, el metoprolol es beta-bloqueador selectivo, el labetadol es un beta-bloqueador no selectivo con selectividad alfa, el carvedilol es un bloqueador beta y alfa.
1018.- En una mujer de 20 años con masa asintomática de 2 cms. En el polo inferior del lóbulo tiroideo derecho, la maniobra inicial mas apropiada:
a)
Biopsia excisional b) Biopsia incisionalc) Aspiración con aguja para citología
d)
Estudio de captación de yodo radioactivo e) Examen de tiroides con ultrasonidoNodular thyroid disease is common, occurring in about 3 to 7% of adults when assessed by physical examination. Using more sensitive techniques, such as ultrasound, it is present in >25% of adults. Thyroid nodules may be solitary or multiple, and they may be functional or nonfunctional. Benign thyroid nodules are common (5 to 10% adults), particularly when assessed by sensitive techniques such as ultrasound. The risk of malignancy is very low for macrofollicular adenomas and normofollicular adenomas. Microfollicular, trabecular, and Hurthle cell variants raise greater concern, and the histology is more difficult to interpret. About one-third of palpable nodules are thyroid cysts. These may be recognized by their ultrasound appearance or based on aspiration of large amounts of pink or straw-colored fluid (colloid). Many are mixed cystic/solid lesions, in which case it is desirable to aspirate cellular components under ultrasound or harvest cells after cytospin of cyst fluid. Cysts frequently recur, even after repeated aspiration, and may require surgical excision if they are large or if the cytology is suspicious. Sclerosis has been used with variable success but is often painful and may be complicated by infiltration of the sclerosing agent.
1019.- Mecanismo mediante el cual la heparina previene la trombosis:
a)
Inhibe la activación del factor Xb)
Inhibe la activación del factor VIIIc)
Inhibe la activación de los factores VIII y Xd)
Incrementa la actividad de antitrombina III e) Inhibe la agregación plaquetariaLa antitrombina, sintetizada en el hígado, inhibe los factores de la coagulación activados: trombina, IXa, Xa, XIa, XIIa y calicreina. La antitrombina III inhibe la trombina sólo en presencia de la heparina, ya que ésta al fijarse a la antitrombina le induce un cambio conformacional que hace más accesible el sitio reactivo a la trombina.
1020.- Virus conocidos como agentes etiológicos del carcinoma del cuello uterino:
Virus Epstein-barr (EBV)
Virus herpes simple tipo 2 (HSV-2) Virus 1 de inmunodeficiencia humana (HIV 1) Poliovirus (PV)
Virus sarcoma Rous (RSV)
Aunque es por todos conocido que la infección por VPH tipo 16 y 18 es característica de lesiones precancerosas para cérvix y vulva, también esta documentado que la
infección por VHS tienen un rasgo de recurrencia del 65% que se relaciona con una mayor incidencia de cáncer de cérvix, y que además facilita el contagio por VIH.
1021.- Tratamiento de elección para síndrome disenteriforme y sospecha de shigella Sp: Ceftriaxona Gentamicina Trimetropin/Sulfametoxasol Colimicina Furazolidona
Siguella: su localización más frecuente es el recto-sigmoides, produce abscesos en las criptas, diarrea con moco y sangre, con DOLOR RECTAL, prototipo de la disentería bacilar (bacilo G -). Se adquiere a través de agua contaminada. La Siguella puede producir síndrome urémico-hemolítico, que en el adulto es mas grave. El tratamiento en los niños es TMP-SMX, en adultos el ciprofloxacino es la mejor opción, también se puede dar ampicilina.
1022.- Edad idónea en la que se debe aplicar la vacuna SPR (sarampión, parotiditis y rubéola), o triple viral:
a) 9 meses b) 12 meses c) 15 meses
d)
Previo al ingreso a la escuela (preescolar) e) Inició de la adolescenciaLa triple viral se aplica al año y a los 6 años de edad.
