Secretion Physio Flashcards

(86 cards)

1
Q

Saliva Functions

A
  • Initial digestion of starches and lipids
  • Dilution and buffering of ingested food
  • Lubrication of ingested food and mucus
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2
Q

Parotid glands

A
  • Serous cells
  • Secrete fluids composed of water, ions and enzymes (ie. amylase)
  • 25% total salivary output
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3
Q

Submaxillary and sublingual glands

A
  • Mixed serous and mucous cells
  • Secrete aqueous fluid and mucin glycoprotein for lubrication
  • 75% total salivary output
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4
Q

Structure of salivary glands

A
  • Acinus
  • Myoepithelial cells
  • Intercalated duct
  • Striated duct
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5
Q

Acinus

A
  • Acinus cells secrete initial (isotonic) saliva

- Blind end of gland

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6
Q

Myoepithelial cells

A
  • Motile extensions

- Contract to eject saliva into mouth when stimulated by neurons

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7
Q

Intercalated duct

A
  • Saliva similar to ionic composition of plasma
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8
Q

Striated duct

A
  • Columnar epithelium (ductal cells)
  • Ductal cells modify initial saliva to produce final (hypotonic) saliva through alteration of electrolyte concentrations
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9
Q

Composition of saliva

A
  • Hypotonic

- Contains H2O, electrolytes (more KHCO3, less NaCl), a-amylase, lingual lipase, kallikrein, and mucus)

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10
Q

Transport mechanisms of salivary electrolytes

A
  • Na/H, Cl/HCO3, H/K exchangers

- Leave cell to lumen via cAMP activated CFTR Cl channel or Cl/HCO exchanger

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11
Q

Unusual features of salivary regulation

A
  1. Salivary secretion exclusively under ANS control

2. Secretion increased by both sympathetics and parasympathetics

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12
Q

Components of gastric juice

A
  • HCl
  • Pepsinogen
  • Mucus
  • Intrinsic factor
  • H2O
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13
Q

HCl (gastric juice)

A
  • Initiates protein digestion
  • Converts pepsinogen to pepsin (which also digests proteins)
  • Kills bacteria entering stomach
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14
Q

Mucus (gastric juice)

A
  • Lines stomach wall/protects from damage
  • Lubricant
  • Along w/ HCO3, neutralizes acid and maintains surface of mucosa @ neutral pH
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15
Q

Intrinsic factor

A

B12 absorption in ileum

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16
Q

H2O (gastric juice)

A
  • Medium for action of HCl and enzymes

- Solubilizes ingested material

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17
Q

Oxyntic gland (type of cells present)

A
  • Proximal 80% of stomach
  • Secretes acid
  • Parietal cells, mucous neck cells, ECF-like cells, D cells, chief cells
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18
Q

Pyloric gland (types of cells present)

A
  • Distal 20% of stomach (antrum)
  • Synthesizes and releases gastrin
  • G cells, D cells, some mucus neck cells
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19
Q

Non-parietal gastric juice secretions

A
  • Basal alkaline secretion of constant/low volume
  • Components = Na, Cl (K present @ same concentration as in plasma)
  • HCO3 secreted @ 30 mEq/L
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20
Q

Parietal gastric juice secretions

A
  • Slightly hyperosmotic
  • 150-160 mEq H+/L
  • 10-20 mEq K/L
  • Cl- only anion present
  • w/ increased secretion rate, concentrations of electrolytes approach those of pure parietal secretions
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21
Q

Direct pathway of vagal stimulation

A

Vagus n. — ACh — parietal cells — HCl released

*Atropine can block

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22
Q

Indirect pathway of vagal stimulation

A
  • Vagus n — GRP — G cells — gastrin — circulation — parietal cells — HCl
  • Antrum distension — ACh — G cells …
  • AAs — G cells …
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23
Q

Gastrin release regulation

A
  • Vagal activation stimulates gastrin release (via GRP)

