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23 Cards in this Set
- Front
- Back
What is the mechanism of atropine?
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competitive antagonist for the muscarinic acetylcholine receptor.... inhibits action of vagal nerve. It's an "anticholinergic."
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How does Gastrin largely mediate it's increase in acid secretion?
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It's released from G cells --> into the circulation.
Increases Histamine release from ECL cells (which in turn ^^H+ from parietal)... only has a small/modest direct effect on parietal cells themselves. |
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If you gave atropine, would it block Gastrin secretion? H+ secretion?
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Blocks H+ secretion from parietal cells because ACh is the vagal nerve's messenger @ jxns with parietal cells.
Gastrin secretion will NOT be affected directly, as the vagal nerve uses GRP to stimulate G cells, not ACh. |
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What is the source of most of the serous salivary secretions?
Mucinous? |
Parotid (most serous)
Submandibular, submaxillary(in the middle) and sublingual (most mucinous) |
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What are the components of saliva?
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- alpha-amylase (ptylain) begins starch digestion and then is inactivated by low pH upon reaching stomach
- Bicarb neutralizes oral bacterial acids, and maintains dental health - Mucins (glycoproteins) lubricate food - Antibacterial secretory products - Growth factors that promote epithelial renewal |
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What stimulates salivary secretion: parasympathetics or sympathetics? How?
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BOTH!!
symp: T1-T3 superior cervical ganglion para: facial, glossopharyngeal nerve |
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What nerve runs through the parotid gland?
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CNVII, can be damaged by local surgery.
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What is the tonicity of saliva when flow is slow? why?
When flow is fast? why? |
hypotonic (there is more time to reabsorb Na and Cl)
closer to isotonic b/c there is less time to reabsorb. |
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What are the three stimulatory receptors on parietal cells?
- which two have clinical useful inhibitors, and what are they? - what intracellular mechanisms do each of the receptors work on? - Which is the most functionally important for H+ production? - What nerve can essentially upregulate ALL three receptors thru a combo of both direct and indirect action? - How do Prostaglandins and Somatostain receptors downregulate acid production? |
- ACh stim M3 receptor
- Gastrin stim CCK-b receptor - Histamine stim H2 receptor - Atropine inhibits ACh M3 receptor - Cimetadine inhibits H2 histamine receptor - H2 is cAMP, and the other two are Gq-->IP3 - H2 receptor. - vagus nerve (ACh direct to M3, Stim G-cells: --> Gastrin to CCK-b; gastrin to ECL --> histamine to H2) - use Gi to \\cAMP. |
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What is the alkaline tide?
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CA is what's combining CO2 and H20 into H+ and bicarb... for every H+ that's secreted, a HCO3 is secreted back into the blood in exchange for a Cl- to excrete w/ the H+!.... so as the Parietal cells rev up acid production, blood becomes alkaline.
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How do parietal cells excrete acid? (what is the pump mechanism)
What drug inhibits this pump? |
ATPase H+/K+ exchanger.
Omeprazole. |
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What are the ONLY GI submucosal gland? what is their fx? Where are they found?
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Brunner's glands. Secrete alkaline mucus to neutralize acid contents entering the duodenum from the stomach.
duodenal submucosa. |
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Hypertrophy of Brunner's glands is seen in what?
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PUD.
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Given the following pancreatic enzymes, give me their fx, and the form in which they're secreted:
- alpha-amylase - Lipase, phospholipase A, colipase - Proteases (trypsin, chymotrypsin, elastase, carboxypeptidase) |
- starch digestion, secreted in active form
- fat digestion (active form) - protein digestion... secreted as proenzymes = ZYMOGENS. |
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How do zymogens become activated?
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trypsinogen (=a zymogen) is secreted, and then is activated by Enterokinase/enteropeptidase (= enz secreted from gastric mucosa).
Once activated, trypsin activates other zymogens and also activates more trypsinogen --> trypsin --> (+) feedback loop. |
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Given the following fx performed, give me the enzyme that does it and it's location:
- starts digestion, hydrolyzes a-1,4 linkages to yield disaccharides (maltose, maltotriose, and a-limit dextrans) - Rate limiting step in CHO digestion, which produces monosaccharides from oligo- and disaccharides - hydrolyzes starch to oligosaccharides and disaccharides. |
- salivary amylase, from saliva.
- brush border of intestine; oligosaccharide hydrolases - Highest concentration in duodenal lumen; pancreatic amylase. |
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What are the CHO absorbed by enterocytes?
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monosaccharides (glucose, galactose, fructose)
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How are Glucose and Galactose absorbed by enterocytes?
Fructose? how are all three transported to blood post-absorption? |
SGLT1 (Na+ dependent)
Facilitated diffusion by GLUT-5 GLUT-2 |
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Where are the following absorbed?
- iron - folate - B12 |
Iron is in the duodenum
Folate in the jejunum ileum along with bile acids. |
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What do Peyer's patches contain?
B cells stimulated in Peyer's patches diff into what and live where? |
They're unencapsulated lymphoid tissue found i/lamina propria and submucosa of small intestine.
Contain specialized "M cells" that tale up antigen. Diff into IgA secreting plasma cells, and take up residence in lamina propria. IgA gets a protective secretory component and then is transported across epithelium to gut to deal with intraluminal antigen. |
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What is Bile made of?
They are the only significant excretion mech for what? |
composed of bile salts (bile acids conjugated to glycine or taurine, amking them water soluble), phospholipids, cho, bilirubin, water, and ions.
excretion of cholesterol |
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What is needed for digestion of TG and micelle formation in the small intestine?
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bile.
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Walk through bilirubin metabolism.
- where is urobilinogen found - in what form is bili excreted in urein? - feces? |
product of heme metabolism. Unconjucated bili is removed from blood by liver, is then conjugated with glucuronate (soluble) and excreted into the lumen in bile.
- found in gut. formed by breakdown of conjugated bilirubin by gut bacteria. - 80% is excreted in feces as stercobilin. - 10% gets excreted in urine as urobilin - 10% goes back into enterohepatic circulation. |