Physiology Flashcards
What is secreted by each of the following salivary glands: parotid, submaxillary/submandibular, and sublingual?
- Parotid: secrete fluid of water, ions, and enzymes
- submaxillary/ submandibular: mixed glands; secrete fluid and mucin glycoproteins
- sublingual: mixed glands; secrete fluid and mucin glycoproteins
How does saliva compare to plasma? What is the difference in ions?
saliva is hypotonic compared to plasma
- higher levels of K and HCO3
- lower levels of Na and Cl
Describe the function of each of the following: salivary acinus, striated duct, and myoepithelial cells?
- acinus: produces initial saliva
- striated duct: modifies saliva (hypotonic)
- myoepithelial cells: contract to eject saliva as stimulated by neuronal inputs
Describe the formation of saliva
initial solution isotonic -> absorption of Na and Cl -> secretion of K and HCO3 -> net absorption of solute b/c ductal cells impermeable to water
What transporter is located on basolateral side of salivary duct cells?
Na/K ATPase (K into ductal cells; Na out)
What 3 transporters are located on apical side of salivary ductal cells?
- Na/H anti porter (Na into cell and H out to saliva)
- Cl/HCO3 antiporter (Cl into cell and HCO3 out to saliva)
- K/H antiporter (H into cell and K out to saliva)
What is the parasympathetic innervation for the 3 types of salivary glands?
Facial N. (CN VII) for submandibular and sublingual
Glossopharyngeal N. (CN IX) for parotid
What stimulates parasympathetic activation of salivary glands? Through which receptors and what NT?
- activated by smell, food, higher brain function
- NT: ACh
- Receptor: Muscarinic
What is sympathetic innervation of salivary glands? What is the result of sympathetic activation? Through what receptor and NT?
- T1-T3 and superior cervical ganglion
- increases salivary secretion (just like parasympathetic)
- NT: NE
- Receptor: beta adrenergic
Name 7 major stomach secretions
Acid, Pepsinogen, Intrinsic factor, Gastrin, Mucus, HCO3, and Water
What is the location of oxyntic glands in the stomach?
proximal 80% of stomach (fundus and body)
Name 6 types of cells located in oxyntic glands
parietal cells, D cells, mucous cells, ECF cells, chief cells, ECF-like cells
What is the location of pyloric glands in the stomach?
distal 20% of stomach (antrum)
Name 4 types of cells located in pyloric glands
G cells, D cells, mucous cells, ECF cells
What is produced by each of the following cells: parietal cells, D cells, ECF cells, Chief cells, ECF-like cells, G cells
- parietal cells: acid
- D cells: somatostatin
- ECF cells: ANP
- Chief cells: pepsinogen
- ECF-like cells: histamine
- G cells: gastrin
Name 2 functions of HCl in the stomach
lower pH to 1-2; converts pepsinogen to pepsin
What are 3 receptors that activate parietal cells?
M3 (ACh), H2 receptors (histamine), CCK-B (gastrin)
What is the optimal pH for pepsin? What happens if the pH becomes too high?
- optimal pH = 1.8 - 3.5
- reversibly inactivated > 5
- irreversibly inactivated > 7-8
Name 4 stimuli for chief cells to release pepsinogen. Which is the most important?
- Vagus N. (most important)
- H triggers local cholinergic (ACh) reflex to stimulate chief cells
- Gastrin and secretin enter circulation and activate chief cells
Describe HCl secretion from parietal cells
- Na reabsorbed into cytoplasm (Na/K ATPase)
- negative charge on canaliculus side -> Na and K passively diffuse into canaliculus
- H2O dissociates into OH and H in parietal cell
- H secreted into canaliculus (H/K ATPase)
- Cl actively transported into canaliculus
- water enters canaliculus via osmosis
Describe an alkaline tide
CO2 reacts w/ OH in cytoplasm of parietal cells to form HCO3 -> secreted into ECF -> slight increase in pH surrounding stomach
How does the vagus N. directly influence parietal cells to secrete HCl?
