#101
¿Cuál de las siguientes complicaciones es más frecuente en el reemplazo valvular aórtico transcatéter (TAVI) respecto del reemplazo valvular quirúrgico?
Pulmonary atelectasis is more related to general anesthesia and open thoracotomy/sternotomy, which is more relevant to surgical AVR, not TAVI (often done with less invasive anesthesia).
Correct. TAVI carries a higher rate of complete AV block requiring permanent pacemaker implantation compared to surgical AVR, because the transcatheter valve frame sits very close to the conduction system (AV node/bundle of His) near the membranous septum.
Pericardial effusion can occur with either approach but is not the classically described more-frequent-with-TAVI complication compared to surgery.
Major bleeding is actually generally LESS frequent with TAVI than with open surgical AVR, given the less invasive access — the opposite of what this option claims.
⭐ High-yield pearl
TAVI's conduction system proximity makes complete AV block / new pacemaker need more common than with surgical AVR.
The transcatheter valve stent frame exerts direct mechanical pressure on the AV node and proximal conduction system, which passes very close to the aortic annulus — this anatomic relationship explains why new-onset complete heart block requiring pacemaker implantation is one of the most characteristic and more frequent complications of TAVI compared to surgical valve replacement.
#102
Señale cuál de las siguientes situaciones se considera indicación de cirugía para el tratamiento de endocarditis infecciosa (EI):
Acute kidney injury alone (without heart failure, uncontrolled infection, or embolic risk) is not by itself a standard indication for surgery in infective endocarditis.
A single embolic event already found at diagnosis is a complication, but by itself (without recurrent embolism or very large/mobile vegetations) is not automatically a surgical indication — it's the ongoing/recurrent embolic risk that typically drives the decision.
For right-sided (tricuspid) endocarditis, surgery is generally reserved for much larger vegetations (typically >20 mm) or recurrent pulmonary emboli — 8 mm is well below the threshold usually used to trigger surgery in isolation.
Correct. Persistently positive blood cultures despite 7-10 days of appropriate, targeted antibiotic therapy indicates uncontrolled infection, which is one of the three classic pillars (heart failure, uncontrolled infection, prevention of embolism) that indicate surgery in infective endocarditis.
⭐ High-yield pearl
Surgery in IE is driven by 3 classic pillars: heart failure from valve dysfunction, uncontrolled infection (e.g., persistent bacteremia despite adequate antibiotics), and prevention of embolism (very large/mobile vegetations, especially with prior embolism).
Remembering these three surgical indication categories (rather than memorizing isolated lab values) helps navigate exam vignettes: persistent bacteremia on appropriate therapy is the clearest single indicator of 'uncontrolled infection' among the choices typically given.
#103
Hombre de 68 años, hipertenso y fumador que acude a urgencias por dolor torácico y disnea desde hace 3 horas. Presenta mal estado general, presión arterial 118/45 mmHg, FC 105 lpm, saturación O2 96%. En la auscultación crepitantes basales finos, tonos cardíacos atenuados, que no permiten identificar soplos. Dímero D 16.000 ng/mL. El ECG muestra taquicardia sinusal y signos de hipertrofia ventricular izquierda. Un ecocardiograma urgente revela un ventrículo izquierdo hipertrófico, no dilatado, con disfunción sistólica global ligera, insuficiencia aórtica moderada, no conocida previamente y derrame pericárdico moderado-grave. Con estos datos, ¿qué patología debe descartar?
Correct. A widened pulse pressure pattern (here narrowed, but with new aortic regurgitation), muffled heart sounds, a new pericardial effusion, and a markedly elevated D-dimer in a hypertensive smoker with acute chest pain and dyspnea is the classic combination pointing to proximal (type A) aortic dissection — dissection into the aortic root can cause acute AR and hemopericardium (pericardial effusion), and D-dimer is characteristically very high.
Papillary muscle rupture from an MI would cause acute, severe MITRAL regurgitation (not aortic regurgitation) and would show more overt regional wall motion abnormalities/infarct pattern rather than global LVH with new AR and effusion.
While massive PE can cause dyspnea, chest pain, tachycardia, and an elevated D-dimer, it wouldn't explain new aortic regurgitation and a pericardial effusion — those specific findings point toward the aortic root/dissection process instead.
Effusive-constrictive pericarditis is typically a more chronic/subacute process and wouldn't explain the acute new aortic regurgitation described — the overall picture fits an acute aortic process better.
⭐ High-yield pearl
New aortic regurgitation + pericardial effusion + markedly elevated D-dimer in a patient with acute chest pain = think proximal aortic dissection.
Proximal (type A) aortic dissection can propagate retrograde into the aortic root, disrupting the aortic valve (causing acute AR) and rupturing into the pericardial space (causing a hemopericardium/effusion, with tamponade risk) — this triad of findings should prompt emergent aortic imaging (CT angiography or TEE) rather than delay for other work-up.
#104
Hombre de 71 años portador de un marcapasos bicameral por bloqueo AV completo. Está en ritmo sinusal a 85 lpm con ritmo ventricular estimulado por el marcapasos. La interrogación del marcapasos muestra un porcentaje de estimulación ventricular del 99%. En el ecocardiograma tiene dilatación y disfunción sistólica de ambos ventrículos. La fracción de eyección del ventrículo izquierdo es del 30% y tiene insuficiencia mitral funcional grave. No tiene lesiones obstructivas en la coronariografía. Está en clase funcional III NYHA a pesar de tratamiento médico óptimo para la insuficiencia cardíaca con fracción de eyección reducida. ¿Cuál de las siguientes es la primera opción de tratamiento?
Valve repair surgery targets the mitral regurgitation directly, but here the MR is FUNCTIONAL (secondary to ventricular dilation/dysfunction from long-term RV pacing) — addressing the underlying dyssynchrony/pacing-induced cardiomyopathy is the more appropriate first step rather than valve surgery.
Similarly, valve replacement surgery doesn't address the root cause (pacing-induced dyssynchrony/cardiomyopathy) and carries more risk than a less invasive first-line option.
Correct. A 99% ventricular pacing burden causing biventricular dilation/dysfunction and severe functional MR describes pacing-induced (dyssynchrony) cardiomyopathy; the first-line treatment is upgrading to cardiac resynchronization therapy (biventricular pacing) to restore synchronous contraction, which often also improves the functional MR.
MitraClip (transcatheter edge-to-edge repair) is generally considered after guideline-directed medical therapy AND addressing reversible causes (like pacing-induced dyssynchrony via CRT) have been optimized — it's not the first-line step here.
⭐ High-yield pearl
Very high RV pacing burden (like 99%) causing new biventricular dysfunction = pacing-induced cardiomyopathy → upgrade to cardiac resynchronization therapy (CRT) first.
Chronic right ventricular-only pacing causes electrical (and eventually mechanical) dyssynchrony similar to LBBB, which can lead to a genuine cardiomyopathy over time — recognizing a very high pacing percentage as the likely cause (rather than coronary disease, which was excluded here) points directly to CRT upgrade as the logical first-line fix, often improving both LVEF and functional MR without needing valve surgery.
#105
Neonato de 10 días de vida que es traído por sus padres a los servicios de urgencias por presentar, desde hace 24 horas, rechazo de las tomas e hipotonía generalizada. Tras pruebas complementarias, se diagnostica de coartación de aorta preductal crítica. El paciente evoluciona en pocas horas hacia el shock cardiogénico. En este contexto, ¿cuál debe ser el primer tratamiento para mejorar la hemodinámica de este paciente?
Correct. In critical (ductal-dependent) coarctation of the aorta, prostaglandin E1 infusion is the essential first-line treatment to reopen/maintain patency of the ductus arteriosus, restoring lower-body perfusion and stabilizing the infant before any definitive intervention.
Ibuprofen (like indomethacin) is used to CLOSE a patent ductus arteriosus (e.g., in preterm infants with a hemodynamically significant PDA) — the opposite of what's needed here, where the ductus needs to stay open.
Emergent surgery might ultimately be needed, but the neonate must first be stabilized hemodynamically with PGE1 to reopen the ductus — rushing to surgery in an unstabilized, shocked neonate carries very high risk.
A Rashkind balloon atrial septostomy is a procedure used for conditions like transposition of the great arteries to improve mixing — it is not the treatment for ductal-dependent coarctation.
⭐ High-yield pearl
Ductal-dependent critical coarctation in cardiogenic shock → PGE1 infusion FIRST to reopen the ductus arteriosus and restore systemic perfusion.
Many critical neonatal cardiac lesions are 'ductal-dependent' (for systemic or pulmonary blood flow), and recognizing this is essential: PGE1 buys time and stabilizes the infant, allowing subsequent definitive surgical repair to happen electively rather than in the setting of active shock.
#106
Mujer de 46 años que tras 10 años de mastectomía derecha con vaciamiento ganglionar seguida de quimioterapia y radioterapia presenta linfedema de brazo derecho de larga evolución con importante edema y empastamiento, sin signos de celulitis. ¿Cuál de las siguientes medidas terapéuticas NO está recomendada?
Physical activity with limb elevation is actually recommended/encouraged in chronic lymphedema management, not contraindicated.
Complex decongestive physiotherapy (manual lymphatic drainage, compression bandaging, exercise, skin care) is the mainstay first-line treatment for lymphedema.
Correct (this is the one NOT recommended). Diuretics are NOT effective for lymphedema — lymphedema is a protein-rich fluid accumulation from impaired lymphatic drainage, not simple fluid overload, so diuretics don't meaningfully reduce it and are not part of standard management.
Liposuction (removing the fibrofatty tissue that develops in chronic, longstanding lymphedema) is a recognized surgical option in selected chronic cases that have failed conservative management, typically combined with ongoing compression therapy.
⭐ High-yield pearl
Diuretics do NOT work for lymphedema — it's protein-rich lymphatic fluid, not a simple volume-overload problem.
This is a classic teaching point: unlike edema from heart failure or venous insufficiency, lymphedema results from impaired lymphatic clearance of protein-rich interstitial fluid, so the mainstay treatments are mechanical/physical (compression, manual lymphatic drainage, exercise) rather than pharmacologic diuresis, which simply doesn't address the underlying problem.
#107
En un paciente que tras una embolectomía por isquemia arterial aguda secundaria a un émbolo en la bifurcación aorto-ilíaca, presenta hipotensión, hipercalciuria, mioglobinuria e insuficiencia renal, ¿cuál de entre los siguientes es el diagnóstico más probable?
Recurrent arterial thrombosis would present with recurrent limb ischemia symptoms, not this systemic metabolic/renal picture following a successful revascularization.
Correct. After revascularizing an acutely ischemic limb, reperfusion syndrome causes systemic release of toxic products (myoglobin, potassium, and other intracellular contents from the previously ischemic, damaged muscle) into the circulation, causing hypotension, myoglobinuria, and acute kidney injury.
