Physiology Block 3 Week 13 04 GI Secretion 02 Flashcards
Pancreas Secretions
Pancreatic secretions in response to chyme in upper small intestine with juice characteristics dependent on type of food
Common opening at sphincter of Oddi
Pancreatic Proteins
Trypsin, Chymotrypsin, and Carboxypeptidase
–all secreted in inactive form
Trypsinogen –> Trypsin by enterokinase
Trypsin activates more trypsinogen, and converts chymotrypsinogen and procarboxypeptidase
Trypsin inhibitor prevents activation until secretions reach small intestines
Protein Breakdown
Proteins broken down by Pepsin
Forms Proteoses, Peptones, and Polypeptides
Further degradation by Trypsin, Chymotrypsin, Carboxypeptidase, and Proelastase
Forms Polypeptides and Amino Acids
Further breakdown by Peptidases
Forms Amino Acids
Carbohydrate Breakdown
Starches broken down to maltose and 3 to 9 glucose polymers
Enzymes:
- Ptyalin (saliva)
- Pancreatic amylase ** 50-80%
Fat Breakdown
Majority we eat are Triglycerides
Pancreatic Lipase (fatty acids and monoglycerides)
Cholesterol esterase (Cholesterol esters)
Phospholiase (splits fatty acids from phospholipids)
Bicarbonate Secretion
To neutralize acid in the upper small intestine
CO2 moves into cell from blood
Carbonic Anhydrase converts to bicarb
Bicarb actively transported out into the lumen
Pancreatic Secretion Stimuli
Acetylcholine–acini
Cholecystokinin–acini
70% of total pancreatic digestive enzyme secretion
Secretin–pancreatic duct
-prosecretin converted to secretin by low pH in small intestine
Phases of Pancreatic Secretion
Cephalic: 20% –mostly digestive enzymes
Gastric: 5%
Intestinal: 75%–bicarbonate rich solution
Water vs Enzyme Secretion
HCl
Soap (Fat)
Peptone
HCl: mostly Water and Bicarb
Soap: equal amounts of Water and Bicarb and Enzymes
Peptones: mostly enzymes
Pancreatic Insufficiency
Multiple causes including chronic alcohol use
Can affect both exocrine and endocrine functions when 90% of function is lost
Exocrine:
- weight loss: can’t break down fats
- steatorrhea: it floats
Endocrine:
-Diabetes Mellitus
Hepatic Histology
Portal Triad–Portal Vein, Hepatic Artery, Bile Duct
Also Lymphatic duct (but discovered later)
Portal Vein and Hepatic Artery feed every corner of the Hepatic LOBULE and drains into central vein
Central Vein drains to the hepatic vein which drain into the IVC
Lobules drain into central vein through sinusoids
Sinusoids are fenestrated–blood can go thru the pores and come in contact with hepatocytes
Toxic stuff are cleaned and sent to central vein
Kupffer cells (surround sinusoids) act as phagocytes and remove bacteria
Substances that carry (like proteins) interact with hepatocytes too
Space of Disse–drain into lymphatic duct
Stellate Cell (within space of Disse)–makes collagen when irritated–leads to cirrhosis
Hepatocytes are arranged in plates joined by tight junctions, and their apical membranes make up the bile canaliculi
Segregated from the blood-filled sinusoids by fenestrated endothelial cells without a basement membrane, and by space of Disse
Kupffer cells reside in the sinusoidal lumen
Stellate cells are found within the space of Disse
Biliary System
Bile assists in fat digestion and absorption as well as to eliminate waste products such as BILIRUBIN
Right and Left Hepatic ducts from liver drain into common hepatic duct
Cystic duct (gallbladder) connects distally with common hepatic forming common bile duct
Pancreatic duct connects with common bile duct distally
Bile secretion at 2nd part of duodenum controlled by Sphincter of Oddi
Storage of Bile in Gallbladder
Mechanism for Concentration:
Absorption of Water
NaCl leads to concentration of bile salts, cholesterol, lecithin, and bilirubin
Cholesterol and lecithin are solubilized by bile salts
Volume goes from 500 ml to 50 ml
Cholesterol Homeostasis
The combined fecal excretion of cholesterol and bile acids is equivalent to input of cholesterol from the DIET plus ENDOGENOUS SYNTHESIS of cholesterol
Bile Salt Formation
Cholesterol broken down by hydroxyase
–Primary Bile Acids
Broken down by dehydroxylase
–Secondary Bile Acids
Conjugated with glycine
–Bile salt (NOW SOLUBLE)
Bile Salt Function
Emulsification
-decreases surface area tension and breaks fat globules into smaller size particles
Forms Micelles
- soluble in chyme
- helps absorption of fat breakdown products (fatty acids, monoglycerides, cholesterol)
Gallstone Formation
Majority of gallstones are cholesterol stones
Bile salts allow cholesterol to remain soluble
Fat, Forty, Fertile, Female
Causes:
- Too much absorption of water from bile
- Too much absorption of bile acids from bile
- Too much cholesterol in bile
- Epithelium inflammation
Acute Pancreatitis
Causes:
- alcohol and gallstones
- medications
- elevated triglycerides
- hypercalcemia
Pt complains of severe upper abdominal pain
Blood tests show elevated lipase and amylase
Need to have pain and elevated lipase and amylase
Biliary Atresia
The bile ducts inside or outside the liver do not have normal openings
With biliary atresia, bile becomes trapped, builds up, and damages the liver. The damage leads to scarring, loss of liver tissue, and cirrhosis.
