Karius Flashcards
ACh, NE, VIP, Enkephalins (opiates) are all what?Be careful of which bc results in what SE when used for pain management?
- all GI NT
Enkephalins - constipation
Gastrin
- stimulus for secretion
- site of secretion
- actions
- distention of stomach, Vagus
- secreted from G cells in stomach
- action - increase gastric acid
Cholecystokinin (CCK)-
- stimulus for secretion
- site of secretion
- ACTIONS(5)**
-aa, peptides, FA
-I cells of duodenum and jejunum
- Fat absorption
1) **GB cxn
2) **Increase pancreatic enzyme secretion
3) Increase pancreatic bicarb secretion
4) growth of exocrine pancreas an dGB
5)decreases GASTRIC EMPTYING/inc emptying time
(also acts on brain/liver to cause satiety)
Secretin:
- stimulus for secretion
- site of secretion
- actions
- Acid or FA in duodenum
- S cells of duodenum
- increase pancreatic bicarb, increased biliary bicarb, dec. gastric acid secretion
Glucose-dependent Insulinotropic Peptide (GIP):
- stimulus for secretion
- site of secretion
- actions
- FA, aa, oral glucose
- duod/jejunum
- inc insulin from pancreatic B cells, dec gastric acid secretion
Pancreatic enzymes:
- somatostatin (D cells) –> when luminal pH decreased to dec. acid
- histamine - stimulate acid
Where is the satiety center located?
VPN - ventromedial nucleus of the hypoth
Where is the feeding center located? Where does the incoming info come from?
LHA - lateral hypothalamic area.
Info comes from the Arcuate Nucleus of the hypothalmus
What is released from the arcuate nucleus to DECREASE appetite. What substances act on arcuate nucleus to cause this.
Anorexigenic Neurons release POMC to dec appetite.
-Release stimulated by LEPTIN, insulin, GLP-1
CCK also acts on brain/liver to cause satiety
What is released from the arcuate nucleus to INCREASE appetite. What substances act on arcuate nucleus to cause this.
Orexgenic Neurons release neuropeptide Y to inc appetite.
-Release of GHRELIN by gastrin cells.
Where is the vomiting center? Afferent info comes from what 4 locations?
Medulla –> NUCLEUS TRACTUS SOLITARIUS (also pharyngeal swallow coordination center)
Info comes from: vstibular system, back of throat, GI, and CTZ
The sequence of the vomiting reflex:
VOMITING:
- Rerverse peristalsis
- relaxation of the stomach and pylorus
- forced inspiration to inc abd pressure
- mvmt of larynx upward and forward and RELAXATION of LES
- glottis closure
- forceful expulsion of gastric –> UES OPEN
RETCHING - UES CLOSED, LES open (gastric contents stay in stomach
GI secretions from the saliva.
- Names
- Factors that increases secretion
- Factors that decrease secretion
- bicarb, potassium, amylase, lipase
- PSNS(major), SNS
- sleep, dehydration, atropine
GI secretions from the Stomach (2)
- Names
- Factors that increases secretion
- Factors that decrease secretion
- HCl (stim by GASTRIN, ACh, HISTAMINE; dec. by acid, chyme in duod, somatostatin, atropine, cimetidine, omeprazole)
- Pepsinogen factor (stim by PSNS)
GI secretions from the Pancrease (2).
- Names
- Factors that increases secretion
- Bicarb (inc by secretin, CCK, PSNS)
- Pancreatic lipase/amylase/proteases (inc. by CCK and PSNS)
GI secretions from the Stomach (4)
- Names
- Factors that increases secretion (same for all 4)
- Factors that decrease secretion (same for all 4)
- Bile salts, Bilirubin, Phospholipids, cholesterol
- inc. by CCK (GB cxn, Oddi relaxation), PSNS
- dec. by ileal resection
Mechanism of HCl secretion by parietal cells: basolateral membrane exchangers and apical membrane channels.
-omeprazole affects what?
- Basolateral exchangers: Na/K ATPase, HCO3/Cl exchangers
- Apical channels - H/K ATPase and Cl channels
Digestion and absorption of carbohydrates
Location of absorption: SI
Digestion: Salivary and Pancreatic amylase, SI sucr/malt/lact/trehalASE
Digestion and absorption of proteins
Location of absorption: SI
Digestion: Stomach pepsin, pancreatic typsin, chymotryp, carboxypeptidase, elastase, SI dipeptidase/enterokinase
Digestion and absorption of lipids
Location - SI
Digestion - lingual lipase. pancreatic lipase-colipase, PLA2, cholesterol ester hydrolase
Diarrhea due to increased motility - 2 ways
- Peristaltic rush - SI irritation, clears irritant. SUBSTANCE P binds to NK-1 receptor
- Ultrapropulsive event - irritation in LI, clears irritant. NEUROKININ B binds to NK3 receptor
What triggers production of bile salts/acids?
Return of bile salts/acids to liver.
Relaxation of hepatopancreatic sphincter of Oddi is produced by?
Wave of relaxation that precedes a peristaltic wave in duodenum
Widened, flattened villi on biopsy associated with what type of diarrhea?
Osmotic
