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Pancreas: Secretory Fxn (exocrine pancreas (acinus (acinar cells (hormonal…

- - - - enzyme-rich, watery, isotonic secretions
        
        NaCl
        
        Na & H2O follows Cl into lumen d/t (-) luminal charge via tight jxns
        
        stimulus: Ach & CCK >> phosphorylation of ion channels
        
        ~15 enzymes
        
        amylase >> carbs {Cl activator}: converts polysaccharides into disaccharide amylase
        
        proteases >> proteins {trypsin activator}
        
        trypsinogen >> (+) itself & other zymogens*
        
        enterokinase: released from brush border membrane by bile salts >> cleaves hexapeptide trypsinogen >> trypsin
        
        chymotrypsinogens* (endo-peptidase)
        
        proelastase* (endopeptidase)
        
        procarboxypeptidases* A & B (exopeptidase)
        
        lipases >> lipids
        
        pancreatic lipase: ONLY fat-digesting enzyme secreted thruout entire GI
        
        nonspecific esterase
        
        pro-phospholipase A2*
        
        nucleases >> nucleotides
        
        ribonuclease
        
        deoxyribonuclease
        
        others
        
        procolipase* (cofactor for lipase) >> fat droplets
        
        monitor peptide (MP) {intestinal contents} >> secretion feedback
        
        trypsin inhibitors & other nondigestive proteases >> (-) trace active enzymes w/in pancreas >> protects acinar/ductal cells
        
        glycoproteins >> protects against protease-mediated mucosal injury
        
        proteins:
        
        stimulus: ACh, CCK, secretin, VIP >> inc. [Ca]i and (+) protein kinases >> inc. acinar cell secretion
        
        protection from autodigestion:
        
        stored & secreted as zymogens (inactive) in sorted granules
        
        protease inhibitors in zymogen granule
        
        condensation of secretory proteins at low pH
        
        enterokinase restricted to intestinal mucosal cells
      - hormonal regulation: CCK (I cells)
        
        regulation of release: CCK-RP & MP
        
        low protein: trypsin degrades CCK-RP/MP >> terminates release of CCK
        
        high protein: too much CCK released >> trypsin degrades dietary proteins & CCK-RP/MP very slowly; other proteins compete for binding site on trypsin
        
        stimulus: FAs & aromatic a.a. in duo
        
        stimulus: small peptides, a.a. & FAs enter duo
        
        results:
        
        inc. secretion of pancreatic digestive enzymes (dominant stimulant during intestinal phase)
        
        contraction of gall bladder & relaxation of sphincter of Oddi
        
        MOA: same as ACh (PKC-PLC) >> inc. [Ca]i & (+) protein kinases
        
        potentiated by ACh via vagovagal reflexes
      - pyramidal
        serous cells
        
        basophilic basal cytoplasm & basal nucleus w/ extensive rER & Golgi
        
        acidophilic granules (w/ zymogens) in apical cytoplasm
        
        "more cuboidal looking"
        
        apical tight jxns & microvilli
  - - - deactivates pepsin
      - neutralize acidic chyme >> buffers pH for max enzymatic activity
      - prevents damage to duo mucosa
    - - stimulus: H+ in duo; fatty acid meal
      - MOA: PKA-cAMP >>>> CFTR >> inc. Cl secretion
      - results:
        
        creates electrical gradient that favors HCO3 secretion
        
        inc. secretion of aq. NaHCO3 by ductal cells, epi cells lining bile ducts & duo
        
        also affect acinar secretions, but to much lesser extent than CCK
        
        (+) liver to produce bile more rapidly (more so by bile salts)
      - potentiated by CCK & ACh
      - as secretory rate rises, pH & [HCO3] also rise; at low rates, Na & Cl predominate
- - - - immunosuppressants
      - anticonvulsants
      - thiazides
    - - celiac disease
      - IgG4
    - - Cystic Fibrosis
        
        dec. Cl, HCO3 & H2O secretion
        
        results: thick secretions >> obstruction >> autodigestion
        
        autosomal recessive; CFTR gene
        
        primarily caucasians
        
        progressive pulmonary & pancreatic insufficiency (chronic)
      - weak SPINK1, CTRC genes
    - - dec. lipase & HCO3 secretion
      - fatty diarrhea: floats, oily appearance, foul smell
      - Tx: supp pancreatic enzymes
      - early sign of pancreatic dysfxn bc fat digestion usually affected most
      - low pH inactivates lipase
    - - dec. enzymatic secretion except amylase
      - severe protein malnutrition
    - - XS aldosterone
      - salivary NaCl ~0
      - salivary K inc. to high levels
    - - dec. enzyme secretion in absence of pancreatic disease
  - - - obstructive (gallstone/malignancy in pancreatic duct)
    - - hereditary (mutated trypsin resistant to inhibitors)
      - alcohol abuse >> inflammation
- - - - amylin >> glycemic control via slow gastric emptying & (+) satiety; not found in urine
      - insulin >> dec. glucose in blood
      - also, proinsulin & C peptide
  - - - beta cells more abundant in center of islet
      - alpha & delta cells more abundant at periphery
      - blood supply courses outward from center
    - - gap jxns
    - - both sympathetic & parasympathetic