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Guyton & Hall Physiology > Ch 62-65 GI Physiology > Flashcards

Ch 62-65 GI Physiology Flashcards

1
Q

What types of electrical activity occur in GI smooth muscle?

A
  1. Slow waves: undulating changes in resting membrane potential, caused by interstitital cells of Cajal. Only causes contractions in the stomach (sometimes)
  2. Spike potentials: True action potentials, when resting mp rises > -40 mv. Caused by stretch, acetylcholine, and parasympathetics that allow Ca++ and Na+ to enter the cell and cause the action potentials
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2
Q

What factors depolarize the membrane in GI smooth muscle?

A
  1. Muscle stretch
  2. Acetylcholine release
  3. GI hormonal stimulation
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3
Q

What factors cause hyperpolarization of the GI smooth muscle?

A
  1. Nor/Epi
  2. SNS stimulation
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4
Q

What causes tonic contraction of GI smooth muscle?

A
  1. Continuous repetitive spike potentials
  2. Hormones
  3. Continuous Ca++ entry into cells
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5
Q

What are the two plexuses comprising the enteric nervous system?

A
  1. Outer/Myenteric (Auerbach’s) plexus between longitudinal and circular muscle layers. Controls GI movement
  2. Inner/submucosal plexus (Meissner’s) in the submucosa. Controls local secretions and blood flow
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6
Q

To where do GI sensory fibers send afferent fibers?

A
  1. The prevertebral ganglia of the SNS
  2. The spinal cord
  3. Vagus nerves (to brainstem)
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7
Q

What are the effects of stimulating the myenteric plexus (4 ways the contactions are modified)?

A
  1. Increased tonic contraction of the gut wall
  2. Increased intensity of rhythmical contractions
  3. Slightly increased rate of the rhythm of contraction
  4. Increased excitatory wave conduction along the GI wall (speedier contractions)
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8
Q

Where does the myenteric plexus have mainly inhibitory effects?

A

Especially at sphincters muscles, via release of inhibitory neurotransmitter

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9
Q

Where does the submucosal plexus have effects in the GI tract?

A

Sensory signals from GI epithelium are integrated into the submucosal plexus to control local intestinal secretion, absorption, and local submucosal muscle contractions

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10
Q

Which are the main neurotransmitters that control GI function? What effects do they have?

A
  1. Acetylcholine excites
  2. NorEpi and Epi inhibit
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11
Q

What parts of the GI tract do the cranial and sacral divisions off the PSNS each control?

A

Cranial: Via vagus. Esophagus, stomach, pancreas, some intestines and a little bit of colon
Sacral: From the pelvic nerves in the 2-4th sacral SC segments. Controls the Distal half of large intestine and to the anus

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12
Q

What effect does stimulation of the postganglionic neurons of the GI PSNS have?

A

These are in the myenteric and submucosal plexuses. Stimulation is excitatory to the whole enteric nervous system

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13
Q

How does the SNS exert its effects on the enteric nervous system?

A
  1. Slightly via direct effect of secreted norEpi to inhibit smooth muscle
  2. Majorly via NorEpi’s inhibitory effect on neurons of the entire ENS
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14
Q

Where do SNS fibers to the ENS originate(which section of spinal cord and which ganglia)?

A

Between segments T5 to L2. Preganglionic fibers enter the sympathetic chains then pass to the celiac and mesenteric ganglia

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15
Q

What stimulates the sensory nerves of the GIT?

A
  1. Gut mucosal irritation
  2. Excessive gut distension
  3. Specific chemicals in the gut
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16
Q

What are the types of gastrointestinal reflexes?

A
  1. Those entirely within the GI wall : secretion, peristalsis, mixing, local inhibition
  2. Those connecting the gut to the prevertebral SNS ganglia: gastrocolic, enterogastric, colonoileal
  3. Those between the spinal cord/brainstem and GI tract: gastric motor and secretory action, pain & corresponding inhibition, defecation reflexes
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17
Q

Gastrin: what stimulates secretion, where is it secreted, and what does it do?