Gallbladder Contraction and Emptying
Vagal stimulation
–causes weak contraction of gallbladder
Secretin via blood stream
–stimulates liver ductal secretion
–produce a solution rich in NaHCO3:
helps neutralize acids and optimize pancreatic function
Cholecystokinin via blood stream (released bc fatty foods in duodenum)** (Major)
- -gallbladder contraction
- -empties in under 1 hour
- -relaxation of sphincter of Oddi
Where are bile salts reabsorbed?
Enterohepatic circulation:
Bile salts reabsorbed mostly in terminal ileum–95%
Bilirubin Metabolism
When RBC old or damaged, sent to spleen for breakdown
Hb released and broken down to heme
Heme converted to unconjugated bilirubin
Not water soluble, so binds albumin and sent to liver
In the liver, bilirubin CONJUGATED with glucuronic acid by glucuronyltransferase–now water soluble
Bile duct:
Large intestine flora break it down further creating urobilinogen
Broken down further to stercobilin (feces brown color) and urobilin
Systemic Circulation:
Some Urobilinogen reabsorbed and excreted in urine and oxidized to urobilin (gives yellow color)
Direct vs Indirect Bilirubin Elevation
Elevated Indirect (unconjugated) Bilirubin:
- increased breakdown of RBC
- inability of bilirubin-albumin adduct to be taken up by hepatocytes (transport mech)
- inability of hepatocytes to conjugate bilirubin (enzyme deficient)
Elevated Direct Bilirubin:
- hepatocyte dysfunction
- biliary obstruction
Amount of light will determine at what total bilirubin value you are able to detect scleral icterus (yellow instead of while sclera)
Small Intestine Secretions
Brunner’s Glands (duodenum):
-secrete alkaline mucus to protect mucosa
Produced in response to:
- tactile or irritating stimuli
- vagal stimulation
- SECRETIN
Inhibited by sympathetic stimulation
Crypts of Lieberkuhn
Found in all parts of the Small Intestine between the villi
Secrete almost pure ECF
Goblet cells: secrete mucus
Enterocytes: secrete water and electrolytes
Digestive enzymes on villi surface
Peptidase on small intestine villi surface
Break down peptides into amino acids
Carbohydrate Digestion
Small intestine
Disaccharides are broken into monsaccharides by sucrase, maltase, isomaltase, and lactase
Large Intestine Secretions
No villi present
Crypts of Lieberkuhn without villi Mucus secretion: -protects mucosa from excoriation, acid -packing of stool -antibacterial properties
Parasympathetic innervation through pelvic nerves (S2-S4) stimulate mucus production
Which of the following has its major effect on the pancreatic duct epithelium?
A. Acetylcholine
B. CCK
C. Secretin
D. Amylase
C. Secretin
True statements regarding bilirubin metabolism include all of the following except?
A. Under normal conditions the majority of bilirubin is derived from the breakdown of RBC
B. Bilirubin binds to albumin once within the hepatocyte
C. Stercobilin is found in feces
D. Conjugated bilirubin flows into bile canaliculi
B. Bilirubin binds to albumin once within the hepatocyte
Happens in the plasma and then transported to the hepatocyte
Ascities
Accumulation of fluid in the peritoneal cavity
Cause:
- umbilical hernia (even an inguinal hernia)
- Caput medusae
