Versión: 0 · Preguntas 151-200 de 210 · Questions in Spanish · Explanations & high-yield pearls in English
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#151
Hombre de 85 años diagnosticado de enfermedad de Alzheimer en tratamiento con donepezilo. Desde hace una semana y coincidiendo con una infección urinaria por germen sensible a amoxicilina/clavulánico, presenta un trastorno grave de conducta; por todo ello, recibe tratamiento con dicho antibiótico y con risperidona 1 mg cada 12 horas. Hoy la familia lo trae a su consulta porque a pesar de mejorar la infección de orina, está muy enlentecido, necesitando ayuda para comer y vestirse, no es capaz de deambular sin ayuda, duerme de día y presenta insomnio de madrugada. Ante esta situación clínica señale la respuesta CORRECTA:
Correct. New functional decline (slowed movement, needing help with feeding/dressing, inability to walk unaided) plus a disrupted sleep-wake cycle shortly after starting risperidone in a frail 85-year-old with dementia is a classic extrapyramidal/over-sedation adverse effect of antipsychotics in the elderly — the appropriate action is to stop the likely offending drug.
Adding a benzodiazepine on top of an antipsychotic in an elderly patient already over-sedated would worsen the drug-induced functional decline and increase fall/delirium risk — the opposite of what's needed.
Waiting for the UTI to fully resolve delays addressing a clear, reversible drug-induced problem that is actively harming the patient's function right now — the medication should be reassessed promptly, not deferred.
Attributing this to dementia progression and adding memantine ignores the much more likely and reversible cause (antipsychotic-induced parkinsonism/over-sedation) temporally linked to starting risperidone.
⭐ High-yield pearl
New functional decline in an elderly patient after starting an antipsychotic = presume a drug adverse effect first, not disease progression.
Elderly patients, especially those with dementia, are highly susceptible to antipsychotic-induced extrapyramidal symptoms and excessive sedation even at low doses; the first step when new functional decline appears temporally linked to starting such a drug is to stop or reduce it, applying the geriatric principle of 'is this a new symptom, or a side effect?' before assuming disease progression.
#152
Los criterios STOPP/START tienen el objetivo de optimizar la medicación y minimizar las reacciones adversas a los medicamentos durante la revisión de la medicación en adultos mayores. En cuanto a los criterios START (versión 3, última versión), ¿cuál deberíamos valorar indicar?
Correct. START criteria (medications that SHOULD be started/considered when indicated and not contraindicated) include topical vaginal estrogens for symptomatic atrophic vaginitis in older women — an evidence-based, often under-prescribed treatment in this population.
Tetanus vaccination for an open wound is a general acute-care recommendation, not one of the specific START criteria items targeted at optimizing chronic medication use in older adults.
Topical lidocaine patches are specifically indicated for localized neuropathic pain (e.g., post-herpetic neuralgia), not generalized joint pain — this doesn't match a START indication.
Inhaled corticosteroids in mild (GOLD 1-2) COPD without frequent exacerbations are generally NOT recommended (this would actually align more with a STOPP-type criterion to avoid overuse), not a START indication.
⭐ High-yield pearl
START criteria highlight evidence-based therapies that are often under-prescribed in older adults — like topical vaginal estrogen for atrophic vaginitis — while STOPP criteria flag ones that should be stopped/avoided.
STOPP/START tools work as a pair: STOPP (Screening Tool of Older Persons' Prescriptions) flags potentially inappropriate medications to stop, while START (Screening Tool to Alert to Right Treatment) flags appropriate, evidence-based medications that are often missed or under-prescribed in older patients — topical vaginal estrogen for symptomatic atrophy is a classic START example precisely because it's frequently overlooked despite being effective and low-risk.
#153
En la actualidad se definen varios estadios o etapas de la diabetes tipo 1 autoinmune. Señale cuál es la definición CORRECTA:
Stage 3 is actually the stage where overt hyperglycemia meeting diabetes diagnostic criteria (with symptoms) appears — not simply autoimmunity plus glucose intolerance, which corresponds to stage 2.
Correct. Stage 1 of autoimmune type 1 diabetes is defined by the presence of ≥2 islet autoantibodies with normal glucose tolerance (normoglycemia) — autoimmunity is present, but there's no glucose abnormality yet.
Stage 2 is characterized by autoimmunity PLUS dysglycemia (abnormal glucose tolerance, not yet meeting full diabetes diagnostic thresholds) — frank diabetes-level hyperglycemia corresponds to stage 3, not stage 2.
The 'honeymoon phase' (partial remission with reduced insulin requirements) occurs AFTER clinical diagnosis (stage 3, once insulin therapy has started), not at stage 2.
⭐ High-yield pearl
Type 1 diabetes staging: Stage 1 = autoimmunity + normal glucose; Stage 2 = autoimmunity + dysglycemia (not yet diabetic-range); Stage 3 = autoimmunity + overt diabetes-level hyperglycemia/symptoms.
This staging system (from Insel et al./ADA) reframes type 1 diabetes as a continuum starting years before clinical diagnosis, which is the basis for newer disease-modifying immunotherapies (like teplizumab) now approved to delay progression from stage 2 to stage 3 in at-risk individuals.
#154
Mujer que acude a consulta de endocrino por secreción láctea por el pezón y una cifra de prolactina en sangre de 45 µg/L (normal <20 µg/L). ¿Cuál es la actitud diagnóstica más apropiada?
Jumping straight to brain MRI assumes a macroadenoma, but this level of prolactin elevation (45, only mildly above normal) is far more consistent with a common, non-tumoral cause than a macroadenoma (which typically produces much higher prolactin levels, often >200-250 µg/L) — imaging isn't the first step.
Correct. Before extensive work-up, common and reversible causes of hyperprolactinemia must be excluded first: dopamine-antagonist medications (antipsychotics, metoclopramide, etc.) and pregnancy are the most common causes of a mild-to-moderate prolactin elevation and must be ruled out with history and a pregnancy test before further testing.
An isolated prolactin measurement alone is insufficient for full work-up — other tests (TSH to rule out hypothyroidism, pregnancy test, medication review, sometimes macroprolactin testing) are needed to properly characterize the etiology.
Primary hypothyroidism (via elevated TRH driving prolactin release) is one recognized cause of mild hyperprolactinemia and should be checked with TSH, but it's not the single most important first step compared to the broader history-taking (medications, pregnancy) that applies to essentially every patient.
⭐ High-yield pearl
Mild-to-moderate hyperprolactinemia: rule out medications and pregnancy first — these are far more common causes than a pituitary tumor.
The magnitude of prolactin elevation is a useful clue: mild-moderate elevations (like 45 µg/L here) are usually from physiologic causes (pregnancy, stress, nipple stimulation), medications (dopamine antagonists), primary hypothyroidism, or a small prolactinoma, whereas very high levels (often >200-250 µg/L) are much more specific for a macroprolactinoma — so history and simple labs come before imaging.
#155
La estrategia de cribado de diabetes gestacional en un solo paso consiste en:
A 50-gram glucose challenge test is the initial screening step of the TWO-step strategy (followed by a confirmatory 100-gram test if the screening result is abnormal), not the one-step approach.
Correct. The one-step strategy for gestational diabetes screening (per IADPSG/current guidelines) uses a single 75-gram oral glucose tolerance test with fasting, 1-hour, and 2-hour glucose measurements, diagnosing gestational diabetes if any one value meets or exceeds the established thresholds.
A 90-gram load is not a standard glucose tolerance test protocol used in gestational diabetes screening.
A 100-gram oral glucose tolerance test is used as the confirmatory (second) step of the traditional TWO-step screening strategy, not the one-step approach.
⭐ High-yield pearl
One-step GDM screening = single 75g OGTT (fasting/1h/2h); two-step = 50g screen followed by 100g confirmatory test if abnormal.
Different professional societies endorse different strategies (one-step vs. two-step), which is a recurring source of confusion — remembering the glucose loads (75g = one-step; 50g screen → 100g confirm = two-step) is the key to keeping them straight.
#156
Está de guardia en urgencias y valora a un hombre de 45 años que consulta por vómitos de 2-3 días de evolución con disconfort abdominal y astenia intensa desde hace 1 mes. La presión arterial en triaje es 85/40 mmHg. Cuando lo explora objetiva hiperpigmentación parcheada en la cavidad oral y en la analítica destaca sodio de 134 mEq/L. ¿Cuál es su primera opción diagnóstica de las expuestas a continuación?
Hemochromatosis causes skin bronzing (diffuse hyperpigmentation from iron deposition), but wouldn't explain hypotension, vomiting, and hyponatremia as an acute presentation, nor patchy oral mucosal pigmentation specifically.
Peutz-Jeghers syndrome causes perioral/oral mucocutaneous pigmented macules, but is associated with GI polyposis and intussusception risk, not this acute adrenal-insufficiency-type presentation with hypotension and hyponatremia.
Correct. Chronic weakness/fatigue, weight loss, GI symptoms (nausea, vomiting), hypotension, hyponatremia, and patchy hyperpigmentation of the oral mucosa (from elevated ACTH cross-reacting with melanocyte receptors) describe primary adrenal insufficiency (Addison's disease), here presenting acutely as an adrenal crisis.
Stevens-Johnson syndrome is an acute severe mucocutaneous drug reaction with skin/mucosal blistering and sloughing, not this chronic constitutional/adrenal insufficiency picture.
⭐ High-yield pearl
Hypotension + hyponatremia + oral/mucosal hyperpigmentation + chronic weakness = primary adrenal insufficiency (Addison's disease) → think adrenal crisis if acutely decompensated.
The hyperpigmentation in Addison's disease is a key distinguishing clue from secondary (pituitary-driven) adrenal insufficiency: in primary adrenal failure, very high ACTH (and its co-secreted peptide, MSH-like activity) drives skin/mucosal hyperpigmentation, especially in sun-exposed areas, scars, and the oral mucosa — a finding that is ABSENT in secondary adrenal insufficiency (low ACTH).
#157
¿Qué fármaco de los mencionados a continuación ha de tenerse en cuenta cuando se evalúa a un paciente con hiperparatiroidismo?
Correct. Thiazide diuretics (hydrochlorothiazide) reduce renal calcium excretion (increase calcium reabsorption), which can raise serum calcium and either unmask or worsen apparent hyperparathyroidism — a very important confounder to consider/exclude when evaluating a patient with elevated calcium/PTH.
Losartan (an ARB) doesn't have a significant clinically relevant effect on calcium homeostasis relevant to hyperparathyroidism evaluation.
Amlodipine (a calcium channel blocker) doesn't meaningfully affect serum calcium levels or parathyroid function.
Doxazosin (an alpha-blocker) doesn't have a significant relevant effect on calcium/PTH homeostasis.
⭐ High-yield pearl
Thiazide diuretics can raise serum calcium (via reduced renal calcium excretion) — always check for thiazide use when working up hypercalcemia/hyperparathyroidism.
When evaluating any patient for primary hyperparathyroidism, a thorough medication history is essential: thiazides can mimic or exacerbate hypercalcemia, so ideally they should be discontinued (if clinically feasible) before confirming the diagnosis, to avoid misattributing a reversible drug effect to true parathyroid disease.
#158
¿Cuál de las siguientes causas de hipertiroidismo puede cursar con TSH normal o elevada?
Factitious thyrotoxicosis (exogenous thyroid hormone intake) causes suppressed TSH, like all other peripheral causes of hyperthyroidism, since the excess hormone suppresses pituitary TSH via negative feedback.
Struma ovarii (ectopic functioning thyroid tissue in an ovarian teratoma) causes peripheral thyroid hormone excess, which also suppresses TSH via negative feedback.
Correct. A TSH-secreting pituitary adenoma is the classic cause of 'inappropriate' hyperthyroidism where TSH is normal or even elevated despite high thyroid hormone levels, because the tumor autonomously secretes TSH, escaping normal negative feedback regulation.
