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  • A

    Stem: 67-year-old woman presents to her GP with 10 days history of vomiting with gastric content. This can occur any time and has no associated factors. At the GP surgery she collapsed but does not lose consciousness. The ambulance takes her to ED, on arrival she has pulse of 105, BP 105/55 and epigastric fullness was noted.

    Why hypokalaemia hypochloremic metabolic alkalosis?

    Persistent vomiting (chloride, hydrogen)
    Bicarbonate used in production of gastric acid secret in blood because of acid is loss more. More bicarbonate in the blood when ability of the gut and kidney to Excrete or saturated
    Increase creatinine, because hypovolemia decreases renal perfusion

    Why hypokalaemia??

    Loss vomiting
    K+/Na+ exchange

    In addition to the fluid resuscitation what bedside procedure can help in the bowel problem?

    NGT
    Catheter

    As surgical registrar, who will be involved ?!

    Surgical consultant
    HDU / level 2 nursing staff or Anaesthesia team (line placement).

    When patient will be fit for the surgery?

    Corrected electrolyte and metabolic disturbance.

    Optimal iv fluid resuscitation??

    I will give this patient sodium chloride, plus potassium supplement to:
    -replace sodium and chloride and potassium
    -correct of the metabolic component better than Hartman (more chloride)

    Clinical picture of hyponatremia?

    Confusion, cerebral oedema
    Seizures
    Cardiac arrhythmia disturbances

    Why aciduria?

    Dehydration will lead to increase aldosterone which happens DCT and collecting duct. Here Na+ reabsorbed in exchange K and hydrogen ion.

    Classification of hyponatremia & give example for each?

    According to Serum osmolarity can be divided to isotonic, hypotonic and hypertonic hyponatremia.
    Then hypotonic hyponatremia can be divided according to volume status to:
    Hypovolemic hyponatremia e.g. diarrhoea, vomiting and diuretics
    Euvolemic hyponatremia e.g. SIADH, hypothyroidism
    Hypervolemic hyponatremia, e.g. heart failure
    Pseudohyponatremia: Multiple myeloma

    Complications of hyponatremia?

    Brain: cerebral oedema, seizures and decrease consciousness level, confusion
    Heart: MI and heart failure
    Respiratory: SOB, Chest pain
    Liver: hepatic encephalopathy
    Kidney: renal failure

    Causes of gastric outlet obstruction?

    Benign -> pyloric stenosis secondary to chronic peptic ulceration.
    Malignant -> (gastric or pancreatic) carcinoma.

    Is NaHCO3 excreted as a whole ion?

    Yes

    What is Chloride shift?

    Is the shift of the chloride ion to the intra-cellular compartment of RBC in exchange of bicarbonate ion excretion.

    What is the single bedside test you should do?

    ABG

    What is the clinical picture of GOO

    Dehydration.
    Non bilious vomiting
    Left hypochondrial fullness
    Visible peristalsis