Muscle necrosis is a component/consequence within reperfusion syndrome, but reperfusion syndrome is the broader clinical syndrome being described (the systemic manifestations after revascularization), making it the more complete and accurate answer.
Ischemic neuropathy would present with sensory/motor deficits in the affected limb, not this systemic metabolic derangement (hypotension, myoglobinuria, renal failure).
⭐ High-yield pearl
Revascularizing a severely ischemic limb can trigger reperfusion syndrome — a systemic release of myoglobin/potassium/toxic metabolites causing hypotension, myoglobinuria, and acute kidney injury.
This is why severely ischemic limbs (especially after prolonged ischemia time) require close monitoring after revascularization: the same restored blood flow that saves the limb can wash out damaging intracellular contents into systemic circulation, sometimes requiring aggressive fluid resuscitation, alkalinization, and even fasciotomy for concurrent compartment syndrome.
#108
Hombre de 55 años con HTA y dislipemia que consulta por disnea de esfuerzo. Presenta en la ecocardiografía válvula aórtica bicúspide con área valvular aórtica de 0,9 cm2, gradiente transvalvular de 45 mmHg, velocidad pico de 5,5 m/seg, raíz aórtica de 6 cm y fracción de eyección de ventrículo izquierdo de 45%. En la analítica, péptido natriurético tipo B el triple de lo normal. ¿Qué opción terapéutica le recomendaría?
This patient is symptomatic (exertional dyspnea) with severe AS (area 0.9 cm², high gradient/velocity) and reduced EF plus elevated BNP — this is clearly not an asymptomatic patient who can simply be observed.
TAVI is generally not the preferred option in a relatively young patient with a bicuspid aortic valve AND a significantly dilated aortic root (6 cm) — bicuspid valve anatomy and concomitant aortopathy requiring root replacement are better addressed with surgery, which can treat both the valve and the root simultaneously.
Balloon aortic valvuloplasty provides only temporary, limited benefit and is not a definitive treatment for severe symptomatic AS in a reasonable surgical candidate — it's typically reserved as a bridge in high-risk/inoperable patients.
Correct. Severe symptomatic aortic stenosis (bicuspid valve) with a significantly dilated aortic root (6 cm, meeting surgical threshold) in a patient who is a reasonable surgical candidate warrants combined surgical aortic valve replacement plus aortic root replacement, addressing both problems in a single operation.
⭐ High-yield pearl
Bicuspid aortic valve + severe AS + dilated aortic root (≥5.5 cm) = combined surgical valve + root replacement, not TAVI.
TAVI trials and guidelines have generally excluded/de-prioritized bicuspid valve anatomy with significant aortopathy, since transcatheter valves are designed and studied predominantly for tricuspid valve anatomy — when the aortic root itself also needs replacing, open surgery addressing both structures at once is the standard approach.
#109
En la respuesta inmune innata, las células más numerosas a nivel pulmonar, que conforman la primera línea defensiva, son:
Neutrophils are recruited rapidly during active infection/inflammation but are not the resident, most numerous first-line innate immune cells in the normal lung.
Correct. Alveolar macrophages are the resident innate immune cells that are most numerous in the lung under baseline conditions, patrolling the alveolar spaces and providing the first line of defense against inhaled pathogens and particles.
Eosinophils are more specifically associated with parasitic infections and allergic/type 2 inflammatory responses, not the baseline first-line pulmonary defense.
Mast cells play an important role in allergic and immediate hypersensitivity responses, but they are not the most numerous resident innate immune cells in the lung.
⭐ High-yield pearl
Alveolar macrophages are the lung's resident first-responders — the most numerous innate immune cells patrolling the airspaces at baseline.
Alveolar macrophages continuously sample the alveolar environment, phagocytosing inhaled particles/pathogens and clearing surfactant turnover products, while also orchestrating recruitment of neutrophils and other immune cells when a stronger inflammatory response is needed.
#110
Hombre de 60 años que acude a consulta por presentar tos y expectoración habitual mucosa, amarillenta, con más de 4-5 episodios de reagudizaciones al año, algunas veces con hemoptisis. ¿Cuál de los siguientes es el diagnóstico más probable?
Asthma typically presents with episodic wheeze/dyspnea related to triggers, not chronic daily purulent sputum production with hemoptysis.
Idiopathic pulmonary fibrosis presents with a dry cough and progressive exertional dyspnea, not chronic purulent sputum production or hemoptysis.
Correct. Chronic daily mucopurulent sputum production with frequent exacerbations (4-5/year) and occasional hemoptysis is the classic presentation of bronchiectasis, from chronically dilated, damaged airways prone to recurrent infection and mucosal vessel bleeding.
Heart failure typically causes exertional dyspnea and possibly pink, frothy sputum from pulmonary edema, not chronic purulent sputum production with recurrent infective exacerbations.
⭐ High-yield pearl
Chronic daily purulent sputum + frequent exacerbations + occasional hemoptysis = classic bronchiectasis.
Bronchiectasis results from irreversible bronchial dilation and impaired mucociliary clearance, creating a cycle of chronic infection and inflammation; hemoptysis occurs because chronically inflamed, hypertrophied bronchial arteries are prone to bleeding — HRCT chest is the diagnostic test of choice to confirm the airway dilation.
#111
¿Qué hallazgos de los descritos a continuación son MENOS probables en la exploración física de un paciente con fibrosis a nivel del intersticio pulmonar?
Correct (this is the LEAST likely finding). Bilateral wheezing is an obstructive airway finding (asthma, COPD), not a typical feature of interstitial pulmonary fibrosis, which is a restrictive process — fibrosis doesn't classically cause wheeze.
Bibasal fine end-inspiratory ('Velcro') crackles ARE a classic, expected finding in pulmonary fibrosis.
Decreased breath sounds with clubbing (acropaquia) ARE classically associated with pulmonary fibrosis.
Decreased vocal fremitus with dry, Velcro-type crackles IS a classic description of pulmonary fibrosis findings.
⭐ High-yield pearl
Pulmonary fibrosis is a restrictive disease with classic dry 'Velcro' crackles and clubbing — wheezing is NOT a typical feature (that's an obstructive-disease finding).
Distinguishing restrictive from obstructive lung disease on exam is high-yield: fibrosis (restrictive) gives fine, dry, end-inspiratory 'Velcro' crackles plus clubbing, while wheeze reflects airway narrowing/obstruction (asthma, COPD, bronchospasm) — a fibrotic lung doesn't produce wheeze from its fibrosis alone.
#112
Paciente que en revisión en consulta refiere tos matutina diaria y disnea de moderados esfuerzos (MRC 2) habitual que limita sus actividades cotidianas en tratamiento con doble terapia broncodilatadora desde hace dos años. La espirometría presenta un FEV1 del 35% del teórico en situación basal con una respuesta broncodilatadora que muestra un incremento del FEV1 de 250 mL y un 13%. En el estudio por TC se identifican áreas de enfisema centroacinar y en la analítica 250 eosinófilos/µL. En el último año ha sufrido dos exacerbaciones respiratorias de las cuales una ha requerido ingreso hospitalario. Indique el tratamiento más adecuado:
Chronic systemic corticosteroids are not standard maintenance therapy for stable COPD (even with frequent exacerbations) due to their long-term side-effect burden — inhaled, not systemic, corticosteroids are added when indicated.
Roflumilast is typically reserved for severe COPD with chronic bronchitis phenotype and continued exacerbations despite triple therapy — it's not the next step before escalating to triple inhaled therapy first.
Correct. A patient already on dual bronchodilator therapy (LABA+LAMA) with continued exacerbations (especially one requiring hospitalization) and a peripheral eosinophil count that isn't very low (around 250-300 cells/µL range, without being clearly 'low' <100) is a reasonable candidate for stepping up to triple therapy by adding an inhaled corticosteroid to the dual bronchodilators.
LABA + ICS alone omits the LAMA component and isn't the recommended escalation pattern in a patient already established on dual bronchodilator (LABA+LAMA) therapy with ongoing exacerbations — the addition should be an ICS on top of the existing LABA+LAMA, not switching to just LABA+ICS.
⭐ High-yield pearl
COPD patient already on LABA+LAMA with continued exacerbations (especially with hospitalization) and eosinophils not clearly low → step up to LABA+LAMA+ICS (triple therapy).
Peripheral eosinophil count is a key biomarker guiding ICS add-on decisions in COPD: higher eosinophil counts predict a greater exacerbation-reduction benefit from adding ICS to bronchodilator therapy, while very low counts (<100) suggest minimal benefit and higher pneumonia risk from ICS — this patient's borderline-elevated count, combined with ongoing exacerbations despite dual bronchodilators, supports triple therapy.
#113
Paciente con asma mal controlada a pesar de una combinación de glucocorticoides inhalados a dosis altas y un broncodilatador β-agonista de acción prolongada. Ha requerido ciclos de corticoides sistémicos sin una respuesta adecuada. Presenta rinosinusitis crónica con poliposis nasal y un recuento de eosinófilos de 400 células/μL en la analítica. Señale la respuesta correcta en cuanto al fenotipo asmático y la mejor opción de tratamiento.
This is indeed T2/eosinophilic asthma, but omalizumab (anti-IgE) is specifically indicated for allergic asthma with an IgE-mediated component, not primarily targeted at the eosinophilic pathway highlighted by this patient's blood eosinophilia and nasal polyposis.
Correct. Elevated blood eosinophils (400 cells/µL) plus chronic rhinosinusitis with nasal polyps describes T2 (eosinophilic) severe asthma; mepolizumab (anti-IL-5) is a well-matched biologic option for this eosinophilic phenotype, and anti-IL-5/IL-5R agents are also beneficial for the associated nasal polyposis.
This patient's phenotype (elevated eosinophils, nasal polyps) is a classic T2-high pattern, not non-T2 asthma, so classifying it as 'non-T2' is incorrect, and antileukotrienes are not the preferred step for severe biologic-eligible eosinophilic asthma.
Again, this presentation is T2-high (not non-T2) — benralizumab (also anti-IL-5 receptor) could actually be a reasonable biologic choice for this phenotype, but the phenotype classification in this option ('non-T2') is what makes it incorrect.
⭐ High-yield pearl
Elevated blood eosinophils + nasal polyposis in severe asthma = T2 (eosinophilic) phenotype → anti-IL-5/IL-5R biologics like mepolizumab are a strong option.
Biologic selection in severe asthma increasingly depends on phenotyping: elevated eosinophils and/or nasal polyps point toward anti-IL-5 pathway agents (mepolizumab, reslizumab, benralizumab) or anti-IL-4/13 (dupilumab, especially good for polyps), while omalizumab targets allergic/IgE-driven asthma specifically — matching the biomarker profile to the right biologic class is a high-yield modern asthma concept.
#114
En el estudio de las enfermedades intersticiales difusas del pulmón, señale en que entidad el lavado broncoalveolar posee valor diagnóstico:
BAL in sarcoidosis typically shows an elevated CD4:CD8 ratio, which is supportive but not diagnostic on its own — biopsy showing non-caseating granulomas remains needed for diagnosis.