Beta-hCG-driven hyperthyroidism (from cross-reactivity with the TSH receptor during pregnancy/gestational trophoblastic disease) suppresses TSH via the elevated peripheral thyroid hormones, just like other peripheral causes.
⭐ High-yield pearl
TSH-secreting pituitary adenoma is the classic cause of hyperthyroidism with a NON-suppressed (normal/elevated) TSH — virtually all other causes suppress TSH via negative feedback.
This is a very high-yield exam concept: any hyperthyroid patient with a TSH that is not suppressed (normal or high) should raise suspicion for either a TSH-secreting pituitary adenoma or (much more commonly) assay interference/resistance to thyroid hormone — a genuinely 'inappropriate' TSH result always deserves further investigation rather than assuming lab error.
#159
Hombre de 58 años, fumador de 30 cigarrillos diarios desde los 19 años, con antecedentes de hipertensión arterial mal controlada, diabetes mellitus tipo 2 y obesidad grado I. En estudio por disnea de 5 meses de evolución, asociando pérdida de peso, astenia e hiporexia. Como parte del estudio se realiza TC toracoabdominal describiéndose la presencia de un nódulo pulmonar inespecífico de 1,1 cm en lóbulo superior derecho sin datos de malignidad y un nódulo en la glándula suprarrenal derecha de 1,9 cm. ¿Qué pruebas complementarias habría que solicitar para el estudio del incidentaloma suprarrenal?
An 8 mg high-dose dexamethasone suppression test is used to differentiate causes of established Cushing's syndrome (pituitary vs. ectopic ACTH), not as an initial screening test for an incidentally found adrenal nodule.
An 18FDG PET-CT isn't part of the standard first-line functional work-up of an adrenal incidentaloma; it's reserved for cases with imaging features suspicious for malignancy, and the aldosterone/renin ratio (not renin/aldosterone) is the correct orientation for the screening test.
Correct. Standard functional work-up of an adrenal incidentaloma includes: screening for autonomous cortisol secretion with a 1 mg overnight dexamethasone suppression test, screening for pheochromocytoma with 24-hour urinary fractionated metanephrines (or plasma free metanephrines), and screening for primary aldosteronism with an aldosterone/renin ratio (particularly relevant given this patient's poorly controlled hypertension); imaging characterization typically continues with dedicated adrenal CT protocol.
Urinary free cortisol is a less standard first-line screening test compared to the 1 mg overnight dexamethasone suppression test for autonomous cortisol secretion, and MRI is not the preferred first-line adrenal imaging modality (dedicated CT protocol with washout characteristics is generally preferred for adrenal incidentaloma characterization).
⭐ High-yield pearl
Adrenal incidentaloma work-up = 1mg overnight DXM suppression test (cortisol) + fractionated metanephrines (pheochromocytoma) + aldosterone/renin ratio (if hypertensive/hypokalemic) + dedicated adrenal CT.
Every adrenal incidentaloma needs a standardized functional screen for the three classic secretory syndromes (Cushing's, pheochromocytoma, and — especially if hypertension or hypokalemia is present — primary aldosteronism) regardless of how the nodule was found, since silent functioning adenomas are common and carry distinct management implications.
#160
Mujer de 25 años, sin enfermedades previas conocidas, que consulta por lesión en labio inferior. No es la primera vez que le sucede desde la adolescencia, siempre en la misma zona, inicia dolor y aparece una lesión vesiculosa que se autolimita en una semana aproximadamente. Respecto al abordaje de la enfermedad de esta paciente, es INCORRECTO que:
True — suppressive antiviral prophylaxis (e.g., valacyclovir 500 mg twice daily or 1g daily) for ~6 months is a recognized approach for patients with frequent (>3/year) recurrences of herpes labialis.
True — mild, isolated recurrent herpes labialis lesions can reasonably be managed with observation alone or simple topical measures (zinc/copper sulfate compresses) without systemic antivirals.
Incorrect statement (so this is the answer). Suspected ophthalmic involvement (herpes zoster ophthalmicus / ocular herpes) is an urgent situation requiring prompt ophthalmology referral and typically higher-dose, longer antiviral therapy than standard labial herpes dosing — this scenario needs specialist urgent management, not simply outpatient oral valacyclovir at the stated dose as a routine approach.
True — UV/sun exposure is a well-known trigger for herpes labialis recurrences, so sun protection of the lips is a reasonable preventive recommendation.
⭐ High-yield pearl
Suspected ocular involvement with herpes (periocular vesicles, eye symptoms) is an ophthalmologic emergency requiring urgent specialist referral, not routine oral antiviral dosing alone.
Herpes simplex/zoster involving the eye (keratitis, uveitis) can threaten vision if not promptly and appropriately treated — this is why any suggestion of periocular or ocular involvement in a patient with recurrent herpetic lesions should prompt urgent ophthalmology evaluation rather than simply treating it like routine cold sores.
#161
Hombre de 50 años que presenta una erupción generalizada especialmente en el tronco. Refiere malestar general desde hace pocos días. Hoy acude porque ha tenido fiebre la noche anterior y se ha visto una mancha negra en la zona abdominal. A la exploración física, la mancha negra corresponde a una pequeña escara. El paciente es cazador y acudió recientemente a una batida. Sobre el abordaje del caso es cierto que:
Correct. This is a rickettsial infection (Mediterranean spotted fever/tick-borne rickettsiosis, suggested by the hunting exposure, a black eschar/tache noire, fever, and generalized rash) — rickettsioses are reportable/notifiable diseases in Spain, making declaration mandatory.
The treatment of choice for rickettsial infections is doxycycline, not amoxicillin — beta-lactams are not effective against intracellular organisms like Rickettsia.
Uncomplicated rickettsiosis in a stable patient can typically be managed as an outpatient with oral doxycycline; hospital referral is not automatically required unless there are signs of severe/complicated disease.
The classic sequence is actually the OPPOSITE: the eschar (tache noire) typically appears FIRST at the tick bite site, followed by fever, and then the generalized maculopapular rash a few days later — not fever preceding the eschar.
⭐ High-yield pearl
Black eschar (tache noire) at a tick bite + fever + generalized rash in someone with outdoor/hunting exposure = think rickettsiosis (spotted fever group); treat with doxycycline.
Mediterranean spotted fever (Rickettsia conorii) is transmitted by tick bites, classically producing the eschar first (at the bite site), followed by fever and a centrifugal maculopapular/petechial rash involving the trunk, palms, and soles; doxycycline is the treatment of choice regardless of age given its clear superiority for rickettsial disease, and these infections are notifiable.
#162
Respecto al tratamiento de la foliculitis, es correcto que:
For localized, mild folliculitis, topical antibiotics/antiseptic measures are generally first-line, not automatically oral cloxacillin — systemic therapy is reserved for more extensive or refractory cases.
Correct. In a patient with penicillin allergy, oral ciprofloxacin (or another agent with activity against Staphylococcus aureus, like clindamycin or trimethoprim-sulfamethoxazole depending on local resistance patterns) is a reasonable alternative when oral therapy for folliculitis is needed.
Simple superficial folliculitis is not itself an indication for oral antibiotic prophylaxis/treatment specifically due to endocarditis risk in valvular disease — this isn't standard practice for a superficial skin infection of this kind.
Folliculitis is fundamentally a Staphylococcus aureus infection, not primarily caused by Streptococcus pyogenes.
⭐ High-yield pearl
Folliculitis is primarily caused by Staphylococcus aureus — treatment should target staph, and localized cases are usually managed topically first.
Knowing the primary causative organism (S. aureus, not S. pyogenes) is what drives correct antibiotic selection: cloxacillin/dicloxacillin (or other anti-staphylococcal agents) for typical cases, with ciprofloxacin, clindamycin, or TMP-SMX as reasonable alternatives in penicillin-allergic patients depending on local susceptibility patterns.
#163
Hombre de 62 años con antecedentes de hipertensión arterial, diabetes mellitus tipo 2 y en tratamiento con infliximab por artritis reumatoide, se presenta en urgencias con fiebre, tos seca, mialgias y disnea leve de 5 días de evolución. A la exploración física, la saturación de oxígeno es del 90% con aire ambiente. Se realiza una radiografía de tórax que muestra opacidades en vidrio deslustrado bilaterales. La PCR en frotis nasofaríngeo para SARS-CoV-2 resulta positiva. ¿Cuál de las siguientes opciones es la conducta más apropiada?
Convalescent plasma is not standard first-line therapy for COVID-19 pneumonia with hypoxemia; prophylactic anticoagulation may be part of supportive management for hospitalized patients but isn't the defining answer here.
Empiric broad-spectrum antibiotics aren't indicated without evidence of bacterial superinfection, and high-dose corticosteroids (rather than standard-dose dexamethasone) aren't the evidence-based approach for COVID-19 pneumonia with hypoxemia.
With hypoxemia (SpO2 90% on room air) and bilateral ground-glass opacities, outpatient management with only symptomatic treatment and phone follow-up is inadequate and unsafe — this patient meets criteria for hospitalization.
Correct. An immunosuppressed patient (on infliximab) with confirmed COVID-19, hypoxemia (SpO2 90%), and bilateral ground-glass opacities on imaging meets criteria for hospitalization and treatment with remdesivir plus dexamethasone, the evidence-based combination for COVID-19 pneumonia requiring supplemental oxygen.
⭐ High-yield pearl
COVID-19 pneumonia with hypoxemia (needing supplemental oxygen) = hospitalize and treat with dexamethasone ± remdesivir — the evidence-based standard-of-care combination.
Recognizing the oxygen-requirement threshold is key: mild COVID-19 without hypoxemia is managed with outpatient supportive care (± outpatient antivirals like nirmatrelvir-ritonavir in eligible patients), while hypoxemic COVID-19 pneumonia requiring supplemental oxygen is the threshold at which hospitalization and dexamethasone (± remdesivir) become standard, evidence-based therapy — especially important to apply promptly in an immunosuppressed patient like this one.
#164
Hombre de 56 años, nacido en Paraguay, acude a consulta, remitido por su médico de familia, por disnea progresiva y palpitaciones. Tiene un ECG en el que se observa extrasístoles ventriculares y bloqueo completo de rama derecha. Aporta una serología por ELISA IgG positiva frente a Trypanosoma cruzy. ¿Cuál de las siguientes respuestas es INCORRECTA?
True — confirming a positive ELISA with a second serologic test using a different technique (e.g., immunofluorescence) is standard practice for Chagas disease diagnosis, since no single serologic test has perfect specificity.
True — PCR has good sensitivity in the acute phase (high parasitemia) but limited diagnostic value in the chronic phase of Chagas disease (as here, with cardiac manifestations years/decades after infection), since parasitemia is low/intermittent by then, making serology the mainstay of chronic-phase diagnosis.
Incorrect statement (so this is the answer). In the CHRONIC phase of Chagas disease with established cardiac involvement (as in this patient with ECG conduction abnormalities), antitrypanosomal treatment with benznidazole has NOT been shown to modify the progression of established cardiomyopathy — trypanocidal treatment benefit is much clearer in the acute phase and in the chronic phase without yet-established organ damage, not once cardiomyopathy has developed.
True — Chagas disease can be transmitted vertically and through shared exposure (vector-borne in endemic areas), so screening close family members (especially children of an infected mother, and those with shared exposure history) is a recommended practice.
⭐ High-yield pearl
Benznidazole's proven benefit is in acute-phase and early chronic-phase Chagas disease — trypanocidal treatment does NOT reverse or clearly modify already-established Chagas cardiomyopathy.
This is an important nuance distinguishing WHEN antitrypanosomal therapy helps: strong evidence supports treatment in acute infection and in the indeterminate/early chronic phase (before organ damage), but once cardiomyopathy or megaesophagus/megacolon has developed, benznidazole does not reliably reverse or halt structural disease progression — management then shifts to standard heart failure/arrhythmia therapy.
