Gastroenterology Flashcards

Question

cleft lip and palate (7 influences, how different types of feeding affected, general mx approach)

Answer 1

some genetic influence but also if during preg mum takes steroids, BZDs, sod val, phenytoin; also maternal smoking or alcohol may have difficulty bottle feeding but breast feeding is usually okay surgery and mdt management to achieve best aesthetics; foetal surgery offers prospect of scarless healing

Answer 2

usually iatrogenic (endoscopy inc dilation for strictures or achalasia) Also boerhaave syndrome from severe vomiting or retching very rarely from other raised abdo pressure inc Heimlich manouevre, defaecation, status eplilepticus, parturition, weight lifting very rarely from blunt or air blast trauma; also from any penetrating injuries to this region; also ingestion of caustic fluids, either accidentally or with suicidal intentions; also cancer acute sudden chest pain radiating to back or left shoulder often; vomiting and sob pos, subcut emphysema also poss; may see pneumomediastinum; haematemesis typically not seen, helps differentiate from eg mallory weiss tear and epigastric/chest pains may have speech problems and cervical pain if perf was in neck, also cervical crepitus pt often distressed with fever and tachy; SIRS can dev and poss bacterial mediastinitis CXR: suspect if pneumoperit, subcut emphy, PTX; water soluble contrast swallow will show and consider CT with oral contrast; endoscopy if suspect strongly but CXR neg NBM, fluids, analgesia, broad spectrum antibiotics iv; iatrogenic, small, contained perfs can have conservative management; also if perf from inoperable malig; operative treatment otherwise

Answer 3

GIT is largest endocrine organ 3 main families: gastrin-CCK, secretins (secretin, glucagon, VIP), somatostatins others: motilin, sub P, ghrelin, and many more gastrin made by G cells in stomach, stimulates the secretion of gastric acid, pepsinogen, intrinsic factor, and secretin; promotes gut motility CCK made by enteric nerves in SI, Stimulates gallbladder contraction and intestinal motility; stimulates secretion of pancreatic enzymes, induces satiety secretin stimulates pancreas enzyme release, reduces motility, decreases gastrin release VIP relaxes sphincters, suppresses gastric acid but promotes bile/pancreas, increases motility and intestinal bloodflow ghrelin - promotes appetite and stomach emptying motilin - increases motility somatostatin - from delta cells in antrum, duodenum, pancreas; decreases intestinal bloodlow, slows gastric emptying, inhibits pancreatic enzyme release inc glucagon and insulin, suppresses other GI hormones

Answer 4

Somatostatin receptors are Gi-protein coupled receptors. Activation of such a receptor inhibits intracellular cAMP production; it also activates potassium channels, hyperpolarising the membranes of excitable tissues; practically speaking, somatostatin (and thus octreotide) prevent secretion from glands depresses secretion of: GH, calcitonin, ACTH, insulin, glucagon, ifn-g, gastrin (+gastric acid); it also reduces splanchnic blood flow can reduce GI bleeding and HRS through splanchnic vasoconstriction, control diarrhoea through less GI secretion, decrease chyle flow in chylothorax, reduce hormone release from neuroendocrine tumours, and slow output through stoma or down pancreas or bowel fistula (by inhibiting CCK, VIP, and secretin that promote motility and GI secretion); induce selective splanchnic vasoconstriction by inhibiting the release of vasodilator glucagon and through blunting of postprandial splanchnic hyperemia - minimal systemic s/e compared to terlipressin but lasts less long biliary stasis may inc risk of gallstones, can get hyperglyc, hypoadrenalism, poor wound healing (GH def), constipation, delayed gastric emptying

Answer 5

used to reduce gastric acid secretion: g cells release gastrin, bind to CCK2r on ECL cells, raising Ca and causing histamine release which acts on H2 on parietal cells: PKA phosphos proteins involved in trafficking of K/H pumps, enhancing their activity to enhance H efflux; somatostatin is negative regulator of this directly via Gi coupled SSTr on parietal cells, indirectly by same r's on G/ECL cells to reduce gastrin/histamine release CCK2r antag proglumide reduces histamine secretion but surpassed by H2r antags like cimetidine (though can inhibit p450 so ranitidine surpassed it); now PPIs like omeprazole used preferentially to H2r antags as irreversible block of last step so more effective; antacids used to counteract stomach pH; cholinergic blockade and vagotomy were used but now obsolete, ACh on M3r on parietal cells enhances acid release which atropine would stop NSAIDs inhibit PGE2 (which acts on ECL EP2/3R to inhibit acid secretion, and EP4R which enhances mucin secretion, and EP1/2R to increase bicarbonate secretion); so stop taking NSAIDs combo pills like arthrotec (mix of NSAID diclofenac and misoprostol (PG analogue binding PGEP2/3/4r), used in treatment of rheumatoid arthritis with the misoprostol prophylactic against peptic ulcer

Answer 6

penetrate the mucosa, may be from distal oesophagus through to duodenum gastric more common in elderly and duodenal more in <40yos present with: epigastric pain (g - after eating and relieved by antacids, d - nocturnal and relieved by food), vomiting (rare for duodenal, common for gastric), gastric common to lose appetite/weight but duodenal may even gain weight, may present with haematemesis endoscopy to diagnose, can biopsy for H pylori or in gastric case to check for malignancy at edge of ulcer, should do second endoscopic scan to check healing of gastric ulcers due to risk of malignancy; duodenal wont go malignant but have higher risk of perforation besides H pylori, risk inc'd by smoking, NSAIDs, stress (esp due to chronic disease eg cirrhosis etc) perforation: severe upper abdo pain rapidly generalising, air under diaphragm, rigid and silent abdo gastric outlet obstruction if near pylorus: distension, vomit old food, dehydration, hypokalaemic alkalosis, NG aspiration of stomach contents then endoscope to investigate; drip n suck (iv nutrition, NG aspiration); treat with balloon dilation

Answer 7

v common cancer death worldwide, esp china and japan; incidence falling in UK often from chronic ulcers, diets with lots of pickled or smoked foods; smoking and alcohol epigastric pain unrelated to meals, relieved by acid suppressants; weight/appetite loss; haematemesis rare except in late disease; supraclavicular lymph node and migratory thrombophlebitis are rare but classic signs endoscopy will show irregular ulcer looking thing, biopsy the edges; FBCs and LFTs, CXR, abdo CT can help with staging

Answer 8

90% ACC, also lymphoma (MALT), GIST, neuroendocrine; ACC subtypes: intestinal type (glands), diffuse type (signet rings - krukenberg, intraperit spread) Gastric MALT lymphoma is frequently associated (72–98%) with chronic inflammation as a result of the presence of Helicobacter pylori GIST looks like dome in stomach wall; often spindle cells on histo; immunohistochem to identify for sure; often have RTK mutations so imatinib endoleak, expanding aneurysm sac, stent fractures and occlusions, graft infection, graft migration, aortoenteric fistula, aortic rupture, and ischaemic complications (limb, visceral and renal inc heart attack and stroke) aorto-enteric fistula rare cause of haemat, after abdo AAA surg - herald bleed then rapid exsanguination, CT +/- OGD

Answer 9

arise in interstitial cells of cajal or other mesenchymal neoplasms, driven by mutation in KIT (CD117 pos), PDGFRA, or BRAF kinase; they are sarcomas and nonepithelial unlike most GI tumours; 70% stomach, 20% SI, 10% oesophagus present with some of: trouble swallowing, GI bleeding, symptoms from mets (oft liver), anemia, blood in stool or vomit; abdominal discomfort; painless abdo lump; vomiting; fatigue; fever, night sweats, weight loss small tumours generally benign, large malign and disseminate to liver, omentum surgical resection potentially curative; most chemo and radio dont help much but imatinib and a couple other targeted drugs do malt lymphoma v often associated with h pylori infection, and if low grade often resolves by itself if you treat the infection

Answer 10

Hiccups are very common in all age groups but especially children and are usually a mild and self-limiting condition requiring no formal treatment. However, if they are persistent (lasting over 48 hours) or intractable (lasting over one month), they can have a profound adverse impact on quality of life Peripheral causes are usually triggered by irritation of the phrenic or vagus nerves. They can be subdivided into gastrointestinal causes such as reflux, gastroparesis, gastric irritation and non-gastrointestinal causes such as pneumonia and other chest infections, asthma, etc. Central causes can be subdivided into neurological causes such as brain tumour, brain infections or brain trauma, non-neurological causes such as infection, metabolic such as electrolyte imbalance, iatrogenic (from use of opiates, dexamethasone, chemotherapy agents for example), or from hypocapnia triggered by over breathing due to stress, fear, or anxiety. Other potential causes should be considered and addressed before pharmacological intervention is considered – correction of metabolic causes where possible, strategies to reduce stress and anxiety, stopping or reducing medication known to potentially exacerbate hiccup such as opioids, dexamethasone, chemotherapy agents and simple strategies to reduce gastric distension such as adjustment of feeds, regular winding, posture to reduce reflux The most common cause of hiccups is gastric reflux and distension – due to ingestion of fizzy drinks, swallowing air, eating too much or too fast, gastrointestinal reflux, or especially in palliative care where gastric stasis or delayed gastric emptying may be present. Other triggers can include emotional stress, sudden temperature changes, spicy foods, alcohol etc Medication should be avoided unless nonpharmacological measures have been tried unsuccessfully. These include breath holding, Valsalva manoeuvre, and other measures to stimulate nasopharyngeal irritation such as sipping iced water, eating granulated sugar off a teaspoon, and rubbing the soft palate with the tip of a swab For PERIPHERAL causes, simple over the counter remedies such as peppermint water or an antifoaming agent such as simethicone may offer simple effective relief, especially with upper gastrointestinal causes. If more formal prescribed medication is required, first line treatment should be a PPI as the most common cause is gastric irritation and reflux. Metoclopramide is an alternative or additional therapy, but only in a palliative care setting as neurological side effects limit its use For CENTRAL causes, Baclofen, for its GABA receptor agonist activity, is usually recommended as the first line agent of choice in adults, although there is little evidence for this in children. It is used widely for other indications in children. Second line drug of choice is Gabapentin, and third line suggestions include Haloperidol and Calcium channel blockers such as Nifedipine, which may block the hiccup reflex arc. For troublesome hiccup in the terminal stages of life, Midazolam is often used

Answer 11

delayed gastric emptying in the absence of mechanical obstruction early satiety, postprandial fullness, nausea, vomiting, weight loss, bloating, and upper abdominal pain idiopathic, diabetes, post-surgical (vagus nerve injury), parkinsons, MS, brainstem CVA/tumour, autonomic neuropathy, SCI, amyloidosis, scleroderma, autoimmune, drugs inc opioids, octreotide, TCAs (anticholinergic) etc can diagnose with SGE (scintigraphic gastric emptying) assessment; gastric emptying breath testing is an alt optimise DM/PD etc control, smaller more freq meals, reduce carbonated beverages, reduce smoking/alcohol (can delay gastric emptying), consider jejunostomy if not meeting nutritional requirements metoclopramide, can try other antiemetics; domperidone better tolerated than metoclop in kids; another option is erythromycin but shows tachyphylaxis, can have some weeks on then some off to counter this; PPIs often also given as overlap in presentation with dyspepsia gastric electric stimulation if refractory to medical mx

Answer 12

indications for PEG feeding: lack of volition, nutritional support (eg CF), unsafe swallow, head/neck/oesoph cancer, oesoph dysmot delayed gastric emptying eg gastroparesis in DM (use jejunal extension) PEG blocked: massage visible blockage and try to aspirate with 20mL syringe, then push and pull syringe with warm water, then again with 8.4% bicarb (let it sit for a couple hours then flush if blockage removed), then try again with creon dissolved in bicarb Redness around PEG: exclude infection, leak, granulation tissue; then if psoriais or contact dermatitis give eumovate ointment for 2 weeks, wash the site twice daily, and apply greasy emollient oil; if allergic reaction refer derm Granulation tissue: wound irrigation solution clean daily for 2 weeks, then salt rx 2 weeks, then hydrocort 2 weeks, then seek advice Leaking: Test pH, if <5 is leaking from stomach; if <72 stop using, make child NBM, call surgeons; otherwise check if fitted right, stoma right etc Infection: If cellulitis (warm, spreading, pus) or candida (satellite lesions) swab and rx with oral abx/fluconazole + clean site, clotri + HC cream, and foam dressing

Answer 13

NBM for 6 hrs prior, no fluids for 2hrs before RIG (radiologically inserted gastrostomy) insertion under sedation, NGT to put air into stomach, then US to locate stomach; local anaesthetic then stitches to secure stomach to abdo wall, and pass tube in; tube changed every 3-6 months PEG (percutaneous endoscopic gastrostomy) is similar, under sedation, but endoscope passed down with light on end that is visible externally then cut made to insert tube contraindications would include INR >1.5 or other bleeding risk, gastric varices, peritoneal dialysis, organomegaly you also need to consider if pt could tolerate the procedure eg lie flat for >30mins

Answer 14

recurrent episodes of intense nausea and vomiting that can last from hours to days without any functional or infectious illness exact cause of CVS is unknown. In the pediatric patient, CVS is considered by many to be a precursor to migraines later in life; Allergies to foods, stressful triggers, and lack of sleep are also associated with CVS. There is an increased frequency during patient menstrual cycles, suggesting a possible hormonal trigger for CVS. Longterm cannabis use has been associated with CVS as well patient will often describe a sudden onset of vomiting. Abdominal pain is a common complaint as well. Many describe prodrome of nausea, anorexia, sweating and fatigue prior to the onset of vomiting. These episodes may last hours to days. In between episodes, patients describe pain-free and symptom-free intervals that last weeks to months. The hallmark of this disease is the recurrence of vomiting cycles dd: Gastroenteritis, gallbladder disease, peptic ulcer disease, appendicitis, pancreatitis, infectious or toxic causes, mechanical obstruction, irritable bowel syndrome, psychiatric causes, neurological causes, metabolic causes, and pregnancy; also consider cannabinoid hyperemesis syndrome, functional dyspepsia (will not have phases), rumination syndrome, and bulimia; gastroenterology input is needed Full blood count, urea and electrolytes, liver function testing, amylase, urinalysis (including a pregnancy test in patients of child-bearing age), and plain film radiography can be undertaken to exclude any obvious organic cause of nausea and vomiting, and can help to eliminate potential complications of CVS exam findings and bloods normally non-specific, may find pt dehydrated triggers can be identified with sx diary and can include stressful events (both positive and negative), travel/motion sickness, sleep deprivation, food, weather changes, menstrual cycle; sleep hygiene and meditation can be helpful as well as trigger avoidance during episodes: IVF/rehydration, anti-emetics, and rest in dark quiet room ondansetron is best anti-emetic choice (SL or PR), can combine with a benzo; intranasal sumatriptan can stop attacks, especially if migrainous features; TCAs are first line prophylaxis, others inc topiramate or aprepitant

Answer 15

taken for malabsorption, histo shows villous atrophy coeliac disease - definitive diagnosis is initial biopsy + normal one after 6 weeks gluten free diet; repeat biopsy more important in child <2yo as transient gluten intolerance more common transient gluten intolerance (usually sec to gastroenteritis) post-gastroenteritis cow's milk/soya milk protein intolerance giardiasis SCID post-chemo hypogammaglobulinaemia (this may be due to giardiasis) kwashikor tropical spruce malabsorption syndrome

Answer 16

pyloric stenosis - projectile vomiting w/o bile in, usually after feeding, usually present when 2-12weeks old; mass may be palpable in abdo; uss can confirm, and surgery will treat gord - effortless regurg of feeds common in infants <1yo, so suspect if accompanied by crying, has chronic cough, an episode of pneumonia, feeding difficulties, faltering growth; if >1yo may have heartburn take feeding history, ensure person with appropriate training does feeding assessment; ask about onset - usually ~8weeks and if after 6mo may be something else eg uti; red flags: if forceful may be stenosis, if bilious may be obstruction, if distension may be obstruction, haematemesis suggests upper gi bleed, bulging fontanelle or lethargy suggests meningitis, headache and vomiting worse in morning w/w-o head circ inc >1cm per week suggests raised icp (tumour, hydrocephalus). blood in stool suggests cows milk allergy or gastroent, chronic diarrhoea or atopy suggests cows milk allergy; dysuria (esp if lethargy, jaundice, irritability, haemat) suggests uti; onset after 6mo or persisting after 1yr suggests cause besides gord reassure (affects 40% babies), becomes less freq over time and resolves; reassess if red flags emerge, new concerns, persists past 1yo if symptoms persist after breastfeeding assessment trial alginate eg childrens gaviscon if formula fed reduce feeds if excessive for childs weight (>150ml/kg/24hrs; trial smaller more freq feeds; trial feed thickener, if unsuccessful trial gaviscon infant added to formula gaviscon fails breast or bottle fed trial PPI or H2RA for 4 weeks, and consider endoscopy

Answer 17

2ww for oesoph if dysphagia or 55yo+ w weight loss and one of reflux, dyspepsia, upper abdo pain; non urgent endoscopy for oesophageal cancer if haematemesis, treatment resistant dyspepsia, upper abdo pain + low Hgb levels; upper abdo pain/weight loss + n&v, or any of those with raised platelets 2ww pancreatic cancer if >40yo have jaundice, or over 60yo with weight loss and any of diarrhoea, back or abdo pain, n&v, constipation, new onset diabetes; early signs are epigastric discomfort or dull backache, usually worse when supine, steatorrhoea; ca19.9 is most useful tumour marker as baseline to guide treatment/follow-up 2ww if upper abdo mass consistent with stomach cancer; or dysphagia, or >55yo w weight loss and 1+ of upper abdo pain, reflux, dyspepsia or any of the other oesophageal criteria; as symptoms vague high threshold for referral of at risk pts with recent onset dyspepsia; PPIs delay diagnosis 2ww for GB cancer if ruq mass consistent with GB cancer; cholangiocarcinoma may cause obstructive jaundice w hepatomeg, maybe courvoisiers sign 2ww if <40 and heptomegaly for liver cancer

Answer 18

acute onset of severe abdo pain (+/- rif pain) oft radiating to back, retching and vomiting; pt lies still or leans forward to relieve pain; recent alcohol binge or problems with biliary colic poss, pyrexia, tachycardia, upper abdo tenderness; if severe may have shock, gen perit (but often milder as deep structure), grey turner and cullens signs, signs of hypocalc it is almost always gallstones or alcohol but remember GETSMASHED: G: gallstones, genetic - cystic fibrosis E: ethanol (alcohol) T: trauma S: steroids M: mumps (and other infections)/malignancy A: autoimmune S: scorpion stings/spider bites H: hyperlipidaemia, hypercalcaemia, hyperparathyroidism E: ERCP D: drugs (tetracyclines, furosemide, azathioprine, thiazides and many others) first confirm, then quantify severity serum amylase >3x normal upper limit (but can be back to normal if pt presents >24hr after onset of pain, also can be up to 4x normal in most acute abdo problems); serum lipase better ecg to exclude ACS; erect CXR to rule out perf and check for complications (ARDS or pleural effusion); supine AXR to rule out obstruction; USS for gallstones, if severe or deteriorating then oral contrast enhanced panc protocol CT to look for pan nec/abscess then quantify disease: def severe if in shock or has organ failure; otherwise obesity, pleural effusion or CRP >150mg/L; or glasgow scoring scale: paO2, age >55, WCC >15x10^9, BM >10, urea >16, hypocalc, albumin <32, LDH >600; hypocalc may be due to fat necrosis around the pancreases releasing FFAs which bind Ca, thus lower Ca means more severe damage mild: admit, enteral feeding (via NG/NJ tube if required), thromboproph, catheter and iv fluids, O2 and insulin if needed, morphine and antiemetics prn; daily bloods for risk surveillance severe: same as above + itu, NG definitely, central line for CVP monitoring; bloods and ABGs twice daily instead of once; note even many severe cases will be managed medically Urgent therapeutic ERCP should be performed in patients with acute pancreatitis of suspected or proven gall stone aetiology who satisfy the criteria for predicted or actual severe pancreatitis, or when there is cholangitis, jaundice, or a dilated common bile duct; cholecystectomy should also be done later All patients with persistent symptoms and greater than 30% pancreatic necrosis, and those with smaller areas of necrosis and clinical suspicion of sepsis, should undergo image guided FNA to obtain material for culture 7–14 days after the onset of the pancreatitis Patients with infected necrosis will require intervention to completely debride all cavities containing necrotic material

Answer 19

Presenting symptoms of pancreatitis include epigastric or diffuse abdominal pain (80-95% of cases), nausea and vomiting (40-80% of cases), abdominal distension, fever, breathlessness, irritability, and impaired consciousness. This can be accompanied by more systemic signs such as pyrexia, low oxygen saturation, tachypnoea, tachycardia, hypotension, abdominal guarding, ileus and/or oliguria. However, it should be noted that often symptoms are vague (especially in younger children) and that pain radiating to the back (which is classically described in older patients) may not always be present causes align with those in adults ie GETSMASHED Serum amylase and/or lipase (NV usually <110 IU/L), triglyceride levels, full blood count, CRP, renal and liver function tests (e.g. ALT/AST, GGT, bilirubin, ALP), glucose, calcium and capillary blood gas should be obtained at presentation consider taking blood cultures if pyrexial and a full coagulation screen (e.g. PT, APTT, Fibrinogen) if there are concerns about DIC/SIRS Immunoglobulins, IgG subclasses (1-4) and autoantibodies (i.e. liver screen [e.g. anti-SMA, anti-LKM1, ANA, anti-mitochondrial] and diabetes screen [e.g. anti-GAD, antiIA2, anti-ZnT8]), especially if suggestive pancreatic imaging and/or past medical or family history of autoimmune disorders Transabdominal ultrasound (fasted) should be performed in all CYP with a clinical diagnosis of pancreatitis looking for evidence of pancreatic abnormalities (parenchymal and ductal) and local complications. * Chest x-ray if clinical concerns to identify any pleural effusion. * If the diagnosis remains uncertain or there is persistence/worsening of clinical and/or biochemical picture, then MRI/MRCP or CT are indicated There is no clear indication for axial imaging (CT/MRI) within the first week of presentation in uncomplicated cases. However, in patients with evidence of chronicity on initial US examination an MRCP would be beneficial within the first 6-8 weeks following presentation as an outpatient. * In contrast, if the child is pyrexial and jaundiced with bile duct dilatation on US, suggestive of cholangitis, early MRCP or endoscopic ultrasound (EUS), with a view or proceeding straight to ERCP, sphincterotomy and stone extraction should be considered. In these cases, early discussion with either a specialist paediatric centre (or local adult colleagues depending on the age/weight of the child) is strongly recommended Based on assessment of hydration status/hemodynamic status, if evidence of hemodynamic compromise, a bolus of 10 to 20 mL/kg is recommended. * Children with diagnosis of acute pancreatitis should be provided 1.5 to 2 times maintenance IV fluids with hourly monitoring of urine output over the initial 24-48 hours. Adjust fluid intake based on overall fluid balance. * Reduction of intravenous fluids and initiation of enteral feeds depending on tolerance and clinical status analgesia, starting with IV para + NSAID and escalate as needed +/- urgent pain team review if PCA needed following discussion with a specialist centre, especially in those with refractory pain, octreotide may be considered. * There is some evidence that octreotide may be useful in the treatment of pancreatic pseudocysts, a common complication of pancreatitis, although again specialist advice should be sought Discuss with a specialist centre about the indication for Endoscopic Ultrasound (EUS) if: the diagnosis is not clear and there is indication for tissue diagnosis (Fine Needle Biopsy) or there is pseudocyst formation that requires draining (cyst gastrostomy) Encouragement with oral intake within the first 24 hours is strongly advised once the patient has been safely fluid resuscitated. If oral intake is not tolerated in this time an alternative safe route of enteral feeding, (e.g. NG tube) should be considered within the first 48-72 hours of presentation unless direct contraindications to enteral feeding (including but not limited to ileus, pancreatic laceration/transection/fracture or duct disruption) In cases of worsening epigastric pain, high gastric aspirates, a significant spike in pancreatic amylase or lipase directly associated with feeding or vomiting with oral or nasogastric (NG) feeding, feeding via the jejunal route (NJ) feeding may be indicated. * Parenteral nutrition should be only considered in cases where enteral nutrition is not possible for a prolonged period (longer than 5–7 days) such as in ileus, complex fistulae, abdominal compartment syndrome

Answer 20

usually a whipple's pancreaticoduodenectomy (pancreas head, duodenum, cbd, gallbladder removed and anastomoses between jejunum and duct in tail of panc, cut hep duct and the first anastomosis, and between stomach and jej complications: suspect anastomotic leak in all patients who become unwell after a whipple: pain, tachy, fever, olig, resp rate inc (oft first sign); wound may discharge - send fluid for amylase measurement; abdo CT, drain, further laparot if needed delayed gastric emptying common after whipple, presents similar to gastric outflow obstruction (high volume vomiting every 1-2 days): NG drain, abdo CT to rule out obstruction, TPN or nasojejunal feeding, prokinetic agent like metoclop, takes several weeks to settle upper gi bleed from anasotomosis sites, or leak of bile into RUQ giving pain

