#201
En la enfermedad por arañazo de gato, señale la INCORRECTA:
Incorrect statement (so this is the answer). Cat scratch disease (typically presenting as regional lymphadenopathy near the scratch/bite site) does not require topical treatment specifically — most mild/localized cases without systemic symptoms are managed with observation alone (since the disease is usually self-limited), not topical antibiotic therapy, which isn't the standard approach here.
True — while cat scratch disease is often a clinical diagnosis, serology (Bartonella henselae antibody testing) is used to help confirm the diagnosis, particularly in atypical or more severe presentations.
True — when antibiotic treatment is indicated (e.g., for larger/painful lymphadenopathy or systemic symptoms), azithromycin with this specific dosing regimen (500 mg loading dose, then 250 mg daily for 4 more days) is the recommended regimen shown to accelerate resolution of lymphadenopathy.
True — most cases of cat scratch disease are self-limited, resolving spontaneously over weeks to a few months without any specific treatment, especially in immunocompetent patients with mild disease.
⭐ High-yield pearl
Mild, localized cat scratch disease is usually managed with observation (it's self-limited) — NOT topical treatment; antibiotics (azithromycin) are reserved for more significant or systemic disease.
Bartonella henselae (transmitted via a cat scratch or bite, often from a kitten) classically causes regional lymphadenopathy near the inoculation site, sometimes with a low-grade fever and malaise; because most cases resolve spontaneously, treatment is reserved for more bothersome or complicated presentations (large/painful nodes, systemic symptoms, or immunocompromised hosts), using the specific short-course azithromycin regimen rather than topical therapy.
#202
Hombre de 45 años que refiere desde hace 3 meses dolor en codo derecho irradiado a antebrazo, no asociado a parestesias ni sensación subjetiva de pérdida de fuerza. La intensidad del dolor va empeorando a lo largo del día, principalmente con trabajo de ordenador y con actividades deportivas. A la exploración física no se observan signos inflamatorios externos, presenta dolor a la palpación de epitróclea humeral y se reproduce su dolor al distender y resistir la musculatura flexora de antebrazo y mano. ¿Cuál de los siguientes es el diagnóstico más probable?
Correct. Pain at the medial epicondyle (epitróclea) reproduced by resisted wrist/finger FLEXION and passive extension/stretching of the forearm flexor-pronator muscle group describes medial epicondylopathy ('golfer's elbow') — the involved muscle group (flexors) and the specific tenderness location (medial epicondyle) both point here.
Lateral epicondylopathy ('tennis elbow') involves the extensor muscle group and lateral epicondyle tenderness, reproduced by resisted wrist EXTENSION — not matching this patient's medial-sided, flexor-muscle-group findings.
Chronic exertional compartment syndrome typically causes diffuse forearm pain/tightness with exertion, often with neurological symptoms (paresthesias) developing during exercise, and doesn't specifically localize to the medial epicondyle with a positive resisted-flexion test.
Ulnar neuropathy at the cubital tunnel would typically cause sensory symptoms/paresthesias (in the ulnar nerve distribution — 4th/5th fingers) and/or motor weakness, which this patient specifically denies, arguing against this diagnosis.
⭐ High-yield pearl
Medial elbow pain reproduced by resisted wrist/finger FLEXION = medial epicondylopathy ('golfer's elbow'); lateral pain with resisted EXTENSION = lateral epicondylopathy ('tennis elbow').
Distinguishing these two common overuse tendinopathies is straightforward once you localize both the tender point (medial vs. lateral epicondyle) and which resisted movement reproduces the pain (flexors = medial/golfer's elbow; extensors = lateral/tennis elbow) — repetitive computer use and certain sports (golf, throwing) classically stress the flexor-pronator origin at the medial epicondyle.
#203
Hombre de 57 años con buen estado general, tiene un PSA de 13 ng/mL y tacto rectal pétreo. El estudio diagnóstico revela cáncer de próstata de alto riesgo, Gleason 9, metastásico, con afectación ósea (más de 8 lesiones en el esqueleto axial) y metástasis hepáticas. ¿Cuál de los siguientes es el tratamiento inicial indicado en la actualidad?
Radical prostatectomy with metastasis resection is a locally-directed curative-intent approach that is not appropriate for widely metastatic disease (bone AND liver metastases) — surgery isn't the standard of care once distant metastatic spread, especially visceral (liver) involvement, has occurred.
Definitive pelvic radiotherapy plus stereotactic radiotherapy to metastases is a local/oligometastatic-directed approach, not appropriate as primary treatment for this widely disseminated (high-volume, visceral-involving) metastatic disease.
