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3002 > 17 Salivary and gastric secretions > Flashcards

17 Salivary and gastric secretions Flashcards

1
Q

Which 4 structures are responsible for secreting fluids, enzymes and mucous into the lumen of the GI tract?

A
  1. Salivary glands (saliva)
  2. Cells of the gastric mucosa (gastric secretion)
  3. Exocrine cells of the pancreas (pancreatic secretion)
  4. Liver (bile)
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2
Q

Saliva characteristics?

A
  • High HCO3-
  • High K+
  • Hypotonic
  • Alpha-amylase
  • Lingual lipase
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3
Q

Factors that increase saliva secretion?

A
  • Parasympathetic (primarily)

* Sympathetic

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4
Q

Factors that decrease saliva secretion?

A
  • Sleep
  • Dehydration
  • Atropine
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5
Q

Function of salivary secretion?

A
  • Initial digestion of starches and lipids
  • Dilution and buffering of ingested foods
  • Lubrication if ingested foods with mucous (mucin)
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6
Q

How much saliva secreted per day?

A

1 L

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7
Q

3 features of the structure of the salivary glands?

A
  1. Paired:
    • Parotid - serous cells secreting an aqueous fluid composed of water, ions and enzymes
    • Sublingual - mostly mucous cells
    • Submandibular - mixed glands containing serous and mucous cells (mucin glycoprotein for lubrication)
  2. High blood flow (10x exercising muscle)
  3. Parasympathetic (dominant) and sympathetic supply both stimulate saliva production
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8
Q

Compounds in mucous responsible for lubrication?

A

Mucin glycoprotein

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9
Q

Role of acinar cells in salivary glands?

A

Produce an initial isotonic saliva composed of water, ions, enzymes and mucus

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10
Q

Role of myoepithelial cells in salivary glands?

A
  • In (and near) the acini

* Stimulated by neural input to eject saliva

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11
Q

Role of ductal cells in salivary glands?

A

Modify the initial saliva by altering electrolyte concentrations

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12
Q

Describe ductal cell transport systems

A

?

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13
Q

What are the 4 methods of salivary modification?

A

Combined action:

  1. Absorption of Na+ and Cl-
  2. Secretion of K+ and HCO-3
  3. Because more NaCl is absorbed than KHCO3 secreted there is net absorption of solute
  4. Low water permeability of ductal cells means that the final saliva is hypotonic
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14
Q

What 4 compounds are secreted by acinar cells?

A
  1. Alpha-amylase
    - begins the initial digestion of carbohydrates
  2. Lingual lipase
    - begins the initial digestion of lipids
  3. Mucus - lubricant
  4. Kallikrein
    - enzymatic cleavage of kininogen —> bradykinin (potent vasodilator)
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15
Q

What is the neural regulation of salivary secretion?

A
  • Salivary secretion is exclusively under neural control by the ANS (no hormonal regulation)
  • Salivary secretion is increased by both the parasympathetic and sympathetic nervous system
  • Neural stimulation results in an increased saliva production, HCO-3 production, enzyme secretion and myoepithelial cell contraction
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16
Q

Difference between PS and sympathetic innervation on salivary secretion?

A
  • PS: Produce fluid/ protein in saliva by binding to muscarinic receptor (IP3, Ca2+)
  • Symp: Produces mainly protein in saliva by binding to beta adrenal receptor (cAMP)
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17
Q

What is sialorrhea?

A
  • Excessive drooling

* Cerebral pasy and complex neurodisability

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18
Q

What are the side effects of anticholinergic medication?

A
  • Drowsiness or sedation
  • Blurred vision
  • Dizziness
  • Urinary retention
  • Confusion or delirium
  • Hallucinations
  • Dry mouth
  • Constipation
  • Reduced sweating and elevated body temperature

(Can’e pee, see, spit, shit)

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19
Q

What are transdermal scopolamine patches (scopoderm TTS)?

A
  • Treat drooling
  • Application of a skin patch behind the ear, at level of mastoid process
  • Patch releases a sustained dose of 0.5 mg of scopolamine per day and must be changed every 72 hrs, alternating between right and left sides
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20
Q

What are ultrasonography-guided Botulinum Toxin type A injections used for?

A
  • Injected into bilateral parotid and submandibular glands

* Treat sialorrhea in children with neurologic disorders

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21
Q

What are the 4 components of gastric juice?

A
  1. HCl - protein digestion
  2. Pepsinogen - protein digestion
  3. Intrinsic factor - vitamin B12 absorption (in the ileum)
  4. Mucus - protects the gastric mucosa and lubricates food
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22
Q

What factor increases HCl secretion?

A

Gastrin

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23
Q

What factor decreases HCl secretion?

A

H+ in stomach

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24
Q

What factor increases pepsinogen secretion?

A

ACh

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25
Q

What factor decreases pepsinogen secretion?

A

Chyme in duodenum

26
Q

What factors increase intrinsic factor secretion?

A
  • Histamine

* Parasympathetic

27
Q

What factors decrease intrinsic factor secretion?

A
  • Somatostatin
  • Atropine
  • Cimetidine
  • Omeprazole
28
Q

What are the locations and secretory products of gastric cells?