M3 receptor (IP3/Ca) via ACh
How does the vagus N. indirectly influence parietal cells to secrete HCl?
- induces gastrin release via GRP directly on G cells
- activates ECL cells to release histamine
How does atropine affect HCl secretion?
blocks muscarinic (cholinergic) receptors - lower HCl secretion; does not shut down the whole system
How does each of the following affect HCl secretion: histamine, gastrin, ACh, somatostatin, prostaglandins?
- histamine: increases
- gastrin: increases
- ACh: increases
- somatostatin: decrease
- prostaglandins: decrease
What cells produce histamine? What receptor does histamine use to increase acid secretion?
produced by ECL-like cells; uses H2 receptors
What 2 things potentiate the release of histamine from ECL-like cells?
gastrin and ACh
How do somatostatin and prostaglandins inhibit acid secretion?
directly and indirectly by inhibiting ECL-like cells
What 3 things does gastrin stimulate the release of?
- acid via CCKB receptors
- histamine from ECL-like cells
- somatostatin (inhibits acid secretion)
How do prostaglandins inhibit acid secretion?
inhibit ECL-like cells (histamine) and parietal cells directly via cAMP
Describe passive feedback of HCl secretion
HCl secretion inhibits gastrin release -> reduces HCl secretion
What is cimetidine? What is it used to treat?
H2 receptor antagonist; treats GERD, duodenal and gastric ulcers
What is the MOA of omeprazole?
inhibits H/K ATPase on parietal cells to prevent them from secreting acid
Explain PSNS regulation of gastrin and somatostatin release? How is somatostatin released?
- Vagus N. stimulates gastrin release via GRP; inhibit somatostatin
- somatostatin released due to gastrin
What is the 1st phase of gastric HCl release? How much HCl is released and what stimulates it?
cephalic phase; 30% of HCl secretion; stimulated by smell, taste, chewing, swallowing, and conditioned reflexes (Vagus N.)
What is the mechanism by which the cephalic phase of HCl release works?
- vagus N. stimulates parietal cells via ACh (direct)
- vagus N. stimulates gastrin secretion via GRP on G cells (indirect)
What is the 2nd phase of gastric HCl release? How much HCl is released and what stimulates it?
Gastric phase; 60% of HCl secretion; stimulated by distention of the stomach and presence of proteins
What is the mechanism by which the gastric phase of HCl release works?
- distention activates mechanoreceptors in mucosa of oxyntic and pyloric glands (activates vagus N.)
- distention of antrum activates local reflex of gastrin release
- AAs and small peptides stimulate gastrin release
What is the 3rd phase of gastric HCl release? How much HCl is released and what stimulates it?
intestinal; 10% of HCl secretion; stimulated by distention of small intestine and presence of digested protein
What is the mechanism by which the intestinal phase of HCl release works?
- distention of small intestine stimulates acid secretion via ENS
- digested protein stimulates gastrin release (hormone mediated)
What is the reverse enterogastric reflex?
small intestine switches roles from activating acid secretion to inhibiting it
What hormones have a role in the reverse enterogastric reflex?
secretin, GIP, VIP, and somatostatin
What is the only essential stomach secretion? What is its function and what happens if it is not secreted?
intrinsic factor from parietal cells; required for absorption of B12 in the ileum; if not secreted -> pernicious anemia
What do mucous neck cells and gastric epithelial cells secrete?
- mucous neck cells -> mucus
- gastric epithelial cells -> HCO3
What are 5 protective factors of the gastric mucosa?
HCO3, mucus, prostaglandins (inhibits acid), blood flow, gastrin (growth factors)
What are 7 damaging factors of the gastric mucosa?
acid, pepsin, NSAIDs/ASA, H. Pylori, alcohol, bile, stress
What are the 2 predominant causes of PUD in the US?