BAL findings in idiopathic pulmonary fibrosis are nonspecific and not diagnostic — the diagnosis relies on the clinical-radiological (HRCT UIP pattern) or biopsy picture instead.
BAL in hypersensitivity pneumonitis typically shows lymphocytosis, which is supportive of the diagnosis but not by itself diagnostic.
Correct. In pulmonary alveolar proteinosis, bronchoalveolar lavage fluid has a characteristic milky, opaque appearance with PAS-positive lipoproteinaceous material on microscopy — this finding is considered diagnostic (not just supportive) for the condition.
⭐ High-yield pearl
BAL is truly diagnostic (not just supportive) in pulmonary alveolar proteinosis, thanks to its characteristic milky, PAS-positive appearance.
For most other diffuse interstitial lung diseases (sarcoidosis, IPF, hypersensitivity pneumonitis), BAL findings are supportive clues that narrow the differential but require additional biopsy or clinical-radiological correlation for definitive diagnosis — alveolar proteinosis is the classic exception where BAL alone can essentially clinch it.
#115
Hombre de 65 años, exfumador, en el que de forma incidental se identifica un nódulo pulmonar solitario (NPS) en radiografía simple de tórax. Diagnosticado de enfermedad pulmonar obstructiva crónica con un FEV1 del 30%. En el estudio por TC se describe un NPS en lóbulo superior derecho de 9 mm de diámetro con cola pleural y calcificaciones excéntricas. Se realiza tomografía por emisión de positrones con captación patológica indicativa de malignidad. ¿Cuál de las siguientes actitudes terapéuticas es la más adecuada?
Given severe underlying COPD (FEV1 30%), jumping straight to surgical biopsy without first assessing functional operability (cardiopulmonary reserve) skips an essential safety step given this patient's very high surgical risk.
With a PET already showing pathologic uptake indicative of malignancy, simple radiologic surveillance would inappropriately delay treatment of a likely cancer — surveillance is for truly low-probability, small nodules, not this PET-positive one.
This option contradicts itself: if cardiopulmonary exercise testing shows a maximal oxygen consumption <10 mL/kg/min, that indicates the patient is TOO HIGH RISK for surgical resection, so referring for surgery in that scenario would be the wrong (unsafe) conclusion.
Correct. Given the high probability of malignancy (PET-positive) but severe COPD, cardiopulmonary exercise testing should be performed to assess surgical fitness; if VO2 max is <10 mL/kg/min (indicating prohibitive surgical risk), the safer alternative to surgery is stereotactic body radiotherapy (SBRT) rather than proceeding with a high-risk resection.
⭐ High-yield pearl
In a high surgical-risk patient (severe COPD) with a likely malignant nodule, assess operability first (cardiopulmonary exercise test); if too high-risk for surgery, treat with stereotactic body radiotherapy instead.
This reflects real-world decision-making for early-stage lung cancer in patients with severe comorbid lung disease: surgical resection remains the gold standard when feasible, but SBRT has become the well-established alternative curative-intent option for patients deemed unfit for surgery due to poor pulmonary reserve.
#116
En una mujer de 72 años con litiasis biliar asintomática se indicaría colecistectomía laparoscópica en caso de:
Microlithiasis being a risk factor for pancreatitis is real, but asymptomatic microlithiasis alone isn't a standard blanket indication for prophylactic cholecystectomy in an asymptomatic patient.
Very large gallstones (often cited around 3 cm, not 2.5 cm) have been associated with increased gallbladder cancer risk in some studies, but this specific size threshold isn't the strongest/most classic indication compared to the option below.
Correct. A porcelain (calcified-wall) gallbladder is a well-established indication for prophylactic cholecystectomy in an asymptomatic patient due to an associated increased risk of gallbladder carcinoma.
The type of stone composition (pigment/bilirubin stones vs. cholesterol stones) doesn't by itself constitute an indication for prophylactic surgery in an asymptomatic patient.
⭐ High-yield pearl
Porcelain gallbladder (calcified wall) is a classic indication for prophylactic cholecystectomy even without symptoms, due to gallbladder cancer risk.
Most gallstones found incidentally in asymptomatic patients are simply observed, but certain features change that calculus: porcelain gallbladder, very large stones, gallbladder polyps >1 cm, and anomalous pancreaticobiliary duct junction are among the recognized exceptions warranting consideration of prophylactic cholecystectomy.
#117
¿En cuál de las siguientes técnicas quirúrgicas para la reparación de una hernia inguinal NO se emplea una malla protésica?
Correct. The Shouldice technique is a pure tissue (non-mesh) repair, reconstructing the inguinal floor using layered suture imbrication of the patient's own tissue rather than a prosthetic mesh.
The Lichtenstein technique is a classic open tension-free mesh repair, placing a synthetic mesh over the posterior inguinal wall.
Laparoscopic TEP repair uses a mesh placed in the preperitoneal space without entering the peritoneal cavity.
Laparoscopic TAPP repair also uses a mesh, placed after entering the peritoneal cavity and creating a peritoneal flap.
⭐ High-yield pearl
Shouldice is the classic pure tissue-based (non-mesh) inguinal hernia repair — all the other listed techniques use mesh.
Mesh-based ('tension-free') repairs like Lichtenstein, TEP, and TAPP have largely replaced pure tissue repairs due to lower recurrence rates, but Shouldice remains a well-regarded tissue-based alternative, particularly valued in settings where mesh is contraindicated (e.g., contaminated/strangulated hernia repair).
#118
Mujer de 42 años que consulta por dolor rectal descrito como una sensación de peso u ocupación continua que se agrava con la deposición. En la exploración física el ano es normal y en el tacto rectal se palpa el músculo puborrectal hipertónico y doloroso a la tracción. ¿Cuál de los siguientes es el diagnóstico más probable?
Solitary rectal ulcer syndrome typically presents with rectal bleeding, mucus discharge, and straining, with a visible mucosal ulcer on endoscopy — not primarily a tender, hypertonic puborectalis muscle finding.
Proctalgia fugax causes brief, intermittent, severe rectal pain episodes (seconds to minutes), not this continuous heaviness/pressure sensation aggravated by defecation.
'Nonspecific proctalgia' is a vague, less specific label, whereas the exam finding described (tender, hypertonic puborectalis on palpation/traction) points to a more specific diagnosis.
Correct. Continuous rectal pressure/heaviness worsened by defecation, with a tender, hypertonic puborectalis muscle on digital rectal exam (pain reproduced with traction on the muscle), is the classic presentation of levator ani syndrome (a chronic pelvic floor muscle tension/spasm disorder).
⭐ High-yield pearl
Continuous rectal heaviness/pressure + tender, hypertonic puborectalis on exam = levator ani syndrome (a pelvic floor tension disorder).
Levator ani syndrome, proctalgia fugax, and nonspecific functional anorectal pain are all considered functional pelvic floor pain disorders, but they're distinguished by their time course and exam findings: levator ani syndrome specifically features a tender, tight puborectalis muscle reproducible on digital exam, unlike the brief self-limited episodes of proctalgia fugax.
#119
Un hombre con diagnóstico de melanoma avanzado y en tratamiento con nivolumab (fármaco anti-PD-1) desarrolla elevación de las transaminasas siete veces los valores normales, junto con elevación de la bilirrubina total (2,3 mg/dL). Se han descartado cuadros infecciosos y no ha mejorado tras suspender el fármaco. ¿Cuál de las siguientes afirmaciones es cierta?
Immune-mediated hepatitis from checkpoint inhibitors shares features with autoimmune hepatitis but often lacks the same specific autoantibody profile and has distinguishing histologic/clinical clues — it's not considered truly indistinguishable in all cases.
Rechallenge with the same or a different checkpoint inhibitor after resolution can sometimes be attempted (especially for milder grades), and recurrence is not described as occurring in 'the majority' of rechallenged patients — this overstates the recurrence risk.
Correct. For significant (grade ≥3, e.g., transaminases >5x ULN with bilirubin elevation) immune-mediated hepatitis from checkpoint inhibitors not improving after holding the drug, systemic corticosteroids (around 1 mg/kg/day prednisone equivalent) are the standard first-line treatment.
Immune-related adverse events like hepatitis can occur at variable times, including relatively early in treatment (weeks), not necessarily 'always late, months in' — the timing is variable rather than uniformly delayed.
⭐ High-yield pearl
Significant checkpoint-inhibitor hepatotoxicity (grade ≥3) not improving after holding the drug → systemic corticosteroids (~1 mg/kg/day prednisone equivalent) are first-line.
Immune-related adverse events (irAEs) from checkpoint inhibitors are managed by a grading system: mild cases may just need drug holding and monitoring, while more severe grades (like this one, with markedly elevated transaminases and bilirubin) require corticosteroids, with further immunosuppression (e.g., mycophenolate) reserved for steroid-refractory cases.
#120
Un paciente con enfermedad de Crohn con antecedente de extirpación de un melanoma precisa iniciar un tratamiento avanzado por corticodependencia. ¿Cuál de los siguientes fármacos se debería evitar al estar descrito un aumento del riesgo de dicha neoplasia?
Correct. Thiopurines (azathioprine/6-mercaptopurine) have been associated with an increased risk of skin cancers, including melanoma, as well as lymphoma — making them the agent to avoid in a patient with a prior melanoma history.
Anti-TNF agents like infliximab carry their own risk profile (e.g., some association with non-melanoma skin cancer and lymphoma in combination therapy), but the specific, well-documented melanoma risk signal is most strongly linked to thiopurines among these options.
Vedolizumab is a gut-selective integrin inhibitor with a more favorable extraintestinal safety profile and is not particularly associated with increased melanoma risk.
Ustekinumab (anti-IL-12/23) also has a relatively favorable safety profile without a strong specific melanoma risk signal like thiopurines.
⭐ High-yield pearl
Thiopurines (azathioprine/6-MP) carry an increased risk of skin cancers including melanoma — avoid them in patients with a prior melanoma history when alternatives exist.
This is why IBD patients with a personal history of melanoma (or significant skin cancer risk factors) are often steered toward biologics with a more favorable dermatologic safety profile (vedolizumab, ustekinumab) rather than thiopurines, when advanced therapy is needed for steroid-dependent disease.
#121
Respecto al divertículo faringoesofágico o divertículo de Zenker, es cierto que:
Zenker's diverticulum is actually a PULSION (false) diverticulum, containing only mucosa and submucosa (not all layers of the esophageal wall), herniating through Killian's triangle — the opposite of what this option describes.
Zenker's diverticulum is in fact the MOST common type of esophageal diverticulum, not less frequent than mid-esophageal (traction) diverticula.
