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What percentage of HCl is produced in the cephalic phase
40%.
What triggers the cephalic phase of HCl secretion
Sight, smell, taste, or thought of food activating vagus nerve.
What percentage of HCl is produced in the gastric phase
50%.
What triggers the gastric phase of HCl secretion
Stomach stretch and peptides.
What percentage of HCl is produced in the intestinal phase
10%.
What triggers the intestinal phase of HCl secretion
Food entering the duodenum.
What hormone from D cells inhibits HCl secretion
Somatostatin.
What triggers somatostatin release
Stomach pH < 3.
What is the effect of somatostatin on parietal cells
Inhibits HCl secretion.
What secretes prostaglandin E2
Surface epithelial cells.
What is the effect of PGE2 on parietal cells
Inhibits HCl via EP3 receptor.
How does H. pylori affect D cells
Inhibits somatostatin → increases HCl.
What do surface epithelial cells produce
Mucus and HCO3−.
What receptors stimulate mucus production
EP3 and mAChR.
What receptors stimulate HCO3− production
EP3 and mAChR.
What is the function of trefoil factor
Cytoprotection after mucosal injury.
What do mucus neck cells do
Produce mucus and act as stem cells.
What is the turnover time of mucus neck cells
1–3 days.
What do mucus neck cells differentiate into
All gastric cell types.
What do parietal cells secrete
HCl and intrinsic factor.
What is the function of intrinsic factor
Protects B12 and allows ileal absorption.
Where is vitamin B12 absorbed
Ileum.
What do chief cells secrete
Pepsinogen.
What activates pepsinogen
HCl.
What does pepsin do
Breaks proteins into peptides.
What enzyme digests casein in infants
Rennin.
What do ECL cells secrete
Histamine and serotonin.
What receptor does serotonin bind in gut
5‑HT3 receptor.
What is serotonin’s effect on motility
Increases motility.
What organism produces serotonin‑like toxin
Enterotoxigenic E.coli (ETEC).
What is the effect of ETEC toxin
Activates 5‑HT3 → diarrhea.
What hormone do I cells release
CCK.
What stimulates CCK release
Fat and protein in duodenum.
What receptor does CCK bind
CCK‑1 receptor.
Where is CCK‑1 receptor for enzyme secretion
Pancreatic acinar cells.
What is CCK’s effect on acinar cells
Releases digestive enzymes.
What effect does CCK have on gallbladder
Contracts it.
What effect does CCK have on sphincter of Oddi
Relaxes it.
What hormone do S cells release
Secretin.
What stimulates secretin release
Acidic chyme in duodenum.
What receptor does secretin bind
Secretin receptor.
Where is secretin receptor located
Pancreatic ductal cells.
What is secretin’s effect on ductal cells
Increases HCO3− secretion.
What is the purpose of pancreatic bicarbonate
Neutralize gastric acid.
What stimulates pancreatic secretion via vagus nerve
Acetylcholine.
What receptor does ACh act on in pancreas
mAChR.
What are zymogens
Inactive enzyme precursors.
How are zymogens identified
“Pro‑” or “‑gen.”
What activates trypsinogen
Enteropeptidase.
What does trypsinogen become
Trypsin.
What enzymes does trypsin activate
Chymotrypsinogen, pro‑elastase, pro‑carboxypeptidase, pro‑aminopeptidase.
What do active proteases produce
Amino acids.
Where is enteropeptidase located
Brush border of duodenum.
What is the function of HCO3− in pancreatic juice
Neutralizes acid.
What are the main components of dietary fat
Triglycerides, cholesterol, phospholipids, fat‑soluble vitamins.
What converts pro‑colipase to co‑lipase
Trypsin.
What is the function of co‑lipase
Helps lipase bind fat droplets.
Why is co‑lipase needed
Bile salts inhibit lipase.
What does pancreatic lipase do
Breaks triglycerides into monoglycerides + FFAs.
What begins cholesterol synthesis
Acetyl‑CoA + aceto‑acetyl‑CoA.
What enzyme forms HMG‑CoA
HMG synthase.
What enzyme converts HMG‑CoA to mevalonate
HMG‑CoA reductase.
What cofactor does HMG‑CoA reductase require
NADPH.
What is the rate‑limiting step of cholesterol synthesis
HMG‑CoA → mevalonate.
What drug class inhibits HMG‑CoA reductase
Statins.
How do statins work
Competitive inhibition.
What molecule forms after mevalonate
Squalene.
What forms after squalene
Lanosterol.
What forms after lanosterol
Cholesterol.
What activates SREBP2
Low intracellular cholesterol.
Where does active SREBP2 go
Nucleus.
What does SREBP2 bind
SRE on LDL receptor gene.
What is the effect of SREBP2 activation
Increases LDL receptors.
What is the effect of increased LDL receptors
More LDL uptake → lower blood cholesterol.
What is one structural function of cholesterol
Maintains membrane fluidity.
What hormones are made from cholesterol
Cortisol, aldosterone, testosterone, estrogen, progesterone.
What organ synthesizes bile salts
Liver.
What enzyme converts cholesterol to 7‑α‑hydroxycholesterol
7‑α‑hydroxylase.
What are primary bile acids
Cholic acid, chenodeoxycholic acid.
What amino acids conjugate bile acids
Glycine, taurine.
What are conjugated bile salts examples
Glycocholic, taurocholic, glycochenodeoxycholic, taurochenodeoxycholic.
Why are conjugated bile salts hydrophilic
Water‑soluble.
Why are unconjugated bile salts hydrophobic
Fat‑soluble.
What is the bile micelle ratio
10 bile salts : 3 phosphatidylcholine : 1 cholesterol.
What creates micelle hydrophobic surface
Bile salts.
What creates micelle hydrophilic core
Phosphatidylcholine.
What causes cholesterol gallstones
Excess cholesterol.
What causes pigment stones
Calcium + bilirubin.
What is the consequence of blocked bile flow
Pale stool, fat malabsorption.
What fills micelle core in duodenum
Monoglycerides, FFAs, cholesterol, vitamins A/D/E/K.
What transporter absorbs free cholesterol
NPC1L1.
What drug inhibits NPC1L1
Ezetimibe.
What does ACAT do
Converts cholesterol → cholesterol ester.
What does DGAT do
Converts monoglycerides + FFAs → triglycerides.
What protein forms chylomicrons
ApoB48.
What protein loads lipids onto ApoB48
MTP.
Where are chylomicrons formed
Enterocytes.
How do chylomicrons exit enterocytes
Exocytosis.
Where do chylomicrons go first
Lacteals.
Why do chylomicrons enter lacteals
Too large for blood capillaries.