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163 Cards in this Set
- Front
- Back
Parietal cells secrete:
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1. H+
2. intrinsic factor |
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3 things that stimulate parietal cells:
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1. Vagus - Ach (M3)
2. Gastrin (CCKb) 3. Histamine (H2) |
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Parietal cells can by inhibited by _
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omeprazole at the H+/K+ ATPase
|
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2 things that inhibit and action:
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SST, Prostaglandins; Gi stimulated, lowers cAMP level
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Histamine stimulates H+ secretion by _
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activating Gs (increase cAMP)
|
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Potentiation effects is possible, because:
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Gastrin and Vagus act thru IP3/Ca+2 and Histamine acts thru cAMP (Gs)
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ACh potentiates _ and _
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gastrin, histamine
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Atropine blocks _ and _
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1. direct action of ACh
2. potentiation effects |
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Gastric H+ secretion can be inhibited by:
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1. low pH (negative feedback)
2. SST (Gi) 3. prostaglandin (Gi) |
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Stimulation of Gi in parietal cell _
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decreases cAMP
|
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3 ways in which SST inhibits:
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1. Gastrin release
2. Histamine release 3. Gi -> decr cAMP |
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low pH (less than _) is usually after _
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3, meal ingestion
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ACh blocker is _, Histamine blocker is _
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atropine, cimetidine
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peptic ulcer is a lesion of the _ or _ mucosa
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gastric, duodenal
|
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2 causes for peptic ulcer:
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1. no protective layer (mucous, bicarb)
2. excess H+, pepsin |
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5 protective factors for stomach:
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1. mucus
2. bicarb 3. prostaglandins 4. mucosal blood flow 5. growth factors |
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5 damaging factors:
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1. H+
2. pepsin 3. H pylori 4. NSAIDs 5. stress, smoking, alcohol |
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H pylori causes peptic ulcers by:
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1. releasing cytotoxins
2. urease (urea -> NH3) |
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Gastric ulcers damages _, leading to gastrin incr/decr?
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gastric mucosa, increased (response to lack of H+)
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prostaglandins: protect or damage gastric mucosa?
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protect (inhibit parietal cells)
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to protect: incr/decre mucosal blood
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increase
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NSAIDs are protective or damaging?
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damaging (inhibit mucous secretion)
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pepsin is damaging or protective?
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damaging
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Vagotomy is _
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cutting off vagus n.
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Vagotomy stimulates/inhibits parietal cells?
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inhibits
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vagus works thru _ receptor on parietal cells
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M3
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Chief cells secrete _
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pepsinogen
|
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Cells located on the stomach body:
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1. parietal
2. chief |
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Cells located on the antrum:
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G cells
|
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BPCAGM (Buena Park, CA, GM)
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body has parietal and chief; antrum has g cells and mucous
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H+ in the parietal cells is produced by _ enzyme
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carbonic anhydrase (HCO3- leaves to the blood side, basolaterally)
|
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Omeprazole inhibits _
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H+/K+ ATPase (on parietal cells)
|
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If vomit, why does your body suffer from alkalosis?
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bicarb is never secreted, because it is not stimulated by the H+ in the duodenum
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Gastrin is released by _
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1. eating a meal
2. small peptides 3. distension of the stomach 4. vagal stimulation |
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Zollinger-Ellison Syndrome is:
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1. gastrin secreting tumor of pancreas
2. increased H+ 3. not subject to - feedback |
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H pylori also causes duodenal ulcer, because it inhibits:
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1. SST
2. intestinal bicarb |
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Atropine:
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1. blocks H+
2. inhibit ACh on parietal |
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Cimetidine:
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1. blocks H2 receptor (histamine)
2. also blocks potentiation |
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Omeprazole:
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inhibits H/K ATPase
|
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Pancreatic juice: low flow _, high flow_
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NaCl; NaHCO3 (but always isotonic)
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Pancreatic juice has much higher _ and lower _ concentration than plasma
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higher: bicarb; lower: Cl-
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Secretin secretes:
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mostly fluid from pacnreas
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CCK secretes:
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mostly pancreatic enzymes
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Secretin is scereted by _ cells in the _
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S, duodenum
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secretin acts on _ cells to increase _ secretion
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ductal, bicarb
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Pancreas: acinar produces _, but ductal replaces _ with _
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Na, Cl; ductal replaces Cl with bicarb
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CCK is secreted by _
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I cells
|
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CCK is in response to _, _, _
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1. peptides
2. a.a. 3. FA |
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CCK's second messenger is _ and _
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IP3 and Ca+2
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CCK has potentiating effects?