Cricopharyngeal myotomy is actually the cornerstone treatment even for SMALL Zenker's diverticula (often performed alone, without diverticulectomy, for smaller pouches) since it addresses the underlying cricopharyngeal dysfunction driving the pulsion diverticulum — this option has it backwards.
Correct. When an open surgical approach is used for diverticulectomy or diverticulopexy, the incision is classically made on the LEFT side of the neck, since the esophagus deviates slightly leftward, providing better surgical access from that side.
⭐ High-yield pearl
Zenker's diverticulum is a pulsion (mucosa/submucosa-only) diverticulum through Killian's triangle, treated with cricopharyngeal myotomy — and open surgical repair uses a left-sided neck incision.
Zenker's diverticulum arises from increased pressure against a poorly relaxing cricopharyngeus muscle (the true underlying motility problem), which is why myotomy — not just removing the pouch — is central to treatment, whether via an open left neck approach or an endoscopic stapling/laser technique.
#122
Mujer de 67 años con antecedentes de infección por VHC que acude a urgencias por hematemesis. A la exploración observamos ascitis y ligera ictericia. ¿Cuál es la actitud diagnóstica y terapéutica más adecuada?
Reserving TIPS as an immediate universal first-line step (rather than after failed endoscopic therapy or in specific high-risk situations) skips the standard first steps of vasoactive drugs and endoscopic band ligation.
Performing a paracentesis is not the priority in an acute GI bleeding emergency — hemodynamic stabilization and addressing the bleeding source come first.
Correct. In suspected variceal hemorrhage in a cirrhotic patient (here, HCV cirrhosis with ascites/jaundice and hematemesis), the standard approach is hemodynamic stabilization, early initiation of a vasoactive drug (terlipressin, octreotide, or somatostatin) even before endoscopy, followed by upper endoscopy with band ligation once the bleeding source is confirmed as variceal.
Waiting for endoscopy results before starting any treatment delays potentially life-saving vasoactive drug therapy, which should be started as soon as variceal bleeding is suspected, not held until endoscopic confirmation.
⭐ High-yield pearl
Suspected variceal bleed in a cirrhotic patient: stabilize, start a vasoactive drug (terlipressin/octreotide) EARLY (before endoscopy), then endoscope and band-ligate.
Early vasoactive drug therapy (started as soon as variceal bleeding is suspected clinically, without waiting for endoscopic confirmation) has been shown to reduce bleeding severity and improve outcomes, working alongside prophylactic antibiotics and subsequent endoscopic band ligation as the cornerstone of acute variceal hemorrhage management.
#123
Mujer de 38 años que presenta nódulo tiroideo indoloro y creciente en el lóbulo derecho de 6 meses de evolución. Ha experimentado recientemente disfagia y cambios de la voz. Se diagnostica de carcinoma medular de tiroides en estadio III con extensión extratiroidea y compromiso de ganglios linfáticos cervicales. De entre los siguientes, ¿cuál es el tratamiento más adecuado?
Subtotal thyroidectomy leaves residual thyroid tissue behind, which is inappropriate for a malignant, locally advanced medullary thyroid carcinoma requiring complete resection.
Hemithyroidectomy alone would leave the contralateral lobe in place and wouldn't adequately address extrathyroidal extension and confirmed lymph node involvement.
Correct. Medullary thyroid carcinoma with extrathyroidal extension and cervical lymph node involvement requires total thyroidectomy with therapeutic cervical lymph node dissection — surgery is the primary and most effective treatment for medullary thyroid carcinoma (which doesn't take up radioactive iodine, unlike differentiated thyroid cancers).
Chemotherapy alone is not the primary treatment for locally advanced but resectable medullary thyroid carcinoma — surgery remains central, with systemic therapy reserved for advanced/metastatic or unresectable disease.
⭐ High-yield pearl
Medullary thyroid carcinoma = total thyroidectomy + cervical lymph node dissection is the primary treatment (it doesn't respond to radioactive iodine like differentiated thyroid cancers do).
Because medullary thyroid carcinoma arises from parafollicular C cells (not follicular cells), it does not concentrate iodine, so radioactive iodine therapy — a mainstay for papillary/follicular thyroid cancer — is not effective here; complete surgical resection (including nodal dissection when involved) is the cornerstone of curative treatment.
#124
Mujer de 58 años que consulta por presentar desde hace varios meses dolor abdominal epigástrico intermitente, náuseas y pérdida de peso involuntaria de 8 kg. Refiere episodios ocasionales de vómitos biliosos, sin haber notado sangre en los vómitos ni en las heces. Ha estado tomando antiácidos sin mucho alivio. En la exploración física se aprecia abdomen blando, con dolor a la palpación profunda en el epigastrio, sin masas palpables ni signos de peritonitis. Los análisis muestran anemia microcítica e hipocrómica y ferropenia. En la gastroscopia lesión ulcerada en la segunda porción del duodeno, que se biopsia. El informe histológico confirma la presencia de adenocarcinoma duodenal. Una TC abdominal muestra la lesión limitada al duodeno, sin evidencia de diseminación a ganglios linfáticos o metástasis a distancia. ¿Cuál es el siguiente paso más adecuado en el manejo de esta paciente?
Simple observation is inappropriate for a confirmed malignant tumor (duodenal adenocarcinoma) — this requires active treatment, typically surgical, not surveillance.
Neoadjuvant chemotherapy before surgery is not the standard first approach for a localized, resectable duodenal adenocarcinoma without nodal or distant spread — upfront surgery is standard for resectable disease.
Correct. For localized duodenal adenocarcinoma involving the second portion of the duodenum without nodal or distant metastasis, the standard treatment of choice is surgical resection — pancreaticoduodenectomy (Whipple procedure), given the duodenum's close anatomic relationship with the pancreatic head and common bile duct.
Radiotherapy alone is not the primary treatment for resectable duodenal adenocarcinoma — surgery is the standard curative-intent approach for localized disease.
⭐ High-yield pearl
Localized, resectable duodenal adenocarcinoma (2nd portion) without nodal/distant spread → Whipple procedure (pancreaticoduodenectomy) is the standard of care.
Because the second portion of the duodenum shares its blood supply and anatomic space with the pancreatic head, ampulla, and distal common bile duct, tumors here typically require the more extensive Whipple resection rather than a simple segmental duodenal resection, even when the tumor itself appears localized.
#125
Mujer de 60 años que tras un esfuerzo refiere la aparición de una tumoración en la zona inguino-crural derecha no reductible y muy dolorosa. Acude a urgencias con un cuadro de vómitos con dolor y distensión abdominal. ¿Cuál es el diagnóstico más probable?
Direct inguinal hernias are more common in older men and have a lower incarceration risk than femoral hernias — less classically fitting this presentation in a woman.
Indirect inguinal hernias are the most common hernia type overall (in both sexes) but are less specifically associated with this inguino-crural location and high incarceration risk compared to femoral hernias.
Obturator hernia is rare and classically presents in thin, elderly women with the Howship-Romberg sign (pain radiating down the medial thigh) rather than a palpable inguino-crural mass.
Correct. A painful, non-reducible mass in the inguino-crural region after exertion in a woman, with signs of bowel obstruction (vomiting, distension), is classic for an incarcerated femoral (crural) hernia — femoral hernias are more common in women and carry a notably higher risk of incarceration/strangulation than inguinal hernias due to the rigid, narrow femoral canal.
⭐ High-yield pearl
Femoral (crural) hernias are more common in women and have a higher incarceration risk than inguinal hernias, due to the narrow, rigid femoral canal.
Any painful, irreducible groin mass — especially in a woman, located just below the inguinal ligament — should raise concern for an incarcerated femoral hernia, given the tighter anatomic space that makes strangulation more likely and surgical urgency higher than with most inguinal hernias.
#126
Hombre de 77 años que acude a urgencias por prurito, ictericia y síndrome tóxico de un mes de evolución. Refiere ingesta de amoxicilina-clavulánico desde hace 10 días por un resfriado. A su llegada se realiza una ecografía que se informa de dilatación de la vía biliar intra y extrahepática con vesícula biliar distendida. ¿Cuál es la sospecha diagnóstica y la actitud a seguir?
Acute cholecystitis typically presents with RUQ pain and fever over days, with a thickened/tender gallbladder wall on imaging, rather than this chronic (1-month) painless jaundice/weight-loss-type picture with a distended, non-tender gallbladder.
While choledocholithiasis is a common cause of biliary dilation, the combination of a distended, non-tender gallbladder (a positive Courvoisier's sign) with painless progressive jaundice and a 'toxic'/constitutional syndrome over a month is more suggestive of a malignant distal obstruction than stones (which usually cause a small, fibrotic, non-distensible gallbladder).
The recent antibiotic use is a distractor — a month-long toxic syndrome with progressive jaundice and a distended gallbladder began before or independent of a 10-day antibiotic course and doesn't fit a straightforward drug-induced cholestasis picture alone.
Correct. Painless jaundice with a palpable/distended, non-tender gallbladder (Courvoisier's sign) plus a constitutional 'toxic' syndrome over weeks strongly suggests a malignant obstruction of the distal common bile duct (e.g., pancreatic head or distal cholangiocarcinoma); the next step is abdominal CT to characterize the mass and stage the disease.
⭐ High-yield pearl
Courvoisier's sign (palpable, non-tender distended gallbladder) + painless progressive jaundice = think malignant distal biliary obstruction, not stones.
Courvoisier's law states that a palpably enlarged, non-tender gallbladder in a jaundiced patient is unlikely to be due to gallstones (since chronic stone disease usually causes gallbladder fibrosis/shrinkage) and instead points toward a malignant obstructive process — classically pancreatic head cancer or distal cholangiocarcinoma — warranting CT imaging for staging and diagnosis.
#127
La forma más eficaz de evaluación preoperatoria de la función del cuerpo esofágico y del esfínter esofágico inferior en un paciente con sospecha de reflujo gastroesofágico es:
Ambulatory pH/impedance monitoring is excellent for confirming and quantifying acid/non-acid reflux itself, but it doesn't directly assess esophageal body motility or LES function/pressure.
Correct. Esophageal manometry directly measures esophageal body peristalsis and lower esophageal sphincter pressure/relaxation, making it the most effective preoperative test specifically for evaluating esophageal motor function before anti-reflux surgery (also important to exclude motility disorders that would change the surgical approach).
Upper endoscopy is useful for visualizing mucosal damage (esophagitis, Barrett's) and excluding other pathology, but it doesn't assess esophageal motor function or LES pressure directly.
Barium esophagography can show gross anatomic/motility abnormalities but is far less precise and quantitative than manometry for assessing esophageal body function and LES parameters.
⭐ High-yield pearl
Before anti-reflux surgery, esophageal manometry is essential — it directly evaluates esophageal body peristalsis and LES function, screening for motility disorders that would change the surgical plan.
Preoperative manometry is critical because certain motility disorders (like achalasia or severe ineffective esophageal motility) can change or even contraindicate a standard fundoplication approach — pH/impedance monitoring confirms that reflux is occurring, but manometry answers the separate, essential question of how well the esophagus and LES are actually functioning mechanically.
