Composition of Saliva
99% water
1% electrolytes and organis substances
organic substances:
- enzymes; lingual lipase, ptyalin (salivary alpha amylase)
- mucin
- antimicrobials; peroxidases, lysozymes, lactoferrin, igA
- others; growth factors, urea, blood grp substances
saliva pH
6.4-6.9
may reach 7.8 when in mouth
functions of saliva
- bolus formation and lubrication
- washing away food substances
- preventing infection
- starting digestion
- speech
- acid buffer
- taste
xerostomia causes + effects
- radiotherapy = salivary gland damage
- autoimmune disorders (sjorgens syndrome)
- drugs (anticholinergics, antidepressants)
- dehydration
- aging
- dry lips, altered taste, impaired digestion, lack of defence
increased risk of dental caries and periodontal disease
composition of gastric juice and source
urease - h pylori
rennin in infants
water - all gastric cells
HCL - parietal cells
Intrinsic factor - parietal cells
pepsinogen, gastric lipase, gelatinase- chief cells
mucus +hco3- - mucuous cells
functions of gastric juice
converts pepsinogen -> pepsin
- provides optimal ph for digestion of;
fats, - gastric lipase
gelatin
urea
proteins - pepsin (also curdles milk)
- kills ingested micororganisms
- mucin protects stomach mucosa
- calcium and iron absorption
- b12 absorption
HCL functions
- pepsinogen -> pepsin
- antibacterial action
- converts fe3+ to fe2+ for improved absorption
mechanism of hcl secretion
- co2 into parietal cell
- co2+h20=h2co3
- h2co3 dissociates into hco3- and h+
- h+ actively pumped out and k+ in
- k+ recycled back through ion channel
- hco3- exchanged for cl- on basolateral membrane
- cl- diffuses into gastric lumen via ion channels
- combine to form hcl
stimulators and inhibitors of hcl secretion
stimulators:
- Ach - from vagus -> m3 receptors
- gastrin - from G cells -> cck-b receptors
- histamine - ecl cels -> h2 receptors
histamine most potent, increases camp activity and therefore proton pump
inhibitors
- somatostatin
- prostaglandin
- secretin
- GIP
- ph<3
achlorhydia
absence of hcl secretion, due to parietal cell destruction or chronic gastritis
- decreased protein digestion,
- dec iron absorption = anaemia
- bacterial overgrowth - excess lactic acid levels shown
gastric ulcer
- imbalance between acid secretion and mucosal defence
causes: - excess hcl
- h pylori
- NSAIDS (decreased prostaglandins)
= mucosal erosion and bleeding
pancreatic juice composition
enzymes:
1. proteolytic
- trypsin
- chymotrypsin
- carboxypeptidases
- nuclease
- elastase
- collagenase
- lipolytic
- pancreatic lipase
- cholesterol ester hydrolase
- phospholipase A
- phospholipase B
- colipase
- bile self activated lipase - pancreatic amylase
other organic substances;
- albumin
- globulin
electrolytes
bicarbonate content of pancreatic juice
110-150mEq/L
ph of pancreatic juice
- 8-8.3 (high hco3-)
pancreatic enzymes functions
see chapt 2 table
acute pancreatitis
premature trypsinogen activation
= severe abdominal pain, enzyme leakage
caused by gallstones and alcohol
cystic fibrosis
- defective cftr leads to thick secretions due to defective cl- transport across epithelial cells
- blocks pancreatic ducts, so enzymes cannot reach intestines = pancreatic insufficiency
- decreased fat digestion = steatorrheoa (greasy foul smelling stools)
how does secretin affect pancreatic secretions
- released by s cells ins tomach in response to hcl -> bloodstream -> pancreas
- increases cAMP
= watery secretion deficient in enzymes high in hco3- - this helps neutraise acidic chyme
- inhibits gastric acid secretion
- increases bile flow
cck effect on pancreatic juice
- stimulates enzyme rich secretion of pancreatic juice
- phospholipase c mechanism
- low volume
bile composition
97% water
3% solids
- bile salts; emulsify fats
- bilirubin; waste excretion
- cholesterol; excretory
- lecithin
- mucin
- phospholipids; micelle formation
- electrolytes; fluidity
ph bile
7.8-8.6
functions of bile
- emulsification + absorption of fats
- absorption of fat soluble vitamins
- cholesterol secretion
- antiseptic and mild laxative effects
- activates pancreatic lipase
cholelithiasis
- bile precipitation = stones
1. cholesterol stones; - yellow, radiolucent
- when bile is supersaturated with cholesterol
2. pigment stones - black stones: calcium bilirubinate - (hemolysis, cirrhosis)
- brown stones; infection of biliary tract
- biliary colic (right upper quadrant pain
- nausea vomiting
- fatty food intolerance
- can lead to obstructive jaundice
cholelithiasis pathogenesis
gallstones form due to imbalance between bile components
- supersaturation of cholesterol
- decreased bile salts or lecithin
- increased cholesterol secretion - nucleation
- cholesterol crystallises , promoted by mucin
- inflammation - gallbladder stasis
- poor emptying,
prolongs crystal growth