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Yes, act thru IP3/Ca+2
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ACh is released in response to:
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H+, peptides, FA
|
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ACh stimulates enzyme secretion by acinar cells, potentiates effect of _
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secretin
|
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Cystic fibrosis is a defect in _ channel
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chlroide (CTFR gene)
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Cystic fibrosis affects pancreatic secretion, because:
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bicarb/Cl- sends Cl- into the cell (if Cl- not work, cannot secrete enzymes)
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Cystic fibrosis can lead to:
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malabsorption, steatorrhea
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Fat soluble vitamins are _
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ADEK
|
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Fat soluble vitamins are incorporated into _ and absorbed with _
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micelles, lipids
|
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Water soluble vitamins are absorbed by _
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Na+ dependent cotransport
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Water soluble vitamins are absorbed by _ dependent
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Na+
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Vit B12 is absorbed in _ and requires _
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ileum, intrinsic factor
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R factor is in the _
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saliva (which has to be removed before reaching ileum)
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Gastrectomy is _
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cutting of GI tract
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intrinsic factor is produced by _
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parietal cell
|
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lack of Vit B12 leads to _
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pernicious anemia
|
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Active form of Vit D is _, produced by _
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1,25 dihydroxy-cholecalciferol; kidney
|
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1,25 dihydroxy-cholecalciferol induces synthesis of _
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ca binding pn., calbindin D-28K
|
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Vit D deficiency causes _ and kids and _ in adults. _ can also cause this.
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rickets; osteomalacia; renal failure
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Calcium may not be absorbed due to _
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renal failure
|
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2 things that increase Ca+ absorption:
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1. PTH
2. thiazide diuretics |
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Ca absorption competes w/ _ in the _ area
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Mg, DAL
|
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90% of calcium is absorbed at _ and _
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proximal tubules, DAL
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loop diuretics will cause calcium excretion/absorption?
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excretion (Na+ secreted, Ca also not absorbed)
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Ca reabsorption is coupled to _ absorption
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Na (that is why loop diuretics cause less Ca absorption)
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Iron is absorbed bound to _ or _ or _
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1. Hb
2. myoglobin 3. Free iron |
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Heme iron is degraded in _, releasing free Fe+2
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intestinal cells
|
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Fe+2 circulates in blood bound to _
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transferrin
|
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Free iron in intestinal cells bind to _ and is released to blood
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apo-ferritin
|
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Iron bound to transferrin transports it from _ to _
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small intestine; liver
|
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Iron is carried from liver to bone marrow for synthesis of _
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Hb
|
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Anemia is most commonly caused by _
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iron deficiency
|
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Gallbladder is contracted by _ and _
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CCK, ACh
|
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CCK is released in response to:
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1. aa, small peptides
2. FA (from I cells) |
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Carbohydrate: only _ are absorbed
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monosaccharides (Glu, Gal, Fru)
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Glu and Gal are transported thru _
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SGLT1 (Na+ depending cotransport)
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SGLT1 uses _ to drive _
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Na+, glucose/galactose into cells
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3 border enzymes are:
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maltase, alpha-dextrinase, sucrase
|
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Fructose is transported by _
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facilitated diffusion (passive); GLUT5
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Fructose is passive/active?
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passive
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lactose intolerance is from deficient _
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lactase (osmotic diarrhea)
|
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Na/K pump on the basolateral keeps the intracellular _ low
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Na+
|
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Poisoning of Na/K ATPase inhibits absorption of:
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glucose, galactose (no Na+ gradient)
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Na+ gradient is used to absorb:
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glucose, galactose
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Sugar is absorbed from lumen to cell by _ and from cell to blood by _
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SGLT1, GLUT2
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Proteins can be done by _ and _
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endopeptidases (interior peptide), exopeptidases (one aa at a time from the C terminus)
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Is pepsin essential for pn digestion?
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no, not essential
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chief cells produce _
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pepsinogen (activated to pepsin by H+)
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optimum pH for pepsin is btw/ _ and _
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1-3
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when the pH is above 5, pepsin is _
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denatured
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Trypsin, chymotrypsin, elastase, carboxypeptidase A, B are:
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pancreatic proteases
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Trypsinogen is activated to _
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trypsin
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trypsin cleaves:
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trypsinogen, chymotrypsinogen, proelastase, procarboxypeptidase A, B
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pepsin is denatured at pH _
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above 5
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Glucose and galactose enter the blood thru _ by active/passive?
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GLUT2, passive
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after digestion, pancreatic proteases _
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degrade each other / absorbed with dietary proteins
|
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Proteins can be absorbed in ___ forms
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aa, di-, tripeptides
|
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aa are absorbed using _
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Na+ dependent cotransport
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Na+ dependent cotransport are used to absorb:
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glucose, galactose, a.a. (separate carriers for each type), [kidneys: glucose, bicarb, a.a., phosphate, lactate]
|
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aa enter cells by _, then enter blood by _
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Na+ dep cotransport; facilitated diffusion
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dipeptides and tripeptides are absorbed faster/slower than free a.a?