#128
Mujer de 34 años con diagnóstico de púrpura trombocitopénica idiopática (PTI) refractaria al tratamiento médico remitida para evaluación quirúrgica. A pesar del tratamiento con corticosteroides y otros inmunosupresores, sus recuentos plaquetarios han permanecido bajos, con episodios recurrentes de sangrado leve. Se decide realizar una esplenectomía laparoscópica como siguiente paso terapéutico. En relación con la planificación y manejo de la esplenectomía laparoscópica, ¿cuál de las siguientes estrategias es la más adecuada?
While controlling the splenic artery is important during splenectomy, early ligation 'in all cases' before any mobilization is stated too absolutely — surgical sequence can vary by approach and case specifics, and this isn't the single most defining correct principle being tested here.
For ITP specifically, complete splenectomy (not partial, spleen-preserving surgery) is the standard approach, since the goal is to remove the primary site of platelet destruction — leaving splenic tissue behind would undermine the therapeutic goal.
The lateral approach is a common and preferred technique for laparoscopic splenectomy, but stating it's 'the only option regardless of spleen size' is too absolute — for markedly enlarged spleens, other approaches or hand-assisted/open techniques may be preferred.
Correct. Because splenectomy removes a key organ for immune defense against encapsulated organisms, preoperative vaccination against Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae type b is essential, ideally completed at least two weeks before elective surgery to allow adequate antibody response.
⭐ High-yield pearl
Splenectomy = increased lifelong risk of overwhelming infection with encapsulated organisms → vaccinate against pneumococcus, meningococcus, and H. influenzae ideally ≥2 weeks before elective surgery.
This vaccination timing matters because antibody responses take time to develop; when splenectomy is urgent/emergent and pre-op vaccination isn't possible, vaccines are instead given postoperatively (typically after 2 weeks), and these patients need lifelong awareness of infection risk (some also receive prophylactic antibiotics, especially in the first years after splenectomy or in children).
#129
¿Cuál de las siguientes medidas aconsejadas para reducir la infección de la herida quirúrgica es INCORRECTA?
Incorrect statement (so this is the answer). Current guidelines recommend hair removal with electric CLIPPERS specifically, and explicitly advise AGAINST razor/blade shaving, since razors cause microabrasions in the skin that increase surgical site infection risk — pairing clippers 'or a razor' as equally acceptable is the error here.
True — maintaining perioperative normothermia (avoiding hypothermia, generally keeping core temperature above ~35.5-36°C) is a well-established measure to reduce surgical site infection risk.
True — maintaining perioperative glucose control below roughly 180 mg/dL (avoiding both marked hyperglycemia and hypoglycemia) reduces infection risk.
True — prophylactic antibiotics should be infused within about 60 minutes before incision (for most agents) to ensure adequate tissue levels at the time of the first cut.
⭐ High-yield pearl
Hair removal for surgery should use electric clippers — razor/blade shaving is specifically discouraged because it increases surgical site infection risk via skin microabrasions.
This is a frequently tested surgical-care bundle concept (part of Surgical Care Improvement Project-type measures): avoid razor shaving (clippers or no hair removal at all if not needed), maintain normothermia, control glucose, and give prophylactic antibiotics within the appropriate window before incision — all evidence-based measures bundled together to reduce SSI rates.
#130
En un paciente diagnosticado de fracaso renal agudo, el tratamiento con hemodiálisis está indicado en todas las siguientes situaciones clínicas, EXCEPTO en una:
True — refractory metabolic acidosis unresponsive to medical (bicarbonate) therapy is a classic indication for urgent hemodialysis.
True — volume overload with pulmonary edema unresponsive to diuretics is a classic indication for urgent hemodialysis.
True — hyperkalemia refractory to medical treatment is a classic indication for urgent hemodialysis.
Correct (this is the exception). Proteinuria of 1 gram/24h is a marker of kidney damage/disease severity, but it is not one of the classic acute indications for emergency dialysis (the classic mnemonic AEIOU covers Acidosis, Electrolyte disturbance, Intoxication, Overload, Uremia — proteinuria alone isn't part of this list).
⭐ High-yield pearl
Remember the AEIOU mnemonic for urgent dialysis indications: Acidosis (refractory), Electrolytes (refractory hyperkalemia), Intoxication (dialyzable toxins/drugs), Overload (refractory fluid overload/pulmonary edema), Uremia (symptomatic) — proteinuria isn't on this list.
Proteinuria is an important marker for assessing chronicity/severity of kidney disease and guiding long-term management (e.g., ACEi/ARB, SGLT2i therapy), but it doesn't reflect an acute, immediately life-threatening derangement the way the AEIOU indications do, which is why it isn't a standalone trigger for emergency dialysis.
#131
Mujer de 54 años diagnosticada de diabetes mellitus tipo 2 hace tres años en tratamiento con metformina y lisinopril con buen control metabólico. Es enviada a consulta de Nefrología por creatinina sérica de 1,7 mg/dL, filtrado glomerular estimado de 49 mL/min/1,73m2 y cociente albumina/creatinina en orina de 250 mg/g. En los siguientes meses se confirma estabilidad de la función renal, las cifras de presión arterial se mantienen alrededor de 125/70 mmHg, en la ecografía se observan riñones de tamaño y morfología normal y en el estudio de fondo de ojo se objetiva una retinopatía diabética grado 2. ¿Cuál de las siguientes es la actitud a seguir?
Simply doing nothing misses an evidence-based opportunity to add nephroprotective therapy given this patient's confirmed diabetic kidney disease (reduced eGFR, moderately increased albuminuria).
Blood pressure is already well controlled (125/70) on an ACE inhibitor — adding an ARB on top of an ACE inhibitor (dual RAAS blockade) is specifically discouraged due to increased risk of hyperkalemia and acute kidney injury without added cardiovascular benefit.
A renal biopsy isn't routinely needed when the clinical picture (long-standing diabetes, concurrent diabetic retinopathy, gradual proteinuric CKD, normal-sized kidneys) is entirely consistent with diabetic kidney disease — biopsy is reserved for atypical features.
Correct. Current guidelines (KDIGO/ADA) recommend adding an SGLT2 inhibitor in type 2 diabetic patients with CKD and albuminuria (like this patient), given its proven nephroprotective effect (slowing CKD progression) independent of glycemic control, on top of existing ACE inhibitor therapy.
⭐ High-yield pearl
T2DM + CKD + albuminuria (even with 'good' BP/glucose control already) → add an SGLT2 inhibitor for its independent nephroprotective effect.
This reflects a major shift in diabetic kidney disease management: SGLT2 inhibitors are now recommended for their kidney (and cardiovascular) protective effects in patients with CKD and diabetes, essentially as a 'fourth pillar' of therapy alongside ACEi/ARB — added specifically because of the CKD/albuminuria, not just for additional glucose lowering, and NOT combined with an ARB on top of an existing ACE inhibitor.
#132
El síndrome de secreción inadecuada de hormona antidiurética (SIADH), se caracteriza por:
Correct. SIADH is characterized by hyponatremia with low serum osmolality alongside an inappropriately concentrated (elevated) urine osmolality relative to the low serum osmolality — the kidney continues concentrating urine despite the body already being 'too dilute,' reflecting inappropriate ADH activity.
SIADH is a euvolemic (not hypovolemic) hyponatremia — patients are clinically euvolemic (no edema, no signs of volume depletion), which is actually a key diagnostic feature distinguishing it from hypovolemic causes of hyponatremia.
Treatment of SIADH is based on fluid restriction plus, when needed, vasopressin receptor ANTAGONISTS (like tolvaptan) — not agonists, which would worsen the problem by increasing water retention further.
While drugs can cause SIADH (including some antibiotics, antidepressants, and other agents), it is not accurate to say that 'most cases' are drug-induced — SIADH has many causes, including malignancy (especially small cell lung cancer), CNS disorders, and pulmonary disease, among others.
⭐ High-yield pearl
SIADH = euvolemic hyponatremia with LOW serum osmolality but INAPPROPRIATELY concentrated urine — treated with fluid restriction ± vasopressin receptor ANTAGONISTS (not agonists).
The key diagnostic insight in SIADH is the mismatch: a normal kidney facing low serum osmolality should produce maximally dilute urine to correct it, but in SIADH the urine remains inappropriately concentrated because ADH is being secreted despite the absence of an appropriate osmotic or volume stimulus.
#133
Hombre de 37 años que se deriva a consulta de Nefrología para estudio de hematuria microscópica persistente. La exploración es normal salvo por presión arterial 160/100 mmHg. Hemograma sin alteraciones, urea 25 mg/dL, creatinina 0,8 mg/dL, Na 139 mEq/L, K 4,5 mEq/L, perfil hepático y lipídico normales, no hipoalbuminemia ni hipoproteinemia; estudio de autoinmunidad normal, complemento, inmunoglubulinas y proteinograma normales; serología vírica negativa; proteinuria de 0,75 g/24h; sedimento urinario con 30 eritrocitos por campo, 90% dismórficos, no leucocituria. Se realiza biopsia renal que muestra depósitos mesangiales de IgA, IgG y C3 con hipercelularidad mesangial (M1) y glomeruloesclerosis segmentaria (S1) pero sin proliferación endocapilar (E0) ni fibrosis túbulo-intersticial (T0) ni presencia de semilunas. ¿En este momento, cuál de entre los siguientes es el tratamiento más recomendado?
Immunosuppression with corticosteroids alone is reserved for higher-risk IgA nephropathy (e.g., persistent significant proteinuria >1 g/day despite optimized supportive care, or more aggressive histologic features like E1/crescents) — this patient's relatively mild picture (proteinuria under 1 g/day, no crescents, no endocapillary proliferation) doesn't yet meet that threshold.
Correct. IgA nephropathy with mesangial hypercellularity and segmental sclerosis but WITHOUT endocapillary proliferation, crescents, or significant proteinuria (here, 0.75 g/day, below the ~1 g/day threshold typically used to consider immunosuppression) is managed initially with optimized supportive therapy — blood pressure control and reducing proteinuria with an ACE inhibitor or ARB — before considering immunosuppression.
Rituximab is not established first-line therapy for IgA nephropathy in this scenario — it's not part of standard first-line management here.
High-dose corticosteroids plus cyclophosphamide induction is reserved for much more aggressive presentations (e.g., crescentic IgA nephropathy with rapidly progressive renal failure) — not this relatively low-risk MEST-C score without crescents and with sub-threshold proteinuria.
⭐ High-yield pearl
Low-risk IgA nephropathy (MEST-C without crescents/endocapillary proliferation, proteinuria <1g/day) → optimize supportive care (BP control + ACEi/ARB) first, before immunosuppression.
