- segmentation (mixing, breaking down)- SI - peristalsis (movement of food)- SI - reverse peristalsis- vomiting - SI? - MMC- between meals, stimulated by motilin between meals - mass movement (moving fecal matter)- colon

GI Flashcards by Kelly A

layers of the gut wall, from inner to outer

lumen

mucosa
submucosa
musclaris externa (circular then longitudinal)
serosa

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layers of the mucosa, from inner to outer

epithelium (specialized)
lamina propria
muscularis mucosae

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2 nerve plexuses in GI mucosa (enteric nervous system) and where they are located

submucosal plexus- in submucosa

myenteric plexus- between two muscle layers

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unit of absorption

villus

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how is the salivary system regulated? what about the rest of the GI tract?

saliva: only neural

- all others: neural, paracrine, endocrine

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5 motility patterns

segmentation (mixing, breaking down)- SI
peristalsis (movement of food)- SI
reverse peristalsis- vomiting - SI?
MMC- between meals, stimulated by motilin between meals
mass movement (moving fecal matter)- colon

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functions of saliva & key enzymes

lubrication
protection
initial digestion - not major

alpha amylase- starches
lingual lipase- lipids
lysozyme- maintains oral hygiene

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final saliva is hypo/iso/hypertonic to plasma; it was initially hypo/iso/hypertonic ; at what flow rate is it most similar to plasma

final= hypotonic (ALWAYS); initially= isotonic

most similar to plasma at high flow rates

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what are the net processes involved in saliva creation? which one is abnormal?

secrete K+, HCO3-
absorb Na+, Cl-

HCO3- stimulated by parasympathetics, increases with flow rate

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describe regulation of saliva secretion - stimulating and inhibiting factors

both result in saliva secretion!

1) parasympathetic (dominant)- releases Ach via CN 7&9 onto muscarininc receptors, Ip3/Ca2+ blocked by atropine

stimulating: conditioning, food, nausea, smell
inhibiting: dehydration, fear, sleep

2) sympathetic- T1-T3, Ne on beta-adrenergics, cAMP

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3 phases of swallowing reflex, which is voluntary

1) oral - voluntary

2) pharyngeal

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what is receptive relaxation?

LES and orad stomach relax at the same time

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roles of the UES and LES, and which one is important for GERD

1) UES- protects airway- keeps food/acid out of airway, keeps air out of esophagus
2) LES- keeps acid out of esophagus - GERD

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what does chronic gastric reflux cause?

change in esophageal mucosa from stratified squamous epithelium

1) to simple columnar (like in stomach) - just metaplasia
2) to simple columnar with goblet cells- barretts esophagus/intestinal metaplasia

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what is the essential factor the the stomach secretes?

intrinsic factor, required for vitamin B12 absorption, don’t produce anywhere else

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6 secretory cells of stomach

1) parietal/oxyntic- HCl, Intrinsic factor
2) mucous neck cells- mucus
3) peptic/chief cells- pepsinogens
4) enterochromaffin-like cells (ECLs)- histamine
5) D cells- somatostatin
6) G cells- gastrin

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where are goblet cells located? where are cholangiocytes located?

goblet: intestinal, mostly large intestine
cholangiocytes: lining the bile duct

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where does a proton pump inhibitor such as omeprazole work? what is lacking when you give this drug?

H+/K+ ATPase on luminal side

see no somatostatin b/c it only responds to low pH, have high levels of gastrin in their blood

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what is the net result of gastric acid secretion?

net secretion: HCl

net absorption: bicarb

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what protects the stomach from ulcers (what causes damage)?

damage caused by H+/pepsins
pepsin only works in low pH
thick layer of mucus with bicarb trapped inside

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stimulating agents for gastric acid secretion and drugs that block them

1) Vagus releasing Ach on M3 receptors (blocked by atropine) - neurocrine- directly working on parietal cells & potentiates
2) G-cells releasing gastrin on CCKb receptors - endocrine
3) ECL cells releasing histamine on H2 receptors (blocked by cimetidine) - paracrine

inhibition of gastric acid secretion

1) somatostatin - inhibits histamine
* direct by blocking cAMP
* indirect by inhibiting histamine and gastrin release
2) prostaglandins- inhibit cAMP

difference between gastric and duodenal ulcer

gastric- defect in mucosa barrier (not hypersecretion)
duodenal- more common- excess H+ (and pepsin) in duodenum overpowers bicarb buffering (if pancreatic secretion isn’t enough)

what major factors contribute to the slowing of gastric emptying? what hormone is this effect mediated by?

fat & AA in duodenum
H+ in duodenum
mediated by CCK released from I cells

what does CCK regulate?