H. Pylori infection and NSAIDs
What is the main reason for gastric ulcers? What is the major causative agent and how is it diagnosed?
mainly due to defective mucosal barrier; causative agent is H. Pylori; dx based on urease activity (alkalizing agent that allows bacteria to colonize)
What are H secretion rates in duodenal ulcers? How does H. Pylori play a role?
H secretion is slightly higher; H. Pylori has an indirect influence by inhibiting somatostatin and HCO3 secretion
What is Zollinger-Ellison Syndrome?
gastrinoma (pancreatic tumor that secretes large amounts of gastrin) cause really high H secretory rates -> increased H secretion by parietal cells and increased proliferation of parietal cells
What is used to dx Zollinger-Ellison syndrome? What is the tx?
Secretin is used to dx (paradoxical increase in gastrin); tx include cimetidine, omeprazole, and surgery
What are 2 types of active enzymes released from the pancreas?
amylases and lipases
What is the organization of the exocrine pancreas?
similar to salivary glands; acinus (secretes enzymes) -> centroacinar cells -> ducts (secretes aqueous solution w/ HCO3)
What is the role of pancreatic ductal cells?
secretion of HCO3 and absorption of H
What is the 1st phase of pancreatic secretion and what is released (and %)? What stimulates it?
cephalic phase produces enzymatic secretion (10-15%); initiated by vagus N., smell, taste, and conditioning
What is the 2nd phase of pancreatic secretion and what is released (and %)? What stimulates it?
gastric phase produces enzymatic secretion (5-10%); imitated by vagus N. and stomach distention
What is the 3rd phase of pancreatic secretion and what is released (and %)? What stimulates it?
intestinal phase produces enzymatic and aqueous secretions (80%); driven by secretin
What is the sympathetic innervation of the pancreas and what does it do?
postglangionic nerves from celiac and superior mesenteric plexus -> inhibitory
What is the parasympathetic innervation of the pancreas and what does it do?
vagus N. -> stimulatory; potentiates secretin and CCK
What is secreted from S cells and I cells of the duodenum?
S cells = secretin
I cells = CCK
What stimuli does secretin respond to and what is its function?
secreted in response to pH < 5.0 in duodenum; stimulates aqueous and HCO3 secretion from ductile cells of pancreas
What stimuli does CCK respond to and what is its function?
secreted in response to fat and protein digestion byproducts in duodenum and jejunum; stimulates enzymatic secretions for pancreatic acini
What is secreted from Brunner’s glands in the small intestine (duodenum)?
mucous -> protects duodenum from acid
What is secreted from crypts of lieberkuhn in small and large intestine?
goblet cells secrete mucus
What effect does excessive alcohol intake cause on the liver?
most common cause of cirrhosis; leads to accumulation of fat within hepatocytes -> steatohepatitis which is fatty liver w/ inflammation -> scarring of the liver
Explain how hepatitis leads to increased portal blood pressure
inflammation causes a thick collagen basement membrane to develop -> free flow of materials is impacted -> less capillaries to spread out the blood (less in parallel) but the same amount is flowing through a smaller space
How does portal HTN affect hydrostatic and oncotic pressures?
increased hydrostatic pressure (pushes fluid out of capillary) and decreased oncotic pressure (pulls fluid back into capillary)
Name 6 consequences of portal HTN
- ascites
- esophageal varices
- hepatic encephalopathy
- malnutrition
- caput medusae
- hemorrhoids
Bile is composed of what 6 things?
bile salts, bile pigments (bilirubin), cholesterol, phospholipids, ions, and water
Where are primary and secondary bile acids synthesized as well as bile salts conjugated?
- primary bile acids = hepatocytes
- secondary bile acids = small intestine
- bile salts = liver
In what form do bile sals transport lipids?
as micelles (amphipathic) which increase the surface area of lipids and expose them to lipases
How does secretin affect bile concentration?
stimulates release of HCO3, water, and Na from ductile cells -> increases the volume and pH of bile and decreases bile salt concentration
What is the state of the gallbladder during the interdigestion period?