Brachytherapy is a local prostate-directed treatment for localized (non-metastatic) disease, not appropriate for this widely metastatic presentation.
Correct. For newly diagnosed high-risk, high-volume metastatic castration-sensitive prostate cancer (with visceral/liver involvement, as here), current standard of care is systemic therapy: androgen deprivation therapy (LHRH analogs, often with initial anti-androgen for flare protection) combined with androgen receptor pathway inhibition (like enzalutamide) plus chemotherapy (docetaxel) — this 'triplet therapy' approach has shown improved outcomes in high-volume/high-risk metastatic disease.
⭐ High-yield pearl
High-volume, visceral (liver) metastatic castration-sensitive prostate cancer = systemic triplet therapy (ADT + androgen receptor pathway inhibitor + docetaxel), not local/surgical treatment.
Modern prostate cancer treatment for newly diagnosed metastatic disease has moved decisively toward early treatment intensification — combining androgen deprivation with either an androgen receptor pathway inhibitor, chemotherapy, or both ('triplet therapy') in high-risk/high-volume disease — rather than sequential single-agent therapy, reflecting improved survival outcomes shown in recent major trials.
#204
Gestante de 36 años primigesta sin factores de riesgo excepto índice de masa corporal de 32 pregestacional, que acude a urgencias a las 28 semanas y presenta una rotura prematura de membranas. En el momento del ingreso la analítica es normal, no presenta dinámica uterina y la longitud cervical es de 38 mm. ¿Cuál de las siguientes afirmaciones es INCORRECTA?
True — antenatal corticosteroids for fetal lung maturation are indicated at 28 weeks with preterm PROM, given the significant risk of preterm delivery within the next 7 days.
True — antibiotic prophylaxis (typically a regimen covering common pathogens, e.g., erythromycin/ampicillin-based protocols) is standard management in preterm PROM to reduce chorioamnionitis risk and prolong latency.
Incorrect statement (so this is the answer). Fetal neuroprotection with magnesium sulfate is indicated when delivery is IMMINENT or actively anticipated within the next 24 hours (typically used when in preterm labor or shortly before a planned preterm delivery), not simply upon admission for PROM without uterine activity or imminent delivery — starting it now, without impending delivery, isn't the indicated approach.
True — pregnancy itself, combined with reduced mobility from hospitalization and an elevated pre-pregnancy BMI (32, obesity), constitutes multiple VTE risk factors, making thromboprophylaxis with LMWH an appropriate consideration during this admission.
⭐ High-yield pearl
Fetal neuroprotection with magnesium sulfate is given when preterm delivery is imminent (active labor or planned delivery within ~24h) — NOT simply upon admission for PROM without signs of imminent delivery.
This question tests recognizing the SPECIFIC timing indication for magnesium sulfate neuroprotection (shown to reduce cerebral palsy risk in preterm infants) — it's reserved for the window immediately before anticipated preterm birth, not started prophylactically at every preterm PROM admission when delivery isn't yet imminent, distinguishing it from corticosteroids (given as soon as preterm risk is identified) and antibiotics (started at admission to prolong latency).
#205
¿Qué autoanticuerpos en las miopatías inflamatorias debería alertarnos de un curso agresivo de una neumonía intersticial asociada?
Anti-TIF-1 (anti-p155/140) is associated with an increased risk of underlying MALIGNANCY in dermatomyositis, not specifically with aggressive interstitial lung disease.
Correct. Anti-MDA-5 antibodies are specifically and strongly associated with rapidly progressive, aggressive interstitial lung disease in dermatomyositis (often amyopathic or hypomyopathic forms), carrying a high risk of severe, sometimes fatal, respiratory failure — recognizing this antibody should prompt close monitoring and aggressive treatment.
Anti-Mi2 is associated with classic dermatomyositis with a relatively good prognosis and good response to treatment, not aggressive ILD.
Anti-PM/Scl is associated with overlap myositis-scleroderma syndrome, and while ILD can occur, it's not specifically linked to the rapidly progressive, aggressive course that anti-MDA-5 is.
⭐ High-yield pearl
Anti-MDA-5 antibody in dermatomyositis = red flag for rapidly progressive, life-threatening interstitial lung disease — requires close monitoring and aggressive early treatment.
Myositis-specific autoantibodies carry distinct clinical associations worth memorizing as a set: anti-TIF-1/anti-NXP2 → malignancy risk; anti-Mi2 → classic DM with good prognosis; anti-MDA-5 → rapidly progressive ILD (often with minimal muscle involvement — 'amyopathic' dermatomyositis); anti-synthetase antibodies (anti-Jo1, etc.) → antisynthetase syndrome with ILD, arthritis, and mechanic's hands.