1) pylorus contraction 2) gallbladder contraction- produce bile 3) relaxes sphincter of oddi- so bile/pancreatic juice can center 4) pancreatic secretion

2 components of exocrine pancreas secretions

1) aqueous- high in bicarb (ductal cells) | 2) enzymatic (acinar cells)

regulation of pancreatic ductal secretion

1) low pH in duodenum 2) stimulates S cells to release secretin 3) secretin increases ductal bicarb secretion via CFTR chloride channel * bicarb from NBC-1 or carbonic anhydrase 4) pH of intestinal lumen increases 5) secretin secretion is inhibited

3 things that trigger CCK release

1) direct action of AAs/Fats 2) fats/AA binding to paracrine cells that release CCKRP 3) pancreatic acinar cells secreting monitor peptide (neural regulation)

how are bile acids recycled?

- enterohepatic circulation | - terminal ileum asbt recycles conjugated bile acids back to liver

difference in Na absorption between jejunum and ileum

jejenum- Na+ transported with sugar/AAs on luminal side, absorbed with bicarb- on basolateral ileum- Na+ transported with sugar/AAs on luminal side, absorbed with Cl- on basolateral side

what is an illeal brake and what does it do?

EECs in terminal ileum secrete *peptide YY* in response to lipids in the lumen - decreases gastric emptying, reduces Cl (and fluid) secretion by intestinal cells - reduces fluidity

final mechaism for the absorption of H20

ENaC - Na+ channel in distal colon, patients w/ bowel inflammation have defects here

major contribution of colonic microflora

production of ammonia from urea; urease activity

what is hepatic triad

hepatic artery, portal vein, bile duct

zone 1 vs zone 2 vs zone 3 cells of liver

- zone 1- periportal- most sensitive to oxidative species, toxins b/c they encounter them first - zone 3- pericentral- close to hepatic vein- most sensitive to ischemia, most active in bile synthesis

what does a gallstone near the sphincter of oddi cause

blocks bile duct and pancreatic flow | can cause pancreatitis and cholangitis

where does bilirubin come from and how is it excreted?

- comes from heme degradation in reticuloendothelial system (macrophages) Hemeoglobin- biliverdin- bilirubin- bilirubin + albumin- taken up by OATP- conjugated in liver with UDPGT, is now water soluble- some secreted in bile - de-conjugated by bacteria to urobilinogen - urobilin & stercobilin excreted in feces

major cause of hyperbilirubinemia that cause jaudice

1) intrahepatic/extrahepatic bile duct obstruction | 2) newborns don't have UDPGT

pathologies of liver

1) hepatic encephalopathy- no urea cycle to get rid of ammonia which can cross BBB 2) liver cirrhosis- activate hepatic stellate cells which produce lots of collagen, leading to fibrosis 3) portal hypertension- increased resistance of vascular system in liver, results in spleenomegaly & fluid accumulation

energy values of food

carbs- 4 kcal/g protein- 4 kcal/g fat- 9 kcal/g

main enzyme for starch digestion and what bonds does it digest

amylase (salivary & pancreatic) | - digests alpha 1, 4 linkages (cellulose is beta 1,4)

disaccharides in food and the monosaccharides they are made up of which we can absorb

trehalose- 2 glucose sucrose- glucose + fructose lactose- glucose + galactose

what products does pancreatic amylase produce? what are they digested by?

a-limit dextrins (isomaltase), maltose (maltase), maltriose (sucrase) digested by brush border enzymes products are glucose

glucose transporter on luminal side?

SGLT1 requires Na/K ATPase

glucose/fructose/galactose transporter on basolateral side?

GLUT2

emulsification vs micelle formation

emulsification- processing before fat digestion has taken place; break down into small pieces; bile acids play big role; most in duodenum micelle formation- after fat digestion, exterior lined with amphipathic bile salts (hydrophilic ends outside)

3 important lipolytic enzymes in pancreatic juice (most of lipid digestion in SI)

- pancreatic lipase (triglycerides), - phospholipase A2 (lysolecthin), - cholesterol ester hydrolase

where does protein digestion start and with what? what is it secreted as? what is it activated by?

stomach with action of pepsin, secreted as pepsinogen; activated by low pH

where is (90% of) protein digestion completed?

duodenal area by pancreatic brush border proteases (endo & exopeptidases)

proenzymes in the pancreatic juice are activated by what? what is that activated by?

trypsin activated from trypsinogen by enterokinase in brush border trypsin in pancreatic juice enterokinase in brush border

what forms of proteins are absorbable? how?

AAs, di & tri peptides | - some symported with Na, H+ (PEPT1)