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249 Cards in this Set
- Front
- Back
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saliva contains:
(4) |
1. HCO3
2. lubricating fluid and mucus 3. amylase and lingual lipase 4. histatin and alpha-defensins |
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what does HCO3 from saliva do?
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protects against gastric reflux
|
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gastric reflux =
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backflow of stomach contents
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histatin =
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wound-healing factor
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a-defensins =
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anti-microbials
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paneth cells:
(2) |
1. found at the base of SI crypts
2. produce defensins |
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parietal cells secrete:
(2) |
1. HCl
2. intrinsic factor |
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another name for HCl =
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gastric acid
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what do the H+ and Cl- of HCl do, respectively?
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H+ (acid) kills bacteria, breaks things up
Cl- enhances Ca2+ absorption |
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what's so important about intrinsic factor?
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it's essential for absorption of B12
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what do chief cells secrete?
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pepsinogen
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what do EC cells of the stomach secrete?
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a specific hormone (per each EC cell)
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enteroendocrine =
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enterochromaffin = EC
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acid secretion is limited by:
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negative feedback
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ECL cell =
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EC-like cell
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**what's the main stimulant of H+ release from parietal cells?**
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**histamine**
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the duodenum is not meant to handle:
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acid
|
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how do proton pumps of parietal cells get to the membrane to release H+?
(2) |
1. ACH and gastrin => Ca2+ => fusion
2. Histamine and SS inhibits cAMP, allowing it to proceed |
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how does the stomach keep from digesting itself?
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a thick layer of mucus
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|
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ulcer =
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breakdown of mucus barrier
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ulcers =>
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digestion of stomach/duodenal wall
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3 causes of ulcers:
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1. excess acid
2. H. pylori 3. NSAIDS, aspirin |
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all 3 causes of ulcers are exacerbated by:
(4) |
caffeine/nicotine/alcohol/stress
|
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excess acid usually occurs via:
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a gastrin-secreting tumor
|
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to diagnose a gastrin-secreting tumor, inject:
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secretin
- if gastrin levels increase, you know it's a tumor (b/c secretin would cause a dec. in gastrin release from G cells) |
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***no acid =
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no ulcer***
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|
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3 treatments for ulcers:
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1. Histamine-receptor blockers
2. proton pump inhibitors 3. pH buffers (like Tums) - only a bandaid |
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up to 20% of people with GERD develop:
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Barrett's esophagus
|
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Barrett's esophagus =
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normal epithelium of the esophagus is replaced with a columnar epithelium, like that of SI
- it's red and inflammed from the outside |
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patients with Barrett's are 40x more likely to develop:
|
esophageal adenocarcinoma
|
|
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adenocarcinoma =
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malignant tumor from glandular structures in epithelial tissues
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venous blood from GI will first go to the:
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liver
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the liver stores many nutrients, preventing:
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oversupply
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which hormones do acinar cells of the pancreas respond to?
(2) |
CCK and ACH
|
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what is the acinar cell response to CCK and ACH?
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secretion of digestive enzymes
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5 phases of eating:
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interdigestive
cephalic gastric early intestinal late intestinal |
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what occurs during the interdigestive phase?
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stomach has lots of H+
=> pH = 1.2 => parietal cells are inhibited from secreting more H+ |
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what happens during the cephalic phase?
(2) |
1. though/smell/sight/taste of food activates the vagus => ACH to chief cells => pepsinogen released
2. stomach pH still low => SS => no HCl release |
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what happens during the gastric phase?
(2 => 1) |
1. food in stomach => G cells activate
2. food buffers pH => dec. H+ **both cause a decrease in SS => inc. gastrin release => /inc. Histamine** |
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what happens during the early intestinal phase?
(2) |
1. chyme in intestine => release of gastrin that travels to the stomach => ***enhanced*** acid release
2. AA/fat digestants cause release of CCK |
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what does CCK do?
(4) |
1. increases constriction of pyloric sphincter, thereby slowing chyme movement
2. causes bile to be pumped out of gallbladder 3. relaxes sphincter of Oddi (to allow pancreatic secretions) 4. acts on acinar cells to cause release of digestive enzymes via Oddi |
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what happens in the late intestinal phase?
