Exocrine Function GI Flashcards

Question

What are features/roles of mucus?

Answer 1

1) Thick secretion → composed mainly of water electrolytes and glycoproteins 2) Adheres tightly to food or other particles → spreads a thin film over surfaces 3) Convers the gut wall → limits direct contact of particles with the mucosa 4) Resistant to GI enzymes → long durability because not broken down by GI enzymes 5) Causes fecal particles to adhere → forming the feces 6) Has amphoteric properties → can buffer small amounts of acids or alkalis

Answer 2

Major organ for digestion → releases pancreatic juices & enzymes - pancreatic juices enter with bile from liver/gall bladder - regulated entry into GIT at spincter of Oddi → Spincter is relaxed by CCK + CCK promotes secretion of pancreatic enzymes by acinar cells + contract gall bladder

Answer 3

Exocrine: (Head/Body) - Tubuloacinar glands → similar to salivary glands - Individual ducts flow into main collecting duct that leads to duodenum Endocrine: (Tail) - "Islet of Langerhans" - Adjacent to and surround Acinar cells - Produce hormones → blood - D cells → secrete Somatostatin *Somatostatin decreases Gastrin production (activated by H+) // Decreases enzyme release by acinar cells

Answer 4

- Ductal region of the pancreas - Stimulated by Secretin Composition = Na+, K+, HCO3-, Mg2+, Ca2+ → similar to plasma - isotonic Functions: - Neutralizes chyme - Protects mucosa form acid - pH necessary for enzyme function

Answer 5

1. Secretion of Cl- via CFTR channels into the lumen 2. Secretion of HCO3- in exchange for Cl- at the lumenal membrane 3. Secretion of H+ via the pumps on the basolateral membrane **Balances "alkaline tide" - No net Cl- secretion - CO2 entry from the basolateral side → H+ + HCO3-

Answer 6

1. Enterokinase is secreted by cells in the duodenum → cleaves Trypsinogen → Trypsin Pancreatic enzymes are released as Zymogen granules by exocytosis → inactive components because they are so powerful they could dammage the pancreas if already active - Activated by proteolytic cleavage with enterokinase from SI 2. Trypsin acts in a positive feedback loop on itself and further cleaves Trypsinogen → trypsin 3. Trypsin cleaves all other pancreatic enzymes into their active form in the SI Chymotrypsinogen → chymotrypsin + peptide Proelastase → Elastase + peptide Procarboxypeptidase → carboxypeptidase + peptide Prophospholipase a → phospholipase A + peptide

Answer 7

1. Enzymes are secreted as Zymogens (inactive form) and are activated by enterokinase which is produced in the SI, not in the intestine 2. The pancreas produces a Trypsin inhibitor to prevent proteolytic cleavage and activation of the enzymes *In the case of blockage of the pancreatic duct, there can be activation of the enzyme that are stuck and this can be very dammaging for the pancreas

Answer 8

Pancreatic cells have Muscarini receptors (activated by ACh) + CCK-A receptor (CCK/Gastrin) + VIP receptor (Secretin/VIP) Cephalic phase → Nervous control (Vagus ACh) Gastric phase → Nervous (stretch) + hormonal (Gastrin) Intestinal phase → APUD cells sense contents of the SI lumen - H+ → Secretin → inhibits parietal cells, stimulates duct cells to secrete HCO3- - Fat → CCK → stimulate acinar cells to secrete enzymes - Somatostatin from D cells in islet of Langerhans → inhibits gastrin release + inhibits pancreatic acinar cells (decrease enzyme secretion)

Answer 9

If the case of pancreatic duct blockage, somatostatin analogues would inhibit pancreatic enzyme secretion → prevent risks of dammaging the pancreas

Answer 10

1. Blockage of secretory ducts + loss of acinar tissue 2. Decrease alkaline secretion (ductal cells) + decrease enzyme secretion (acinar cells) Has 3 possible major effects: - Decreased enzyme activity → reduced digestion, poor absorption and weight loss - Decreased micelle formation (change in pH and loss of lipases) → steatorrhea - Increase acidity → ulcers, fiborsis of pancreas (not always the case, but can be)