A
  1. Parietal cells:
    • Body
    • Intrinsic factor + HCl
  2. Chief cells:
    • Body
    • Pepsinogen
  3. G cells:
    • Antrum
    • Gastrin (to circulation)
  4. Mucus:
    • Antrum
29
Q

Structure of an oxyntric/gastric gland?

Compounds secreted by cells?

A
  • Surface epithelium
  • Mucous neck cells: Secrete mucous
  • Oxyntric/ parietal cells: Secrete HCl and intrinsic factor
  • Peptic/chief cells: Secrete pepsinogen
30
Q

What cells secrete HCl?

What is the consequence of HCl secretion?

A
  • Parietal cells secrete HCl which acidifies the gastric contents to pH 1-2
  • Secretes into lumen: H+ (via ATPase protein) and Cl- => HCl
  • Low gastric pH converts inactive pepsinogen –> pepsin (active form)
  • Pepsin is a protease which initiates protein digestion
31
Q

How is the H+ ion produced in parietal cells?

A

Carbonic anhydrase catalyses the combination of metabolic:

CO2 + H2O => H2CO3 => H+ + HCO3-

32
Q

Describe HCl secretion at the apical surface of gastric parietal cell

A
  • H+ is secreted into the lumen via the H+ K+ ATPase

* Cl- follows by diffusion through an apical channel

33
Q

Describe HCl secretion at the basolateral surface of gastric parietal cell

A
  • HCO3- is exchanged for Cl+ via the chloride-bicarbonate exchanger (alkaline tide)
  • Eventually HCO3- is secreted back into the GI tract in pancreatic secretions
34
Q

List the 3 phases of gastric HCl release

A
  1. Cephalic phase - 30% of secretion
  2. Gastric phase - 60% of secretion
  3. Intestinal phase - 10% of secretion
35
Q

Describe the cephalic phase of gastric HCl release:
• % of HCl secretion?
• Stimuli?
• Mechansim?

A
  • 30% of secretion
  • Stimuli: Smell, taste, chewing, swallowing, conditioned reflexion anticipation of food
• Direct stimulation:
vagus --> parietal cell
• Indirect stimulation:
vagus --> gastrin --> parietal cell
- vagal gastrin releasing peptide (GRP) stimulates gastrin release from G cells. Gastrin hormone enters the circulation and stimulated parietal cells to release HCl
36
Q

Describe the gastric phase of gastric HCl release:
• % of secretion?
• Stimuli?
• Mechanism?

A
  • 60% of secretion
  • Stimuli: Distension of the stomach and the presence of breakdown products of proteins, amino acids and small peptides in the stomach

• Distension causes:
1. Direct vagal stimulation of parietal cells
(vagus –> parietal cell)
2. Indirect stimulation via gastrin
(vagus –> gastrin –> parietal cell)
3. Local reflexes in the antrum that stimulate gastrin release
(local reflex –> gastrin –> parietal cell)
• Direct effect of amino acid and small peptides on G cells stimulates gastrin release
(gastrin –> parietal cell)

37
Q

What does vagal GRP stimulate?

A

Gastrin release from G cells

38
Q

Distension causes?

A
  1. Direct vagal stimulation of parietal cells
  2. Indirect stimulation via gastrin
  3. Local reflexes in the antrum that stimulate the gastrin release
39
Q

What are the direct and indirect methods of regulation of HCl secretion?

A
  1. Direct vagal pathway
    - vagal release of ACh activates parietal cells
  2. Indirect vagal pathway
    - vagal stimulated release of gastrin from G cells (by GRP neuropeptide transmitter)
40
Q

What are the types of vagotomy?

A
  1. Truncal vagotomy:
    • Section of the vagus nerve
    • Reduces the maximal acid output by ~50%
  2. Selective vagotomy:
    • Gastric branches are severed
    • Hepatic branches are preserved
  3. Highly selective vagotomy:
    • Fibres supplying the parietal cells are ligated
    • Nerve of Latarjet which supplies and rum is retained
    • So no drainage procedure is required in HSV
41
Q

Describe the intestinal phase of gastric HCl release

A
  • 10% of secretion

* Presence of breakdown products of proteins in the duodenum

42
Q

List the substances which stimulate HCl secretion

A
  1. ACh (neurocrine)
  2. Histamine (paracrine)
  3. Gastrin (hormone)
43
Q

Acetylchloline (neurorcrine) in the stimulation of HCl secretion:
• Origin
• Action
• 2nd messenger

A
  • Origin: vagus nerve
  • Action: binds to muscarinic (M3) receptors on parietal cells
  • 2nd messenger: IP3/ Ca2+
44
Q

Histamine (paracrine) in the stimulation of HCl secretion:
• Origin
• Action
• 2nd messenger

A
  • Origin: enterochromaffin like cells (ECL) in the gastric mucosa
  • Action: diffuses to and binds to H2 receptors on parietal cells
  • 2nd messenger: cyclic AMP
45
Q

Gastrin (hormone) in the stimulation of HCl secretion:
• Origin
• Action
• 2nd messenger

A
  • Origin: G cells in the stomach antrum
  • Action: binds to CCKb receptors on parietal cells
  • 2nd messenger: IP3/Ca2+
46
Q

How is HCl secretion inhibited?