Answer 21

often may be difficult to distinguish chronic panc from some of these, even after surgery rare tumours are neuroendocrine, producing some mix of glucagon, insulin, somatostatin, serotonin, gastrin, VIP, ACTH (cushings); can be associated with MEN insulinoma gives hypoglyc (weak, sweat, tremble, confusion, hemiplegia, seizures, coma) + hunger, abdo pain, diarrhoea; often present when pt hungry esp first thing in morning, and relieved by eating; gross weight gain common w/excessive appetite, and commonly misdiagnosed as psyche problem; exercise can also induce symptoms gastrin producing ones trigger zollinger-ellison syndrome: excess production of gastric acid leading to diarrhoea, oesophagitis, very commonly peptic ulcer (present with bleeding or perf and multiple duodenal ulcers), malabsorption; gastromas can also be in duodenum or rarely in stomach; part of MEN 25% time, can be malig

Answer 22

60% in head, 25% body, 15% tail middle aged and elderly (50% cases in >75s) may get obstructive jaundice spread into duod giving obstruction or occult/gross upper GI bleed portal vein giving thromb or ascites and portal hypertension SMA giving thrombosis or h+ ivc giving bilat leg oedema Can spread via lymph, or via blood to liver and lungs; peritoneal seeding and ascites generally can occur painless progressive jaundice if tumour near CBD/ampulla; >50% pts have dull ache in epigastrium which may radiate to back; recent onset DM in elderly is suspicious; migrating thrombophlebitis; anorexia and weight loss; GB may be palpable via Courvoisier's law, hepatomeg oft, epigastric mass maybe CT to visualise tumour, endoscopic USS to give info about its relationship to SMA and portal vein plus local lymph nodes to define operability, needle aspiration; serum amylase rarely elevated; elevated levels of Ca 19.9 (but not specific) only 15% cases operable, with whipple; follow-up chemo; chemo and palliative operations for the rest

Answer 23

chronic: 80% due to alcohol abuse but also duct obstruction from strictures, metabolic disease eg hypercalcaemia or hypertriglyceridaemia, mutations in CFTR or spink1, autoimmune pain: epigastric, radiating to back often (10-15% patients have no pain) malabsorption: rec inflam gives gland destruction until exocrine insufficiency; carbs/proteins/fats not absorbed properly, weight loss and steatorrhoea diabetes: linked to above but endocrine insufficiency, may see polyuria, polydipsia, malaise blood tests after convalescent phase (so acute attack doesnt alter blood results) look for high TGs and Ca as well as LFTs for biliary obstruction; fasting glucose can be tested, and faecal elastase to test exocrine function US (exclude a biliary disease cause), CT to assess calcification; MRCP to investigate parenchyma and ducts; ERCP if cholelithiasis not ruled out

Answer 24

usually adenocarcinoma, 2x more common in men, mean age 55 CT or MRCP preferred scan, ERCP if obstructive jaundice; fine needle aspiration under CT or endoscopic US guidance <6% survival, presents late and extensive lymphatic drainage so hard to completely resect; chemo and radiotherapy palliation

Answer 25

associated with pancreatitis, more oft chronic than acute but can be either may be asymp, but as get larger cause pain, dyspepsia, nausea and vomiting, bloating, weight loss may become infected, block part of the SI, or rupture; rarely can cause jaundice or sepsis abdo trauma or neoplasm may also sometimes cause these CT for initial assessment and follow up endoscopic USS guided drainage or transpap drainage if in panc head, for any symptomatic or non-symp but pressure on great vessels, risk of infection or rupture if EUS unsuitable or fails then laparoscopic or open drainage can be performed

Answer 26

one fifth to one third is supplied by the hepatic artery; two thirds of the hepatic blood supply is portal venous blood; liver receives 25% of CO in total hepatic arterial resistance is proportional to portal venous blood flow, such that a reduction in portal venous flow causes a decrease in hepatic arterial resistance and increases hepatic arterial flow This is probably mediated by adenosine; symp innervation of hep artery and PVT, with alpha action on PVT helping to mobilise blood; VIP, glucagon, secretin help to inc blood flow; sinusoids are low pressure, low flow to maximise time for metabolism and prevent backflow into PVT high pressure, well-oxygenated arterial blood mixes completely with the low-pressure, less well-oxygenated, but nutrient-rich, portal venous blood within the hepatic sinusoids (capillaries); the sinusoids then lead to the liver lobules liver lobules are roughly hexagonal, and consist of plates of hepatocytes, and sinusoids radiating from a central vein towards an imaginary perimeter of interlobular portal triads consisting of branches of hep art, portal vein, and common bile duct; bile canaliculi run between hepatocytes back to merge into bile ducts at the perimeter; Hepatocytes possess a toolbox of genes which encode enzymes that can modify a huge range of different types of compounds (for example, the cytochrome p450 family of enzymes), and they perform metabolic functions while blood passes between them; because the characteristics of the blood and the liver environment (ie, amount of bile or oxygenation) change as it passes from the portal to the central vein, the liver cells at different places on the journey perform different metabolic tasks. This is a property called zonation. For example, because oxygen is more freely available near the portal veins (because there is also a branch of the hepatic artery here), metabolic tasks requiring oxygen are carried out here (such as oxidizing fats) perisinusoidal space (or space of Disse) is a location in the liver between a hepatocyte and the sinusoid endothelium; Microvilli of hepatocytes extend into this space, allowing proteins and other plasma components from the sinusoids to be absorbed by the hepatocytes. Fenestration and discontinuity of the endothelium facilitates this transport; perisinusoidal space also contains hepatic stellate cells (also known as Ito cells), which store fat or fat soluble vitamins including vitamin A). A variety of insults that cause inflammation can result in the cells transforming into myofibroblasts, resulting in collagen production, fibrosis, and cirrhosis Kupffer cells are liver-specific macrophages that reside in the sinusoidal lumen where they are exposed to the systemic circulation via the hepatic artery and to the splanchnic circulation via the portal vein. straddle inside the sinusoidal space like a spider in ambush for particulate substances passing through the hepatic circulation. Kupffer cells account for approximately 15% of the liver cell population; clear circulating endotoxin from the blood and secrete cytokines, prostanoids etc into the blood

Answer 27

Bile flows out of the liver through the left and right hepatic ducts, which come together to form the common hepatic duct. This duct then joins with a duct connected to the gallbladder, called the cystic duct, to form the common bile duct. The common bile duct enters the small intestine at the sphincter of Oddi (a ring-shaped muscle), located a few inches below the stomach. About half the bile secreted between meals flows directly through the common bile duct into the small intestine. The rest of the bile is diverted through the cystic duct into the gallbladder to be stored. In the gallbladder, up to 90% of the water in bile is absorbed into the bloodstream, making the remaining bile very concentrated. When food enters the small intestine, a series of hormonal and nerve signals triggers the gallbladder to contract and the sphincter of Oddi to relax and open. Bile then flows from the gallbladder into the small intestine to mix with food contents and perform its digestive functions. After bile enters and passes down the small intestine, about 90% of bile salts are reabsorbed into the bloodstream through the wall of the lower small intestine. The liver extracts these bile salts from the blood and resecretes them back into the bile. Bile salts go through this cycle about 10 to 12 times a day. Each time, small amounts of bile salts escape absorption and reach the large intestine, where they are broken down by bacteria. Some bile salts are reabsorbed in the large intestine. The rest are excreted in the stool. thus you can also see that the gallbladder, though useful, is not necessary

Answer 28

a cause of chronic diarrhoea. This may be primary, due to excessive production of bile acid, or secondary to an underlying gastrointestinal disorder causing reduced bile acid absorption. It can lead to steatorrhoea and vitamin A, D, E, K malabsorption. Secondary causes are often seen in patients with ileal disease, such as with Crohn's. Other secondary causes include: cholecystectomy coeliac disease small intestinal bacterial overgrowth Investigation the test of choice is SeHCAT nuclear medicine test using a gamma-emitting selenium molecule in selenium homocholic acid taurine or tauroselcholic acid (SeHCAT) 2 scans are done 7 days apart to assess the retention/loss of radiolabelled 75SeHCAT; >15% retention normal, less suggests excessive loss Management bile acid sequestrants e.g. cholestyramine

Answer 29

bilirubin - normal adult makes 450 micromol/day; serum conc up when biliary track blocked; usually <21micromol/L and when >~35 get jaundice aminotransferase activity is sensitive but non-specific indicator of acute hepatocyte damage (infection, toxicity/overdose, cardiac failure/shock) - AST/ALT alkaline phosphatase activity up indicates cholestasis (>2x the normal upper limit of activity range), as well as indicating infiltrating lesions eg tumours, and in cirrhosis - note though that if cause such as above not indicated by other stuff too, alkaline phosphatase activity is found in other structures like the bone so cant just use this gamma-GT activity raised with cholestasis, alcohol, phenytoin, and also parallel the changes in aminotransferases; note GGT is not always raised in congen cholestasis due to bili metab defect hypoalbuminaemia suggests advanced chronic liver disease or notably severe acute liver disease AFP conc increased in 80-90% hepatocellular carcinoma cases, prothrombin has v short half life, so prothrombin time increase may be earliest indicator of reduced hepatic synthesis and is preferred to albumin usually AST:ALT scores >2 are, therefore, strongly suggestive of alcoholic liver disease and scores <1 more suggestive of NAFLD/NASH

Answer 30

4 isoenzymes: intestinal, placental, germ cell, and tissue non-specific (liver/bone/kidney) bone normally contributes half normal level, and esp when bone being laid down eg children (esp growth spurt), pagets, hyperparathyroid, fracture, bone mets; other reasons to be raised inc CKD, IBD, coeliac, rickets, liver disease, pregnancy (can be 3x normal upper limit) low if postmenopause on oestrogen, hypophos or hypomag, hypothyroid, achondroplasia, after severe enteritis in children, if taking OCP, if malnourished deficiency of TNSALP gives IEM hypophosphatasia (rickets or osteomalacia, seizures) you can test for specific ALP subtypes

Answer 31

R value is a proposed score aimed to aid physicians in determining the pattern of liver injury based on the upper limit of normal (ULN) of certain enzymes. R value = (ALT ÷ ULN ALT)/(ALP ÷ ULN ALP). R value > 5 is suggestive of hepatocellular pattern, > 2 to < 5 is suggestive of a mixed pattern, and < 2 suggestive of cholestatic pattern with HC pattern causes: ALT-predominant: Acute or chronic viral hepatitis, steatohepatitis, acute Budd-Chiari syndrome, ischemic hepatitis (aka shocked liver), hemochromatosis, medications/toxins, autoimmune, alpha1-antitrypsin deficiency, Wilson disease, Celiac disease AST-predominant: Alcohol-related, steatohepatitis, cirrhosis with cholestatic pattern: Bile duct obstruction, primary biliary cirrhosis, primary sclerosing cholangitis, medication-induced, infiltrating diseases of the liver, cystic fibrosis, hepatic metastasis; also consider bone and renal causes, infection/inflam, lymphoma

Answer 32

Alcohol is thought to cause injury to the mitochondria which contains AST but not ALT (both present in cytoplasm). In addition, in chronic alcoholics, pyridoxine (vitamin B6) deficiency may reduce the synthesis of ALT more than AST because the former is more B6-dependent however also note that the raised AST:ALT ratio is generally only once disease is advanced, and in early stages you might not see this even if pt is drinking very large amount of alcohol

Answer 33

post-mature erythrocytes -> removed by reticuloendothelial system w globin broken down to aa and iron reutilised to make haem -> biliverdin (water soluble) -> biliverdin reductase converts it to unconj bilirubin (water insoluble) -> bound to albumin and taken to liver binding affinity for albumin to bilirubin is extremely high, and under ideal conditions, no free (non-albumin bound) unconjugated bilirubin is seen in the plasma taken up by hepatocytes and in smooth ER UDP glucuronyl transferase conjugates with 2x glucuronic acid to make it water soluble conj bili then active transport into bile canaliculi thence to intestine where in terminal ileum /colon hydrolysed by bacti to release free bilirubin which is reduced to urobilinogen which has 3 fates most oxidised to stercobilin (faecal pigment), some absorbed by terminal ileum then back to liver by enterohepatic circulation, and some reabsorbed into blood and excreted by kidney

Answer 34

as water insoluble no bilirubin in urine, but inc'd urobilinogen in urine can be inc'd production: haemolysis, sepsis, haematoma, polycythaemia decreased bili uptake or metab: gilbert syndrome, crigler-najjar, lucey-driscoll, hypothyroidism, sepsis/acidosis/hypoxia, heart failure, physiological jaundice altered enterohep circulation - breast milk jaundice, intestinal obstruction, abx

Answer 35

intrahep causes mainly mixed picture, extrahep mainly conj picture conj bilirubin is water soluble and so found in urine, so dark urine and pale stools + pruritus neonatal hepatitis (rubella, CMV, toxoplasmosis, A1AT def, CF, metabolic disorders inc wilsons, gaucher etc), idiopathic giant cell hepatitis abnormal bilirubin excretion by hepatocyte: dubin-johnson, rotor syndrome; note GGT is not always raised in these cholestatic conditions (and ALP may also be normal) non-neonatal hep (A B C, ECHO, CMV, EBV, leptospirosis; chemical and drug induced, autoimmune) intrahep cholestasis (various congen syndromes) and extrahep (biliary atresia, choledochal cyst, mass/neoplasia, stone, high intestine obstruction)

Answer 36

prehep: inc production of bilirubin due to eg RBC haemolysis exceeds livers ability to conjugate, unconj up in blood; other cause may be reabsorption of large haematoma hep: from hepatocyte damage, unconj and conj build up in blood; hepatitis, EBV, cholestasis from drugs (flucloxacillin, chlorpromazine), toxicity eg paracetamol, tumours, sepsis, cirrhosis posthep/obstructive: stools pale, conj in blood excreted in urine turning it dark (may see in hep type too); hep and posthep can coexist if eg stone in CBD, as both outflow obstruct and biliary cirrhosis; tumour deposits in liver or cirrhosis may also both cause both as damage liver tissue and compress intrahep duct posthep causes: cholelithiasis, CBD atresia or traumatic stricture, sclerosing cholangitis, tumour of CBD, tumour of head of pancreas, tumour of ampulla of Vater, pancreatitis, liver hilar lymphadenopathy painless jaundice of sudden onset with tenderness in younger person usually viral; severe colic + intermit jaundice suggests stone important: in all cases after bloods etc USS needed to see if ducts dilated before moving on to other scans and management

Answer 37

urine: prehep/hep urobilinogen, post hep bilirubin serum bilirubin: prehep unconj, posthep conj, hep mixed ALT/AST: prehep normal, hep raised, posthep normal/raised a bit ALP: prehep normal, hep normal/raised a bit, posthep raised (but ALP may also be raised if concurrent bone disease inc eg bone mets) blood glucose: prehep normal, hep normal or low if liver failure, posthep normal or high if panc tumour prothrombin time: prehep normal, hep prolonged due to poor synthetic functino, posthep prolonged due to poor vit K absorption USS: prehep normal, hep may have abnormal liver texture, posthep dilated bile ducts inc accurate at spotting stones haemat investigation for haemolysis: coomb's test, raised reticulocyte count CT/MRI can then spot hep lesions for biopsy, or panc lesions; in posthep MRCP/ERCP can be handy

Answer 38

bacterial infection of an obstruction within biliary tract (partial obstruction higher risk than complete) charcot's triad: fever, jaundice, RUQ pain (may be absent in elderly); severe cases may also have confusion and hypotension (reynolds pentad) FBC, LFTs; ALT and AST may be elevated in early stage before bile duct dilated on US, so may be mistaken for viral hep transabdo US has v high specificity but poor sensitivity for gallstones MRCP and endoscopic ultrasonography are more sensitive ERCP is gold standard and can procede to therapeutic stone removal etc, but is invasive 80-90% patients respond well to broad spectrum antibiotics

Answer 39

chemical or bacti inflam of gallbladder following gallstones (calculous cholecystitis) but 5% dont (acalculous) unremitting RUQ pain, anorexia, nausea/vomiting, fever in severe acute cases get necrosis of the gallbladder complications: perforation, pericholecystic abscess, fistulae cholecystectomy to treat; antibiotics, low fat diet, and observation can be used in patients where surgery would be risky (eg a comorbidity)

Answer 40

usually young men (40yo), linked to IBD; chronic progressive with inflam and stricture formation of intra/extrahepatic bile ducts jaundice, steatorrhoea, pruritus, weight loss, reduced Ca and fat soluble vitamin absorption; though many patients no symptoms or just vague ruq discomfort conjugated bilirubin and GGT up, ALP often 3x normal, xanthomas may be present liver transplant only treatment to extend life

Answer 41

autoimmune attack on epithelial cells lining intrahepatic bile duct; 10x more women than men, from late teens on but usually ages 30-65 fatigue, pruritus, hyperpigmentation, xanthelasmas, splenomegaly; may have other autoimmune diseases liver transplant again only life extending treatment

Answer 42

UDCA is commonly used to treat patients with primary biliary cholangitis and may have a role in PSC has also found use in the treatment of cystic fibrosis, graft vs. host disease involving the liver, liver allograft rejection, bile duct-paucity syndromes such as biliary atresia, and non-alcoholic steatohepatitis bile acids damage cells by causing mitochondrial dysfunction. UDCA offers cytoprotection in hepatic epithelia by preserving cell structures, including plasma membranes and mitochondria while stimulating anti-apoptotic pathways. Additionally, UDCA can prevent Kupffer cells, the resident macrophages in the liver, from generating reactive oxygen species UDCA competitively displaces the endogenous bile acids at the level of ileal absorption or the hepatocyte level, thus decreasing the concentration of toxic hydrophobic bile acids UDCA induces vesicular exocytosis in cholestatic hepatocytes by indirectly increasing intracellular calcium levels leading to increased secretion of bile acids DCA has been shown to reduce the expression of class I MHC antigens in several cholestatic liver disorders

Answer 43

abdo pain, palpable mass, hepatomegaly, weight loss; progressive obstructive jaundice; advanced disease may have cholangitis or acute cholecystitis, or anaemia from blood loss ultrasonography first line investigation; abdo CT if mass like tumor, MRCP or ERCP if stricture causing tumour complete surgical resection only chance of cure but stent, chemo etc for palliation

Answer 44

either toxins, ischaemia, sepsis, or viruses - and of toxins, v oft paracetamol hyperacute: 0-7 days, severe encephalopathy coagulopathy, and raised intracranial pressure; LFTs oft very deranged; best recovery chance acute: 7-28 days subacute: 28 days +, gradual, worst outcome right heart failure, budd chiari, hepatic ischaemia (global or embolic), viral hep, EBV, CMV, HSV, VZV, HCC/mets/lymphoma, paracetamol, alcohol, TB meds, amanita mushroom, drugs of abuse, reye's syndrome, reaction to NSAIDs or anticonvulsants, wilson's, haemophagocytic syndrome, vasculitis, crush injury, hyperthermic injury, acute fatty liver of pregnancy, HELLP ix: LFTs, FBC (eosins for drug reaction or autoimmune), paracetamol level, LDH, CK, anti HAV and HAV IgM, HBV core IgM (and other ix), coags, caeruloplasmin, urinary copper; EBV, CMV, HSV, VZV serology if immunocomp, dengue and yellow fever serology, anti SM ab/ANA/anti-mi ab + serum Ig (and in kids also anti liver-kidney-microsomal ab and coeliac screen) echo, liver uss, CT abdo with contrats

Answer 45

damage allows shunt of 'dirty' portal blood into systemic circulation, exposing bowel bacti endotoxin to iNOS + cytokines and vasoactive GIT hormones wash through all leading to hyperdynamic circulation (+ failing liver not removing as much); SIRS or sepsis often also develops ARDS will dev as part of SIRS, however due to ammonia causing raised ICP you can't do permissive hypercapnoea; ascites may impair ventilation, and get portopulmonary shunt and hepatopulmonary syndrome hepatic enceph: short attention span, tremor, then incoordination, lethargy, disorientation, then somnolence, asterixis, ataxia, coma; ICP monitoring if young, confused or worse on above scale, serum ammonia >150 hypercatabolic state will inc daily caloric requirements; hypoglyc common as less glycogen storage or release and elss gluconeogenesis lactate will be raised as broken down in liver normally; higher levels suggest worst failure, may take a while to come down even after shock resolved relative adrenal deficiency, may need hydrocort; HRS may dev but not all AKI will be this -> CRRT may be needed raised INR in acute liver failure may overestimate bleeding risk as protein C/S also not made bone marrow suppressed in 10% of ppl by cytokines, can range from mild too full aplastic anaemia; have dec'd complement so impaired opsonisation and phagocytosis, also have worse chemotaxis and neut function note that liver cells store large amounts of B12, so damage to them (cirrhosis, carincoma/mets, PVT. liver abscess etc) causes high serum b12 level -> so if level high and not on replacement this is a sign of badness

Answer 46

urea cycle broken -> ammonia up astrocytes combine it with glutamate to make glutamine but end up making massive amounts and swelling, giving cerebral oedema; also inc's distance between neurons and caps giving nutrient diffusion defect excess glutamine also made in BBB which inc's transport of aas that exchange with glutamine to cross and impairs transfer of others, meaning less 5HT and DA made, and the excess wrong aa are made into unusual NTs like insect norad equiv, and these derange synaptic transmission ammonia inhibs a-ketoglut dehydrogenase so stops TCA, and inhibs PDH; thus brain produces more lactate alcoholics often don't dev raised ICP as brain atrophied and due to chronic adaptation; however in certain conditions ICP is monitored stroke, sepsis/CNS infection, CNS neoplasm, drugs (eg benzos for withdrawal regime), trauma eg SDH, hypoglyc, hyponat, UGIB, seizures/NCSE, alcohol toxicity high calory diet, high protein intake (to stop catabolism of body protein), give branched chain aa as can enter TCA at later stage than alpha ketoglu dehydro ammonia may be normal, as other neurotoxins also involved in HE eg manganese, short chain fatty acids EEG can show high-amplitude low-frequency waves and triphasic waves but not specific, is still useful to exclude other things like NCSE

Answer 47

identify and remove causes eg NAC for paracet, l-carnitine for valproate etc if HE: intubate and ventilate, keeping paCO2 low/normal, norad, propofol to sedate; consider ICP monitoring and get hypernat 145-155, consider therapeutic hypothermia, continuous haemodiafiltration to remove ammonia dextrose infusion + crystalloid (careful not to fluid overload), PPIs to avoid bleed, drain ascites, vit K 10mg, daily blood cultures to watch for sepsis, give phosphate (new liver cells will hoover up and needed for ATP synthesis); NAC has been shown in newer trials to likely benefit even non-paracetamol acute liver failure, but can get advice on this MELD score to decide if to do transplant (+ king's college score); absolute contras are sepsis, malignancy, severe cardioresp disease, ongoing alcohol or IVDU, AIDS, likely poor compliance; liaise with transplant centre early

Answer 48

antibiotic-induced hepatotoxicity can often be detected early from elevations in ALT to >2x upper limit of normal adverse effects may develop almost immediately, late in the course of prolonged antibiotic treatment or several months after the cessation of therapy co-amox: cholestatic or mixed ceftriaxone: biliary sludge as precipitates with Ca, normally asymp but occasionaly can course cholelithiasis type sx w/o LFT derangement, v rarely can dev cholestatic jaundice co-trimox, macrolides are intermediate risk TB drugs also high risk, and nitrofurantoin, fluclox, interferons and nevirapine need to work-up inc abdo US, and basic liver blood screen; if suspect then stop the drug and rpt LFTs, they should improve; if they dont then consider biopsy if bloods might also support an autoimmune hep diagnosis, or if fails to regress or even worsens after abx stopped Liver injury caused by unintentional rechallenge in clinical practice can confer a higher risk of mortality/liver transplantation and so shouldnt be done deliberately

Answer 49

transudates: hydrostatic (portal hypertension), oncotic (hypoalbuminaemia), fluid retention (portal hypertension leads to renal hypoperfusion, renin release, secondary hyperaldosteronism, salt and water retention) exudates: inflam or malignancy of peritoneal surface (inc panc, bowel obstruction) calculate serum albumin conc - ascites albumin conc; if >11g/L then portal hypertension is the cause treat underlying condition low Na diet (or fluid restriction) spironolactone if tense ascites: paracentesis with 10g albumin given for each litre of fluid removed to minimise fluid shifts and subsequent haemodynamic consequences ciprofloxacin if cirrhosis + ascites and ascitic protein 15g/L or less