(3) |
1. less food in the stomach = pH falls again => inc. SS => dec. gastrin/dec. Histamine release
2. acid in duodenum => inc. secretin => dec. H+ release, inc. HCO3 from the pancreas 3. CCK continues digestive actions |
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2 kinds of pancreatic secretions in response to a meal:
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1. acinar cells release digestive enzymes and NaCl
2. duct cells/centroacinar cells release NaHCO3 |
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acinar cell release is mediated by:
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Ca2+-activated Cl channels and Ca2+-mediated exocytosis of vesicles
|
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duct cell release is mediated by:
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cAMP-activated chloride channels
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what GI hormone increases cAMP?
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secretin
|
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if Cl leaves the cell, then:
|
Na+ leaves
=> water follows |
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**relationship of parietal cells to duct cells:**
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they *oppose* each other
|
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***how do parietal cells and duct cells oppose each other?***
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1. parietal cells release H+; duct cells release HCO3 down the line
2. parietal cells cause alkaline tide in blood, via release of HCO3; duct cells cause acid tide in blood, via release of H+ |
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***results of parietal and duct cells opposing each other:***
(2) |
1. duodenal lumen is neutral
2. blood coming into liver is neutral |
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bile is sent from the liver to:
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the intestines, to aid in the digestion of fats
|
|
|
the vast majority of bile components is:
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recycled; returned to the liver to be used again
|
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capillaries of the liver are sinusoidal; bile components return though them, which is a signal for:
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the hepatocytes to stop making bile
|
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components of bile:
(6) |
1. bile acids
2. phospholipids 3. cholesterol 4. bile pigments 5. xenobiotics 6. water |
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bile acids:
(3) |
1. made in hepatocytes
2. only 0.5% is excreted 3. amphipathic => spontaneously form micelles |
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bile acids that pass through the kidney are:
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reabsorbed and returned to the liver
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"xenobiotics" =
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drugs, AB's, toxins
|
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old RBC's die and release:
(3) |
1. globin
2. bilirubin 3. iron |
|
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bilirubin circulates bound to:
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albumin
=> too big for kidneys => excreted into the intestines |
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what is the result of an abnormal composition of bile?
|
gallstones
|
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cholecystectomy =
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removal of gall *bladder*
|
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75% of gallstones are _____________________; 25% are ___________________________________
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cholesterol stones;
pigment stones (both insoluble components of bile) |
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first symptoms of gallstones =
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inflammation and pain
|
|
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prolonged obstruction of bile duct due to gallstones =>
(2) |
1. liver problems (e.g. jaundice due to accumulation of bilirubin)
2. pancreatitis |
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pancreatitis means:
|
the pancreas begins to digest itself
|
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pancreatitis =>
|
loss of pancreatic functions => diabetes, lack of digestion, etc.
|
|
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treatment of gallstones:
(3) |
1. removal of stones followed by cholecystectomy
2. ultrasound to pulverize 3. oral bile salts => dissolves stones |
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what do oral bile salts do to gallstones?
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dissolve them
|
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generic layers of the GI tract:
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1. mucosa
2. submucosa 3. muscularis externa 4. external layer |
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mucosa =
(3) |
1. epithelium
2. lamina propria 3. muscularis mucosae (SM) |
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submucosa =
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CT
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muscularis externa =
(2) |
inner circular SM, outer longitudinal SM
|
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external layer =
(2) |
1. adventitia (loose CT)
2. serosa |
|
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serosa =
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CT with mesothilial lining from peritonium
|
|
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histology of esophagus:
(3) |
1. stratified squamous
2. glands in lamina propria 3. glands in submucosa |
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the stomach's muscularis externa has:
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3 layers of SM, instead of the usual 2
|
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histology of stomach:
(3) |
1. simple columnar epithelium with gastric pits
2. gastric *glands* in the lam. prop. 3. mucous cells are found in the glands of *every* region |
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facets of gastric glands:
(3) |
1. very short in the cardiac region
2. very long in the fundic/body region 3. just long in the pyloric region |
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"fundic glands" ~
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glands of fundus AND body
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parietal cells:
(2) |
1. located at isthmi or necks of gastric glands
2. lots of mit. |
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chief cells:
(3) |
1. located at bases of glands
2. abundant RER 3. LOTS of secretory granules |
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***chief cells are localized to:***
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glands of the fundus/body region of the stomach
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histology of the SI:
(2) |
1. simple columnar with goblet cells and microvilli
2. **lacteals and crypts** in the lam. prop. |
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which region of the SI has the most goblet cells?