A
  1. protein, distension, and nerves stimulate. Acid inhibits.
  2. Secreted at G cells of antrum, duodenum, and jejunum
  3. Action: stimulates gastric acid secretion and mucosal growth
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18
Q

Cholecystokinin: what stimulates secretion, where is it secreted, and what does it do?

A
  1. Stimulated by protein, fat, and acid
  2. Secreted at the I cells of the small intestine
  3. Action: Stimulates pancreatic enzyme and bicarb secretion, gallbladder contraction, exocrine pancreatic growth, and inhibits gastric emptying
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19
Q

Secretin: what stimulates secretion, where is it secreted, and what does it do?

A
  1. Acid and fat
  2. S cells of whole sm intestine
  3. Stimulates pepsin and pancreatic bicarb secretion, biliary bicarb secretion, exocrine pancreas growth, and inhibits gastric acid secretion
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20
Q

Gastric inhibitory peptide: what stimulates secretion, where is it secreted, and what does it do?

A
  1. Protein, fat, carbs
  2. K cells of duodenum and jejunum
  3. Stimulates insulin release. Inhibits gastric acid secretion
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21
Q

Motilin: what stimulates secretion, where is it secreted, and what does it do?

A
  1. Fat, acid, nerves
  2. M cells of duodenum and jejunum
  3. Stimulates gastric motility and intestinal motility
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22
Q

What causes GI peristalsis and how does it normally occur?

A

Stimulated by GIT distension, chemical or physical irritation of the epithelial lining or strong PSNS signals.

Effectual peristalsis requires an active myenteric plexus

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23
Q

What kind of GIT movement would occur, if any, if forward propulsion was blocked?

A

Mixing movement would still occur to churn the contents but no forward propulsion could occur

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24
Q

How does blood flow through the splanchnic circulation, and to what benefit?

A

Blood flows through the gut itself, through the spleen and pancreas, and then immediately into the liver via the portal vein. From there, it passes through liver sinusoids and leaves through hepatic veins to empty into the vena cava. By flowing through the liver, the reticuloendothelial cells can remove bacteria and harmful particulates before they enter systemic circulation

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25
Q

How are water soluble nutrients vs fat soluble nutrients absorbed from the GIT?

A
  1. nonfat/cho’s and proteins: through portal venous blood. Absorbed and stored by hepatic cells there
  2. Fats: absorbed into intestinal lymphatics and into systemic circulation via the thoracic duct (bypasses liver!)
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26
Q

What factors modify/increase blood flow to the GIT?

A
  1. Mucosal-originating vasodilators (cholecystokinin, vasoactive intestinal peptide, gastrin, secretin)
  2. GI glands release kallidin and bradykinin to vasodilate
  3. Decreased oxygen increases blood flow by vasodilation and release of adenosine
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27
Q

Why are the tips of intestinal villi especially susceptible to perfusion-reducing disease states?

A

Because most blood oxygen diffuses out of arterioles and into the venules via countercurrent exchange before reaching the villus tips. Explains blunting!

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28
Q

How does the autonomic NS influence GI blood flow? What is autoregulatory escape?

A

PSNS nerves to the stomach and lowewr colon can increase local blood flow while increasing glandular secretion

SNS stimulation has a direct effect on ALL of the GIT to cause intense vasoconstriction. AND causes intense vasoconstriction of the large volume intestinal and mesenteric veins

Autoreg escape = when SNS reduces blood flow, local metabolic vasodilatres override the sns vasoconstriction

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29
Q

What is the chewing reflex? Which cranial nerve is involved?

