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Physiology > Unit 6 - Salivation and Gastric Function > Flashcards

Unit 6 - Salivation and Gastric Function Flashcards

1
Q

how do hormones get to GIT?

A

peptides released from endocrine cells of GIT

  • secreted into portal circulation, pass thru liver, enter systemic circulation
  • delivers hormones to target cells
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2
Q

how are paracrines related to GIT?

A

secreted by endocrine cells of GIT

-act locally in same tissue that secretes them

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3
Q

what is paracrine control of GIT exerted by? (3 factors)

A
  1. serotonin - made by enterochromaffic cells (EC) in intestine in response to distension; indirectly excites ENS to increase motility and secretions
  2. somatostatin - peptide made by D cells, and potent inhibitor of many processes (pancreatic/gastric secretions, motility)
    - acts in endocrine and paracrine manner
  3. histamine - made by EC-like cells in stomach, stimulating HCl secretion via H2 recceptors
    - acts in paracrine fashion, but not a peptide
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4
Q

how are neurocrines related to GIT?

A

made in neurons in GIT, released following AP

  • after release, diffuse across synaptic cleft to act on target cell
  • ACh, NE, VIP, GRP, and substance P
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5
Q

location, relative amounts, and action of gastrin

A

secreted by antral mucosal cells via G-cells in response to food, distension, and vagus

  • increase acid secretion by parietal cells
  • stimulate growth of gastric mucosa
  • tapers off in jejunum, no longer in ileum
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6
Q

location, relative amounts, and action of cholecystokinin

A

CCK; secreted by mucosa of intestine (I cells in duodenum and jejunum) in response to fats, PRO, peptides, AA

  • increase GB contraction
  • increase pancreatic enzyme and bicarbonate secretion (trypsin, chymotrypsin, lipase, amylase)
  • inhibits gastric emptying
  • tapers off in ileum
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7
Q

location, relative amounts, and action of secretin

A

secreted by mucosa of small intestine (S-cells in duodenum) in response to acidic chyme from stomach

  • increases bicarbonate (HCO3-) and fluid secretion by pancreas
  • decreases gastric acid secretion in stomach by decreasing gastrin
  • inhibits gastric emptying
  • tapers off in ileum
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8
Q

location, relative amounts, and action of motlin

A

secreted by mucosa of SI (M cells in duodenum and jejunum) during fasting period

  • promotes contractions in distal stomach and intestines to ‘clear” tract of indigestible materials (MMC)
  • only in duodenum and jejunum
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9
Q

location, relative amounts, and action of glucose-dependent insulinomic peptide

A

secreted by mucosa of SI (K-cells in duodenum and jejunum) in response to fat and CHO

  • acts on pancreas to stimulate insulin secretion
  • inhibits HCl secretion by parietal cells
  • only in duodenum and jejunum
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10
Q

what is membrane digestion?

A

complete digestion of CHO and PRO via enzymes on luminal surface of SI

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11
Q

when is digestion of PRO initiated?

A

in stomach via pepsins; continued in intestines via pancreatic enzymes

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12
Q

when is digestion of fat initiated?

A

in mouth via lingual lipase; continued with swallowed lingual lipase in stomach, and finished in intestines via pancreatic enzymes

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13
Q

what is the physiological secretory unit of salivary glands? how much is secreted? what are components of the salivary system?

A

salvion; similar in structure to pancreas
-1.5 L saliva secreted per day from parotid, submandicular, and sublingual glands (other glands dispersed thruout submucosa of oral cavity)

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14
Q

what kinds of saliva do acinar cells of parotid, sublingual, and submandibular glands secrete?

A

parotid: serous 9watery) substance rich in alpha-amylase (~25% of saliva/day)
sublingual (5%) and submandibular (70%) secrete sero-mucous product rich in mucin glycoPRO

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15
Q

what are saliva functions for

  • lubrication
  • protection
  • digestion
A

L: moistens mouth to prevent dehydration of oral mucosa, and lubricates food for swallowing
-depends on presence of mucous in saliva (sublingual and submandibular)
P: flows across teeth to clear bacteria and reduce bacterial growth (lysozyme, IgA-binding PRO)
D: amylase (ptyalin) that converts starch to sugar at optimum pH = 7 (denatured below 4 in stomach); lingual lipase hydrolyzes TG and secreted by small salivary glands on tongue

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16
Q

Sjogren syndrome

A

chronic and progressive autoimmune disease that destroys salivary and lacrimal glands

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17
Q

xerostomia

A

dry mouth; from inadequate saliva production

  • typically leads to difficulty speaking due to poor lubrication
  • dental carries, and halitosis from bacteria
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18
Q

how is the composition of saliva modified?

A

“primary secretion” contains amylase, Na, K, Cl, HCO3 like plasma

  • at low flow rates, NaCl is absorbed and KHCO3 is secreted by duct cells of salivary glands
  • -creates K+ rich, hypotonic secretion at rest
  • -“tightness” of ductal epithelium inhibits paracellular water movement, contributing to hypotonic product
  • at high flow rates, saliva is like plasma, b/c transport processes cannot handle increased load
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19
Q

what does high [HCO3-] do to fresh saliva?

