Flashcards in GI Session 4 Deck (92):
What are gastric pits?
Indentations on gastric mucosa which denote entrances to tubular gastric glands
Where are tubular gastric glands deepest?
What cell types make up tubular gastric glands?
What cells are found between gastric pits?
What is secreted by each cell type in the gastric pit?
Surface and neck mucus cells secrete mucus and alkali
What do the endocrine cells between gastric pits secrete?
What is secreted by the cell types in the gastric gland?
Parietal --> acid
Chief --> enzymes
How is acid secreted by parietal cells in the gastric glands?
Mitochondria split H2O --> H+ and OH- releasing ATP and CO2
OH-+CO2 --> HCO3- flows down concentration gradient into ECF
H+ actively pumped out of cell using ATP released
What is the canaliculus of a parietal cell?
Invagination of cell wall with proton pump
What shape are the parietal cells?
What are the 3 main factors which overlap to control gastric acid c
How does gastrin control gastric acid secretion?
Secreted by G-cells --> blood --> surface receptor on parietal cells --> secondary messenger --> acid and intrinsic factor secretion
How does a lack of gastrin release from G-cells lead to aneamia?
Lack of intrinsic factor secretion stimulation from parietal cells so vitamin B12 cannot be absorbed
How does histamine control gastric acid secretion?
Local release from mast cells scattered in gastric mucosa like endocrine cells --> H2 receptor on parietal cells --> cAMP --> acid secretion
What is different about the histamine receptors in the stomach?
H2 compared to H1 elsewhere, therefore H2 are almost unique to stomach parietal cells
How does ACh control gastric acid secretion?
Local release from post-ganglionic parasympathetic neurones of stomach wall plexuses --> muscarinic receptor on parietal cell--> secondary messenger --> acid secretion
What do G-cells sense and why?
Peptides and low pH due to proximity to surface of mucosa
What stimulates mast cells in the stomach to amplify the original signal for acid secretion?
What antagonises histamine action on parietal cells and therefore provides an effective mechanism of decreased acid secretion?
What can activate intrinsic neurones to release ACh to act directly on parietal cells to stimulate acid secretion?
Distension on stretch receptors
What are the three phases of acid secretion control?
What happens in the cephalic phase of acid secretion control?
Smelling/tasting/chewing food causes brainstem to use ANS to fire efferent impulses --> ACh stimulates parietal cells directly and indirectly via histamine to secrete acid
What happens in the initial surge of the gastric phase of acid secretion control?
Food bolus reaches stomach --> buffers stomach acid due to alkaline saliva and amine groups covering food --> increases stomach pH --> G-cells release gastrin --> stimulates acid secretion
Stomach distends --> intrinsic nerves --> ACh
What happens in the secondary surge of gastric phase of acid secretion control?
Initial digestion releases peptides --> gastrin released --> acts with previously released ACh --> histamine release
What ensures acid secretion continues when buffering and distension are acting at max stimulatory effect?
Secondary surge in gastric phase of acid secretion control
What happens in the intestinal phase of acid secretion control?
Stomach slowly empties chyme into duodenum --> G-cells stimulate further gastrin secretion in duodenum --> rapidly counteracted by duodenal hormones --> signal stomach function is complete
Accumulation of acid in empty inhibits gastrin secretion
What is the characteristic history of stomach ulcer?
Epigastric pain at 2-3am eased by eating
How does the mucus in the stomach compare to that in the saliva?
Much more viscous
What halogens to the mucus layer of the stomach when it is disrupted?
What is the unstirred layer in the stomach?
Surface epithelial cells secrete mucus and HCO3- which absorb and react with H+ to prevent damage to cells
What do H+ react with in the unstirred layer?
HCO3- and basic groups on mucus glycoproteins
What causes stimulation of secretion of the components of the unstirred mucus layer?
Prostaglandins which are promoted by most factors that stimulate acid secretion so defences match attack
What are the stomach secretions for defence against self-digestion?
Mucus and HCO3-
What causes persistent alcoholic gastritis?
Ongoing alcohol consumption causing mucus to be repeatedly dissolved
How does H.pylori infection lead to gastritis at least and peptic ulcer at worst?
Inhibits self-healing mechanisms of mucus
How can NSAIDs breach stomach defences?
Inhibit prostaglandins so decrease mucus and alkali secretion
Some converted into benign non-ionised form by stomach acid so they can pass through mucosa and be re-ionised in surface epithelial cells and become harmful
What are the stages of stomach motility?
Relax to accommodate food --> rhythmically contract to break down large particles --> slow delivery of chyme to duodenum
How is receptive relaxation of the stomach brought about?
On swallowing a neural reflex via the vagus nerve and nerve plexuses --> active relaxation of tension in stomach wall
What is the purpose of receptive relaxation in the stomach?
Prevent pressure increase within the stomach to reflux is limited
How is the wave of peristalsis in the stomach brought about?
Pacemaker in the cardia region fires about 3x a minute to cause contraction of longitudinal and circular muscle
How does the wave of peristalsis change as it moves across the stomach?