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di-, tri-peptides are absorbed FASTER
|
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di-, tri-peptides are absorbed using _
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H+ dependent cotransport
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di-,tri-peptides enter the cell by _, then leave as _
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H+ dependent cotransport; free a.a (facilitated diffusion)
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Lipid begins digestion in _
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mouth (lingual lipases)
|
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most lipids are digested in the _ by _
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intestines, pancreatic lipases
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CCK functions are BIG P
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1. bicarb secretion
2. inhibit gastric emptying 3. gallbladder (enzyme, growth) 4. pancreatic enzymes |
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CCK is activated by
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1. aa/peptides
2. FA |
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Lipids are emulsified by _ and then digested by _
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bile acids, pancreatic lipases
|
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CA Salt:
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conjugated bile acid = bile salt
|
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6 causes of steatorrhea:
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1. pancreatic disease (pancreatitis CF)
2. gastrin secretion (i.e. ZE) 3. ileal resection (deplete bile due to low reabsorption) 4. bacterial growth (deconjugate bile early, not efficient in lipid emulsification) 5. tropical sprue (decreased # of intestinal cell for absorption) 6. apoB not synthesized (inability to form chylomicrons) |
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bile salt is deconjugated by _
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bacteria (deconjugated so that it can be absorbed)
|
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tropical sprue causes _
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decreased # of intestinal cells
|
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chylomicrons require _
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apoprotein B48 (specifically for chylomicron)
|
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Micelles bring lipid digestion products to the _
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absorptive surface of intestinal cells
|
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FA, monoglycerides, and choleserol _ across the lumninal membrane.
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diffuse
|
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is glycerol contained in the micelles?
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no, glycerol is hydrophobic
|
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Lipid enter the cell by _, then become re-esterified to _, then exit by _ to _
|
diffusion, chylomicrons, exocytosis, lymph vessels (thoracic duct)
|
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bile contains (4 components):
|
1. bile salts
2. phospholipid 3. cholesterol 4. bile pigment |
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bile is produced by _
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liver (hepatocytes)
|
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primary bile is converted to secondary by _
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bacteria in intestines
|
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secondary bile acids are (2 types):
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1. deoxycholic acid
2. lithocholic acid |
|
CA salt:
|
conjugated bile acid forms bile salt
|
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bile acids are conjugated with _ or _
|
glycine, taurine
|
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Gallbladder functions to _
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concentrate and store bile
|
|
Choleretic agents incr/decr the formation of bile?
|
increase
|
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Tight epithelium is seen on _, while leaky is seen on _
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colon; SI and gallbladder
|
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_ bind the epithelial cells to one another
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tight junctions
|
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Electrolytes and water can cross intestinal epithelial cells by either: _ or _ pathways
|
1. transcellular
2. paracellular |
|
I Kiss Meg's Pn's
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ICF has K, Mg, and Pn's
|
|
ENaCh'l Bicar
|
ECF has Na, Cl, Bicarb
|
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K+ is actively/passively secreted in the _
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actively; colon
|
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K+ secretion is stimulated by _, in both colon and kidneys
|
aldosterone
|
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Diarrhea: _ is lost, causing _
|
K+, hypokalemia
|
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Dietary K+ is absorbed in _ by active/passive thru para/transcellular route?
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SI, passive, paracellular
|
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Water is secondary to _ absorption
|
solute
|
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Colon has higher/lower water permeability than SI?
|
colon has lower water permeability
|
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water is absorbed isomotically in the _ and _
|
SI, gallbladder
|
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GI tract secretes electrolytes from _ to _
|
blood to lumen
|
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GI tract: secretion is in _, absorption in _
|
crypts, villi
|
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Primary ion secreted into the SI is _
|
Cl-
|
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Na+ is secreted into the lumen by passively following _
|
Cl-
|
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Vibrio cholerae is aka _
|
cholera toxin
|
|
cholera toxin causes _, by stimulating _
|
diarrhea, Cl- secretion
|
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Cholera catalyzes _, the alpha subunit of Gs pn coupled to adenylyl cyclase to _
|
ADP ribosylation; permanently activated
|
|
cholera: intracellular cAMP increases/decreases; opening _ channels
|
cAMP incresases; Cl-
|
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_ and _ follow Cl- into the lumen, leading to secretory diarrhea
|
Na, water
|
|
_ cause diarrhea in a similar fashion as cholera
|
some strains of E Coli
|
|
Na is absorbed thru 4 ways:
|
1. passive diffusion (thru Na+ channels)
2. Na+/glucose and Na+/a.a. 3. Na/Cl cotransport 4. Na/H exchange |
|
In the small intestines, 3 paths are most imp. for Na+ absorption:
|
1. Na/glucose
2. Na/a.a 3. Na/H exchange (similar to renal proximal tubule) |
|
Colon: Na+ is absorbed by _
|
passive diffusion
|
|
Na+ absorption is stimulated by _
|
aldosterone (K+ secretion is also stimulated by this)
|
|
Na+ is pumped out against its gradient by _
|
Na/K ATPase (this creates the gradient for other absorption)
|
|
Na/K ATPase is on the _ membrane
|
basolateral
|
|
Cl- absorption accompanies _ absorption
|
Na+
|
|
Cl- absorption accompanies Na+ absorption by 3 ways:
|
1. passive diffusion paracellularly
2. NaCl cotransport 3. Cl-/HCO3- exchange |