Answer 50

SAAG > 11g/L (indicates portal hypertension) prophylactic oral ciprofloxacin if cirrhosis and ascites, total protein<15 autoimmune hep has ANA and anti smooth muscle antibodies, may present acutely but usually chronic ferritin + transferrin sat up suggest iron overload (HH or multiple transfusions) hepatic encephalopathy: lactulose first-line, with the addition of rifaximin (promote excretion/gut bacti metabolism of ammonia) in NAFLD: enhanced liver fibrosis (ELF) blood test to check for advanced fibrosis, then refer for biopsy

Answer 51

leave on free drainage for 4-6 hours patients should be administered 100ml of human albumin solution 20% (HAS) for every 2-3 litres of ascitic fluid drained generally remove when stops draining or after 4-6 hours (to reduce risk of SBP) some patients with malignant ascites get radiologically-guided drains that can stay in so that they can drain some fluid off each day removal: if straight/normal then pull out, if pigtail cut the string then pull out after removal apply dressing and keep it dry for 48hrs; if draining a lot may need to place stoma bag over hole for over days to weeks For persistent leak following drain removal, consider placing a suture (ask gastro)

Answer 52

besides portal hypertension from compression by scarred tissue or general venous congestion, liver function may be down (hypoalbuminaemia); also cirrhosis causes splanchnic vasodilation as vasodilators (nitric oxide) accumulate in the splanchnic circulation when liver fails; systemic hypotension and renal hypoperfusion thus renin-ang activation, aldosterone release giving salt and water retention; sometimes this exacerbates as renal vasocons cant compensate so renin-ang system stays activated, inc'g renal vasocontriction until AKI; hepatorenal syndrome is result as renal hypoperfusion continues, this has high mortality via AKI diagnosed if liver disease, AKI, not responding to fluids, not shocked, no nephrotoxics or abnormal renal USS - essentially diagnosis of exclusion; this also means must fail to respond to standard care and volume expansion for 48h in order to diagnose; how to differentiate it from ATN: use fractional excretion of sodium and urinary microscopy usually HRS is due to acute decompensation of cirrhosis due to infection eg spont bacti peritonitis, GI bleed, alcohol intake - type 1, cr doubles in 2 weeks a slower form with diuretic resistant ascites (as kidney function unable to excrete enough sodium to clear the fluid, this slower kind of HRS may be the end stage of ascites can also occur due to acute liver failure mx: HAS + terlipressin, can consider octreotide; definitive mx is transplant; can do TIPS but oft has poor outcome

Answer 53

For PVT "nothing" or "vague unwellness" may actually be the only clinical findings, but more generally people will present either with features of portal venous hypertension (such as ascites) or with abdominal pain. May see variceal bleeding, haemorrhoids, worsening features of portal hypertension; may get venous infarct of liver or spleen contrast CT abdo will show PVT inflam near vessel: pancreatitis, cholecystitis, inflamed bowel inc diverticula, TB lymphadenitis, duodenal ulcer, neonatal omphalitis injury to portal system from any abdo surgery any abdo malig cirrhosis or retroperitoneal fibrosis/mass giving venous stasis congen or acquired prothromb states 90% will recanalise with time, and bear in mind bleeding risks in these pt; however if no varices and pro-thromb state then can do rx dose LMWH or warfarin; BB, spiro, TIPS are options budd chiari: abdominal pain, ascites, and liver enlargement; may dev liver failure hypercoag esp polycythemia, pregnancy, post partum, OCP, congen, then others; secondary due to compression by eg tumour CT abdo with contrast, give hep/warf

Answer 54

Chronic EtOH NAFLD/NASH Chronic HCV (and HBV) Rare: Genetic: Wilson's, α1ATD, HH, CF Auto Immune: AH, PBC, PSC Drugs: Methotrexate, amiodarone etoh/nafld -> fatty liver disease; first Steatosis: Fat deposition in hepatocytes, Nuclei displaced then Steatohepatitis: Neutrophil infiltrates Hepatocyte swelling/necrosis Mallory-Denk bodies; finally cirrhosis

Answer 55

cirrhosis consequences: Breakdown Bilirubin → Jaundice Ammonia → Encephalopathy Synthesis Carbohydrate metabolism → Hypoglycaemia Protein synthesis → Hypoalbuminaemia → oedema Clotting factors → coagulopathy: PT affected more Acute phase and other immune proteins -> immunodef Storage Iron → anaemia (small bleeds, hypersplenism from port hyp) PVP up, and HCC risk; former: varicosities, organomegaly, ascites, hepatorenal syndrome also hyperdynamic circuation (spider naevi, tachy, palmar erythema), na/fluid retention through hyperaldos investigate with LFTs, Hepatitis serology and viral screen Ferritin and iron studies Alpha 1 antitrypsin Autoantibodies (PBC, PSC, autoimmune hep) AFP Serum copper and caeruloplasmin conjugated hyperbili: BR made it to liver but not into bile due to cholestasis, hepatocellular damage, disorders of secretion unconj hyperbili: BR isnt reaching liver or is but not then conj eg haemolysis or impaired conj eg gilberts syndrome ALT and AST are aminotransferases in many hepatocytes, some released all the time but more upon cell injury/death; thus highest levels in severe acute, then mild acute; in chronic conditions inc eg mild chronic HCV or cirrhosis there is little ongoing injury and so the levels are lower

Answer 56

to be done if jaundice of hepatic origin; hepatitis screen, autoantibody profile (high levels IgM suggest PBC, high levels of IgG poss autoimmune hep), ferritin and transferrin saturation (haemochromatosis), alpha1 antitrypsin (def results in emphysema and/or chronic liver disease inc cirrhosis and failure), afp (raised in HCC often), caeruloplasmin, TFTs

Answer 57

childs-pugh uses bili, albumin, INR, ascites, encephalopathy; somewhat subjective, but predicts mortality well; should be done on admission; class A is well compensated, class B is compromised and class C is worst MELD developed as more objective (weighted function of cr, INR, bili), used for transplant listing and eg TIPS procedures; it and child's pugh have different strengths

Answer 58

at risk: T2DM/metabolic syndrome in children do USS if above and no alcohol use, if normal keep repeating every 3 years; generally is suggested by deranged LFTs with suggestive US or negative liver screen for adults, calculate NAFLD/FIB4 score and based on result can either be managed in primary care (Q risk and lifestyle factors), get ELF test, or straight referral to hepatology - or can go straight to ELF test ELF every 3 years (2 if kids) for fibrosis; patients with NAFLD and suspicion for advanced fibrosis should have a liver biopsy to confirm findings lose weight, exercise; adults can try pioglitazone or vit E (not if heart failure, previous or active bladder cancer, haematuria), kids could also try vit E -refer to paeds hepatology, liraglutide may also be used

Answer 59

wilsons: Clinical features – CLANK Cornea – Kayser-Fleischer rings Liver – acute failure or eventual cirrhosis Arthritis Neurology – Ataxia, parkinsonism, psychosis Kidney – Fanconi’s syndrome (prox tubule affected, giving type 2 RTA, ricketts/osteomalacia (due to loss of phosphate not vit d/ca problems), glycosuria (so polyur/dip/dehydration) Ix: Serum/urine copper (serum low as caeruloplasmin would carry most, urine high over 24 hr collection) and caeruloplasmin (low, unless active inflam as is acute phase protein) Once suspected, liver biopsy +/- genetic testing to confirm Mx: Penicillamine lifelong (30% pts need to stop due to reaction inc skin, renal, lupus like), other binders and zn salts available + low copper diet advised for all; family screening will be performed; will need referral to paediatric hepatology Copper enters the body through the digestive tract. A transporter protein on the cells of the small bowel, carries copper inside the cells and in response to rising concentrations of copper, an enzyme called ATP7A (Menkes' protein) releases copper into the portal vein to the liver. Here, ATP7B links copper to ceruloplasmin and releases it into the bloodstream, as well as removing excess copper by secreting it into bile - does neither of these functions in wilsons disease Copper accumulates in the liver tissue; ceruloplasmin is still secreted, but in a form that lacks copper that is rapidly degraded; When the amount of copper in the liver overwhelms the proteins that normally bind it, it causes oxidative damage to the liver giving hepatitis and cirrhosisliver also releases copper into the bloodstream that is not bound to ceruloplasmin. This free copper precipitates throughout the body, but particularly in the kidneys, eyes, and brain. In the brain, most copper is deposited in the basal ganglia, particularly in the putamen and globus pallidus and damage here gives neuropsych sx haemochromatosis: MEALS Myocardial: dilated cardiomyopathy Endocrine: hypopituitarism (hypogonadism - ED, amenorrhoea), hypoparathyroid, hypopancreas (T2DM due to poor insulin secretion and insulin resistance related to liver disease) Arthritis: MCP joints, knees, shoulder Liver: Cirrhosis Skin: Bronze/ Slate Grey colour ED Ix: Ferritin and iron studies Mx: Venesection: 2 weekly initially (depletion) → 6 weekly (maintenance)

Answer 60

wilsons, nephrotic syndrome, malabsorp/nutrit, protein losing enteropathy

Answer 61

adults get early emphysema, infants neonatal cholestasis + cirrhosis A1AT is acute phase protein and so levels may be normal if inflam going on for whatever reason, so also do protease inhibitor typing types are ZZ, MZ, MM with co-dominant inheritance so ZZ have, MZ may or may not, MM don't treatment is liver transplant which converts recipient to protease inhibitor type of the donor

Answer 62

hepatic steatosis: echogenicity up on USS so walls of hept and portal veins cant be seen, looks more echogenic comp to kidneys/spleen; liver attenuation down in CT so look darker than spleen on unenhanced CT; MRI diagnostic with in phase and out of phase imaging, parenchymal signal reduction on out phase as water and fat signal cancel cirrhosis: ascites, nodular margin, heterogeneous texture visible on USS, and fat suppressed in T2 weighted image; but generally imaging insensitive for fibrosis in early stages; possible solution: MR elastography- but biopsy ultimately used

Answer 63

Flu-like prodrome RUQ pain Fever Jaundice (mixed) Deranged LFTs: >20x normal in acute disease, AST

Answer 64

chronic liver disease = any dysfunction lasting >6mo; acute decomp may present with any of jaundice, ascites, encephalopathy, AKI, GI bleed, sepsis/hypovol sepsis, sbp, HBV/HCV reactivation, alcohol, drug toxicity, GI bleed, portal thrombosis, ischaemic insult (eg shock), surgery, autoimmune, dehydration, constipation, HCC FBC, CRP, U&Es, LFTs, glucose, coags, bone profile, Mg, AFP, blood cultures, urine dip + MC&S, CXR, USS abdo ascitic tap if any ascites present for culture, WCC, albumin - needs to be done before abx, within a few hours of starting abx culture may not grow anything and you've lost the chance to diagnose it; neut count raised but not massive, if very high consider perf record recent daily alcohol can get ammonia but not useful as not always raised in hepatic enceph - may be good if pt sedated/no other way to tell has encephalopathy if >8 units a day alcohol (M) or 6 (F) or unclear then 2 vials pabrinex TDS, CIWA scoring, consider reducing chlordiazepoxide if suspect sepsis start abx, if ascitic PMNs >250/mm^3 then abx and IV 20% HAS if AKI then hold nephrotoxics, 250ml boluses saline or HAS 5% up to 1-2L, fluid balance chart + daily weights, aim for UO >0.5ml/kg.hr and if not reached by 6 hrs escalate to ITU GI bleeding mx as for varices, and if PT prolonged give IV vit K 10mg stat; if INR >2 or PT >20 give 2-4 units FFP if encephalopathy then lactulose, can request CTH to exclude SDH LMWH prophylaxis unless plats <50 or actively bleeding, and needs GI/liver r/v, even if INR raised as still pro-thrombotic state until INR gets up to somewhere between 2.1-2.5 (only way to tell when the balance has been crossed is to do TEG, and when more likely to bleed is when LMWH should be stopped) liaise with transplant team and consider early transfer based on king's criteria: INR >6.5 or 3 out of: <11yo or >40yo, serum bili >300, time between jaundice onset and coma >7d, INR >3.5, drug toxicity; in paracetamol overdose it's pH <7.3 + enceph, cr >300, INR >6.5 - >90% of cirrhotic patients are sarcopenic, which is an independent predictor of mortality - need 1.5g/kg of protein per day and 30kcal/kg per day - NG feed if not meeting within 48h

Answer 65

Platelet counts are often low in cirrhosis due to portal hypertension and "pooling" in the spleen, and PT/INR tends to be raised patients with liver disease are at a high risk of thromboembolism even with a prolonged prothrombin time - only withhold VTE proph if actively bleeding or plats <50 (or if INR >2.5, discuss with seniors/haem) generally can use LMWH omit dose day before procedures: ERCP, TIPSS, biopsy etc As long as there is no sign of post-procedure bleeding, VTE prophylaxis can commence 24 hours after the procedure if the patient remains in hospital pre-procedure you can generally continue aspirin, and can continue DAPT for simple procedures (OGD, EUS, biliary stents) - for more complex (FNA, oesoph stent, ERCP, PEG, varices therapy), stop the second antiplat if IHD with no stent, PVD, CVA 5 days before procedure, liaise with cardio if IHD with stents but generally only stop the second agent if >1mo since metal stent or >12mo since drug eluting stent inserted low risk procedures continue warfarin, omit DOAC morning of; for high risk omit DOACs for 48hrs before, stop warf 5 days before and ensure INR <1.5 (restart evening of procedure day)(if prosthetic mitral valve or any prosthetic valve and AF then bridge with LMWH until 24hrs pre-procedure)

Answer 66

at risk: anorexia nervosa, chronic alcoholism, malignancy, HHS, HIV/AIDS, chronic panc, bariatric surgery, elderly/frail, hyperemesis gravidarum - in short, anyone who is chronically malnourished for any reason (inc homeless etc) criteria: one of BMI <16, unintentional weight loss >15% in past 3-6mo, minimal nutrient intake in past 10 days, refeeding picture in bloods; or two of BMI <18.5, unintent weight loss >10% in past 3-6mo, minimal nut intake for past >5days, history of drug or alcohol abuse With the restoration of glucose as a substrate, insulin levels rise and cause cellular uptake of these ions. Depletion of adenosine triphosphate (ATP) and 2,3-diphosphoglyceric acid (2,3-DPG) results in tissue hypoxia and failure of cellular energy metabolism. This may manifest as cardiac and respiratory failure, with paraesthesiae and seizures; thiamine deficiency also contributes phosphate stores are depleted during starvation while serum levels initially maintained, so vulnerable to fall with inc'd insulin that other pt groups aren't to prevent: slow refeed (10kcal/kg/d then build up 10% each day), pabrinex and vitamin B co-strong + multivit, daily refeeding bloods and replace electrolytes as required, dietician r/v

Answer 67

contain thiamine, riboflavin, pyridoxine, and nicotinamide people at high risk of developing refeeding syndrome should be prescribed the following vitamins for the first 10 days of feeding. They should be prescribed oral thiamine 200mg to 300 mg daily, vitamin B compound strong 1 or 2 tablets, three times daily or a full dose daily intravenous vitamin B preparation, if necessary, and a balanced multivitamin and trace element supplement once daily. not much thiamine stored in body, can be depleted in 2-3 weeks, so anyone at risk of refeeding should be on prophylaxis of 100mg a day; also note if any hints of WE (inc alcohol detox delirium as you can't fully tell the difference) will need pabrinex; pabrinex can be given IM if pt non-cooperative Vitamin B compound strong may be prescribed if there is a medically diagnosed deficiency, chronic malabsorption, or following surgery that results in malabsorption. This should be prescribed only under the advice of a specialist clinician or dietitian. Please note that neither vitamin B compound nor vitamin B compound strong contain vitamin B12 so they should not be prescribed for vitamin B12 deficiency doesn't have enough thiamine for prophylaxis of WE, so offer prophylactic oral thiamine at a dose of 200mg to 300mg per day in divided doses, to harmful or dependent drinkers: * if they are malnourished or at risk of malnutrition * if they have decompensated liver disease * if they are in acute withdrawal * before and during a planned medically assisted alcohol withdrawal (note, reason why such high doses of thiamine needed is firstly as no specific transporter across BBB so need to establish high gradient, and needs to be IV as oral bioavailability reduced in alcoholics)

Answer 68

Thiamine is crucial for the formation of thiamine pyrophosphate - required for glycolysis and TCA cycle (inc needed for PDH and a-KGase to function) - so if deficient keto-acids and lactic acid formed pentose phosphate pathway also needs thiamine to generate NADPH, so failure to synthesise this giving glucose allows for much more lactic acid production as depletes whatever thiamine reserves there are quickly, combined with failure to generate NADPH to protect from ROS; this leads to cellular damage and ultimately apoptosis or necrosis thus before giving glucose, TPN, or dextrose long-term you must make sure a refeeding risk pt is given thiamine -> HOWEVER, a single bolus of glucose alone won't precipitate WE, if a pt has a hypo then treat it without waiting for thiamine

Answer 69

You order with a paper form as it is made from donor blood Nephrotic Syndrome – in combination with diuretics. During drainage of ascitic fluid to prevent renal dysfunction due to increased renin activity and hyponatraemia (thereby preventing post-paracentesis circulatory dysfunction). The dose is as per the ascitic fluid drainage protocol – 100 ml of 20% HAS for every 2 litres of ascites drained. Severe burns after the first 24 hours (usage before this time has been demonstrated to cause paradoxical pulmonary oedema). Acute Respiratory Distress Syndrome where use of diuretics has caused fall in effective plasma volume. Acute liver injury to support plasma oncotic pressure and bind excessive bilirubin, activated plasmin, toxins etc. (you might try and evaluate resus with eg hartmanns first) Renal dialysis if the patient becomes hypotensive. Hepatorenal Syndrome (HRS) The dose is as per HRS guideline – 1g/kg (Max 100g /day) per day for two or more days until improvement in renal function. Either 4.5% or 20% concentrations may be used depending on the fluid status of the patient; note also that patients with SBP may be at high risk of getting HRS and so should be given HAS Inappropriate indication Intravascular volume expansion after trauma or major surgery. As part of total parenteral nutrition. In long term supplementation of albumin in nephrotic syndrome

Answer 70

ciclosporin, tacrolimus, sirolimus most common chemo drugs ketoconazole/itraconazole clari/erythromycin TCAs, SSRIs, venla, mirtaz many antipsychotics many opioids diaz/clonaz/midaz Z drugs donepezil statins (except prava/rovu) CCBs amiodarone sex hormones chlorphen/terfen -vir and nevirapine antivirals hydrocort/dexameth warfarin omeprazole domperidone/ondansetron eplerenone propran, salmet, losartan, montelukast some anti-epileptics

Answer 71

two main forms of cardiac hepatopathy are acute cardiogenic liver injury (ACLI) (also referred as hypoxic hepatitis) and congestive hepatopathy (CH) passive venous congestion in the setting of chronic right-sided HF; leads to sinusoidal hypertension, centrilobular fibrosis, and ultimately, cirrhosis and maybe HCC oft asymp, but may have dull right upper quadrant pain and nausea. Other symptoms include anorexia, early satiety, and malaise. Of note, all of them may occur in the absence of overt ascites or lower extremity oedema hepatomegaly, an irregular and nodular liver, dilation of inferior vena cava and hepatic veins with absence or attenuation of the normal variation of their diameter with respiratory movements mx the underlying cardiac disease

Answer 72

congenital (riedel's lobe, polycystic liver disease (devs in adult life, cystic liver often associated with PCKD)) acquired: steatosis (fatty liver disease or poorly controlled DM), neoplasm (prim or mets), early cirrhosis, venous outflow limitation (heart failure, budd-chiari), infiltration (lymphoma, amyloidosis, glycogen storage/gaucher disease, histiocytosis, sarcoidosis) if can feel liver see if can feel enlarged spleen, lymph nodes, any abdo masses; if spleen big too consider cirrhosis, haemat malig, amyloid, unusual infections; if lymph nodes also big consider lymphoma but could be EBV

Answer 73

focal nodular hyperplasia (2nd) haemangioma (1st), adenoma (rare), abscess, mets (specific imaging sequence shows liver tissue - primovist) primovist MRI; PET-CT - prior to operating on liver malignancy scoring systems: UKELD/MELD, childs-pugh - UKELD 49+ means eligible for liver transplant management for HCC (2 conditions - cancer and chronic liver disease) so assess: perf status, liver function (scoring system above), TNM/cancer status barcelona clinic management criteria

Answer 74

mostly arises from ppl with cirrhosis (and so who will already have liver symptoms), due to eg HBC, HCV, haemochromatosis, alcohol, nonalcoholic steatohepatitis, a1 antitrypsin etc; haemophilia/haemoglobinopathy pt more likely as more likely to get hepatitis as many blood transfusions over life + poss iron overload, DM2 incs risk poorly defined hypoechoic lesion, AFP produced oft (though not great sensitivity) 5-15% pts suitable for surgical resection (>40% cirrhotic volume, equiv to >25% normal healthy volume, has to be left and all the malignancies have to be removed); resection is of some combination of the 9 liver segments eg right hemi-hepatectomy is segments V-VIII, left II-IV, sometimes also I; this is bc each segment has its own vascular supply and so can be safely excised w/o damaging remaining segments radio and chemotherapy are options if non-resectable, alongside liver transplantation

Answer 75

the most common primary liver tumor in children, and is usually diagnosed during the first 3 years of life pretreatment extent of disease (PRETEXT) staging system has become a consensus classification Most HBLs are sporadic, but some are associated with constitutional genetic abnormalities and malformations, such as the Beckwith-Wiedemann syndrome and familial adenomatous polyposis and other risk factors are extreme prematurity and birth weight <1kg most common sign is abdominal distension or abdominal mass. Some children present with abdominal discomfort, generalized fatigue, and loss of appetite, due to tumor distension or secondary anemia. Children with a ruptured tumor usually present with vomiting, symptoms of peritoneal irritation, and severe anemia. Rare cases manifest precocious puberty/virilization due to β-human chorionic gonadotropin (hCG) secretion by the tumor AFP levels almost always raised and used for monitoring rx and relapse; Abdominal ultrasonography usually reveals a large mass in liver, sometimes with satellite lesions and areas of hemorrhage within the tumor. The most useful diagnostic modality is multiphase computed tomography (CT) or magnetic resonance imaging (MRI) tumor resection remains the cornerstone of definitive cure for HBL; pretext I/II/III without extrahepatic features gets surgical removal then post-op chemo; moderate or high risk patients get pre op chemo, op, post op chemo; very high risk (mets, normally in lung) get preop chemo, op, metastetctomy, and post op chemo

Answer 76

often insidious w/ 1mo+ general malaise before rigors, high swinging fever, palpable tender liver, and jaundice; infection elsewhere in portal territory eg appendicitis, suppurative cholangitis, or diverticulitis may be in recent history blood cultures often positive and USS or CT may find one or multiple abscesses

Answer 77

lymphoma and some leukaemias, myeloprolif diseases, haemolytic anaemias portal hypertension ebv, malaria, endocarditis, rarer infection RA (felty), SLE sarcoidosis, amyloidosis, glycogen storage disorders

Answer 78

Indications: trauma, infection (EBV), hypersplenism (hereditary spherocytosis, elliptocytosis; PVT), malignancy (lymphoma, leukaemia) At high risk from sepsis due to encapsulated organisms (post-splenectomy sepsis, PSS) S. pneumoniae H. influenzae N. meningitidis Prevention penicillin V for at least 2 years Immunization against HiB, meningitis A+C (meningococcus), influenza (annual), pneumococcal (every 5 years) see howell-jolly bodies

Answer 79

overwhelming post splenectomy infection - encapsulated bactis, 5% lifetime risk penV or clarithromycin for at least 2 yrs + vaccines for encap bacti, annual flu cipro + present to A&E if get a fever due to risk it may be opsi

Answer 80

congen due to iem - primary if defects of urea cycle enzymes, most common orrnithine transcarbamylase def; sec if defects of enzymes not involved in urea cycle or of cells eg liver failure acquired causes: acute or chronic liver failure eg hepatotoxins, infectious hepatitis, cirrhosis. HCC; lactulose or rifaximin can treat this valproic acid overdose causes carnitine def, mx by replacing, can also just have carnitine def uti by urease producing organisms (proteus, klebsiella, pseudomonas, corynebacterium) severe dehydration SIBO glycine toxicity (TURP syndrome) protein load or steroids (inc protein catab) AML, MM if urea cycle enzyme defects can limit dietary protein dialysis needed if levels v high

Answer 81

always abnormal haem: rhesus, ABO, anti C, E, Kell, duffy; hereditary spherocytosis; G6PD def; haemoglobinopathies not now as HbF predominates sepsis: inc UTI, TORCH ix: fbc + film, group of baby and mum + mum antibodies, directcoombs test, G6PD assay, TORCH screen (esp if conjugated bili), infection screen (blood culture, urine MC&S etc)

