Versión: 0 · Preguntas 51-100 de 210 · Questions in Spanish · Explanations & high-yield pearls in English
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#51
¿Cuál de los siguientes escenarios podría suponer una contraindicación para el uso de un injerto de piel parcial como cobertura de un defecto cutáneo?
Large surface area is actually where split-thickness skin grafts (STSGs) excel compared to flaps — a big defect isn't a contraindication, it's a typical indication.
Medical comorbidities affect overall surgical risk/wound healing broadly, but they're not a specific structural contraindication to grafting itself.
Correct. A split-thickness graft needs a vascularized bed to survive by imbibition/inosculation. Exposed tendon without its paratenon (like bone without periosteum, or cartilage without perichondrium) has no local blood supply to support graft take — a flap (not a graft) is needed here.
Active infection is a relative, treatable contraindication (the wound can be debrided/controlled first, then grafted) — it's not the same category of absolute structural problem as an avascular bed.
⭐ High-yield pearl
Grafts need a vascular bed — exposed tendon without paratenon, bone without periosteum, or cartilage without perichondrium won't support a skin graft.
Skin grafts survive initially by plasmatic imbibition and then inosculation/neovascularization from the wound bed. Structures stripped of their vascularized covering layer (paratenon, periosteum, perichondrium) cannot supply this, so a vascularized flap is required instead of a simple graft.
#52
Un enfermo diabético de reciente diagnóstico acude a revisión oftalmológica. A las pocas horas vuelve con un cuadro bilateral de edema y eritema palpebral, quemosis, hiperemia conjuntival, lagrimeo y picor. Su actitud debe ser:
Ordering glucose/HbA1c/ESR doesn't address the acute allergic reaction that just developed hours after an ophthalmology visit — it doesn't fit the acute timeline.
Correct. Bilateral eyelid edema/erythema, chemosis, conjunctival hyperemia, tearing, and itching appearing within hours of an eye exam is a classic acute allergic reaction (likely to mydriatic/diagnostic drops); treatment is a topical antihistamine or low-potency corticosteroid.
OCT for diabetic macular edema is a reasonable diabetic follow-up test, but it doesn't address this acute allergic reaction happening right now.
Gonioscopy to check for neovascularization of the angle is relevant in advanced diabetic retinopathy, but is unrelated to this acute allergic eye reaction.
⭐ High-yield pearl
Bilateral itchy, watery, swollen eyes right after an eye exam = acute allergic conjunctivitis, likely reaction to the drops used.
Diagnostic mydriatic/anesthetic eye drops can trigger acute allergic conjunctivitis within hours of instillation. It's a clinical diagnosis based on the acute onset and classic signs (chemosis, itching, tearing), treated symptomatically with topical antihistamines or a mild corticosteroid.
#53
En relación al tratamiento quirúrgico de las cataratas, señale cuál de los siguientes enunciados es correcto:
This has the direction backwards — index (lenticular) myopia from a denser cataractous lens classically IMPROVES near vision transiently ('second sight'), while worsening distance vision, not the reverse.
Cataract/lens surgery actually INCREASES the risk of retinal detachment, especially in young myopic patients — the opposite of what this option states.
Current cataract surgery indications consider functional impact and quality of life broadly, not simply a visual acuity threshold in isolation.
Correct. Alpha-blockers like tamsulosin are associated with Intraoperative Floppy Iris Syndrome (IFIS) — a well-known complication of cataract surgery causing a flaccid, prolapsing iris that increases surgical difficulty and complication risk.
⭐ High-yield pearl
Tamsulosin (and other alpha-blockers) → Intraoperative Floppy Iris Syndrome during cataract surgery.
IFIS is important to recognize preoperatively: surgeons need to know about current or past alpha-blocker use (even if stopped) so they can adjust technique (e.g., pupil expansion devices, iris hooks) to manage the floppy, poorly-dilating iris and reduce complications.
#54
Hombre de 72 años exfumador, acude a consulta por visión borrosa y dificultad para leer, especialmente en el ojo derecho, situación que ha progresado lentamente en los últimos seis meses. En la exploración del segmento anterior no se encuentran alteraciones clínicamente relevantes. En el ojo derecho se observan múltiples drusas en la región macular (una de tamaño grande) y alteraciones pigmentarias. En la tomografía de coherencia óptica se muestra un adelgazamiento del epitelio pigmentario de la retina y áreas de acumulación de material subretiniano en la mácula del ojo derecho. ¿Cuál es el manejo inicial indicado para este paciente?
Intravitreal dexamethasone is used for macular edema from causes like retinal vein occlusion or uveitis, not for dry age-related macular degeneration.
Correct. Multiple drusen (including a large one) with pigmentary changes and OCT findings of RPE thinning and drusenoid subretinal material describe intermediate dry AMD; initial management is AREDS2-type vitamin/antioxidant supplementation to slow progression.
There's no mention of a visually significant cataract driving this presentation — the findings described are specific to the macula (AMD), not the lens.
Anti-VEGF injections are reserved for neovascular (wet) AMD with active exudation/hemorrhage — the findings here (drusen, RPE thinning, drusenoid material) describe the dry, non-neovascular form.
⭐ High-yield pearl
Intermediate dry AMD (large drusen + pigmentary changes) → AREDS2 vitamin supplementation, not anti-VEGF.
AREDS2 supplementation (vitamin C, E, zinc, copper, lutein/zeaxanthin) has been shown to reduce progression risk in intermediate dry AMD. Anti-VEGF therapy is reserved specifically for the neovascular (wet) form, which presents with subretinal/intraretinal fluid or hemorrhage from choroidal neovascularization, not simple drusen.
#55
Hombre de 26 años que presenta otorrea unilateral derecha de una semana de evolución desde su regreso de vacaciones en la playa donde una ola le arrolló provocando inmersión. Refiere haber sido tratado en la infancia con colocación de drenajes transtimpánicos bilaterales y ha evitado la entrada de agua en los oídos desde entonces. No presenta dolor, pero sí molestias y leve hipoacusia. Tampoco tiene vértigo, pero sí sensación de taponamiento ótico. En la otoscopia se evidencia una perforación timpánica central de bordes lisos y otorrea que proviene de oído medio. ¿Cuáles son el diagnóstico y tratamiento del paciente?
Correct. A residual central tympanic perforation (from childhood tympanostomy tubes) that gets contaminated by seawater causes reactivation of simple chronic otitis media; treatment is topical ciprofloxacin drops (safe in a non-intact tympanic membrane, unlike aminoglycosides) with ENT follow-up.
Acute otitis media typically occurs behind an intact tympanic membrane with bulging, not through a pre-existing perforation with water-triggered otorrhea; also, gentamicin drops are ototoxic and avoided with a non-intact eardrum.
Cholesteatoma classically shows a marginal (not central) perforation, often with foul-smelling otorrhea and retraction pockets — not the smooth-bordered central perforation described here; also gentamicin is ototoxic and should be avoided.
External otitis affects the ear canal, not otorrhea originating from the middle ear through a tympanic perforation, so this doesn't match the described findings.
⭐ High-yield pearl
Water exposure through an old central perforation = reactivated chronic otitis media, treated with a non-ototoxic drop like ciprofloxacin.
Any topical ear drop used with a known or possible non-intact tympanic membrane should avoid aminoglycosides (gentamicin, neomycin) due to ototoxicity risk — fluoroquinolone drops like ciprofloxacin are the safe choice in this setting.
#56
Hombre de 40 años que acude a urgencias por presentar un cuadro de mareo con giro de objetos acompañado de náuseas, vómitos, palidez y sudoración de varias horas de evolución. Nunca había presentado un cuadro similar. No refiere hipoacusia ni acúfeno ni sensación de taponamiento. La otoscopia es normal. Se observa un nistagmo horizonto-rotatorio hacia el lado derecho grado III que aumenta la velocidad cuando dirige la mirada a la derecha, maniobra oculocefálica positiva izquierda, test de Skew y el test de Romberg positivo a la izquierda. ¿Cuál de los siguientes es el diagnóstico más probable?
A cerebral infarct causing an isolated acute vestibular syndrome without other focal neurologic deficits, and with a unidirectional, gaze-enhanced (Alexander's law), horizontal-torsional nystagmus, is less typical than a peripheral cause fitting the same pattern.
Correct. Acute, isolated, severe vertigo lasting hours with nausea/vomiting, no hearing loss/tinnitus, and a unidirectional horizontal-torsional nystagmus that increases in the direction of the fast phase (Alexander's law) is the classic presentation of vestibular neuritis.
Meniere's disease requires the triad of episodic vertigo WITH hearing loss and tinnitus/aural fullness — explicitly absent here.
BPPV is triggered by specific position changes and lasts seconds, not the continuous hours-long vertigo described in this vignette.
⭐ High-yield pearl
Isolated acute vertigo (hours, no hearing loss) + unidirectional nystagmus that grows with gaze toward the fast phase = vestibular neuritis.
Vestibular neuritis is thought to result from viral or post-viral inflammation of the vestibular nerve, sparing the cochlear branch (hence no hearing loss), presenting as a single, severe, isolated episode of vertigo lasting days, distinguishing it from the recurrent episodes of Meniere's or the brief positional triggers of BPPV.
#57
Mujer de 54 años consulta por hipoacusia unilateral derecha de horas de evolución que se ha presentado de manera brusca. Presentó un cuadro viral de vía aerodigestiva superior hace unos días. Sin antecedentes de interés, no presenta vértigo ni sensación de taponamiento ótico ni acúfeno. No refiere dolor ni presenta parálisis facial. La otoscopia es normal. En la acumetría la prueba Rinne es positiva bilateral y la pruebas Weber lateraliza al lado izquierdo. ¿Cuál es la sospecha diagnóstica y el manejo?
