Based on the clinical scenario, the most likely risk factor in this child to develop gallstones is sickle cell disease.Note:Haemolysis is the most frequent cause for gallstones in children and the likeliest cause because of his ethnicity would be sickle cell disease. The gallstones are pigmented which form from bilirubin. 70% of patients with sickle cell disease will develop gallstones| the prevalence of gallstones is related to the rate of haemolysis.Other options:- Gilbert’s syndrome: it is a common condition in which bilirubin glucuronidation (i.e. converting bilirubin into a water-soluble form) is affected. During times of stress (viral illness, fasting, etc.) there is an excess bilirubin production, and jaundice may develop. It is a benign condition but there is some evidence of an increased risk of developing gallstones. However, sickle cell disease is a more likely risk factor in this case.- Hereditary spherocytosis: Hereditary spherocytosis is a disease of the white population and is less likely to be the underlying cause in this case.- Male gender: After puberty, the incidence of gallstones is higher in women. Before puberty, the incidence is equal.- Obesity: Obesity is a risk factor for gallstones and is thought to be behind the rising incidence among young adults. Nevertheless, haemolytic states remain the most common reason for gallstones in children.

Food poisoning is defined as an illness caused by the consumption of food or water contaminated with bacteria and/or their toxins, or with parasites, viruses, or chemicals. The most common pathogens are Norovirus, Escherichia coli, Salmonella, Clostridium perfringens, Campylobacter, and Staphylococcus aureus.The following are some of the salient features of food poisoning:Acute diarrhoea in food poisoning usually lasts less than 2 weeks. Diarrhoea lasting 2-4 weeks is classified as persistent. Chronic diarrhoea is defined by duration of more than 4 weeks.The presence of fever suggests an invasive disease. However, sometimes fever and diarrhoea may result from infection outside the GI tract, as in malaria.A stool with blood or mucus indicates invasion of the intestinal or colonic mucosa.Reactive arthritis can be seen with Salmonella, Shigella, Campylobacter, and Yersinia infections.A profuse rice-water stool suggests cholera or a similar process.Abdominal pain is most severe in inflammatory processes. Painful abdominal cramps suggest underlying electrolyte loss, as in severe cholera.A history of bloating should raise the suspicion of giardiasis.Yersinia enterocolitis may mimic the symptoms of appendicitis.Proctitis syndrome, seen with shigellosis, is characterized by frequent painful bowel movements containing blood, pus, and mucus. Tenesmus and rectal discomfort are prominent features.Consumption of undercooked meat/poultry is suspicious for Salmonella, Campylobacter, Shiga toxin E coli, and C perfringens.Consumption of raw seafood is suspicious for Norwalk-like virus, Vibrioorganism, or hepatitis A.Consumption of homemade canned foods is associated with C botulinum.Consumption of unpasteurized soft cheeses is associated with Listeria, Salmonella, Campylobacter, Shiga toxin E coli, and Yersinia.Consumption of deli meats notoriously is responsible for listeriosis.Consumption of unpasteurized milk or juice is suspicious for Campylobacter, Salmonella, Shiga toxin E coli, and Yersinia.Salmonella has been associated with consumption of raw eggs.

CUTANEOUS DISORDERS OR DERMATOSIS ASSOCIATED WITH IBD- Psoriasis- Secondary amyloidosis- Vitiligo- Acquired epidermolysis bullosaIn some cases, non-granulomatous skin disorders occur as a reaction to the intestinal disease. These include:- Pyoderma gangrenosum- Neutrophilic dermatosis / Sweet syndrome, typically with pustules- Pyodermatitis-pyostomatitis vegetans, a purulent erosive dermatosis characterised by snail-track ulcers- Erythema multiforme- Erythema nodosum- Acneiform eruptions including nodulocystic acne, hidradenitis suppurativa and folliculitis- Palisaded neutrophilic and granulomatous dermatitis- Necrotizing and granulomatous small vessel vasculitis.

Based on the history and clinical presentation, she most likely has iron toxicity.Iron can cause scarring of the gut mucosa. This explains her pyloric stenosis. This typically occurs at the pylorus as this is where iron tablets tend to pool and cause maximal tissue damage.Other options:- Citalopram: Selective serotonin reuptake inhibitors (SSRIs) ingestion rarely causes serious consequences. It can rarely lead to serotonin syndrome (autonomic instability, mental status change, and increased neuromuscular tone).- Ibuprofen: While it may cause gastritis, ibuprofen does not cause pyloric/intestinal stenosis.- Thyroxine: An overdose of thyroxine will cause features of hyperthyroidism which are not present in the patient in question.- Zinc: High doses of zinc can cause abdominal cramps, nausea, vomiting and diarrhoea.