- gallbladder fills w/ bile
- gallbladder is relaxed
- sphincter of Oddi is closed
What mediates the contraction of the gallbladder and opening of the sphincter of Oddi upon ingesting food?
CCK
How does CCK mediate the contraction of the gallbladder?
- directly by acting on the gallbladder
- indirectly but communicating w/ Vagus N. afferents -> efferents cause gallbladder to contract through ACh
Name 4 things that decrease gallbladder contractility
SNS, secretin, pancreatic polypeptide, and somatostatin
What is the purpose of enterohepatic circulation? What organs are involved?
recycles bile acids/salts
- involves the liver, gallbladder, bile duct, duodenum, ileum, and portal circulation
Name 2 channels that uptake bile acids into hepatocytes
NTCP and OATP (also plays a role in bilirubin transport)
Name 2 channels that uptake bile acids into canaliculi
BSEP and MRP2 (mutations associated w/ liver diseases and hyperbilirubinemia)
How much of bile acids are recycled per day as opposed to being excreted in feces? How is this affected by removing the ileum?
90-95% recycled; 5-10% excreted
- if the ileum is removed, cannot recycle bile acids and production must go up
How is bilirubin made and by what system? How is it transported in blood?
- bilirubin is released during RBC breakdown by the reticular endothelial system (RES)
- circulates bound to albumin
What is the key enzymes in the conjugation of bilirubin in the liver?
UDP-glucuronyl transferase (UGT)
What is bilirubin converted to in the intestines?
urobilinogen
What 3 routes can urobilonogen take once in the small intestine?
- reabsorbed to the kidney (excreted as urobilin)
- reabsorbed back to the liver (enterophatic circulation)
- excreted in the feces (as stercobilin)
What 3 liver enzymes are measured in serum using LFTs?
- alanine aminotransferases (ALT)
- aspartate aminotransferase (AST)
- alkaline phosphatase (AlkPhos)
What do elevated aminotransferases or AlkPhos generally mean?
- aminotransferases: hepatocyte injury
- AlkPhos: gallstones (damage to bile duct)
What are 3 abnormal values that may be seen w/ impaired hepatic function?
- bilirubin
- albumin
- prothrombin time (PT)
Difference between direct and indirect bilirubin?
indirect = uncogjugated direct = conjugated
What could impaired liver function do to albumin levels?
decrease albumin levels -> decrease oncotic pressure
What could impaired liver function do to PT?
increases PT as the ability of the liver to form new clotting factors decreases
What is Jaundice a sign of?
hyperbilirubinemia
Name 5 causes of hyperbilirubinemia and whether the excess bilirubin is conjugated or uncojugated
- excess production of bilirubin (hemolytic anemia)(unconjugated)
- decrease uptake of bilirubin into hepatocytes (uncojugated)
- defective UGT enzyme (uncojugated)
- disturbed secretion of bilirubin into canaliculi (conjugated)
- bile duct obstruction (conjugated)
What is hemolytic anemia and what type of bilirubin will be increased?
excessive breakdown of RBCs -> uncojugated
What are the 2 main causes of neonatal jaundice? What type of bilirubin in increased?
- increased bilirubin production due to breakdown of fetal erythrocytes
- low activity of UGT enzyme
- uncojugated
What is the purpose of phototherapy to help with neonatal jaundice?
light changes trans-bilirubin to cis-bilirubin (more water soluble and can be excreted)
What is Gilbert’s syndrome? What usually causes flare ups? What type of bilirubin is increased?
- mutation in the gene that encodes UGT (defect in conjugation of bilirubin)
- uncojugated increases
- flare ups caused by physiological stress (seen by adolescence)
What is Crigler-Najjar Syndrome? Which type is more severe? What type of bilirubin is increased?
- loss of function mutations in UGT
- unconjugated increases
- Type 1 is much more severe than Type 2
Explain Type 1 Crigler-Najjar Syndrome compared to Type 2?
What is the treatment?
