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Physiology Unit 6 > Salivary Glands > Flashcards

Salivary Glands Flashcards

1
Q

hormones

A
  • peptides released from endocrine cells of the GI tract

- secreted into portal circulation pass through liver and enter systemic circulation

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2
Q

paracrines

A
  • secreted by endocrine cells of GI tract
  • act locally on same tissue that secretes them
  • somatostatin is a peptide, histamine isn’t a peptide
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3
Q

serotonin

A
  • produced by enterochromaffic cells in response to distension
  • indirectly excites the ENS to increase motility and secretions
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4
Q

somatostatin

A
  • produced by D cells and potent inhibitor of several processes-pancreatic and gastric secretions, motility
  • can act in endocrine and paracrine matter
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5
Q

histamine

A
  • released by EC like cells in the stomach

- might stimulate HCl secretion

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6
Q

neurocrines

A
  • synthesized in neurons in the GI tract and released following an AP
  • they diffuse across the synaptic cleft and act on the target cell
  • Ach, Norepi, VIP, gastrin releasing peptide, substance P
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7
Q

gastrin

A
  • secreted by antral mucosa cells (G cells in stomach) in response to food, distension, vagus
  • increase acid secretion by parietal cells
  • stimulates growth of gastric mucosa
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8
Q

cholecystokinin (CCK)

A
  • secreted by mucosa of intestine (I cells in duodenum and jejunum) in response to fats and proteins/peptides/ aa
  • increases gal bladder contraction
  • increase pancreatic enzyme and bicarbonate secretion (trypsin, chymotrypsin, lipases, amylases)
  • inhibits gastric emptying
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9
Q

secretin

A
  • secreted by mucosa of small intestine (S cells in duodenum) in response to arrival of acidic chyme from the stomach
  • increases bicarbonate and fluid secretion by pancreas
  • decreases gastric acid secretion in stomach by decreasing gastrin, inhibits gastric emptying
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10
Q

motilin

A
  • secreted by M cells in the duodenum and jejunum during the fasting period
  • promotes contractions in distal stomach to clear tract of indigestible materials
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11
Q

glucose dependent insulinomic peptide

A
  • secreted by K cells in duodenum and jejunum in response to fat and carbs
  • acts on pancreas to stimulate insulin secretion
  • inhibits HCl secretion by parietal cells
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12
Q

carbs and lipids

A
  • digestion initiated in the mouth by salivary and lingual enzyme
  • amylase for carbs and lipase for lipids
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13
Q

proteins

A
  • digestion is initiated in the stomach by gastric proteases-pepsins
  • additional lipid digestion in the stomach due to swallowed lingual lipase
  • some gastric lipase
  • gastric enzymes don’t do carbs
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14
Q

enzymes in small intestine

A
  • lipase, chymotrypsin, amylase are critical for lipids, proteins, and carbs (pancreas)
  • enzymes on luminal surface of SI complete carb digestion and proteins
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15
Q

salivary secretions

A
  • lubricate, protect, and digest
  • salivon similar to pancreas
  • secrete 1.5 L saliva/day
  • acinar cells of parotid secrete serous substance rich in alpha amylase
  • sublingual and submandibular secrete sero-mucous product rish in mucin glycoproteins
  • other minor glands dispersed throughout the submucosa of the oral cavity
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16
Q

ptyalin

A

-converts starch to sugar at pH 7, denatured below 4

17
Q

lingual lipase

A

-hydrolyzes triglycerides and is secreted by small salivary glands on the tongue surface

18
Q

sjogren syndrome

A
  • chronic and progressive autoimmune disease that destroys the salivary and lacrimal glands
  • xerostomia-dry mouth- difficulty speaking, dental caries and halitosis
19
Q

primary salivary secretion

A
  • modified by transport processes of duct
  • depends on flow rate
  • at low rates, Na and Cl are absorbed and K is secreted
  • at high rates, more like plasma
  • high HCO3 makes fresh saliva more alkaline than plasma and neutralizes gastric acid that refluxes into the esophagus as well as acid produced by oral bacterial
20
Q

salivary acinar cells

A
  • during secretion, blood flow to acini is increased by PNS stimulation and ultrafiltrate from plasma enters acini
  • filtrate from cells enters the lumen of the acinar cells
  • mixes with secreted mucous and alpha amylase, creates primary secretion
  • secretion is modified as it passes through ducts into mouth
  • lipase from von ebners glnads
21
Q