Celiac disease is classified as a Type IV hypersensitivity mediated by T-cell response. Negatively charged gliadin has been shown to induce interleukin 15 in the enteric epithelial cells, stimulating the proliferation of the natural killer cells and intraepithelial lymphocytes to express NK-G2D, a marker for natural killer T lymphocytes.

Meckel’s diverticulum is 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 2’s- occurs in 2% of the population- it is located 2 feet proximal to the ileocaecal valve- it is 2 inches long- it is 2 times more common in men- there are 2 tissue types involvedIt is typically asymptomatic. Symptomatic presentation indicates inflammation of the diverticulum. The symptoms include:- Abdominal pain mimicking appendicitis- Rectal bleeding- Intestinal obstruction: secondary to an omphalomesenteric band (most commonly), volvulus and intussusceptionManagement:Surgical removal if the neck of the diverticulum is narrow or symptomatic. Surgical options are excision or formal small bowel resection and anastomosis.

Celiac disease has characteristic shortened intestinal villi. When patients with celiac disease eat products containing gluten, they are unable to absorb the nutrients due to flattened or shortened intestinal villi. The blistering rash present on the patient’s elbows strongly suggests celiac disease. This rash is a sign of the condition Dermatitis Herpetiformis which is associate with celiac disease. Therefore, it is also often called ‘gluten rash’.

Most experts suggest that parents reassurance in case of infantile gastro-oesophageal reflux (GOR) is a sufficient initial measure that involves education about regurgitation and lifestyle changes.

The clinical picture suggests that the child is severely dehydrated. IV fluid bolus then IV maintenance fluids is the correct option.

Colonic Polyposis and neoplasia are often seen in Cowden Syndrome which is a hamartomatous polyposis syndrome. Patients with Cowden syndrome have an increased risk for colorectal cancer.

The initial symptoms of spasmodic abdominal pain, rectal bleeding and vomiting might point towards intussusception, but the peak incidence is in children aged 6–9 months. Considering that this child has additional symptoms of haematuria, proteinuria and a purpuric rash, it is more likely that the child has Henoch–Schönlein purpura (HSP). HSP is an identifiable cause of intussusception. It is an IgA-mediated, autoimmune hypersensitivity vasculitis that targets the small vessels of the skin, GI tract, kidneys, and joints. It is most commonly seen in children aged 3 – 6years and is twice as common in boys than girls. Preceding viral URTI with low-grade pyrexia is common. The most common organism associated with HSP is, however, Group A streptococcal infection. A purpuric rash is seen on the back of the legs and buttocks and can less frequently, affect the arms. Arthralgia is common (usually knees/ankles) in these patients. Abdominal pain and bloody diarrhoea may occur. And half of the children with HSP have renal involvement. Rarely, it can lead to end-stage renal failure. Treatment includes adequate hydration, occasionally steroids, and other immunosuppressants. The disease can recur in 1 in 3 children.

H. pylori release the enzyme urease that has the ability to split urea releasing nitrogen. This process increases the pH in the gastric antrum making the gastric pH less acidic.Helicobacter pylori:It is a spiral, microaerophilic, gram-negative bacterium. It is one of the most common causes of antral gastritis in children. Ulcers are less common in children compared with adults| however, when they occur, they are more common in the duodenum.The presence of H.pylori can be confirmed by:- Stool antigen test (preferred)- Serology- Endoscopy with biopsy and culture- Rapid urease testsH.pylori gastritis may be associated with:- Iron deficiency anaemia- Gastric malignancy Management:The treatment is with triple therapy- two antibiotics, and an antacid.Treatment failure is often attributed to a possible worldwide increase in macrolide resistance. Interestingly, children have higher antibiotic resistance compared with adults.Note:Zollinger-Ellison syndrome (ZES) causes gastrin-secreting tumours and can present as a part of multiple endocrine neoplasia type 1 (MEN1)- an autosomal dominant disorder.

The structure in question is the rectus sheath. This sheath encloses the rectus abdominis muscle and thus, will be encountered by the surgeon.Note:- Midline incision: It is the most common approach to the abdomen. The structures divided during this incision are linea alba, transversalis fascia, extraperitoneal fat, and peritoneum ( with care taken to avoid the falciform ligament above the umbilicus).The bladder can be accessed via an extraperitoneal approach through the space of Retzius.- Paramedian incision: It is an incision that is made parallel to the midline. The structures divided or retracted are anterior rectus sheath, rectus (retracted), posterior rectus sheath, transversalis fascia, extraperitoneal fat, and peritoneum.- Battle incision: It is similar to a paramedian but the rectus is displaced medially (and thus denervated).- Kocher’s incision: It is an incision made under the right subcostal margin, e.g. cholecystectomy (open).- Lanz incision: It is an incision in the right iliac fossa, e.g. appendicectomy.Gridiron incision: It is an oblique incision centred over the McBurney’s point – usually used for appendicectomy (less cosmetically acceptable than LanzPfannenstiel’s incision: It is a transverse suprapubic incision, primarily used to access pelvic organs.McEvedy’s incision: It is a groin incision used for emergency repair strangulated femoral hernia.Rutherford Morrison incision: It provides an extraperitoneal approach to left or right lower quadrants. It provides excellent access to iliac vessels and is the approach of choice for first-time renal transplantation.