Answer 82

circulating unconjugated bilirubin, which is lipid-soluble, passes the blood-brain barrier and enters neuronal and glial membranes. In the brain, bilirubin has a special affinity for the globus pallidus, the hippocampus, and the subthalamic nucleus; Bilirubin attaches to cell membranes and is toxic to neurons and oligodendroglia. It damages the mitochondria, inhibits oxidative phosphorylation, and causes calcium release promoting apoptosis; presence of neurologic symptoms like altered mental status, hypotonia, and decreased reflexes, especially in a preterm infant, should arouse the suspicion of kernicterus. The infants can also present with non-specific symptoms like reduced feeding from the inability to suck efficiently Acute bilirubin encephalopathy can be further divided into three phases: Weakness, lethargy, and poor feeding are seen in this phase. These are not specific to this condition and are seen in a variety of diseases, thus making it difficult to identify the condition at this stage. Prompt administration of treatment at this stage will stop the progression of the condition. Extensor hypertonia, retrocollis, opisthotonus are generally seen in this phase. Hypotonia is typically seen in infants aged more than one week. A bilirubin level should be measure in all jaundiced babies. When measuring the bilirubin level: use a transcutaneous bilirubinometer in babies with a gestational age of 35 weeks or more and postnatal age of more than 24 hours. if a transcutaneous bilirubinometer is not available, measure the serum bilirubin if a transcutaneous bilirubinometer measurement indicates a bilirubin level greater than 250 micromol/litre a serum bilirubin should be obtained. if the transcutaneous bilirubin is within 25micromols/l of the treatment line a serum bilirubin should be obtained (use treatment threshold graph). always use serum bilirubin measurement to determine the bilirubin level in babies with jaundice in the first 24 hours of life. always use serum bilirubin measurement to determine the bilirubin level in babies less than 35 weeks gestational age. In addition to a full clinical examination by a suitably trained healthcare professional, carry out all of the following tests in babies with significant (i.e. requiring treatment) hyperbilirubinaemia: serum bilirubin (for baseline level to assess response to treatment) Full blood count blood group (mother and baby) DAT (Coombs’ test). Interpret the result taking account of the strength of reaction, and whether mother received prophylactic anti-D immunoglobulin during pregnancy. When assessing the baby for underlying disease consider whether the following tests are clinically indicated: blood glucose-6-phosphate dehydrogenase levels, taking account of ethnic origin microbiological cultures of blood, urine and/or cerebrospinal fluid (if infection is suspected). timing of repeat samples for infants of 38 weeks gestation or more to the following: Within 50micromols/l of the treatment line: No additional risk factors- recheck within 24 hours Additional risk factors- recheck within 18 hours Testing frequency guidance is not given for more immature infants. Given their greater susceptibility to kernicterus it would be prudent to ensure that they are retested within 18 hour Treatment (phototherapy) should be commenced one a serum bilirubin has confirmed that the bilirubin level is over the treatment threshold NICE suggests the following as evidence that the bilirubin is not coming under control and suggests moving to multiple phototherapy: the serum bilirubin level is rising rapidly (more than 8.5 micromol/litre per hour) the serum bilirubin is at a level that is within 50 micromol/litre below the threshold for which exchange transfusion is indicated after 72 hours the bilirubin level fails to respond to single phototherapy (that is, the level of serum bilirubin continues to rise, or does not fall, within 6 hours of starting single phototherapy). Care must be taken to ensure that phototherapy is being adequately delivered at all times. Single phototherapy can be reverted back to once the serum bilirubin has fallen greater than 50micromol/litre below the exchange transfusion threshold and is stable/falling Care while receiving phototherapy place the baby in a supine position unless other clinical conditions prevent this ensure treatment is applied to the maximum area of skin monitor the baby’s temperature and ensure the baby is kept in an environment that will minimise energy expenditure (thermoneutral environment) monitor hydration by daily weighing of the baby and assessing wet nappies support parents and carers and encourage them to interact with the baby. Give the baby eye protection and routine eye care during overhead phototherapy. During conventional ‘blue light’ phototherapy: using clinical judgement, encourage short breaks (of up to 30 minutes) for breastfeeding, nappy changing and cuddles continue lactation/feeding support During multiple phototherapy: do not interrupt phototherapy for feeding but continue administering intravenous/enteral feeds continue lactation/feeding support so that breastfeeding can start again when treatment stops NICE recommend checking an initial bilirubin 4-6 hours after commencing phototherapy, and 6-12 hourly thereafter if the bilirubin is falling Stop phototherapy once serum bilirubin has fallen to a level at least 50 micromol/litre below the phototherapy threshold NICE recommend a check for rebound of significant hyperbilirubinaemia with a repeat serum bilirubin measurement 12–18 hours after stopping phototherapy. Babies do not necessarily have to remain in hospital for this to be done Use intravenous immunoglobulin (IVIG) (500 mg/kg over 4 hours) as an adjunct to continuous multiple phototherapy in cases of Rhesus haemolytic disease or ABO haemolytic disease when the serum bilirubin continues to rise by more than 8.5 micromol/litre per hou Use a double-volume exchange transfusion to treat babies: whose serum bilirubin level indicates its necessity (see treatment charts). and/or with clinical features and signs of acute bilirubin encephalopathy. During exchange transfusion do not : stop continuous multiple phototherapy

Answer 83

conj causes: neonatal hepatitis, intra or extrahep cholestasis, disorder of bilirubin secretion unconj causes: hypothyroid, haemolytic anaemia, breast milk, sepsis, gilbert, crigler-najjar, lucey-driscoll, transient familial ix: fbc, blood group, direct coombs, LFTs, U&Es, blood culture, urine MC&S, urine reducing substances, TFTs if jaundice unconj and ix normal + baby clinically well then wait and see - if mum breastfeeding that's usually the cause; if conj then need bacti and viral cultures, metabolic screening tests, hepatic uss and if still no cause then radioisotope studies +- biopsy to differentiate biliary atresia and neonatal hep 99Tc labelled HIDA scan w <5% excretion in 72hrs suggesting biliary atresia; kasai procedure must be done within 6 weeks of life for max chance of success; this is hepatic portoenterostomy between porta hepatis and bowel lumen postop comps inc int obs, ascending cholangitis, peristomal breakdown, biliary cirrhosis; 50% cases unsuccesful with ongoing inflam/cirrhosis -> liver transplant

Answer 84

most likely ABO incomp - this is milder jaundice and less likely to need transfusion than rh haemolysis may see inc'd retics, reduced serum hapto, drop in Hb conc

Answer 85

may well infectious hep -> A most likely in UK but consider EBV, CMV; HBV/HCV blood-borne so look in history also good to see if recent transfusions/injectons, contact with jaundiced individuals, urine dark/stools pale, recent medications, period from sx to jaundice (2-6 weeks for HAV and 2-6mo for HBV), abdo pain (hep, stones), recent surgery (halothane toxicity), and FH (eg gilberts)

Answer 86

haemolytic disorders where haemolysis provoked by stressors like infection, medication, surgery; eg sickle cell, G6PD inherited disorders of bili metabolism - if unconj gilbert or crigler-najjar, if conj dubin-johnson or rotor syndrome gilbert is AD, rest AR; gilbert 1-2% pop, bilirubin not very high, dx of exclusion CN type 1 AR 2 AD, v rare, high neonatal bili can give kernicterus, type 1 completely deficient in conjugating enzyme so death, type 2 partial def may respond to phototherapy DJ usually after puberty, liver stained black by centrilobular melanin, due to dec'd hepatic excretion; bromosulphthalein elimination rises late at 90min but normal at 45, cholecystogram abnormal rotor presents at younger age; BSP raised at 45, no sec rise at 90; cholescystogram normal; defect unknown

Answer 87

if mum hepB SAg +ve look at e Ag and ig, if pos former neg latter high infectivity, 80% chance baby has; if no e markers intermediate infectivity; if neg former pos latter low infectivity, 10% chance in first two cases active and passive immunisation into diff thighs, in latter just active; in all cases imm in first 12h of life, active doses repeated at 1 and 6mo w seroconversion tested at 1yr, and if neg booster of active given; another booster at 5yo this important to reduce risk of cirrhosis and hepatoma later in life

Answer 88

portal htn -> oesophageal varices now bleeding vit K deficiency -> raised INR liver disease -> raised INR haemoptysis mistaken for haematemesis portal htn -> hypersplenism -> thrombocytopenia

Answer 89

hepatic failure -> enceph but also: reye syndrome (viral urti then 5-6 days later intractable vomiting, confusion, agitation, deepening unconsciousness due to raised ICP, usually no jaundice/fever bili normal, NH3 up, PT up, hypoglyc in 15% of cases, aetiology unknown but linked to HiB, varicella, aspirin in <12yo; histo of liver will show fatty accumulation w no necrosis or inflam, mitos will be swollen treatment supportive -> fluid restriction, treat hep failure also consider fatty acid oxidation and mito etc defects, urea cycle defects, salicylate or carbon tetrachloride poisoning, sepsis, hypothermia

Answer 90

chronic active hepatitis, commonly autoimmune test for ANA, anti smooth muscle, anti liver microsomal ig treat w steroids +/- azathioprine 70% normal 5 yrs post therapy, rest dev cirrhosis and liver failure

Answer 91

extrahep bile ducts obliterated by inflam (maybe viral origin); jaundice, pale stools, dark urine, though normal meconium may be initially passed; failure to thrive, with cirrhosis and portal hypertension + splenomegaly by 2mo Portal findings in BA simulates those of large-duct obstructive cholangiopathy due to any other etiologies. Portal tracts show expansion and demonstrate edematous fibroplasia with bile ductular proliferation, consisting of anastomosing ductules located at the periphery of the portal tracts; Duct/ductal bile plugs and portal stromal edema are strong histologic predictors of BA. Proliferation of fibroblasts, as well as a variable amount of inflammatory cells, especially neutrophils are usually present Experimental and clinical studies have suggested that viral infection initiates biliary epithelium destruction and release of antigens that trigger a Th1 immune response, which leads to further injury of the bile duct, resulting in inflammation and obstructive scarring of the biliary tree. It has also been postulated that biliary atresia is caused by a defect in the normal remodelling process. Genetic predisposition has also been proposed as a factor Type 1: Atresia of the common bile duct with patent proximal ducts. Type 2: Atresia involving the hepatic duct but with patent proximal ducts. Type 3: Atresia involving the right and left hepatic ducts at the porta hepatis. Type 3 is the most common (88%) and has the worst prognosis conjugated hyperbili, with uss to help diagnose, but consider other obstructive causes like gallstones etc; surgery to treat, otherwise fatal by 18mo neonatal hep - by 2-3mo old clear infant not gaining weight, irritable, prolonged bleeding, ascites, liver failure; any jaundice beyond 21 days old needs investigating in case its this; if unconj bili is physiological (decreased excretory capacity secondary to low levels of ligandin in hepatocytes, and low activity of the bilirubin-conjugating enzyme uridine diphosphoglucuronyltransferase (UDPGT), more rbcs in neonates) or related to breast feeding

Answer 92

20% cholesterol, 5% pigment, 75% mixed if bile supersaturated with cholesterol risk inc's eg OCP, age, pregnancy inc risk as does crohns, esp resection of terminal ileum (interruption of enterohepatic circulation means deficiency of bile salts) haemolytic anaemias inc risk of pigment stones as excess bile pigment deposits in biliary tract, suspect haemolysis if find these esp in young person; mixed has same aetiology as cholesterol silent when in gallbladder, may become impacted in cystic duct, water reabsorbed and remaining conc stone produces chemical cholecystitis which may become infected, or in pouching of gallbladder may impact either causing inflam or getting mucous secreted around it forming a mucocele which is then infected to give empyema of gallbladder; may migrate into CBD and produce jaundice, or sometimes ascending cholangitis or acute panc; large gallstone rarely ulcerates through into adjacent duodenum and either pass per rectum or impact at terminal ileum producing gallstone ileus (actually a mech obstruction) when in cystic duct if blocking can get biliary colic w/o jaundice, pain 2-3hrs after eating often wakes pt, pain cont, lasts for hours, radiate to scapula common, also vomiting and sweating; also biliary colic as part of stone in CBD can occur accompanying a temp attack of posthep jaundice if remains blocked the bile concs and produces chemical cholecystitis, fever and gallbladder filled with sterile pus, mass as inflamed GB adheres to omentum, empyema devs and may rarely perf; GB can press against CBD producing mild posthep jaundice stones in duct w/ jaundice 75% cases painless palpable GB + jaundice is unlikely due to a stone, as if stone present GB usually thickened and fibrotic so doesnt distend

Answer 93

early intervention good as inflam adhesions make it harder to remove GB later, although can often treat acute chole medically with elective removal later due to high risk of recurrence impacted stones can be removed by ERCP, this an emergency if acute cholangitis as toxaemia and often bacteraemia inc risk of sepsis iv vit K should be given as lack of bile salts in gut from obstructive jaundice means vit k def so bleeding risk if surgery - can check coags first gallstones may not show up in CBD if behind duodenum as air in the SI can hide them, so USS can be good for cholecystitis and stones in GB but if obstructive jaundice then a CT scan has greater sensitivity

Answer 94

common hepatic duct compression, leading to obstructive jaundice, from a stone lodged in cystic duct or neck of GB then externally compressing the CHD may present with jaundice and RUQ pain + fever (cholecystitis picture); it is rare but associated with GB cancer (likely biliary stasis and chronic inflam incs risk of both conditions) important to be aware of as exploration of CBD may not reveal any source of obstruction

Answer 95

3 phases in sequence: Zero point (before contrast) Arterial phase Portal venous phase All three of these phases occur within the first 1.5 minutes of the exam most common time point in abdominal CT is the portal venous phase, which is obtained around 70–80 seconds after contrast is injected. This phase provides the best balance of solid organ, bowel, and vascular enhancement for general imaging arterial phase is the second most common sequence to obtain and can range from 20–35 seconds after contrast injection. The exact timing depends on whether you want to evaluate the vessels or check the organs for abnormalities, such as tumors with a rich arterial blood supply - in art phase aorta bright, liver/spleen dark and grey, whereas in venous phase the organs are brighter as they are full of blood containing contrast In multiphasic exams, images are obtained at several different time points, both before and after IV contrast is injected in the patient, rather than just in the portal venous phase

Answer 96

The first (superior) part of the duodenum begins as a continuation of the duodenal end of the pylorus. It passes laterally to the right, superiorly and posteriorly, for approximately 5 cm, before making a sharp curve inferiorly into the superior duodenal flexure second (descending) part of the duodenum begins at the superior duodenal flexure. It passes inferiorly to the lower border of vertebral body L3, before making a sharp turn medially into the inferior duodenal flexure - this part contains ampulla of vater third (inferior/horizontal) part of the duodenum begins at the inferior duodenal flexure and passes transversely to the left, crossing the vertebral column fourth (ascending) part passes superiorly, either anterior to, or to the left of, the aorta, until it reaches the inferior border of the body of the pancreas. Then, it curves anteriorly and terminates at the duodenojejunal flexure where it joins the jejunum. The duodenojejunal flexure is surrounded by a peritoneal fold containing muscle fibres: the ligament of Treitz

Answer 97

only if other options unsuitable, most hospitals will have team based consultation and collection of baseline measurements before starting if patients cant absorb food from GI tract may consider, so eg IBD like crohns, or short bowel syndrome due to mesenteric artery infarction short 1-2 weeks by peripheral veins, or long term via central venous catheter (can stay in for years) often inpatients but some central catheter peeps admin their own TPN at home, often at night TPN contains calories, amino acids, vitamins, trace elements; often get a prepackaged TPN mix but sometimes tailored to specific patient problems: catheter site sepsis so aseptic technique when dealing with the catheter; misplaced catheter can lead to serious problem of extravascular infusion so place under x-ray control; metabolic complications, most common hyperglycaemia esp as background often has inc'd stress level; also hypokalaemia/phosphataemia/magnesaemia, hypercalcaemia/lipidaemia, acid base disorders, re-feeding syndrome, esp be aware for chronic alcoholics starting TPN

Answer 98

malaise, anorexia, bloating, diarrhoea (esp stool bulk change rather than freq so much), weight loss specifics: steatorrhoea (fat malabsorption), oedema and ascites (protein), paraesthesia or tetany (mg/ca), skin rash (zn, vit B), cheilitis/glossitis (vit B), neuropathy and psych changes (B12), night blindness (vit A), bruising (vit K or vit C), bone pain or osteoporosis (vit D) investigations to find cause: serology (FBC, Fe, B12, folate, albumin, U&Es, coeliac antibodies), barium follow through, capsule endoscopy, lactose and glucose breath tests, other specific tests if cause suspected

Answer 99

syndrome where there is an excess loss of proteins in the gastrointestinal tract; should be suspected in patients with low serum proteins and in whom other causes of hypoproteinemia (severe malnutrition, nephrotic syndrome, or chronic liver diseases) have been ruled out Primary Erosive/Ulcerative gastrointestinal Disorders - inc IBD, GI malignancy, peptic ulcer, c diff colitis, carcinoid, GVHD Non-Erosive/Non-Ulcerative Gastrointestinal Disorders, inc tropical Sprue, coeliac disease, Menetrier disease, amyloidosis, eosinophilic gastroenteritis, SIBO, parasitic infections, Whipple disease*, collagenous colitis, AIDS, mixed connective tissue diseases, systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) Disorders Causing Increased Interstitial Pressure or Lymphatic Obstruction - primary intestinal lymphangiectasia, right-sided heart failure, constrictive pericarditis, congenital heart disease, Fontan procedure for single ventricle, portal hypertension gastropathy, hepatic venous outflow obstruction, mesenteric tuberculosis or sarcoidosis, retroperitoneal fibrosis, lymphoenteric fistula, lymphoma, and thoracic duct obstruction may present with any of periph oedema, ascites, pleural effusions, immunocompromise due to loss of Ig and leucs; may have sx of cause too albumin and globulins should be low as protiens lost regardless of weight; A1AT intestinal clearance commonest test to demonstrate it; then workup for cause treat cause (may lead to complete resolution)and mx with diet - may need 2 to 3g/kg/day of protein, generally diet rich in protein and medium chain triglycerides and low in fat is considered the best diet in this condition; micronuts etc may need supplementing - dietician review can be helpful

Answer 100

T cell inflam of small bowel against a-gliadin infants: diarrhoea, malabsorption, failure to thrive upon weaning children: abdo pain, anaemia, short stature, delayed puberty adults: bloating, lethargy, diarrhoea or constipation, Fe deficiency anaemia, malabsorption, sometimes oral ulcers and psych disturbance often linked to other autoimmune diseases esp sjogrens syndrome, prim bil cirr, thyroid disease, ins dep diabetes, dermatitis herpetiformis duodenal biopsy gold standard (villous atrophy and crypt hyperplasia and intraepithelial lymphocytosis) look for IgA to TTG but false neg if patient has IgA deficiency, can screen for it and monitor response to treatment FBC (anemia), U&Es; (ca, vit B12 and K, vit D, albumin) dietician to support lifelong gluten free diet, correct deficiencies often hyposplenic which may lead to rec encapsulated bacti infections There are 3 types of cancer associated with celiac disease: enteropathy-associated T-cell lymphoma (EATL), non-Hodgkin’s lymphoma, and adenocarcinoma of the small intestine EATL is aggressive non hodgkin lymphoma type arising from sites of chronic inflam in the gut epithelium afflicted individuals present with worsening coeliac disease symptoms of abdominal pain, malabsorption, diarrhea, weight loss, fever or night sweats - often quite acute; or bowel obstruction and/or bowel perforation caused by bulky EATL masses

Answer 101

note: coeliac strongly linked to HLA-DQ2 (95% of cases) and HLA-DQ8 (5%) conditions that have inc'd risk of also having coeliac: T1DM, selective IgA nephropathy, TS21, williams/turner syndromes, other autoimmune disease, unexplained transaminitis, relatives with coeliac Gastrointestinal -indigestion, diarrhoea, abdominal pain, bloating, constipation, nausea and vomiting. Dermatological- dermatitis herpetiformis, apthous stomatitis Endocrine- delayed puberty, amenorrhoea, recurrent miscarriage Neurological- peripheral neuropathy Growth/Ortho- failure to thrive, short stature, arthralgia Haematological- anaemia, unexplained iron, B12 or folate deficiency. Hepatic- deranged LFT’s should be on gluten containing diet for 3mo prior to testing otherwise risk false negatives Bloods: FBC, ferritin, vitamin D, liver and renal profile bloods, folate, iron, vitamin B12, thyroid function, Total IgA (deficiency if <0.05g/l) and IgA anti-tTG antibodies at this point you also need to refer to paeds GI specialist if anti-tTG >10x ULN then test for antiendomysial antibodies, if test positive then coeliac confirmed; if test negative or anti-TTG <10x ULN then will need biopsy if total IgA is low then will need tertiary centre advice, if normal but serology discordant with sx consider if risk of false negative (has been avoiding gluten, on immunosuppresants, has primarily extra-intestinal manifestations) - if no risk of these then doesn't have coeliac, if there is a risk will need tertiary advice biopsy takes >4 samples from distal duodenum; if marsh score 2-3 then CD confirmed; if 0-1 then do additional tests like anti-endomysial antibodies, HLA type etc - will need tertiary guidance if HLA-DQ2/8 negative then CD unlikely, if positive then can do normal gluten intake and re-test; if total IgA low then IgG tests (endomysial, anti-TTG, DGP) and if these positive proceed to biopsy note patients can have a non-coeliac gluten intolerance, possibly a non IgE mediated food intolerance strict gluten free diet and will need clinic review at 1mo and 6mo then annually at each check height, weight Gluten challenges should not be completed routinely and only undertaken under the recommendation of the consultant gastroenterologist in cases where there is diagnostic uncertainty. Timing of the gluten challenge should be carefully considered on a case-by-case basis and it is not advised in children under 5 years of age or during periods of rapid growth such as pubertal growth spurt

Answer 102

relapsing/remitting crohns: non-continuous skip lesions: mostly in ileal-colonic region (40% of cases), SI (30%), purely colonic (20%), purely perianal (10%); inflam involves full thickness of the wall with deep ulcers giving cobblestone appearance, somtimes fistulae and abscesses through to bladder, vagina, other parts of gut; get giant cell granuloma on histology UC: always rectum and can extend in continuous fashion to sigmoid (40%) or whole colon (20%); other 40% have extensive colitis past sigmoid but not a full pancolitis; inflam confined to mucosa with crypt abscesses; chronic inflam incs dysplasia which incs carcinoma risk 35% of people get extra-intestinal manifestations of these diseases

Answer 103

failure to thrive, thin, wasting (esp buttocks), pale, diarrhoea (soft, pale, sticky), bloating; may have oedema, rickets, fe def anaemia and child oft depressed and irritable onset usually by 2yo, sx most commonly start when cereal introduced ~5-6mo of age - growth chart may show weight fallingaround then vomiting more common the earlier the onset; HLA-B8 association late complications inc GI lymphoma (worsening clinical state), myopathies, neuropathies, hyposplenism, and later gastric and oesophageal carcinoma; also dermatitis herpetiformis important diff is giardiasis (repeat stool microscopy, as secreted at intervals risk of missing it), treat with metro - may give empirically ix - IgA antigliadin, antiendomysial, entireticulin but bear in mind IgA def; jejunal biopsy +/- aspirate for giardia other diffs inc cows milk protein intolerance (d&v - may have blood in stool, failure to thrive, rash, wheeze, eczema)

Answer 104

generally abdo pain and diarrhoea ileal crohns: inflam abscess causing (post prandial) pain giving anorexia, weight loss and non-bloody diarrhoea; can get malabsorption and SBO prox crohns: more likely to get vomiting crohns colitis: bloody diarrhoea, malaise, fever but sigmoidoscopy often shows rectal sparing perianal crohns: skin tags, anal fissures or fistulas UC: bloody diarrhoea; proctitis and proctosigmoiditis give fresh rectal bleeding, tenesmus, only get constitutional symptoms if severe; extensive or pancolitis give more abdo pain and constitutional symptoms, severe may have raised pulse and temp plus >6poos daily toxic megacolon: severe colitis giving abdo distension and strong constitutional symptoms with high risk of perforation; can occur in crohns colitis but usually is UC

Answer 105

uveitis, scleritis, angular stomatitis and mouth ulcers (crohns), erythema nodosum/multiforme, pyoderma gangrenosum, ankylosing spondylitis, arthropathy, osteoporosis, oxalate kidney stones, amyloidosis, glomerulonephritis, gallstones, autoimmune hepatitis, primary sclerosing cholangitis, fatty liver, pericarditis, fibrosing alveolitis, pulmonary vasculitis, neuropathy, myopathy

Answer 106

inflammation of the anterior portion of the uvea - iris and ciliary body. It is associated with HLA-B27 and may be seen in association with other HLA-B27 linked conditions (see below). Features acute onset ocular discomfort & pain (may increase with use) pupil may be small +/- irregular due to sphincter muscle contraction photophobia (often intense) blurred vision red eye lacrimation ciliary flush: a ring of red spreading outwards hypopyon; describes pus and inflammatory cells in the anterior chamber, often resulting in a visible fluid level visual acuity initially normal → impaired Associated conditions ankylosing spondylitis reactive arthritis ulcerative colitis, Crohn's disease Behcet's disease sarcoidosis: bilateral disease may be seen Management urgent review by ophthalmology cycloplegics (dilates the pupil which helps to relieve pain and photophobia) e.g. Atropine, cyclopentolate steroid eye drops

