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GIGU > Secretions of the GI and Pancreas > Flashcards

Secretions of the GI and Pancreas Flashcards

1
Q

What is the function of saliva?

A
  • Initial digestion of starches and lipids
  • Dilute and buffer food
  • Lubrication of food with mucous
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2
Q

Describe the parotid gland?

A
  • Composed of serous cells
  • secretes water ions and enzymes (amalyase)
  • 25% of output of saliva but largest gland
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3
Q

Submaxillary and sublingual gland?

A
  • Mixed glands
  • Secrete aqueous fluid and mucin glycoprotein for lubriation
  • secretes most of saliva (mandibular) (lingual contributes little)
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4
Q

Describe structure of salivary glands and ionic composition comapred to plasma.

A
  • Has acinar cellssecreting the initital saliva
  • Myoepithelial cells have motile extensions & can be stimulated by neural input to contract releasing saliva into mouth
  • Saliva in the intercalated ducts have same ionic composition as plasma
  • Striated duct lined by columnar cells, ductal cells modify the saliva to produce hypotonic solution and ductal cells alter the concentration of other electorolytes
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5
Q

What makes up saliva?

A
  • water
  • Electrolytes
  • alpha amylase
  • lingual lipase
  • kallikrein
  • mucous
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6
Q

How does saliva compare to plasma?

A
  • Hypotonic compared to plasma it has an increased K and bicarb concentration and decreased sodium and chloride concentration
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7
Q

What are the two main steps for forming saliva?

A
  1. Formation of isotonic plasma like solution by the acinar cells
  2. Modification of isotonic solution by the ductal cells
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8
Q

NOT ANSWERED What is the mechanism of salivary excretion?

A

no idea……slide 365

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9
Q

how does saliva become hypotonic as it flows through the ducts?

A

the ductal cells are water impermeable

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10
Q

What stimulates salivary secretion?

A

Food nausea and smell via parasympathetics (CN VII and IX) with ACh through muscarinic ACh receptors

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11
Q

How do sympathetis stimulate saliva secretion?

A

Norepinephrine binds Beta adrenergic forming cAMP resulting in increase of saliva secretion, production, bicarb and enzyme secretions and contraction of myopeithelial cells

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12
Q

What happens if you block the mAChR?

A

Atropine is a muscarinic ACh receptor blocker. If this is blocked saliva production is not stimulated

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13
Q

What are two unique features of the regulation of saliva secretion?

A
  • exclusively under control of ANS
  • Salivary secretion is increased by both parasympathetic and sympathetic stimulation
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14
Q

What are the main componenets of gastric juice?

A
  • HCl
  • Pepsiogen
  • Mucous
  • Intrinsic factor
  • Water
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15
Q

What does HCl do?

A
  • With pepsin it initiates protein digestion and is necessary for the conversion of pepsinogen to pepsin
  • kills bacteria that enters stoamch
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16
Q

What is the role of mucous in the gastric mucosa?

A
  • lines wall of stomach and prevents damage
  • lubricates
  • nutralizes acid and maintains surface of mucosa at neutral pH
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17
Q

What is the significance of intrinsic factor?

A

neeed for absorption of B12 in ileum

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18
Q

Where are Oxyntic glands located and what do they secrete?

A
  • Proximal 80% of stomach (body and fundus)
  • secretes acid
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19
Q

Pyloric gland location and secretion

A

Distal stomach (antrum) and synthesizes and releases gastrin

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20
Q

what do chief cells secrete?

A

pepsinogen

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21
Q

what do parietal cells secrete?

A

HCl

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22
Q

Where is HCl formed?

A

Villus like membranes of the canaliculi of parietal (oxyntic) cells

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23
Q

What are the two separate secretions that make up gastric juice?

A
  • Non parietal secretions which is an alkaline secretion of constant and low volume mostlhy made up of Na and Cl, but K is present in concentrations = to plasma and bicarb is secreted of ~30mEq/L
  • Parietal secretions which are hyperosmotic containing H, K and Cl
    • as secretion rate increases the concentrations of electroytes gets closer to concentration of parietal cell secretion
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24
Q

What agents stimulate acid secretion from parietal cell

A

Ach Gastrin via Gq and Histamine via Gs

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25
Q

What inhibits parietal cells?

A

Somatostatin and prostaglandins via Gi

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26
Q

As pH falls ___ release is inhibitied causing a __ in HCl secretion.

A

gastrin, decrease

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27
Q

What is the role of the vagus nerve on HCl secretion?