- starts earlier in life; jaundice appears at birth; results in kernicterus - form of brain damage caused by accumulation of uncojugated bilirubin
- tx is a liver transplant
Explain Type 2 Crigler-Najjar Syndrome compared to Type 1?
What is the treatment?
- starts later in life and survival goes into adulthood; less likely to develop kernicterus
- tx is phenobarbitol (no response in Type 1)
What is Dubin-Johnson Syndrome? What may worsen it? What type of bilirubin is increased?
What is unique about the liver?
- defect in ability of hepatocytes to secrete conjugated bilirubin into bile (mutations in MRP2)
- mild jaundice throughout life; may be worsened by alcohol, BC, infection, or pregnancy
- conjugated
- liver has black pigmentation
What is Rotor Syndrome?What type of bilirubin is increased? What is unique about the liver?
- gene mutations in OATP (bilirubin cannot leave enterocytes - recycling compromised)
- conjugated and unconjugated can be increased
- lack of liver pigmentation
Name 4 causes of gallstones?
- too much water absorption from bile
- too much absorption of bile acids
- too much cholesterol in bile
- inflammation of epithelium
What stimulates bile acid independent bile formation?
secretin
Why are microvilli the longest in the duodenum?
absorption occurs most in the duodenum and then lessens as it moves through the small intestine
What are enterocytes and what is there function?
epithelial cells of the small intestine that play a role in absorption of nutrients and secretion of HCO3 as protection
Goblet cells vs Paneth cells
Goblet cells: mucus-secreting cells
Paneth cells: secrete defensins as part of mucosal defenses against infection
Name 4 routes of passage into enterocytes
pinocytosis, passive diffusion, facilitated diffusion, and active transport
Describe the layers solutes must cross moving from enterocyte to lumen of blood (7)
- unstirred layer of fluid (mucus layer w/ immunological products)
- glycocalyx
- apical membrane
- cytoplasm of cell
- basolateral membrane
- basement membrane
- wall of blood capillary/wall of lymphatic vessels
Which nutrient is mainly absorbed into the lymphatics?
fats
What cannot be absorbed if the ileum is resected?
bile salts and vitamin B12
What are the 3 primary sugars of the human diet? What starts digesting them in the mouth?
- sucrose, lactose, and starch
- salivary amylase breaks down starch into maltose starting in the mouth
What starts breaking sugars down in the duodenum?
pancreatic amylase
What are the brush border enzymes that break down sugars? What forms are they broken into?
- maltase = maltose -> glucose + glucose
- trehalase = trehalose -> glucose + glucose
- lactase = lactose -> glucose + galactose
- sucrase = sucrose -> glucose + fructose
What transporter bring glucose and galactose into intestinal epithelial cells? What process?
SGLT1; active transport
What transporter bring fructose into intestinal epithelial cells? What process?
GLUT5; facilitated diffusion
What transporter moves glucose, fructose, and galactose into the blood?
GLUT2
How does lactase deficiency cause osmotic diarrhea?
lactose remains in intestine and unabsorbed -> holds H2O in the lumen -> diarrhea
What is used to test the ability of the intestines to break down a sugar vs absorb it?
D-xylose -> 25 grams ingested during fast and urine collected for the next 5 hours -> if you collect less than 4 grans after 5 hours, it means the intestines are not absorbing
Endopeptidases vs Exopeptidases
Endopeptidases - hydrolyse interior bonds between peptides
Exopeptidases - hydrolyze one AA at a time
Which endopeptidase is secreted from the stomach rather than the pancreas? Is it essential?
pepsin; responsible for 10-20% protein breakdown in stomach -> not essential (can still break down protein in small intestine if pepsin not available)
What is the brush border enzyme for protein breakdown and what is its function?
enterokinase -> activates trypsinogen to trypsin -> trypsin activates all other endopepidases an exopeptidase from pancreas
What stimulates activation of the pancreas to secrete enzymes?