- Somatostatin inhibits gastrin release

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24
Q

Gastrin negative feedback loop

A

Increases in gastrin (and H+) increases somatostatin

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25
Potentiation
Combined response to two stimulants exceeds the sum of their individual responses
26
Potentiation with HCl
- Histamine potentiates actions of HCl and gastrin - ACh potentiates actions of histamine and gastrin * Antagonists along pathway block direct effects (and potentiated effects)
27
Cephalic phase (of HCl secretion)
- Stimuli: smelling/tasting, chewing/swallowing, conditioned reflexes - Mechanisms: 1. Vagus n — parietal cell 2. Vagus n — gastrin — parietal cell - 30% HCl secreted * Vagotomy abolishes!
28
Gastric phase (of HCl secretion)
- Stimuli: distension of stomach, presence of proteins, AAs, small peptides - Mechanisms: 1. Distension — activates mechanoreceptors in mucosa of oxyntic and pyloric gland — direct and indirect pathways 2. Distension of antrum — local reflexes — ACH — parietal cells/G cells 3. AA/small peptides — gastrin — peptides - 60% HCl secreted * Coffee stimulates gastric HCl secretion
29
Intestine Phase
- Distension of SI — stimulates acid production - Digested protein — stimulates acid production (direct and indirect) - 5-10% HCl secretion
30
Protective factors for gastroduodenal mucosa
- HCO3/mucus - Prostaglandins - Mucosal blood flow - Growth factors
31
Damaging factors to gastroduodenal mucosa
- H+/pepsin - H. Pylori - NSAIDS - Stress - Smoking - Alcohol
32
Growth of gastric mucosa
- Gastric epithelium secretes HCO3 and mucus to form mucosal barrier - Mucous cells secrete mucus - Surface epithelial cells secrete HCO3
33
Zollinger-Ellison syndrome
- Very high H+ levels - D/t tumor (usually in pancreas) secreting large amounts of gastrin — increased H+ and increased parietal cell mass (trophic effect) - Excess H+ in duodenum overwhelms buffer capacity of HCO3 and creates ULCER * low duodenal pH inactivates pancreatic lipases — steatorrhea
34
Gastric ulcers
- Form on stomach lining - D/t defective gastric mucosal barrier (NOT increased acid secretion) - Gastrin levels increased b/c H+ is decreased
35
Duodenal ulcers
- Form on duodenal lining - More common than gastric ulcers - Increased H+ secretion - Increased gastrin d/t ingestion of food - Increased parietal cell mass (d/t increased gastrin)
36
Peptic Ulcer Disease
- Predominant causes: H. Pylori and NSAID use - Mechanism: loss of protective mucosal barrier, excessive H+ and pepsin secretion - Results in gastric and duodenal ulcers
37
Secretin stimulation test
- Secretin used in dx of gastrin-secreting tumors - Secretin usually inhibits gastrin release - W/ gastrinomas, secretin injection causes increase in gastrin release
38
Helicobacter pylori
- Acquired factor in origin of gastric and duodenal ulcers - H. Pylori releases cytotoxins that breakdown mucosal barrier and underlying cells - Urease allows bacteria to colonize gastric mucosa
39
Role of urease w/ H. Pylori
- Allows bacteria to colonize gastric mucosa - Urease converts urea to ammonia (alkalinizes local environment) - Resulting production of NH4+ is major cause of cytotoxicity - Dx test based on urease activity
40
Pepsinogen
Released by chief cells and mucus cells in oxyntic glands (which requires H+ secretion from parietal cells to lower gastric pH)
41
Stimuli for pepsinogen secretion
* Vagal nerve stimulation | - Also low gastric pH (otherwise pepsinogen won’t convert to pepsin)
42
Protein degradation via pepsin
- Optimal pH is 1.8-3.5 - Reversibly inactivated above 3.5-5.0 - Irreversibly inactivated above 7-8 - Proteolytic enzyme splits interior peptide linkages
43
Intrinsic Factor
- Required for absorption of B12 in ileum - Mucoprotein secreted by parietal cells * failure to secrete IF associated with achlorhydria and absence of parietal cells * *only “essential” secretion by the stomach
44
Pernicious Anemia
Stomach does not produce enough IF (low B12 levels)
45
Causes of Pernicious Anemia
1. Atrophic gastritis: chronic inflammation of stomach mucosa leading to loss of parietal cells 2. Autoimmune metaplastic atrophic gastritis: immune system attacks IF protein or gastric parietal cells
46
Pancreatic juice contents