The Oxford MEST-C classification (Mesangial hypercellularity, Endocapillary proliferation, Segmental sclerosis, Tubulointerstitial fibrosis, Crescents) helps risk-stratify IgA nephropathy; current guidelines emphasize maximizing supportive therapy (RAAS blockade, BP/proteinuria control, and now increasingly SGLT2 inhibitors) for at least several months before considering immunosuppression, reserving the latter for higher-risk features or inadequate response to supportive care.
#134
Hombre de 65 años que presenta un episodio de infección respiratoria y es tratado con amoxicilina/clavulánico. Una semana después comienza con fiebre y aparición de rash cutáneo por lo que acude a Urgencias. En la analítica se objetiva deterioro de función renal con creatinina sérica 3,2 mg/dL (previa 1,2 mg/dL), eosinofilia y presencia de proteinuria y microhematuria en el sistemático de orina. Indique cuál de estas actitudes es la más correcta:
A skin biopsy isn't needed to establish this diagnosis — the clinical picture (temporal relationship to a new drug, fever, rash, eosinophilia, and AKI with an active urine sediment) is characteristic enough to make a clinical diagnosis of drug-induced acute interstitial nephritis without requiring skin biopsy.
Increasing the antibiotic dose would be exactly the wrong move — the clinical picture (fever, rash, eosinophilia, AKI after starting a new antibiotic) points to a drug-induced hypersensitivity reaction (acute interstitial nephritis), not worsening infection needing more antibiotic.
Correct. Fever, rash, eosinophilia, and AKI with an active urine sediment (proteinuria, microhematuria) occurring about a week after starting a new antibiotic (a classic AIN-inducing drug class) describes drug-induced acute interstitial nephritis; management is stopping the offending drug first, with corticosteroids considered if renal function doesn't improve within a few days.
Jumping straight to high-dose steroid bolus and renal biopsy skips the reasonable first step of simply stopping the likely offending drug and observing for a short interval, which often leads to improvement without needing steroids or biopsy at all.
⭐ High-yield pearl
Fever + rash + eosinophilia + AKI with an active sediment, temporally linked to a new drug (classically beta-lactams, NSAIDs, PPIs) = acute interstitial nephritis → stop the drug first.
AIN's classic hypersensitivity triad (fever, rash, eosinophilia) is actually only present together in a minority of cases, but when present (as here) it's highly suggestive; the first and most important intervention is simply discontinuing the offending agent, with a renal biopsy and/or corticosteroids reserved for those who don't recover renal function within days of stopping the drug.
#135
Hombre de 72 años, remitido a consulta tras un hallazgo en una TC solicitada para el estudio de molestias digestivas inespecíficas. Se objetiva una lesión sólida, exofítica, heterogénea, con realce intenso tras la administración de contraste, de 4,9 cm de diámetro, dependiente del polo inferior renal derecho; en el riñón izquierdo litiasis piélica de 3 cm que condiciona hidronefrosis y atrofia cortical. Antecedentes personales de hipertensión, sobrepeso (mide 1,6 m y pesa 95 kg) y fumador habitual. En la analítica destaca creatinina sérica de 1,5 mg/dL. Señale de entre las siguientes opciones de tratamiento la que considera más adecuada:
Bilateral nephrectomy would leave the patient anephric/dialysis-dependent, which is completely disproportionate for a likely resectable, localized right renal mass with a functionally compromised (but not absent) contralateral kidney.
Correct. A likely renal cell carcinoma (~4.9 cm, exophytic, enhancing) in a patient whose contralateral kidney already has compromised function (hydronephrosis and cortical atrophy from a stone) should be managed with nephron-sparing surgery — partial nephrectomy — to preserve as much renal function as possible given the at-risk solitary functional reserve.
Percutaneous biopsy followed by neoadjuvant chemotherapy isn't standard management for a resectable renal mass suspicious for RCC — renal cell carcinoma is not particularly chemo-sensitive, and surgery remains the primary treatment for localized disease.
Radical (complete) nephrectomy would remove the entire right kidney, which is an unnecessarily aggressive approach when partial nephrectomy is technically feasible, especially critical here given the compromised function of the left kidney (making preservation of every possible nephron on the right side more important).
⭐ High-yield pearl
When the contralateral kidney's function is already compromised, favor nephron-sparing (partial) nephrectomy over radical nephrectomy for an otherwise resectable renal mass.
Partial nephrectomy has become the preferred approach for many localized renal masses (especially ≤7 cm, and particularly when nephron preservation matters more, as with a solitary kidney, bilateral tumors, or, as here, a contralateral kidney with reduced function from chronic obstruction) — preserving renal function is a key consideration alongside oncologic control.
#136
Hombre de 53 años acude a urgencias por anuria de 48 horas de evolución. Presenta dolor abdominal difuso de varios días de evolución que no se modifica con la posición ni con la ingesta. No ha presentado fiebre pero sí náuseas con dos vómitos escasos biliosos sin productos patológicos, además de estreñimiento. En la analítica sanguínea presenta ligera leucocitosis con desviación izquierda, creatinina 7 mg/dL con FG<15mL/min, sodio 132 mmol/L y potasio 5,7 mmol/L, bilirrubina 1 mg/dL, amilasa 100 U/L, AST 30 U/L, ALT 45 U/L, fosfatasa alcalina 60 U/L, y GGT 70 U/L. En el sedimento de orina únicamente se evidencian 5-10 hematíes/campo y leve piuria. En la ecografía abdominal dilatación pielocalicial y ureteral moderada-severa bilateral con leve disminución del parénquima en el riñón izquierdo y múltiples imágenes hiperecoicas con sombra acústica posterior en todos los grupos caliciales así como en el uréter proximal izquierdo. ¿Cuál es la actitud más correcta a seguir?
Aggressive IV fluids to 'force diuresis' won't relieve the underlying mechanical obstruction and won't resolve anuria caused by bilateral obstructive uropathy — the obstruction itself must be addressed.
IV diuretics also won't fix a mechanical (obstructive) cause of anuria and could theoretically worsen volume status without addressing the actual problem.
Correct. Anuria with bilateral hydronephrosis/hydroureter and stones seen throughout the collecting systems (obstructive uropathy, here bilateral) is a urologic emergency requiring urgent bilateral urinary tract decompression (via nephrostomy tubes or ureteral stents) to relieve the obstruction and allow renal recovery.
Ordering a CT scan for 'acute abdomen' work-up would delay the urgent, clearly indicated intervention (urinary diversion) — the diagnosis (bilateral obstructive uropathy from stones) is already established by ultrasound, and further imaging shouldn't delay definitive treatment of this emergency.
⭐ High-yield pearl
Anuria + bilateral hydronephrosis from stones = obstructive uropathy, a urologic emergency requiring URGENT bilateral urinary decompression (nephrostomy or stents), not more fluids or imaging.
Post-renal (obstructive) acute kidney injury is one of the few immediately reversible causes of severe AKI, but only if the obstruction is relieved promptly — recognizing bilateral hydronephrosis with anuria as a time-sensitive urologic emergency (rather than treating it like typical prerenal or intrinsic AKI) is essential to avoid unnecessary, function-threatening delay.
#137
Hombre de 28 años que consulta por haberse despertado por dolor en la región genital y tumefacción en el pene. No recuerda con detalle lo sucedido en las últimas 12 horas. En las últimas 48 h ha consumido alto volumen de alcohol, varias drogas (mefedrona, cocaína, anfetamina), junto con sildenafilo y se ha autoinyectado en el pene 20 µg de alprostadil. A la exploración destaca, pene flácido, glande no visible en su totalidad por edema y hematoma expansivo de partes blandas. Presenta restos hemáticos en el meato uretral. ¿Cuál de las siguientes opciones NO formaría parte de su plan terapéutico?
Correct (this is what would NOT be part of the plan). Corpus cavernosum blood gas sampling is used to distinguish ischemic from non-ischemic priapism — but this patient has a FLACCID penis with an expanding hematoma and blood at the meatus (suggesting penile fracture/urethral injury from trauma during a drug-fueled sexual encounter combined with intracavernosal injection), not a persistently erect (priapic) penis, so this test doesn't apply to this clinical picture.
Urgent surgical exploration IS appropriate here given the expanding hematoma and suspected penile fracture/urethral injury — timely surgical repair improves outcomes.
Avoiding urethral catheterization IS appropriate given blood at the meatus, which raises concern for urethral injury — attempting catheterization could worsen a partial urethral tear, so a retrograde urethrogram or careful specialist assessment should precede any catheter attempt.
Penile ultrasound IS a useful, appropriate imaging tool to assess for tunical (corpus cavernosum) rupture / hematoma extent in suspected penile fracture.
⭐ High-yield pearl
This is a suspected penile fracture with urethral injury (flaccid penis, expanding hematoma, blood at meatus) — NOT priapism, so corpus cavernosum blood gas sampling (a priapism-specific test) doesn't apply.
Don't confuse penile fracture (traumatic rupture of the tunica albuginea, presenting with detumescence, an expanding hematoma, and often a 'crack'/pop sound during vigorous intercourse or manipulation) with priapism (a persistent, painful erection) — they require very different diagnostic tests and are managed differently, even though both can occur in the context of erectile dysfunction drugs and intracavernosal injections.
#138
Hombre de 51 años que consulta preocupado por la aparición de leve goteo postmiccional. Tiene dislipemia, hipertensión arterial y alopecia androgénica incipiente. Sigue tratamiento con simvastatina, enalapril, minoxidil y dutasteride. Padre y hermano fallecidos por cáncer de próstata. En los reconocimientos de salud laboral realizados en 2.021 y 2.023 se observa PSA de 0,3 y de 3,8 ng/mL respectivamente (valores de referencia <4 ng/mL). Una RMN prostática multiparamétrica muestra una próstata de 55 mL y en secuencia T2 un nódulo hipointenso moderado y homogéneo de 1,7 cm, con restricción de la difusión y realce precoz en perfusión en el límite entre el estroma fibromuscular anterior y la zona transicional del lóbulo izquierdo prostático. Repetimos una nueva determinación de PSA 3,5 ng/mL. A la vista de estos hallazgos, ¿qué recomendación propondría al paciente como la más adecuada?
A purely systematic (random) transrectal biopsy without MRI-targeted sampling would risk missing the specific suspicious lesion already identified on mpMRI, and the transperineal route also carries a lower infection risk than transrectal.
There's no clinical indication of prostatitis/infection here to justify empiric antibiotics before biopsy — this would just delay appropriate diagnostic work-up of a suspicious MRI lesion.
Simple reassurance would be inappropriate given: a dramatic PSA rise (0.3→3.8, notably a >10x increase even though still 'normal' range) plus a family history of prostate cancer deaths in both father and brother, plus a discrete suspicious MRI lesion with restricted diffusion — these all warrant tissue diagnosis, not reassurance alone.