1023.- En los pacientes pediátricos, la osteoporosis puede ser causada por el uso prolongado de:
a) Isoniazida b) Rifampicina c) Fenobarbital
d) Trimetoprim-sulfametoxazol e) Difenilhidantoina
Se ha informado de raquitismo y osteomalacia en quienes reciben fenilhidantoina y fenobarbital como terapia anticonvulsiva prolongada. Con mayor frecuencia, los fármacos inducen un estado de osteoporosis con recambio alto, a consecuencia de disminución de la absorción intestinal de Ca+.
1024.- Se producen reacciones de temor o miedo cuando se aplican estímulos en: a) Hipotalamo b) Núcleos amigdalinos c) Hipocampo d) Lóbulo frontal e) Núcleo anterior
La reacción de temor puede producirse en animales conscientes, por estimulación del hipotálamo y núcleo amigdaloide. A la inversa, las reacciones de miedo y sus
manifestaciones autónomas y endocrinas faltan cuando se ha destruido la amígdala, en situaciones en las que serían evocadas normalmente. Hay una cantidad considerable de pruebas de que el núcleo amigdaloide se ocupa de la codificación de las memorias que evocan temores.
1025.- La causa más frecuente de muerte posterior a un infarto del miocardio es la presentación de:
a) Nuevo infarto del miocardio b) Insuficiencia cardiaca progresiva c) Taquiarritmias ventriculares d) Bloqueo auriculoventricular e) Aneurisma ventricular
La causa más común de muerte en las primeras 48 hrs posteriores a un infarto agudo del miocardio es la fibrilación ventricular (FV). Entre otras causas se mencionan la rotura cardiaca, bombeo insuficiente debido a infarto masivo, complicaciones mecánicas agudas como la rotura del tabique ventricular o regurgitación mitral aguda y choque cardiogénico.
1026.- El mecanismo de daño en el lupus eritematoso generalizado más importante es:
a) Anafilaxia
b) Citotoxicidad por anticuerpos c) Deposito de complejos inmunes d) Hipersensibilidad retardada
e) Daño tisular mediado por células
SLE1 is caused by interactions between susceptibility genes and environmental factors, resulting in abnormal immune responses. The immune responses include hyperreactivity and hypersensitivity of T and B lymphocytes and ineffective regulation of antigen availability and of ongoing antibody responses. Hyperreactivity of T and B cells is indicated by increased surface expression of molecules such as HLA-D and CD40L, showing that cells are easily activated by antigens that induce first-activating signals and by molecules that drive cells to full activation via second signals. The end result of these abnormalities is sustained production of pathogenic autoantibodies and formation of immune complexes that bind target tissues, resulting in (1) sequestration and destruction of Ig-coated circulating cells; (2) fixation and cleaving of complement proteins; and (3) release of chemotaxins, vasoactive peptides, and destructive enzymes into tissues. Many autoantibodies in persons with SLE are directed against DNA/protein or RNA/protein complexes such as nucleosomes, some nucleolar RNA, and spliceosomal RNA (Table 300-1). During apoptosis these antigens migrate to cell surfaces, where they are enclosed in blebs, and membrane phospholipids change orientation so that antigenic portions are near the surface. Intracellular molecules altered during cell activation or damage migrate to the cell surface. All these antigens near or in cell surfaces probably activate the immune system to produce autoantibodies. In individuals with SLE, phagocytosis and removal of apoptotic cells and of immune complexes are impaired. Thus, in SLE, antigens are available; they are presented in locations recognized by the immune system; and the antigens, autoantibodies, and immune complexes persist for prolonged periods of time, allowing tissue damage to accumulate to the point of clinical illness. SLE is a multigenic disease. It is likely that alleles of multiple normal genes each contribute a small amount to the abnormal immune responses; if enough variations accumulate, disease results. Some predisposing genes are located in the HLA region (particularly HLA class II DR and DQ