    What are the common causes of gastric outlet obstruction in adults? SpoilerThe causes can be divided into benign and malignant. Benign Peptic ulcer disease causing pyloric stenosis Chronic pancreatitis Caustic ingestion Post-surgical strictures Crohn’s disease Malignant Distal gastric cancer (most common modern cause) Pancreatic head cancer Duodenal carcinoma Periampullary tumours Historically peptic ulcer disease was the commonest cause, but malignancy is now more common. Why does gastric outlet obstruction cause vomiting of undigested food? SpoilerThe obstruction occurs at the pylorus or proximal duodenum, preventing gastric emptying. Food therefore remains in the stomach for prolonged periods and is vomited before reaching the small intestine, so it appears undigested. What electrolyte and acid–base abnormalities are classically seen? SpoilerThe classical abnormality is: Hypochloraemic Hypokalaemic Metabolic alkalosis Often associated with hyponatraemia and volume depletion. Why does vomiting lead to metabolic alkalosis? SpoilerGastric secretions contain hydrochloric acid (HCl). Vomiting causes loss of: Hydrogen ions Chloride ions Loss of hydrogen ions leads to metabolic alkalosis, and loss of chloride contributes to hypochloraemia, which also impairs renal bicarbonate excretion and worsens the alkalosis. Why does hypokalaemia occur in gastric outlet obstruction? SpoilerHypokalaemia occurs due to: Renal potassium loss from activation of the renin–angiotensin–aldosterone system due to dehydration. Hydrogen–potassium exchange in the kidney during metabolic alkalosis, where potassium is excreted to retain hydrogen ions. What clinical signs might you find on examination? SpoilerPossible signs include: Epigastric distension Succussion splash (if stomach contains retained fluid) Visible gastric peristalsis Signs of dehydration (tachycardia, hypotension) Possible weight loss if chronic What investigations would you perform to confirm the diagnosis? SpoilerInvestigations include: Blood tests: FBC, U&E, LFTs, ABG Nasogastric aspiration (large residual volume) Upper GI endoscopy (OGD) – confirms obstruction and allows biopsy CT abdomen – helps identify malignancy or extrinsic compression OGD is the key diagnostic test. How would you manage this patient initially? SpoilerInitial management is resuscitation and decompression: Nil by mouth Nasogastric tube for gastric decompression IV fluids to correct dehydration Correct electrolyte abnormalities IV proton pump inhibitor Arrange urgent endoscopy Definitive treatment depends on the cause (e.g., endoscopic dilation, surgery, or oncological treatment).
  • A

    Scenario: 24-year-old male, Day 1 post-op emergency laparoscopic appendectomy for perforated appendicitis
    Vitals: HR 128 bpm, BP 88/52 mmHg, RR 26/min, SpO2 93% (room air), Temp 38.6 °C, Urine Output 15 mL/hr over 3 hours (Weight: 70 kg).

    Q1 What is your immediate structured assessment and initial management plan for this patient?

    I would immediately assess this patient using a structured CCrISP / ABCDE approach while simultaneously initiating resuscitation and escalating to senior support.
    Airway: Assess patency and voice. Administer high-flow oxygen via a non-rebreathe mask at 15 L/min to target SpO2 >= 94%.
    Breathing: Auscultate chest, check respiratory rate and trachea position.
    Circulation: Establish two wide-bore (16G/14G) peripheral IV cannulae. Send urgent baseline lab bloods (FBC, U&Es, LFTs, Coagulation, CRP, Group & Save/Crossmatch) and blood cultures. Obtain an immediate Venous/Arterial Blood Gas to check lactate, pH, and base excess.
    Resuscitation: Immediately deliver a rapid fluid bolus of 500 mL warmed balanced crystalloid (Hartmann's solution) over 15 minutes and reassess.
    Disability: Assess GCS/AVPU, check pupils, and measure blood glucose.
    Exposure: Expose and examine the abdomen for peritonitis or distension, inspect laparoscopic port sites for hemorrhage/leakage, check drains, and measure temperature.
    Monitoring: Insert a urinary catheter with an hourly urometer to monitor fluid balance accurately (aiming for > 0.5 mL/kg/hr)

    Q2 What is your primary clinical working diagnosis, and what targeted microbiology and antibiotic plan would you initiate?

    My primary working diagnosis is septic shock secondary to an intra-abdominal source, such as persistent pelvic contamination, an early post-operative pelvic collection, or an appendiceal stump leak.
    Differential diagnoses to exclude include intra-abdominal hemorrhage, pulmonary embolism, and chest infection/atelectasis.
    Microbiology & Antibiotic Plan:
    Draw two sets of peripheral blood cultures prior to antibiotic administration, alongside wound or drain fluid cultures if accessible.
    Administer empiric, broad-spectrum IV broad-spectrum antibiotics within 1 hour as per the Sepsis Six protocol (e.g.,
    IV Piperacillin/Tazobactam (Tazocin) 4.5 g, or
    IV Co-amoxiclav 1.2 g + IV Metronidazole 500 mg, adjusted for renal function and local trust guidelines).