An urgent CT scan isn't the diagnostic test of choice for sudden sensorineural hearing loss — audiometry is needed first to confirm and characterize it, and MRI (not CT) is used to look for retrocochlear causes if indicated.
A bilaterally positive Rinne (air conduction > bone conduction on the affected side) argues against a conductive hearing loss — serous otitis media would show a negative Rinne on the affected ear.
Correct. Sudden unilateral hearing loss with a positive Rinne bilaterally (ruling out conductive loss) and Weber lateralizing to the unaffected (left) ear is sudden sensorineural hearing loss; management is urgent pure-tone audiometry to confirm/quantify it, followed by systemic and/or intratympanic corticosteroids.
There's no mention of vesicular ear lesions or facial palsy, which are required for Ramsay Hunt syndrome (herpes zoster oticus) — this doesn't fit the presentation.
⭐ High-yield pearl
Sudden unilateral hearing loss + Weber lateralizing to the GOOD ear = sensorineural loss → urgent audiometry + corticosteroids.
Remember the Rinne/Weber logic: in sensorineural hearing loss, Rinne stays positive (air > bone) on the affected side, but Weber lateralizes AWAY from the affected ear (toward the healthy ear) because the damaged cochlea perceives bone-conducted sound less well overall.
#58
Mujer que acude a ecografía de rutina de segundo trimestre a las 22 semanas de gestación. Las biometrías corresponden a un feto de 19 semanas. ¿Cuál es el siguiente paso para orientar el caso?
Jumping straight to genetic testing is premature before ruling out the much simpler explanation of incorrect dating.
Correct. Before assuming true fetal growth restriction, the first step is always to confirm gestational age against the first-trimester crown-rump length (the most accurate dating method) — a biometric 'lag' may simply reflect incorrect dating rather than pathology.
Repeating the scan in 2 weeks without first checking the dating just delays addressing the more fundamental question of whether the pregnancy is even correctly dated.
There's no clinical information here (blood pressure, proteinuria, symptoms) suggesting preeclampsia — this doesn't fit the presenting problem of a biometric discrepancy.
⭐ High-yield pearl
Any apparent growth discrepancy on ultrasound → first confirm dating against the first-trimester CRL before assuming pathology.
First-trimester crown-rump length is the most accurate method for gestational age dating, with much less variability than later biometric parameters — discrepancies discovered later in pregnancy should always be checked against it before invoking fetal growth restriction or genetic work-up.
#59
¿Cuál de los siguientes métodos anticonceptivos es el más adecuado para una mujer de 35 años con migraña con aura?
Combined oral contraceptives are contraindicated in migraine with aura due to increased ischemic stroke risk from the added estrogen.
The contraceptive patch also delivers estrogen systemically and carries the same contraindication in migraine with aura.
A combined injectable (estrogen + progestin) also carries systemic estrogen exposure and the same contraindication.
Correct. A levonorgestrel-releasing IUD is a progestin-only, non-estrogen method, making it appropriate for a woman with migraine with aura, where estrogen-containing methods are contraindicated due to stroke risk.
⭐ High-yield pearl
Migraine WITH aura = avoid estrogen-containing contraceptives (stroke risk); progestin-only or non-hormonal methods are preferred.
This is one of the WHO Medical Eligibility Criteria's clearest absolute contraindications: combined hormonal contraception (pills, patch, ring, injectable) in migraine with aura is a category 4 (unacceptable risk) due to synergistic increased ischemic stroke risk — progestin-only methods (including the LNG-IUD) remain safe.
#60
Mujer con gestación monocorial biamniótica de 22 semanas que acude a urgencias por dinámica uterina ocasional. En la ecografía se observa feto 1 con peso estimado en el percentil 80 y columna máxima vertical de líquido amniótico de 11 cm, vejiga urinaria distendida y aumentada de tamaño y feto 2 con un peso en el percentil 25 con una columna máxima de líquido amniótico de 0,5 cm y vejiga urinaria no visible. Exploración vaginal anodina. La longitud cervical es de 36 mm. ¿Cuál es el diagnóstico más probable?
Correct. In a monochorionic diamniotic twin pregnancy, one twin with polyhydramnios (deepest pocket 11 cm) and a distended bladder (the 'recipient') alongside the other with severe oligohydramnios (0.5 cm) and an invisible bladder (the 'donor') is the classic diagnostic picture of twin-to-twin transfusion syndrome via unbalanced placental vascular anastomoses.
Selective fetal growth restriction is defined primarily by growth discordance, not by this striking discordant amniotic fluid/bladder pattern, which is the specific hallmark of TTTS.
Isolated PROM of one twin wouldn't produce a distended bladder and polyhydramnios in the co-twin — this pattern is specific to unbalanced blood flow between twins.
A renal malformation in twin 2 could cause oligohydramnios/anhydramnios alone, but wouldn't explain the reciprocal polyhydramnios and bladder distension seen in twin 1 — the paired findings across both twins is what defines TTTS.
⭐ High-yield pearl
Monochorionic twins + one polyhydramnios/full bladder + one oligohydramnios/empty bladder = twin-to-twin transfusion syndrome.
TTTS results from unbalanced blood flow through shared placental vascular anastomoses in monochorionic twins: the 'donor' twin becomes hypovolemic (oliguria → oligohydramnios, empty bladder), while the 'recipient' twin becomes hypervolemic (polyuria → polyhydramnios, distended bladder) — diagnosed and staged (Quintero staging) by exactly this fluid/bladder discordance pattern.
#61
Puérpera de parto eutócico sin complicaciones hace 4 días que acude a urgencias por cefalea de 12 horas de evolución y edemas maleolares. A la exploración presenta cifras tensionales de 165/100 mmHg en dos ocasiones y en la analítica se observa una cifra de plaquetas de 254.000/µL, AST 172 UI/L, ALT 154 UI/L y LDH 345 UI/L, creatinina 0,9 mg/dL y cociente prot/creat 235 mg/g. ¿Cuál de las siguientes opciones terapéuticas forma parte de la primera línea de tratamiento inmediato?
Correct. This is postpartum preeclampsia with severe features (BP ≥160/110, headache, elevated transaminases, significant proteinuria) — IV magnesium sulfate is first-line for seizure (eclampsia) prophylaxis in preeclampsia with severe features, regardless of the antihypertensive chosen.
Oral labetalol may be used for blood pressure control, but with severe-range BP and severe features, IV antihypertensives (labetalol or hydralazine IV) plus magnesium sulfate for seizure prophylaxis are the priority — oral therapy alone isn't the immediate first-line step here.
High-dose corticosteroids aren't first-line treatment for preeclampsia itself (they're used in specific HELLP syndrome protocols in some settings, but aren't the core immediate intervention being tested here).
IV diuretics aren't part of first-line preeclampsia management and could worsen the intravascular volume depletion often present in preeclampsia.
⭐ High-yield pearl
Preeclampsia with severe features (even postpartum) → IV magnesium sulfate is first-line for seizure prophylaxis.
Preeclampsia can present or worsen up to several weeks postpartum, and severe features (BP ≥160/110, symptoms like headache, elevated liver enzymes, or significant proteinuria) mandate magnesium sulfate for eclampsia prophylaxis plus prompt blood pressure control — this doesn't change just because delivery has already occurred.
#62
¿Cuál es la vía de diseminación más frecuente y característica del cáncer de ovario en el momento del diagnóstico?
Lymphatic spread does occur in ovarian cancer (particularly to pelvic/para-aortic nodes) but is not the most characteristic/frequent route at diagnosis.
Hematogenous spread is uncommon and typically a late-stage finding in ovarian cancer, not the primary or most frequent route.
Direct contiguous invasion of adjacent pelvic organs does occur, but it's not the dominant/most characteristic dissemination pattern of ovarian cancer overall.
Correct. Ovarian cancer's most characteristic and frequent route of spread is peritoneal (transcoelomic) dissemination — malignant cells exfoliate from the ovarian surface and spread throughout the peritoneal cavity, seeding the omentum and peritoneal surfaces, often already present at diagnosis.
⭐ High-yield pearl
Ovarian cancer's signature spread pattern is peritoneal/transcoelomic seeding, not lymphatic or hematogenous.
Because ovarian cancer often presents at an advanced stage with peritoneal carcinomatosis (ascites, omental caking, diffuse peritoneal implants), understanding this transcoelomic spread pattern explains both the diagnostic imaging findings and the rationale behind cytoreductive surgery aiming to remove all visible peritoneal disease.
#63
¿Cuál de las siguientes es una de las características que condiciona de modo crucial e independiente la elección del tratamiento adyuvante del cáncer de endometrio?
Tumor size is not a primary independent driver of adjuvant treatment selection in the current endometrial cancer risk-stratification framework.
Correct. The molecular classification of endometrial cancer (POLE-mutated, mismatch-repair-deficient/MSI-H, p53-abnormal, and no specific molecular profile — the ESGO/ESMO/ESTRO molecular classification) is now a crucial, independent factor guiding adjuvant treatment decisions, sometimes overriding traditional histologic risk factors.
Isolated tumor cells in lymph nodes are a nodal staging nuance, but not the dominant independent factor driving current adjuvant treatment algorithms compared to molecular classification.
Presence of postmenopausal bleeding is a presenting symptom that led to diagnosis, not a factor used to guide adjuvant treatment decisions.
⭐ High-yield pearl
Modern endometrial cancer management is built around molecular classification (POLE, MMR-d/MSI-H, p53abn, NSMP), not just histology/stage alone.