Answer 107

FBC, U&Es, CRP, ESR (CRP more acute inflam marker, ESR good as more chronic marker of inflam) endoscopy/sigmoidoscopy; full colonoscopy to assess extent of disease abdo x-ray if suspect toxic megacolon or crohns SBO barium follow through for crohns disease, if this and CT fail to spot then capsule endoscopy; if patients too unwell for these procedures can do radiolabelled white cell scan (for areas of inflam, less accurate though) oral steroids in crohns help induce remission; oral 5-ASA may help maintain remission if freq relapses; surgical resection of affected area suppository steroids to induce remission in UC, enemas if severe and oral if still not responding; start with oral if extensive; oral 5-ASA to maintain remission if freq relapses note 90% UC is relapsing remitting but other 10% have chronic active disease and these are esp likely to have surgery

Answer 108

Faecal calprotectin Raised inflammatory markers Deficiencies: B12, folate Antibody testing UC: ANCA +ve CD: ASCA +ve Imaging AXR: drainpipe colon (UC) Small bowel barium enema - Crohn’s: stricture (Kantor’s string sign), proximal bowel dilation, rose thorn ulcers, fistulae UC: loss of haustrations, superficial ulceration, pseudopolyps Diagnostic: colonoscopy + biopsy Terminal ileal biopsy UC - inflam confined to mucosa, crohns is fully transmural - cobblestone UC: crypt abscesses, Depletion of goblet cells and mucin crohns: More goblet cells, caseating granulomas with giant cells Lifestyle Stop smoking Diet change UC remission: step-up (1) Proctitis (2) Proctosigmoiditis (3) Left-sided UC (4) Severe Topical aminosalicylate: mesalazine, suphasalazine Oral aminosalicylate Topical/oral corticosteroid IV corticosteroids + IV ciclosporin (or infliximab (TNFa inhib)) Maintain remission Topical/oral aminosalicylate Severe or >2 exacerbations in 12 months: Oral azathioprine Oral mercaptopurine Biologics Infliximab Adalimumab (both TNFa inhibs) Emergency presentations that don’t respond to medical therapy 🡪 subtotal colectomy with end ileostomy (or perf, toxic mega etc) crohns remission: First line: Steroids (e.g. oral prednisolone or IV hydrocortisone) If steroids alone don’t work, consider adding immunosuppressant medication under specialist guidance: Azathioprine Mercaptopurine Methotrexate Infliximab Maintain remission Monotherapy Azathioprine Mercaptopurine Methotrexate Biologics Adalimumab Infliximab surg: intractable disease with growth failure, obstruction, abscess drainage, fistula, intractable haemorrhage, perforation aminosalicylates - Sulphasalazine a combination of sulphapyridine (a sulphonamide) and 5-ASA many side-effects are due to the sulphapyridine moiety: rashes, oligospermia, headache, Heinz body anaemia, megaloblastic anaemia, lung fibrosis other side-effects are common to 5-ASA drugs (see mesalazine) Mesalazine a delayed release form of 5-ASA sulphapyridine side-effects seen in patients taking sulphasalazine are avoided mesalazine is still however associated with side-effects such as GI upset, headache, agranulocytosis, pancreatitis*, interstitial nephritis; pan risk 7x higher than for sulf FBC key investigation in unwell pt taking either due to agranulocytosis risk

Answer 109

salofalk - tablets and granules containing mesalazine, for treatment and maintenance of IBD budenofalk - contains budesonide, used mostly for IBD but also eg eosinophilic oesophagitis and autoimmune hepatitis too

Answer 110

Pred works best orally, budesonide’s very potent so good for inhaled use but has extensive first pass metabolism so less good if you’re wanting it to go from the gut to somewhere other than the gut (good for IBDs though!) - side effects are less likely than with some other steroid medicines if budesonide taken orally

Answer 111

stool culture and c diff toxin to rule out infective cause initial flexisig, but full colonoscopy needed to define extent of disease 2 biopsies from 5+ sites inc rectum and ileum needed for histology can classify severity using mayo score oral 5ASA is standard mx for active UC (eg salofalk); also offer 5ASA enema; monitor U&Es, including pre-treatment as IBD can affect renal function anyway; if flare while on 5ASA then escalate dose and add enemas first if don't respond to/tolerate 5ASA then oral budenofalk or pred is next line; mod/severe flare can get weaning course of pred first line if 2+ flares requiring steroid in past yr, dependent on steroid, or resistant to steroid, then start thiopurine (azathioprine or 6MP), anti TNF (infliximab, adalimumab), vedolizumab, or tofacitinib (latter 2 are options if anti TNF fails) if acute severe colitis (6+ bloody stools a day + one of fever >37.8, HR >90, Hb <105, or CRP >30) admit to hospital with bloods, stool cultures, CT, flexi sig; give IV hydrocort - dont delay for culture results, if not responding by day 3 then rescue therapy with infliximab or ciclosporin; if still not responding then surg rv for if emergency colectomy needed, and give accelerated induction regime of infliximab; also emerg surg if perforate, toxic megacolon, or severe h+; planned surg if chronic ative sx despite optimal medical mx

Answer 112

The ileal pouch-anal anastomosis (“pouch”) is the most common way patients who require surgery to remove their colon are able to avoid a permanent ileostomy (“ostomy”). This pouch, created from the small intestines, serves as a reservoir to hold stool - up to 80% of these patients will experience pouchitis commonly presents with a constellation of symptoms such as increased stool frequency, watery stool, bloody stool, tenesmus, abdominal cramps, incontinence, and pelvic pressure important to consider alternative etiologies that may mimic idiopathic pouchitis such as infection (particularly cytomegalovirus and Clostridiodes difficile), ischemia, non-steroidal anti-inflammatory drugs (NSAIDs), pre-existing versus de novo Crohn’s disease, pelvic sepsis, anastomotic leak if acute <4 weeks then give cipro or metro, if no response speak to micro about alternatives; if chronic >4 weeks look into steroids and immunomodulators; as soon as abx course completes start probiotics

Answer 113

colonoscopy w biopsy is first line; small bowel imaging needed alongside as may be beyond reach of scope - MR enterography may be best, but CT and US are options if normal/equivocal imaging then can do capsule endoscopy (if clinical picture suggestive and faecal calprotectin raised) mild-mod active disease treat with budesonide, or oral pred if severe; both are 8 week courses; exclusive enteral nutrition is an alternative if you want to avoid steroids for that long (so is preferred option in kids if mild-mod); can resect if ileocaecal and failing on initial induction therapy (or prefer surgery) if mod-severe then oral steroids; if aggressive, extensive, or poor prognostic factors then early biologics if mod-sev and pred responsive then introduce thiopurines or methotrexate as maintenance while pred is weaning so there is cover; if refractory to this for induction or remission then anti-TNF, vedolizumab, or ustekinumab - combo of infliximab with thiopurine is good choice if jejunal or extensive small bowel disease then consider early biologics; oesophageal or gastroduodenal can be treated with PPI if mild, steroids if worsens, but mod-sev get early anti-TNF; in all cases encourage pt to stop smoking strictureplasty is alternative to resection if strictures short and need to preserve bowel length; balloon dilation if accessible and short stricture; intra-ab abscess needs IV abx and radiological drainage; enterovaginal or enterovesical fistulae need medical mx and surgical resection; low volume enterocutaneous fistulae get biologics, high volume usually need surgery; perianal fistulae get pelvic MRI, surgery, seton, infliximab following ileal resection watch for bile acid malabsorption and consider cholestyramine trial, SeHCHAT study if fails to respond or unclear diagnosis if lived/born in endemic areas also consider intestinal TB which may look v similar but more weight loss, less apthous ulcers and skip lesions; test for extrapulm TB if suspect; stool cultures, c diff toxin, and if relevant travel history dysentery screen + amoebiasis; if colitis mod-sev, esp if immunsupp'd or disease steroid resistant, then histo should look for CMV - ganciclovir + continue crohns mx (stop crohns mx only if meningoenceph, pneumonitis, hepatitis, oesophagitis) anti-TNF therapy may be withdrawn in patients with prolonged corticosteroid-free remission and mucosal healing. Retreatment in the event of relapse is usually successful; faecal calprotectin monitoring for relapse may be helpful

Answer 114

mucosal healing demonstrated on endoscopy is a common treatment target, commonly defined by a decrease in Simple Endoscopic Score for Crohn’s Disease [SES-CD] or Crohn’s Disease Endoscopic Index of severity [CDEIS] of at least 50% from baseline - no evidence that histological remission is superior to MH in achieving long-term clinically important outcomes In patients with luminal CD in clinical remission, a significant rise of faecal calprotectin should trigger further investigations and consideration of treatment escalation if eg CRP also raised (but shouldn't alone trigger escalation of rx) In children with active luminal CD, dietary therapy with exclusive enteral nutrition [EEN] (6-12 weeks of formula only, no solids) is recommended as first line for induction of remission -> as long as low to moderate risk on assessment with Paris classification; Considering the reduced palatability, the risk of early withdrawal, and the high costs associated with elemental diets, the primary choice of a polymeric formula is justifiable. Use of a nasogastric feeding tube may be considered to overcome aversion to the formula or not achieving the required daily intake. when EEN is not an option, corticosteroids may be considered for inducing remission, likewise if poorly tolerated or is ineffective after 2 to 4 weeks of good compliance; budesonide for milder ileo-caecal disease, if colonic may need pred In new-onset patients with high risk for a complicated disease course, anti-TNF therapy is recommended for inducing remission. Infliximab or adalimumab In patients with fistulising perianal disease, anti-TNF therapy is recommended as the primary induction and maintenance therapy, in combination with antibiotic therapy (cipro or metro), surgical treatment, or both

Answer 115

Methotrexate can be used to maintain clinical remission as a first-choice immunomodulator, or after thiopurine failure methotrexate is usually administered in practice SC once weekly at a dose of 15 mg/m2 [body surface area] to a maximum dose of 25 mg. If sustained clinical remission with mucosal healing is achieved, an attempt can be made to decrease the dose to 10 mg/m2 once a week to a maximum of 15 mg; Oral administration of folate [5 mg 24–72 h after methotrexate once weekly or 1 mg once daily for 5 days per week] is advised to reduce hepatotoxicity and gastrointestinal side-effects; Nausea and vomiting are major problems both at start of methotrexate therapy and during maintenance use; administration of ondansetron 1 hour before dosing, and for 1 [occasionally more] days afterwards from the outset, may reduce nausea, and as extremely teratogenic an effective birth control method [if appropriate] must be used during therapy and for 6mo afterwards before starting - exclude pregnancy, get baseline FBC, LFTs, U&Es then recheck every 1-2 weeks until stable on rx, then every 2-3mo and advise report any sx of unwell due to blood dyscrasia risk; folinic acid if toxicity suspected thiopurines [azathioprine or 6-mercaptopurine] can be used to maintain remission - latter is pro-drug for former; Haematological toxicity occurs in 2–14% of cases, typically in the first months of treatment. Pancreatitis develops in up to 7% of patients, is usually idiosyncratic, occurs within the first weeks after treatment initiation, and typically requires cessation of the drug; Increased transaminases up to twice the upper limit of normal may be transient or resolve after drug tapering or discontinuation. If newly raised transaminases are observed, treatment should be discontinued and thiopurine metabolites should be assessed, if available. Thiopurines should be withheld until transaminases are in the normal range again; if unresolved, further investigations for liver disease should be performed. In patients with nausea and vomiting due to azathioprine therapy, interventions include split dosing, switch to 6-mercaptopurine, and use of low-dose thiopurine in combination with allopurinol patients with low or absent TPMT activity are at an increased risk of developing severe, life-threatening myelotoxicity from thiopurines if conventional doses are given so TPMT testing should be done before starting the drug; patients initiating thiopurine therapy should have baseline complete blood counts and liver enzymes measurements. Close blood and liver monitoring should be performed monthly in the first 3 months and then at least once every 3 months thereafter. Thiopurine dose reduction is required in patients who are heterozygous for TPMT also low but definite malignancy risk -> lymphomas and non-melanoma skin cancers patients with perianal disease, stricturing or penetrating behaviour, or severe growth retardation should be considered for up-front anti-TNF agents in combination with an immunomodulator, with the latter possibly stopped after 6-12 mo patients with CD treated with adalimumab have their first proactive TDM just before the third injection [ie, 4 weeks after the first dose]. Patients treated with infliximab should have their first proactive TDM just before the fourth infusion to ensure trough conc in therapeutic range if inadequate clinical response, changes should be based on TDM results and the consequent stratification to immunogenic [presence of ADA - anti drug antibodies], pharmacokinetic [low trough concentrations without ADA], and pharmacodynamic loss of response [adequate trough concentrations]; Patients with low ADA titres may restore response following dose escalation, addition of an immunomodulator, or both, whereas patients with high ADA titre should be switched in-class [from infliximab to adalimumab or vice versa]. Patients with low trough levels without ADA should have a dose increase, and patients with trough levels that are well in range should be switched to an out-of-class biologic In patients who fail to achieve or maintain clinical remission on anti-TNF agents, despite anti-TNF dose optimisation and immunomodulator use, ustekinumab or vedolizumab can be considered

Answer 116

for crohns and UC, before starting immunomodulators screen for r HBV, HCV and HIV (and VZV if no history of chicken pox, shingles or varicella vaccination), screen for TB prior to anti TNF therapy with CXR and IGRA, and check thiopurine methyltransferase status (check in all pts before starting thiopurine therapy); if lived in endemic areas then check strongyloides seroloy and eosinophil count; get vaccine history and ensure up to date - cant have live vaccines while on immunomod therapy; should get annual flu vaccine and pneumococcal + booster; infants exposed in utero get no live vaccines for 6mo before starting thiopurines: ► Baseline FBC, U&E and LFT measurement ► If available test NUDT15 genotype ► Screen for HCV, HBV, HIV, refer if positive, consider HBV vaccination if naïve ► Check VZV immunity and vaccinate if low ► Vaccinate for influenza and pneumococcal vaccine ► Check cervical screening up to date ► Check TPMT and start at target dose once result available thiopurine monitoring: FBC, U&E and LFT at least at weeks 2, 4, 8, and 12, and then at least 3-monthly adult IBD patients on triple immunosuppression and using more than 20mg prednisolone may be offered prophylactic antibiotics for Pneumocystis jirovecii Ulcerative colitis patients who continue to smoke cigarettes should be encouraged to stop. There is an increased risk of flare after stopping, and patients should be made aware of this the mainstay of symptom relief for IBD-associated arthropathy which is related to IBD activity should be through control of intestinal inflammation, physiotherapy and simple analgesia; Local injection of corticosteroids may be required if symptoms don’t resolve rapidly for IBD-related arthropathy which is not related to IBD activity, rheumatology referral, physiotherapy and simple analgesia should be offered; consider other causes of joint pain which can include non-specific arthralgia, osteonecrosis, lupus-like syndrome in relation to anti-TNF therapy, and corticosteroid withdrawal arthralgia. Azathioprine-related arthralgia usually occurs early in treatment and resolves rapidly on stopping the drug; note that short-term use of NSAIDs is safe if IBD is in remission, but long-term use or use in active disease carries more risk of worsening IBD symptoms IBD patients with colonic disease should be offered ileocolonoscopy 8 years after symptom onset to screen for neoplasia, to determine disease extent and decide on the frequency of ongoing surveillance

Answer 117

may be constipation predominant, diarrhoea predominant, or mixed-stool pattern (40:20:40%) cramping abdo pain and symptoms dont occur at night, incomplete evacuation can occur TCAs, CBT may help; antispasmodics in some cases if postprandial cramp usually, fodmap diet classical presentation: pain relieved by diarrhoea with alternating diarrhoea and constipation; usually disease of under 40s so beware diagnosing in older people as may be a malignancy

Answer 118

weight loss, intermittent abdominal pain + bloating, chronic diarrhoea, failure to thrive; Gliadin is deaminated by tissue transglutaminase (tTG) It can then bind to APCs, which interact with CD4+ T cells, which then interact with B cells B cells create anti-endomysial and anti-TTG antibodies Gliadin also causes the release of IL-15/ IL-8 from enterocytes🡪 activating local immune response Crypt hyperplasia Villous atrophy Intraepithelial lymphocytosis Gluten free diet One-off pneumococcal vaccination There are 3 types of cancer associated with celiac disease: enteropathy-associated T-cell lymphoma (EATL), non-Hodgkin’s lymphoma, and adenocarcinoma of the small intestine

Answer 119

At least 6 months of recurrent abdominal pain plus 2 of: Relief by defecation Change in bowel habit Change in bowel frequency Also: urgency, bloating, mucus Management Conservative: fodmap diet, manage stress; regular meals, do not miss meals, restrict caffeine alcohol and fizzy drinks, limit high-fibre food 1st line: anti-motility (loperamide) 2nd: SSRI, amitryp

Answer 120

FODMAPs = fermentable Oligosaccharides, Monosaccharides, Disaccharides and Polyols; a group of dietary short-chain carbohydrates that are slowly absorbed in the small intestine or non-digestible due to inactivity or lack of hydrolases they have ability to induce abdominal symptoms when consumed at usual dietary amounts in patients with irritable bowel syndrome (IBS) and avoidance reduces symptoms Prebiotics are compounds in food that foster growth or activity of beneficial microorganisms such as bacteria and fungif FODMAPs are defined by their molecular size, absorptive characteristics in the small intestine and fermentability. Prebiotics are defined by their effects on microbiota and health, and are substrates that are selectively utilised by host microorganisms conferring a health benefit. Many dietary carbohydrates that have prebiotic actions are members of the FODMAP group of carbohydrates. This has led to fear-mongering that reducing FODMAP intake will lead to a dysbiotic gut microbiota with associated adverse health effects. Apart from reduced relative abundance of Bifidobacteria associated with extreme restriction of FODMAPs, changes to microbial communities have generally been overinterpreted and are not alarming

Answer 121

An infant delivered vaginally has colonization representative of the mother’s vaginal tract, including Lactobacillus, Prevotella, or Sneathia spp. Infants born via cesarean section have colonization more consistent with maternal skin and oral microbes Breast-fed infants have a microbiome predominantly consisting of Lactobacillus, Staphylococcus, and Bifidobacterium, whereas infants that are formula-fed have microbiomes consistent with Roseburia, Clostridium, and Anaerostipes An infant’s neonatal microbiome matures into a more complex one within the first year of life Weaning signals a significant change in diet, after which Proteobacteria become far less abundant. During childhood years the diversity increases as does the stability. By adolescence the gut microbiome does not yet resemble that of an adult but does show a shift toward an overall decrease in numbers of aerobes and facultative anaerobes, as well as concurrent increases in anaerobic species

Answer 122

Chronic watery diarrhoea 10% chronic diarrhoea cases, age 50-70y, women >men Associated with drugs (NSAIDs, PPIs) and coeliac disease Biopsy Lymphocytic colitis Collagenous colitis Management: stop offending drug, treat with budesonide

Answer 123

jejunum for digestion, and absorption of carbs, fats, and aa's; ileum for absorption of salt, fluids, bile salts, calcium, magnesium, B12 fat malabsorption: luminal (panc insufficiency, certain bacti inc bact overgrowth, zollinger-ellison), mucosal (giardia, coeliac), post-mucosal (radiotherapy, lymphoma, lymphangiectasis); longitudinal (short bowel syndrome) so again to be clear lymphoma can present as malabsorption if abdominal lymphoma when screening for malabsorption you might want to look for: MCV, CRP, B12, folate, ferritin, albumin, Ig, Mg, ALP, vit D, PTH; beware also def of fat soluble vits ADEK bacti and panc insuff both give fat malbsorb, but bacti make vit K so will have that in excess (also folate for same reason) but may have mg deficiency instead histologically similar to coeliac may be giardiasis, sibo, whipples; in first see little bug/specks in the lumen coeliac cant eat wheat, barley, rye; corn, potatoes, rice are okay exocrine panc insuff: most common causes are chronic panc and CF crohns and coeliac disease can also cause, and zollinger-ellison PERT to treat (+ for chronic panc endocrine replacement eg diabetes management, also pain management eg denervation of splanchnic nerves or gabaergic pain killers) faec elastase, TTG, CT abdo and pelvis; endoscopic uss best way to look at panc, MRCP also if you want to see the ducts; on uss panc will be hyperechoic, with parenchymal and ductal calcifications; histo see loss of lobular archtecture, lymphocytes, fibrosis - FNA as hard to biopsy alcohol, smoking, panc cancer, developmental duct problems cause also duct obstruction by things not cancer eg CF, trauma pancreatic exocrine insuff can be caused by coeliac disease due to altered CCK release

Answer 124

pathophysiology of intestinal lymphangiectasia is centered around the dilation of the lymphatic vessels in the intestinal mucosa, submucosa, and sometimes the mesentery which impedes the normal flow of lymph from the intestines back to the circulatory system overflow of lymphatic fluid into the intestines leads to the loss of lymphocytes, immunoglobulins, and proteins, causing lymphopenia, hypogammaglobulinemia, and hypoalbuminemia Chronic diarrhea and malabsorption are common symptoms. The loss of protein can lead to edema, particularly in the legs and abdomen, due to decreased oncotic pressure. Nutritional deficiencies may develop due to malabsorption, leading to growth retardation in children and weight loss in adults as well as fat soluble vit deficiency. Immune abnormalities resulting from lymphocyte loss can predispose patients to recurrent infections Diagnosis is through biopsy. The presence of hypoproteinemia, decreased blood lymphocytes, and decreased cholesterol support the diagnosis. Hypocalcemia (low calcium) is also seen due to poor absorption of vitamin D and calcium, and secondary to low protein binding of calcium In the case of primary intestinal lymphangiectasia, a diet of low-fat and high-protein aliments, supplemental calcium and certain vitamins has been shown to reduce symptom effects; diet must be continued for life to keep the symptoms under control. In some rare situations, surgery might be considered. small bowel transplant has been performed for people who did not respond to other treatments

Answer 125

causes of exocrine insuff may inc: acute pancreatitis chronic pancreatitis cystic fibrosis post gastric and/or pancreatic surgery pancreatic cancer other conditions such as diabetes mellitus, coeliac disease, Crohn's disease Steatorrhoea occurs when over 90% of normal enzyme secretion is lost - so is a severe/late stage finding creon is a brand of pancreatic enzyme replacement correct dose is that which successfully controls bowel symptoms and maintains good nutritional status recommended starting dose for adults is 2 x Creon® 25,000 per meal and 1 x Creon® 25,000 per snack; there are dosing guidelines for children too

Answer 126

Giardiasis: non-bloody. Recent travel to Spain. Can get malabsorption and lactose intolerance following infection. Metronidazole. E. coli Commonest cause of traveller’s diarrhoea; 3-4 days incubation (can be 1-10) 0157: shiga-toxin-producing. Contact with livestock. Kids>adults. think bloody diarrhoea, HUS Campylobacter: flu-like prodrome, diarrhoea may be bloody. Can cause GBS, reactive arthritis. 2-5 days incubation though up to 10 poss Amoebiasis (Entamoebia histolytica): bloody diarrhoea, incubation 2-4 weeks up to months. Stool microscopy: warmed or within 15 min. Liver abscesses with anchovy sauce. Metronidazole. Enteric fever: typhoid/paratyphoid: Salmonella (para)typhi. (Relative) bradycardia, abdominal pain+distension, CONSTIPATION, rose spots. Shigella: bloody diarrhoea. MSM. antibiotic-induced colitis and diarrhoea: pseudomembranous colitis Exotoxins: TcdB: disrupts tight junctions Due to CLINDAMYCIN, cephalosporins, co-amoxiclav Ix Raised WCC! C diff toxin (CDT) in stool Mx First line: oral metronidazole Second line/severe infection: vancomycin +/- metro Third line: faecal transplant