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the ileum
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which region of the SI contains Brunner's glands?
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the duodenum
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Brunner's glands are located in:
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the duodenal submucosa
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Brunner's glands produce:
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alkaline fluid, to offset acidic chyme from the stomach
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the SI contains lymphoid nodules, which are:
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collections of immune cells
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in the SI, lymphoid nodules are found in the lamina propria of:
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all 3 sections
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***in the ileum, the lymphoid nodules extend into the:***
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submucosa
- form large aggregates called Peyer's Patches |
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3 tricks that inc. the SA in the SI:
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1. plicae circulares
2. intestinal villi 3. microvilli |
|
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plicae circulares =
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visible, circular folds of tissue
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plicae circulares are most prominent in the:
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jejunum
|
|
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intestinal villi =
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evaginations that contain lacteals
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goblet cells secrete:
|
mucus
|
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enterocytes =
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the regular, microvillied absorbing cells of the SI
|
|
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enterocytes:
(2) |
1. columnar
2. also called surface-absorptive cells |
|
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Paneth cells:
(3) |
1. located at bases of crypts
2. secrete lysozyme 3. contain LARGE granules |
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lysozyme =
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antibacterial enzyme
|
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like the stomach, the SI has:
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EC cells
|
|
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histology of the LI:
(3) |
1. simple columnar with goblet cells
2. crypts, but NO villi 3. lymphoid nodules |
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**histology of the appendix:**
|
just like LI, except with LARGER lymphoid nodules
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the myenteric plexus controls:
|
the muscularis externa layer
|
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the submucosal plexus controls:
|
the muscularis mucosae layer
|
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coordination betwen the myenteric and submucosal plexi is achieved via:
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the intrinsic cells of Cajal
|
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liver disease =>
(5) |
1. jaundice (of sclera and otherwise)
2. ascites/edema 3. gynecomastia 4. palmer erythema (redness of palms) 4. spider angiomas |
|
|
gynecomastia is the result of:
|
excessive EST
|
|
|
spider angioma =
|
dilation of superficial blood vessels on chest wall/arm
- along with palmar erythema, a result of cirrhosis |
|
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which blood does the portal vein receive?
|
all of the blood from the GI and spleen
|
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splanchnic and splenic veins =>
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portal vein => liver => hepatic vein
|
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splanchnic means:
|
of the visceral organs
|
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the liver is designed to maximize exchange with the blood that comes through it; =>
|
wide, low-Resistance caps for slow flow
|
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portal hypertension =
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backup of blood due to inability to pass through liver
|
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portal hypertension is usually the result of:
|
cirrhosis
|
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cirrhosis =
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scarring/fibrosis of the liver
|
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effects of cirrhosis =
(2) |
1. portal HTN (due to increased R via fibrosis)
2. encephalopathy |
|
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immediate effects of portal hypertension:
(3) |
1. large, hemorrhoidal veins
2. splenomegaly 3. esophageal varices |
|
|
hemorrhoidal just means:
|
swollen
|
|
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varices are at risk for:
|
rupture
=> bleed out |
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later effects of portal HTN:
(3) |
1. ascites
2. edema 3. shunting of blood around the liver |
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edema occurs because:
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vessels dilate due to increased fluid => low BP => NaCl/water retention
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encephalopathy is the result of:
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a decreased ability to biotransform ammonia
|
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encephalopathy has 2 immediate causes:
|
1. fewer functional cells to perform biotransformation
2. shunting of blood *around* the liver => no detox |
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2 important proteins secreted by the liver:
|
1. albumin
2. all coagulation factors (save VIII) |
|
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lack of albumin =>
|
decreased COP in caps
|
|
|
cirrhosis ~~
|
liver failure
=> decreased conversion of NH3 into NH4+ |
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what's the result of a decreased conversion of ammonia (NH3) into ammonium (NH4+)?
