Step 1: Gi Iii

Front 1

What is the mechanism of atropine?

Back 1

competitive antagonist for the muscarinic acetylcholine receptor.... inhibits action of vagal nerve. It's an "anticholinergic."

Front 2

How does Gastrin largely mediate it's increase in acid secretion?

Back 2

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.

Front 3

If you gave atropine, would it block Gastrin secretion? H+ secretion?

Back 3

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.

Front 4

What is the source of most of the serous salivary secretions?

Mucinous?

Back 4

Parotid (most serous)

Submandibular, submaxillary(in the middle)

and sublingual (most mucinous)

Front 5

What are the components of saliva?

Back 5

- 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

Front 6

What stimulates salivary secretion: parasympathetics or sympathetics? How?

Back 6

BOTH!!
symp: T1-T3 superior cervical ganglion
para: facial, glossopharyngeal nerve

Front 7

What nerve runs through the parotid gland?

Back 7

CNVII, can be damaged by local surgery.

Front 8

What is the tonicity of saliva when flow is slow? why?

When flow is fast? why?

Back 8

hypotonic (there is more time to reabsorb Na and Cl)

closer to isotonic b/c there is less time to reabsorb.

Front 9

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?

Back 9

- 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.

Front 10

What is the alkaline tide?

Back 10

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.

Front 11

How do parietal cells excrete acid? (what is the pump mechanism)

What drug inhibits this pump?

Back 11

ATPase H+/K+ exchanger.

Omeprazole.

Front 12

What are the ONLY GI submucosal gland? what is their fx? Where are they found?

Back 12

Brunner's glands. Secrete alkaline mucus to neutralize acid contents entering the duodenum from the stomach.

duodenal submucosa.

Front 13

Hypertrophy of Brunner's glands is seen in what?

Back 13

PUD.

Front 14

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)

Back 14

- starch digestion, secreted in active form
- fat digestion (active form)
- protein digestion... secreted as proenzymes = ZYMOGENS.

Front 15

How do zymogens become activated?

Back 15

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.

Front 16

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.

Back 16

- salivary amylase, from saliva.
- brush border of intestine; oligosaccharide hydrolases
- Highest concentration in duodenal lumen; pancreatic amylase.

Front 17

What are the CHO absorbed by enterocytes?

Back 17

monosaccharides (glucose, galactose, fructose)

Front 18

How are Glucose and Galactose absorbed by enterocytes?

Fructose?

how are all three transported to blood post-absorption?

Back 18

SGLT1 (Na+ dependent)

Facilitated diffusion by GLUT-5

GLUT-2

Front 19

Where are the following absorbed?
- iron
- folate
- B12

Back 19

Iron is in the duodenum

Folate in the jejunum

ileum along with bile acids.

Front 20

What do Peyer's patches contain?

B cells stimulated in Peyer's patches diff into what and live where?

Back 20

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.

Front 21

What is Bile made of?

They are the only significant excretion mech for what?

Back 21

composed of bile salts (bile acids conjugated to glycine or taurine, amking them water soluble), phospholipids, cho, bilirubin, water, and ions.

excretion of cholesterol

Front 22

What is needed for digestion of TG and micelle formation in the small intestine?

Back 22

bile.

Front 23

Walk through bilirubin metabolism.
- where is urobilinogen found
- in what form is bili excreted in urein?
- feces?

Back 23

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.