Answer 127

5 step approach to diarrhoea: 1. Does the patient really have diarrhea? Beware of fecal incontinence and impaction. 2. Rule out medications as a cause of diarrhea (drug-induced diarrhea). 3. Distinguish acute (<2 weeks, likely infectious) from chronic diarrhea. 4. Categorize the diarrhea as inflammatory, fatty, or watery. 5. Consider factitious diarrhea. for 2: key to diagnosing drug-induced diarrhea is to establish the temporal relationship between starting use of the drug and onset of diarrhea. The medications that most frequently cause diarrhea include antacids and nutritional supplements that contain magnesium, antibiotics, proton pump inhibitors, selective serotonin reuptake inhibitors, and nonsteroidal anti-inflammatory drugs for 4: Inflammatory diarrhea is characterized by frequent, small-volume, bloody stools and may be accompanied by tenesmus, fever, or severe abdominal pain. Inflammatory diarrhea is suspected with the demonstration of leukocytes or leukocyte proteins (eg, calprotectin or lactoferrin) on stool examination. Other laboratory studies that may indicate an inflammatory diarrhea include elevated C-reactive protein level or sedimentation rate and low serum albumin level. Inflammatory diarrhea fundamentally indicates disrupted and inflamed mucosa, such as that caused by idiopathic inflammatory bowel disease (Crohn disease or ulcerative colitis), ischemic colitis, and infectious processes, such as C difficile, cytomegalovirus, tuberculosis, or Entamoeba histolytica. Radiation colitis and neoplasia are uncommon causes of inflammatory diarrhea. When history or stool analysis suggests chronic inflammatory diarrhea, flexible sigmoidoscopy or colonoscopy should be the initial study to look for structural changes Fatty stools are suggested by a history of weight loss, greasy or bulky stools that are difficult to flush, and oil in the toilet bowl that requires a brush to remove; suggest malabsorption or maldigestion, with malabsorption is caused by mucosal diseases, most commonly celiac disease, whereas the maldigestion results from pancreatic exocrine insufficiency (eg, chronic pancreatitis) or inadequate duodenal bile acid concentration (eg, small intestinal bacterial overgrowth [SIBO] or cirrhosis); test for coeliac inc OGD and biopsy, consider H breath test and CT looking at pancreas, can try empiric creon trial Watery diarrhea can be further classified as osmotic or secretory in origin. Osmotic diarrhea is due to the ingestion of poorly absorbed ions or sugars. Secretory diarrhea is due to disruption of epithelial electrolyte transport. Two ways to distinguish an osmotic from a secretory process is by response to fasting and calculating the fecal osmotic gap. An essential characteristic of osmotic diarrhea is that stool volume decreases with fasting, whereas secretory diarrhea typically continues unabated with fasting. Another way to clinically differentiate osmotic diarrhea from secretory diarrhea is by calculating the fecal osmotic gap. The fecal osmotic gap is calculated by adding the stool sodium and potassium concentration, multiplying by 2, and subtracting this amount from 290 mmol/L. Measured stool osmolality should not be used because it largely reflects bacterial metabolism in vitro, not intraluminal osmolality. A fecal osmotic gap greater than 50 mmol/L suggests an osmotic cause for diarrhea, whereas a gap less than 50 mmol/L supports a secretory origin. Osmotic diarrhea is usually due to ingestion of poorly absorbed cations (eg, magnesium) or anions (eg, phosphate, or sulfate), which are often contained in laxatives and antacids, or to carbohydrate malabsorption from ingestion of poorly absorbed sugars or sugar alcohols (eg, sorbitol or xylitol). Lactose intolerance is by far the most common type of carbohydrate malabsorption; most common cause of secretory diarrhea is infectious, however if chronic need to consider bile acid malabsorption, IBD, peptide-secreting endocrine tumors (eg, carcinoid or gastrinoma), neoplasia (carcinoma, lymphoma), disordered regulation (neuropathy inc diabetic, post-vagatomy etc), addisons, mastocytosis, hyperthyroidism note you can calculate faecal osmotic gap: raised is osmotic, low is secretory, normal is functional; stool pH is useful for osmotic as if low then is carbohydrate malabsorption (broken into fatty acids by gut bacteria) 5: factitious diarrhoea due to laxative ingestion, suspect if no diagnosis after thorough investigation; note may be accidental eg senna is in some herbal teas, so ask about diet including drinks and supplements; also consider functional ie IBS and trial FODMAP diet, if no improvement test for coeliac

Answer 128

FH of bowel/ovarian cancer, >60 + change in bowel habit (looser, more freq), rectal bleeding entamoeba can give abscesses in liver, brain; pinkish large macro looking cells embedded among other cells is the amoeba itself diarrhoea >7 days think giardia, cryptosporidium CMV can cause diarrhoea if immunosupd; microscopic colitis esp if elderly! dont forget public health notification

Answer 129

intestinal insuff: reduction in absorptive capacity not needing iv supp; intestinal failure when do need iv supp eg short bowel (esp <1m), obstruction, dysmotility (scleroderma, hirchsprungs, radiation), parenchymal disease (crohns, coeliac, autoimmune enteropathy, radiation enteritis etc) high output stoma produces more than 1500ml effluent per day complications of parenteral nutrition: local infection, septicaemia, renal failure from repeat AKI, liver disease (IFALD), micronut def/excess, hyperglycemia

Answer 130

vomiting - low Na, K, CL persistent vomiting - hypochloraemic hypokalaemic metabolic alkalosis; may also be signs of dehydration (raised urea, hypernat) malabsorption - low fe, ca, phos, ADEK, ferritin, albumin, folate, raised ALP and INR (vit K) diarrhoea - hypo/hypernat poss, initially hyperkal due to bicarb loss so met acidosis, but later falls congenital chloridorrhoea - abnorm cl absorption in ileum gives low plasma cl and K, high plasme HCO3, confirmed with low urinary cl, excessive faecal cl (normal is 5-15mmol/l); get growth and dev delay and treat with KCl

Answer 131

abetalipoproteinaemia blood film will show acanthocytosis (also seen post splenectomy) - this the ret pig may be sec to vit E def caused by defect in apoprotein B production giving defective LDL, VLDL, chylomicron synthesis and failure of lipid transport from intestine and liver, thus fat malabsorption and along with that vit ADEK def cholesterol and triglyc levels will be v low, INR raised etc replace lipids and vitamins to treat

Answer 132

acute: usually viral gastroent (esp rotavirus, norovirus); bacti infections suggested by high fever and bloody/pussy/mucousy stool (campylobacter, shigella, salmonella); may be antibiotic associated (as side effect), rarely c diff; may be lactose or cows milk intolerance or food allergy; malabsorption (CF, coeliac); inflam (crohns, UC); constipation with overflow, HUS, toddlers diarrhoea, hyperthyroidism, ischaemia from intussusception, volvulus etc, HSP assess for dehydration; pain shouldnt be focal or increase on palp; animal exposure (camp), travel (e coli), swimming (parasite or ameoba) admit if dehydration severe, systemically quite unwell, intractable or bilious vomiting, acute onset painful and bloody; suspect HUS or sepsis; inadequate response or cant take ORS; continue regular feeds, ors if at risk of or has dehydration; avoid giving solid food until rehydrated, discourage fruit juice and carbonation until stopped; if suspect bacti cause can send stool sample for culture and sensitivity stop spread by ensuring washing of hands (and potties), cleaning door handles etc, wash soiled linen separate from other clothes at 60deg; no school or socialising outside home until 48hrs after last episode of d&v vomiting usually 1-2 days, diarrhoea usually 5-7 and stops in a couple of weeks; follow up if symptoms change; if doesnt resolve then c&s notifiable diseases: bacti, protazoa, amoeba diarrhoea, HUS, enteric fever (typhoid, paratyphoid), cholera antibiotic advice from local health protection team

Answer 133

>2 weeks well child with no weight loss: toddlers diarrhoea (usually in second year of life, undigested food eg peas or carrots in stool, resolves by 4 years); breast fed babies oft have liquid stools, doesnt need investigating if baby otherwise well and thriving unwell with weight loss: food intolerance, panc insuff, coeliac, short bowel syndrome, inborn error of digestion, giardiasis, drugs eg laxatives, hyperthyroid, chronic infection stool MC&S, sweat test, faecal calprotectin (IBD), coeliac investigation, basic bloods, may need endoscopy or barium follow through

Answer 134

vomiting, hypotension, thrombocytopenia, temp instability, apnoeas, lethargy antenatal doppler report may exist of reversed end-diastolic flow

Answer 135

Spontaneous intestinal perforation of the newborn, also known as focal intestinal perforation or isolated perforation, is a single intestinal perforation typically occurring at the terminal ileum. It is a life-threatening condition that affects very low birth weight infants (birth weight <1500 g) Infants present with acute onset of abdominal distension. A blue-black discoloration of the abdominal wall may be seen. As the condition progresses, metabolic acidosis and systemic signs, including tachycardia and hypotension, may be evident Laboratory findings are usually non-specific and may include: Leukocytosis Anemia Thrombocytopenia Elevated liver function tests, including serum alkaline phosphatase and bilirubin levels Diagnosis of spontaneous intestinal perforation can be confirmed by the typical radiographic findings of pneumoperitoneum Spontaneous intestinal perforation appears earlier in life than necrotizing enterocolitis. The median age of presentation for spontaneous intestinal perforation is seven days compared to 14 days for necrotizing enterocolitis. In general, infants with spontaneous intestinal perforation are significantly more premature and have a smaller birth weight than infants with necrotizing enterocolitis. Antenatal infection and medications have been reported as risk factors for developing spontaneous intestinal perforation. Early enteral feeding has been associated with necrotizing enterocolitis, whereas early feeding with colostrum and breast milk has reduced the incidence of spontaneous intestinal perforation. Spontaneous intestinal perforation usually presents with acute abdominal distension and bluish-black discoloration of the abdomen, whereas necrotizing enterocolitis usually presents will initial signs such as emesis, bloody stools, and abdominal wall oedema, crepitus, and induration. While necrotizing enterocolitis usually presents with radiographic findings such as pneumatosis intestinalis, portal venous air, thickening of the intestinal wall, and fixed dilated small bowel loops, the typical radiographic finding of spontaneous intestinal perforation involves pneumoperitoneum. On histopathologic exam, coagulative necrosis is observed in cases of necrotizing enterocolitis, whereas isolated hemorrhagic necrosis is the typical finding in spontaneous intestinal perforation. Necrotizing enterocolitis involves a variable degree of inflammation and ischemia of the bowel with extensive peritoneal contamination and bacterial translocation, whereas spontaneous intestinal perforation involves a focal area of perforation with normal-appearing proximal and distal intestines All enteral feeds and medications must be discontinued, and a nasogastric tube or orogastric tube must be inserted at low intermittent or continuous suctioning to decompress the abdomen. Total parenteral nutrition must be started In cases of hypotension, inotropic medications should be started. Intravenous empiric antibiotics should be initiated Laparotomy with resection of the affected intestine and creation of a stoma is the traditional surgical approach

Answer 136

Gram positive anaerobe that can be spread via spores ◦ Diarrhoea (≥3 x T5-7 stools per day) ◦ May be described as foul smelling/green-yellow in colour ◦ Known use of recent or recurrent antibiotics ◦ Typical antibiotic associations are Clarithromycin, Clindamycin, Ciprofloxacin, Co-amoxiclav key signs: ◦ Observations – fevers, tachycardia/hypotension (if severe/dehydrated) ◦ Dry mucous membranes ◦ Abdominal tenderness on palpation or they may have a tense/distended abdomen, if there is an ileus investigations: ◦ Bloods (Hb/WCC/CRP/U&Es/LFTs…) ◦ Stool cultures (stating a request for C. difficile) ◦ GDH+ / toxin –ive = equivocal result, may have previously had it ◦ GDH + / toxin +ive = need to treat (currently have it) ◦ Imaging may be appropriate = AXR/CT severity: ◦ Mild = WCC not typically raised, usually <3 per day (T5-7) ◦ Moderate = WCC may be raised, but usually <15, with around 3-5 motions per day ◦ Severe = Significantly raised WCC (>15), temperature >38.5, acute rising creatinine (>50% in baseline creatinine)… ◦ Life-threatening = Hypotension, signs of complete ileus/toxic megacolon management: ◦ Discontinue all unnecessary antibiotics, PPIs ◦ Low threshold for imaging (CT/AXR) to look for any signs of megacolon/obstruction ◦ If stool is confirmed as positive + moderate severity = start Metronidazole 400mg PO TDS for 10-14 days ◦ If this fails/relapse/severe signs = Vancomycin 125mg PO QDS for 10-14 days ◦ If no oral route is available = 500mg Metronidazole IV TDS ◦ Continued failure = Fidaxomicin or Faecal transplant

Answer 137

admit, stool culture x3, IV/rectal steroids, DVT prophylaxis, stool chart, daily AXR, flexible sigmoidoscopy within 24 hrs besides IBD inc infectious colitis; colitis caused by methotrexate, TNFa antagonists

Answer 138

fever, flushed skin, headache, itchiness, blurred vision, palpitations or tachycardia, breathlessness or wheeze (in severe cases - may also have distributive shock) abdominal cramps, and diarrhoea, usually onset 10-20 mins after eating; may develop florid erythema due to histamine toxicity from eating food with large amount of histamine in it comes from fish including common fish like tuna, that hasn't been processed properly antihistamines help sx resolve quickly - want H1 and H2 blockade (eg chlorphenamine and ranitidine); if shock, bronchospasm, or airway oedema then treat as anaphylaxis with adr

Answer 139

collection of indigestible material, may be made up of undigested milk proteins or eg hair (in trichotillomania, oft in adolescent girls and poss psych disturbance) important as may result in obstruction, and should form part of differential for obstruction

Answer 140

M>F may present as: delay in passing meconium in first 24hrs, intermittent bowel obstruction or chronic constipation, failure to thrive, severe enterocolitis which may perforate can be a short segment or more extensive involvement anal canal and rectum usually free of faeces rectal biopsy may find absence of ganglion cells, and nerve fibres may be abnormally prominent internal anal sphincter always involved defunctioning colostomy, remove aganglionic segment, pull-through repair at older age

Answer 141

70 calories, 1.1g protein, casein:whey ratio 3:7, fat 4.2g, sodium 15mg, potassium 60mg, phosphorous 15mg, calcium 35mg note cows milk has more of all ions + protein, less fat and 67 calories, much higher casein:whey ratio (ie whey is main protein in breast milk, more digestible and less curdle prone than cows milk casein other proteins in breast milk inc IgA, IgM, lysozyme, lactoferrin, lactalbumin milk at end of feed (hindmilk) contains more fat than foremilk breast milk has less vit K but more vits ACE than cows milk colostrum is milk made in first 48 hrs after birth and is straw coloured, more protein and less carbs/fat low iron and vit content means defer cows milk until 1 yr; 1mo infant needs 100kcal/kg/day and standard cows milk formula has 100kcal/100ml

Answer 142

recomended to breastfeed for first 6mo of life: Breastfeeding has been linked to reduced infections in the neonatal period, better cognitive development, lower risk of certain conditions (obesity) later in life and a reduced risk of sudden infant death syndrome On formula feed, babies should receive around 150ml of milk per kg of body weight. Preterm and underweight babies may require larger volumes Acceptable for breast fed babies to lose up to 10% and formula fed babies to loose up to 5% of their body weight by day 5 of life. They should be back at their birth weight by day 10. most common cause of excessive weight loss or not regaining weight is dehydration due to under feeding, weaning usually starts at 6mo

Answer 143

breast pain, nipple pain, true or perceived reduced milk supply; latter perceived may be insuff breast access (giving short infreq feeds or sometimes giving dummy or other milk sources), mat dep/anx/stress may cause dec response to infant feeding cues so infreq feeding so reduced stim for milk production; ineff infant positioning (feeds >every 2 hours, for <5mins or >40mins; true reduced supply due to prolactin production def (drugs, thyroid/eating disorders) breastfeeding specialist should observe feeding also consider infant factors: developmental, illness

Answer 144

maternal: untreated TB, hep sag+ve, amiodarone, cytotoxics, indometacin, lithium, tetracyclines, theophylline, colchicine, senna, carbimazole, chloramphenicol, dapsone, thiouracil, sulphonamides, maternal HIV neonatal: cleft palate/lip, IEM

Answer 145

<3 stools a week, rabbit dropping stool, overflow soiling in children >1yo (bad smell, loose, may be thick and sticky or dry and flaky and passed w/o awareness); bleeding associated hard stool, pain or distress passing stool, straining; poor appetite improved after passing stool, waxing/waning abdo pain with stool faecal impaction if combo of severe constipation +/- overlow stool +/- abdo mass - dre not routinely recommended rule out red flags: during first weeks of life or delay in passing meconium (hirchsprungs, CF), abdo distension + vomiting (hirchsprungs, obstruction), FH of hirchsprungs, ribbon stool pattern (anal stenosis), leg weakness (tone, gait, power, reflex) or motor delay (neuro origin), abnormal appearance of anus, signs of spina bifida (inc naevus), scoliosis, glut muscle assym rule out amber flags (need specialist referral but not urgent, can commence treatment while waiting): faltering growth or dev delay (coeliac, hypothyroid, CF), constipation triggered by cows milk (allergy), signs of child mistreatment check for psychosocial causes (stress eg new school, change in family circumstances, fears/phobias) if ruled these and medication induced causes out, may be idiopathic may have perianal strep infection causing if erythema around anus double check for impaction, then prescribe laxative (macrogol) and give diet and lifestyle advice inc schedule toileting attempts, toilet diary, rewards system for going etc depending on the child, physical activity, recommended daily fluid intake levels impaction: may inc symptoms initially, review in a week, give movicol for 2wks, then add stimulant lax; if not tolerated go straight to stim lax (eg senna), with stool softener (lactulose, docusate) if stools hard similar treatments but half dose if no impaction, reduce dose if get diarrhoea (risk of hypokal), continue for up to months until soft consistent stool achieved; follow up in both cases to check adherence, check for reimpaction, use bristol stool chart, reduce laxatives gradually stopping one at a time refer if flags or cant shift impaction, child distressed, not responding to treatment in general after 3mo, or after 4 wks if <1yo (hirchsprung exclusion)

Answer 146

1 per 10,000 births, most diagnosed by age two; 2:1 men:women neonatally may present with obstruction, no meconium in 48 hrs, repeated vomiting; older infants and children may have constipation that's hard to treat: abdo discomfort, early satiety, poor weight gain may develop eneterocolitis (pain, fever, d&v - d possibly blood stained, v possibly bilious) which can give necrosis, perf, sepsis neonatally main differential is meconium ileus (prob CF) AXR (w/contrast), biopsy to confirm diagnosis; surgery, while waiting maybe ng tube decompression, bowel washouts, and if enterocolitis antibiotics and fluid resus

Answer 147

Surgical management for idiopathic constipation is reserved for those patients who are refractory to medical management proposed algorithm that starts with less invasive procedures, such as Botox injection for suspected anal sphincter dysfunction, and progresses stepwise toward more invasive procedures, including antegrade enemas, temporary diversion, and bowel resection. 38 Permanent diversion is reserved as an option of last resort If identified by ARM, IAS hypertonicity and/or achalasia should be treated. Children with idiopathic constipation have a normal IAS resting pressure and RAIR, but have increased sphincter thickness, frequency, and amplitude of IAS contraction—possibly due to the constant stimulus of stool in the rectum—which may perpetuate the vicious cycle of fecal retention and difficult defecation; botox injection very helpful here, and though the effect of Botox is transient, usually lasting 6 months, the symptomatic improvement can last indefinitely, which may be due to Botox leading to improved evacuation and diminished rectal distention, thereby allowing recovery of normal rectal sensation and motor function next step or if no sphincter problem/voluntary withholding then antegrade colonic enema aka ACE: laparoscope is placed through the umbilicus and the cecum is accessed colonoscopically to provide a route for administration of antegrade enemas Intestinal diversion, either via ileostomy or colostomy, can be very effective in relieving symptoms of constipation. Though permanent intestinal diversion is considered by many to be a last resort, temporary diversion may be beneficial in select patients. This may be especially true for patients with marked pan-colonic dilatation, in whom ACE is unlikely to be effective. Some studies also suggest that temporary diversion is superior to ACE in younger children (<5 years of age) since ACE requires a cooperative and compliant patient; Like ACE, temporary diversion can decrease colonic dilatation and improve colonic motility, with many children successfully reestablishing intestinal continuity may consider colorectal resection with primary reanastomosis; especially useful to remove megacolon from dilation after large amount of stool retained in eg hirschprungs or if manometry demonstrates an area of colon that isn't functioning properly

Answer 148

Gastroenteritis main risk is severe dehydration most common cause is rotavirus - typically accompanied by fever and vomiting for the first 2 days. The diarrhoea may last up to a week treatment is rehydration Chronic diarrhoea Infants most common cause in the developed world is cows' milk intolerance toddler diarrhoea: stools vary in consistency, often contain undigested food; affected children have three or more watery loose stools (bowel motions) per day but they can have more than 10 episodes a day. The stools are often smellier and more pale than usual; child with toddler's diarrhoea is otherwise well, grows normally and behaves normally. Examination does not find any abnormalities. Symptoms usually settle by the age of 5-6; It is thought that the balance of fluid, fibre, undigested sugars and other undigested foods that reach the colon may be upset in affected children. This can increase the amount of fluid (water) that is kept in the colon - it is not due to malabsorption or food intolerance, and resolves as colon becomes more efficient; reduce sugary drinks and sweets, ensure not drinking too much; fat slows colonic transit speed so giving a small amount of a high fat food at the end of a meal can help to reduce loose stools e.g. yogurt, ice-cream, full fat mousse and other dairy desserts, full fat milk or even a cube of cheese;a lower fibre and higher fat diet is usually needed while your child is experiencing loose stools and they should grow out of toddler diarrhoea by 4 – 5 years. The recommended healthy diet for children of 5 years and over is to have plenty of fibre and not eat too much fat; if changes not working after a month and still BO >2x a day may need further paeds workup for chronic diarrhoea coeliac disease post-gastroenteritis lactose intolerance For the last one: a common complication of viral gastroenteritis, seen weeks after the infection. Removal of lactose from the diet for a few months followed by a gradual reintroduction usually resolves the problem

Answer 149

majority of benign intussuscepion 6-24mo, if older or enlarged liver must consider enlarged mesenteric nodes or eg cancer commonest benign intuss is ileum into caecum/ascending colon - may give pseudokidney sign LDH raised high big indicator of lymphoid malignancy, but may be haem anaem, acute panc, heart failure, infection and more very non specific at low levels children acutely AXR and USS; then progress to CT (high radiation burden so dont dish out as readily as for adults) children always get oral/IV contrast for CT

Answer 150

bone marrow trephine and biopsy of mass -from mass flow cytometry best as get diagnosis rapidly (2hours); other methods take longer -histo may see mass of lymphocytes giving starry sky appearance (indicates rapid turnover) -B cell (CD20+), germinal centre (CD10+), high proliferation index (so fast growth rate), c-myc positive (and prove translocation) -marrow filled with tumourous B cells (Intrabdo with intuss, and rapidly growing neck mass, are two commonest ways burkitt lymphoma presents) initially give iv steroids then chemo (watch for tumour lysis syndrome)

Answer 151

obstruction, ascites, enlarged organ (inc haemangiomas and tumours)

Answer 152

viral URTI oft precedes intussusception; therapeutic enema, surgery if fails or its perforated

Answer 153

a congenital diverticulum of the small intestine. It is a remnant of the omphalomesenteric duct (also called the vitellointestinal duct) and contains ectopic ileal, gastric or pancreatic mucosa. . Rule of 2s occurs in 2% of the population is 2 feet from the ileocaecal valve is 2 inches long Presentation (usually asymptomatic) abdominal pain mimicking appendicitis rectal bleeding Meckel's diverticulum is the most common cause of painless massive GI bleeding requiring a transfusion in children between the ages of 1 and 2 years intestinal obstruction secondary to an omphalomesenteric band (most commonly), volvulus and intussusception Investigation if the child is haemodynamically stable with less severe or intermittent bleeding then a 'Meckel's scan' should be considered uses 99m technetium pertechnetate, which has an affinity for gastric mucosa mesenteric arteriography may also be used in more severe cases e.g. transfusion is required Management removal if narrow neck or symptomatic options are between wedge excision or formal small bowel resection and anastomosis Pathophysiology normally, in the foetus, there is an attachment between the vitellointestinal duct and the yolk sac. This disappears at 6 weeks gestation the tip is free in the majority of cases associated with enterocystomas, umbilical sinuses, and omphaloileal fistulas. arterial supply: omphalomesenteric artery. typically lined by ileal mucosa but ectopic gastric mucosa can occur, with the risk of peptic ulceration. Pancreatic and jejunal mucosa can also occur.

