GI physiology passmed

Question 1

A 33-year-old female is referred to the endocrine clinic. She has missed her last two periods and has been lactating. She has gained weight and complains of vaginal dryness. The endocrinologist chooses to measure her prolactin levels. Which hormone is responsible for inhibiting prolactin release from the pituitary gland?

Thyrotropin releasing hormone
Oestrogen
Gonadotropin releasing hormone
Luteinising hormone
Dopamine

Answer 1

Prolactin release is persistently inhibited by dopamine

Dopamine persistently inhibits prolactin. Prolactin release is upregulated by thyrotropin-releasing hormone and oestrogen. Prolactin has an inhibitory effect on gonadotropin-releasing hormone and luteinising hormone.

Question 2

A 23-year-old frequent gym-goer has been injecting growth hormone to increase his muscle mass. Which of the following is he now at an increased risk of?

Hypercholesterolaemia
Diabetes mellitus type II
Psoriasis
Thyroid disorders
Hypotension

Answer 2

Diabetes mellitus type II

The correct answer is that an excess of growth hormone will increase the risk of developing diabetes mellitus type II. This is because the hormone mobilises glucose from fat stores (to build muscle), thus increasing its concentration in the blood. Subsequently, the pancreas has to secrete greater amounts of insulin to combat the increased levels of glucose.

Other symptoms of excess growth hormone may include thickened skin, enlarged hands and feet, a prominent jaw, carpal tunnel syndrome, tiredness, muscle weakness and hypertension.

Question 3

Which one of the following is not an effect of somatostatin?

It stimulates pancreatic acinar cells to release lipase
It decreases gastric acid secretion
It deceases gastrin release
It decreases pepsin secretion
It decreases glucagon release

Answer 3

It stimulates pancreatic acinar cells to release lipase

It inhibits pancreatic enzyme secretion.

A working knowledge of gastric secretions is important for surgery because peptic ulcers are common, surgeons frequently prescribe anti secretory drugs and because there are still patients around who will have undergone acid lowering procedures (Vagotomy) in the past.

Gastric acid
Is produced by the parietal cells in the stomach
pH of gastric acid is around 2 with acidity being maintained by the H+/K+ ATP ase pump. As part of the process bicarbonate ions will be secreted into the surrounding vessels.
Sodium and chloride ions are actively secreted from the parietal cell into the canaliculus. This sets up a negative potential across the membrane and as a result sodium and potassium ions diffuse across into the canaliculus.
Carbonic anhydrase forms carbonic acid which dissociates and the hydrogen ions formed by dissociation leave the cell via the H+/K+ antiporter pump. At the same time sodium ions are actively absorbed. This leaves hydrogen and chloride ions in the canaliculus these mix and are secreted into the lumen of the oxyntic gland.

Phases of gastric acid secretion
There are 3 phases of gastric secretion:

1. Cephalic phase (smell / taste of food)
   30% acid produced
   Vagal cholinergic stimulation causing secretion of HCL and gastrin release from G cells
2. Gastric phase (distension of stomach )
   60% acid produced
   Stomach distension/low H+/peptides causes Gastrin release
3. Intestinal phase (food in duodenum)
   10% acid produced
   High acidity/distension/hypertonic solutions in the duodenum inhibits gastric acid secretion via enterogastrones (CCK, secretin) and neural reflexes.

Regulation of gastric acid production
Factors increasing production include:
Vagal nerve stimulation
Gastrin release
Histamine release (indirectly following gastrin release) from enterchromaffin like cells

Factors decreasing production include:
Somatostatin (inhibits histamine release)
Cholecystokinin
Secretin

The diagram below illustrates some of the factors involved in regulating gastric acid secretion and the relevant associated pharmacology