#206
Avisan de paritorio por recién nacido pretérmino tardío (35+3 semanas de edad gestacional) sin otros factores de riesgo. Al nacimiento no presenta esfuerzo respiratorio y se decide monitorización con pulsioximetría. No inicia esfuerzo por lo que a los 30 segundos se ventila con presión positiva intermitente (VPPI) (presión inspiratoria 20 cm H20 y PEEP 6 cm H20 y FiO2 0,21) durante 1 minuto. Inicia llanto y esfuerzo respiratorio pero con signos de dificultad respiratoria en torno a los 3 minutos de vida con cianosis asociada. En la monitorización presenta frecuencia cardíaca de 170 lpm y Sat O2 del 75%. ¿Cuál es su actuación en este momento?
Withdrawing respiratory support entirely would be inappropriate given ongoing signs of respiratory distress with cyanosis — support should be adjusted, not removed.
Continuing full positive-pressure ventilation (rather than stepping down to CPAP, appropriate now that the infant has spontaneous effort and a good heart rate) at 21% oxygen wouldn't address the hypoxemia (SpO2 75%, which at 3 minutes of life is below the expected target range for that time point).
Correct. At 3 minutes of life, a heart rate >100 (170 here) with spontaneous respiratory effort but ongoing distress and an SpO2 (75%) that is below the expected target range for 3 minutes of life (expected roughly 70-75% at 2 min, rising further, so being AT the low end/below target at 3 min) warrants stepping down from PPV to CPAP (since the infant now has adequate spontaneous effort and heart rate) while increasing supplemental oxygen to bring saturations toward target.
Switching to CPAP while KEEPING FiO2 at 21% wouldn't adequately address the hypoxemia; supplemental oxygen should be increased given the SpO2 is below target for this time point.
⭐ High-yield pearl
Neonatal resuscitation target SpO2 values rise progressively minute-by-minute after birth — use the appropriate CPAP/oxygen-titration step once spontaneous effort and heart rate are adequate, rather than continuing full PPV or removing support entirely.
The neonatal resuscitation algorithm uses target preductal SpO2 ranges that climb steadily over the first 10 minutes of life (roughly 60-65% at 1 min, 65-70% at 2 min, 70-75% at 3 min, 75-80% at 4 min, 80-85% at 5 min, 85-95% at 10 min); once the infant has adequate heart rate and spontaneous effort, the appropriate step-down from PPV is to CPAP (for ongoing distress) with oxygen titrated to reach these targets, rather than continuing full ventilation or withholding oxygen when saturations are below target.
#207
En relación con el estudio de la causalidad en epidemiología, solo uno de los siguientes es un criterio o consideración causal de Bradford Hill. Señálelo:
Correct. Biological gradient (dose-response relationship — where increasing exposure correlates with increasing risk/effect) is one of Bradford Hill's classic nine considerations supporting a causal interpretation of an association.
Absence of bias is a general methodological quality consideration for any study, but it is not one of Bradford Hill's specific named causal criteria.
Absence of confounding is also a general methodological consideration for valid causal inference, but again is not one of Hill's specific nine named criteria.
Statistical significance of an association is explicitly NOT one of Bradford Hill's criteria — Hill himself was skeptical of relying on statistical significance testing as a marker of causality, emphasizing the totality and pattern of evidence instead.
⭐ High-yield pearl
Bradford Hill's causal considerations include biological gradient (dose-response) — statistical significance, absence of bias, and absence of confounding are NOT among his named criteria (though they matter for general study validity).
Bradford Hill's classic nine considerations are: strength of association, consistency, specificity, temporality, biological gradient (dose-response), plausibility, coherence, experiment, and analogy — a frequently tested detail is that 'temporality' (cause precedes effect) is the only one Hill considered essential/mandatory, while the others (including biological gradient) are supportive but not individually required.
#208
Hombre de 80 años con antecedentes de hipertensión arterial y diabetes mellitus, así como un accidente isquémico cerebral transitorio 2 años antes. Hospitalizado actualmente tras presentar un infarto de miocardio sin elevación del segmento ST (IAMSEST). En la coronariografía se observa enfermedad arterial coronaria multivaso no revascularizable. En la analítica la función renal es normal, sin anemia. ¿Cuál es el tratamiento antiagregante que debiera recomendarse como primera opción?
Aspirin monotherapy alone would undertreat this patient — dual antiplatelet therapy (DAPT) is standard after an NSTEMI regardless of revascularization status, to reduce recurrent ischemic events.