genes, and HLA class III genes encoding C´2 and C´4). The relevant HLA DR/DQ genes increase risk for SLE by approximately twofold if one susceptibility haplotype is present and by four- to sixfold if two or more are present. Some proteins important in clearing apoptotic cells play a role in genetic susceptibility; for example, homozygous deficiencies of early components of complement Clq, C´2, and C´4 and certain alleles of mannose-binding ligand increase the risk for SLE. Clq deficiency confers the highest genetic risk known but is rare. There are at least five chromosomal regions independent of HLA that contain susceptibility genes. Within one of these regions on chromosome 1 are alleles encoding Fc? receptors that bind subsets of IgG (IgG1, -2, or -3): African Americans inheriting one allele of Fc?RIIA have a receptor that binds the Ig in immune complexes weakly; those persons have increased risk for lupus nephritis. Caucasians and Asians in some populations with alleles of Fc?RIIIA that bind Ig weakly are predisposed to SLE. A region on chromosome 16 contains genes that predispose to SLE, rheumatoid arthritis, psoriasis, and Crohn's disease, suggesting the presence of "autoimmunity genes" that, when interacting with other genes, predispose to different autoimmune diseases. Thus, SLE is modified by multiple susceptibility genes, some of which interact. There are likely to be protective gene alleles as well. These gene combinations influence immune responses to the external and internal environment; when such responses are too high and/or too prolonged, autoimmunity results. Female gender is permissive for SLE; females of many mammalian species make higher antibody responses than males. Women exposed to estrogen-containing oral contraceptives or hormone replacement have an increased risk of developing SLE (approximately twofold). Estradiol binds to receptors on T and B lymphocytes, increasing activation and survival of those cells, thus favoring prolonged immune responses. Several environmental stimuli may influence SLE1. Exposure to ultraviolet light causes SLE flares in approximately 70% of patients, possibly by increasing apoptosis in keratinocytes and other cells or by altering DNA and intracellular proteins to make them antigenic. It is likely that various infections that stimulate immune responses (antibodies and activated T lymphocytes) that cross-react with self or responses that, as they mature, develop the ability to recognize self can promote autoimmune responses that lead to SLE. The observation that children and adults with SLE are more likely to be infected by Epstein-Barr Virus (EBV) than age-, gender-, and ethnically matched controls without SLE is intriguing, because EBV activates B lymphocytes and also contains amino acid sequences that mimic sequences on human spliceosomes — a common autoantibody specificity in people with SLE. Thus, interplay between genetic susceptibility, gender, and environmental stimuli may result in autoimmunity. For maximal production of harmful autoantibodies, B cells require help from T cells, and those functions of T and B cells are normally downregulated by several mechanisms. In murine SLE models, many downregulating networks are abnormal, including generation of multiple types of regulatory and natural killer T cells and of humoral idiotypic downregulating networks. In SLE, biopsies of affected skin show deposition of Ig at the dermal-epidermal junction (DEJ), injury to basal keratinocytes, and inflammation dominated by T lymphocytes in the DEJ and around blood vessels and dermal appendages. Clinically unaffected skin may also show Ig deposition at the DEJ. In renal biopsies, the pattern of injury is important in diagnosis and in selecting the best therapy. The World Health Organization (WHO) has classified lupus nephritis as grade I (no histologic changes), II (proliferative changes confined to the mesangium), III (proliferative changes in tufts of 10 to 50% of glomeruli; higher proportions of glomeruli affected suggest worse prognosis), IV [diffuse proliferative glomerulonephritis (DPGN) affecting >50% of glomeruli], V (predominantly membranous changes with various degrees of proliferation), and VI (end stage, scarred glomeruli). In addition, pathologists report the extent of inflammatory (potentially reversible) and chronic (irreversible scarring in glomeruli, renal tubules, and blood vessels) changes. In general, treatment for lupus nephritis is not recommended in patients with class I or II disease or with extensive irreversible changes. In contrast,
aggressive immunosuppression is recommended for patients with class III, IV, or V inflammatory proliferative lesions because the majority of those individuals, if untreated, develop end-stage renal disease (ESRD) within 2 years. In children, a diagnosis of SLE can be established on the basis of renal histology without meeting additional diagnostic criteria. Histologic abnormalities in blood vessels are not specific for SLE: leukocytoclastic vasculitis is most common. Lymph node biopsies show nonspecific diffuse chronic inflammation.