A
  1. direct pathway: stimulate vagus releasing Ach directly to parietal cells
  2. Indirect path: vagus releases Gastrin releasing Peptide GRP which stilmulates G cells to release gastrin to circulation which then will activate parietal cells
28
Q

How does atropine impact vagal pathways stimulating HCl secretion?

A
  • Direct pathway is blocked
  • Indirect pathway is not blocked because it is not using mAChR as the neurotransmitter released is GRP
29
Q

Describe the regulation of gastrin release.

A
  • Somatostatin inhibits Gastrin release
  • Vagal activation stimulates Gastrin with GPR and inhibits somatostatin
  • Gastrin has NFB on itself, increasing somatostatin
  • H in the lumen stimulates release of somatostatin which will inhibit gastrin release
30
Q

What does histamine potentiate?

A

Actions of ACh and gastrin

31
Q

What does ACh potentiate?

A

actions of histamine and gastrin

32
Q

What do antagonists of H2 receptors such as cimetidine do?

A

Blocks direct action of histamine and blocks potentiated effects of ACh and gastrin

33
Q

What do antagonists of mAChRs such as atropine do?

A

blcok direct effects of ACh and ACh potentiated effects of gastrin and histamine

34
Q

Clinically what is Cimetidine used for?

A
  • H2 receptor antagonist used to treat duodenal and gastric ulcers and GERD
35
Q

What is Omeprazole used for?

A

It inhibits the H/K ATPase used for treatment of ulcers to reduce H secretion

36
Q

What are the three phases of gastric HCl secretion?

A
  1. Cephalic phase via vagus
    1. Goal is to prepare stomach for food
  2. Gastric phase
    1. production of gastrin is key, via local reflexes, vagovagal reflex, results in gastrin and histamine stim
  3. Intestinal phase
    1. nervous and hormonal regulations
37
Q

Describe the cephalic phase of gastric secretion.

A
  • stimulated by smelling,tasting,chewing,swallowing food
  • Mechanism is via vagus nerve releasing ACh to parietal cells or stimulating G cells to release gastrin to circulation to stimulate parietal cells
38
Q

What phase of gastric secretion will a vagotomy get rid of?

A

Cephalic

39
Q

Gastric phase?

A
  • Stimulated by distension of stomach and presence of proteins AA and small peptides
  • Mechanism:
    • distension activates mechanoreceptors
      • local reflex–ACh–parietal and G cells
    • vagus nerve stimulates HCl seccretion from parietal cells
    • Gagus nerve stimulates HCl via indirect path

60% of HCl secretion in response to a meal

40
Q

Describe the intestine phase

A
  • is 5-10% of total HCl in response to a meal
  • Distension of small intestine stimulates acid secretion
  • Digested proteins stimulate acid secrtion via direct effect on parietal cells or Gastrin on parietal cells
41
Q

What is the most important stimulus for pepsinogen secretion

A

Vagus nerve

42
Q

How does pepsin affect pepsinogen?

A

It converts more pepsinogen to pepsin

43
Q

What is Intrinsic factor?

A
  • The only secretion by the stomach that is essential
  • Mucoprotein secreted by parietal cells binding B12
  • Failure to secrete IF is associated with acholorydria and absence of parietal cells
44
Q

What is the mechanism for absorbing B12?

A

Food enters lumen of stomach and pepsin breaks down proteins and Vitamin B12. R protein secreted from salivary gland and stomach and it is a shuttle for Vit. B12 through stomach and SI once it reaches duodenum there are proteasaes that facilitate breakdown of the B12 and R protein. IF is secreted and transports B12 through the rest of the small intestine and tehre is inactive absorption of B12. B12 is stored in the liverWh

45
Q

What causes pernicious anemia?

A

Stomach doesnt make enough IF and there is decreased absorption of B12

  • Atrophic gastritis-chronic inflammation of stomach mucosa leadds to loss of parietal cells
  • Autoimmune metaplastic atrophic gasgtritis- immune system attacks IF protein or gastric parietal cells
46
Q

What surgeries can disrupt B12 absorption?

A

Gastrectomy and Gastric bypass

47
Q

What protects the gastric mucosa?

A

The epithelium secretes bicarb and mucous to form gel mucosal barrier. The mucosal barrier protects the gastric mucosal epithelium against HCl and pepsin

  • Bicarb
  • Mucous
  • Prostaglandins
  • Mucosal blood flow
  • Gastrin
  • Growth factors
48
Q

What damages gastric mucosa?