- HCO3 to neutralize H+ from stomach | - Enzymes to digest carbs, lipids, proteins
47
Exocrine Pancreas parasympathetic innervation
Vagus N - Preganglionic fibers synapse in ENS - Postganglionic fibers synapse on exocrine pancreas * Stimulates pancreatic secretion
48
Exocrine pancreas sympathetic innervation
Postganglionic nerves from celiac and superior mesenteric plexuses *Inhibits pancreatic secretion
49
Components of exocrine pancreas secretions
1. Aqueous solution with HCO3- | 2. Enzymatic secretion
50
Acinar cells (of pancreas)
1. Pancreatic amylase/lipases (ACTIVE form) | 2. Pancreatic protease (INACTIVE zymogens) — activated in lumen of duodenum
51
Centroacinar and ductal cells
- Secrete HCO3-rich fluid that alkalinizes and hydrates protein-rich secretions from acinar cell - Initial secretion modified by transport processes in ductal epithelial cells
52
Cephalic phase (pancreatic secretions)
- Initated by smell, taste, conditioning - Mediated by vagus n. - Produces mainly enzymatic secretion
53
Gastric phase (pancreatic secretion)
- Initiated by distension of stomach - Vagus n - Produces mainly an enzymatic secretion
54
Intestinal phase (pancreatic secretion)
- 80% of pancreatic secretion | - Enzymatic and aqueous secretions are stimulated
55
Cystic Fibrosis and pancreas
- D/t mutations in CFTR (regulated Cl- channel in apical surface of duct cell) - Associated with loss of HCO3 secretion (ability to flush active enzymes out of duct may be lost) - Acute/chronic pancreatitis may result * Pancreas one of 1st organs to fail w/ CF
56
Net result of initial pancreatic secretion by ductal cells
- Secretion of HCO3 | - Absorption of H+
57
Parasympathetic (preganglionic) salivary gland
Originate @ facial n. (CN 7) and glosspharyngeal n. (CN 9)
58
Parasympathetic (postganglionic) salivary gland
Autonomic ganglia innervate individual glands
59
Sympathetic (preganglionic) salivary gland
Originate @ cervical ganglion
60
Sympathetic (postganglionic) salivary gland
Extend into glands in the periarterial spaces
61
Factors stimulating salivary secretion
- Conditioning - Food - Nausea - Smell
62
Factors inhibiting salivary secretion
- Dehydration - Sleep - Fear
63
Mechanism of parasympathetic salivary secreton
CN VII/IX -- ACh -- mAChR -- IP3 and increased Ca2+ (acinar and ductal cells) -- SALIVA
64
Mechanism of sympathetic salivary secretion
T1-T3 -- NE -- beta AR -- cAMP -- SALIVA
65
Effects of salivary cells stimulated
- Increased saliva production - Increased HCO3- and enzymatic secretions - Contraction of myoepithelial cells
66
Effect of ADH and Aldosterone on saliva
Decrease [Na+] and increase [K+]
67
Salivary transporters on BL side
- Na+/K+ ATPase | - HCO3-/Na+
68
Salivary transporters on apical side
- Na+/H+ - HCO3-/Cl- - H+/K+ - cAMP-activated CFTR Cl-
69
Effect of atropine on gastrin secretion
Atropine will NOT block vagal effects on gastrin b/c neurotransmitter on G cells is GRP
70
H+ effect on somatostatin
Stimulates release
71
Vagal activation effect on somatostatin
Inhibits release
72
Somatostatin effect on G cells
Inhibits gastrin release
73
Effect of increased gastrin on somatostatin
Increases somatostatin (via negative feedback loop)
74
Effect of atropine
Inhibits M3 receptor (Vagus n./ACh)
75
Effect of cimetidine
Inhibits H2 receptor (ECL cells/histamine) | - Tx of duodenal/gastric ulcers, GERD
76
Effect of omeprazole
Inhibits H+/K+ ATPase (for H+ secretion) | - Tx of ulcers to reduce H+ secretion
77
Effect of coffee on HCl secretion
Increases
78
Formation of mucosal barrier
- Gastric epithelium releases HCO3- and mucus
79
What do the surface epithelium cells secrete?
HCO3-
80
Main function of gastric mucosal epithelium?
Protects against HCl and pepsin
81
Pancreatic proteases... active or inactive?
Secreted inactive, converted to active in doudenum
82
Pancreatic amylases/lipases... active or inactive?
Secreted active
83
HCO3- secretion into lumen? explain process
Occurs via Cl-/HCO3- exchanger and cAMP-activated CFTR Cl- channel
84
Process of pancreatic secretion (I cells)
I cells -- CCK (Ach potentiates) -- IP3/increased Ca2+ (acinar cells) -- Enzymes released
85
Stimulatory effect of I cells
- Phe, Met, Trp, small peptides, FAs
86
Process of pancreatic secretion (S cells)
S cells -- secretin (ACh, CCK potentiate) -- cAMP (ductal cells) -- Aqueous secretion (HCO3- and Na+)