Correct. In an elderly patient (80 years old) with a prior history of ischemic stroke/TIA, clopidogrel is the preferred P2Y12 inhibitor to pair with aspirin — both ticagrelor and prasugrel carry higher bleeding risk profiles that are particularly concerning in this combination of advanced age and prior cerebrovascular event, making clopidogrel the safer, guideline-preferred choice here despite non-revascularized multivessel disease.
Ticagrelor is generally preferred over clopidogrel in ACS for its greater potency, but a prior history of intracranial hemorrhage is an absolute contraindication to ticagrelor, and prior ischemic stroke/TIA combined with advanced age raises significant bleeding risk concerns that favor the safer clopidogrel option instead.
Prasugrel is explicitly CONTRAINDICATED in patients with a prior history of stroke or TIA (per its label, due to significantly increased intracranial hemorrhage risk in this population) — an absolute contraindication given this patient's TIA history 2 years ago.
⭐ High-yield pearl
Prasugrel is contraindicated with a history of prior stroke/TIA; ticagrelor also carries relatively higher bleeding risk in this context — clopidogrel is the safer preferred P2Y12 inhibitor in elderly patients with a cerebrovascular history.
Choosing among the P2Y12 inhibitors after ACS requires weighing potency against bleeding risk in the individual patient: while ticagrelor and prasugrel are generally more potent than clopidogrel and preferred in many ACS scenarios, prasugrel's explicit contraindication in prior stroke/TIA and the heightened bleeding risk with either more potent agent in elderly, cerebrovascular-disease patients make clopidogrel the safer, guideline-supported default here.
#209
Hombre de 34 años con poliposis intestinal y manifestaciones extraintestinales como hipertrofia congénita de retina y osteomas mandibulares. Para hacer el diagnóstico genético se debe analizar el gen:
MYH (MUTYH)-associated polyposis is an autosomal recessive polyposis syndrome, but it doesn't classically present with this specific combination of congenital hypertrophy of the retinal pigment epithelium (CHRPE) and mandibular osteomas.
PTEN mutations cause Cowden syndrome (hamartomatous polyposis with macrocephaly, mucocutaneous lesions, and breast/thyroid cancer risk), not this specific presentation with CHRPE and osteomas.
Correct. Intestinal polyposis with extraintestinal manifestations including congenital hypertrophy of the retinal pigment epithelium (CHRPE) and mandibular osteomas describes Gardner syndrome, a variant of familial adenomatous polyposis (FAP) caused by APC gene mutations.
p53 mutations are associated with Li-Fraumeni syndrome (a broad hereditary cancer predisposition syndrome), not this specific polyposis-plus-CHRPE-and-osteomas presentation.
⭐ High-yield pearl
CHRPE (congenital hypertrophy of retinal pigment epithelium) + osteomas + intestinal polyposis = Gardner syndrome, an APC-gene-mutation FAP variant.
Gardner syndrome is essentially FAP (APC gene mutation) plus distinctive extraintestinal manifestations — osteomas (especially mandibular), CHRPE, epidermoid cysts, and desmoid tumors — recognizing this specific extraintestinal symptom cluster should immediately point to APC gene testing rather than the other polyposis-associated genes (MYH/MUTYH, PTEN, STK11 for Peutz-Jeghers, etc.).
#210
Acude por primera vez a la consulta una paciente de 17 años con anorexia nerviosa de un año de evolución. En la exploración física y analítica son característicos los siguientes signos EXCEPTO:
True — lanugo (fine, downy body hair) is a classic physical finding in anorexia nervosa, thought to be a compensatory response to hypothermia/malnutrition.
Incorrect fit (so this is the answer). Anorexia nervosa classically causes BRADYCARDIA (not tachycardia) as an adaptive response to chronic starvation/reduced metabolic demand — tachycardia would be atypical and should actually raise concern for another process (e.g., significant dehydration, cardiac complications, or refeeding syndrome) rather than being a 'classic' expected sign.
True — hypokalemia is a classic and clinically important finding when purging behaviors (self-induced vomiting, laxative misuse) are present, reflecting significant electrolyte loss.
True — hypothalamic suppression of gonadotropins (LH/FSH) is a classic finding in anorexia nervosa, clinically manifesting as amenorrhea.
⭐ High-yield pearl
Anorexia nervosa classically causes BRADYCARDIA (an adaptive starvation response), not tachycardia — tachycardia is the atypical finding that should prompt looking for another explanation.
The classic anorexia nervosa physical/lab picture reflects the body's adaptation to chronic starvation: bradycardia, hypotension, hypothermia, lanugo, and hypothalamic-pituitary-gonadal axis suppression (amenorrhea) are all expected findings — recognizing that tachycardia does NOT fit this pattern (and instead suggests a superimposed problem) is a frequently tested distinguishing point.