A
  • H and pepsin
  • H. Pylori
  • NSAIDs
  • Stress
  • Smoking
  • Alcohol
49
Q

What is Zollinger Ellison syndrome?

A
  • Large secretion of gastrin by duodenal or pancreatic neuorendocrine tumors
  • Increase in H secretion by parietal cells and their cell mass
  • Inhibit absorption of sodium and water by the small intestine (secretory diarrhea)
  • The excessive H overwhelms the duodenum’s buffer capacity of HCO3 in the pancreatic juice causing an ulcer
  • The intestine has a low pH
50
Q

In Zollinger Ellison syndrome, what are the effects of having a low intestinal pH?

A

It will inactivate the pancreatic enzymes, disrupt emulsification of fats, damage intestinal epi cells and villi, and lead to maldigestioni and malabsorption, which will lead to steatorrhea (oily stool)

51
Q

What is the Secretin stimulation test?

A
  • It is used to diagnose gastrin secreting tumors
  • With normal conditions, secretin will inhibit gastrin secretion
  • With gastriniomas injection of secretin causes an increase in gastrin release
52
Q

What is the mechanism for peptic ulcer disease?

A
  • loss of protective mucosal barrier
  • excessive H or pepsin secretion
  • Combo of both

Caused by NSAIDs and H. Pylori predominantly

53
Q

How does H.Pylori break down mucosal barriers?

A
  • It uses Urease which converts urea to ammonia making the environment more alkaline and this is a major cacuse of the cytotoxicity of H.Pylori. It damages epithelial cells and breaks the mucosal barrier
  • Diagnostic test is done to see urease activity
54
Q

What is the main reason Gastric ulcers form?

A

Gastric mucosal barrier is defective rather than increasing acid secretion

55
Q

What type of ulcer is more common?

A

Duodenal ulcers

Usually H secretions are higher than normal and these ulcers dont’t become malignant

56
Q

Compare H secretion and gastrin levels in Duodenal and Gastric ulcers and ZE synddrome.

A

Gastric:

  • Decreased H secretion and increased Gastrin due to the low H levels

Duodenal:

  • Increased H secretion and increased gastrin due to food ingestion

ZE:

  • very increased H secretion and gastrin
57
Q

What does pancreatic juice contain and what is the purpose?

A
  • Bicarb for neutralizing H from stomach and enzymes to digest carbs proteins and lipids
58
Q

What innervates the exocrine pancreas?

A
  • Sympathetic postganglionic nerves from celiac and superior mesenteric plexues
  • Parasym vagus nerve
    • pregang fibers synapse in the ENS and post in the exocrine pancreas

Parasymp increases activity and symp decreases

59
Q

What are the two main components of the exocrine pancreas?

A

Enzyme secretion by the acinar cells:

  • pancreatic amylases and lipases active
  • Proteases secreted inactive and converted to active in the duodenum lumen

Aqueous solution by centroacinar and ductal cells:

  • secrete bicard fluid that alkalinizes and hydrates protin rich secretions of acinar cell
  • initial secretion is modified in ductal epithelial cells
60
Q

How is the exocrine pancreas organized?

A
  • Similar to salivary glands
    • Acinus which synthesizes and secretes major enzymes for digestion
    • Ducts whic hhave ductal and centroacinar celsl secreting the aqueous solutin with bicarb
61
Q

How does CF impact the pancreas?

A
  • Pancreas is one of the first organs to fail in CF
  • CF is caused by CFTR mutations which is a Cl channel in the apical surfacec of duct cells
  • CTFR mutations are associated with a loss of bicarb secretion which results in a loss of the ability to get rid of active enzymes in the duct and can lead to chronic and recurrent acute pancreatitis
62
Q

What is the cephalic phase of pancreatic secretion?

A
  • Mediated by vagus nerve initiated by smell taste and conditioning
  • produces an enzymatic secretion
63
Q

Gastric phase of pancreatic secretion?

A
  • initiated by distension of the stomach
  • mediated by vagus nerve
  • produces enzymatic secretion
64
Q

Intestinal phase of pancreatic secretion?

A
  • Accounts for 80% of pancreatic secretions and enzymatic and aqueous secretiosn are stimulated
65
Q

What does CCK induce?

A

Release of pancreatic enzymes into duodenal lumen

66
Q

What does secretin induce in the pancreas?

A

Secretion of bicarb from pancreatic cells into the duodenum

67
Q
A

GIGU (17 decks)

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