- vagus N. through ACh
- secretin -> works on ductal cells
- CCK -> works on acinar cells
What activates pepsin from pepsinogen?
low pH in stomach
What enzymes does trypsin activate?
- trypsin
- chymotrypsin
- elastase
- carboxypeptidase A and B
By what mechanism are proteins absorbed into small intestine and into blood?
- Na-AA co-transporters on apical side (brings AAs into cell)
- facilitated diffusion into the blood (Na/K ATPase creates Na gradient)
What is chronic pancreatitis caused by?
deficiency in pancreatic enzymes -> ductal and acinar cells lose ability to produce HCO3 -> improper pH -> won’t secrete enzymes
In what 2 ways could you have a congenital absence of trypsin?
- if pancreas is not producing trypsinogen
- could have problem w/ enterokinase and can’t convert trypsinogen to trypsin
What is cystinuria caused by?
defect or absence in Na/AA cotransporters in small intestine -> di-basic AAs all excreted
What is Hartnup disease?
AR defect in neutral AA co-transporter; cannot absorb neutral AAs (such as tryptophan) and sx include pellagra (4Ds)
How is cystic fibrosis connected to pancreatic defects?
loss of Cl channels -> not able to secrete HCO3 -> cannot neutralize acid -> activate trypsin before reaching small intestine -> auto digestion of pancreas
What enzyme converts cholesterol to primary bile acids?
7a-hydroxylase
What enzyme converts primary bile acids into secondary bile acids?
7a-dehydroxylase by bacteria in small intestine
What are bile acids conjugated w/ to produce bile salts in the liver?
taurine and glycine
How is pancreatic lipase secreted? What is needed for it be be activated? What is its function once it is activated?
- secreted as active enzyme
- requires colipase to be activated (colipase is activated by trypsin)
- displaces bile salts from fats
How is cholesterol ester hydrolase secreted? What is its function?
- secreted as active enzyme
- catalyzes production of free cholesterol
How is phospholipase A2 secreted? What activates it and what is its function?
- secreted as proenzyme
- activated by trypsin
- phospholipid breakdown
What are the 5 steps of fat absorption?
- solubilization by micelles
- diffusion of micelles across apical membrane
- re-esterification (add back on FFA to reform fat)
- chylomicron formation (for circulatory transport)
- exocytosis of chylomicrons into lymphatics
Why would small intestinal bacterial overgrowth (SIBO) cause a deficiency in bile salts?
bacteria deconjugate bile salts which impares micelle formation
What deficiencies occur if you lose intestinal microvilli?
folate, vitamin B12, and fat soluble vitamins (ADEK)
Fat soluble vs water soluble vitamin absorption
- Fat soluble: same mechanism as lipids
- Water soluble: Na-dependent cotransporters except B12 (intrinsic factor)
What does a deficiency in vitamin B12 cause? Common cause of vitamin B12 deficiency?
- pernicious anemia -> failure of RBC maturation
- stomach does not produce enough IF
What does calcium absorption depend on ?
presence of vitamin D as well as calcitriol and PTH
How could you develop vitamin D deficiency?
lack of vitamin D in diet and by sunlight
Explain how iron is absorbed? What facilitates iron entry into enterocytes?
- liver secretes apotransferrin into bile -> duodenum
- apotransferrin binds to free Fe and w/ hemoglobin to produce transferrin
- transferrin binds to receptors on membranes of intestinal epithelial cells
- Fe enters enterocytes w/ help of ferric reductase which requires vitamin C
In which part of the intestines is calcium absorbed?
duodenum, jejunum, and colon
Which part of the intestine is important for sodium absorption?
jejunum
Which part of the brain is key in regulation of food intake?
hypothalamus
What are the 2 anorexigenic signals in the arcuate nucleus and what is their function?