A

Food into mouth > inhibits muscles of mastication > jaw drops and stretches muscles > rebound contraction. CN V (trigeminal) innervates muscles of mastication, and the chewing process is ultimately controlled by brainstem nuclei

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30
Q

What are the stages of swallowing, and what occurs during each? Include significant stimuli and controllers of actions

A
  1. Voluntary stage: food bolus is voluntarily squeezed back into the pharynx by the tongue
  2. Pharyngeal stage:
    -Stimulate epithelial swallowing receptor areas
    -Soft palate pulls upward
    -Palatopharyngeal folds pull medially and allow small, chewed particles to pass
    -Vocal cords strongly approximate each other, the neck muscles pull the larynx upward and anteriorly, and upward epiglottis movement is inhibited to close the larynx
    -Upward laryngeal movement enlarges the esophageal opening and the upper esophageal sphincter (pharyngoesophageal) relaxes
    -Muscular pharynx contracts once sphincter relaxes and larynx raises to propel food to the esophagus
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31
Q

What parts of the nervous system control the pharyngeal stage of swallowing?

A
  1. Sensory portions of the glossopharyngeal and trigeminal nerves transmit through the tractus solaris to the medulla oblongata
  2. Deglutition/swallowing center of the medulla
  3. Motor impulses from the swallowing center travel by the 5th, 9th, 10th, and 12th cranial nerves to pharynx and upper esophagus
    *the swallowing center inhibits the respiratory center to allow swallowing
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32
Q

What types of peristalsis comprise the esophageal stage of swallowing?

A
  1. Primary: continuation of the wave started in the pharynx
  2. Secondary: results from esophageal distension that continues until food deposits in the stomach.
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33
Q

What controls the secondary peristalsis of the esophagus?

A

Intrinsic neural circuits initiate, followed by transmission to vagal afferent fibers, then back down via glossopharyngeal and vagal efferent fibers?

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34
Q

How does musculature of the esophagus in a monogastric animal differ along its length?

A

Pharyngeal wall and upper 1/3 = striated muscle

Lower 2/3 is smooth muscle, controlled by the myenteric nerve plexus

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35
Q

What is achalasia?

A

Failure of the gastroesophageal sphincter (cardia) to relax

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36
Q

How is acid reflux normally prevented?

A

-tonic contraction of the lower esophageal sphincter
-Valvelike mechanism of the distal esophagus that closes it when intra-abdominal pressure increases

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37
Q

What are the motor functions of the stomach? What stimulates these?

A
  1. Food storage
  2. Food mixing to form chyme
    -basic electrical rhythm (slow waves) stimulates this
    -because the pylorus is small, most chyme squeezed toward it becomes retropulsed toward the body, mixing chyme
  3. Slow emptying of chyme
    -As constrictor waves progress from body to antrum, they become more intense and provide peristaltic action potentials
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38
Q

What factors stimulate stomach emptying?

A
  1. Intense peristaltic contractions in the antrum “pyloric pump”
  2. Increased food volume to the extent that it stretches the stomach wall and elicits local reflexes to enhance the pyloric pump and inhibit the pyloris
  3. Gastrin enhances the pyloric pump and stimulates motor function
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39
Q

What factors inhibit stomach emptying?

A

-Degree of duodenal distension
-Presence of irritants in the duodenum
-Degree of chyme acidity
-Degree of chyme osmolality (hypo or hyper)
-Presence of breakdown products

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40
Q

How are the duodenal reflexes controlling gastric emptying mediated?

A
  1. Duodenum signals to stomach through ENS
  2. Extrinsic nerves to the prevertebral SNS ganglia and back
  3. Slight…vagus nerves to the brainstem.
    They inhibit the pyloric pump AND increase the tone of the pyloric sphincter
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41
Q

What are the roles of fats and cholecystokinin on gastric emptying?

A
  1. CCK released from jejunal mucosa in response to fats in the chyme inhibits stomach motility caused by gastrin
  2. Fats extract hormones from the duodenal and jejunal epithelium by binding with “receptors” , and then travel by circulation to the stomach perfusion to inhibit the pyloric pump and increase strength of the pyloric sphincter contractions

Other possible contributors: secretin, Gastric inhib peptide,

42
Q

What determines the frequency of small intestinal segmentation contractions?