|
NH3 crosses the blood brain barrier
=> toxicity to brain |
|
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encephalopathy =
|
worsening of brain function
(confusion, coma) |
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NH4+ can't cross into the brain because of:
|
its charge
|
|
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dec. conversion of ammonia is treated with:
|
oral lactulose
=> converted => excreted as NH4+ |
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the liver transfroms both:
(2) |
endogenous cmpds (bilirubin, sterol) and xenobiotics
|
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Phase I of transformation =
|
making cmpds more water-soluble
|
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Phase II of transformation =
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making cmpds *highly* water-soluble
|
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the liver makes hydrophobic cmpds hydrophilic, so as to:
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enhance excretion in urine or bile
|
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dead RBC => unconjugated bilirubin =>
|
liver => conjugated bilirubin => more soluble => secreted into bile
|
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the ileum and colon metabolize conjugated bilirubin (found in bile) into:
(2) |
1. urobilogen
2. stercobilin |
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stercobilin is the:
|
dark pigment of feces
|
|
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urobilogen is further metabolized by the kidneys into:
|
the yellow urobilin of urine
|
|
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cholestasis =
|
blocked flow of bile from the liver
=> non-colored stools (because bilirubin is never metabolized into stercobilin) |
|
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immune function of the liver is achieved via:
|
Kuppfer cells
|
|
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Keppfer cells:
(5) |
1. actually macrophages
2. metabolize aged RBC's 3. secrete immuno-proteins 4. digest Hb 5. destroy bacteria |
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acinus =
|
small cavity surrounded by secretory cells
|
|
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*compound* exocrine glands have:
|
>1 shaft
- they are branched |
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parenchyma =
|
functioning portions of a tissue/organ, as opposed to CT
|
|
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serous cells of salivary glands secrete:
(2) |
amylase and lipase
|
|
|
mucus cells of salivary glands secrete:
|
mucin
(protein component of mucus) |
|
|
myoepithelial cells of the salivary glands are ______________
|
*contractile*
|
|
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what do myoepithelial cells of the salivary glands do?
(2) |
1. accelerate saliva secretion
2. prevent distention of secretory unit |
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what do striated duct cells and intercalated duct cells of the salivary glands do?
(2) |
1. modify and conduct saliva
2. form the exocrine ducts |
|
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parotid gland:
(2) |
1. cmpd acinar
2. made of ONLY serous cells |
|
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submandibular gland:
(3) |
1. cmpd tubuloacinar
2. 80% serous, 20% mucus 3. **contains serous demilunes** |
|
|
serous demilune =
|
serous-cell cap on mucous cells
|
|
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what do serous demilunes do?
|
secrete lysozymes, which destroy bacteria
|
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sublingual gland:
(2) |
1. cmpd tubuloacinar
2. 50% serous, 50% mucous |
|
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pancreatic acini:
(3) |
1. surround islets of Langerhans
2. secrete digestive enzymes, as zymogens or otherwise 3. composed of acinar cells |
|
|
acinar cells have LOTS of:
|
secretory vesicles
|
|
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centroacinar cells form the beginning of the:
|
intercalated ducts that come out of pancreatic acini
|
|
|
the liver receives gets a dual blood supply:
|
1. the hepatic artery, from the heart
2. the portal vein, from the GI tract |
|
|
portal vein => branches of portal vein (venules) =>
|
sinusoids => central veins (venules) => sublobular veins => hepatic vein => IVC
|
|
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***portal triad = ***
(3) |
1. branches of portal vein (venules)
2. hepatic arterioles 3. bile ductules |
|
|
**portal triads flow into:**
|
the central vein of each hepatic lobule
|
|
|
in terms of size, what's the ranking of the portal triad members?
|
venules > arterioles > bile ductules
|
|
|
sinusoids of the liver:
(3) |
1. discontinuous endo
2. discontinuous basal lamina 3. large fenestrations |
|
|
space of Disse is found between:
|
hepatocytes and sinusoidal endothelium
|
|
|
space of Disse allows free flow of plasma in and out, =>=>
|
easy exchange of *macromlcls*b/w sinusoids and hepatocytes
|
|
|
3 roles of hepatocytes:
|
1, absorptive
2. endocrine 3. exocrine (release of bile into bile canaliculi) |
|
|
stellate cells:
(3) |
1. aka hepatic lipocytes aka Ito cells
2. live in space of Disse 3. store fat and lots of other stuff |
|
|
flow of bile from liver: hepatic ducts (right and left) =>
|
common hepatic duct => common bile duct => duodenum
or: common bile duct => cystic duct => gallbladder (if bile isn't needed) |
|
|
gall bladder:
(2) |
1. simple columnar with sporadic microvilli
2. lamina propria contains lymphocytes |
|
|
what does CCK do at the GB?