POMC/CART; decreases food intake and increases EE
What are the 2 orexigenic signals in the arcuate nucleus and what is their function?
neuropeptide Y (NPY) and AgRP); increases food intake and decreases EE
What is the function of the NTS?
nucleus tractus solitarius regulates sympathetic activity and energy expenditure
Where does a-MSH come from? What does it target and what is its function?
released from POMC/CART neurons -> binds to MCR-4 (neurons) or MCR-3 (NPY/AgRP) and inhibits their activity -> decreases food intake
What 3 things activate the POMC/CART pathway and inhibit the AgRP/NPY pathway?
Insulin, leptin, and CCK
What activates the AgRP/NPY pathway?
ghrelin
What is released by NPY/AgRP neurons? What does it target and what is its function?
release NPY which binds to Y1Rs on second order neurons to stimulate food intake
What is the function of AgRP?
MCR-4 antagonist that blocks the action of a-MSH
What is the role of the vagus N. in satiety and feeding?
vagal afferents talk to NTS -> vagal efferents talk to stomach to control energy homeostasis
What secretes ghrelin? What is its function?
- secreted by oxyntic cells of stomach
- stimulates neurons that release NPY, increases appetite, gastric motility, gastric acid secretion, and adipogenesis
How does insulin affect NPY/AgRP and POMC/CART systems? What is its overall function?
- activates POMC/CART
- inhibits NPY/AgRP
- overall decreases appetite and increases metabolism
What secretes peptide YY (PYY) and what is its function?
- released by L cells of the ileum and colon after a meal
- binds to Y2R on NPY/AgRP neurons to inhibit food intake
What secretes leptin? What is its function?
- secreted by adipocytes
- inhibits NPY pathway and stimulates POMC pathway
- overall, decreases appetite and increases metabolism
What is adulthood obesity usually associated with?
leptin resistance
What secretes CCK and what is its function in feeding behaviors?
- secreted by I cells of duodenum
- elicits satiety
What secretes GLP-1 and what is its action?
co-secreted w/ PTT from L cells of intestine
- reduces food intake, suppresses glucagon secretion, and delays gastric emptying
What affect do pancreatic polypeptide, Amylin, and glucagon all have?
reduce food intake
Describe an adjustable gastric band (lap band)
an adjustable band around the upper portion of the stomach -> activates ENS due to premature distention of stomach
Describe a sleeve gastrectomy
left lateral portion of stomach is removed which leaves a banana shaped and sized stomach
Describe a duodenal switch
sleeve gastrectomy is performed and large portion of small intestine is bypassed -> decreased absorption of nutrients
Describe a Roux-en-Y. What does it do the levels of GLP-1 and PYY
involves creating a small stomach pouch and bypassing 3-5 ft of small intestine
- increases hormone levels (decrease desire to eat)
What type of hormonal changes are seen in anorexia nervosa?
ghrelin resistance (fasting, so chronically elevated); increased levels of PYY
Name 4 apical membrane transporters in the jejunum
Na-glucose, Na-galactose, Na-AA, Na-H
What happens to HCO3 in the cells of the jejunum?
transported into blood via HCO3 transporter on basolateral membrane
Which part of the intestine has a net absorption of NaCl? How does this occur?
- ileum
- Na-H exchanger and Cl-HCO3 transporter move H and HCO3 into the lumen and Na and Cl into the cell
Which electrolyte is absorbed in the colon and which is secreted? What affect does aldosterone have on the Na channels?
- Na absorbed; K secreted
- aldosterone induces synthesis of Na channels -> more Na absorbed and more K secreted
What affect does diarrhea have on K?
increased K loss in the colon -> hypokalemia
What activates Cl channels on the apical membrane of intestines? How do they do this?
ACh and VIP -> generates cAMP to open the Cl channels and secrete Cl
What 2 electrolytes are mainly lost during diarrhea? What does this cause?
mainly HCO3 (metabolic acidosis) and K (hypokalemia)
What type of diarrhea does lactase deficiency cause?
Osmotic diarrhea -> lactose remains in intestines and retains water
What can cause secretory diarrhea?
overgrowth of pathogenic bacteria such as E. Coli and cholera -> causes excessive secretion of fluid by crypt cells