A
  • HCl secretion is inhibited when HCl is no longer needed to convert pepsinogen to pepsin
  • Occurs after the chyme moves into the small intestine and the H+ buffering capacity of the food is no longer a factor

• Somatostatin:

  1. Direct pathway - binds to receptors on parietal cells and inhibits adenylate cyclase via G9 protein
  2. Indirect pathway - inhibits histamine release from ECL cells and gastrin release from G cells
47
Q

How does somatostatin inhibit HCl secretion?

A
  1. Direct pathway - binds to receptors on parietal cells and inhibits adenylate cyclase via G9 protein
  2. Indirect pathway - inhibits histamine release from ECL cells and gastrin release from G cells
48
Q

What cells secrete pepsinogen? Stimulation of secretion?

A

• Vagal stimulation
- chief and mucous cells in the oxyntic glands secrete pepsinogen

• H+ triggers local reflexes
- chief cells secrete pepsinogen

49
Q

Intrinsic factor secretion:
• What is intrinsic factor?
• Absence causes…
• Relevance in gastrectomy patients?

A
  • Mucoprotein released from parietal cells required for Vitamin B12 absorption in the ileum
  • Lack of intrinsic factor causes pernicious anaemia
  • Following gastrectomy, patients receive injections of Vitamins B12 to bypass the absorption defect
50
Q

What is the only essential secretion of the stomach?

A

Intrinsic factor secretion - required for Vitamin B12 absorption in the ileum

51
Q

What does lack of intrinsic factor cause?

A

Pernicious anaemia

52
Q

What injections do patients receive following gastrectomy?

A

Injections of Vitamins B12 - to bypass absorption defect

53
Q 
Pernicious anaemia:
• What is it?
• Responsible for?
• Prevalence?
• Biologically characterised by?
• Treatment?
A
  • Autoimmune atrophic gastritis - predominantly of the fundus
  • Responsible for a deficiency in vitamin B12 dues to its malabsorption
  • Prevalence: 0.1% (general population; 1.9% (>60 y.o)
  • Represents 20-50% of the causes of vitamin B12 deficiency in adults
  • Biologically characterised by presence of anti-intrisinc factor antibodies
  • Treatment - administration of parenteral vitamin B12
54
Q

What is Zollinger-Ellison syndrome?

A

• Gastrinoma - gastrin secreting tumour

  • Non-beta-cell of the pancreas
  • High circulating levels of gastrin
55
Q

What does high circulating levels of gastrin result in?

A
  • Increased H+ secretion by parietal cells
  • Hypertrophy of the gastric mucosa
  • Duodenal ulcers (constant secretion of gastric H+)
  • Acidification of the intestinal lumen (inactivation of pancreatic lipases)
56
Q

What are the clinical symptoms of Zollinger-Ellison syndrome?

A
  • Abdominal pain
  • Chronic diarrhoea
  • Dyspepsia
  • Weight loss
  • GI bleeding
57
Q

What is Hypertrophic Pyloric Stenosis (HPS)

A
  • Repeated episodes of vomiting following attempts to feed the infant cause progressive dehydration and loss of hydrogen chloride from the gastric juices
  • Exchange of extracellular potassium with intracellular hydrogen ions in an attempt to correct pH imbalance
  • Infants with severe committing can develop hypochloremia and hypokalaemia
  • Vomiting of PS may begin any time after birth but doesn’t assume its characteristic pattern before the 2nd - 3rd week
58
Q

What are the statistics of Hypertrophic Pyloric Stenosis?
• Prevalence
• More common in?
• % with family history

A
  • Affects 3/ 1000 babies born
  • More likely to affect full-term, 1st-born male infants
  • More common in caucasian infants
  • ~15% of infants born with HPS have a family history
59
Q

What is the classic biochemical abnormality in Hypertrophic Pyloric Stenosis (HPS)?

A

Hypochloremic, hypokalemic metabolic alkalosis

60
Q

How to diagnose Hypertrophic Pyloric Stenosis (HPS)?

A
  1. Test feed
  2. Ultrasonography
    • standard technique
    • reliable, highly sensitive/ specific and easily performed
    • > 3mm of muscular layer of pylorus - hypertrophy
    • Abnormal pyloric channel length: >15 - 19mm
  3. Barium upper GI (UGI)
61
Q

Preoperative management of infants with HPS

A
  • Preoperative management is directed at correcting the fluid deficiency and electrolyte imbalance
  • Adequate amounts of both Cl and K are necessary to correct metabolic alkalosis
  • Before induction of anaesthesia, aspirate the infant’s stomach with a large-caliber suction tube to remove any residual gastric fluid or barium
62
Q

Treatment of Pyloric Stenosis

A
  • Surgical Pyloromyotomy
  • Known as Ramstedt’s procedure - dividing the muscle of the pylorus to open up the gastric outlet
  • Done through a single incision (3-4 cm long: tiny circular incision) or laparoscopically

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