This molecular classification has become central to prognostication and adjuvant therapy decisions: POLE-mutated tumors have an excellent prognosis and may be de-escalated, while p53-abnormal tumors carry a poor prognosis and often warrant more aggressive adjuvant therapy, independent of traditional grade/stage in many cases.
#64
Niña de 13 años con desaceleración en el crecimiento en el último año. En la exploración detectamos un bocio con tiroides aumentado de tamaño de forma difusa, firme y no doloroso a la palpación. La madre de la niña comenta que en su adolescencia ella había tenido una enfermedad del tiroides de la que se recuperó espontáneamente. De las siguientes pruebas complementarias, ¿qué considera indicado realizar en primer lugar?
A percutaneous biopsy is invasive and not the first step for a diffuse, firm, painless goiter with growth deceleration and a family history suggestive of autoimmune thyroid disease.
A thyroid ultrasound is useful but doesn't establish the functional/autoimmune diagnosis, which should be checked first with simple blood tests.
A thyroid scan is more useful for evaluating nodules or hyperthyroidism (e.g., toxic nodule), not the first step in a diffuse goiter with suspected autoimmune (Hashimoto) thyroiditis.
Correct. A diffuse, firm, painless goiter with growth deceleration in an adolescent girl, especially with a family history of thyroid disease, should first be evaluated with thyroid function tests (TSH, free T4) and thyroid autoantibodies (anti-TPO, anti-thyroglobulin) to diagnose Hashimoto thyroiditis.
⭐ High-yield pearl
Diffuse, firm, painless goiter + growth deceleration + family history of thyroid disease in a girl → screen for Hashimoto thyroiditis first with TSH/T4/antibodies.
Hashimoto (chronic lymphocytic) thyroiditis is the most common cause of acquired hypothyroidism and goiter in children/adolescents, often with a genetic/familial predisposition to autoimmune thyroid disease; growth deceleration is a classic sign of underlying childhood hypothyroidism that should prompt early testing.
#65
Niña de 10 meses, correctamente vacunada para su edad, tiene fiebre alta, fotofobia y tos. Tras 4 días de fiebre se aprecian unas manchas blancas, como un espolvoreado de harina en mucosa malar a nivel del 2º molar. Al día siguiente de detectarse estas manchas, todavía con fiebre y tos, se detecta un exantema eritematoso, maculo-papuloso morbiliforme, con tendencia a la confluencia en algunas zonas, de aparición craneocaudal. La fiebre persiste hasta 3 días más. Al 5º día de iniciar el exantema el niño se encuentra afebril pero inicia en la piel una fase de descamación fina, furfurácea. El diagnóstico clínico más probable es:
Correct. High fever with photophobia and cough, followed by Koplik spots (whitish 'flour-dusted' spots on the buccal mucosa opposite the molars), then a cephalocaudal, confluent morbilliform rash with continuing fever, and later fine desquamation, is the classic clinical course of measles (rubeola).
Rubella causes a milder illness with a fine, non-confluent rash, minimal fever, and posterior auricular/occipital lymphadenopathy — it does not produce Koplik spots or this degree of fever/cough or desquamation.
Varicella presents with pruritic vesicular lesions in different stages ('dew drops on a rose petal'), not a morbilliform confluent rash with Koplik spots.
Scarlet fever presents with a sandpaper-like rash, strawberry tongue, and follows streptococcal pharyngitis — not the described prodrome with Koplik spots and cephalocaudal morbilliform rash.
⭐ High-yield pearl
Fever + cough/coryza/conjunctivitis + Koplik spots + cephalocaudal confluent rash + later desquamation = measles.
Koplik spots are pathognomonic for measles and typically appear 1-2 days before the rash, providing an early clinical clue. The classic sequence (the 3 C's: cough, coryza, conjunctivitis) plus high fever, followed by the cephalocaudal spreading morbilliform rash and later fine desquamation, is a very high-yield clinical vignette.
#66
El síndrome de Guillain-Barré es considerado una polineuropatía postinfecciosa que presenta todas las características siguientes, EXCEPTO una:
Incorrect statement (so this is the answer). Guillain-Barré syndrome classically causes HYPOreflexia or AREFLEXIA in the weak limbs, not hyperreflexia — hyperreflexia would suggest an upper motor neuron/central process instead.
True — GBS is predominantly a motor disorder, though sensory symptoms (paresthesias) commonly accompany it.
True — the classic CSF finding is albuminocytologic dissociation: elevated protein without pleocytosis (normal cell count) and normal glucose.
True — IVIG (or plasmapheresis) speeds recovery and reduces the time on ventilatory support, but doesn't necessarily change the ultimate long-term functional outcome for all patients.
⭐ High-yield pearl
Guillain-Barré causes hyporeflexia/areflexia, NOT hyperreflexia — this is a classic exam trap.
GBS is an acute inflammatory demyelinating (or axonal) polyradiculoneuropathy — a peripheral nervous system disease, so reflexes are diminished or absent, distinguishing it from central causes of weakness. The albuminocytologic dissociation on LP (high protein, normal cell count) is a key supportive finding.
#67
Un lactante de 6 meses acude a urgencias por presentar vómitos y diarrea en las últimas 12 horas. Su peso es de 6 kg. Hace 24 horas su peso era de 6,5 kg. Presenta frecuencia cardíaca 140 lpm, frecuencia respiratoria 30 rpm, presión arterial 90/40 mmHg. En la gasometría venosa se observa pH 7,25, pCO2 33 mmHg, pO2 45 mmHg, bicarbonato 17 mmol/L, exceso de bases -7, lactato 2,5 mmol/L. El sodio es 143 mmol/L. ¿Cuál es su situación en el equilibrio ácido base?
The pCO2 is already reduced (33, below normal ~40), showing that respiratory compensation (hyperventilation blowing off CO2) IS occurring — so this isn't uncompensated.
Correct. Low pH (7.25) with low bicarbonate (17) and negative base excess (-7) indicates a primary metabolic acidosis (from dehydration/diarrhea-related losses); the low pCO2 (33, below the expected ~40) shows the expected respiratory compensation (hyperventilation), and since the pH remains abnormal, it's partial (not full) compensation.
A primary respiratory acidosis would show an elevated pCO2, not a reduced one as seen here — this doesn't fit a respiratory-primary process.
Alkalosis would show an elevated pH; this patient's pH is clearly acidotic (7.25), ruling out an alkalotic process.
⭐ High-yield pearl
Low pH + low HCO3 + low pCO2 (below normal, but pH still abnormal) = metabolic acidosis with partial respiratory compensation.
In simple acid-base analysis: identify the primary disorder from the pH direction and the value that matches it (here, low pH matches low bicarbonate → metabolic acidosis), then check if the other parameter (pCO2) has moved in the expected compensatory direction — it has (decreased), but pH hasn't normalized, so compensation is partial, not complete.
#68
Avisan de paritorio por parto a término. Se explora a recién nacida, sin esfuerzo de llanto, flácida y cianótica. Se seca y estimula y ante la ausencia de inicio de llanto se traslada a cuna térmica. Inicia llanto intenso y eficaz a los 30 segundos de vida, donde ya se podía observar recuperación del tono de forma completa con movimiento activo, frecuencia cardíaca por encima de 100 lpm y estornudo tras aspiración de secreciones faríngeas espesas. Sin embargo, persiste cianosis generalizada hasta 1 minuto y 20 segundos de vida a partir del cual presenta solamente acrocianosis. A los 4 minutos de vida inicia dificultad respiratoria (esfuerzo respiratorio irregular) consistente en polipnea, tiraje subcostal e intercostal leve-moderado, leve aleteo nasal y quejido espiratorio (con frecuencia cardíaca por encima de 100 lpm, movimiento activo, recuperación completa del color con coloración completamente rosada y reflejos de tos y estornudo), que se resuelve tras colocar presión positiva durante 2 minutos. ¿Qué puntuación de Apgar tiene esta recién nacida?
A score of 4 at 1 minute is too low given the description — by 1 minute the infant already has a strong cry, good tone, heart rate >100, and a sneeze reflex; only color remains abnormal (still generally cyanotic right at the 1-minute mark).
Correct. At 1 minute: heart rate >100 (2) + strong effective cry (2) + good active tone (2) + sneeze/cough reflex (2) + still generally cyanotic at exactly 1 minute (0) = 8. At 5 minutes: heart rate >100 (2) + irregular respiratory effort with grunting/retractions (1) + good tone (2) + reflex present (2) + fully pink color (2) = 9.
A 9/9 would require full respiratory scoring (2) at 5 minutes, but the described grunting/retractions/irregular effort at that point corresponds to a partial (1), not full, respiratory score.
A 9/10 would require a perfect score of 10 at 5 minutes, but the respiratory distress (grunting, retractions) described at that time point means the respiratory component can't score the maximum 2.
⭐ High-yield pearl
Apgar is scored at 1 and 5 minutes across 5 components (HR, respiratory effort, tone, reflex irritability, color) — work through each individually rather than eyeballing 'looks fine.'
This vignette is a good drill for the Apgar components: at 1 minute, everything but color has normalized (giving 8); by 5 minutes, color has normalized but new mild respiratory distress appears, capping the respiratory sub-score at 1 (giving 9 total) — a useful reminder that Apgar can 'move around' between components at different time points.
#69
Respecto a las medidas a tomar ante un niño diagnosticado de tos ferina, en relación a sus contactos, indique la respuesta INCORRECTA:
This is a true, standard recommendation — chemoprophylaxis is given to all household (close) contacts regardless of age/vaccination/symptom status, since household exposure is considered high-risk regardless of these factors.
Incorrect statement (so this is the answer). Prophylaxis for healthcare workers is targeted at those with unprotected close exposure to respiratory secretions, not blanket treatment of 'all staff who attended the child' regardless of the type/level of exposure or protection used.
