Pancreas AND salivary gland

Which salivary gland is most likely to become malignant and which is most likely to have a tumor

Most malignant = sublingual; most common is parotid

What makes up salivon

Acinus, intercalated duct, striated duct, excretory duct

What are the functions of the cells in the acinus

Serous cell: secrete watery secretion; mucous cell: secrete mucus rich secretion

Describe the viscosity of saliva from each salivary gland

Parotid → High serous cell → Watery; submandibular → Mostly serous → Semi viscous (normal saliva); sublingual → Mostly mucous → Viscous

What is primary secretion

Isotonic saliva: Serous cell release water that travel through the duct

What is secondary secretion

Hypotonic saliva; at striated duct there is Na and Cl reabsorption + K and HCO3 secretion

What is the characteristic of low flow rate

Hypotonic, acidic saliva → Na, Cl decrease, K increase, HCO3 decrease

What is the characteristic of high flow rate

Near isotonic, alkaline → High HCO3 reabsorption

What controls salivary secretion

PNS → INCREASE watery saliva, vasodilation and flow; SNS → DECREASE volume, saliva is protein rich

Which glands are controlled by CN IX and VII

Parotid controlled by IX, submandibular and sublingual by CN VII

Function of acinar cells

Release digestive enzyme

What stimulate acinar cells

CCK from I cell and ACh from vagus nerve

What is the characteristic of acinar cells in histology

Basophilic cytoplasm (acidic, has many RER), zymogen granules that are red (basic, has a lot of protein)

Centroacinar cell function

Start HCO3 release into pancreas

How is HCO3 brought into the lumen

Secretin from S cell activate CFTR → CTFR allows Cl- to move into cell lumen → Cl in lumen exchange with HCO3 in cell → HCO3 in lumen

What is the difference between the Cl and HCO3 concentrations at centroacinar and duct

Centroacinar has highest Cl, low HCO3; duct has high HCO3, low Cl

What is the pathology of CFTR dysfunction

Cl cannot center cell → No exchange of Cl and HCO3 → The secretion is viscous → Can cause obstruction

What are the consequence of CFTR dysfunction

Obstruction → Pancreatic enzymes retained → Acinar cell damaged → Lack pancreatic enzyme → Steatorrhea and ADEK def (fat soluble vitamin)

When is exocrine pancreatic secretion the highest

Intestinal phase → Acid and fatty acid in duodenum causes secretin and CCK release

What happens during the first (rapid) phase of insulin secretion

Glucose enters cell by GLUT2 → Glycolysis occurs → ATP closes K channel → K accumulates (depolarization) → Opens Ca channel → Ca influx → Insulin exocytosis; peak because it is using insulin reserve

What happens during the second (steady) phase of insulin secretion

Incretin trigger pathway that amplify first phase + insulin generation

Appearance of C peptide in blood indicates what

Patient is able to produce their own insulin; C peptide is product of insulin modification

Sulfonylurea function

Block K channel without needing glucose → Depolarization → Ca enters → Insulin exocytosis; causes weight gain and hypoglycemia

What is DDP4

Inhibits incretin; DDP4 inhibitor allow incretin to work fully

What is T2DM not respond to

GIP; T2DM patients need to be given GLP-1

Why can incretins only be given through injection

Peptide hormone → Needs to be injected or else it will be digested

Why does secretin not cause salivary HCO3 secretion

Saliva controlled by SNS/PNS rather than hormone