A

Slow waves

43
Q

How is chyme propelled through the small intestines?

A

-peristaltic waves in the small intestine
-the gastroenteric reflex is conducted through the myenteric plexus
-Gastrin, CCK, insulin, motilin, and serotonin enhance intestinal motility
-**Secretin and glucagon inhibit SI motility
-Segmentation movements (isolated, regular, irregular, weak regular) move it to the ileocecal valve
-Chyme waits at the ileocecal valve until the gastroilieal reflex causes movement into the cecum

44
Q

What is peristaltic rush?

A

Intense irritation of the SI mucosa (infectious diarrhea) causes powerful and rapid peristalsis to relieve the SI of irritant and excessive distenstion

45
Q

How is the ileocecal sphincter controlled?

A

-Cecal reflexes: sphincter contractions intensify when the cecum distends. Irritants in the cecum delay emptying
-Mediated by the myenteric plexus and gut wall with extrinsic and nerves esp by pervertebral sns ganglia

46
Q

What is the peritonealintestinal reflex?

A

Peritoneal irritation strongly inhibits excitatory enteric nerves and causes ileus.

47
Q

What are the renointestinal and vesicointestinal reflexes?

A

Inhibition of intestinal activity via kidney and bladder irritation, respectively

48
Q

What are the principal functions of the colon?

A
  1. Absorb water and electrolytes from chyme
  2. Storage of fecal matter until expulsion
49
Q

What is a “mass movement” and what function does it serve in the colon?

A

modified type of peristalsis that occurs as follows:
-Constrictive ring forms due to distension or irritation of colon
-Rapidly, the immediately distal portion of colon loses its haustrations and contracts as a unit to propel fecal matter
-Mass movements are caused by the gastrocolic and duodenocolic reflexes.

IBD can exacerbate mass movements

50
Q

What are haustrations and what purposed do they serve?

A

Large circular constrictions of the colon and combine with contractions of the longitudinal muscles (teniae coli) to propel contents which bulge out of the sacs created (haustra). Rolls and mixes material

51
Q

How is defecation controlled, initiated, or inhibited?

A

Controlled because of an internal anal sphincter (smooth muscle, circular) and an external anal sphincter (striated muscle)

Pudendal nerve: External sphincter control
Defecation reflexes:
-Intrinsic reflex via local ENS spread through the myenteric plexus. Weak
-Parasympathetic defecation reflex: controlled by the pelvic nerves, intensifies peristaltic waves, relaxes the internal sphincter

52
Q

Which type of stimulus can both inhibit and induce glandular secretion?

A

The SNS – mildly stimulatory on its own, inhibitory via vasodilation when overriding PSNS
PSNS, tactile stim, chemicals, and distension all stimulate secretion

53
Q

What type of glands are found in the salivary glands and pancreas?

A

Acinous glands: contains millions of acini lined with secreting glandular cells that feed into a duct system

54
Q

In which part of the GIT is secretion controlled mainly by the PSNS?

A

Salivary, esophageal, gastric, pancreas, Brunner’s glands in the duodenum and some distal glands in the colon

55
Q

Briefly, what steps comprise the basic mechanism of glandular secretion?

A
  1. Substrate for secretion is transported or diffuses into the glandular cell’s base
  2. ATP provides energy to synthesize substance in the endoplasmic reticulum and golgi apparatus
  3. Transported through the ER, modified and packaged at the golgi apparatus
  4. Vesicles of secretion are released by exocytosis when a control signal increases cell permeability to calcium, and influx of calcium causes vesicular fusion to the apical membrane
56
Q

Describe the type of secretion made by the different salivary glands

A
  1. Parotid glands: serous secretion with ptyalin (alpha amylase)
  2. Buccal glands: mucus
  3. Submandibular and sublingual glands: both mucus and serous
57
Q

Briefly, how is saliva modified as it is secreted through a duct?