True — Tdap vaccination of household contacts is recommended regardless of prior pertussis infection, since natural immunity (like vaccine immunity) wanes over time.
True — the standard isolation recommendation is at least 5 days of appropriate antibiotic treatment (or about 3 weeks from cough onset if untreated).
⭐ High-yield pearl
Pertussis chemoprophylaxis for household contacts is universal; for healthcare workers, it's based on the type/level of exposure, not a blanket policy.
This distinction matters clinically: household members share prolonged, unavoidable close contact (hence blanket prophylaxis), while healthcare exposure risk varies enormously depending on PPE use and contact type — so occupational prophylaxis decisions are individualized to actual exposure risk.
#70
Indique la respuesta FALSA respecto a la invaginación intestinal en pediatría:
Incorrect statement (so this is the answer). Most pediatric intussusception cases are idiopathic, with lymphoid hyperplasia (e.g., from a preceding viral infection, such as Peyer's patch enlargement) acting as the lead point — congenital adhesions are not the typical cause; a pathologic lead point (Meckel diverticulum, polyp, etc.) is more common in older children/adults but still isn't 'adhesions.'
True — intussusception shows a seasonal pattern with peaks in autumn/winter, paralleling viral illness seasonality.
True — an association with preceding or concurrent adenovirus (especially type C) infection is well documented, likely via lymphoid (Peyer's patch) hyperplasia acting as a lead point.
True — a small, transient increased risk of intussusception in the 1-3 weeks after rotavirus vaccination (particularly after the first dose) has been observed and is monitored, though the benefits of vaccination clearly outweigh this small risk.
⭐ High-yield pearl
Most pediatric intussusception is idiopathic (viral-triggered lymphoid hyperplasia acting as lead point) — NOT due to congenital adhesions.
Congenital adhesions (Ladd's bands) are associated with malrotation/volvulus, a different pediatric surgical emergency — don't confuse the two. Intussusception's lead point in infants is usually just hypertrophied Peyer's patches from a recent viral illness (like adenovirus), not a structural/congenital band.
#71
Todas las siguientes pueden ser manifestaciones tardías de sífilis congénita, habitualmente no evidentes clínicamente en los 2 primeros años de vida. Indique la manifestación que NO es habitual en esta patología:
Hutchinson teeth (notched, peg-shaped upper central incisors) are a classic late manifestation of congenital syphilis.
Saddle nose deformity (from destruction of nasal cartilage) is a classic late manifestation of congenital syphilis.
Interstitial keratitis is a classic late ocular manifestation of congenital syphilis, part of the Hutchinson triad along with Hutchinson teeth and 8th nerve deafness.
Correct (this is the one that's NOT typical). Congenital heart disease is not a characteristic feature of congenital syphilis — the classic late findings involve teeth, bone (saber shins, saddle nose), eyes (interstitial keratitis), and 8th cranial nerve (deafness), not cardiac malformations.
⭐ High-yield pearl
Congenital syphilis's classic late triad (Hutchinson triad): Hutchinson teeth + interstitial keratitis + 8th nerve deafness, plus bony changes like saddle nose and saber shins.
Congenital cardiac defects are not part of the classic congenital syphilis picture — this is a useful exclusion to remember, since the disease's late stigmata are concentrated in teeth, bone, eyes, and hearing rather than the heart.
#72
Mujer de 35 años que hace dos días sufrió un accidente de coche sin apenas consecuencias físicas acude a su médica de atención primaria, por insomnio con pesadillas, expresa también recuerdos vívidos de detalles del accidente y síntomas de hiperactivación. El diagnóstico más probable es:
Correct. Intrusive memories, nightmares, insomnia, and hyperarousal beginning within days of a traumatic event, and lasting under a month, define acute stress reaction/disorder — PTSD requires symptoms to persist beyond one month.
An adjustment disorder with depressed mood would center on low mood/depressive symptoms rather than this specific trauma-related intrusion/hyperarousal symptom cluster.
PTSD requires the symptom duration to exceed one month; at only two days post-trauma, the timeline doesn't yet meet PTSD criteria, even though the symptoms are similar.
Generalized anxiety disorder involves chronic, diffuse worry unrelated to a specific precipitating traumatic event, not this acute, trauma-linked symptom cluster.
⭐ High-yield pearl
Trauma-related symptoms <1 month after the event = acute stress reaction; only after 1 month does it become PTSD.
The symptom clusters (intrusion/re-experiencing, hyperarousal, avoidance) are similar between acute stress reaction and PTSD — the key differentiator on exams is simply the timeline: under a month is acute stress reaction, beyond a month (with continued symptoms) becomes PTSD.
#73
Los mecanismos de defensa que con mayor frecuencia se presentan en el trastorno delirante son los siguientes, EXCEPTO:
Projection (attributing one's own unacceptable feelings/impulses to others) is a classic, frequently described defense mechanism in delusional (paranoid) disorder.
Denial is also commonly described as operating in delusional disorder, helping the person avoid the underlying unacceptable feelings that the delusion defends against.
Correct (this is the exception). Reaction formation (converting an unacceptable impulse into its opposite) is not among the defense mechanisms classically emphasized in delusional disorder, unlike projection, denial, and regression.
Regression (reverting to earlier, less mature patterns of functioning) is also classically described as operating in delusional disorder.
⭐ High-yield pearl
Delusional disorder's classic defense mechanisms are projection, denial, and regression — reaction formation is not part of this classic trio.
These psychodynamic concepts occasionally appear on exams as a memorization point: know that paranoid/delusional disorder is classically linked to projection (turning internal threat into external threat), with denial and regression also commonly cited, while reaction formation is more associated with obsessive-compulsive personality patterns.
#74
Sobre los factores de mal pronóstico en la esquizofrenia, señale la respuesta INCORRECTA:
True — early age of onset is a recognized poor prognostic factor in schizophrenia.
True — prominent negative symptoms are associated with a worse prognosis in schizophrenia.
Incorrect statement (so this is the answer). Acute (sudden) onset is actually a GOOD prognostic factor in schizophrenia, not a poor one — insidious/gradual onset is the poor prognostic pattern, the opposite of what this option claims.
True — a history of aggressive behavior has been associated with a worse prognosis/course.
⭐ High-yield pearl
Acute onset predicts a BETTER prognosis in schizophrenia — insidious onset is the poor prognostic pattern, the opposite of what's often assumed.
Classic favorable prognostic factors in schizophrenia include: acute/sudden onset, later age of onset, a clear precipitating stressor, good premorbid functioning, prominent mood symptoms, and a family history of mood disorder (rather than schizophrenia) — remembering these as a set helps avoid this common trap.
#75
Adolescente de 16 años que es traída a la consulta por sus padres debido a cambios drásticos en su comportamiento en los últimos seis meses. Ha mostrado síntomas de depresión, irritabilidad y recientemente ha comenzado a autolesionarse realizándose cortes en los brazos. También se ha aislado socialmente y ha tenido dificultades para mantener su rendimiento académico. ¿Cuál de los siguientes factores es el más significativo para indicar desregulación emocional y riesgo de conducta suicida en esta paciente?
Correct. Self-harm behavior (cutting) is the single most significant marker here of emotional dysregulation and elevated suicide risk — it's a direct behavioral indicator, carrying much more specific risk weight than the other, more nonspecific symptoms listed.
Social withdrawal is a concerning but nonspecific symptom seen across many conditions (depression, anxiety, normal adolescent adjustment difficulties) and carries less specific weight than actual self-harm behavior.
Irritability is also nonspecific and common in many adolescent mood presentations, without the same direct risk signal as self-harm.
Academic difficulties are a general functional impact marker, not a specific indicator of emotional dysregulation or suicide risk the way self-harm is.
⭐ High-yield pearl
Among nonspecific mood/behavioral changes, actual self-harm behavior is the strongest, most specific red flag for suicide risk.
When multiple concerning symptoms are present, self-harm behavior should always be weighted most heavily and explored directly (method, frequency, suicidal intent, access to means) — it is a much stronger predictor of future risk than nonspecific symptoms like irritability or social withdrawal, which are common across many adolescent presentations.
#76
Mujer de 28 años con diagnóstico de trastorno bipolar tipo I embarazada de 12 semanas. Ha tenido episodios maníacos y depresivos en el pasado. Actualmente, está preocupada por el impacto de su tratamiento en el feto. ¿Cuál de los siguientes tratamientos es más seguro y recomendado durante el embarazo, y qué tipo de psicoterapia es apropiada como complemento?
Valproic acid is one of the most teratogenic mood stabilizers (neural tube defects, other major malformations, and neurodevelopmental effects) and should be avoided in pregnancy whenever possible.
Correct. Lamotrigine has a comparatively more favorable reproductive safety profile among mood stabilizers and is often preferred for maintenance treatment of bipolar disorder in pregnancy, particularly for depressive-pole prevention, combined with cognitive-behavioral therapy as an adjunct.
Lithium carries its own teratogenic risk (notably cardiac malformations such as Ebstein's anomaly, especially with first-trimester exposure), making it a less favorable first choice than lamotrigine when an alternative is reasonable, though it can still be used cautiously in some cases.
Carbamazepine is also teratogenic (neural tube defects among other risks) and is not preferred during pregnancy when better-tolerated alternatives exist.
⭐ High-yield pearl
Among mood stabilizers, lamotrigine has a relatively more favorable reproductive safety profile compared to valproate, carbamazepine, and lithium.
Medication choice in bipolar disorder during pregnancy always requires weighing teratogenic risk against the risk of untreated illness (relapse can itself harm mother and fetus) — this is why an individualized risk-benefit discussion with psychiatry/obstetrics is essential, but among the options given, lamotrigine plus CBT represents the more favorable combination.