ANS and saliva

A
  • secretion controlled by autonomic innervation
  • PNS stimulation promotes increased and sustained salivary secretion in which flow is increased 10x over the basal rate
  • SNS causes and lesser and more transient stimulation (from superior cervical ganglion)
  • activation of glands causes release of kallikrein, which leads to production of bradykinin and vasodilation
  • increases cap hydrostatic pressure and cap filtration, supplies fluid for secretion
  • salivation reflex can be conditioned
  • salivatory nuclei in junction of medulla/pons- excited by taste and tactile stimulation from tongue and other areas of mouth/pharynx
  • can also be influenced by higher centers-near PNS centers of ant hypothal
  • reflexes from stomach
22
Q

gastric juice

A
  • from gastric mucosa
  • oxyntic glands in body of stomach
  • duct empty into pits
  • pits contain parietal cells and chief cells
  • pyloric glands in antrum of stomach
  • G cells and mucous cells in their pits
23
Q

oxyntic glands

A
  • acid forming
  • inside surface of body and fundus
  • mucous neck cells, chief cells (pepsinogen and gastric lipase), and parietal cells (HCl and intrinsic factor)
24
Q

destroy parietal cells

A

-achlorhydria and pernicious anemia due to failure of maturation of RBCs in absence of B12 stimulation of the bone marrow

25
Q

pyloric glands

A
  • secrete mucous
  • secrete gastrin from G cells
  • somatostatin from D cells
  • few peptic and almost no parietal cells
26
Q

cardiac glands

A
  • near esophageal orifice

- secrete mucous

27
Q

pepsin

A
  • initiates breakdown of ingested protein, attack internal bonds
  • derived from pepsinogen and is most active at acidic pH (more spontaneous below 3.5)
  • secreted from oxytinic glands and stimualted by vagus and ENS
  • digest collagen in CT
28
Q

protection of gastric mucosa

A
  • alkaline mucous layer
  • mucous layer traps HCO3, which titrates any H+ that diffuse into the gel layer
  • inactivates pepsin
  • if H gets in, hurts mast cells and release histamine
  • IF response
  • renews itself every 3-4 days
29
Q

erosive gastritis

A
  • chronic use of NSAIDs

- inhibit prostaglandin synthesis in stomach, which maintains physiochemical barrier by stimulating mucous and HCO3

30
Q

gastric parietal cells

A
  • net secretion of HCl and net absorption of HCO3
  • hydrogen potassium pump (ATPase)
  • carbonic anhydrase takes CO2 and water and makes H2CO3
  • dissociates into HCO3
  • HCO3 transported across basolateral membrane into ECM in exchange for Cl
  • HCl ends up outside
31
Q

apical membrane

A
  • H secreted into lumen in exchange for K

- Cl follows by diffusion

32
Q

basolateral membrane

A
  • HCO3 absorbed from cell into blood

- cl HCO3 exchanger

33
Q

parietal cell HCl production

A
  • 160 mmol/L HCl
  • isotonic nearly
  • 0.8 pH
  • concentration 3 million times bigger than arterial blood
  • 1500 calories of energy per liter of gastric juice
  • as hydrogen ions are secreted, bicarbonate enters the blood so that gastric venous blood has a higher pH than arterial blood when the stomach is secreting acid- alkaline tide
  • eventually go back to GI tract
34
Q

prolonged vomiting

A
  • causes dehydration, alkalosis and hypokalemia
  • vomiting center in medulla
  • stimuli induce salvation and retching
  • reverse peristalsis from mid small intestine to pylorus
  • retching until UES opens
  • irritants in stomach or SI, enteric virus/bacteria
  • systemic irritant by chemoreceptor in 4th ventricle
  • head injury
  • abdominal stimulation of vestibular organs
35
Q

HCl secretion regulation

A
  • vagus, gastrin, and histamine stimulate secretion
  • vagus and gastrin stimulate histamine release from ECL cells
  • vagus inhibits secretion of somatostatin
  • acid turned on by insulin, caffeine, stress
  • turned off by somatostatin, GIP, secretin
36
Q

parietal cell signals

A

-Ach and gastrin bind to specific receptors (M3 and CCK) coupled to Gq
-PLC and then PKC activated
-increase Ca
-histamine binds to H2-Gs increases cAMP and PKA
^both lead to acid secretion
-somatostatin and prostaglandins inhibit linked to Gi (H2 receptor antagonists are antacids) and proton pump inhibitors

37
Q

HCl in cephalic and gastric phases

A
  • cephalic is smelling, tasting, conditioned reflexes
  • direct stim of vagus nerve (Ach on parietal cell) and indirect of parietal cell by gastrin
  • vagus releases gastrin releasing peptide onto G cells

gastric phase:

  • distension of the stomach and presence of breakdown products of proteins
  • same as above plus distension of antrum activates local reflexes to enhance gastrin release plus aa and small peptides stimulate G cells to release gastrin

intestinal phase:
-10% of Hcl secretion and mediated by products of protein digestion

HCl is inhibited when no longer needed for activation of pepsinogen, majorly through somatostatin

38
Q

last slide

A
  • corpus of stomach-vagus stimulates parietal cells via Ach and stimulates ECL cells (histamine) and D cells (dec somatostatin)
  • antrum-vagus stimulates G (gastrin) and D cells
  • G cells via GRP (gastrin releasing peptide)-promoting gastrin release-gastric acid secretion by parietal cells and ECLs
  • D cells- dec somatostatin (less inhibition)
  • luminal H+ stimulates D cells to release somatostatin-neg feedback
  • products of protein digestion directly stimulate G cells to release gastrin

Physiology Unit 6 (12 decks)

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