#165
Una mujer de 45 años con antecedentes de pleuritis hace 3 años y episodios ocasionales de poliartritis en los últimos 8 meses, fue diagnosticada de LES hace un mes tras un ingreso por fatiga y dolor torácico opresivo de esfuerzo, donde se objetivó una Hb de 5,8 g/dL y VCM de 109 fL por una anemia hemolítica autoinmune. El resto de la analítica mostró una linfopenia de 900/mm3, plaquetas en rango de normalidad, función hepática, creatinina y ionograma normales, tiempo de protrombina 85%, TTPA se muestra prolongado (ratio de 1,8). Existe hipocomplementemia C3 y C4, ANA 1/640, con Anti-DNA +. Fue dada de alta con corticoides, hidroxicloroquina y belimumab semanal subcutáneo. A las tres semanas del alta refiere sensación disneica de 48 horas de evolución sin otros síntomas acompañantes, la Hb de urgencias es de 10,2 gr/dL. ¿Cuál de las siguientes determinaciones de laboratorio deberíamos realizar en primer lugar?
Correct. This patient has SLE with a prolonged aPTT (suggesting a lupus anticoagulant/antiphospholipid antibody, a recognized SLE-associated finding), and now presents with new-onset dyspnea — in this context, pulmonary embolism must be prioritized in the differential, making D-dimer (as an initial screening step, recognizing its limitations in inflammatory states) and subsequent imaging the appropriate first-line work-up direction.
Urine protein would be relevant for assessing lupus nephritis activity, but doesn't address the acute new symptom (dyspnea) that needs urgent evaluation for a potentially life-threatening cause first.
NT-proBNP would help evaluate for heart failure, but given the strong antiphospholipid-syndrome-suggestive history (prolonged aPTT in an SLE patient), a thromboembolic cause should be prioritized in the initial work-up.
A repeat Coombs test would help re-assess hemolysis, but her hemoglobin has actually improved (5.8 → 10.2), making a hemolytic flare less likely to be the primary explanation for this new, isolated dyspnea.
⭐ High-yield pearl
SLE + a prolonged aPTT (unexplained by bleeding) = think lupus anticoagulant/antiphospholipid syndrome; new dyspnea in this context should prioritize a pulmonary embolism work-up.
A prolonged aPTT that does NOT correct with a mixing study, combined with a clinical history of pregnancy morbidity or thrombosis, points toward antiphospholipid syndrome (often associated with SLE) — this patient's new dyspnea, in that context, should trigger urgent evaluation for venous thromboembolism (starting with D-dimer/imaging) given the markedly elevated thrombotic risk this population carries.
#166
Mujer de 72 años, procedente del medio rural que acude al servicio de urgencias por un cuadro de dolor abdominal, vómitos y diarrea líquida, que posteriormente se hace sanguinolenta, de 6 días de duración. No refiere fiebre ni tratamiento antibiótico previo. Se toman muestras para hemocultivo y estudio microbiológico de las heces y se inicia tratamiento con fluidoterapia intensiva. 48 horas después se observa disminución del nivel de conciencia y la presencia de anemia (hematocrito de 25%, hemoglobina de 7,9 g/dL), trombopenia (plaquetas de 60.000/mL), creatinina de 3,2 mg/dL, hematuria y hemoglobinuria. En el estudio de sangre periférica se aprecian abundantes esquistocitos circulantes (más del 10%). Señale la respuesta INCORRECTA:
True — the clinical picture (bloody diarrhea evolving to a hemolytic-uremic-syndrome-type presentation with schistocytes, thrombocytopenia, AKI) should prompt specific testing for Shiga toxin-producing E. coli (STEC), including PCR for Stx1/Stx2 genes.
Incorrect statement (so this is the answer). Antibiotic treatment should NOT be started in suspected Shiga toxin-producing E. coli infection — killing the bacteria can release additional preformed Shiga toxin, worsening endothelial damage and increasing the risk/severity of hemolytic uremic syndrome, a well-established contraindication.
True — this presentation (bloody diarrhea progressing to a thrombotic microangiopathy picture with schistocytes, thrombocytopenia, and AKI) is not consistent with C. difficile infection, which doesn't typically cause this hemolytic-uremic-syndrome pattern.
True — plasmapheresis has not shown clear benefit in typical (Shiga-toxin-associated) hemolytic uremic syndrome, unlike its established role in atypical HUS or TTP — so it is not considered useful here.
⭐ High-yield pearl
Antibiotics are AVOIDED in suspected Shiga toxin-producing E. coli infection — killing the bacteria releases more toxin and can precipitate/worsen HUS.
This is a classic, frequently tested exception to 'always treat the infection': in bloody diarrhea suspicious for STEC (especially in a patient developing microangiopathic hemolytic anemia, thrombocytopenia, and AKI = HUS), antibiotics are withheld because bactericidal killing releases additional Shiga toxin — supportive care and close monitoring for HUS complications is the mainstay instead.
#167
Mujer de 54 años de edad que acude a su consulta para estudio y evaluación del riesgo vascular. Entre sus antecedentes más relevantes, destacan un infarto agudo de miocardio a los 51 y a los 53 años de edad, hipertensión arterial controlada y un perfil lipídico con tratamiento hipolipemiante de alta intensidad de: colesterol total 120 mg/dL, cHDL 60 mg/dL cLDL 50 mg/dL, TG 128 mg/dL. HB1AC de 5.2% y glucemia plasmática en ayunas normal. Nunca ha fumado. Índice de masa corporal de 23 Kg/m2. De las siguientes pruebas o determinaciones que se exponen a continuación, ¿qué es más útil para determinar el riesgo y la etiología de eventos recurrentes en esta paciente?
ApoB is a useful marker of atherogenic particle number, but given that this patient's LDL is already very well controlled (50 mg/dL) on high-intensity therapy, ApoB wouldn't add much additional information about a residual, unexplained cause of recurrent events.
ApoA reflects HDL particle number, which is less clinically actionable and not the key test to explain recurrent cardiovascular events in a patient with excellent conventional lipid control.
Correct. In a relatively young woman with recurrent myocardial infarctions despite excellent conventional lipid control (very low LDL) on high-intensity therapy, and no other major risk factors (non-smoker, normal glucose, normal weight), lipoprotein(a) — a largely genetically determined, independent atherogenic risk factor not addressed by standard lipid-lowering therapy — is the most useful test to explain residual/recurrent risk.
CRP reflects general inflammatory risk and can be used for risk stratification, but it doesn't specifically explain an unusually strong genetic/lipid-related predisposition to premature, recurrent MI the way Lp(a) does in this exact clinical scenario.
⭐ High-yield pearl
Recurrent premature MI despite excellent LDL control and few conventional risk factors → check lipoprotein(a), a genetically determined, independent cardiovascular risk factor.
Lp(a) levels are largely genetically determined (not significantly modified by diet, exercise, or statins) and represent a distinct, additional atherogenic and prothrombotic risk factor; elevated Lp(a) is increasingly recognized as an important explanation for 'unexplained' premature or recurrent cardiovascular disease despite otherwise well-controlled conventional risk factors, and its identification can also prompt cascade screening in family members.
#168
Mujer de 28 años sin enfermedades previas, recién llegada de los Estados Unidos de América, donde ha estado practicando espeleología en el valle del Ohio durante un par de semanas, presenta clínica de infección respiratoria consistente en tos, fiebre, sensación disneica y artralgias, lesiones cutáneas nodulares y dolorosas, eritematosas y calientes en la zona pretibial. ¿En qué enfermedad hay que pensar?
Aspergillosis typically affects immunocompromised patients or those with underlying lung cavities/structural lung disease, and doesn't have this specific geographic/exposure (caving in the Ohio Valley) and erythema-nodosum-type presentation.
Sporotrichosis classically causes a lymphocutaneous infection (nodular lesions along lymphatic channels) from a plant/soil inoculation injury, not this respiratory + erythema nodosum presentation tied to cave exposure.
Cryptococcosis is classically linked to bird droppings (pigeon exposure) rather than cave/bat guano exposure, and doesn't typically cause this respiratory illness plus erythema nodosum presentation.
Correct. Respiratory symptoms (cough, fever, dyspnea) plus erythema nodosum (painful, warm, erythematous pretibial nodules) and arthralgias in someone with recent caving exposure in the Ohio/Mississippi River Valley region (endemic area, exposure to bat guano) is the classic presentation of acute pulmonary histoplasmosis.
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Caving/spelunking exposure in the Ohio/Mississippi River Valley + respiratory symptoms + erythema nodosum = classic acute pulmonary histoplasmosis.
Histoplasma capsulatum is endemic to soil enriched with bird or bat droppings in the Ohio and Mississippi River valleys of the United States; caving ('spelunker's disease') is a classic exposure history, and the combination of acute pulmonary symptoms with erythema nodosum and arthralgias reflects an immune-mediated hypersensitivity reaction accompanying the acute infection.
#169
Hombre de 53 años, sin antecedentes patológicos, acude al hospital por fiebre de 10 días de evolución, con intensa cefalea retroorbitaria y una importante sensación de fatiga. No refiere dolor musculoesquelético, lesiones cutáneas ni ningún otro síntoma acompañante. A lo largo de 15 días de ingreso se objetiva fiebre persistente y la aparición de discreta ictericia conjuntival. La exploración respiratoria, cardíaca, abdominal y neurológica es normal. La analítica muestra VSG 97 mm/h, PCR 24,5 mg/dL, GOT 156 U/L, GPT 148 U/L, FA 410 U/L, GGT 794 U/L, bilirrubina total 5,5 mg/dL a expensas de la bilirrubina directa, hemoglobina 11,5 g/dL, recuento leucocitario normal, plaquetas 648.000/mm3, función renal e ionograma normales, tiempo de protrombina normal pero TTPA ratio 1,8. Los anticuerpos antinucleares (ANA) son positivos a títulos 1/160. Una ecografía abdominal no muestra ninguna alteración destacable. Desde el punto de vista clínico y a la vista de los datos analíticos, ¿cuál de las siguientes enfermedades es la que se ajusta mejor con nuestro paciente?
COVID-19 typically presents with respiratory symptoms and doesn't classically produce this pattern of prolonged fever, cholestatic liver injury, and a positive ANA/prolonged aPTT — this combination doesn't fit well with COVID-19.
Correct. Prolonged fever, severe retro-orbital headache, marked systemic inflammation (very high ESR/CRP), a cholestatic pattern of liver injury (elevated GGT/ALP with conjugated hyperbilirubinemia), thrombocytosis, and a positive ANA with a prolonged aPTT (from a transient lupus-anticoagulant-like phenomenon associated with the infection) is a classic presentation of acute Q fever (Coxiella burnetii) — a well-recognized clinical picture in this disease.
Weil's disease (severe leptospirosis) typically presents with more acute, severe illness including significant renal impairment, more pronounced jaundice, and often a history of water/animal exposure — the normal renal function and relatively indolent 10+ day course here fit less well.
Primary sclerosing cholangitis is a chronic autoimmune cholangiopathy typically associated with inflammatory bowel disease, presenting more insidiously — it wouldn't explain this acute febrile illness with marked systemic inflammatory markers.
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Prolonged fever + retro-orbital headache + cholestatic hepatitis + a transient positive ANA/prolonged aPTT = classic acute Q fever (Coxiella burnetii) presentation.
Acute Q fever is a zoonotic infection (from livestock exposure, often unrecognized) that classically causes a triad of prolonged fever with severe headache, an atypical/granulomatous hepatitis (often cholestatic pattern), and sometimes pneumonia; a positive ANA and a prolonged aPTT (from a transient antiphospholipid-like antibody) are well-documented, somewhat distinctive laboratory associations that can help point toward this diagnosis on exams.