#77
Respecto a la enfermedad de Alzheimer, señale la respuesta INCORRECTA:
True — the ApoE ε4 allele is a well-established genetic risk factor for late-onset Alzheimer's disease.
Incorrect statement (so this is the answer). CSF tau (total tau and phospho-tau) is actually INCREASED in Alzheimer's disease (reflecting neuronal injury), not decreased — it's CSF amyloid-beta42 that decreases, not tau.
True — amyloid PET and tau PET are useful biomarkers supporting early/preclinical diagnosis of Alzheimer's disease.
True — medial temporal lobe (hippocampal) atrophy is a classic structural MRI finding in Alzheimer's disease.
⭐ High-yield pearl
CSF biomarkers in Alzheimer's: amyloid-beta42 goes DOWN, but total tau and phospho-tau go UP — don't mix up the direction for tau.
The classic Alzheimer's CSF biomarker profile is 'low amyloid, high tau': decreased Aβ42 (reflecting its deposition into plaques, so less is free in CSF) paired with increased total tau and phospho-tau (reflecting ongoing neuronal/axonal injury) — remembering this opposite-direction pairing prevents this exact type of exam trap.
#78
Un paciente acude a la consulta porque tiene un trastorno de la marcha, tropieza y tiene caídas frecuentes. En la exploración presenta temblor de reposo en el miembro superior derecho, rigidez en rueda dentada al movilizarle las extremidades superiores y marcha alterada desplazando el tronco hacia delante con pasos cortos. ¿Cuál de las siguientes afirmaciones apoyaría el diagnóstico de enfermedad de Parkinson?
Lack of initial response to levodopa would argue AGAINST idiopathic Parkinson's disease (which is typically levodopa-responsive) and would instead suggest an atypical parkinsonian syndrome.
Correct. A dopamine transporter (DAT) SPECT scan showing reduced uptake in the nigrostriatal pathway supports a diagnosis of Parkinson's disease, reflecting loss of dopaminergic nigrostriatal neurons — a supportive imaging biomarker.
A normal cardiac MIBG scintigraphy would argue AGAINST Parkinson's disease — an abnormal (reduced uptake) MIBG scan supports Parkinson's disease (reflecting cardiac sympathetic denervation), so a normal result doesn't support the diagnosis.
Early, prominent autonomic symptoms would raise suspicion for an atypical parkinsonian syndrome like multiple system atrophy, not idiopathic Parkinson's disease, where autonomic features typically appear later.
⭐ High-yield pearl
DAT-SPECT showing reduced nigrostriatal dopamine transporter uptake supports Parkinson's disease; early dysautonomia or a normal MIBG scan argue AGAINST it.
Atypical features that should make you doubt idiopathic Parkinson's disease and consider an atypical parkinsonian syndrome instead include: poor/absent levodopa response, early falls, early prominent autonomic failure, early dementia, and symmetric onset — the vignette here (asymmetric tremor, rigidity, good fit with classic gait) plus a supportive DAT-SPECT points toward classic Parkinson's disease.
#79
Mujer de 35 años consulta por cuadro de diplopia y debilidad proximal progresivas que empeora a lo largo de día. En la exploración neurológica se aprecia voz nasal, ptosis bilateral sin afectación pupilar, limitación para la abducción de ojo derecho y debilidad proximal con reflejos miotáticos conservados. Respecto a esta paciente señale la opción INCORRECTA:
True — anti-AChR antibody titers correlate poorly with disease severity across patients (though changes within an individual patient can sometimes track disease activity).
True — myasthenia gravis is commonly associated with other autoimmune diseases (thyroid disease, other autoimmune conditions).
True — some degree of familial clustering/genetic predisposition is recognized in myasthenia gravis.
Incorrect statement (so this is the answer). Patients are generally either anti-AChR-positive OR anti-MuSK-positive (these are largely mutually exclusive antibody profiles, not both together), and anti-MuSK-positive myasthenia typically responds LESS predictably to standard immunosuppressants/pyridostigmine compared to anti-AChR-positive disease, not more.
⭐ High-yield pearl
Anti-AChR and anti-MuSK positive myasthenia gravis are largely distinct, mutually exclusive subgroups with different treatment response profiles — they don't occur 'both positive' with better combined response.
Anti-MuSK-positive myasthenia has distinct clinical features (often more bulbar/facial/neck weakness, less thymic pathology) and a different treatment response pattern (often poorer response to pyridostigmine, sometimes better response to rituximab) compared to the more classic anti-AChR-positive disease — recognizing them as separate immunologic subgroups is key.
#80
Con respecto a la parálisis facial, ¿cuál de los siguientes signos y síntomas nos haría pensar en un origen central?
Ageusia (taste loss) reflects involvement of the chorda tympani/facial nerve peripherally, which is a peripheral (not central) sign.
Ear pain/hypoesthesia in the peripheral distribution of the facial nerve is a feature of peripheral facial palsy (e.g., from herpes zoster/Ramsay Hunt), not a central sign.
Correct. Sparing of the forehead/eyelid closure (only lower facial muscles weak) reflects bilateral cortical innervation of the upper face, so an upper motor neuron (central) lesion spares upper facial movement while causing lower facial weakness — a peripheral (Bell's-type) palsy would affect the WHOLE hemiface, including the forehead.
Decreased lacrimation reflects greater superficial petrosal nerve/peripheral facial nerve involvement (a proximal peripheral lesion), not a central process.
⭐ High-yield pearl
Sparing of the forehead/eye closure (only lower-face weakness) = central (UMN) facial palsy; full hemiface weakness = peripheral (LMN) facial palsy.
This is one of neurology's most classic localizing exam points: the forehead has bilateral cortical (UMN) innervation, so a central lesion (affecting only one cortical hemisphere/corticobulbar tract) spares the forehead, while a peripheral facial nerve lesion (affecting the nerve itself, past where the two sides' innervation has already diverged) paralyzes the entire hemiface, including the forehead and eye closure.
#81
Hombre de 75 años con antecedentes de fibrilación auricular e hipertensión arterial es traído a urgencias por hemiparesia derecha, dificultad para hablar y fiebre de 38,5°C. La tomografía computarizada (TC) de cráneo revela un infarto cerebral en la región parietal izquierda e ingresa en la unidad de ictus. A las 48 h del ingreso se informa de presencia de Streptococcus viridans en hemocultivo. ¿Cuál es el diagnóstico más probable y el enfoque diagnóstico-terapéutico adecuado en este caso?
Simply attributing this to AF-related cardioembolic stroke ignores the new finding of Streptococcus viridans bacteremia, which points to a different (infective) embolic source requiring specific work-up and treatment — anticoagulation alone would miss the underlying infection.
There's no mention of meningeal signs, CSF findings, or a clinical picture supporting bacterial meningitis — the positive blood culture with a stroke points toward an embolic infectious source (endocarditis) rather than primary CNS infection.
Correct. A viridans group streptococcus bacteremia (a classic endocarditis-causing organism) in a patient with a new embolic-appearing stroke should raise strong suspicion for infective endocarditis with septic embolization; work-up should include echocardiography to look for vegetations, with targeted antibiotics per susceptibility.
Nothing in the vignette (fever, positive blood culture with a typical endocarditis organism, embolic-type stroke) points toward malignancy — this doesn't fit a paraneoplastic/tumor explanation.
⭐ High-yield pearl
Fever + stroke (embolic pattern) + a typical endocarditis organism (viridans strep) in blood culture = think infective endocarditis with septic embolism.
Streptococcus viridans is one of the classic causative organisms of subacute bacterial endocarditis (often on previously damaged/native valves). A new stroke plus positive blood cultures for such an organism should prompt echocardiography (transthoracic, then transesophageal if needed) to look for vegetations, in addition to targeted IV antibiotics — anticoagulation is typically avoided or used very cautiously in this setting due to hemorrhagic transformation risk in septic emboli.
#82
Mujer de 55 años que consulta por una cefalea con sensación de presión bilateral, que no asocia fotofobia, náuseas ni vómitos. La paciente puede realizar sus actividades habituales porque el dolor es de intensidad moderada. El dolor es prácticamente diario en los últimos 6 meses. Desde el punto de vista terapéutico, ¿cuál es la opción más adecuada?
Daily simple analgesic use for near-daily headache risks causing medication-overuse headache and doesn't address the underlying chronic tension-type headache pattern needing preventive therapy.
Triptans are specific to migraine treatment and are not appropriate for tension-type headache (which lacks the migrainous features — no photophobia, nausea, or significant disability described here).
Propranolol is a preventive option more specifically indicated for migraine prophylaxis, not the first-line preventive choice for chronic tension-type headache.
Correct. Bilateral, pressure-type headache without migrainous features (no photophobia/nausea/vomiting), occurring almost daily for 6 months, describes chronic tension-type headache; first-line preventive treatment is low-dose amitriptyline (25-50 mg/day) continued for 3-6 months.
⭐ High-yield pearl
Bilateral, non-disabling, pressure-type headache without migrainous features, occurring almost daily = chronic tension-type headache → low-dose amitriptyline as first-line prevention.
Distinguishing tension-type headache from migraine is largely clinical: tension-type is typically bilateral, pressing/tightening, mild-moderate, and not worsened by routine activity, without the associated photophobia/phonophobia/nausea that define migraine — and their preventive drug choices differ (amitriptyline for tension-type vs. propranolol/topiramate/CGRP-targeted agents for migraine).