1027.- Caso clínico seriado: Paciente masculino de 50 años que presenta súbitamente dolor intenso en primer ortejo de pie derecho durante la noche posterior, tras ingesta de alcohol. Primer enunciado con los datos clínicos anteriores usted pensaría que el paciente cuenta con:
a) Hiperuricemia crónica sintomática b) Síndrome de Reiter
c) Artritis reumatoide d) Monoartritis infecciosa e) Artritis gotosa
1028.- Segundo enunciado. Se sabe que en esta patología existe una alteración que consiste en:
a) Disminución en la eliminación del ácido úrico
b) Complejo antígeno-anticuerpo a nivel de la articulación afectada c) Degradación de cuerpos cetonicos
d) Reacción cruzada contra los condrocitos e) Inflamación viral
1029.- Tercer enunciado. El tratamiento de elección es: a) AINEs
b) Alopurinol y glucocorticoides c) Colchicina y AINEs
d) Pirazona y alopurinol
e) Cirugía para extracción de tofos
Monosodium urate (MSU) gout is a metabolic disease most often affecting middle-aged to elderly men and postmenopausal women. It is typically associated with an increased uric acid pool, hyperuricemia, episodic acute and chronic arthritis, and deposition of MSU crystals in connective tissue tophi and kidneys. Acute arthritis is the most frequent early clinical manifestation of MSU gout. Usually, only one joint is affected initially, but polyarticular acute gout is also seen in male hypertensive patients with ethanol abuse as well as in postmenopausal women. The metatarsophalangeal joint of the first toe is often involved, but tarsal joints, ankles, and knees are also commonly affected. In elderly patients, finger joints may be inflamed. Inflamed Heberden's or Bouchard's nodes may be a first manifestation of gouty arthritis. The first episode of acute gouty arthritis frequently begins at night with dramatic joint pain and swelling. Joints rapidly become warm, red, and tender, and the clinical appearance often mimics a cellulitis. Early attacks tend to subside spontaneously within 3 to 10 days, and most of the patients do not have residual symptoms until the next episode. Several events may precipitate acute gouty arthritis: dietary excess, trauma, surgery, excessive ethanol ingestion, adrenocorticotropic hormone (ACTH) and glucocorticoid withdrawal, hypouricemic therapy, and serious medical illnesses such as myocardial infarction and stroke. After many acute mono- or oligoarticular attacks, a proportion of gouty patients may present with a chronic nonsymmetric synovitis, causing potential confusion with
rheumatoid arthritis. Less commonly, chronic gouty arthritis will be the only manifestation and, more rarely, the disease will manifest as inflamed or noninflamed periarticular tophaceous deposits in the absence of chronic synovitis. Women represent only 5 to 17% of all patients with gout. Premenopausal gout is a rare occurrence and accounts for only about 17% of all women with gout; it is seen mostly in individuals with a strong family history of gout. A few kindreds of precocious gout in young females caused by decreased renal urate clearance and renal insufficiency have been described. Most women with gouty arthritis are postmenopausal and elderly, have arterial hypertension causing mild renal insufficiency, and are usually receiving diuretics. Also, most of these patients have underlying degenerative joint disease, and inflamed tophaceous deposits may be seen on Heberden's and Bouchard's nodes. The mainstay of treatment during an acute attack is the administration of an anti-inflammatory drug such as colchicine, nonsteroidal anti-anti-inflammatory drugs (NSAIDs), or glucocorticoids depending on the age of the patient and comorbid conditions. Both colchicine and NSAIDs may be quite toxic in the elderly, particularly in the presence of renal insufficiency and gastrointestinal disorders. In elderly patients, one may favor the use of intraarticular glucocorticoid injections for attacks involving one or two larger joints or ice pack applications along with lower oral doses of colchicine for gouty synovitis affecting small joints. Colchicine given orally is a traditional and effective treatment, if used early in the attack, in at least 85% of patients. One tablet (0.6 mg) is given every hour until relief of symptoms or gastrointestinal toxicity occurs, or a total of four to eight tablets may be given in accordance with the age of the patient. The drug must be stopped promptly at the first sign of loose stools, and symptomatic treatment must be given for the diarrhea. Intravenous