#170
Hombre de 38 años con dependencia alcohólica grave. Ha tenido varios ingresos por pancreatitis aguda en el contexto de ingesta de alcohol e hipertrigliceridemia grave. Acude a consulta 12 meses después del último episodio de pancreatitis. No presenta clínica que sugiera insuficiencia pancreática exocrina. Niega reiteradamente ingesta de alcohol. Sigue tratamiento con estatinas y fibratos que asegura tomárselos. Aporta un análisis básico reciente de su empresa con los siguientes datos: colesterol 300 mg/dL, cHDL 42 mg/dL, TG 1102 mg/dL, cLDL no calculable por Friedewald. Colesterol no-HDL 258 mg/dL, ApoB 90 mg/dL, Lp(a) 38 nmol/L (normal <125 nmol/L). En dicho análisis hay un dato, además de la hipertrigliceridemia, que sugiere que el paciente continúa ingiriendo alcohol. Señálelo.
ApoB reflects the number of atherogenic (LDL/VLDL/IDL) particles and isn't a specific marker suggesting ongoing alcohol consumption in this context.
Correct. This patient's HDL cholesterol (42 mg/dL) is relatively HIGH given his severe hypertriglyceridemia (typically severe hypertriglyceridemia is associated with LOW HDL) — chronic alcohol consumption is a well-known cause of elevated HDL, so a disproportionately 'normal-to-high' HDL in the setting of extreme hypertriglyceridemia is a clue suggesting ongoing drinking despite his denial.
Lp(a) is a largely genetically determined lipoprotein not significantly affected by alcohol intake, so it doesn't provide a clue about ongoing consumption.
Total cholesterol being elevated is a nonspecific finding driven mainly by the severe hypertriglyceridemia itself (via VLDL) and doesn't specifically indicate ongoing alcohol use.
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Chronic alcohol use raises HDL cholesterol — a disproportionately preserved/elevated HDL alongside severe hypertriglyceridemia (which usually LOWERS HDL) is a subtle clue for ongoing drinking.
This is a clinically useful pattern-recognition pearl: alcohol independently raises HDL cholesterol through several mechanisms (increased ApoA-I production, altered lipid transfer protein activity), so when HDL doesn't show the expected inverse relationship with severe hypertriglyceridemia, it should raise suspicion that an external factor (like ongoing alcohol intake, contrary to what the patient reports) is influencing the lipid profile.
#171
Respecto a las infecciones de las heridas quirúrgicas, señale la respuesta INCORRECTA:
True — diabetes, malnutrition, obesity, and immunosuppression are all well-established patient-related risk factors for surgical site infection.
True — perioperative glycemic control is a recognized, evidence-based measure to reduce surgical site infection risk.
Incorrect statement (so this is the answer). Current recommendations for surgical antibiotic prophylaxis (including cardiac surgery) generally favor a SHORT duration — typically limited to the perioperative period/within 24 hours of surgery — rather than routinely extending prophylaxis to 48 hours or beyond, since prolonged prophylaxis doesn't reduce infection rates further and increases the risk of resistance/adverse effects.
True — local (topical/intra-wound) antibiotic therapy, such as antibiotic-loaded cement or beads, is used both prophylactically and therapeutically, particularly in the context of infected joint prostheses.
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Surgical antibiotic prophylaxis should generally be SHORT duration (perioperative/≤24h) — prolonging it (e.g., to 48h) doesn't further reduce SSI risk and is not recommended practice.
This reflects a broader antimicrobial stewardship principle: unnecessarily prolonged surgical prophylaxis doesn't improve outcomes and instead increases risks (C. difficile, resistance, cost, adverse effects) — current guidelines across most surgical specialties, including cardiac surgery, favor limiting prophylactic antibiotics to a short perioperative window.
#172
Hombre de 37 años con infección VIH ha dejado de tomar el tratamiento por razones personales hace 3 meses; estaba tomando una combinación de dos inhibidores de transcriptasa inversa y un inhibidor de la integrasa. En la evaluación llevada a cabo en este momento tiene 120 linfocitos CD4/mm3 y una carga viral de VIH-1 de 80.000 copias/mL. Estamos pendientes del estudio de resistencias. ¿Qué debemos recomendarle en este momento?
Correct. Given a low CD4 count (120/mm3, indicating significant immunosuppression and risk of opportunistic infection) and a high viral load, restarting antiretroviral therapy promptly is a priority — resuming the previous regimen while awaiting resistance testing results is reasonable, since significant resistance is less likely after only a relatively short interruption, and treatment shouldn't be delayed in a patient at high risk.
Waiting for resistance testing results before restarting therapy would unnecessarily delay treatment in a patient with a low CD4 count and high viral load who is at significant risk of opportunistic infections/clinical progression — urgent restart of therapy takes priority.
Switching empirically to a protease-inhibitor-based regimen isn't the recommended default approach; restarting the prior effective regimen while resistance testing is pending is more appropriate.
Starting integrase inhibitor dual therapy isn't the standard recommended empiric approach here without a specific indication — restarting the previous effective regimen is preferred while awaiting resistance data.
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In a patient off ART with a low CD4 count and high viral load, restart therapy promptly (don't wait for resistance testing) — treatment delay carries real clinical risk.
The urgency of restarting therapy in an immunosuppressed, high-viral-load patient generally outweighs the theoretical benefit of waiting for resistance results, especially after a relatively short treatment interruption — therapy can always be adjusted later once resistance data return, but the priority is not leaving a CD4 <200 patient untreated and at risk for opportunistic infections.
#173
Hombre de 55 años con antecedentes de cáncer de pulmón (estadio IV). Su madre murió a los 65 años por un episodio de broncoaspiración. Consulta por debilidad muscular en los muslos y disfagia. Exploración física: fuerza en psoas 4+/5, cuádriceps 3/5, deltoides 5/5. Presenta ptosis palpebral bilateral y no tiene diplopía. Los valores de CPK eran 900 UI/L (normal <150 UI/L) y los de aldolasa, 7 UI/L (normal <6 UI/L). Se practicó una biopsia en el músculo vasto lateral externo del muslo derecho, en la cual se objetivó variabilidad en el tamaño de fibras, aumento del tejido conectivo, imágenes de pseudodivisión celular y vacuolas ribeteadas; no se observó infiltrado inflamatorio. ¿Qué es lo más probable que le suceda al paciente?
Oculopharyngeal muscular dystrophy is an inherited condition typically presenting with progressive ptosis and dysphagia starting in mid-adulthood, but it wouldn't produce this specific biopsy pattern (rimmed vacuoles, pseudo-cell-division) nor would it fit as well with the asymmetric quadriceps-predominant weakness.
Mitochondrial myopathy can cause ptosis and weakness, but the specific biopsy finding of rimmed vacuoles without inflammatory infiltrate is more classic for inclusion body myositis, and mitochondrial disease typically shows ragged red fibers on special stains rather than this description.
Myasthenia gravis causes fatigable weakness and often diplopia along with ptosis, but wouldn't explain this markedly elevated CPK or the described muscle biopsy findings (rimmed vacuoles) — MG is a neuromuscular junction disorder without primary myopathic muscle damage.
Correct. Asymmetric, distal-and-proximal weakness (notably quadriceps-predominant, often greater than hip flexors — matching the pattern here where quadriceps is weaker than psoas), dysphagia, and a muscle biopsy showing rimmed vacuoles without significant inflammatory infiltrate are classic for inclusion body myositis, which characteristically affects older patients and can be a slowly progressive, sometimes underrecognized condition.
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Rimmed vacuoles on muscle biopsy + quadriceps-predominant asymmetric weakness + dysphagia in an older patient = inclusion body myositis.
Inclusion body myositis is distinguished from the other inflammatory myopathies (polymyositis, dermatomyositis) by its characteristic biopsy findings (rimmed vacuoles, inclusions, often without prominent inflammatory infiltrate), its typically asymmetric and distal-plus-proximal weakness pattern (with quadriceps and finger flexors classically affected early and often disproportionately), and its generally poor response to immunosuppressive therapy compared to the other inflammatory myopathies.
#174
Mujer de 81 años consulta por cuadro de 1 mes de duración de astenia, febrícula, pérdida de unos 4 kg de peso, cefalea hemicraneal izquierda y dolor en la zona de los hombros y de las caderas, que le dificulta los movimientos después de estar en reposo. Se palpa una zona engrosada y dolorosa en el territorio de la arteria temporal izquierda. Respecto al proceso diagnóstico de esta paciente, señale la opción INCORRECTA:
True — this clinical picture (unilateral headache, temporal artery tenderness/thickening, constitutional symptoms, and features suggestive of polymyalgia rheumatica) is classic for giant cell arteritis, a large/medium-vessel vasculitis.
Incorrect statement (so this is the answer). A NORMAL ESR would actually argue AGAINST giant cell arteritis, not support it — ESR (and CRP) are typically markedly elevated in GCA, and while rare cases with normal inflammatory markers exist, a normal ESR does not support the diagnosis; this option has it backwards.
True — imaging (CT angiography, MR angiography, or PET-CT) frequently reveals involvement of the aorta and its major branches in GCA, reflecting its classification as a large-vessel vasculitis.
True — a temporal artery biopsy showing inflammatory infiltrate in the arterial wall (often with giant cells) is the classic confirmatory test for GCA.
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Elevated (not normal) ESR/CRP supports the diagnosis of giant cell arteritis — a normal ESR argues against it, though rare exceptions exist.
GCA is a systemic inflammatory disease and virtually always presents with markedly elevated acute-phase reactants (ESR often >50-100 mm/h, elevated CRP); while treatment (especially corticosteroids) should never be delayed for biopsy in a high-suspicion case with vision at risk, normal inflammatory markers should prompt reconsideration of the diagnosis rather than being cited as supportive evidence.
#175
¿Cuál de las siguientes manifestaciones clínicas es la más característica de la miopatía de la dermatomiositis?
Difficulty walking can occur with more advanced/severe proximal weakness, but it's a less specific, later finding compared to the classic early symptom of proximal lower-extremity weakness.
Correct. Difficulty climbing stairs (or rising from a seated position) reflects proximal LOWER extremity muscle weakness (hip girdle/thigh muscles), which is the classic, most characteristic early symptom of the proximal myopathy in dermatomyositis/polymyositis.
Difficulty with fine motor tasks like buttoning reflects DISTAL hand weakness, which is atypical for classic dermatomyositis/polymyositis (a proximal myopathy) — distal weakness would be more suggestive of inclusion body myositis instead.
Muscle pain can occur in inflammatory myopathies but is a less specific and less consistently present feature than the characteristic proximal weakness pattern; many patients with dermatomyositis have prominent weakness with little or no pain.
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Dermatomyositis/polymyositis classically causes PROXIMAL, symmetric muscle weakness (difficulty climbing stairs, rising from a chair, raising arms overhead) — distal weakness is atypical and points elsewhere (like inclusion body myositis).
The proximal-vs-distal weakness pattern is a key distinguishing feature among the inflammatory myopathies: classic dermatomyositis/polymyositis affects proximal muscles (hip and shoulder girdles) symmetrically, while inclusion body myositis characteristically also involves distal muscles (finger flexors, and often asymmetrically) — recognizing 'trouble with stairs' as proximal weakness is a frequently tested pattern-recognition point.
#176
Mujer de 38 años que consulta por la presencia de dolor ocular, ojo rojo bilateral, hipersensibilidad a la luz y disminución de la agudeza visual. La historia clínica se completa con antecedentes de aftas bucales dolorosas y recidivantes y un diagnóstico previo de eritema nodoso hace 2 años. En la exploración oftalmológica se observa panuveitis bilateral con signos de vasculitis retiniana bilateral. Señale la respuesta correcta sobre el diagnóstico y tratamiento de la enfermedad que sospecha en esta paciente:
HLA-B*51 is associated with an increased risk of Behçet disease and can support the diagnosis, but it is not diagnostic/confirmatory on its own — Behçet disease remains a clinical diagnosis based on established criteria (recurrent oral ulcers plus other features), not a genetic test result.
