Gastrology Flashcards
What is a choledochal cyst
sever liver dysfunction
+ / - abdominal mass
large common channel drainage pancreatic and bile duct - juices cause wall destruction this with stenosis cause cysts
What would be seen in protein-losing enteropathy
high levels of alpha-1 antityrptase in stool
Hypoalbuminae
Name a type of protein-losing enteropathy
lymphangiectasis
high levels of alpha1 antitryptase in stool
Hypoalbuminae
Loose stools
Embryology of diaphragm
formed between 5th and 7th week
Fusion of septum transverse, pleuroperitoneal folds, cervical somites
Septum transverse - central tendon
Pleuroperitoneal folds - parietal membranes surrounding viscera
Cervical somites - C5-C7 muscular components
Embryology of GI tract
Endoderm - epithelial lining of GI tract
Mesoderm - smooth muscle
ectoderm - enteric nervous system
What structures make up the foregut
Pharynx
Oesophagus
Stomach
Proximal duodenum
What structures make up mid gut
forming distal duodenum
Small bowel
Distal colon
What structures Make up hind gut
Distal colon
Rectum
Timeline of rotation of GI tract
5th week - intestine elongates and form loop - protrudes into umbilicus
6th week - stomach and duodenum rotate 90 degrees
8th week - duodenum and jejunum herniate further from superior mesenteric artery
11th week - GI retracts into abdomen
What is villous atrophy
Villi surrounding small intestine erode away
What causes villious atrophy
Coeliac disease
NSAIDS
Giardsis
H. pylori gastritis
What produces gastric acid
Parietal cells in the stomach
Maintained by H+ / K+ / ATPase pump
What is stomach pH ?
around 2
1.5-3.5
Pathophysiology of gastric acid production
Sodium and chloride cells secreted from parietal cells to canniculis
Negative gradient - K+ and Na cells move down into it
H20 and CO2 from to make carbonic anhydrase
Carbonic anhydrase dissociates - H + move out of cells into stomach lumen, Na and K+ move into cells - leaves Cl and H+ ions in cannaiculis
What increases gastric cell production
Vagal nerve stimulation
Gastrin release
Histmaine release
Where is the gastrin released from
Released from G cells in pyloric antrum and duodenum
How does gastrin work
Directly- Stimulates parietal cells to release HCL
Indirectly work on enterochromaffin cells - binds to CCK2 receptors -> releases histamines -> parietal cells
Where is pepsinogen released
chief cells
Other functions of gastrin
Causes chief cells to release pepsinogen -> pepsin
Promotes muscle contraction
Strengthens antrum contractions - > increases rate of gastric emptying
Induces pancreatic secretions
What factors increase gastrin
partially digested proteins
Hypercalcaemia
Stomach distension
Vagal stimulation
What inhibits gastrin
Too much HCl - negative feedback
Glucagon
Somatostatin
GIP / VIP
What pH of the duodenum
7-8