A
  1. Sodium is actively reabsorbed
  2. Potassium is actively secreted in exchange
  3. Chloride is passively reabsorbed
  4. Bicarbonate is secreted

This “reconditioning” reduces when the rate of salivation increases

58
Q

How is salivary secretion controlled?

A
  1. Mainly by PSNS
    Stimulates it: tastes, tactile, appetite, nausea, swallowing irritating foods, SNS stimulation (minor), PSNS causes vasodilation and kallikrein secretion
59
Q

What types of glands exist in the esophagus?

A

Upper portion: some complex mucus glands
Body: simple mucus
Distal: more complex mucus glands

60
Q

What is the function of Parietal cells?

A
  1. Water inside the cell becomes H+ and OH-
  2. H+ used by the K/H ATPase to excrete in exchange for K+ on the basolateral side
  3. K+ leaks out, but is also being brought into the cell by a Na/K ATPas on the other side of the cell
  4. Creates a gradient to pull Na+ into the cell from the lumen side
  5. H+ is pumped out, so OH- accumulates in the cell and combines with CO2 to form bicarbonate (thanks, carbonic anhydrase)
  6. Bicarb is transported into the extracellular fluid in exchange for Cl- from the ECF
  7. Cl- are secreted through channels into the lumen to form HCl

Final secretion contains HCl, water, KCl, and some NaCl

61
Q

What stimulates gastric acid secretion?

A

Acetylcholine via PSNS, gastrin, histamine

62
Q

What stimulates secretion of pepsinogen? What stimulates mucus cell secretion?

A

PSNS stimulation

63
Q

What is the function of pepsinogen?

A

Secreted and when contacts HCl, becomes pepsin, a proteolytic enzyme. Must be at a pH < 5

64
Q

What is intrinsic factor, and how is it made

A

Parietal cells secrete intrinsic factor, which is essential for absorbing vitamin B12 in the ileum

65
Q

How is mucus produced in the stomach?

A

Surface mucous cells secrete viscid mucus, which is alkaline and forms a thick gel

66
Q

What is produced from oxyntic glands?

A

Deepest: ECL cells
Deep: peptic or chief cells
“neck” : Parietal cells
Near surface: mucous cells

67
Q

How is histamine secreted in the stomach?

A

From enterochromaffin-like cells (ECL cells) release histamine in direct contact with the parietal cells’ production of HCl, and stimulated by gastrin. Histamine stimulates HCl secretion

68
Q

What is Gastrin and its function?

A

Secreted by g cells of the pyloric glands
Polypeptide secreted in a large and smaller form. Stimulates ECL cells, which stimulate parietal cells to make HCl

Stimulated by presence of proteins in the stomach

69
Q

How is pepsinogen secretion regulated?

A

Stimulated by:
1. Acetylcholine from the vagus or gastric enteric plexus
2. In response to acid in stomach

70
Q

What are the phases of gastric secretion?

A
  1. Cephalic phase:
    perception of food originates in the cerebral cortex, activates the dorsal motor nuclei, then vagus, and causes gastric secretions (30%)
  2. Gastric phase:
    Food enters the stomach and stimulates secretion (60%) by local and vagal reflexes and gastrin-histamine
  3. Intestinal phase:
    Food in the upper SI continues to cause secretions in stomach by nervous and hormonal routes …10%
71
Q

What enzymes does the pancreas produce? What else?

A

Protein-digestors: trypsin, chymotrypsin, carboxypolypeptidase. They start out as inactive forms (trypsinogen, chymotrypsinogen, proxcarboxypolypeptidase)
CHO digestor: pancreatic amylase
Fat digestor: Pancreatic lipase, cholesterolesterase
Phospholipase
And bicarb

72
Q

How are the proteolytic enzymes activated?

A
  1. Secreted into SI tract
  2. Enterokinase activates trypsinogen to trypsin
  3. Trypsin activates itself and all the other proteases
73
Q

How is the timing of proteolytic enzymes controlled?

A

Secreted alongside the proteolytic enzymes is trypsin inhibitor, that prevents trypsin’s activation inside the secretory cells and in the acini and ducts

74
Q

How is bicarbonate secreted by the pancreas?