Oral ulcers in Behçet disease are typically recurrent and painful but generally heal WITHOUT scarring in most cases, unlike the description here.
Correct. Recurrent painful oral aphthae, erythema nodosum, and now bilateral panuveitis with retinal vasculitis describe Behçet disease with sight-threatening ocular involvement; this requires prompt, aggressive treatment with systemic corticosteroids plus an immunosuppressant (such as azathioprine) to control inflammation and prevent vision loss.
Anti-TNF biologics (like infliximab/adalimumab) and cyclosporine ARE effective and commonly used add-on treatments for Behçet-associated uveitis refractory to or requiring more than corticosteroids/azathioprine alone — this statement incorrectly claims they don't help.
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Recurrent oral aphthae + erythema nodosum + bilateral panuveitis with retinal vasculitis = classic Behçet disease presentation; sight-threatening uveitis needs prompt aggressive immunosuppression.
Behçet disease's ocular involvement (panuveitis with retinal vasculitis) is one of its most feared manifestations because it can rapidly cause irreversible vision loss; because of this, treatment is more aggressive than for many other uveitis causes — combining systemic corticosteroids with a steroid-sparing immunosuppressant (azathioprine classically, though anti-TNF agents are increasingly used as effective options) from the outset rather than a stepwise, conservative approach.
#177
Mujer de 80 años que ingresa en el hospital para estudio de anemia tras ser llevada por sus hijos a urgencias por rectorragia y decaimiento físico. Clínicamente se encuentra estable. Está diagnosticada de un deterioro cognitivo, con ideación y juicio frecuentemente incoherentes y alteraciones conductuales para lo que toma risperidona. Se sospecha neoplasia maligna de colon y se plantea realizar una colonoscopia. Usted verifica que la paciente es incapaz de entender adecuadamente lo que se le explica sobre tal prueba, su naturaleza, objetivos, posibles complicaciones, o sus consecuencias diagnósticas y eventualmente terapéuticas. En tal caso, ¿cuál de las siguientes respuestas es correcta?
The physician is NOT exempted from obtaining informed consent simply based on their own judgment alone — when a patient lacks decision-making capacity, consent must be obtained by proxy (representation), following a defined legal process, not simply bypassed.
Judicial authorization is not the standard first step required for routine medical decisions in an incapacitated patient with available family members who can act as legal representatives — that pathway is reserved for more specific/contested situations, not routine diagnostic procedures.
Correct. When a patient lacks the capacity to understand and decide, informed consent must be obtained by representation (from family members/legal representative) — and per Spanish law (Ley 41/2002), this consent by representation must be documented in WRITING on the informed consent form, not simply given informally.
A verbal agreement alone is not legally sufficient for informed consent by representation in this context — written documentation is required, especially for a procedure like colonoscopy that carries recognized risks.
⭐ High-yield pearl
When a patient lacks decision-making capacity, informed consent by representation (family/legal representative) is required — and per Spanish law, it must be documented in WRITING, not simply verbal.
Spanish patient autonomy law (Ley 41/2002) establishes that when a patient cannot understand or decide due to their clinical condition, consent is obtained from their legal representative (family member acting on their behalf), always leaving written documentation of this — this differs from situations requiring judicial intervention, which are reserved for specific circumstances like disputes among family members or refusal of treatment with serious health consequences.
#178
Atiende a una paciente ingresada desde hace tres semanas en la unidad de cuidados intensivos por un cuadro de shock séptico respiratorio. Su evolución durante el ingreso no ha sido favorable y todavía continúa dependiente de ventilación mecánica invasiva. En los últimos días, tras recibir la información de que probablemente precise ventilación mecánica a medio-largo plazo, durante los periodos en que la paciente ha estado despierta, ha manifestado de forma clara su deseo de no continuar utilizando el ventilador. La paciente afirma comprender las consecuencias de esta decisión. Este caso habla de:
Correct. A competent, informed patient who clearly expresses her wish to discontinue an ongoing treatment (mechanical ventilation), understanding the consequences, is exercising her right to refuse treatment — a fundamental patient autonomy right, distinct from limitation of therapeutic effort (which is a medical team decision based on futility) or assisted dying processes.
Limitation of therapeutic effort (adequacy of care) refers to a clinical decision, typically made by the medical team (often with patient/family involvement), to withhold or withdraw treatments considered futile or disproportionate — here, the driving factor is the patient's own autonomous refusal, not a medical futility judgment.
Assisted suicide involves a physician providing the means for a patient to end their own life directly — this scenario describes withdrawal of an ongoing treatment at the patient's request, a legally and ethically distinct category (treatment refusal).
Euthanasia involves a deliberate act by a third party to directly end a patient's life at their request — again distinct from a patient exercising their right to refuse or discontinue an unwanted medical treatment.
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A competent patient refusing ongoing treatment (even life-sustaining treatment like mechanical ventilation) is exercising the right to refuse treatment — legally and ethically distinct from euthanasia, assisted suicide, or limitation of therapeutic effort.
Respecting a competent, adequately informed patient's decision to refuse or discontinue treatment — even when that decision will lead to death — is a well-established patient autonomy right, fundamentally different from euthanasia/assisted suicide (which involve an external agent's active intervention to end life) and from limitation of therapeutic effort (a clinical futility judgment initiated by the care team rather than by patient refusal).
#179
Respecto al tratamiento del dolor en cuidados paliativos, indique, de las siguientes afirmaciones, cuál es correcta:
Morphine remains a mainstay, first-line opioid in palliative care, not a 'relegated to testimonial role' drug — no other opioid has been shown to be uniformly superior in both efficacy and side-effect profile across the board.
Genuine addiction (as opposed to physical dependence/tolerance, which is expected and different) is NOT a significant clinical concern in patients receiving opioids for pain control at end of life — this is an important, frequently tested distinction in palliative care pharmacology.
Transmucosal fentanyl is specifically designed and indicated for BREAKTHROUGH pain (rapid-onset, short-duration episodes), not for chronic baseline/non-breakthrough pain — this statement has the indication backwards.
Correct. Methadone undergoes primarily hepatic metabolism with minimal renal excretion, making it a useful opioid option in patients with reduced renal clearance/renal failure, where many other opioids (like morphine, with renally-cleared active metabolites) can accumulate and cause toxicity.
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Methadone's minimal renal excretion makes it a preferred opioid choice in renal impairment — unlike morphine, whose active metabolites can accumulate and cause toxicity in kidney failure.
This distinction matters practically: morphine's active metabolites (morphine-6-glucuronide) are renally cleared and can accumulate in renal impairment, causing neurotoxicity (myoclonus, sedation, delirium) — methadone (and to a lesser extent fentanyl) is often preferred in this setting due to its predominantly hepatic elimination, though methadone requires careful titration due to its unpredictable, variable half-life and QT-prolongation risk.
#180
En relación con la atención en urgencias al paciente menor de edad y de acuerdo con la Ley de protección integral a la infancia y la adolescencia frente a la violencia, cuando el profesional sanitario advierta indicios de una situación de violencia ejercida sobre un menor, en un contexto en el que no exista una amenaza evidente sobre su salud o seguridad, tendrá obligación de comunicarlo de forma inmediata:
Correct. Per Spain's Law on comprehensive protection of children and adolescents against violence, when there is suspicion of violence against a minor WITHOUT an immediate/evident threat to health or safety, the healthcare professional's obligation is to communicate this to the competent social services, who coordinate further assessment and protective action.
Reporting to the on-call court via an injury report (parte de lesiones) is generally reserved for situations with clearer evidence of a criminal act or more urgent/severe circumstances, not the primary first-line pathway for non-urgent suspected cases under this specific law's framework.
Direct notification to law enforcement is not the primary designated first channel under this framework for non-urgent suspected cases — that pathway is reserved for situations involving more immediate risk or clear criminal urgency.
The Institute of Legal Medicine and Forensic Sciences is not the primary designated first point of contact for this type of non-urgent suspected case under the referenced law.
⭐ High-yield pearl
Suspected child abuse without an immediate safety threat → report to social services first, per Spain's child protection law framework.
This reflects a graduated response system: cases with immediate danger to a minor's health/safety typically escalate directly to judicial/law enforcement channels, while suspected but non-urgent situations are first routed through social services, allowing coordinated multidisciplinary assessment and follow-up rather than an immediate judicial/police intervention.
#181
En relación con la marca producida por el paso de la corriente eléctrica a través de la piel (también conocida como lesión electroespecífica o "marca de Jellinek"), ¿cuál de las siguientes afirmaciones es cierta?
Most household and occupational electrical injuries actually come from LOW-voltage sources (standard household current), not high-voltage sources, which are less common exposures overall.
Correct. The characteristic skin lesion (electrical mark/Jellinek mark) results from localized heat generation as current passes through the skin's electrical resistance, causing thermal (Joule heating) injury to the dermis at the contact point.
This has it backwards: HIGH-voltage current tends to cause deeper tissue damage (following the path of least resistance through deeper structures), while LOW-voltage current tends to produce more localized, superficial injury at the contact point — the statement reverses the typical pattern.
The electrical mark indicates a point of skin contact with current, but it is NOT reliably diagnostic of which point was specifically the 'entry' versus 'exit' point — current can leave marks at multiple contact points, and distinguishing true entry from exit isn't reliably possible from the mark's appearance alone.
⭐ High-yield pearl
Electrical skin marks (Jellinek marks) result from localized Joule heating as current meets skin resistance — most household/occupational injuries are actually LOW-voltage, and high voltage tends to cause deeper injury than low voltage.
Two classic exam traps here: (1) don't assume high voltage is the more common source of injury — everyday low-voltage household/occupational exposure is actually more frequent; and (2) don't assume low voltage causes only superficial injury — high voltage classically causes deeper, more extensive tissue damage due to the current following deeper, lower-resistance pathways.
#182
Hombre de 85 años con enfermedad de Alzheimer de 6 años de evolución, actualmente en estadio GDS-FAST 7c. Está institucionalizado en centro sociosanitario desde hace 1 año. En los últimos 6 meses tiene frecuentes episodios de broncoaspiración por los que ha acudido a Urgencias y han sido tratados con antibioterapia de amplio espectro con mejoría clínica. Acude nuevamente a urgencias por disnea en relación con nuevo episodio de broncoaspiración y negativa a la ingesta. ¿Cuál debe ser la actitud a seguir?
Nasogastric tube placement does NOT reliably prevent aspiration (aspiration of secretions/reflux can still occur) and isn't the recommended approach in advanced, terminal-stage dementia — this represents inappropriately aggressive intervention at end of life.
PEG tube placement has NOT been shown to reduce aspiration risk or improve survival/quality of life in advanced dementia, and is generally not recommended in this context — again, inappropriately aggressive care for a patient at the terminal stage of dementia (GDS-FAST 7c).
Correct. A patient with very advanced dementia (GDS-FAST 7c, essentially end-stage) with recurrent aspiration pneumonia episodes despite treatment, and now refusing oral intake, has a very limited prognosis; evidence does not support enteral feeding tubes in this context (they don't reduce aspiration or improve outcomes), and the appropriate approach shifts to adequacy of therapeutic effort — focusing on comfort-oriented palliative care rather than further aggressive antibiotic treatment or invasive feeding.
While curing the infection might transiently help, in end-stage dementia with recurrent aspiration episodes despite prior antibiotic courses, continuing to treat each recurrence aggressively doesn't change the underlying trajectory and isn't aligned with goals-of-care in this terminal stage — comfort-focused care is more appropriate.
⭐ High-yield pearl
End-stage dementia (GDS-FAST 7c) with recurrent aspiration pneumonia and food refusal = a signal to shift toward comfort-focused palliative care, not escalating tube feeding or repeated aggressive antibiotic courses.