    Q3 You give a 500 mL fluid bolus. His BP remains low at 90/55 mmHg, HR is 124 bpm, and lactate returns at 4.2 mmol/L. How is Septic Shock defined, and what are your immediate escalation steps?

    According to the Sepsis-3 definitions, Septic Shock is defined as a subset of sepsis in which underlying circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality. Clinically, it is identified by:
    Persistent hypotension requiring vasopressors to maintain a Mean Arterial Pressure (MAP) >= 65 mmHg, AND
    A serum lactate level > 2.0 mmol/L despite adequate fluid resuscitation.
    Escalation Steps:
    Escalate: Inform the Consultant Surgeon and request an immediate ICU / Senior Anaesthetic review for level 2/3 care admission.
    Hemodynamic Support: Prepare for vasopressor therapy (e.g., Noradrenaline) via a central venous catheter to restore MAP.
    Invasive Monitoring: Request arterial line placement for continuous blood pressure tracking and central venous line insertion for vasopressor delivery and CVP monitoring.
    Ongoing Fluids: Continue fluid challenge cautiously (20-30 mL/kg total) while monitoring for fluid responsiveness and pulmonary edema.

    Q4 What radiological investigation would you order once the patient is hemodynamically stabilized, and what specific findings are you looking for?

    Once initial resuscitation establishes sufficient hemodynamic stability, I would request an urgent contrast-enhanced CT Scan of the Abdomen and Pelvis (CT AP) with IV contrast.
    Key Findings to Assess:
    Intra-abdominal Collection/Abscess: Look for ring-enhancing fluid collections in the pelvis, rectovesical pouch, or subphrenic spaces.
    Appendiceal Stump Leak: Presence of focal free air, extraluminal contrast, or fluid tracking near the cecal pole.
    Interloop Abscess or Peritonitis: Diffuse fat stranding, thickened bowel loops, or complex free fluid.Intra-abdominal Hemorrhage: Hyperdense free fluid or active arterial extravasation (contrast blush).

    Q5 The CT scan demonstrates a 6cm x 5cm fluid collection with ring enhancement in the pouch of Douglas, containing small pockets of gas. How would you manage this collection?

    Management depends on clinical stability and technical accessibility:
    Radiological Intervention (First-line): For a localized, 6 cm pelvic collection accessible via a transabdominal, transrectal, or transgluteal window, the primary management is image-guided percutaneous drainage (ultrasound or CT-guided) along with targeted antimicrobial coverage based on aspirate cultures.
    Surgical Re-exploration: Laparoscopic or open washout and drainage would be indicated if:
    Percutaneous drainage is non-feasible or fails to yield clinical improvement within 24-48 hours.
    The patient continues to deteriorate hemodynamically despite maximal therapy.
    There is generalized peritonitis suggesting widespread breakdown or uncontained perforation.

    The patient’s urine output remains 15mL/hr over the past 4 hours. His urea is 14.2mmol/L and creatinine is 185mol/L (baseline 70).
    Q6 Classify this Acute Kidney Injury (AKI) and state the physiological classification of causes you consider.

    This represents Stage 2 Acute Kidney Injury (AKI) under the KDIGO criteria (creatinine elevated 2.0-2.9 times baseline, or urine output < 0.5 mL/kg/hr for >= 12 hours).
    Physiological Causes:
    Pre-renal (Primary Cause): Renal hypoperfusion secondary to septic vasodilatation, intravascular volume depletion, and third-space fluid sequestration.
    Intrinsic Renal: Acute Tubular Necrosis (ATN) triggered by prolonged hypotension/ischemia or nephrotoxic medications (e.g., NSAIDs, aminoglycosides, contrast dye).
    Post-renal: Urinary catheter obstruction, urinary retention, or accidental iatrogenic ureteric injury during appendectomy.
    Immediate Action: Ensure catheter patency (flush line), optimize renal perfusion pressures with vasopressors/fluids, perform an urgent renal ultrasound to exclude obstruction, and hold all nephrotoxic agents.

    Q7 What are the key physiological criteria for safe transfer of this patient from the HDU to the Intensive Care Unit (ICU)?