Peutz-Jeghers syndrome (PJS) is an autosomal dominant inherited disorder characterized by intestinal hamartomatous polyps in association with a distinct pattern of skin and mucosal macular melanin deposition (freckles on the lips, face, palms and soles). Patients with Peutz-Jeghers syndrome have an estimated 15-fold increased risk of developing intestinal cancer compared to the general population.Management: conservative unless complications develop.

Based on the clinical scenario, the most probable diagnosis is Wilson’s disease. Elevated serum ceruloplasmin levels can confirm the diagnosis.Serum ceruloplasminWilson’s disease causes reduced binding of copper to ceruloplasmin, which is the body’s primary copper carrying protein. As a result, copper cannot be excreted into the bile. Copper, therefore, builds up in the liver, causing toxicity and is secreted into the bloodstream unbound to ceruloplasmin. This free copper is deposited around the body, especially the brain, eyes and kidneys. The genetic defect means that ceruloplasmin is not released into the bloodstream| therefore, ceruloplasmin is low in Wilson’s disease.Other options:- Microscopic evaluation of the hair is performed in Menke’s disease, which is a disease of copper absorption leading to copper deficiency. This causes kinky hair, failure to thrive and neurological symptoms (such as hypotonia).- Magnetic resonance imaging (MRI) scan of the brain: An MRI brain may show features of Wilson’s disease (especially in the basal ganglia), but it is not diagnostic.- Serum ferritin: Serum ferritin becomes high in haemochromatosis. This classically causes cirrhosis, bronzing of the skin, cardiomyopathy and diabetes.- Ultrasound scan of the abdomen: While it is useful in any case of hepatomegaly| it is not going to provide the diagnosis in this case.

Coeliac disease is associated with the following conditions:- Dermatitis herpetiformis- Autoimmune disorders (e.g. thyroid disease, pernicious anaemia, diabetes)- IgA deficiency- Small-bowel malignancy, particularly lymphoma, if the gluten-free diet is not followed.Serology testing: The IgA tissue transglutaminase antibody is the most sensitive and specific, compared with the anti-endomysial antibody. However, false negatives will occur in children who are IgA-deficient, and IgA levels should be taken at the same time. Other options:Distal obstruction syndrome, meconium ileus, pancreatitis and rectal prolapse are all gastrointestinal manifestations of cystic fibrosis.

Based on the presentation, the patient is probably a case of Crohn’s disease. The first-line treatment of Crohn’s disease is exclusive enteral nutrition.Exclusive enteral nutrition (EEN)This involves drinking a protein-based formula exclusively for 6–8 weeks. It has been shown to have superior mucosal healing when compared with steroids. Furthermore, it is nutritionally advantageous when compared to steroids and does not have the side-effect profile of steroids.Other options:- Intravenous steroids: This is the first-line treatment for ulcerative colitis (UC) or Crohn’s disease if there is rectal disease (which is not the case here). Side-effects include adrenal suppression, behavioural effects, osteopenia and changes in adipose tissue distribution.- Oral steroids: This can be used if EEN is not possible. However, the side-effect profile is less favourable and is not as effective concerning mucosal healing.- Parental nutrition and surgery: They may be occasionally required in severe cases that have failed first-line therapy.

The patient has bloody diarrhoea that sounds like a food poisoning in the clinical scenario. Campylobacter is the most common cause of this in the United Kingdom. This is then followed by Salmonella and Shigella. The symptoms are usually self limiting. This is more likely to be bacterial from the food than a viral gastroenteritis.

From the midgut derives most of the small intestine as well as some parts of the large intestine, including the appendix. The appendix is at the base of caecum, up to 10cm long and mainly comprised of lymphoid tissue (Hence mesenteric adenitis may mimic appendicitis).

The most probable diagnosis in this patient is lead poisoning.Lead poisoning: While it is not common, it can be potentially fatal. One of the key presenting features here is pica, the ingestion of non-nutritive substances such as soil, soap, paper or wood. Pica can also be observed in children in iron-deficiency anaemia, developmental delay and pregnancy. However, in a child who is exposed to lead in their environment (e.g. from lead paint or pipes), lead poisoning is most likely. It is commonly associated with iron deficiency which in turn increases the lead absorption. Treatment is either with oral D-penicillamine or intravenous sodium calcium edetate.