Correct. Given a significant PSA rise, strong family history, and a discrete PI-RADS-type suspicious lesion on multiparametric MRI, the recommended next step is a transperineal prostate biopsy combining systematic sampling with MRI-fusion targeted biopsy of the identified lesion — this approach improves cancer detection accuracy while lowering infection risk compared to the transrectal route.
⭐ High-yield pearl
Rising PSA (even within 'normal' range) + strong family history + a discrete suspicious lesion on mpMRI = biopsy, ideally transperineal with MRI-fusion targeting (systematic + targeted).
Note that dutasteride (a 5-alpha-reductase inhibitor, being taken here for hair loss) roughly halves PSA levels after chronic use, meaning the 'true' PSA-equivalent value is higher than reported — this makes the observed rise even more concerning and reinforces why proceeding to biopsy is appropriate despite PSA remaining under the standard <4 ng/mL cutoff.
#139
¿Cuál de estas afirmaciones es cierta sobre los subtipos moleculares de cáncer de mama?
Triple-negative breast cancer is NOT the most common subtype — luminal A (hormone receptor-positive, HER2-negative, low proliferation) is the most common molecular subtype overall.
HER2-positive breast cancer is generally considered more aggressive (higher proliferation, historically worse prognosis) than luminal A, not less aggressive — though targeted anti-HER2 therapy has dramatically improved outcomes.
Luminal A is actually the MOST common molecular subtype, not the rarest — this statement has it backwards.
Correct. Triple-negative breast cancer (lacking ER, PR, and HER2 expression) is generally considered the most aggressive molecular subtype, with higher proliferation rates, a greater tendency for early relapse/visceral metastasis, and fewer targeted therapy options compared to hormone receptor-positive or HER2-positive subtypes.
⭐ High-yield pearl
Luminal A is the most common (and generally best-prognosis) breast cancer subtype; triple-negative is the least common major subtype but the most aggressive.
Molecular subtyping (luminal A, luminal B, HER2-enriched, triple-negative/basal-like) has become central to both prognosis and treatment selection: triple-negative cancers lack the targets for hormone therapy or anti-HER2 agents, largely explaining their historically more aggressive course and reliance on chemotherapy (and now increasingly immunotherapy) as mainstays of treatment.
#140
Mujer de 60 años con diagnóstico reciente de cáncer de mama metastásico con alta carga tumoral. Acude a Urgencias 48 horas después de haber recibido el primer ciclo de tratamiento, con cuadro de náuseas, vómitos, diarrea, dolor abdominal, astenia intensa y letargia. En la analítica sanguínea presenta alteración de la función renal. ¿Cuál de las siguientes alteraciones analíticas esperaría encontrar también?
Tumor lysis syndrome causes HYPERuricemia (from massive purine release/breakdown), not hypouricemia — this is the opposite direction of what actually occurs.
Correct. This clinical picture (high tumor burden, symptoms starting 48 hours after the first cycle of chemotherapy, GI symptoms, lethargy, and new renal impairment) is classic for tumor lysis syndrome, which classically causes hyperkalemia (from massive intracellular potassium release as tumor cells lyse), alongside hyperuricemia and hyperphosphatemia.
Tumor lysis syndrome causes HYPERphosphatemia (from released intracellular phosphate), not hypophosphatemia.
Tumor lysis syndrome causes HYPOcalcemia (calcium gets bound/precipitated with the excess released phosphate as calcium-phosphate complexes), not hypercalcemia — this is the opposite direction.
⭐ High-yield pearl
Tumor lysis syndrome's classic tetrad: hyperkalemia, hyperuricemia, hyperphosphatemia, and (secondary) hypocalcemia — with acute kidney injury from urate and calcium-phosphate crystal deposition.
Recognizing high-tumor-burden malignancies and rapidly proliferating cancers as high-risk for tumor lysis syndrome after starting cytotoxic therapy is important for prevention (prophylactic hydration, allopurinol or rasburicase) — once established, it requires aggressive supportive management and sometimes urgent dialysis for severe electrolyte derangements or renal failure.
#141
¿A cuál de las siguientes proteínas presentes en la superficie celular se une el fármaco pembrolizumab?
Correct. Pembrolizumab is an anti-PD-1 monoclonal antibody, binding the PD-1 receptor on T cells to block its inhibitory interaction with PD-L1/PD-L2, thereby restoring T-cell-mediated antitumor immune activity.
PD-L1 is targeted by different checkpoint inhibitors (like atezolizumab, durvalumab, avelumab), not pembrolizumab, which targets the receptor (PD-1) rather than its ligand.
CTLA-4 is targeted by a different class of checkpoint inhibitor (ipilimumab), acting at an earlier stage of T-cell activation than the PD-1/PD-L1 axis.
HER2 is targeted by drugs like trastuzumab and pertuzumab — an entirely different target/mechanism from checkpoint inhibition.
⭐ High-yield pearl
Pembrolizumab and nivolumab target PD-1 (on T cells); atezolizumab/durvalumab/avelumab target PD-L1 (on tumor cells); ipilimumab targets CTLA-4 — three distinct checkpoint inhibitor classes.
Keeping these checkpoint inhibitor-target pairings straight is high-yield oncology/immunology knowledge, since the specific target (PD-1 vs. PD-L1 vs. CTLA-4) determines the mechanism of action and helps distinguish drug names on exams.
#142
¿Cuál de estos pacientes en tratamiento con quimioterapia cumple criterios de neutropenia febril?
Correct. Febrile neutropenia is defined as a single temperature ≥38.3°C (or ≥38.0°C sustained over 1 hour) with an absolute neutrophil count <500/mm3 (or expected to fall below that). This patient has both: fever of 38.5°C and neutrophils of 400/mm3 — she meets criteria regardless of her overall good clinical appearance or seemingly mild URI-type symptoms.
This patient's temperature (37.8°C) doesn't reach the 38.0-38.3°C fever threshold required, even though her neutrophil count (300/mm3) does meet the neutropenia criterion — both criteria must be met together.
This patient's neutrophil count (600/mm3) is above the <500/mm3 threshold, and the temperature (37.5°C) also doesn't meet the fever definition — neither criterion is met.
This patient's neutrophil count (700/mm3) is above the <500/mm3 cutoff, so despite having a qualifying fever (38.6°C), the neutropenia criterion isn't met.
⭐ High-yield pearl
Febrile neutropenia requires BOTH criteria together: ANC <500/mm3 AND fever ≥38.3°C (or ≥38.0°C sustained) — regardless of how well or unwell the patient otherwise looks.
This is an important safety point: even a patient who 'looks well' with a mild-seeming viral-type syndrome must be treated as having febrile neutropenia (with urgent empiric broad-spectrum antibiotics) if they meet both numeric criteria, since neutropenic patients can deteriorate rapidly and lack the usual inflammatory signs of severe infection.
#143
En un paciente con cáncer colorrectal metastásico irresecable RAS nativo y con pérdida de expresión de proteínas reparadoras del ADN (MSI-H). ¿Cuál debe ser el tratamiento de elección de primera línea?
Anti-EGFR therapy (cetuximab/panitumumab) requires RAS wild-type status (present here) but is not the preferred first-line choice over immunotherapy specifically in MSI-H/dMMR tumors, which respond exceptionally well to checkpoint inhibition.
Correct. Metastatic colorectal cancer with MSI-H/deficient mismatch repair (dMMR) status responds remarkably well to immune checkpoint inhibitors (per pivotal trials like KEYNOTE-177), making immunotherapy the preferred first-line treatment for this specific molecular subgroup, regardless of RAS status.
Chemotherapy alone would be the standard approach for microsatellite-stable (MSS) colorectal cancer, but MSI-H tumors specifically do dramatically better with immunotherapy as first-line treatment.
Adding an anti-VEGF agent (bevacizumab) to chemotherapy is standard first-line therapy for MSS metastatic colorectal cancer, but for MSI-H tumors, immunotherapy is now preferred over chemotherapy-based regimens in the first-line setting.
⭐ High-yield pearl
MSI-H/dMMR metastatic colorectal cancer responds remarkably well to checkpoint immunotherapy — a landmark exception where immunotherapy, not chemotherapy, is now preferred first-line.
MSI-H tumors accumulate very high mutational burdens due to defective DNA mismatch repair, generating many neoantigens that make them exceptionally immunogenic and responsive to PD-1/PD-L1 blockade — this is one of the clearest examples in oncology where a specific biomarker (MSI-H/dMMR status) completely changes the standard treatment algorithm.
#144
Hombre de 48 años, exfumador hasta el 2.020, con antecedente de nefrectomía parcial izquierda en el 2.020 por carcinoma de células renales, tipo célula clara, grado 2/4, pT1b, que acude por autopalparse una adenopatía laterocervical alta hace 4 meses. En la ecografía de cuello se identifican 2 lesiones nodulares submaxilares y en el TC de cuello se informa de una lesión nodular de partes blandas derecha que corresponde probablemente a una adenopatía sospechosa. Se indica biopsia de la lesión donde se observa una proliferación neoplásica constituida por células con marcada atipia citológica que se disponen con un patrón de crecimiento difuso. El estudio inmunohistoquímico es positivo para CD20, y negativo para CD3, CD30, CD15 y CKAE1-AE3. En estos casos se completa el estudio con CD10, Bcl6 y MUM1 para indicar el fenotipo de la neoplasia. ¿Cuál es el diagnóstico anatomopatológico?
Classic Hodgkin lymphoma would typically show CD30-positive (and often CD15-positive) Reed-Sternberg cells, whereas this tumor is CD30-negative and CD20-positive, pointing away from Hodgkin lymphoma.
Correct. A diffuse growth pattern of large, markedly atypical cells that are CD20-positive (a B-cell marker), with negative CD3 (T-cell), CD30 and CD15 (Hodgkin/anaplastic markers), and negative cytokeratin (ruling out carcinoma), describes diffuse large B-cell lymphoma — the additional CD10/Bcl6/MUM1 panel is used to further subclassify it into germinal-center vs. non-germinal-center (activated B-cell) phenotypes (Hans algorithm), which carries prognostic significance.
Peripheral T-cell lymphoma would be expected to show CD3 positivity (a T-cell marker), but this tumor is CD3-negative and CD20-positive, pointing toward a B-cell, not T-cell, lymphoma.
Carcinoma metastasis would be expected to stain positive for cytokeratin (CKAE1-AE3), but this tumor is cytokeratin-negative and instead expresses the B-cell marker CD20, ruling out a carcinoma and confirming a lymphoid origin.
⭐ High-yield pearl
CD20+, CD3-/CD30-/CD15-/cytokeratin-negative diffuse large atypical cells = diffuse large B-cell lymphoma; CD10/Bcl6/MUM1 further subclassify it (Hans algorithm: germinal center vs. non-GC subtype).
This immunohistochemistry panel logic is classic exam material: CD20 marks B cells (ruling in DLBCL here), CD3 marks T cells, CD30/CD15 suggest Hodgkin/anaplastic lymphoma, and cytokeratin (CKAE1-AE3) marks epithelial/carcinoma cells — working through each marker's presence or absence systematically narrows the differential to the correct diagnosis.