Answer 154

occurs in around 3-6% of all children and typically presents in the first 3 months of life in formula-fed infants, or around 7mo when formula is introduced; rarely it is seen in exclusively breastfed infants via mums diet Both immediate (IgE mediated) and delayed (non-IgE mediated) reactions are seen. The term CMPA is usually used for immediate reactions and CMPI for mild-moderate delayed reactions. IgE mediated reaction within 2 hours with stridor, angio-oedema, pruritus, erythema, urticaria, vomiting, diarrhoea, sneezing, anaphylaxis, and skin prick and IgE RAST positive; non-IgE mediated >2 hours, sometimes up to 48 hrs, mediated by T cells, diarrhoea or constipation with bloody stools and abdo pain, faltering growth, pruritus, erythema, and atopic eczema with skin prick and IgE RAST usually negative Features regurgitation and vomiting diarrhoea urticaria, atopic eczema 'colic' symptoms: irritability, crying, 3 hours a day at least 3 days a week for at least 3 weeks wheeze, chronic cough rarely angioedema and anaphylaxis may occur Investigations include: skin prick testing - results immediately. but suppressed ir recent antihistamine, topic steroid, beta blocker, TCA use total IgE and specific IgE (RAST) for cow's milk protein - days to weeks to come back, can be used if equivocal results from skin prick note both tests confirm antibodies which suggests sensitisation only, needs to be combined with history to confirm allergy If the results of allergy testing do not correspond with the clinical history, or the history is equivocal, an oral food challenge in a supervised setting may be needed to confirm the diagnosis if non IgE medaiated eliminate cows milk from mother diets or switch to eHF/AAF for 2-4 weeks, see if sx improve, then reintroduce and see if they return; if they disappear and return this confirms the diagnosis if sx don't disappear either consider different ddx +/- refer to paeds, or if think it may be CMPA still then trial AAF and refer to allergy clinic Management if formula-fed extensive hydrolysed formula (eHF) milk is the first-line replacement formula for infants with mild-moderate symptoms amino acid-based formula (AAF) in infants with severe CMPA or if no response to eHF around 10% of infants are also intolerant to soya milk Management if breastfed continue breastfeeding eliminate cow's milk protein from maternal diet. Consider prescribing calcium supplements for breastfeeding mothers whose babies have, or are suspected to have, CMPI, to prevent deficiency whilst they exclude dairy from their diet; and for all refer to dietician for advice on what to eat use eHF milk when breastfeeding stops, until 12 months of age and at least for 6 months other types of milk are nutritionally poor so shouldnt be uced, and rice milk shouldn't be used by any kids <4.5yo due to arsenic content CMPI usually resolves in most children in children with IgE mediated intolerance around 55% will be milk tolerant by the age of 5 years in children with non-IgE mediated intolerance most children (80-90%) will be milk tolerant by the age of 3 years a challenge is often performed in the hospital setting as anaphylaxis can occur; otherwise gradually reintroduce at term

Answer 155

Intolerance to carbohydrates is the most common type of non-immune-mediated adverse food reaction Symptoms of intolerance to carbohydrates are primarily due to deficiency of enzymes or transporters or overloading of a transport system located on the brush border of the epithelium; Non-absorbed carbohydrates in the intestinal tract drive fluids into the lumen through an osmotic force, causing osmotic diarrhea. Moreover, non-absorbed carbohydrates are fermented by gut microbiota to gas and produce a lowered stool pH sx such as distension of the small bowel, non-focal abdominal pain associated with bloating and flatulence, nausea, increased gut motility, and diarrhea; Extraintestinal symptoms, such as headache, vertigo, memory impairment, and lethargy have been described in less than 20% of subjects with carbohydrate intolerance and may be due to altered cell signalling from toxic metabolites congenital sucrase-isomaltase deficiency means can't properly absorb sucrose/starch, so sx normally on weaning, needs low sucrose diet; genetic testing can confirm glucose-galactose malabsorption have problem with a Na-gluc co-transporter, and have life threatening chronic diarrhoea, onset soon after birth, with reducing substances in stool, which doesn't improve on lactose free and aa based formula; genetic analysis of SLC5A1 to confirm lactose intolerance may be congenital, secondary (after gastroent, coeliac, crohns, radiation colitis, SIBO), or adult-type (lactase activity decreases around 2-4yo - this is the common type); breath testing to confirm, also used for sorbitol and fructose intolerances; cut out lactose for 2-4 weeks for sx to remit then re-introduce small amounts to find tolerance, often eg 1 cup of milk equiv would be okay; otherwise avoid lactose products, or try eg lactase tablets available otc breath test process: fast from food and drink for 12 hours, then 5 mins before get breath baseline H2 level, then give a dose of the sugar in question, collect breath at 20min intervals for 2 hours and monitor H2 and CH4 levels, looking for two fold increase across 3 samples or increase by more than a specific value also can have FODMAPs intolerance (Fermentable oligosaccharides, disaccharides, monosaccharides, and polyols) which include lactose and fructose but also fructans, galactans, and polyols; paediatric dietician to guide elimination diet for 4-6 weeks, then re-introduction of specific groups to liberalise diet as much as possible

Answer 156

class I (sensitisation to antigens in the gut, giving sx like IgE and non-IgE mediated CMPA in response to food exposure) and class II (IgE against pollen with cross reaction in the mouth/throat against botanically similar foods) history inc possible triggers, personal and family atopy, sx (inc onset speed, type, frequency, repeatability), any response to elimination or re-introduction, and weaning details examine for growth (height, weight, head circ), signs of malnutrition, and any signs of atopy IgE mediated needs skin prick or RAST test in allergy clinic; if non-IgE suspected then eliminate for 2-6 weeks then re-introduce (with dietician support); skin prick 3mm greater than control usually considered positive common triggers are egg, nuts, sesame, fish, shellfish, wheat, soya, kiwi Some food allergies (i.e. milk and egg) have a good prognosis with between 40-90 % of children ‘growing out’ of these allergies between 1 and 5 years of age (3-5). Other food allergies (i.e. peanuts, tree nuts and sesame) have a poorer prognosis and tolerance to these foods is achieved in only the minority of children mild acute reaction give cetirizine or chlorphenamine and can go home from ED, if mod-severe then mx as anaphylaxsis any child who has had anaphylaxis, or has a nut allergy and asthma, or seems to have unstable symptoms, or appear sensitive to very small amounts of a food, should be given 2 adrenaline auto-injectors and school should be informed Egg allergy is unique in that 70 to 80 percent of egg-allergic patients may tolerate egg that has undergone extensive baking and are thus able to consume baked egg in pastries, breads, and cakes. Ovalbumin in particular is broken down and not able to bind IgE after such heating. However, ovomucoid is heat-stable, and patients who are allergic to ovomucoid tend to not tolerate baked egg. One study noted that patients who were baked-egg tolerant and regularly consumed baked egg were able to tolerate all forms of egg faster than those who could not tolerate baked egg. class II: oral allergy syndrome often in ppl with hayfever; most common reaction is an itching or burning sensation in the lips, mouth, ear canal, or pharynx. Sometimes other reactions can be triggered in the eyes, nose, and skin. Swelling of the lips, tongue, and uvula, and a sensation of tightness in the throat may be observed. Once the allergen reaches the stomach, it is broken down by the acid, and the allergic reaction does not progress further grass pollen: figs, tomatoes, melons, oranges and peaches birch pollen: apples, pears, and most berries and fruits alder pollen: as above other pollen types too latex: kiwi, avocado, banana, and some others

Answer 157

lack of dietary fibre, impaired colonic motility, mechanical intestinal obstruction, impaired rectal sensation impairing the process of defecation. Constipation is common in irritable bowel syndrome. Other important causes include colorectal cancer, hypothyroidism, hypercalcaemia, drugs (opiates, iron) and immobility (Parkinson’s disease, stroke). Absolute constipation (no flatus or bowel movements) suggests intestinal obstruction and is usually associated with pain, vomiting and distension. Tenesmus suggests rectal inflammation or tumour.

Answer 158

Look for 2+ of the following: Child < 1 year Child > 1 year Stool pattern Fewer than 3 complete stools per week (type 3 or 4 on Bristol Stool Form Scale) (this does not apply to exclusively breastfed babies after 6 weeks of age) Hard large stool 'Rabbit droppings' (type 1) Fewer than 3 complete stools per week (type 3 or 4) Overflow soiling (commonly very loose, very smelly, stool passed without sensation) 'Rabbit droppings' (type 1) Large, infrequent stools that can block the toilet Symptoms associated with defecation Distress on passing stool Bleeding associated with hard stool Straining Poor appetite that improves with passage of large stool Waxing and waning of abdominal pain with passage of stool Evidence of retentive posturing: typical straight-legged, tiptoed, back arching posture Straining Anal pain History Previous episode(s) of constipation Previous or current anal fissure Previous episode(s) of constipation Previous or current anal fissure Painful bowel movements and bleeding associated with hard stools

Answer 159

Look for 2+ of the following: Child < 1 year Child > 1 year Stool pattern Fewer than 3 complete stools per week (type 3 or 4 on Bristol Stool Form Scale) (this does not apply to exclusively breastfed babies after 6 weeks of age) Hard large stool 'Rabbit droppings' (type 1) Fewer than 3 complete stools per week (type 3 or 4) Overflow soiling (commonly very loose, very smelly, stool passed without sensation) 'Rabbit droppings' (type 1) Large, infrequent stools that can block the toilet Symptoms associated with defecation Distress on passing stool Bleeding associated with hard stool Straining Poor appetite that improves with passage of large stool Waxing and waning of abdominal pain with passage of stool Evidence of retentive posturing: typical straight-legged, tiptoed, back arching posture Straining Anal pain History Previous episode(s) of constipation Previous or current anal fissure Previous episode(s) of constipation Previous or current anal fissure Painful bowel movements and bleeding associated with hard stools

Answer 160

Usually idiopathic but could be: dehydration low-fibre diet medications: e.g. Opiates anal fissure over-enthusiastic potty training hypothyroidism Hirschsprung's disease hypercalcaemia learning disabilities Exclude secondary causes (can be enough to have no red/amber flags in the hx) Indicates idiopathic constipation 'Red flag' suggesting underlying disorder Timing Starts after a few weeks of life Obvious precipitating factors coinciding with the start of symptoms: fissure, change of diet, timing of potty/toilet training or acute events such as infections, moving house, starting nursery/school, fears and phobias, major change in family, taking medicines Reported from birth or first few weeks of life Passage of meconium < 48 hours > 48 hours Growth Generally well, weight and height within normal limits, fit and active Faltering growth is an amber flag Neuro/locomotor No neurological problems in legs, normal locomotor development Previously unknown or undiagnosed weakness in legs, locomotor delay Rule out impaction: overflow soiling faecal mass palpable in the abdomen

Answer 161

If faecal impaction is present polyethylene glycol 3350 + electrolytes (Movicol Paediatric Plain) using an escalating dose regimen as the first-line treatment add a stimulant laxative if Movicol Paediatric Plain does not lead to disimpaction after 2 weeks substitute a stimulant laxative singly or in combination with an osmotic laxative such as lactulose if Movicol Paediatric Plain is not tolerated inform families that disimpaction treatment can initially increase symptoms of soiling and abdominal pain Maintenance therapy very similar to the above regime, with obvious adjustments to the starting dose, i.e. first-line: Movicol Paediatric Plain add a stimulant laxative if no response substitute a stimulant laxative if Movicol Paediatric Plain is not tolerated. Add another laxative such as lactulose or docusate if stools are hard continue medication at maintenance dose for several weeks after regular bowel habit is established, then reduce the dose gradually General points do not use dietary interventions alone as first-line treatment although ensure the child is having adequate fluid and fibre intake consider regular toileting and non-punitive behavioural interventions for all children consider asking the Health Visitor or Paediatric Continence Advisor to help support the parents. The NICE guidelines do not specifically discuss the management of a very young child. The following recommendations are largely based on the old Clinical Knowledge Summaries recommendations. Infants not yet weaned (usually < 6 months) bottle-fed infants: give extra water in between feeds. Try gentle abdominal massage and bicycling the infant's legs breast-fed infants: constipation is unusual and organic causes should be considered Infants who have or are being weaned offer extra water, diluted fruit juice and fruits if not effective consider adding lactulose

Answer 162

when to admit? Suspect and confirm faecal impaction through: History of soiling, bowels not opening despite active treatment Palpable stools on abdominal examination Dilated rectum with large amount of stool if rectal examination done. (An abdominal X-ray may be needed in those in which faecal impaction is suspected but a physical examination is unreliable or who are difficult to examine. (e.g. autism) Has first-line outpatient oral disimpaction therapy proved unsuccessful? (e.g. Movicol escalation regime +/- combination therapy). Check compliance. Consider appropriate limited enema therapy either as day case (or Inpatient (after counselling and consent) followed by re-trial of first line disimpaction course. Arrange ward admission (NOT suitable for outpatient) o Check for contraindications o Liase with GI lead consultant for admission plan Then give enema and klean-prep: Usually via NGT, Consider Ondansetron if the patient experiences nausea, Avoid directly mixing macrogol-based laxatives with starch-based thickeners (ie stop movicol if theyre on it); Klean-Prep contains aspartame, which is metabolised to phenylalanine. This may be relevant when treating patients suffering from phenylketonuria.  Hypovolemia should be corrected before administration of bowel cleansing preparations and adequate hydration should be maintained during treatment; contraind if perf, megacolon, CHF, phenylketonuria No solid food for 2 hours before starting or during infusion Baseline Urea and electrolytes, bone profile and magnesium prior to commencement.  Daily U+Es, bone profile, magnesium, and blood sugar levels per CLINCIAL Judgement Nausea, vomiting, transient abdo pain common If not working: discuss with consultant with gastro interest, Options to try Bowel Prep Solutions (Picolax), add further enemas, or discuss with Surgical team for Manual Disimpaction gastrografin: oral contrast agent, can be used as osmotic laxative in SBO and constipation resistant to klean-prep, surgery didnt help (tertiary centre to start)

Answer 163

stimulant + osmotic, can add softener, titrate dose to effect; naloxegol if opioid induced and moderately severe sx after taking laxatives for at least 4 days) stimulant: senna 7.5-15mg, or bisacodyl 5-20mg osmotic: laxido (macrogol) 1-3 sachets BD, or if can't take that volume then 15ml lactulose BD (watch for bloating); if neither works or inadequate fluid intake then go to softener (docusate, initially 100mg BD but can titrate up); lactulose is gentler than docusate so preferred if you can use it disimpaction: macrogol (large volumes), if impacted PR then bisacodyl supp if soft stools or glycerin if hard; or docusate/citrate (microlax) mini-enema; if still retain then phosphate or arachis oil enema shouldn't stop laxatives suddenly: can be slowly withdrawn once bowel movements occur easily e.g. 2–4 weeks after defecation has become comfortable and a regular bowel pattern with soft, formed stools has been established; reduce and stop one at a time (stimulant first), can take months to fully wean but may need long term if on constipating drug/medical cause

Answer 164

congenital, or secondary to a malrotation or gastroenteritis damaging the nerves/muscles of the gut Newborn babies with suspected CIPO often have a swollen abdomen and vomiting, and have difficulty passing faeces. Infants and childrenpresent as bowel obstruction (but with no actual obstruction), may have difficulty feeding, with vomiting. constipation, abdo pain and may have GORD over time may have poor growth; sx can settle and flare dd includes Ogilvie syndrome, true mechanical obstruction, IBS, gastroparesis, functional dyspepsia, Crohn’s disease, and cyclic vomiting syndrome Occasionally, CIPO can be suspected after prenatal ultrasound, showing enlarged bowel loops or a large bladder. In infancy and childhood, a series of tests are used to diagnose CIPO, including abdo US, AXR (+ contrast swallow), possibly scintigraphy, endoscopy, manometry and biopsy smaller more freq meals. low fat, low fibre; supplements given, sometimes gastrostomy or jejunostomy needed; occasionally TPN may be indicated; stoma formation may need to happen to decompress bowel; resection of section of bowel can be done if limited to a certain region (though risk of SBS), intestinal transplant can be done may also occur secondary to RA/SLE/scleroderma, parkinsons, MSA, duchenne and other muscle diseases, and more

Answer 165

Loss of <3 kg (0.5 stone) in the previous 6 months is rarely significant. Weight loss is usually the result of reduced energy intake, not increased energy expenditure. It does not specifically indicate gastrointestinal disease, although it is common in many gastrointestinal disorders, including malignancy and liver disease Reduced energy intake arises from dieting, loss of appetite, malabsorption or malnutrition. Increased energy expenditure occurs in hyperthyroidism, fever or the adoption of a more energetic lifestyle. A net calorie deficit of 1000 kcal/day results in weight loss of approximately 1 kg/week (7000 kcal ≅ 1 kg of fat). Greater weight loss during the initial stages of energy restriction arises from salt and water loss and depletion of hepatic glycogen stores, not from fat loss. Rapid weight loss over days suggests loss of body fluid as a result of vomiting, diarrhoea or diuretics (1 L of water = 1 kg).

Answer 166

failure to thrive, acute illness, catch-down growth (when intraut factors mean born at higher centile than genetically determined)

Answer 167

fat, flatus (obstruction), faeces, fluid (ascites, tumours - esp ovarian, distended bladder), fetus, functional (ibs)

Answer 168

High-volume diarrhoea (>1 L per day) occurs when stool water content is increased (the principal site of physiological water absorption being the colon) and may be: * secretory, due to intestinal inflammation, as in infection or inflammatory bowel disease * osmotic, due to malabsorption, drugs (as in laxative abuse) or motility disorders (autonomic neuropathy, particularly in diabetes). If the patient fasts, osmotic diarrhoea stops but secretory diarrhoea persists. The most common cause of acute diarrhoea is infective gastroenteritis due to norovirus, campylobacter (2-10 days) or Salmonella (12-72 hours) species or Clostridium difficile. Infective diarrhoea can become chronic (>4 weeks) in cases of parasitic infestations (such as giardiasis (Giardia lamblia), amoebiasis or cryptosporidiosis). Steatorrhoea is common in coeliac disease, chronic pancreatitis and pancreatic insufficiency due to cystic fibrosis. Bloody diarrhoea may be caused by inflammatory bowel disease, colonic ischaemia or infective gastroenteritis. Change in the bowel habit towards diarrhoea can be a manifestation of colon cancer, in particular cancer of the right side of the colon and in patients over 50 years. Thyrotoxicosis is often accompanied by secretory diarrhoea or steatorrhoea and weight loss. Low-volume diarrhoea is associated with irritable bowel syndrome

Answer 169

Inflammatory bowel disease is more common in patients with a family history of either Crohn’s disease or ulcerative colitis. Colorectal cancer in a first-degree relative increases the risk of colorectal cancer and polyps. Peptic ulcer disease is familial but this may be due to environmental factors, such as transmission of Helicobacter pylori infection. Gilbert’s syndrome is an autosomal dominant condition; haemochromatosis and Wilson’s disease are autosomal recessive disorders. Autoimmune diseases, particularly thyroid disease, are common in relatives of those with primary biliary cirrhosis and autoimmune hepatitis. A family history of diabetes is frequently seen in the context of NAFLD.

Answer 170

25% thrombus (from atheroscle), 50% embolism (from arrhythmias, post MI mural thrombus, prosthetic heart valve, or aortic aneurysm (note these are the risk factors for arterial emboli more generally too)), 20% from shock, <10% from mesenteric venous thrombosis (coagulopathy, malignancy, inflam) rarer causes inc aortic dissection, diff types of vasculitis, certain infections besides pain out of prop with symptoms and nausea/vomiting, take note of sources of potential emboli, past history of DVT/PE, causes of hypercoaguable state (eg malig, anti-phos syndrome) VBG urgently for lactic acidosis extent, sec to extent of bowel infarction (but can be falsely reassuring); FBCs, U&Es, coag screen, amylase, LFTs (liver may be affected if coeliac trunk involved), glucose CT with iv contrast is definitive diagnosis: oedematous bowel, then loss of enhancement; eCXR for perf may be wise surgical emergency with early senior involvement: iv fluids, catheter in, fluid balance chart started, early ITU input to optimise acidosis and guard against multiorgan failure; start broad spec antibiotics for abdominal sepsis (inc metronidazole), make NBM, analgesia If embolic then angioplasty or open embelectomy is ideal; if necrotic bowel or otherwise unsuitable then bowel resection, with maybe another look 24-48hrs later in relook laparotomy; oft will end up with stoma and risk of short bowel syndrome

Answer 171

2nd most common cancer in UK, 30,000 cases a year risk factors: genetic, red meat, sat animal fats, chronic inflam, smoking 65% rectosigmoid, 10% LC or TC, 25% RC rectal bleeding, altered bowel habit; anorexia, weight loss, abdo mass, anaemia; tenesmus if in rectum; non-specific abdo pain flexible sigmoidoscopy (any patient with fresh rectal bleeding); colonoscopy if bowel habit altered, sigmoidoscopy shows polyps, family history barium enema less sensitive but may show strictures serum CEA can be supportive (but false positives and negatives); FBC and iron studies can support diagnosis for staging: CT of abdo, LFTs, pelvic MRI management through MDT with surgery, chemo for palliation or adjuvant to the surgery faecal occult blood test every 2yrs age 60-74 (expanding to 50-74)

Answer 172

loss of appetite, change in bowel habit, weight loss, unexplained abdo pain (could point to many types 2ww if anal mass or unexplained ulceration, iron def anaemia if 60yo+ (crc), iron def anaemia w rectal bleeding if <50yo (crc), abdo mass, abdo pain w rectal bleeding <50yo, change in bowel habit 60yo+ or w rectal bleeding and <50yo, occult blood in faeces, rectal bleeding >50yo FIT test if >60 w anaemia (even if not fe def), <60 w change in bowel habit or iron def anaemia, 50+ with abdo pain or weight loss resection (anterior resection for low sigmoid/high rectum), abdominoperineal if lower than this if metastatic then chemo: capecitabine + oxaliplatin

Answer 173

50% of over 50s have some diverticula diverticulosis: colicky left iliac fossa pain relieved by defaecation; pellet stools; bloating; must exclude colorectal cancer if these present; colonoscopy though has risk of perforation, rigid sigmoidoscopy an alternative; inc fluid and fibre intake diverticular bleeding: can occur, and may ultimately lead to anaemia and altered bowel habit but rule out IBD, coeliac and bowel cancer first; high fibre diet and fluids diverticulitis: fever, raised white count and inflam markers, pain usually in LIF, no colonoscopy, do contrast CT to look for an abscess; co amox or cefalexin + metro and analgesia if mild (if systemically well may not even need antibiotics); stricture, perforation, fistula, abscess may need surgery

Answer 174

blood here will be fresh and bright, or at least red-brown haemorrhoids > fissures > colorectal polyps > colorectal cancer > UC > crohns > rectal prolapse > diverticular disease > ischaemic colitis also angiodysplasia which may be painless occult bleed or acute h+, usually in caecum/ascending colon, endoscopic argon/electric treatment FBC LFT clotting status flexible sigmoidoscopy, colonoscopy if bleeding changes; CT angio +/- intervention to stop bleeding if large volume

Answer 175

an abnormal, tortuous, dilated small blood vessel in the mucosal and submucosal layers of the GI tract - commonest in caecum, then, rectosigmoid, then rest of colon, then SI, then stomach; common cause of obscure GI bleeding in >50yo cause unclear, maybe age related degen or hypo-oxy due to cardiac or pulm disease, inc eg aortic stenosis, as well as ESRD as a result of increased contractility at the level of muscular propria, submucosal veins may become obstructed; congestion of caps leads to formation of arteriovenous collaterals; angiogenesis occurs as a result of hypoxia asymp or obscure lower GI bleeding, maybe IDA; can sometimes have large bleed colonoscopy/endoscopy oft pick up; capsule endoscopy may be needed; if still can't find bleeding source then ix include CT angio, MRA, technetium scintigraphy, or if bleeding and unstable then angiography incidental may be ignored if no bleeding; you can ablate, inject with sclerosing chemicals, clip, do angiography, bowel resection if major bleeding; octreotide and bevacizumab have been used in small studies

Answer 176

pneumonia (esp lower lobe), pharyngitis, pyeloneph, renal colic, nephrotic syndrome, pericarditis, haemolutic crisis, migraine (FH), mono, hypoglyc, diabetes esp dka, hypokal and addisons, hypercalcemia, porphyria, lead poisoning

Answer 177

90% of time no organic cause - the further the pain from the umblicus the more likely path is present may be abdo migraine - diagnose if child thriving, periumb pain + maybe rec n&v, pos FH of migraine or rec abdo pain; episodes usually not long or severe and may have triggers IBS suggested by rec abdo pain, bloating, alternating diarrhoea and constipation might consider FBC, ESR, AXR, urine MC&S