A
  1. CO2 enters the cells and becomes carbonic acid that dissociates into H+ and HCO3-
  2. Bicarb is actively transported in association with Na+ into the luminal cell border
  3. The H+ ions formed in the cell are exchanged for Na+ through the blood border of the cell by secondary active transport (hey look, it’s your Na+ supply!)
  4. Creates an osmotic pressure greadient to draw water by osmosis into the pancreatic duct and form isosmotic solution
75
Q

How are pancreatic secretions regulated?

A
  1. Acetylcholine: from the PSNS and ENS
  2. Cholecystokinin: food in the duodenum and upper jejunum stimulates
  3. Secretin: SI contents with acidic pH below 5.0 stimulate this. Especially responsive to the intestinal phase of secretion.

1&2 stimulate acinar cells of the pancreas
3 stimulates secretion of water and sodium bicarbonate to neutralize chyme. Sodium bicarb allows creation of CO2 and water, and the CO2 can be removed by blood > lungs

76
Q

What are the functions of bile acids?

A
  1. Emulsify large fat particles to increase surface area
  2. Aid in absorption of digested fat end products

Bonus: bile is a means of excretion of bilirubin and excess cholesterol

77
Q

How is bile secreted?

A
  1. Hepatocytes secrete bile acids, cholesterol, and etc into bile canaliculi
  2. Bile flows from canaliculi toward terminal bile ducts, then finally the common bile duct. Watery sodium bicarb is added per stimulation by secretin
  3. Either empties directly into duodenum or diverted through the cystic duct to the gallbladder
78
Q

How is bile stored and released?

A

In a gallbladder in some species, where electrolytes can be reabsorbed through gallbladder mucosa and bile is concentrated

Gallbladder emptying and relaxation of sphincter of Odi (to duodenum) is stimulated by CCK, which is stimulated by the presence of fatty foods

79
Q

What are the functions of bile salts?

A

Precursor is cholesterol
1. Detergent action on fat particles to decrease surface tension and emulsify
2. IMPORTANT, help to absorb fatty acids, monoglycerides, cholesterol, and lipds by forming micelles to ferry the lipids into the intestinal mucosa for absorption into the blood

80
Q

How are bile salts circulated and processed?

A
  1. Diffuse or actively transported into the portal blood to return to the liver
  2. 95% recycled by the liver
    quantity of secretion is controlled by the quantity of bile salts available, and secretin to a lesser degree
81
Q

The brunner’s glands: what do they produce, what controls them, and where are they?

A

Mucous glands at the start of the duodenum
Secrete alkaline mucus in response to tactile or irritating stimuli, vagus, or secretin
*Inhibited by SNS
Function: protect duodenum from digestion

82
Q

Crypts of lieberkuhn: what are they, what do they produce, and what controls them?

A

-Crypts between the intesinal villi comprised of goblet cells and enterocytes that secrete water and lytes, and reabsorb water and lytes at the end of digestion (at the villus tip)

-Produces alkaline secretion: active secretion of Cl- and bicarbonate, dragging Na+ along the gradient and osmotic draw of water
-Facilitates absorption of nutrients

83
Q

What is the lifespan of an intestinal epithelial cell?

A

5 days

84
Q

What are the digestive enzymes secreted from enterocytes for digestion? What regulates them?

A

Peptidases, sucrase, maltase, isomaltase, and lactase, and small amounts of intestinal lipase.
Regulated by local enteric nervous reflexes

85
Q

How is secretion by the large intestine unique?

A

There are no villi and no digestive enzymes, but lots of mucus. It is regulated by direct tactile stimulation of the lining and local nervous reflexes.
*Stimulation of the pelvic nerves (PSNS) can increase mucus secretion too

86
Q

How are carbohydrates digested in the monogastric?