A

makes it more alkaline than plasma, and functions to neutralize gastric acid that refluxes into esophagus, plus acid made by oral bacteria

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20
Q

what is the only humoral agent to activate salivation?

A

aldosterone

-stimulates Na+ reabsorption and K+ secretion by salivary glands

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21
Q

how is blood flow changed during salivary secretion?

A

blood flow to acinar cells is increased by PNS stimulation, and ultrafiltrate from plasma (mostly serous fluid) enters

  • filtrate from cells enters lumen of acinar cells, mixing with secreted mucus and ptyalin, creating primary secretion
  • lingual lipase (from Von Ebner’s glands on tongue) is added in mouth
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22
Q

how do the GI hormones, PNS, and SNS control salivary secretion

A

unaffected by GI hormones

  • PNS promotes increased and sustained salivary secretion, where flow is increased 10x over basal rate
  • SNS causes lesser and more transient stimulation
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23
Q

what does activation of salivary glands cause?

A

release of kallikrein, causing production of vasodilator bradykinin from precursors
-vasodilation increases capillary hydrostatic pressure and capillary filtration, thus supplying fluid for secretion

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24
Q

where are the salivary nuclei and how are they excited?

A

near juncture of medulla and pons, and are excited by taste and tactle stimuli from tongue and other areas of mouth/pharynx

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25
Q

how can rate of salivation be changed by stimuli?

A

taste and tactile
-sour or smooth objects cause increased salivation
-rough causes less or inhibits
also occurs in response to reflexes from stomach and upper SI (irritating foods, or nausea; saliva removes irritating factor)

26
Q

where are oxyntic glands and what do they secrete (from 3 types of cells)

A

acid-forming; on inside surfaces of body and fundus of stomach (proximal 80%); have 3 cell types

  1. mucous neck cells secrete mainly mucus
  2. peptic (chief) cells secrete pepsinogen and gastric lipase
  3. parietal (oxyntic) cells secrete HCl and intrinsic factor
27
Q

what happens when parietal cells are destroyed?

A

happens in chronic gastritis
-develop achlorhydria (lack of stomach acid secretion) and pernicious anemia (failure of RBC maturation in absence of B12 stimulation of bone marrow)

28
Q

where are pyloric glands and what do they secrete?

A

in antrum (distal 20%), with deeper pits than oxyntic glands

  • secrete mucus for protection of pyloric mucosa from stomach acid
  • secrete gastrin (G-cells), and somatostatin (D cells)
  • fewer peptic cells and no parietal cells compoared to oxyntic glands
  • have mostly mucous cells
29
Q

what are cardiac glands?

A

mucus secreting glands in limited area near esophageal orifice

30
Q

what do pepsins digest in meat? what happens if there is a deficiency?

A

collagen of connective tissue; if lack it in stomach juices, digest meat poorly

31
Q

how is pepsinogen activated?

A

pH from 3 to 5 will spontaneously activate by removing N-terminal “activation peptide”; even faster at pH lower than 3
-newly formed pepsins are active only at pH below 3.5, helping catalyzing activation of pepsinogens

32
Q

digestion of proteins in stomach

A

initiated in stomach to make proteoses, peptones, and polypeptides

  • occurs mainly in intestine via pancreatic proteolytic enzyme secretion
  • HCl secreted by parietal cells at pH 0.8, but after mixing with stomach contents becomes 2-3 for pepsin activity
33
Q

what is the location and primary secretion of:

  • parietal cells
  • chief cells
  • G cells
  • mucous cells
A
  1. body (oxyntic glands) - HCl, intrinsic factor
  2. body (oxyntic glands) - pepsinogen
  3. antrum (pyloric glands) - gastrin
  4. antrum (pyloric glands) - mucus, pepsinogen
34
Q

how is the gastric mucosa protected?

A

alkaline mucus layer that lines gut

  • acts as diffusion barrier for H+ and pepsins
  • includes HCO3-, mucus, prostaglandins, mucosal blood flow, and growth factors
  • -HCO3 titrates any H+ that diffuses, and inactivates pepsin that penetrate mucus
35
Q

what happens if H+ penetrates gastric epithelium

A

damaged mast cells, releasing histamine for inflammatory response

  • if mild injury, increased blood flow promotes production of mucus and HCO3 by mucus cells
  • if severe, causes decreased blood flow and cell injury
36
Q

what is erosive gastritis?

A

results from chronic use of NSAIDs (inhibits prostaglandin synthesis in stomach)

37
Q

what does prostaglandin do?

A

maintains physiochemical barrier by stimulating secretion of mucus and HCO3-

38
Q

how frequently does the GIT mucosa renew itself?

A

every 3 to 4 days from stem cells

39
Q

what is the main driving force for hydrochloric acid secretion by parietal cells?