|
contracts its SM, propelling bile to release
|
|
|
intestines have both absorptive AND secretive capabilities; which part of the intestines does what?
|
villi absorb;
crypts secrete |
|
|
**crypts also proliferate**;
|
germinal layer at the base of crypts creates new cells => feed up and up, eventually reaching tops of villi => old cells at the top are shed into the lumen
|
|
|
3 axes of cell differentiation in the GI:
|
1. from mouth to rectum
2. from bottom of crypts to top of villi 3. from one end of the cell (apical) to another (basolateral) |
|
|
what allows movements of particles though the epithelium?
|
epithelial polarity (difference between membranes)
|
|
|
brush border cells contain:
|
digestive enzymes
|
|
|
mouth/stomach/pancreatic digestion = _________ digestion
|
crude
- brush border digestion is refined |
|
|
what kind of transportation does the brush border use to bring nutrients into the epithelium?
|
**active** transport
|
|
|
carb digestion: polysaccharides =>
|
disaccharides => brush border => monosaccharides (fructose, glucose, galactose) => transported into cell (SGL1 for g and g, GLUT5 for fructose) => fructose converted to glucose => g and g => blood
|
|
|
when glucose hits the blood, which messenger is activated?
|
GLP1
|
|
|
what does GLP1 do?
|
goes to pancreas, tells it to release insulin
|
|
|
lactose is a dimer of:
|
glucose and galactose
|
|
|
lactose is normally broken down by lactase at:
|
the brush border
|
|
|
no lactase =>
|
non-absorbable lactose continues down the GI tract =>
1. water pulled in => diarrhea 2. bacteria in colon convert it to acid and H2 => breath |
|
|
protein digestion: proteins =>
|
small peptides / AA's => specific transporters on apical membrane => down concentration gradient and into blood
|
|
|
small peptides are also broken down into AA's, at:
|
the brush border
|
|
|
what activates trysinogen?
|
enterokinases
|
|
|
what does the active trypsin activate?
(2) |
1. chymotrypsinogen
2. precarboxypeptidase |
|
|
fat digestion: fats => MG's and FA's =>
|
enter lacteals in villi => reformed into TG's => secreted into *lymph* in chylomicrons => systemic circulation
|
|
|
exception to normal fat digestion process =
|
short FA's
- released directly into the blood |
|
|
water is actually __________ into the lumen
|
secreted
|
|
|
why is water secreted into the lumen of the intestines?
|
to create the aqueous environment necessary for digestive enzymes and transporters to work
|
|
|
water is also _____________ from the lumen
|
reclaimed
to prevent dehydration |
|
|
diarrhea =
|
massive loss of fluid and electrolyte
|
|
|
diarrhea =>
(4) |
1. dehydration
2. low BP 3. hypokalemia 4. acidosis (via loss of HCO3) |
|
|
one solution to diarrhea's maleffects =
|
oral solution
|
|
|
oral solution means ingesting:
(5) |
NaCl, AA's, glucose, K+, and bicarb
|
|
|
4 kinds of diarrhea:
|
1. fatty
2. osmotic 3. inflammatory 4. secretory |
|
|
which of the 4 kinds of diarrhea are a result of inadequate absorpion?
|
fatty, osmotic, and inflammatory
|
|
|
secretory diarrhea is caused by:
|
pathologies
|
|
|
fatty diarrhea ~~
|
unable to digest/absorb fat properly
|
|
|
osmotic diarrhea is caused by:
(3) |
1. enzyme deficiencies
2. transporter deficiencies 3. unabsorbable foods |
|
|
inflammatory diarrhea is caused by:
(2) |
1. Crohn's disease
2. infectious diseases |
|
|
both Crohn's and infectious diseases cause a loss of:
|
mucosae => loss of ability to absorb
|
|
|
secretory diarrhea is a function of:
|
secretion being greater than absorption
|
|
|
3 causes of secretory diarrhea:
|
1. cholera
2. VIPoma 3. enterotoxic E. Coli |
|
|
how does cholera cause secretory diarrhea?
|
releases cholera toxin => stimulates VIP receptor to continually make cAMP => PKA => Cl channel => Cl continually released into the lumen => water follows
|
|
|
VIPoma =
|
tumor of a non-B islet cell
|
|
|
how does a VIPoma cause secretory diarrhea?
|
constant release of VIP to intestines => producion of cAMP => PKA => Cl channel => Cl continually released into the lumen => water follows
|
|
|
treatment for VIPoma =
|
SS analog
(lasts longer than natural SS) |
|
|
what does the SS analog do?
