Cushing’s syndrome is a collection of symptoms and signs caused by prolonged exposure to elevated levels of either endogenous or exogenous glucocorticoids.The most common cause of Cushing’s syndrome is the iatrogenic administration of corticosteroids. The second most common cause of Cushing’s syndrome is Cushing’s disease.Cushing’s disease should be distinguished from Cushing’s syndrome and refers to one specific cause of the syndrome, an adenoma of the pituitary gland that secretes large amounts of ACTH and, in turn, elevates cortisol levels. This patient has a diagnosis of Cushing’s disease, and this is, therefore, the underlying cause in this case.The endogenous causes of Cushing’s syndrome include:Pituitary adenoma (Cushing’s disease)Ectopic corticotropin syndrome, e.g. small cell carcinoma of the lungAdrenal hyperplasiaAdrenal adenomaAdrenal carcinoma

A scatterplot is a useful summary of a set of bivariate data (two variables), usually drawn before working out a linear correlation coefficient or fitting a regression line. It gives a good visual picture of the relationship between the two variables, and aids the interpretation of the correlation coefficient or regression model. Each unit contributes one point to the scatterplot, on which points are plotted but not joined. The resulting pattern indicates the type and strength of the relationship between the two variables.

The stages of wound healing are: haemostasis, inflammatory, proliferative and remodelling (maturation) phases in that order. The first stage in the healing process of a laceration is haemostasis. Haemostasis is the process of the wound being closed by clotting. The inflammatory phase occurs just after and up to 48 hours after injury– Blood vessels dilate to allow white blood cells, antibodies, growth factors, enzymes and nutrients to reach the wounded area leading to the characteristic signs of inflammation seen. Epithelialisation and angiogenesis are not phases of wound healing but occur during the proliferative phase. This ia after haemolysis and inflammation phases have occurred.The maturation phase is the final phase and occurs when the wound has closed. It involves remodelling of collagen from type III to type I. Apoptosis remove unwanted cells, cellular activity reduces and the number of blood vessels in the wounded area regresses and decreases. This can continues for up to 1 year after injury.

Antibiotics that are bactericidal kill bacteria, while antibiotics that are bacteriostatic limit their growth or reproduction. The antibiotics grouped into these two classes are summarized in the table below:Bactericidal antibioticsBacteriostatic antibioticsVancomycinMetronidazoleFluoroquinolone, such as ciprofloxacinPenicillins, such as benzylpenicillinCephalosporin, such as ceftriaxoneCo-trimoxazoleTetracyclines, such as doxycyclineMacrolides, such as erythromycinSulphonamides, such as sulfamethoxazoleClindamycinTrimethoprimChloramphenicol

Gastric emptying is decreased by: Enterogastric inhibitory reflexes stimulated by – Distension of the duodenum, The presence of fats in the duodenum (by stimulating release of cholecystokinin), A fall in the pH of chyme in the duodenum, An increase in the osmolality of chyme in the duodenum, Irritation of the mucosal lining of the duodenum, Hormones: Cholecystokinin, Secretin

Achlorhydria is an autoimmune illness of the gastric parietal cells that causes insufficient stomach acid production. The parietal cells that have been injured are unable to create the necessary amount of stomach acid. As a result, the pH of the stomach rises, food digestion suffers, and the risk of gastroenteritis rises.The secretion of hydrochloric acid and intrinsic factor is controlled by the gastric parietal cells, which are epithelial cells in the stomach. These cells can be found in the gastric glands, the fundus lining, and the stomach body.In response to the following three stimuli, the stomach parietal cells release hydrochloric acid:H2 Histamine receptors are stimulated by histamine (most significant contribution)Acetylcholine stimulates M3 Receptors via parasympathetic action.CCK2 receptors are stimulated by Gastrin.Intrinsic factor, which is essential for vitamin B12 absorption, is also produced by stomach parietal cells.Omeprazole is a proton pump inhibitor that is both selective and irreversible. It inhibits the H+/K+-ATPase system present on the secretory membrane of gastric parietal cells, which lowers stomach acid secretion.Ranitidine inhibits histamine H2-receptors in a competitive manner. The reversible inhibition of H2-receptors in gastric parietal cells reduces both the volume and concentration of gastric acid.

Insulin is produced by beta cells, located centrally within the islets of Langerhans, in the endocrine tissues of the pancreas. Insulin is a polypeptide hormone consisting of two short chains (A and B) linked by disulphide bonds. Proinsulin is synthesised as a single-chain peptide. Within storage granules, a connecting peptide (C peptide) is removed by proteases to yield insulin. Insulin release is stimulated initially during eating by the parasympathetic nervous system and gut hormones such as secretin, but most output is driven by the rise in plasma glucose concentration that occurs after a meal. The effects of insulin are mediated by the receptor tyrosine kinase.

Somatostatin-producing cells present in the pyloric antrum, duodenum, and pancreatic islets are known as D-cells or delta-cells. Somatostatin inhibits gastric acid secretion by acting directly on acid-producing parietal cells in the stomach via a G-protein coupled receptor. By suppressing the release of other hormones such as gastrin, secretin, and histamine, somatostatin can indirectly reduce stomach acid output, slowing the digesting process.The table below summarizes the many cell types found in the stomach, as well as the substances secreted by each cell type and the function of the secretion:Cell type/ Substance secreted/ Function of secretionParietal cells/ Hydrochloric acid/ Kills microbes and activates pepsinogenParietal cells/ Intrinsic factor/Binds to vitamin B12 and facilitates its absorptionChief cells/ Pepsinogen/ Protein digestionChief cells/ Gastric lipase/ Fat digestionG-cells/ Gastrin/ Stimulates gastric acid secretionEnterochromaffin-like cells (ECL cells) /Histamine/ Stimulates gastric acid secretionMucous-neck cells/ Mucous and bicarbonate/ Protects stomach epithelium from acidD-cells/ Somatostatin/ Inhibits gastric acid secretion

Nitric oxide (NO) production by the endothelium is increased by factors that elevate intracellular Ca2+, including local mediators such as bradykinin, histamine and serotonin, and some neurotransmitters (e.g. substance P). Increased flow (shear stress) also stimulates NO production and additionally activates prostacyclin synthesis. The basal production of NO continuously modulates vascular resistance; increased production of nitric oxide acts to cause vasodilation. Nitric oxide also inhibits platelet activation and thrombosis.

Megaloblastic anemia results from inhibition of DNA synthesis during red blood cell production. When DNA synthesis is impaired, the cell cycle cannot progress from the growth stage to the mitosis stage. This leads to continuing cell growth without division, which presents as macrocytosis, with an increase in mean corpuscular volume (MCV). The defect in red cell DNA synthesis is most often due to hypovitaminosis, specifically vitamin B12 deficiency or folate deficiency.Folate is an essential vitamin found in most foods, especially liver, green vegetables and yeast. The normal daily diet contains 200 – 250 μg, of which about 50% is absorbed. Daily adult requirements are about 100 μg. Absorption of folate is principally from the duodenum and jejunum. Stores of folate are normally only adequate for 4 months and so features of deficiency may be apparent after this time.