    The safe intra-hospital transfer of a critically ill surgical patient follows ICS (Intensive Care Society) guidelines:Airway & Ventilation: Secure airway with adequate oxygenation (PaO2 / FiO2 ratio acceptable); if intubated, confirmed ET tube position and portable ventilator secured.Hemodynamic Stability: Continuous arterial blood pressure monitoring; vasopressor/inotrope infusions running reliably via dedicated central lines with adequate IV access.Escort & Staffing: Accompanied by a minimum of a trained critical care doctor (anaesthetist/intensivist) and an ICU/HDU nurse equipped with a transfer bag, defibrillator, and full monitoring equipment.Communication: Structured handover completed using SBAR (Situation, Background, Assessment, Recommendation) to the receiving ICU consultant and nursing team.

    Q8 Where does qSOFA fit into this patient's assessment?

    In this patient, the qSOFA score is 2 (RR 26 and Systolic BP 88), which correlates with a high risk of mortality and ICU admission. However, while qSOFA is a useful bed-side risk-stratification tool under Sepsis-3, in UK practice, NEWS2 is the preferred screening tool for early deterioration. I would use full lab markers (lactate, arterial blood gas, organ function tests) to score formal SOFA and guide organ support in HDU/ICU.


  • A

    Stem 1: 78-year-old diabetic woman undergoing temporal artery biopsy, she has shoulder pain & a tender scalp.
    When temporal artery biopsy was taken, a skin ulcer was found on her cheek.

    c43a8b57-ea0e-4a9e-840b-a9743615a3b6-image.jpeg
    Describe what you see?

    Pearly papule
    Central ulcer
    Granulation tissue on base
    Inverted edges
    Surrounding telangiectasia

    What is your differential diagnosis?

    BCC
    SCC
    TB
    Actinic keratosis

    Natural Hx of BCC?

    Indolent with slow progression
    Locally destructive
    but limited potential to metastasize

    Examiner gives you histology report. What will you look for in the report?

    Deep margin involvement (i.e. clear margin or not)
    Size and Invasion

    If unclear margins, what to do?

    Re-excision with safety margin, with frozen section or MOHs micrographics surgery.

    If there is lymph node involvement, what to do?

    Lymph nodes biopsy (FNAC or excisional biopsy)

    What is frozen section?

    It is a laboratory procedure that allows for a quick microscopic examination of tissue to help diagnose disease

    What are advantages of frozen section?

    Give rapid intraoperative pathological diagnosis

    Can you explain the steps?

    The surgeon takes a small piece from a tissue or tumour and send it for analysis
    The pathologist freezes it and section it and immediately cut it
    The section will be stained and reported immediately when the results come out

    How do malignant cells reach lymph nodes?

    Cancer cells and the secrete growth factors which are taken up by the lymphatic capillaries and transported towards the LN.
    These growth factors induce lymph-angiogenesis thereby promoting LN metastasis

    Skin graft was done, and the patient had graft failure subsequently. What are the possible causes for graft failure?

    Wound infection
    Hematoma
    Rejection

    Common organisms for wound infection?

    Staph. aureus.
    Streptococcus.

    What to do to diagnose it?

    Swab for C&S
    Blood test (CRP, WCC)

    What is MRSA?

    Methicillin-resistant Staphylococcus aureus.

    What to do if swab for MRSA is positive?

    Isolation of patient
    Inform infection control team and follow infection control protocol
    Wound debridement. I&D if abscess
    Give antibiotics according to trust/local protocol / microbiology advice

    How to decolonise MRSA in a carrier patient (not infected)?

    With mupirocin nasal
    Chlorhexidine body wash / shampoo

    Who will you involve in the management?

    Ward nurse
    Microbiologist
    infection control team

    Patient developed axillary LN enlargement. LN biopsy showed large cells with bilobed nucleus with prominent eosinophilic inclusion with nuclei resembling an owl's eye appearance.
    What is your diagnosis now?

    Reed-Sternberg cells (owl eye appearance) therefor Hodgkin's lymphoma

    Define carcinoma?