#83
Mujer de 18 años sin antecedentes de interés ni consumo de tóxicos que ingresa en planta por un cuadro de alteración conductual con ansiedad, agresividad e ilusiones visuales. Durante su ingreso presenta una crisis convulsiva junto con discinesias orolinguales y distonía del pie izquierdo. Dos semanas previas había presentado un cuadro de diarrea, náuseas y vómitos autolimitados. Respecto a este síndrome señale la respuesta INCORRECTA:
True — anti-NMDA receptor encephalitis is the most common autoimmune encephalitis overall (and the most common in young women).
Incorrect statement (so this is the answer). MRI is frequently NORMAL in anti-NMDAR encephalitis, and when abnormal (e.g., hippocampal/mesial temporal hyperintensity), the finding is nonspecific and not pathognomonic — the diagnosis relies on clinical features plus antibody testing (CSF/serum), not a characteristic MRI pattern.
True — anti-NMDAR encephalitis has a well-recognized association with tumors, classically ovarian teratoma in young women, so tumor screening is part of the standard work-up.
True — with prompt immunotherapy (and tumor removal if present), the prognosis is generally favorable, though recovery can be slow and some patients have relapses.
⭐ High-yield pearl
MRI is often normal in anti-NMDAR encephalitis and is NOT diagnostic — the diagnosis rests on clinical picture + antibody testing (CSF preferred over serum).
This is the most common autoimmune encephalitis, classically presenting in young women with psychiatric symptoms, seizures, movement disorders (orofacial dyskinesias), and autonomic instability, often following a preceding viral-like prodrome — always screen for an underlying tumor (especially ovarian teratoma) as part of the work-up.
#84
Hombre de 81 años con antecedentes de HTA, dislipemia y enfermedad de Alzheimer leve. Avisa su familia porque lo han encontrado en su casa caído en el suelo y no es capaz de movilizar extremidades derechas. Llega al hospital trasladado por emergencias como código ictus. A la exploración física destaca paresia facial derecha supranuclear, afasia global, hemianopsia derecha y hemiplejia de miembros derechos. La TC craneal se informa como ASPECTS 8 sin datos de sangrado. En angioTC oclusión de segmento M2 de división anterior de ACM izquierda. ¿Cuál de los siguientes es el mejor tratamiento inicial para este paciente?
IV alteplasa may also be given (if within the time window and no contraindications) alongside thrombectomy, but for a large-vessel occlusion like this M2 segment, mechanical thrombectomy is the key definitive intervention that fibrinolysis alone often cannot achieve.
Dual antiplatelet therapy and statins are secondary prevention measures, not the acute reperfusion treatment needed for an acute large-vessel occlusion stroke.
Mild Alzheimer's disease alone is not a reason to withhold appropriate acute stroke reperfusion therapy in an otherwise reasonable candidate — conservative management would deny a beneficial intervention.
Correct. A large-vessel occlusion (M2 segment of the left MCA) with a favorable ASPECTS score (8) and no hemorrhage is an indication for mechanical thrombectomy, the most effective treatment for restoring perfusion in this setting.
⭐ High-yield pearl
Large-vessel occlusion (like an M2 MCA segment) with a good ASPECTS score and no hemorrhage → mechanical thrombectomy is the key acute treatment.
Thrombectomy has transformed acute stroke care for large-vessel occlusions, often combined with IV thrombolysis when eligible (not either/or) — ASPECTS score helps assess how much salvageable brain tissue remains and guides eligibility, with higher scores (less early infarction) favoring intervention.
#85
Sobre el tratamiento quirúrgico de la enfermedad de Parkinson señale la opción correcta:
The main modern DBS targets are the subthalamic nucleus (STN) and globus pallidus internus (GPi) — the ventral intermediate thalamic nucleus is used mainly for tremor-predominant cases (including essential tremor), not as one of the two main standard targets described here.
Deep brain stimulation (DBS), not ablative/lesional surgery, is by far the most commonly used surgical approach today — lesional surgery has become far less common.
Correct. Symptoms/signs that do NOT respond to levodopa (such as significant gait freezing, dysarthria, or cognitive impairment) generally do not improve with DBS either and predict poor surgical outcome — levodopa responsiveness is a key selection criterion for surgical candidacy.
High-frequency stimulation is generally thought to functionally disrupt/inhibit abnormal basal ganglia firing patterns (a 'functional lesion' effect), not simply activate the stimulated nucleus in a straightforward excitatory sense.
⭐ High-yield pearl
Levodopa responsiveness predicts DBS outcome — symptoms that don't respond to levodopa generally won't respond to DBS either.
This is why a formal levodopa challenge test is part of the standard pre-surgical work-up for DBS candidacy: the degree of improvement with levodopa strongly predicts the degree of improvement expected from surgery, and non-levodopa-responsive features (axial symptoms, cognitive decline) are a red flag against proceeding.
#86
El APACHE-II (Acute Physiologic Assessment and Chronic Health Evaluation II) es un índice cuantitativo de gravedad que se calcula en el paciente crítico utilizando las siguientes variables, EXCEPTO:
White blood cell count IS one of the physiologic variables included in the APACHE II score.
Glasgow Coma Scale IS one of the variables included in APACHE II (as part of the neurologic component).
Correct (this is the one NOT included). Blood lactate is NOT one of the standard APACHE II variables — APACHE II uses temperature, mean arterial pressure, heart rate, respiratory rate, oxygenation, arterial pH, sodium, potassium, creatinine, hematocrit, WBC count, GCS, age, and chronic health points, but not lactate specifically.
Arterial pH IS one of the variables included in APACHE II.
⭐ High-yield pearl
APACHE II does NOT include lactate as one of its scoring variables — a detail worth memorizing since many other critical-care scores do use lactate.
APACHE II combines 12 acute physiologic variables (temperature, MAP, heart rate, respiratory rate, oxygenation, arterial pH, sodium, potassium, creatinine, hematocrit, WBC, GCS) with age points and chronic health points — lactate, despite its prognostic importance in sepsis/shock, isn't part of this particular composite score (unlike, say, some newer sepsis scoring systems).
#87
Mujer de 57 años ingresada en la Unidad de Cuidados Intensivos por hipotensión persistente y fracaso multiorgánico. Tras monitorización hemodinámica avanzada, la paciente presenta frecuencia cardíaca de 105 lpm, resistencias vasculares sistémicas de 400 din-seg-m2/cm5, gasto cardíaco de 8 L/min, presión venosa central de 5 mmHg, variación del volumen sistólico del 9% e índice de agua pulmonar extravascular indexado de 5 mL/kg. ¿A qué tipo de shock orienta dicha monitorización hemodinámica avanzada?
Correct. A markedly LOW systemic vascular resistance (400, well below normal) combined with a HIGH/normal-high cardiac output (8 L/min) is the classic hemodynamic signature of distributive (e.g., septic) shock — vasodilation is the primary problem, with the heart compensating by pumping more.
Cardiogenic shock would show a LOW cardiac output with HIGH systemic vascular resistance (compensatory vasoconstriction) — the opposite pattern from what's described here.
Hypovolemic shock would show low cardiac output, low CVP, and high SVR (compensatory vasoconstriction) — again the opposite of the low-SVR, high-CO pattern seen here.
Obstructive shock (e.g., tamponade, massive PE) typically shows low cardiac output with elevated filling pressures/CVP from the obstruction — not matching this low-SVR, high-CO profile.
⭐ High-yield pearl
Low SVR + high/normal cardiac output = distributive shock (the body compensates for vasodilation by increasing cardiac output).
Learning the hemodynamic 'fingerprints' of each shock type is high yield: distributive (↓SVR, ↑CO), cardiogenic (↓CO, ↑SVR, ↑filling pressures), hypovolemic (↓CO, ↑SVR, ↓filling pressures/CVP), and obstructive (↓CO, ↑filling pressures from the mechanical obstruction) — matching the numbers to the pattern, rather than memorizing shock names alone, is the transferable skill being tested.
#88
Mujer de 63 años, diabética en tratamiento con antidiabéticos orales que consulta por dolor en hombro derecho de 3 meses de evolución sin antecedente traumático. El dolor le limita el movimiento completo del hombro y desde hace una semana le impide el descanso nocturno. En la exploración el médico constata limitación para el movimiento activo de la abducción a más de 100º, de la flexión a 110º, rotación externa a 45º e interna lleva la mano al glúteo con dificultad. No presenta limitación en la movilidad pasiva de la extremidad. La orientación diagnóstica más probable y la actuación inicial es:
A sling for a week would promote stiffness and isn't the recommended conservative approach for rotator cuff tendinopathy with preserved passive motion — early mobilization/exercise is preferred.
Assuming calcific tendinosis specifically isn't warranted without imaging confirmation; also jumping straight to physiotherapy without simpler first-line measures (analgesia/NSAIDs, home exercise) skips the usual conservative stepwise approach.
Jumping straight to injection and MRI is more aggressive than warranted as the FIRST step for an uncomplicated presentation that hasn't yet failed simple conservative measures.
Correct. Limited ACTIVE range of motion (abduction, flexion, external/internal rotation) with FULLY PRESERVED PASSIVE range of motion points to rotator cuff tendinopathy (not adhesive capsulitis, which limits both active AND passive motion); appropriate first-line management is conservative — cryotherapy, oral NSAIDs, and a home exercise program, with a follow-up visit and imaging reserved for those who don't improve.
⭐ High-yield pearl
Limited ACTIVE but normal PASSIVE range of motion = rotator cuff pathology (tendinopathy/tear); limited active AND passive motion = adhesive capsulitis (frozen shoulder).
This active-vs-passive ROM distinction is one of the highest-yield shoulder exam findings: it separates a soft-tissue/tendon problem (weakness limits active movement, but the joint itself still moves fully when someone else moves it passively) from a true joint capsule/capsular restriction problem (both active and passive motion are limited, as in adhesive capsulitis) — guiding both diagnosis and initial conservative-first management.