A

H+/K+ ATPase in luminal membrane exchanges K+ into cell for H+ to lumen

  • H+ comes from CO2 + H2O (carbonic anhydrase) –> H2CO3 –> H+ + HCO3
  • HCO3 to blood and Cl- to cell via passive exchange
  • K+ enters cell and Na+ exits to blood via ATPase
  • Cl- exits to lumen via passive channel and combines to make HCl
40
Q

what happens at the apical membranes of parietal cells?

A

H+ is secreted into lumen for K+ via active exchange process catalyzed by H+/K+ ATPase

Cl- follows via passive Cl- channels

41
Q

what happens at basolateral membrane of parietal cells?

A

HCO3 is absorbed from cell into blood via Cl-HCO3 exchanger (alkaline tide; righted by pancreatic bicarbonate)

42
Q

how does water pass into canaliculus?

A

by osmosis, b/c of extra ions secreted into canaliculus

-so final secretion contains water, HCl at 150 mEq/L, KCl at 15 mEq/L, and some NaCl –> very acidic

43
Q

how much energy is needed to concentrate H+ ions from parietal cells?

A

need more than 1500 kcal/liter

44
Q

what does prolonged vomiting cause?

A

dehydration, alkalosis, and hypokalemia

45
Q

where does the vomiting center lie?

A

medulla

46
Q

what is retching?

A

gastric and intestinal contents reach esophagus, but EUS is closed
-precedes vomiting

47
Q

what is reverse peristalsis?

A

occurs from mid-small intestine to pylorus, which relaxes so chyme can enter stomach

  • stomach fills, and strong abdominal contractions force gastric contents to esophagus to cause retching
  • further stimulation relaxes the UES, so that there is expulsion of contents thru mouth
48
Q

what stimuli initiate vomiting reflex?

A
  • irritants in stomach or SI, enteric virus, bacteria
  • systemic irritant sensed by chemoreceptor trigger zone in 4th ventricle of brain
  • head injury (concussion) a central effect
  • abnormal stimulation of vestibular organs (central effect via ANS to chmoreceptor trigger zone, then to vomiting center)
49
Q

what can impaired renal function lead to?

A

azotemia (elevated urea and creatinine in blood)

50
Q

how is HCl secretion regulated?

A

Directly: vagus (ACh, gastrin, and histamine)
Indirectly: vagus and gastrin stimulate histmaine release from ECL cells
-vagus also stimulates gastrin release, and inhibits somatostatin secretion

51
Q

how do these stimulators effect acid secretion?

  • histamine
  • vagus
  • gastrin
  • insulin
  • caffeine
  • stress
A
  1. from ECL cells; diffuses thru mucosa to act on adjacent parietal cells
  2. via direct and indirect cells
  3. carried thru blood to act directly on parietal cells and stimulate histamine release
  4. carried thru blood to act directly on parietal cells and stimulate HCl secretion
  5. phosphodiesterase inhibitor increases cAMP in parietal cells, increasing proton pump activity
  6. increases acid secretion in some people, and may be cofactor in ulcer formation
52
Q

how do these inhibitors of acid secretion work?

  • somatostatin
  • GIP
  • secretin
A
  1. released from endocrine cells in gastric pit, acting in paracrine manner on parietal cells and G cells to inhibit gastrin
  2. glucose insulinotropic or gastric inhibitory peptide; released from duodenum and jejunum, acting directly on parietal cells
  3. released from duodenum and jejunum, acting at G-cells to suppress gastrin
53
Q

how many receptors for acid secretagogues does a parietal cell have?

A

3

  • M3 receptor for ACh
  • CCK-B receptor for gastrin
  • H2 receptor for histamine
54
Q

what does binding to M3 (ACh) and CCK-B (gastrin) do?

A

coupled to G-alpha-q, which activates PLC

-leads to activation of PKC and release of Ca++

55
Q

what does binding to H2 (histamine) do?

A

coupled through G-alpha-s to AC

-increased cAMP and activation of PKA

56
Q

what do somatostatin and prostaglandins activate?

A

both bind to separate receptors linked to G-alpha-I

-oppose actions of histamine, in that it decreased cAMP to decrease activation of PKA

57
Q

what do H2 receptor antagonists (cimetidine) do?

A

effective as OTC antacid agents b/c strong cooperativity of ACh, gastrin, and histamine in stimulating HCl production

58
Q

what do proton pump inhibitors (omeprazole, prilosec) do?

A

more effective than histamine receptor antagonists b/c block final common pathway (H+/K+ ATPase)

59
Q

what phases is gastric secretion divided into? how much is secreted each tiem?

A
  1. cephalic - 30%
  2. gastric - 60%
  3. intestinal - 10%
60
Q

what are the stimuli and mechanisms for the cephalic phase?

A

smell, taste, and conditioning

  • vagus –> parietal cell
  • vagus –> gastrin –> parietal cell
61
Q

what are the stimuli and mechanisms for the gastric phase?

A 
distension
-vagus --> parietal
-vagus --> gastrin --> parietal cell
amino acids, small peptides
-local reflex --> gastrin --> parietal cell
-gastrin --> parietal cell
62
Q

what are the stimuli and mechanisms for the intestinal phase?

A

products of PRO digestion

-gastrin –> parietal cell

Physiology (60 decks)

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