A

Mouth: amylase from parotid glands hydrolyzes starch into mainly maltose

Small intestines: lactase, sucrase, maltase, and alpha dextrinase in the enterocyte brush border. Splits into constituents until all are monosaccharides

86
Q

Briefly, explain how the process of hydrolysis allows breakdown of nutrients

A

In hydrolysis, a water molecule is added to a fat/carbohydrate/protein , and then the respective digestive enzyme returns the hydroxyl and hydrogen ions from water to the CHO/fat/AA and in doing so splits the nutrient molecule into their constituents

87
Q

How are proteins digested in the monogastric?

A

Stomach: pepsin digests collagen

Upper SI: trypsin, chymostrypsin, carboxypolypeptidase, proelastase (then elastase). Elastase digests elastin. Most proteins remain as tri/dipeptides

Duodenum/Jejunum brushborder: aminopolypeptidase and dipeptidases split proteins into forms easily absorbed

Intracellular: peptidases break final bonds so all proteins are now single amino acids

88
Q

How are fats digested in the monogastric?

A

Stomach: lingual lipase (trace)
Agitation of the fats to mix up

Duodenum: bile salts and lecithin have polar ends and fat soluble middles, so they dissolve the surface of fat globules, making the fat now soluble, making nonmiscible fluid. This is broken up into tinier globs aka micelles

Agitation in the SI breaks them up further.
Pancreatic lipase then splits emulsified fat into fatty acids and monoglycerides

Brush border: cholesterol ester hydrolase and phospholipase A2 respectively hydrolyze the cholesterol ester and phospholipid

89
Q

How is sodium transported through the small intestinal membrane?

A

A Na/K ATPase on the basolateral membranes drive Na out to create low intracellular Na and create a steep electrochemical gradient to drive the Na/amino acid, Na/glucose, and Na/H transporters.

Aldosterone increases intestinal AND renal Na+ absorption, causing secondary increase in Cl and water

90
Q

How is bicarbonate absorbed?

A

When Na+ is absorbed, some H+ is secreted into the luen of the gut in exchange, and the H+ combines with bicarb to from carbonic acid and then dissociate into water and CO2 so CO2 is expired and H20 stays in chyme

91
Q

How is bicarb secreted?

A

Exchanged for Cl- via an exchanger on the apical membrane

92
Q

How does cholera cause such extreme diarrhea?

A

-Subunit of toxin stimulates excess cAMP, opening lots of Cl- channels and loss into the lumen
-This activates a Na+ pump = loss of Na+ along with Cl-
-Osmosis of water from the blood follows
-Meant to wash away bacteria, but causes rapid and serious dehydration

93
Q

How are Ca++, Iron, K+, Mg2+, and phosphate absorbed?

A

Actively!
Calcium: from duodenum. Controlled by vit D and PTH
Iron: from the SI
Others: actively, but Mg++ (bivalent) only in small amounts

94
Q

How is glucose absorbed?

A

By a sodium co-transport mechanism
1. Na is actively transported through basolateral membranes to deplete the intracellular environment
2. Sodium is moved by secondary active transport from the intestinal lumen into the cell , and glucose from the SI combines with the transporter

  1. Once in the cell, facilitated diffusion takes glucose into the paracellular space
95
Q

How is fructose transported?

A

By facilitated diffusion all the way through. No transporter

96
Q

How are proteins absorbed?

A

Co-transport/secondary active transport with a sodium cotransporter

97
Q

How are fats absorbed?

A

Via bile micelles, diffusion into cells. Then processed by endoplasmic reticulum to form new triglycerides

98
Q

What absorption occurs in the large intestines? Where

A

Proximal first half is absorbing, second half is storage.
Secretes bicarbonate and absorbs sodium and chloride

99
Q

What do LI bacteria produce?

A

Vit K, Vit B12, thiamine, riboflavin, CO2, hydrogen gas, and methane

100
Q

What comprises feces?

A

dead bacteria, fat, inorganic matter, protein, roughage. Colored by stercobilin and urobilin

101
Q
A

Guyton & Hall Physiology (26 decks)

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