#89
Jugador de baloncesto de 42 años que acude a urgencias por dolor de tres días de evolución en cara anterior de muslo derecho de tipo lancinante. Inicia el dolor tras mal gesto en flexión de la columna lumbar, presentando primero lumbalgia y después este dolor irradiado. En la exploración presenta un Lasegue invertido positivo, con un reflejo osteotendinoso rotuliano derecho 2/4. No hay déficit motor. La orientación diagnóstica más probable es:
A migrated central disc herniation causing cauda equina/saddle anesthesia would present with bilateral symptoms, saddle sensory loss, and bowel/bladder dysfunction — none of which is described here.
Correct. Anterior thigh pain with a positive reversed (femoral) straight leg raise test and a reduced (not absent) patellar reflex points to L4 nerve root involvement, consistent with a foraminal L4-L5 disc herniation compressing the exiting L4 root — the L4 root supplies the patellar reflex and anterior thigh/knee sensation.
L5 root compression classically causes lateral leg/dorsal foot pain and weakness in ankle/great toe dorsiflexion, plus a normal patellar reflex (L5 doesn't mediate the patellar reflex) — this doesn't match the anterior thigh distribution and reduced patellar reflex described.
Meralgia paresthetica involves purely sensory symptoms (numbness/burning) in the lateral thigh from lateral femoral cutaneous nerve entrapment, without a reduced reflex or a clear link to a lumbar flexion injury — it doesn't match this presentation.
⭐ High-yield pearl
Anterior thigh pain + reduced patellar reflex + positive reversed (femoral) straight leg raise = L4 radiculopathy, typically from a foraminal L4-L5 disc herniation.
Remember the reflex-root pairings: patellar reflex = L4 (with quadriceps weakness and anterior thigh symptoms in L4 radiculopathy), Achilles reflex = S1 (with calf/lateral foot symptoms); L5 radiculopathy has NO classically associated deep tendon reflex change, which is itself a useful localizing clue when a reflex IS affected.
#90
Paciente de 75 años con estancia prolongada en UCI. En una exploración rutinaria se observa dificultad para la flexión dorsal del pie izquierdo con un tibial anterior a 1/5, una dificultad para la extensión de los dedos 1/5 y dificultad para la eversión con peroneos 3/5. No presenta otro foco neurológico, ni dolor en la región lumbar ni en la extremidad. ¿Cuál de las siguientes es la actitud más correcta?
Correct. Isolated foot drop (weak tibialis anterior/dorsiflexion and toe extension) with relatively preserved eversion strength, no back pain, and no other neurologic findings in a bed-bound ICU patient is classic for common peroneal (fibular) nerve compression at the fibular head (from prolonged pressure/positioning); management is a foot-drop (ankle-foot) orthosis and physiotherapy.
An urgent EMG isn't necessary as the immediate first step for this classic clinical presentation, and simply resting without addressing positioning/bracing wouldn't prevent worsening or aid recovery.
There's no ascending, symmetric weakness or other systemic features suggesting Guillain-Barré — this isolated, unilateral, purely motor deficit localized to one peripheral nerve's distribution doesn't fit a polyradiculoneuropathy picture.
There's no back pain or other findings suggesting a central/spinal cause requiring MRI or corticosteroids — the presentation is classic for a peripheral compressive mononeuropathy, not a central process.
⭐ High-yield pearl
Isolated foot drop in a bed-bound patient, without back pain, = classic common peroneal nerve palsy from compression at the fibular head — manage with bracing and physiotherapy.
The common peroneal nerve winds superficially around the fibular neck, making it especially vulnerable to compression in immobilized, bed-bound, or thin patients (as well as from leg crossing or tight casts) — recognizing this classic 'foot drop with preserved reflexes and no back pain' pattern avoids unnecessary invasive work-up.
#91
Mujer de 19 años que, practicando patinaje sobre ruedas, sufre un traumatismo indirecto de la rodilla derecha, con luxación de rótula tratada en urgencias. Acude a revisión 2 meses más tarde y refiere que nota dolor y sensación de inestabilidad y subluxación frecuente con la actividad física. De los siguientes elementos, señale el que NO favorece la inestabilidad fémoro-patelar:
Femoral anteversion increases the Q angle and lateral pull on the patella, favoring patellofemoral instability — this IS a recognized risk factor.
Correct (this is the exception, so it's the answer). Internal tibial torsion does NOT favor patellar instability — it's EXTERNAL tibial torsion that increases the effective Q angle and predisposes to lateral patellar instability; internal torsion works in the opposite direction.
Genu valgum increases the Q angle, favoring lateral patellar subluxation/dislocation — this IS a recognized risk factor.
Patella alta (a high-riding patella) reduces the patella's engagement in the trochlear groove early in flexion, favoring instability — this IS a recognized risk factor.
⭐ High-yield pearl
Increased Q angle factors (femoral anteversion, genu valgum, EXTERNAL tibial torsion, patella alta) favor patellofemoral instability — INTERNAL tibial torsion does not.
All the true risk factors for patellar instability share a common mechanism: they increase the lateral vector pulling the patella out of the trochlear groove (higher effective Q angle) or reduce bony/ligamentous restraint (patella alta, trochlear dysplasia) — internal tibial torsion doesn't fit this mechanism and is the outlier.
#92
Desde el punto de vista fisiopatológico la osteonecrosis de la cabeza femoral se puede desencadenar por todos los mecanismos aquí descritos EXCEPTO:
Genetic factors affecting vascular flow (e.g., thrombophilias, abnormal coagulation regulation) are a recognized contributing mechanism to femoral head osteonecrosis.
Intravascular occlusion by emboli (fat emboli, nitrogen bubbles in decompression sickness, abnormal sickle red blood cells) is a well-recognized mechanism of femoral head osteonecrosis.
Correct (this is the exception). Arterial intimal dehiscence/tearing is not a classically described mechanism of femoral head osteonecrosis — the recognized mechanisms involve vascular occlusion (embolic, genetic/coagulation-related) or extravascular compression, not primary arterial wall tearing.
Extravascular compression from fat cell hypertrophy/accumulation within the bone marrow (as seen with corticosteroid use or alcohol) raising intraosseous pressure and compressing the microvasculature is a recognized mechanism of osteonecrosis.
⭐ High-yield pearl
Femoral head osteonecrosis mechanisms cluster into vascular occlusion (embolic/genetic) or extravascular compression — arterial intimal tearing is not one of the classic mechanisms.
Remembering osteonecrosis pathophysiology as a checklist helps on exams: (1) direct vascular disruption (trauma, fracture), (2) intravascular occlusion (fat/nitrogen/sickle cell emboli, thrombophilia), and (3) extravascular compression (fat hypertrophy from steroids/alcohol raising intraosseous pressure) — arterial intimal dehiscence doesn't fit any of these established categories.
#93
Mujer de 68 años con IMC 28 kg/m2 que consulta por dolor crónico en rodilla derecha. Refiere que el dolor empeora con la actividad física, especialmente al subir y bajar escaleras, y mejora con el reposo. En la exploración física se observa crepitación en la rodilla derecha y leve deformidad en ambas. Una radiografía de rodilla derecha muestra estrechamiento del espacio articular y formación de osteofitos. ¿Cuál es la opción de tratamiento más adecuada en este caso?
Immobilization with a brace isn't first-line for knee osteoarthritis and can actually worsen muscle weakness/deconditioning through disuse.
Correct. For symptomatic knee osteoarthritis (activity-related pain, crepitus, joint space narrowing, osteophytes) in an overweight patient, first-line management is weight loss and supervised exercise to strengthen the quadriceps, which reduces pain and improves function.
Intra-articular corticosteroid injection is a reasonable option for flares or when conservative measures are insufficient, but it's not the first-line initial approach before trying weight loss/exercise.
Tramadol (an opioid) is reserved for cases not adequately controlled by first-line conservative and simple analgesic measures — it's not the initial treatment of choice.
⭐ High-yield pearl
Knee OA first-line treatment is weight loss + supervised quadriceps-strengthening exercise, before injections or opioids.
Non-pharmacologic measures (weight loss, structured exercise programs targeting quadriceps strength) have strong evidence for reducing pain and improving function in knee osteoarthritis and are recommended as first-line therapy before escalating to intra-articular injections or systemic analgesics like opioids.
#94
Hombre de 30 años que acude a consulta por dolor lumbar crónico que empeora en la noche y mejora con el ejercicio. Refiere rigidez matutina de más de una hora. La exploración física revela una disminución de la movilidad en la columna lumbar y dolor a la palpación y exploración de las articulaciones sacroilíacas. La resonancia magnética muestra edema en las articulaciones sacroilíacas compatible con sacroileitis. ¿Cuál es el tratamiento inicial más indicado para este paciente?
Methotrexate has limited efficacy for the axial (spinal/sacroiliac) manifestations of spondyloarthritis and is not first-line for this presentation.
Oral corticosteroids are not standard first-line therapy for axial spondyloarthritis and don't have strong evidence supporting long-term use in this setting.
Correct. Inflammatory back pain (worse at night, improves with exercise, morning stiffness >1 hour) with MRI-confirmed sacroiliitis describes axial spondyloarthritis; first-line treatment is physiotherapy plus NSAIDs, escalating to biologics only if this fails.
Anti-TNF biologic therapy is reserved for patients who fail an adequate trial of NSAIDs plus physiotherapy first — it's not the initial treatment choice.
⭐ High-yield pearl
Inflammatory back pain pattern (worse at night, improves with exercise, morning stiffness) + sacroiliitis on MRI = axial spondyloarthritis → NSAIDs + physiotherapy first-line.