Answer 178

very common in children and adolescent, most will have some kind of functional pain as defined by rome criteria, of which there are 4 kinds: IBS, functional dyspepsia, abdo migraine, functional abdo pain syndrome alarm sx and resultant ix: weight loss, growth deceleration, or delayed puberty - CRP, FBC, calprotectin, and coeliac testing excessive vomiting, RUQ pain, steatorrhea - LFTs, amylase, lipase, urine dip, abdo USS haematochezia, right lower quadrant pain, severe chronic diarrhoea or diarrhoea at night, perianal disease, systemic features like arthritis or fever, family history of bowel disease - FBC, CRP, calprotectin and coeliac testing dysphagia/odynophagia - contrast study or OGD ?eosinophilic oesophagitis, h pylori association with menses - endometriosis inc ectopic tissue, PCOS, mittelschmerz, normal period pain, refer to specialty if needed examine for rashes, clubbing, jaundice, organomegaly, abdo mass, spine tenderness and joint swelling or heat -> ix as appropriate also consider whether any suspicion of food allergy or non-allergic food intolerance, take full history about bowel habit to consider constipation (more likely if abdominal pain is constant and happens daily, esp if worsened with meals as food stimulates peristalsis), consider if pelvic inflam disease possible consider chronic pancreatitis if malabsorption or risk factors present in younger kids consider intussuception bloating, flatulence, belching, halitosis, intermittent diarrhoea - discuss with GI colleague ?SIBO if confident not any of above (may have sent one stop test of CRP, FBC, calprotectin, coeliac screen +/- pregnany test and abdo USS only if indicated) then apply rome criteria: functional dyspepsia: *Persistent/recurrent epigastric pain *No relief on opening bowels *No change in stool frequency or form IBS: *Abdominal pain present for 1 day per week in the last 3 months with symptoms present for at least 6 months prior to diagnosis. Associated with 2 of more of the following at least 25% of the time: - Pain related to defecation - Associated change in stool frequency or form Abdo migraine: Paroxysmal episodes of intense, acute, peri-umbilical pain lasting more than 1 hour * Intervening periods of usual health lasting weeks to months * Pain interferes with normal activity *Associations (2+): anorexia, nausea, vomiting, photophobia, pallor Must occur more than 2 times in the preceding 12 months Functional abdo pain: Episodic or continuous abdominal pain occurring at least 4 times per month *Insufficient criteria for IBS, functional dyspepsia or abdominal migraine *Cannot fully be explained by another medical condition after appropriate evaluation Does not solely occur with physiological events e.g. menses *Can coexist with other medical conditions such as inflammatory bowel disease mx: explain children do tend to grow out of it analgesia can be tried but often not helpful as doesn't address visceral hypersensitivity, likewise poor evidence for antispasmodics Difficult cycle to break: pain perception  worry about the pain and anticipation  worsening of pain / up-regulation of pain  pain perception can trial dietary exclusion inc FODMAP diet if appropriate, can trial probiotics, and if dyspepsia trial PPI (lanso/omep, liquid omep if feeding tube) but set expectations may not work due to different mechanism for pain distraction and addressing concomitant anxiety is most helpful thing

Answer 179

nephrotic syndrome, abdo pain is due to splanchnic ischamia due to vacular volume depletion diabetes, esp dka addisons - k may be raised, may have hypotension or even shock acute intermittent porphyria - abdo pain during attacks, hyponat from SIADH due to hypothal involvement; may have dark urine and neuro features hyponat sec to d&v

Answer 180

lead poisoning - pain, vomiting, constipation + raised icp, seizures, ataxia, periph neuropathy, microcytic anaemia or haem anaemia with basophilic stippling; may have fanconi syndrome and lead lines (growth arrest lines at metaphysis) acute intermitten porphyria - neuro signs might inc personality changes, spectrum from periph neuropathy to quadriplegia and resp failure; raised urinary porphobilinogen (normal in lead poisoning) and raised delta aminolaevulinic acid (may be raised in lead poisoning) wilsons disease hypoglycaemia sickle cell crisis (may have preceding history) Hypercalcemia

Answer 181

umbilical sepsis patent urachus (urine) patnt vitello-intestinal duct (faeces) umbilical granuloma

Answer 182

former herniates into sac made of amnion and peritoneum and due to def of umbilical ring; umb cord attached to vertex of sac; minor just gut, major gut + liver associated with BW syndrome, tof, imperforate anus, ts13/18 gastroschisis - bowel gerniates through defect to right of umb cord in ant abdo wall, no peritoneal covering; bowel at risk of infarction complications of both: loss of protein, fluid, heat; infection risk place occlusive film, drain gastric contents to prevent gut distension, IV fluids + plasma (monitor urine output and haemodynamic status), then closure in 2 stages; complications of returning bowel into abdo inc bowel infarction, occlusion of ivc

Answer 183

Omphalocele may be repaired quickly or in stages and often a staged repair is preferred (especially with larger defects) as returning the abdominal contents can cause respiratory insufficiency or inability to close the abdomen, both of which can result in death. Therefore gradual closure allows the pulmonary system to adapt to the increased abdominal contents over 6-12 months. There is no need for a cling-film covering as the peritoneum will already be protecting the bowel in omphalocele differential is gastroschisis in which a paraumbilical abdominal wall defect results in abdominal contents being outside the body, without a peritoneal covering. The prognosis is good if operated on as soon as possible and whilst waiting the bowel should be protected with cling-film. Intestinal function will take time to normalise and thus the child may require TPN for a few weeks.

Answer 184

consider bleeding: oesophagitis, swallowing maternal blood at birth or through cracked nipples (both may cause apparent rectal bleeding in neonates), MW tear, gastritis, peptic ulcer, meckels diverticulum (technetium isotope scan), IBD, foreign body, haemangioma, gastroenteritis (esp salmonella, EHEC, e coli, campylobacter, shigella, yersinia), intuss, NEC, volvulus, polyps, cow's milk protein intol, vasculitis (eg HSP), anal fissure, sexual abuse, coagulopathies, lead poisoning note many of these may also be painless

Answer 185

may also have excoriation and erythema must consider sexual abuse, but, esp where labira minora or vaginal orifice itself not involved, also consider: irritation, such as allergy to washing detergent; threadworms

Answer 186

pelvic appendix abscess

Answer 187

familial mediterranean fever medit origin (arab, turkish, sephardic jewish etc) disorder of polymorphonuclear cells attacks usually start between 5 and 15 yo and consist of fevers, serositis (mainly abdo pain but also pleuritis, large joint arthritis, pericarditis) occuring approx monthly for a few days, freq decreasing w age erysipelas may occur WCC and esr up in attacks, not between genetic testing to confirm, treatment with colchicine serious complication is amyloidosis

Answer 188

10-15% school age children get at some point no fever, weight loss, vomiting, blood in stool; may have diarrhoea or constipation but not caused by those headache, limb pain, difficulty sleeping may accompany; it's due to overactive gut-brain axis and can be worsened by stress pain may come on gradually or be sudden; may be constant or come in waves; usually periumbilical; avoiding carbonated drinks, lactose, spicy foods, eating more slowly may all help often gets better on its own with time, try to focus on relaxing and doing things that make the child happy

Answer 189

Children are more likely than adults to suffer with a condition called abdominal migraine. This may occur in young children before they develop traditional migraines as they get older. Abdominal migraine presents with episodes of central abdominal pain lasting more than 1 hour. Examination will be normal. There may be associated: Nausea and vomiting Anorexia Pallor Headache Photophobia Aura NSAIDs/para/triptan + dark quiet room during attack; pizotifin (5HT agonist) main preventative but also eg propranolol

Answer 190

Umbilical hernias are relatively common in newborn children, and in 80% will spontaneously close by 4-5 years of age. Usually, hernias are observed until 4-5 years of age. If a hernia persists beyond this age, it should be managed with elective outpatient surgical repair due to the risk of incarceration. For a large or a symptomatic umbilical hernia, surgeons advocate elective repair at 2-3 years of age. This applies to hernias >1.5 cm (as this size fascial defect is unlikely to resolve spontaneously), or to hernias causing intermittent symptoms of incarceration or recurring pain. If a hernia incarcerates during the observation period, it should be manually reduced with pressure and surgically repaired within 24 hours. If it can't be reduced, an emergency operation is required.

Answer 191

hernia is commonest - may have dragging sensation and oft reducable others: lymph nodes, skin/subcut lumps, saphena varix, hydrocele of spermatic cord, undescended testis, femoral aneurysm, psoas abscess

Answer 192

layers: Skin Subcutaneous fatty layer Membranous fascia External oblique Internal oblique Transversus abdominis Transversalis fascia Preperitoneal fat Parietal peritoneum midline laparatomy: utilises the relatively avascular nature of the linea alba; advantages include the ease with which the incision may be extended either cephalad or caudally in order to improve access. Disadvantages include patients experiencing more pain than they would from a transverse incision, particularly during deep breathing postoperatively, and the incision is perpendicular to the Langer’s skin tension lines resulting in poorer cosmesis. This approach is commonly used for procedures requiring emergency laparotomy, such as in faecal peritonitis secondary to malignant intestinal perforation or in cases of ischaemic bowel. Limited midline incisions are also employed to assist laparoscopic cases such as bowel resections, where the dissection and mobilisation of the specimen to be excised are performed laparoscopically but then a larger port is required for retrieval gridiron incision: entred over McBurney’s point two-thirds of the distance between the umbilicus and the right anterior superior iliac spine (ASIS), where the base of the appendix is most likely to be found; risk of injury to the ilioinguinal and iliohypogastric nerves; lanz is similar, lower down, same disadvantages Pfannenstiel incision is a firm favourite of obstetricians for accessing the gravid uterus for which a curvilinear incision is made through the skin and subcutaneous fat, then a longitudinal incision made in the linea alba. It is also used by general and urological surgeons for some pelvic procedures such as radical open prostatectomy or cystectomy transverse incision is higher up than pfannenstiel, nearer to the umbilicus, and is used in paeds and for repair of AAA kocher is subcostal for open cholecystectomy, on other side for spleen, bilaterally is rooftop/chevron incision to access pancreas and biliary tree as well as gastrectomy, adrenalectomy, oesophagectomy, hepatic resection or liver transplant; risk to intercostal nerves and superior epigastric vessels modified rooftop aka mercedes benze for liver transplants,reverse L another option rutherford morrison/hockey stick is extended lanz, often used for kidney transplants

Answer 193

recent onset abdo pain needing surgical assessment; non-spec 35% cases (diagnosis of exclusion), acute app in 20% cases, int ob in 15%, biliary pain in 10% then urological (torsion), acute colonic diverticulitis, perf, acute panc, ruptured AAA, mesenteric ischaemia, gynae emergency parietal peritoneum involvement is sharper, localised, more intense, worsened by coughing or moving, and leads to guarding dont formally test for rebound tenderness as can cause great pain if has peritonitis - instead elicit it via cough test history and abdo exam(inc rosving, murphy's, maybe psoas sign if think retrocaec appendix) DRE for mass, blood/melaena, press against sacrum shouldnt hurt, press ant might hurt if pelvic peritonitis so eg appendicitis rather than gastroent urinalysis is key; if abnormal send urine for microscopy, culture, and sensitivity MC&S repeat 2-4 hr later (gives timecourse for decline etc) always check glucose as DKA may cause ecg in all patients with upper abdo pain, eAXR if peritonitis to check for perf, pregnancy test, CT with contrast, VBG for lactate

Answer 194

admit keep NBM start iv fluids paracetamol and codeine PO reg and prn morphine iv plus prn antiemetic (not metoclop if obstruction poss) if sick pt: ABCDE, O2, 2x iv large bore cannulae (blood for labs and culture), urinary catheter culture blood/urine if septic, and after can start antibiotics (dont start otherwise until diagnosis made, unless immunosuppressed in which case empiric treatment)

Answer 195

obstruction by faecolith or foreign body, stricture (prev inflam), lymph follicles swelling sec to inflam, or rarely a carcinoid tumour; sometimes prox to obstruction in caecum or ascending colon eg tumour; closed loop so bacti prolif and invade wall, thrombosis in end a's then necrosis and perf, dev from <12hrs to >3-4 days after obstruction non-obstrutive forms eg direct lympoid invasion or haemat spread, more likely to resolve than obstructed form; after any resolve more acute attacks likely; after perf may get localised abscess or genealised peritonitis; perf often improves pain as distended organ relieved, but this followed by more severe pain and profuse vomiting as gen perit devs

Answer 196

mesenteric adenitis (confirmed during appendicectomy), meckel's (exclude if appendix normal), crohn's ileitis, acute obstruction (bowel will be loud and distended instead of quiet as with perf perit); gastroent (more diffuse, less severe), perf pep or acute panc (fluid tracks down), acute cholecyst (colicky visceral epigastric/foregut pain, then localise usually ruq but can be rif), diverticulitis (if sigmoid mobile or occasionally caecal divert) ureteric colic/pyeloneph (urinalysis but inflam app adhere to bladder or ureter can give dysuria, freq, mic haematuria/pyuria so exploratory laparoscopy if unsure); test torsion giving the initial periumb pain ruptured/torted ovarian cyst give severe if pain radiating to loin, salpingitis more diffuse lower abdo pain and vaginal discharge, ectopic; preg test but pelvic laparotomy may be done (appendicectomy at same time) pain preceding herpes zoster of T11/12, irritation of these same roots in spinal disease eg TB/tumour, lightning pains of tabes dorsalis all may sometimes mimic

Answer 197

laparoscopic (confirm diagnosis) appendicectomy; not done immediately if patient moribund with advanced peritonitis (needs fluid resus, antibiotics, analgesia) or if attack resolves (can advise appendicectomy as an elective procedure but no immediate rush), also not done if appendix mass formed w/o gen perit antibiotic proph preop, keep it going if perit found during op; culture the pus and adjust regimen based on results appendix mass - mass in RIF with 4-5 days of abdo pain usually, no evidence of gen perit; adhesions to viscera and omentum, with or w/o local abscess, has walled off the inflam app; surgery in this case may damage bowel loops so mark outlines of mass, pt on fluid diet, metronidazole but not prolonged antibiotics (risk of chronic inflam mass with honeycomb of abscesses); 80% time resolves then appendicectomy 3mo later; if doesnt then drain abscess so doesnt burst into rectum or peritoneal cavity in preg enlarged uterus displaces pain/tenderness more high and lat - MRI abdo safe for foetus and can be used if diagnosis in doubt

Answer 198

BBBPP - blocked (obstruction), bleeding (ruptured aneurysm), broken (trauma), perforation, purulent (appendicitis) also: if in shock may well need surgery always resus the pt before surgery

Answer 199

colicky abdo pain (periumb or suprapub, post-op may be disguised by opiates) + distension (esp chronic LBO, in SBO only small dilated area so less obvious) + absolute constipation (early onset in LBO, late in SBO as even when obstruction fully established 1 or 2 + vomiting (late or even absent in LBO, faeculent due to bacti in static gut contents); not all 4 need be present, sequence in which they appear may help localise to SI or LI adhesion, hernia, volvulus; tumour, strictures (crohns), diverticula, atresia; faecal impacation, gallstone, food bolus, worms, intussusception, appendicolith copius fluid secretion into bowel as well as obstructed swallowed air leads to build up and distention prox to lesion, circulation to distended wall impaired leading to ulceration, necrosis, perf fluid and electrolyte depletion from vomiting and fluid sec into bowel pulse up but freq not pyrexic, if are suggests strangulation occurring; always look for a strangulated hernia which may be hard to find if small femoral in big person and look for abdo scars (post surgical adhesions)

Answer 200

preop: NG gastric aspiration to relieve pressure and dec risk of aspiration during induction; fluid resus; antibiotics if strangulation likely resection of relevant part with anastomosis paralytic ileus - functional obstruction when peristalsis stops; due to peritonitis (toxic shock of nerve plexi), severe hypokalaemia, uraemia, diabetic coma, large doses of anticholinergics or parkinsons medication, also post-op (after all abdo ops for 24-48hrs to some degree); paralytic ileus will ofc have absent bowel sounds and has no pain, but distension, vomiting, and absolute constipation will occur; treat cause (or wait if surgical), NG aspiration, IV fluid, antinausea med; gently reintroduce enteral feeding

Answer 201

usually no symptoms; they may bleed giving bloody stools and/or anaemia, and may cause constipation or diarrhoea, but usually are found at a screening for CRC may dev into adenoma then colorectal carcinoma arises there (most CRC come from initial adenoma), so removal of polyps dramatically decs incidence of CRC 1 in 4 ppl have them, esp if >60, male, family history of CRC, IBD colonoscopy to remove them once found (wire snare or cauterising electric burn); it will be analysed and may have follow up if cancerous change certain types of polyps can recur so if have those then regular colonoscopy every 3-5 years If bleed after then relook sigmoidoscopy, keep overnight to monitor, check Hb, and keep NBM until the morning

Answer 202

autosomal dom, dev hundreds or thousands of colorectal polyps esp in LI, which may bleed into stool; may be silent in some individuals until has dev'd into CRC colonoscopy better as can reach right side of colon; genetic testing often provides ultimate diagnosis, and genetic counselling for families known to carry the genes close colonoscopy surveillance(every 1-2 years), sometimes upper endoscopy too as polyps can grow in upper GI tract and is a risk factor for duodenal cancer most ppl with the mutation will dev CRC by age 40 so try to prevent or remove before reaches that point

Answer 203

mutations in MLH1, MSH2/6, PMS2 lead to potential CRC, endometrial, gastric, or ovarian cancers, and slightly inc'd risk for small bowel breast, and panc cancers too mean age of CRC in this condition is early 40s as opposed to >60 for CRC generally genetic testing for this in everyone diagnosed with bowel cancer, genetic testing for families; may also test for it if 3+ ppl in family have had one of the related cancers and at least 1 person was <50 when happened

Answer 204

in ppl with IBD, infectious or ischaemic colitis esp c diff, sometimes (rarely) CRC pain, swelling, fever, tachy, diarrhoea, high risk of perf, sepsis or bleeding AXR should show treat cause with eg antiinflams or antibiotics, iv fluids, if doesn't reduce in 72hrs or complications dev then colectomy

Answer 205

sigmoid: LBO w/ pain and vomiting occurring late and eventually necrosis dev'g; AXR, CT if unclear; correct dehydration, decompress with sigmoidoscopy + flatus tube; surgery if ischaemia/strangulation or non-op means fail; is main type of LBO that doesnt need surgery initially caecal: distal SBO; AXR and CT if unclear; right hemicolectomy

Answer 206

leaks from anastomoses or suture lines: varies from prolonged ileus to sudden peritonitis and septic shock suspect whenever pt unwell or not progressing as expected; fever, tachy, hypotension, oliguria, abdo pain/distension eCXR but air under diaphragm may be normal 3-7 days post laparotomy; FBCs, U&Es, contrast enema to show leak, maybe CT broad spectrum antibiotics, iv fluids; emergency laporot if gen periton; if localised and systemically well med treatment only unless fail to improve

Answer 207

local vs general; immediate (first 24hrs) vs early (first 30 days) vs late immediate: reactionary local H+, asphyxia from vomit or airway obstruction, anatomical injury early: paralytic ileus, thromboembolism, bed sores, wound dehiscence, secondary H+, obstruction from fibrinous adhesions, c diff from antibiotic use, atelectasis late: obstruction due to fibrous adhesions, incisional hernia, persistent wound sinus, malabsorption after bowel resection; sarcopenia/nutritional deficiency; AKI; cardiac event eg MI/stroke

Answer 208

community acquired mild biliary sepsis treated with co-amoxiclav 625mg po tds and due to overlap in pathogens this is also good choice for most intra-ab infections eg cholecystitis, cholangitis, diverticulitis; cipro + metro if pen allergic tazocin if hosp acquired or severe, or if pen al then as above + vanc

Answer 209

breast is all women between 50- 71 years Mammogram every 3 years. Can request if over 71 just not automatically allocated cervical is women from age 25 to 64 every 3 years between 25-49 50-64 every 5 years can ask for one over 65 if never had before. colon is: All aged between 60-74y Faecal immunochemical test (FIT) test every 2 years. Can request over the age of 74

Answer 210

most likely is viral gastroent could also be IBD, feed intolerance, intestinal hurry (aka toddlers), coeliac, bacterial colitis dont miss intussusception (bloody) or severe dehydration

Answer 211

most likely is viral urti (central, mild, soft abdo) but could be constipation (colicky), appendicitis, other surgical causes dont miss DKA, pyeloneph (may not localise or have urinary sx)

Answer 212

1 Physiological jaundice. 2 Breast milk jaundice. 3 Hepatitis. 4 Biliary atresia or other obstructive cause. 5 Antibody-mediated haemolytic disorders (rhesus, ABO incompatibility). 6 Red cell instability disorders (e.g. pyruvate kinase defi - ciency, spherocytosis, glucose-6 phosphate dehydrogenase (G6PD) defi ciency). 7 Infection (e.g. urinary tract infection). 8 Congenital hypothyroidism. 9 Metabolic disorders (e.g. galactosaemia, α1-antitrypsin defi ciency, Crigler–Najjar syndrome) need to know age, ethnic origin, how old when jaundice started, how marked, what colour are urine/stools, any systemic unwell? any bruising? breast or bottle fed? obstetric and delivery history inc mums blood group and rh status get a FH examine for amount of jaundice, drowsiness, dehydration, pallor, palpate for organomegaly, examine contents of nappy (urine, stool colour), and dip urine to screen for UTI total + conj and unconj bili, FBC and film, TFTs, LFTs, A1AT, plasma galactose, purivate kinase, bilirubin UDP glucuronyl transferase; urine MC&S if dipstick pos manage for kernicterus, where unconj bili crosses BBB (as fat soluble) damaging brain, esp BG - poor feeding, lethargy, cerebral palsy or death; UV light, maybe plasma exchange manages depending on level

Answer 213

dd - Pyloric stenosis. 2 Gastro-oesophageal refl ux. 3 Posseting. 4 Gastroenteritis. 5 Bowel obstruction. 6 Respiratory tract infection. 7 UTI or other systemic infection. hx - Find out more about the vomiting: * Frequency. * Forcefulness. * Relation to feeding. * Relation to coughing. * Colour. * Duration. Associated symptoms * Abdominal distension. * Fever. * Stool colour and consistency. * Respiratory symptoms. Feeding history * Breast or bottle? * How much? * How often? * Does he appear hungry? * Does feeding precipitate the vomiting? * Has he been gaining weight; obstetric history, PMH (any prev episodes), FH assess for dehydration and shock, check for weight loss on growth chart, examine abdo for obstruction (distension), listen for bowel sounds, while feeding assess for olive mass in ruq and visible peristalsis; also check hernial orifices (commonest worldwide cause of childhood bowel obstruction) first mx any dehydration with fluid resus; take FBC, CRP, U&Es, G&S, and blood gas; rehydrate over 24h (calc cluid deficit to make up as follows - lost eg 0.3 kg, This equates to a 300 ml deficit; consider abdo USS for obstruction, refer to surgeons

Answer 214

dd - failure to thrive; Organic causes 1 Inability to get feed into the intestine (e.g. cleft palate or coordination problems in cerebral palsy). 2 Gut malfunction – severe gastro-oesophageal refl ux. 3 Malabsorption (e.g. cystic fi brosis, coeliac disease). 4 Energy wastage in chronic disease (e.g. congenital heart disease, renal failure, cystic fi brosis). 5 Problems with control of growth (e.g. hypothyroidism, congenital adrenal hyperplasia, syndromes). Non-organic causes The lack of intake could be due to: * Poor breastfeeding technique. * Inappropriate or inadequate diet. * Poor meal time environment, e.g. hurried meals, distractions, force feeding. * Child abuse. Other possibilities are erroneous: such as a mischarted weight, or a small but normal child any GI sx? full feed history - input/output for typical 24h day, breast or bottle, any problems latching/suckling? when/what for weaning? current diet and any recent changes? any difficulty swallowing, choking, dyspnoea, milk through nose when feeding? does she seem hungry? meal time history - when, are they rushed, do family eat together, what happens if kid doesnt eat? obs/labour history, any rec chest infections/dyspnoea/cyanosis? assess for dev delay 10% failure to thrive kids have organic cause so take detailed social history - who lives at home, whats housing like? finanicial and work pressures? social/family support? any other kids and how are they? any involvement w social services?

Answer 215

appearance, age-appropriate behaviour, interactins with parent, small or thin (and any muscle wasting?), seem unwell? any dysmorphic features? confirm height and weight plotted right; check for anaemia, look for bruises; abdo exam in mouth/palate, resp system, heart, dev assessment can consider FBC for anaemia, other bloods based on dd if non-organic cause and advice isnt helping may need to admit for observation and hospital diet, and poss social services referral to support mother

Answer 216

ABS stems from the widespread proliferation of gut microorganisms, which, in turn, leads to endogenous production of ethanol. This phenomenon is preceded mostly by the intake of carbohydrate-rich meals or antibiotic use, which can disturb the gut ecosystem causative organisms implicated in ABS include fungi and bacteria, with the most common yeasts being Saccharomyces and Candida species. present with alcohol intoxication without intake of alcohol need to rule out neuro/psych causes of similar presentation eg encephalitis or psychosis, and get stool culture for yeasts; confirmatory test is a glucose challenge mx inc antifungals (or antibacterials if they are the causative organism)

Answer 217

gap between two sides of rectus abdominis due to stretching of the linea alba, most commonly in newborns and pregnant women In the newborn, the rectus abdominis is not fully developed and may not be sealed together at midline. Diastasis recti is more common in premature newborns. A diastasis recti may appear as a ridge running down the midline of the abdomen, anywhere from the xiphoid process to the umbilicus. It becomes more prominent with straining and may disappear when the abdominal muscles are relaxed. - must differentiate it from hernias (look at difference in size between contraction and relaxation of abdo muscles - USS can confirm) In infants, they typically result from a minor defect of the linea alba between the rectus abdominis muscles. This allows tissue from inside the abdomen to herniate anteriorly. On infants, this may manifest as an apparent 'bubble' under the skin of the belly between the umbilicus and xiphisternum (bottom of the breastbone). physio and exercise can generally improve/treat, with surgery an option in extreme cases

Gastroenterology Flashcards

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