(2) |
1. decreases VIP release from pancreas
2. inhibits VIP receptor in intestinal epithelium |
|
|
how does enterotoxic E. Coli cause secretory diarrhea?
|
makes a stable toxin => continual production of cAMP => PKA => Cl channel => Cl continually released into the lumen => water follows
|
|
|
diagnosis for fatty diarrhea =
|
fat in stool
|
|
|
diagnosis for inflammatory diarrhea =
(2) |
1. WBC's in stool
2. parasites/bacteria in stool |
|
|
diagnosis for osmotic diarrhea =
(3) |
1. H2 in the breath (due to lactose in colon)
2. pH < 7 3. osmotic gap >125 |
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|
diagnosis for secretory diarrhea =
(3) |
1. pH about 7
2. osmotic gap <50 3. ***persists in absence of food intake*** |
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|
osmotic gap formula:
|
290 - (2 x [K+] + [Na+])
where concentrations of K+ and Na+ are taken from the **diarrheal fluid** |
|
|
an orange stain ~~
|
**pituitary only**
|
|
|
examples of cells of the anterior pituitary:
(4) |
1. somatoropes
2. lactotropes 3. gonadotropes 4. thyrotropes |
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|
somatotropes are:
|
tall
|
|
|
***lactotropes form a:***
|
***cap around gonadotropes***
|
|
|
what do lactotropes make?
|
prolactin
|
|
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what do gonadotropes make?
|
FSH *and* LH
|
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what do thyrotropes make?
|
TSH
|
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islets of Langerhans: Beta cells are in:
|
the center, alpha cells on on the periphery
|
|
|
what do pancreatic alpha cells make?
|
glucagon
|
|
|
white vesicles within cells =
|
*steroid hormones*
|
|
|
primordial follicles are NOT:
|
primary follicles
|
|
|
the zona pellucida is a:
|
blue membrane UNDER cells
|
|
|
antral follicle is another name for:
|
secondary follicle
Graafian follicle |
|
|
theca interna =
|
cells
|
|
|
theca externa =
|
collagen fibers
|
|
|
mammilary gland =
|
modified sweat gland
|
|
|
spermatids are either:
|
round or elongated
|
|
|
the appendix often has:
|
crud in the lumen
|
|
|
metabolic acidosis is the result of loss of bicarb via:
|
diarrhea
|
|
|
Vomiting => loss of acid =>
|
metabolic alkalosis
|
|
|
***Secretin causes tumor cells to release:***
|
gastrin
|
|
|
secretin is a system-wide ____________ of **hormones**
(as opposed to acid) |
***releaser***
|
|
|
secretin ultimately causes a ____________ in gastrin secretion b/c the local paracrine effect of D cells/SS is stronger than the long endocrine effect of secretin
|
decrease;
The negative of D cells is greater than the positive of secretin |
|
|
Somatostatin is a system-wide _____________
|
inhibitor;
Inhibits G cells, parietal cells, ECL cells, and GH release |
|
|
a positive Urea breath test indicates:
|
presence of active H. pylori
|
|
|
secretin inhibits release of:
|
HCl from parietal cells
|
|
|
conjugated bilirubin:
(3) |
1, more soluble
2. secreted into bile 3. converted into uribilinogen and stercobilin in the colon |
|
|
what does CCK do to your food intake?
|
decreases it
- tells CNS to stop eating |
|
|
what does ghrelin do to food intake?
|
increases it
- tells CNS you're hungry, by raising appetite |
|
|
**both CCK and ghrelin do NOT:**
|
change the food intake set-point
- they only create transient changes in food intake |
|
|
what's an important factor in controlling the food intake set-point?
|
LEPTIN
|
|
|
***Leptin:***
(3) |
1. circulating weight-control peptide
2. tells CNS you're done eating 3. also affects other areas of metabolism |
|
|
many obese people actually have INCREASED leptin in the blood, b/c they are:
|
leptin-RESISTANT
|