Multiple studies have shown that feeding tubes (NG or PEG) do not reduce aspiration risk, improve survival, or improve quality of life in patients with advanced dementia — recognizing recurrent aspiration pneumonia in end-stage dementia as a marker of the terminal phase of the disease, rather than a series of independent treatable infections, is central to appropriate goals-of-care discussions and adequacy of therapeutic effort.
#183
La telemonitorización domiciliaria ha demostrado beneficios en pacientes con insuficiencia cardíaca. Una mujer de 82 años con insuficiencia cardíaca y diabetes tratada con insulina está en programa de telemonitorización y remite cada semana una serie de parámetros a su médico de familia. La semana pasada presentaba presión arterial 140/85 mmHg. Glucemia capilar basal 120 mg/dL. Glucemia postprandial 2 h tras la comida 160 mg/dL. Peso 83 kg. Frecuencia cardíaca 72 lpm. Al recibir los parámetros de esta semana que se exponen a continuación, su médico decide citar a la paciente en consulta. ¿Cuál de los siguientes parámetros ha motivado dicha decisión?
A blood pressure of 135/82 mmHg is actually slightly improved/similar to the prior reading and doesn't represent a concerning change warranting evaluation.
Correct. A weight gain of 2 kg in one week in a patient with heart failure is a red-flag sign of fluid retention/decompensation, warranting closer clinical evaluation to assess for worsening heart failure before it progresses to overt decompensation.
A basal glucose rise from 120 to 130 mg/dL is a small, clinically insignificant fluctuation that wouldn't by itself prompt an urgent visit.
A postprandial glucose rise from 160 to 190 mg/dL is a modest change that, while worth monitoring, is less acutely concerning than a rapid weight gain in a heart failure patient, which signals possible fluid overload.
⭐ High-yield pearl
Rapid weight gain (e.g., ≥2 kg in a week) in a heart failure patient is a classic early warning sign of fluid retention/decompensation — a key telemonitoring red flag.
Daily/weekly weight tracking is one of the most useful and actionable telemonitoring parameters in heart failure management, since fluid accumulation (and resulting weight gain) often precedes overt clinical decompensation (dyspnea, edema) by several days, allowing for early diuretic adjustment and potentially preventing hospitalization.
#184
En un paciente con diabetes y obesidad en prevención secundaria cardiovascular, tratado con metformina y iSGLT2, que presenta mal control glucémico, ¿cuál es el fármaco de elección para mejorar dicho control?
Insulin is effective for glucose control but is not the preferred next step in this patient profile (obesity, established cardiovascular disease) when a GLP-1 receptor agonist offers similar or better glycemic benefit plus weight loss and cardiovascular risk reduction.
Correct. In a patient with type 2 diabetes, obesity, and established cardiovascular disease already on metformin and an SGLT2 inhibitor with inadequate control, a GLP-1 receptor agonist is the preferred next agent — it provides additional glycemic control, promotes weight loss (beneficial given the obesity), and has proven cardiovascular benefit in secondary prevention populations.
Sulfonylureas can cause hypoglycemia and weight gain, making them a less favorable choice in an obese patient with cardiovascular disease when a GLP-1 agonist (weight loss + cardiovascular benefit) is available.
Repaglinide, like sulfonylureas, carries hypoglycemia risk and doesn't offer the weight and cardiovascular benefits of a GLP-1 receptor agonist, making it a less preferred choice in this specific patient profile.
⭐ High-yield pearl
In diabetes + obesity + established cardiovascular disease, GLP-1 receptor agonists are preferred add-on therapy — they improve glycemic control, promote weight loss, AND reduce cardiovascular events.
Modern type 2 diabetes management increasingly moves beyond simply choosing the drug that lowers glucose the most, favoring agents with proven benefits matched to the patient's comorbidity profile: SGLT2 inhibitors and GLP-1 receptor agonists both have cardiovascular/renal benefits, but GLP-1 agonists specifically add substantial weight-loss benefit, making them particularly well-suited to an obese patient with cardiovascular disease needing better glycemic control.
#185
Mujer de 61 años con adenocarcinoma rectal avanzado. Presenta dolor neuropático con irradiación perineal y molestias urinarias en relación con masa presacra. Mejoró con tratamiento con opioides (morfina 60 mg cada 12h) pero no tolera más aumento de dosis ni fármacos adyuvantes. ¿Cuál es el tratamiento de elección?
Celiac plexus block is used for pain from upper abdominal visceral malignancies (pancreatic, gastric, hepatobiliary cancers), not for perineal/pelvic pain from a presacral rectal mass.
Correct. The ganglion impar (a single retroperitoneal sympathetic ganglion located anterior to the sacrococcygeal junction) mediates sympathetically-maintained pelvic/perineal pain, and blocking it is the treatment of choice for perineal pain from pelvic malignancies like advanced rectal cancer, especially when opioid therapy has reached its practical dose limit.
Splanchnic nerve block is used similarly to celiac plexus block, for upper abdominal visceral pain, not perineal pain from a pelvic/presacral tumor.
Pudendal nerve block can help with somatic perineal pain but is less specifically indicated for this visceral/sympathetically-mediated perineal pain pattern from a presacral mass compared to ganglion impar block, which specifically targets the relevant sympathetic pathway.
⭐ High-yield pearl
Perineal/pelvic pain from advanced pelvic malignancy (like rectal cancer) not adequately controlled by opioids = ganglion impar block is the interventional treatment of choice.
Different visceral/sympathetic nerve blocks target pain from different anatomic regions: celiac plexus/splanchnic nerve blocks address upper abdominal visceral pain (pancreatic/gastric cancer), while ganglion impar block specifically addresses perineal and pelvic pain, making it the appropriate choice when systemic opioid therapy alone is insufficient or has reached practical dosing limits for pelvic malignancy pain.
#186
En una guardia de centro de salud avisan para atender a un hombre de 63 años, que ha sido sometido a bajas temperaturas, sin precisar cuánto tiempo ha estado en exposición. A su llegada, tiene una temperatura corporal de 28ºC. ¿Cuál de los siguientes hallazgos NO cabría esperar en este cuadro?
Correct (this is the finding NOT expected). At this degree of moderate-to-severe hypothermia (28°C), respiratory rate progressively DECREASES (bradypnea), not increases — tachypnea would be an early/mild hypothermia finding at best, not something expected at this more advanced stage.
Ventricular fibrillation is a well-recognized, feared cardiac complication of moderate-to-severe hypothermia (typically becoming a significant risk below ~28-30°C), so this IS an expected potential finding at this temperature.
Altered mental status, including confusion and hallucinations, IS a recognized feature of hypothermia at this degree of severity, reflecting CNS depression/dysfunction.
Miotic (constricted) pupils CAN be seen in hypothermia (though pupillary findings can vary), and are a recognized, expected finding at this stage rather than an atypical one.
⭐ High-yield pearl
Severe hypothermia causes progressive BRADYPNEA (decreased respiratory rate), not tachypnea — a common exam trap where people assume all physiologic parameters simply 'speed up' with any stress.
As core temperature drops, hypothermia progressively suppresses metabolic rate and vital functions across the board: heart rate slows (bradycardia), respiratory rate slows (bradypnea), and consciousness declines — the risk of malignant arrhythmias (like VF) increases as temperature falls further, making cardiac monitoring essential in moderate-to-severe hypothermia.
#187
En cuanto al uso de anticonceptivos en mujeres jóvenes en las consultas de Atención Primaria, es importante tener en cuenta diversos aspectos para la prescripción. ¿Cuál de las siguientes es INCORRECTA?
True — structured contraceptive counseling using the WHO Medical Eligibility Criteria, addressing both pregnancy prevention and STI protection, is recommended standard practice.
True — levonorgestrel, ulipristal acetate, and the copper IUD are all recognized, recommended options for emergency contraception.
Incorrect statement (so this is the answer). Routine universal screening for thrombophilia, dyslipidemia, and annual cytology is NOT recommended before/during combined oral contraceptive prescription in the absence of specific risk factors or clinical indications — such screening should be targeted based on personal/family history, not applied routinely to all women starting oral contraceptives.
True — the absolute risk of venous thromboembolism with combined oral contraceptives is low overall, and second-generation progestins carry a lower relative risk than third/fourth-generation progestins, an important consideration in contraceptive choice.
⭐ High-yield pearl
Routine thrombophilia/dyslipidemia screening and annual cytology are NOT required before prescribing oral contraceptives — screening should be targeted to personal/family risk factors, not applied universally.
Over-testing before oral contraceptive prescription can create unnecessary barriers to access without evidence-based benefit; current guidelines instead recommend a thorough personal and family history (for VTE risk factors, migraine with aura, etc.) and blood pressure measurement as the key routine screening steps, reserving thrombophilia testing for those with a suggestive personal/family history.
#188
¿Cuál de los siguientes fármacos debería evitarse en un paciente que presenta diabetes y obesidad por ser un fármaco que puede inducir aumento de peso?
Metformin is generally weight-neutral to modestly weight-reducing, making it a favorable (not a problematic) choice in an obese diabetic patient.
DPP-4 inhibitors like sitagliptin are essentially weight-neutral, so they don't pose the weight-gain concern being asked about here.
Semaglutide (a GLP-1 receptor agonist) actively promotes significant weight LOSS, making it a favorable, not problematic, choice in this patient.
Correct. Pioglitazone (a thiazolidinedione) is well known to cause weight gain (through fluid retention and adipogenesis), making it a less favorable choice specifically in a patient with diabetes and obesity where weight gain is an important consideration to avoid.
⭐ High-yield pearl
Thiazolidinediones (pioglitazone) cause weight gain and fluid retention — a drug class to generally avoid or use cautiously in obese diabetic patients.
When choosing diabetes medications in an obese patient, favor weight-neutral or weight-reducing agents (metformin, SGLT2 inhibitors, GLP-1 receptor agonists) over agents associated with weight gain (sulfonylureas, thiazolidinediones, and insulin) whenever clinically appropriate, since managing obesity is itself a key therapeutic goal in this population.
#189
Hombre de 69 años con adenocarcinoma de páncreas avanzado que presenta como principal sintomatología dolor de características mixtas tratado desde hace 3 meses con opioides con buen control (morfina 60 mg cada 12 horas) + adyuvantes (duloxetina 60 mg/día). Asocia astenia e hiporexia graves tratadas con corticoides desde hace 2 semanas (dexametasona 8 mg/día). Acude a consulta refiriendo somnolencia intensa y alucinaciones táctiles. En la analítica presenta como datos más destacables anemia de trastornos crónicos (Hb 10,6 g/dL) y empeoramiento de la función renal (CKD-EPI 26 mL/min). ¿Cuál es el diagnóstico más probable y la actitud a seguir?
Brain metastases could theoretically explain new neurological symptoms, but the clear temporal link to worsening renal function (which reduces opioid metabolite clearance) makes opioid neurotoxicity a much more likely explanation than a new structural brain lesion, and increasing corticosteroid dose would be inappropriate here regardless.
Corticosteroid-induced psychosis is possible but is less specifically explained by the concurrent renal function decline, which is the key clue pointing toward opioid metabolite accumulation as the more likely culprit.
This describes hyperactive symptoms (somnolence plus tactile hallucinations, which can occur in opioid toxicity) rather than classically 'hypoactive' delirium, and starting neuroleptics would treat a symptom without addressing the underlying reversible cause (opioid accumulation from worsening renal clearance).
Correct. Worsening renal function (CKD-EPI dropping to 26 mL/min) impairs clearance of morphine's active, renally-excreted metabolites (morphine-3-glucuronide and morphine-6-glucuronide), which accumulate and cause opioid-induced neurotoxicity — presenting with sedation, myoclonus, confusion, and hallucinations (classically tactile) as seen here; the appropriate management is to reduce the opioid dose (and consider opioid rotation to a less renally-dependent agent like fentanyl or methadone if needed).
⭐ High-yield pearl
Worsening renal function + a patient on morphine + new confusion/hallucinations/sedation = suspect opioid-induced neurotoxicity from accumulated renally-cleared active metabolites.