#145
Hombre de 17 años con hemofilia A grave e inhibidor de alto título frente al FVIII que presenta sangrado agudo a nivel articular. ¿Cuál de los siguientes tratamientos es el más indicado para controlar la hemorragia?
Desmopressin (DDAVP) works by releasing endogenous factor VIII/von Willebrand factor and is useful in mild hemophilia A or von Willebrand disease — it's ineffective in severe hemophilia A, and completely irrelevant when a high-titer inhibitor against factor VIII is present.
Emicizumab is a bispecific antibody used for ROUTINE PROPHYLAXIS in hemophilia A (including inhibitor patients), mimicking factor VIII's cofactor function — but it is not the treatment for an acute bleeding episode, where a bypassing agent is needed instead.
Tranexamic acid is a useful adjunct (especially for mucosal bleeding) but is not sufficient alone to control an acute joint bleed in a patient with a high-titer factor VIII inhibitor — it doesn't replace the need for a bypassing hemostatic agent.
Correct. In hemophilia A patients with a high-titer inhibitor against factor VIII (making standard factor VIII replacement ineffective), acute bleeding is treated with a 'bypassing agent' — recombinant activated factor VII (or activated prothrombin complex concentrate) — which achieves hemostasis by bypassing the factor VIII-dependent step of the coagulation cascade.
⭐ High-yield pearl
High-titer FVIII inhibitor + acute bleed in hemophilia A = need a bypassing agent (recombinant activated factor VII or aPCC), NOT standard factor VIII replacement.
Emicizumab has transformed long-term prophylaxis in inhibitor patients (given as a subcutaneous injection mimicking FVIII's function), but for treating an acute breakthrough bleed, bypassing agents remain the go-to acute treatment, since emicizumab's mechanism and dosing aren't designed for rapid, high-intensity hemostatic correction of an active bleed.
#146
Hombre de 76 años que es intervenido por recambio protésico de cadera derecha tras traumatismo. Entre los antecedentes personales destaca hipertensión arterial en tratamiento farmacológico y recambio protésico de rodilla izquierda hace 3 meses por artrosis evolucionada. Al cuarto día del postoperatorio se detecta trombopenia de 52.000/mm3 con cifras de hemoglobina y leucocitos normales. El estudio de coagulación y la bioquímica es normal. ¿Cuál es el diagnóstico más probable?
TTP typically presents with the classic pentad features (microangiopathic hemolytic anemia with schistocytes, thrombocytopenia, neurologic symptoms, renal impairment, fever) — the isolated thrombocytopenia with normal hemoglobin and normal coagulation/biochemistry here doesn't fit TTP.
DIC would typically show abnormal coagulation studies (prolonged PT/aPTT, low fibrinogen, elevated D-dimer) — here the coagulation studies are explicitly normal, arguing against DIC.
Correct. Isolated thrombocytopenia developing around day 4-10 after surgery, in a patient with recent/repeated heparin exposure (perioperative prophylaxis, and especially given a recent prior surgery 3 months ago likely with heparin exposure too), with otherwise normal hemoglobin, WBC, and coagulation studies, is the classic presentation of heparin-induced thrombocytopenia (HIT).
Hemolytic uremic syndrome would be expected to show hemolytic anemia (low hemoglobin, schistocytes) and renal impairment alongside thrombocytopenia — none of which is described here, arguing against HUS.
⭐ High-yield pearl
Isolated thrombocytopenia around day 4-10 post-op in a patient with heparin exposure (especially with repeat/recent prior exposure) = classic heparin-induced thrombocytopenia (HIT) until proven otherwise.
HIT's typical timeline (thrombocytopenia onset 5-10 days after starting heparin, or faster with recent prior exposure, as in this patient with surgery 3 months ago) is a key diagnostic clue, and it's critical to recognize because HIT paradoxically causes a prothrombotic state requiring immediate cessation of all heparin products and switching to an alternative (non-heparin) anticoagulant, rather than platelet transfusion.
#147
Los siguientes tipos de linfoma pueden ser originados por virus. ¿Cuál de ellos es producido por el virus herpes humano tipo 8 (KSHV/HHV8)?
Adult T-cell leukemia/lymphoma is caused by HTLV-1 (human T-lymphotropic virus type 1), not HHV-8.
Correct. Primary effusion lymphoma is classically caused by HHV-8 (Kaposi sarcoma-associated herpesvirus), typically presenting as malignant lymphomatous effusions in body cavities (pleural, pericardial, peritoneal) without a discrete tumor mass, most often in immunocompromised patients (e.g., HIV/AIDS).
Burkitt lymphoma is classically associated with Epstein-Barr virus (EBV), particularly the endemic African variant, not HHV-8.
Lymphomatoid granulomatosis is an EBV-driven B-cell lymphoproliferative disorder with angiocentric/angiodestructive features, not caused by HHV-8.
⭐ High-yield pearl
HHV-8 (KSHV) causes primary effusion lymphoma (and Kaposi sarcoma and multicentric Castleman disease) — distinct from the EBV-driven lymphomas (Burkitt, lymphomatoid granulomatosis) and HTLV-1-driven adult T-cell leukemia/lymphoma.
Matching oncogenic viruses to their associated lymphomas is a classic high-yield pairing: EBV → Burkitt lymphoma, Hodgkin lymphoma (some cases), lymphomatoid granulomatosis, PTLD; HHV-8 → primary effusion lymphoma, Kaposi sarcoma; HTLV-1 → adult T-cell leukemia/lymphoma — grouping them this way makes recall much easier than memorizing each in isolation.
#148
Mujer de 50 años diagnosticada de síndrome mielodisplásico con monosomía del cromosoma 7 (45 XX -7 [20]) es sometida a un trasplante hematopoyético alogénico con sangre de cordón umbilical de un hombre compatible procedente de un banco de otro país. A los tres meses del trasplante con recuperación completa de las cifras hematológicas periféricas se realiza una punción de médula ósea, que no presenta alteraciones morfológicas y un estudio cromosómico con un cariotipo 47 XXY [20]. ¿Cuál es la explicación de estos hallazgos?
An undiagnosed Klinefelter syndrome in the donor is a far less likely and unnecessarily complicated explanation compared to the straightforward, expected phenomenon of mixed chimerism after transplant.
Correct. After allogeneic transplant, it's expected (and monitored for) that both donor-derived (male, XY) and residual recipient-derived (female, XX) hematopoietic cells can coexist in the marrow — conventional cytogenetics analyzing a mixed population can report a combined/composite result reflecting this coexistence (mixed chimerism), which is a key post-transplant monitoring parameter (full donor chimerism is generally the goal, especially to ensure the MDS clone hasn't persisted).
Cell fusion between donor and recipient cells generating a genuinely new combined karyotype is not a recognized or expected physiological phenomenon after transplant — mixed chimerism (coexisting separate donor and recipient cell populations) is the standard, well-established explanation instead.
This isn't a transient, clinically insignificant artifact — chimerism status (donor vs. recipient percentage) is an actively monitored, clinically meaningful parameter after transplant, since decreasing donor chimerism can signal impending relapse of the original disease.
⭐ High-yield pearl
After allogeneic transplant, donor and recipient cells can coexist in the marrow (mixed chimerism) — chimerism testing is a standard, clinically important part of post-transplant monitoring, not a meaningless transient artifact.
Chimerism analysis (using more specific molecular techniques like STR-PCR in real practice, though conventional karyotype can sometimes hint at it as in this vignette) is routinely tracked after transplant because a falling donor-cell percentage (increasing mixed or recipient-predominant chimerism) can be an early warning sign of disease relapse, prompting closer monitoring or early intervention (e.g., donor lymphocyte infusion).
#149
Mujer de 90 años sin alergias medicamentosas conocidas, con HTA y gonalgia nocturna por gonartrosis derecha de intensidad leve-moderada de tres meses de evolución. Refiere que no toma ninguna medicación y se confirma que realiza las medidas higiénicas del sueño correctamente. Consulta a su médico de atención primaria por insomnio de conciliación y mantenimiento que le interfiere con sus actividades diarias. ¿Qué fármaco es más adecuado iniciar en este caso?
Paracetamol addresses the underlying knee pain but doesn't directly treat the insomnia itself as a standalone hypnotic strategy, and doesn't reflect the best answer choice for the specific complaint of sleep-onset and sleep-maintenance insomnia.
Benzodiazepines like diazepam are generally avoided in elderly patients due to increased risks of falls, fractures, cognitive impairment, and prolonged sedation from reduced drug clearance — a poor choice in a 90-year-old.
Mirtazapine is more specifically indicated when depression is also present (given its antidepressant mechanism with sedating properties) — it's not typically the first choice purely for insomnia without a depressive component, and its appetite-stimulating/weight gain profile is an additional consideration.
Correct. In an elderly patient with insomnia (both sleep-onset and sleep-maintenance difficulty), trazodone is a favored option due to its relatively favorable safety profile in older adults compared to benzodiazepines, with a lower risk of falls, dependence, and cognitive side effects.
⭐ High-yield pearl
For insomnia in the elderly, trazodone is generally preferred over benzodiazepines, which carry higher fall/cognitive risk in this population.
Choosing sleep medications in older adults requires weighing efficacy against the anticholinergic, sedative-hangover, and fall-risk burden common to many hypnotics; low-dose trazodone has become a common preferred choice in geriatric practice for this reason, reserving benzodiazepines and non-benzodiazepine 'Z-drugs' for very selected, short-term situations given their less favorable risk profile in the elderly.
#150
En los pacientes mayores con síndrome de inmovilidad una de las siguientes manifestaciones clínicas o consecuencias NO es atribuible al mismo:
True — cognitive decline (including features that can resemble intellectual deficit) is a recognized consequence of immobility syndrome, related to sensory deprivation and deconditioning.
True — resting heart rate typically increases with prolonged immobility/deconditioning, as cardiovascular fitness declines.
True — immobility is associated with reduced insulin sensitivity (insulin resistance), contributing to glucose intolerance in immobilized patients.
Correct (this is the one NOT attributable). Immobility causes a NEGATIVE nitrogen balance (increased muscle protein catabolism exceeding synthesis, driving muscle wasting/sarcopenia), not a positive nitrogen balance — this option has the direction backwards.
⭐ High-yield pearl
Immobility syndrome causes a NEGATIVE nitrogen balance (muscle protein breakdown > synthesis, driving sarcopenia) — NOT a positive one.
Immobility syndrome's cluster of consequences (muscle atrophy/negative nitrogen balance, cardiovascular deconditioning with resting tachycardia and orthostatic intolerance, insulin resistance, cognitive decline, pressure injuries, contractures) reflects a systemic 'disuse' physiology across nearly every organ system — remembering the DIRECTION of each metabolic change (negative, not positive, nitrogen balance) is what these exam questions often test.