    Is a type of cancer that develops from epithelial cells

    Features of malignant cells?

    Increased number of mitotic figures
    Abnormal mitoses
    Hyperchromatism (nuclei are darkened due to increased concentration of DNA)
    Pleomorphism (varied size and shape of cell)
    Increased nuclear to cytoplasmic ratio


    Stem2: 78-year-old diabetic woman referred for temporal artery biopsy, having shoulder pain and tender scan for one week. When performing a temporal artery biopsy, you find nodular lesion with some ulcerations in the cheek of the patient suggestive of primary skin carcinoma probably Basal cell carcinoma. Why is temporal artery being biopsy in this case? SpoilerTo test of presence of giant cell arthritis. What is the usual medical treatment of this condition which is started before the biopsy? SpoilerLarge dose of corticosteroid. Why is steroid therapy often started before biopsy is taken? SpoilerTo protect vision from ophthalmic artery insolvent from arthritis. What 4 items of data would you want to see in skin pathology summary report? SpoilerThe type of tumour verification. Tumor diameter. Tumor thickness. Margin clearance, lateral and deep margin. What features of that tumour may give insight into the risk of metastatic disease? SpoilerPresence or absent blood or lymphatic invasion. Six months later the patient readmitted following a mechanical fall in the community. Radiology revealed a fracture neck of femur, requiring surgical intervention. What factors in the scenario can predisposed to this osteoporotic fracture? SpoilerFemale. Age and post menopause. Steroid. From the biochemical perspective, what do you expect the serum calcium and phosphate levels to be, considering this patient is osteoporotic? SpoilerBoth of them will be normal. During surgery, the bone matrix appears to be soft and fragile. A sample sent to the histology and revealed plasmacytoma or myeloma. What will you find in this? SpoilerNeuroplastic, monoclonal, perforations of plasma cell. What may such tumours commonly secrete into the serum? SpoilerMyeloma, immunoglobulins or fragmentation of immunoglobulins. What is Bence Jones protein? SpoilerA light chain or paraprotein, which may be identified in urine. Apart from osteoporosis, what may be the cause of fracture of this patient? SpoilerTumour itself. Bone lysis by the tumour. The screw is required to repair the fracture and some radiotherapy is planned. However, the wound decide heals poorly with a septic breakdown. What 4 factors likely to contribute wound sepsis? SpoilerSteroid. Diabetic. Immunocompromise because plasmacytoma. Foreign body processes. Despite antibiotic treatment, the hip infection persists; excision of the hip, and the fracture site repair followed by a full hip replacement. Patient arrested 24 hours after surgery. What is the cause of this? SpoilerVenous thromboembolism
  • V
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    It's good to see the old imperium continuing the ideals of the new imperium./s
  • throws_lemy@lemmy.nzT
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    read more →
    Scientists should probably caution that more research is needed. But to clarify, it's n=16. Half of those who received the treatment responded and started producing immune cells. Six years later 7 of the 8 who responded are still alive, while only 2 of the 8 who didn't respond are alive. This is one of the deadliest cancers, so having 9 out of 16 still alive after 6 years is an incredible success. More work is needed to find out why half didn't respond, but going from a 13% survivability rate to 56% is a pretty great result for an early trial.
  • V
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    We already have pregnancy vaccines that reduce the incidence of contracting a baby (and with it, that non-existent baby's ability to contract RSV) to close to 100%!
  • V
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    This is a different class of medication than the new thing from Cuba, right? https://pubmed.ncbi.nlm.nih.gov/38093366/
  • I
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    The open-access Nature Microbiology article since I wouldn't trust a Gizmodo author to correctly diagnose a skeleton with death.
  • V
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    Hi, it's vegetative me from the future. If I'm gone and unaware of anything, then it makes no difference to me if you pull the plug or not. If I'm aware, but so vegged to the point where nobody will ever know, for fucks sake yank that plug with the swiftness. My head is torture, and I'd kindly like to be relieved of it. Miss you (maybe), MelodiousFunk
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