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
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
3
Q
serotonin
A
- produced by enterochromaffic cells in response to distension
- indirectly excites the ENS to increase motility and secretions
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
5
Q
histamine
A
- released by EC like cells in the stomach
- might stimulate HCl secretion
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
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
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
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
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
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
12
Q
carbs and lipids
A
- digestion initiated in the mouth by salivary and lingual enzyme
- amylase for carbs and lipase for lipids
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
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
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
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
pyloric glands
- secrete mucous
- secrete gastrin from G cells
- somatostatin from D cells
- few peptic and almost no parietal cells
26
cardiac glands
- near esophageal orifice
| - secrete mucous
27
pepsin
- 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
protection of gastric mucosa
- 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
erosive gastritis
- chronic use of NSAIDs
| - inhibit prostaglandin synthesis in stomach, which maintains physiochemical barrier by stimulating mucous and HCO3
30
gastric parietal cells
- 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
apical membrane
- H secreted into lumen in exchange for K
| - Cl follows by diffusion
32
basolateral membrane
- HCO3 absorbed from cell into blood
| - cl HCO3 exchanger
33
parietal cell HCl production
- 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
prolonged vomiting
- 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
HCl secretion regulation
- 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
parietal cell signals
-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
HCl in cephalic and gastric phases
- 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
last slide
- 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