The classic inflammatory back pain pattern (age <40, insidious onset, improvement with exercise but not rest, night pain, morning stiffness >30-60 min) distinguishes axial spondyloarthritis from mechanical back pain. Treatment follows a step-up approach: NSAIDs plus physical therapy first, with anti-TNF/other biologics reserved for inadequate responders.
#95
Mujer de 83 años hospitalizada por neumonía adquirida en la comunidad por neumococo. Presenta una artritis aguda de carpo derecho. Sospechamos enfermedad por depósito de pirofosfato pero no se observa condrocalcinosis en la radiografía de carpos ni se ha conseguido obtener líquido sinovial durante la artrocentesis. ¿Qué radiografías añadiremos al cribado con el objetivo de identificar condrocalcinosis?
Correct. When screening for chondrocalcinosis (CPPD deposition disease) beyond the wrists, the additional standard radiographic views are the knees and the pubic symphysis — the classic sites where chondrocalcinosis is most reliably visualized.
Shoulders are not part of the classic standard screening set for chondrocalcinosis (knees and pubic symphysis are the standard additional sites, not shoulders).
Similarly, shoulders are not part of the standard screening combination — pubic symphysis is correct, but shoulders should be replaced by knees.
Elbows are not part of the classic standard chondrocalcinosis screening views — knees, not elbows, is the correct pairing with pubic symphysis.
⭐ High-yield pearl
Chondrocalcinosis screening beyond the wrists = knees + pubic symphysis, the two classic additional radiographic sites.
CPPD deposition disease preferentially calcifies fibrocartilage structures — the knee menisci, the triangular fibrocartilage complex of the wrist, and the pubic symphysis fibrocartilage — which is why these specific sites (not just any joint) form the standard screening radiograph combination when chondrocalcinosis is suspected clinically but not yet confirmed.
#96
Uno de estos hallazgos anatomopatológicos sugiere el diagnóstico de enfermedad por IgG4:
Arterial thrombosis is not a characteristic histologic feature that suggests IgG4-related disease.
Arterial intimal proliferation without vasculitis is a described (though less specific) feature in some IgG4-related disease vasculopathy, but it's not the classic, most specific pathologic hallmark being tested here.
Correct. Storiform ('woven mat'-pattern) fibrosis is one of the classic, most characteristic histopathologic hallmarks of IgG4-related disease, typically accompanied by dense lymphoplasmacytic infiltrate (rich in IgG4+ plasma cells) and obliterative phlebitis.
A perivascular polymorphonuclear (neutrophilic) infiltrate suggests an acute inflammatory/infectious process, not the characteristic lymphoplasmacytic infiltrate of IgG4-related disease.
⭐ High-yield pearl
Storiform fibrosis + dense lymphoplasmacytic (IgG4+) infiltrate + obliterative phlebitis = the classic histologic triad of IgG4-related disease.
IgG4-related disease is a fibroinflammatory condition that can affect nearly any organ (pancreas — autoimmune pancreatitis, salivary/lacrimal glands, retroperitoneum, biliary tree, kidneys, and more), unified by this shared histopathologic signature, and it typically responds well to glucocorticoids.
#97
¿Cuál de los siguientes hallazgos NO esperaría encontrar en una mujer de 28 años con una comunicación interauricular evolucionada?
A mesosystolic (pulmonary flow) murmur is a classic auscultatory finding in ASD, from increased flow across the pulmonic valve due to the left-to-right shunt.
Cardiomegaly on chest X-ray (from right heart chamber enlargement due to chronic volume overload) is a classic finding in longstanding ASD.
Right bundle branch block (from right ventricular volume overload/conduction system involvement) is a classic ECG finding in ASD.
Correct (this is the finding NOT expected). ASD causes chronic RIGHT heart volume overload (RA/RV dilation), not left ventricular hypertrophy — LV hypertrophy doesn't fit the pathophysiology of a left-to-right shunt at the atrial level.
⭐ High-yield pearl
ASD causes RIGHT heart volume overload (RA/RV enlargement, RBBB) — NOT left ventricular hypertrophy.
The shunt direction determines which side of the heart bears the chronic volume load: ASD (left-to-right shunt at atrial level) overloads the right atrium and ventricle, producing RBBB, right heart enlargement, and a pulmonary flow murmur — very different from lesions that load the left ventricle (like aortic regurgitation or a VSD, which can eventually affect the LV).
#98
Joven de 16 años con astenia desde hace 1 mes, que durante un partido de fútbol sufre un síncope. A su llegada al hospital inconsciente y hemodinámicamente inestable presenta síntomas y signos de accidente cerebrovascular, de isquemia mesentérica y de isquemia arterial periférica, en miembro superior izquierdo y de ambos miembros inferiores. ¿Cuál cree que es el diagnóstico de sospecha?
Complete heart block would cause syncope from bradycardia/asystole, but wouldn't explain simultaneous embolic phenomena (stroke, mesenteric ischemia, and multi-limb peripheral arterial ischemia) — this pattern points to a source of systemic emboli.
Acute mitral regurgitation would cause acute pulmonary edema/hemodynamic collapse, but wouldn't specifically explain this pattern of widespread simultaneous embolic events to brain, gut, and multiple limbs.
Correct. Simultaneous embolic phenomena affecting multiple vascular territories (stroke, mesenteric ischemia, and peripheral arterial ischemia in several limbs) plus syncope with hemodynamic instability suggests a mobile intracardiac mass showering emboli and intermittently obstructing flow — the classic culprit is a left atrial myxoma, which can prolapse through the mitral valve, causing obstructive syncope, and shed embolic fragments causing widespread systemic embolization.
A ruptured MCA aneurysm would explain a stroke/subarachnoid hemorrhage picture, but wouldn't explain the mesenteric and multi-limb peripheral arterial ischemia occurring simultaneously — this doesn't fit a single-vessel intracranial cause.
⭐ High-yield pearl
Simultaneous embolic events across multiple organs (brain + gut + several limbs) plus syncope = think a mobile cardiac mass (classically left atrial myxoma) as the embolic source.
Left atrial myxoma is the classic 'great mimicker' cardiac tumor: it can cause obstructive symptoms (syncope, mimicking mitral stenosis when it prolapses through the valve) AND multi-territory embolic phenomena simultaneously — a combination that should immediately raise suspicion for an intracardiac mass rather than a single-organ vascular event.
#99
Hombre de 65 años, hipertenso desde hace 12 años, que acude por primera vez a la consulta de su médico de familia para una revisión rutinaria. La exploración física es normal y el electrocardiograma muestra ritmo sinusal a 68 lpm, con bloqueo de la rama izquierda del haz de His y duración del QRS de 150 ms. ¿Cuál de las siguientes situaciones implica este hallazgo?
Correct. A wide QRS from left bundle branch block (150 ms) inherently implies delayed, non-simultaneous activation of the two ventricles — that is, ventricular dyssynchrony — regardless of whether an underlying structural heart disease is also present.
LBBB can be associated with dilated cardiomyopathy, but the finding itself doesn't necessarily imply that specific diagnosis — an incidentally found LBBB in an asymptomatic patient doesn't automatically mean dilated cardiomyopathy is present.
LBBB is an intraventricular conduction delay, not an AV conduction abnormality — it doesn't imply AV dissociation, which is a different electrophysiologic phenomenon (seen in complete heart block or some ventricular arrhythmias).
There's no clinical or ECG evidence here (no chest pain, no ST changes described) suggesting acute myocardial ischemia — LBBB alone in an asymptomatic patient with a routine exam doesn't imply an acute ischemic event.
⭐ High-yield pearl
A wide QRS from bundle branch block directly implies ventricular dyssynchrony — the two ventricles no longer contract in a coordinated, simultaneous fashion.
This concept underlies why patients with LBBB and heart failure with reduced ejection fraction may benefit from cardiac resynchronization therapy (biventricular pacing) — restoring synchronous ventricular contraction directly addresses the mechanical inefficiency created by the dyssynchronous activation pattern that a wide LBBB QRS represents.
#100
Un entrenamiento aeróbico intenso y prolongado produce una serie de adaptaciones cardiovasculares que suelen denominarse "corazón de deportista". Entre las siguientes adaptaciones fisiológicas, señale la respuesta INCORRECTA:
True — sinus bradycardia from increased vagal tone is a classic, benign finding in trained athletes.
True — increased vagal tone in athletes can produce first-degree AV block, Mobitz I (Wenckebach) second-degree block, and even transient third-degree block during sleep, all considered benign physiologic findings in this context.
Incorrect statement (so this is the answer). Complete LBBB is NOT considered a benign physiologic adaptation of athlete's heart — unlike the vagally-mediated conduction findings above, a new complete LBBB in an athlete is considered a pathological/abnormal finding that warrants further cardiac work-up, not a normal training adaptation.
True — physiologic right ventricular dilation from endurance training can produce incomplete or complete right bundle branch block, a recognized benign adaptation in endurance athletes.
⭐ High-yield pearl
Athlete's heart classically causes vagally-mediated bradyarrhythmias and physiologic RBBB — but a new complete LBBB is NOT a benign training adaptation and should be worked up.
This is a key distinction on ECG interpretation in athletes: benign 'athletic' findings (sinus bradycardia, Mobitz I, nocturnal high-grade block, RBBB from RV remodeling) don't need further work-up in an asymptomatic athlete, but new LBBB, pathologic Q waves, marked ST-segment abnormalities, or Mobitz II/complete AV block while awake are red flags requiring cardiology evaluation to exclude underlying structural heart disease.
Resultado del examen
Preguntas 51–100 · Cuaderno de Examen Medicina 2024 (v.0)