Morphine's active metabolites (M3G, M6G) are renally excreted and can accumulate rapidly when renal function declines, producing a recognizable opioid neurotoxicity syndrome (myoclonus, hyperalgesia, sedation, and confusion/hallucinations, often tactile) — management is dose reduction and/or opioid rotation to an agent less dependent on renal clearance, rather than simply treating the hallucinations symptomatically or assuming an unrelated new diagnosis.
#190
Hombre de 36 años sin antecedentes de interés que ingresa en observación de urgencias en espera de intervención quirúrgica por fractura de fémur a nivel diafisario por accidente de tráfico. El paciente llega algo taquicárdico 102 lpm, con gafas nasales para mantener saturación de oxígeno en torno al 96%, 20 respiraciones por minuto y presión arterial 100/60 mmHg. Se procede a ajuste de analgesia y a las 20 horas de estancia en observación indican que el paciente puede ir a quirófano pero presenta un aumento de disnea con saturación del 89% con mascarilla tipo Venturi, 28 respiraciones por minuto, taquicardia a 110 lpm, fiebre de 38ºC y se encuentra algo obnubilado. En la analítica destaca anemia y trombocitopenia. No presenta aumento de volumen en ninguna de las 2 piernas. ¿Qué prueba complementaria tiene mayor sensibilidad y especificidad para la sospecha diagnóstica de este paciente?
CT pulmonary angiography is the standard test for pulmonary EMBOLISM, but this clinical picture (long bone fracture, onset ~24-72h post-injury, hypoxemia, fever, altered mental status, thrombocytopenia, anemia) is more classic for fat embolism syndrome, not thromboembolism — and for fat embolism specifically, echocardiography (looking for right heart strain/emboli or using specific criteria) has higher sensitivity/specificity in this context than CTPA.
A V/Q perfusion scan is also oriented toward diagnosing pulmonary thromboembolism, not the fat embolism syndrome suggested by this clinical picture.
Chest X-ray can show nonspecific bilateral infiltrates in fat embolism syndrome but has low sensitivity and specificity for the diagnosis compared to other options.
Correct. This presentation — long bone (femoral shaft) fracture, symptom onset 12-72 hours after injury, respiratory distress/hypoxemia, neurologic symptoms (confusion), fever, thrombocytopenia, and anemia, WITHOUT leg swelling to suggest DVT — is the classic triad/pentad of fat embolism syndrome. Echocardiography (particularly transesophageal, sometimes showing intracardiac fat globules or signs of right heart strain) has the highest sensitivity and specificity among the listed options for this specific diagnosis.
⭐ High-yield pearl
Long bone fracture + delayed-onset (12-72h) triad of respiratory distress + neurologic symptoms + petechiae/thrombocytopenia (without leg swelling suggesting DVT) = classic fat embolism syndrome, not pulmonary thromboembolism.
Fat embolism syndrome is a distinct clinical entity from venous thromboembolism, typically occurring after long bone or pelvic fractures, with a delayed onset (usually 12-72 hours post-injury, distinguishing it from immediate post-traumatic hypoxemia) and a classic triad of respiratory distress, neurologic dysfunction, and a petechial rash, often accompanied by thrombocytopenia and anemia from marrow fat/fibrin embolization — recognizing this distinct syndrome (rather than defaulting to a PE work-up) changes the diagnostic approach.
#191
Hombre de 72 años sin alergias medicamentosas, no fumador y con antecedentes de hipertensión, dislipemia y diabetes. En tratamiento con ácido acetilsalicílico, atorvastatina, enalapril y metformina. Acude a urgencias por agudización de lumbalgia crónica de meses de evolución. Refiere que el dolor no es irradiado, y no mejora mucho en reposo. Ha tomado varios analgésicos sin ninguna mejoría. A la exploración no presenta dolor en espinosas dorsolumbares, el signo de Lasegue es negativo, no presenta limitación a la movilidad, reflejos normales y no hay alteración de sensibilidad o fuerza. Pulsos pedios ausentes y tibiales débiles. No edemas de miembros inferiores. Ante la sospecha diagnóstica, ¿qué prueba nos daría el diagnóstico más rápidamente con mayor sensibilidad y especificidad?
Abdominal ultrasound can detect an abdominal aortic aneurysm but has lower sensitivity/specificity than CT for fully characterizing it (size, extent, any complications like rupture/leak) and is more operator/body-habitus dependent.
Correct. Chronic, non-radicular low back pain that doesn't improve with rest, combined with absent pedal pulses and weak tibial pulses (signs of peripheral arterial disease/possible aortic pathology), and a completely normal neurological/spinal exam (no radiculopathy signs), should raise suspicion for an abdominal aortic aneurysm eroding into or compressing nearby structures, or significant aortoiliac occlusive disease — thoraco-abdominal CT (with contrast/angiography) provides the fastest, most sensitive and specific diagnostic evaluation of the aorta and its branches in this scenario.
MRI could also evaluate the aorta but is generally slower to obtain in the acute/urgent setting and is not the fastest, most practical first-line test compared to CT in this scenario.
A normal spinal/neurological exam (no tenderness, negative Lasègue, no motor/sensory deficits) argues AGAINST a primary spinal cause, and a plain lumbosacral X-ray wouldn't evaluate the vascular pathology suggested by the absent pulses.
⭐ High-yield pearl
Chronic low back pain with a normal spinal exam BUT absent/weak lower extremity pulses = think vascular (aortic/aortoiliac) pathology, not a spinal cause — CT angiography is the fastest, most sensitive test.
This vignette is designed to redirect you away from the 'obvious' diagnosis (mechanical low back pain) using two key clues: the neurological exam is completely normal (arguing against radiculopathy), and the vascular exam is abnormal (absent pedal pulses, weak tibial pulses) — pointing to an atypical presentation of vascular disease (aortic aneurysm, aortoiliac occlusive disease) masquerading as chronic back pain.
#192
Acude a urgencias un hombre de 34 años, sin diagnósticos previos, con antecedente de consumo de drogas por vía parenteral, con fiebre, tos no productiva y disnea progresiva de varias semanas de evolución. Se realiza radiografía de tórax que muestra infiltrado intersticial bilateral. En analítica sanguínea destaca linfopenia y lactato deshidrogenasa elevada. La saturación de oxígeno es del 88% respirando aire ambiente en reposo. ¿Cuál de las siguientes aseveraciones le parece INCORRECTA?
Incorrect statement (so this is the answer). This presentation (IV drug use as an HIV risk factor, subacute progressive dyspnea, bilateral interstitial infiltrates, lymphopenia, elevated LDH, and significant hypoxemia) is classic for Pneumocystis jirovecii pneumonia in an undiagnosed HIV-positive patient — treating empirically with ceftriaxone (targeting typical bacterial pneumonia) would miss the much more likely diagnosis and fails to provide appropriate PCP-directed therapy.
True — this is exactly the appropriate treatment for suspected/confirmed PCP: TMP-SMX (first-line), adjunctive corticosteroids (given the significant hypoxemia, PaO2 <70 or SpO2 <92% criteria), and supplemental oxygen.
True — given the IV drug use risk factor and this classic PCP-suggestive clinical picture, HIV testing is an essential, appropriate step in the work-up.
True — sputum microbiological studies (including specific staining/PCR for Pneumocystis, and to rule out other infections like TB) are an appropriate part of the diagnostic work-up.
⭐ High-yield pearl
IV drug use (HIV risk factor) + subacute dyspnea + bilateral interstitial infiltrates + lymphopenia + elevated LDH + significant hypoxemia = classic Pneumocystis jirovecii pneumonia (PCP) presentation, often the first sign of undiagnosed HIV.
Elevated LDH is a particularly useful supportive clue for PCP (reflecting the degree of lung tissue turnover/damage), and significant hypoxemia (SpO2 <92% or PaO2 <70 mmHg) is the specific threshold that triggers adjunctive corticosteroid therapy alongside TMP-SMX, in addition to confirming the diagnosis with HIV testing and CD4 count.
#193
Hombre de 46 años sufre accidente de tráfico a alta velocidad con varios vuelcos del vehículo y necesidad de extricación por parte del equipo de bomberos. El paciente es trasladado en una UVI móvil al servicio de urgencias más próximo, con inmovilización en colchón de vacío. A su llegada al hospital se encuentra inestable a pesar de sueroterapia intensiva. A la exploración presenta los siguientes signos vitales: frecuencia respiratoria 35 rpm. Saturación de oxígeno 100% con mascarilla reservorio. Frecuencia cardíaca 140 lpm. Presión arterial 60/30 mm Hg. Temperatura 35,5ºC y glucemia 110 mg/dL. De las siguientes, indique la exploración o prueba complementaria clave del árbol de decisión en este paciente:
Blood count and chemistry are useful baseline labs but are not the immediate KEY decision-making test in a hemodynamically unstable trauma patient — they don't provide the rapid, actionable information needed to guide immediate management the way a bedside ultrasound does.
CT scanning is inappropriate for a hemodynamically UNSTABLE trauma patient (they should never be sent to CT while unstable) — CT is reserved for stable patients; an unstable patient needs a rapid bedside assessment first.
Correct. In a hemodynamically unstable trauma patient, e-FAST (a rapid bedside ultrasound assessing for free fluid in the abdomen/pelvis and pericardial effusion, plus pneumothorax) is the key, immediately actionable test — it's fast, doesn't require moving the unstable patient, and directly guides the decision for emergent surgery (e.g., laparotomy for hemoperitoneum) versus other management.
Diagnostic peritoneal lavage has been largely superseded by e-FAST in modern trauma protocols, since ultrasound is faster, non-invasive, and provides comparable or better information for this purpose.
⭐ High-yield pearl
Hemodynamically unstable trauma patient → e-FAST at the bedside (not CT, which requires an unstable patient to leave the resuscitation area) is the key initial test to guide immediate management.
The fundamental trauma principle 'never send an unstable patient to CT' underlies this question: e-FAST can be performed rapidly at the bedside during ongoing resuscitation, directly answering the critical question of whether there is free intraperitoneal or pericardial fluid requiring emergent surgical intervention, without the delay and risk of transporting an unstable patient to the CT scanner.
#194
En un paciente diagnosticado de una lesión tumoral ósea maligna que ha recibido tratamiento neoadyuvante, se realiza resección de la pieza y posterior biopsia para su análisis anatomopatológico. Indique, de las siguientes, ¿cuál es la información más relevante para el pronóstico del paciente?
Correct. The percentage of tumor necrosis induced by neoadjuvant chemotherapy (assessed on the resected specimen, e.g., using Huvos grading) is one of the most important prognostic factors in malignant bone tumors like osteosarcoma — a high percentage of necrosis (typically ≥90%) indicates a good response to chemotherapy and correlates with significantly better prognosis/survival.
The number of tumor cells in G0/interphase isn't a standard, clinically used prognostic parameter reported on post-neoadjuvant bone tumor pathology assessment.
The percentage of giant cells is relevant to specific diagnoses like giant cell tumor of bone, but isn't the standard prognostic marker assessed after neoadjuvant therapy for a malignant bone tumor like osteosarcoma.
The amount of non-stromal cells composing the tumor isn't a standard, clinically used prognostic parameter for this scenario.
⭐ High-yield pearl
Percentage of tumor necrosis after neoadjuvant chemotherapy (Huvos grading) is the single most important prognostic factor in resected malignant bone tumors like osteosarcoma.
Huvos grading (or similar necrosis-based grading systems) classifies chemotherapy response from grade I (minimal necrosis) to grade IV (no viable tumor cells identified), with ≥90% necrosis (grade III-IV) associated with markedly improved survival — this is why post-neoadjuvant surgical specimens are carefully assessed for necrosis percentage, and it can also inform decisions about adjusting postoperative chemotherapy regimens.