Slow at top where the stomach is wider as more cells have to be stimulated --> antrum accelerates as fewer cells
What does the acceleration of the wave of peristalsis across the stomach cause to happen to the stomach contents?
Inertia or larger lumps means they are overtaken by the wave and pushed back into fundus
How is chyme delivered slowly to the duodenum?
Initially Pylorus is open so a small squirt of chyme is ejected but the peristaltic wave shuts Pylorus so chyme is returned to the stomach
How is the control of gastric emptying exerted?
Intestinal hormones signal to stomach how much chyme it can facilitate and rate of peristaltic wave acceleration is altered to change the volume of chyme ejected
What is detected in the duodenum which causes it to signal to the stomach that it can accommodate a large volume of chyme?
Is the frequency of peristaltic wave in the stomach constant?
Why does the midgut have to make a loop as it develops?
Runs out of space due to the rapid enlargement of itself and the liver
What does the midgut use as its axis when forming a loop?
SMA connected to the yolk sac via the vitelline duct
What does the formation of a loop by the midgut result in?
Cranial and caudal limbs
Does the cranial or caudal midgut limb elongate more?
What are the adult derivatives of the cranial midgut limb?
What are the adult derivatives of the caudal midgut limb?
Proximal 2/3 transverse colon
What happens in physiological herniation in the 8th week of development?
Intestinal loops --> umbilical cord during which small intestinal loops and caecum form
When do the cranial and caudal limbs of the midgut form during development?
How does the midgut rotate during physiological herniation?
3x90 degree rotations counter clockwise
What happens during the first 90 degree rotation of the midgut?
During herniation results in limbs running parallel --> cranial limb elongates and child to form large jejunal loops
What happens during the second 90 degree rotation of the midgut?
During hernia resolution caudal limb moves in front of cranial so caudal derivatives lie anteriorly
What happens during the third 90 degree rotation of the midgut?
During hernia resolution the cranial limb with extensive looping retracts to the L side first as ceacal bud stops caudal limb --> transverse colon anterior to duodenum
What is the ceacal bud?
Small conical dilation of the caudal limb of the primary intestinal loop
What is the last part to enter the abdominal cavity on hernia resolution?
How is the appendix formed?
Distal end of ceacal bud forms a narrow diverticulum
What causes the ascending colon and hepatic flexure to be in the R side?
Movement of caecal bud from directly below R lobe of liver in RUQ --> RIF
What is sub-hepatic caecum?
Where the caecal bud does not move during development leading to a short p/absent ascending colon
What is the clinical relevance of sub-hepatic caecum?
In acute appendicitis tenderness is not located at McBurney's point
What happens in incomplete rotation of the midgut?
Midgut loop only makes one 90 degree rotation --> L sided colon as colon and caecum return first and late loops must move to R
What happens in reversed rotation of the midgut?
Midgut loop makes one 90 degree rotation clockwise --> transverse colon posterior to duodenum lying posterior to SMA
What is a major complication of midgut abnormalities?
Volvulus due to abnormal mobility
SMA compression of transverse colon
What can persistence of the vitelline duct result in?
Vitelline cyst or fistula
What causes increased risk of volvulus in Meckel's diverticulum?
Attachment by fibrous cord
What is the difference between atresia and stenosis?
When can atresia or stenosis occur during development of the GI tract?
When recanalisation of the oesophagus, bile duct or small intestine is wholly or partially unsuccessful
Describe the incidence of aterisa/stenosis in the duodenum, jejunum, ileum and colon.
What is atresia/stenosis of the upper duodenum most likely to be due to?
Failure of recanalisation
What is atresia/stenosis of the lower duodenum most likely to be due to?
Vascular accident leading to tissue necrosis
What is pyloric stenosis?
Hypertrophy of pyloric sphincter circular muscle
Is pyloric stenosis a failure of recanalisation?
What is the characteristic presentation of pyloric stenosis?
Projectile vomiting in neonate
Why does omphalocoele have a lower survival rate than gastroschisis?
Associated with other abnormalities and chromosomal disorders
Why does tissue above the pectinate line have poorly localised pain?
Organisation of afferents giving visceral innervation
What happens to the hindgut at 6 weeks?
Has swollen into cloaca which undergoes anteroposterior subdivision to give rise to the urogenital sinus and anorectal canal
Describe the process that leads to perforation of the anus.
Urogenital septum grows down to meet cloacal membrane and proctodeum ectoderm pushes up to meet gut tube --> perineal body forms as urogenital septum reaches cloacal membrane --> anus perforates with perineal body anteriorly
What is the importance of the perineal body?
Crucial for integrity of the pelvic floor
Which organs retain their mesenteries?
Which organs develop fixed mesenteries?
Where is there no peritoneal covering in the rectum?
What is the fate of the dorsal mesentery?
Jejejunal and ileal loops
What is the fate of the ventral mesentery?
What gives innervation to the midgut?
S: superior mesenteric ganglion and plexus
What gives innervation to the hindgut?
PS: pelvic (S2-4)
S: inferior mesenteric ganglion and plexus
When do the primordia of the liver, pancreas and trachea appear?
When do the pancreatic buds fuse?