colchicine is sometimes used and can reduce, though not eliminate, the gastrointestinal side effects. Intravenous colchicine is most reliable for pre- or postoperative prophylaxis in 1- to 2-mg doses when patients cannot take medications orally. Life-threatening colchicine toxicity and sudden death have been described with the administration of >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 <300 umol/L (5.0 mg/dL) to prevent recurrent gouty attacks and eliminate tophaceous deposits entail a commitment to long-term hypouricemic regimens and medications that generally are required for life. Hypouricemic therapy should be considered when the hyperuricemia cannot be corrected by simple means (control of body weight, low-purine diet, increase in liquid ingestion, limitation of ethanol intake, and avoidance of diuretic use). The decision to initiate hypouricemic therapy is usually made taking into consideration the number of acute attacks, family history of gout, presence of MSU1 tophaceous deposits, uric acid excretion >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 <600 mg in a 24-hour urine sample. Urine volume must be maintained by ingestion of 1500 mL of water every day. Probenecid can be started at a dosage of 200 mg twice daily and increased gradually
as needed up to 2 g in order to maintain a serum uric acid level <300 umol/L (5 mg/dL). Probenecid is the drug of choice to treat elderly patients with hypertension and thiazide dependence; however, probenecid is not effective with a renal creatinine clearance <1 mL/s. These patients may require allopurinol or benzbromarone (not available in the United States), which is another uricosuric drug that is effective in patients with renal failure and who are receiving diuretics. Allopurinol is the best drug to lower serum urate in overproducers, stone formers, and patients with advanced renal failure. It can be given in a single morning dose, 300 mg initially and increasing up to 800 mg if needed. In most patients, it is not necessary to start at a lower dose; however, in patients with renal failure, the dosage should be adjusted depending on the serum creatinine concentration in order to minimize side effects. Patients with frequent acute attacks may require lower initial doses to prevent exacerbations. Toxicity of allopurinol has been recognized increasingly in patients with renal failure who use thiazide diuretics and in those patients allergic to penicillin and ampicillin. The most serious side effects include skin rash with progression to life-threatening toxic epidermal necrolysis, systemic vasculitis, bone marrow suppression, granulomatous hepatitis, and renal failure. Urate-lowering drugs should not be initiated during acute attacks. This is especially important in patients who have refractory acute arthritis or who had a flare-up previously with hypouricemic drugs. Colchicine prophylaxis in doses of 0.6 mg one to two times daily is usually continued, along with hypouricemic therapy, until the patient is normouricemic and without gouty attacks for 3 months. However, prophylactic colchicine treatment may be necessary as long as tophi are present. Recombinant urate oxidase uricase can be used in the short-term prophylaxis and treatment of chemotherapy-associated hyperuricemia in patients with lymphoproliferative and myeloproliferative disorders.
1030.- Paciente masculino de 37 años de edad que acude a urgencias por fiebre, dolor abdominal difuso. A la exploración física se encuentra Giordano bilateral. EGO: leucocitos 10 x campo, bacterias ++, Rx de abdomen con silueta renal, presencia de aire de forma bilateral. Con estos datos establece el Dx de:
a) Litiasis urinaria
b) Infección de vías urinarias c) Pielonefritis enfisematosa d) Cistitis
e) Prostatitis
Formación de gas, en el parenquimatoso renal (rayos X de abdomen o TAC), en el contexto de una pielonefritis aguda, típica en pacientes diabéticos (fermentación mixta de la glucosa). Su mortalidad es del 100% si no se somete el paciente a un tratamiento y del 9 al 40% con un tratamiento óptimo. Este consiste en un drenaje inmediato y en la administración de antibióticos sensibles a los gérmenes gram-negativos, que son los habitualmente responsables.
1031.- Paciente femenino de 27 años con antecedente de infección de vías urinarias recurrentes, por cultivo se identifico Proteus. Hace 24 horas cursa con un lito en vía urinaria. El componente más probable de este lito es:
a) Ácido úrico
b) Pirofosfato de calcio c) Hidroxiapatita d) Estruvita