#195
Mujer de 60 años que acude al hospital por hematuria, mal estado general y fiebre. Se orienta clínicamente de insuficiencia renal progresiva y se decide realizarle una biopsia renal donde se observa una glomerulonefitis necrotizante con reacción extracapilar (semilunas) que afecta a más del 50% de los glomérulos. La inmunofluorescencia directa es negativa. Hay un dato del laboratorio de inmunología que nos ayudará a confirmar el diagnóstico, pero ¿cuál es el diagnóstico más probable?
Correct. Crescentic (necrotizing) glomerulonephritis affecting >50% of glomeruli with a NEGATIVE immunofluorescence (i.e., no significant immune complex or linear staining — 'pauci-immune') is the classic pattern of pauci-immune (ANCA-associated) crescentic glomerulonephritis; the confirmatory immunology lab test would be ANCA (p-ANCA/MPO or c-ANCA/PR3), which is why the vignette specifically flags 'a lab test that will help confirm the diagnosis.'
Tubulointerstitial nephritis affects the tubules/interstitium, not glomeruli with crescents — this doesn't match the biopsy description at all.
Goodpasture syndrome (anti-GBM disease) would show LINEAR immunofluorescence staining for IgG along the glomerular basement membrane, not a NEGATIVE immunofluorescence — the negative IF specifically argues against Goodpasture/anti-GBM disease and points to pauci-immune GN instead.
IgA nephropathy would show characteristic MESANGIAL IgA deposits on immunofluorescence (positive, not negative), so a negative immunofluorescence argues against this diagnosis.
⭐ High-yield pearl
Crescentic GN + NEGATIVE immunofluorescence = pauci-immune (ANCA-associated) glomerulonephritis — confirm with ANCA serology (p-ANCA/MPO or c-ANCA/PR3).
The immunofluorescence pattern is the key to classifying crescentic glomerulonephritis into its three main categories: linear IgG staining = anti-GBM (Goodpasture) disease; granular immune complex deposits = immune-complex-mediated GN (lupus nephritis, IgA nephropathy, post-infectious GN); and negative/pauci-immune staining = ANCA-associated vasculitis — each category has a distinct confirmatory serologic test and treatment approach.
#196
Niño de 3 años de edad con antecedentes de dermatitis atópica leve, sin alergias conocidas. Acude a la consulta con su madre quien comenta que en la última semana le han aparecido unas lesiones en la piel de la cara y la región glútea. Estas lesiones comenzaron como pequeñas máculas eritematosas que en pocos días pasaron a vesículas y erosiones superficiales cubiertas por costras amarillentas y que han ido aumentando en número y tamaño, extendiéndose rápidamente a la piel de alrededor. Ha estado rascándose las lesiones, lo que parece haberlas empeorado. También comenta que en la guardería hay otros niños que han presentado lesiones similares en la piel. El niño tiene buen estado general y no tiene fiebre, sólo se queja de picor en las lesiones. Ante este cuadro clínico, ¿cuál es el diagnóstico más probable?
Correct. Rapidly spreading vesicles/erosions that develop honey-colored ('yellowish') crusts, occurring in a young child with mild atopic dermatitis (a predisposing factor, since scratching/skin barrier disruption facilitates infection), with similar cases in daycare contacts (highly contagious) and good general health without fever, is the classic presentation of non-bullous impetigo.
Molluscum contagiosum presents with characteristic firm, umbilicated papules, not vesicles/erosions with honey-colored crusting — a very different morphology from what's described here.
Herpes virus infection would typically cause grouped vesicles on an erythematous base, often painful, without the classic honey-colored crusting appearance described.
Mucocutaneous candidiasis typically presents in moist, intertriginous areas with satellite lesions, not this honey-crusted, rapidly spreading pattern on the face and buttocks.
⭐ High-yield pearl
Honey-colored ('yellowish') crusted lesions spreading rapidly in a young child, especially with similar cases among daycare contacts, is the classic presentation of impetigo (usually Staphylococcus aureus and/or Streptococcus pyogenes).
Impetigo is highly contagious among young children in close-contact settings (daycare, school), classically starting as vesicles/pustules that rupture to form the pathognomonic honey-colored crust; predisposing factors like atopic dermatitis (impaired skin barrier) and scratching facilitate spread, and treatment is typically topical (mupirocin) for limited disease or oral antibiotics for more extensive involvement.
#197
Hombre de 50 años que acude a la consulta por una lesión pigmentada en su pierna derecha que ha cambiado de tamaño y color en los últimos 4 meses. La lesión es de 8 mm de diámetro, asimétrica, con bordes irregulares y con varias tonalidades de marrón y negro. Además, refiere prurito ocasional en la zona. No tiene antecedentes personales de cáncer, ni otros de interés, pero su madre fue diagnosticada de melanoma a los 60 años. Se realiza una dermatoscopia que revela un patrón de red irregular, puntos negros, áreas de regresión y vasos sanguíneos irregulares. ¿Cuál es el manejo más apropiado?
A punch biopsy of only the most pigmented part risks sampling error, potentially missing the deepest/most invasive part of the lesion and interfering with accurate staging (Breslow thickness) — complete excision is preferred when melanoma is suspected.
Correct. A pigmented lesion with the ABCDE features of melanoma (asymmetry, irregular border, color variegation, changing size, plus dermoscopic red flags: irregular network, black dots, regression areas, irregular vessels) and a family history of melanoma should undergo complete excisional biopsy with narrow (1-3 mm) margins for definitive histopathologic diagnosis, including accurate Breslow depth measurement — this is the standard of care for a suspicious pigmented lesion.
Given the clear ABCDE criteria and concerning dermoscopic findings (plus a documented recent change and family history), watchful waiting/monitoring would inappropriately delay diagnosis and potentially allow progression of a likely melanoma.
Photodynamic therapy is not an appropriate treatment for a lesion suspicious for melanoma and should never precede definitive tissue diagnosis of a pigmented lesion with these concerning features.
⭐ High-yield pearl
Suspicious pigmented lesion (ABCDE features + worrying dermoscopy) → complete excisional biopsy with narrow margins is the standard first step, allowing accurate Breslow depth measurement.
Excisional biopsy (rather than a partial/punch biopsy) is preferred for suspected melanoma specifically because accurate microstaging (Breslow thickness, ulceration status) — critical for determining prognosis and subsequent management (margins for definitive excision, need for sentinel lymph node biopsy) — requires assessment of the entire lesion, which a partial sample cannot reliably provide.
#198
Una lactante prematura de 32 semanas, consulta al mes de nacimiento por 3 hemangiomas infantiles superficiales que han crecido en las 2 últimas semanas en el antebrazo derecho, en el tórax y en la espalda. Respecto a los hemangiomas infantiles que presenta la paciente, señale la respuesta INCORRECTA:
True — infantile hemangiomas classically follow this three-phase course: rapid proliferation, a plateau/stable phase, and then gradual involution.
True — GLUT-1 positivity is a distinctive immunohistochemical marker specific to infantile hemangiomas, useful for distinguishing them from other vascular anomalies/tumors that are GLUT-1 negative.
Incorrect statement (so this is the answer). Routine imaging to screen for visceral hemangiomas is NOT indicated for every infant with cutaneous hemangiomas — it is specifically indicated in patients with MULTIPLE (typically ≥5) cutaneous hemangiomas, given the increased association with hepatic hemangiomas in that specific subgroup; simply having 3 lesions in a preterm infant doesn't automatically meet this threshold, making a blanket statement that imaging 'is necessary' overly broad without specifying the number-based indication.
True — most infantile hemangiomas follow a predictable, self-limited course, and if there's no functional impairment (e.g., vision, airway) or significant cosmetic concern, observation without active treatment is a perfectly reasonable management approach.
⭐ High-yield pearl
Imaging screening for visceral (hepatic) hemangiomas is specifically indicated for infants with ≥5 cutaneous hemangiomas, not for every infant with hemangiomas regardless of number.
This numeric threshold (5 or more cutaneous hemangiomas) is a well-defined, high-yield indication for hepatic ultrasound screening in infantile hemangioma management, since infants with multiple cutaneous lesions have a meaningfully increased risk of associated visceral (particularly hepatic) hemangiomas that could otherwise go undetected.
#199
Hombre de 45 años con antecedentes personales de hipertensión arterial, dislipemia, hígado graso y esclerosis múltiple y en tratamiento con fingolimod, enalapril y simvastatina, presenta una psoriasis con afectación de más del 10% de la superficie corporal y un índice de la severidad del área de psoriasis (PASI) de 14. Había realizado previamente tratamiento con acitretina durante 15 meses con escasa mejoría. El paciente pregunta por otra alternativa terapéutica que consiga mejorar su psoriasis. ¿Cuál considera que es la mejor opción de tratamiento?
Phototherapy would be a reasonable option in many patients, but combining UV light with fingolimod (which affects lymphocyte trafficking and immune surveillance) raises theoretical skin cancer risk concerns, and given failed prior systemic therapy with significant disease burden (PASI 14, >10% BSA), a targeted biologic is generally preferred over phototherapy at this stage.
Anti-TNF biologics carry a risk of triggering or worsening demyelinating disease (including multiple sclerosis) — a well-established contraindication in a patient with pre-existing MS, making this an inappropriate choice here.
Cyclosporine can worsen hypertension and renal function and isn't ideal for long-term use, and doesn't have the same targeted, favorable long-term safety profile as a modern biologic for a patient needing an alternative after failed acitretin.
Correct. In a patient with moderate-to-severe psoriasis (BSA >10%, PASI 14) who failed acitretin and has comorbid multiple sclerosis (where anti-TNF agents are contraindicated due to demyelination risk), an anti-IL-23 biologic is an excellent choice — IL-23 inhibitors have a favorable safety profile that doesn't carry the demyelinating disease risk associated with anti-TNF agents, making them well-suited to this specific patient.
⭐ High-yield pearl
Anti-TNF biologics are contraindicated (or used very cautiously) in patients with multiple sclerosis due to demyelination risk — anti-IL-23 (or anti-IL-17) biologics are safer alternatives for psoriasis in this population.
This is an important drug-selection principle: anti-TNF therapy has a well-documented association with new-onset or worsening demyelinating disease, so in any psoriasis patient with pre-existing MS (or a strong family history of demyelinating disease), biologics targeting other pathways (IL-17, IL-23, IL-12/23) are preferred first-line over anti-TNF agents.
#200
Indique, de los siguientes, ¿cuál es un criterio de malignidad radiológica de los tumores óseos?
Reactive perilesional sclerosis is generally a feature suggesting a slower-growing, more benign process (the bone has time to react and wall off the lesion), not a malignancy indicator.
Punctate ('popcorn') calcifications are classically associated with benign cartilaginous lesions (like enchondroma), not a malignancy indicator.
Correct. Cortical destruction/breakthrough (loss of the bone's outer cortical boundary, often with extension into adjacent soft tissue) is a classic radiological red flag for an aggressive, malignant bone lesion, reflecting rapid growth that outpaces the bone's ability to contain or react to it.
Epiphyseal location is a descriptive anatomic feature relevant to certain specific diagnoses (like giant cell tumor or chondroblastoma, which characteristically arise in the epiphysis), but epiphyseal location alone is not itself a general radiological criterion indicating malignancy.
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Cortical bone destruction/breakthrough is a classic radiological red flag for malignancy — reactive sclerosis and 'popcorn' calcifications instead suggest a more indolent, benign process.
When assessing a bone lesion radiologically for aggressiveness, look for the pattern of bone destruction (permeative/moth-eaten = aggressive vs. well-defined sclerotic margin = more indolent), the presence and character of periosteal reaction (aggressive patterns like Codman triangle/sunburst vs. solid benign patterns), and cortical integrity (breakthrough/destruction = concerning for malignancy) — these together, not any single isolated finding, build the overall radiological impression of malignant potential.
Resultado del examen
Preguntas 151–200 · Cuaderno de Examen Medicina 2024 (v.0)