(a) Discuss the stomach under the following headings: (i) Peritoneal relations (ii) Blood supply (iii) Lymphatic drainage (15…

(a) Stomach: peritoneal relations, blood supply and lymphatic drainage

(i) Peritoneal relations: the stomach is intraperitoneal, covered by peritoneum on both surfaces, which meet at the curvatures.

• Lesser curvature: lesser omentum (hepatogastric ligament) to the liver, containing the left and right gastric vessels.
• Greater curvature: greater omentum (gastrocolic part) below, gastrosplenic ligament on the left, gastrophrenic ligament above.
• Bare area: a small posterior area near the cardia in contact with the left crus of the diaphragm, between the layers of the gastrophrenic ligament.
• Posterior surface forms the anterior wall of the lesser sac and rests on the stomach bed (diaphragm, spleen, left kidney and suprarenal, pancreas, transverse mesocolon, splenic artery). Anteriorly: liver, diaphragm and anterior abdominal wall.

(ii) Blood supply: all from the coeliac trunk.

• Lesser curvature: left gastric artery (direct branch, also gives oesophageal branches) and right gastric artery (from the common or proper hepatic).
• Greater curvature: right gastroepiploic (from gastroduodenal) and left gastroepiploic (from splenic).
• Fundus: short gastric arteries (5–7, from splenic) and posterior gastric artery.
• Veins accompany the arteries and drain into the portal system. The left gastric vein has oesophageal tributaries forming a portosystemic anastomosis (varices in portal hypertension).

(iii) Lymphatic drainage: follows the arteries in four zones, all reaching the coeliac nodes.

• Left gastric nodes (upper two-thirds of lesser curvature side).
• Pancreaticosplenic nodes (left upper greater-curvature side and fundus).
• Right gastroepiploic and subpyloric nodes (lower greater-curvature side).
• Right gastric, hepatic and pyloric nodes (pyloric part of lesser curvature). Clinical note: spread to the left supraclavicular (Virchow) node and the basis of D1/D2 lymphadenectomy in gastric cancer.

(b) Growth hormone: regulation and functions

Regulation: GH is secreted in pulses by somatotrophs, largest in slow-wave sleep. GHRH stimulates and somatostatin inhibits secretion, and gastric ghrelin stimulates it. IGF-1 and GH feed back negatively. Stimuli: hypoglycaemia, fasting, exercise, stress, amino acids (arginine), sleep, oestrogens. Inhibitors: hyperglycaemia, free fatty acids, obesity, glucocorticoid excess. Functions:

• Growth: via IGF-1, stimulates chondrocyte proliferation at epiphyseal plates (linear growth) and growth of soft tissues.
• Protein: anabolic, increases amino acid uptake and protein synthesis, positive nitrogen balance.
• Fat: lipolysis and fatty acid mobilisation.
• Carbohydrate: anti-insulin (diabetogenic), raises blood glucose.
• Others: retention of sodium, phosphate and calcium absorption. Excess causes gigantism or acromegaly, deficiency causes short stature.

(c) Physiological jaundice of the newborn

Definition: transient unconjugated hyperbilirubinaemia in a healthy newborn, appearing after 24 hours (usually days 2–3), peaking on days 3–5 and clearing by about 2 weeks in term babies, with bilirubin usually below about 12–15 mg/dL and no underlying disease. Predisposing causes (mechanisms):

• High red cell mass and shorter red cell life (70–90 days), increasing bilirubin load.
• Immature hepatic uptake (low ligandin) and low UDP-glucuronyl transferase activity.
• Increased enterohepatic circulation (β-glucuronidase, sterile gut, delayed passage of meconium).
• Contributing factors: prematurity, inadequate breastfeeding, bruising or cephalhaematoma, polycythaemia, delayed cord clamping. Effects: yellow skin and sclera, usually harmless and self-limiting. If bilirubin rises excessively, unbound unconjugated bilirubin crosses the blood–brain barrier and can cause acute bilirubin encephalopathy and kernicterus (deafness, choreoathetosis), so levels are monitored and phototherapy given when indicated, and pathological causes (onset within 24 hours, rapid rise, conjugated fraction, persistence) are excluded.

(d) Developmental anomalies of the kidney and ureters

Kidney (metanephros): renal agenesis (failure of ureteric bud, bilateral form causes Potter sequence), hypoplasia, ectopic or pelvic kidney (failure of ascent), horseshoe kidney (lower-pole fusion, trapped under the inferior mesenteric artery), malrotation, crossed ectopia, multicystic dysplastic kidney. Ureter (ureteric bud): duplex ureter (bifid or complete), ectopic ureteric opening, pelviureteric junction obstruction, ureterocele, megaureter, vesicoureteric reflux, retrocaval ureter. They present with hydronephrosis, infection or calculi, often detected on antenatal ultrasound.

(e) Placental hormones in pregnancy

• hCG (syncytiotrophoblast): maintains the corpus luteum and its progesterone in early pregnancy, peaks at 8–10 weeks, stimulates fetal testicular testosterone and has mild TSH-like action. Basis of pregnancy tests.
• hPL (human chorionic somatomammotropin): anti-insulin, lipolytic effects, ensuring glucose and amino acid supply to the fetus, and helps breast development.
• Progesterone: maintains the decidua, keeps the myometrium quiescent, prevents rejection, prepares breast alveoli and raises respiratory drive.
• Oestrogens (mainly oestriol, via the feto-placental unit): uterine growth and blood flow, ductal growth of breasts, relaxation of pelvic ligaments.
• Others: placental CRH (timing of labour), relaxin (with corpus luteum, softens cervix), leptin and growth factors.