Answer 11

Secretin test (stimulates bicarbonate secretion from ductal cells) showed loss of bicarbonate output Glucose Tolerance test showed loss of blood sugar control - pancreas is involved in regulation of blood sugar through release of Glucagon by a-cells and release of insulin through b-cells (in Islet of Langerhans) *One could also detect higher CCK secretion to try to stimulate enzyme secretion from acinar cells, but this can be dangerous because enzymes are being produced, but are stuck in the pancreas → can be damaging → Give a Somatostatin analogue to inhibit enzyme secretion from acinar cells

Answer 12

1. Production of alkaline juices → to neutralize chyme 2. Production of Bile acids → for fat digestion and absorption 3. Degrade products of metabolism 4. Detoxify poisonous and harmful subtances (ex: breakdown product of Heme) 5. Excrete waste materials in bile

Answer 13

1. Opens the sphincter of Oddi (allows entry of contents in the duodenum) 2. Contraction of the gall bladder

Answer 14

- 2 lobes - Largest gland in the body - Can remove ~3/4 and still have adequate function Right and left hepatic ducts → join into the common bile duct - In the absence of a meal, the sphincter of Oddi is closed, the bile goes into the gall bladder and is concentrated - Cystic duct connected Gall bladder to Common bile duct

Answer 15

~ 500 mL much less than pancreas (1500 mL/day)

Answer 16

Periportal hepatocytes: - closer to the portal vein - handle glucose (Gluconeogenesis + Glycogen deposition) - oxidize metabolites - produce bil salts (new + recycling/conjugation) → common bile duct and duodenum Perivenous hepatocytes: - closer to the other end (common bile duct?) - transform toxins to excrete in the bile and enter the feces (Biotransformation) - Glycolysis/ketogenesis/fat deposition - Toxic metabolites → Commone bile duct and duodenum

Answer 17

- Made from cholesterol - Essential for digestion and absorption of fats Primary Bile Acids: - Made by hepatocytes - Soluble in water → can be reabsorbed (at ileum) - Conjugation of Glycine or Taurine residues to Cholesterol → increases water solubility Secondary Bile Acids: - Modified by bacteria in intestines - Decarboxylation of bile salts - Insoluble in water (unconjugated) → excreted in feces

Answer 18

Lack of absorption of fats → fats in feces Due to: - Lack micelle formation - Lack of bile acid production

Answer 19

1. Detoxification of drugs in perivenous hepatocytes (Ethanol) 2. Breakdown of Heme in perivenous hepatocytes (Conjugated bilirubin)

Answer 20

Ethanol → {Aldehyde} → Acetaldehyde → Acetic Acid → Acetyl-CoA (used for energy in cells)

Answer 21

Heme comes from RBC destruction or myoglobin from a meal of meat Heme → Biliverdin (green bile) → Bilirubin (red-orange) Bilirubin ~ Bile pigments (gives color to feces) *Not soluble → conjugated in perivenous hepatocytes *Water soluble Bilirubin diglucuronide = conjugated bilirubin which can move into the bile

Answer 22

The right upper quadrant of the abdomen

Answer 23

1. Stores and concentrates bile 2. Delivers bile to the SI during a meal Concentration of hepatic bile = 26.0 mM vs Gallbladder bile = 145.0 mM Gallbladder contraction is stimulated by CCK and Gastrin

Answer 24

Cholesterol Gallstones (80%): - Caused by too much cholesterol in the liver due to high fat/sugar diet → can't be fully processed into soluble bile acids or held into micelles → precipitates - Decrease concentration of bile acids and phospholipids → cholesterol is not held within icelles and precipitates as crystals Pigment Gallstones (20%): - Overload of unconjugated bilirubin (hemolysis, burns) - Bile becomes supersaturated and precipitates - Free bilirubin combines with Ca++ - Burn patients → high hemolysis → lots of heme to breakdown

Answer 25

meal → Gallbladder contraction (due to CCK secretion) → Bile flows through cystic duct, but presence of gallstones causes distension and pain

Answer 26

Pale color: absence of bile pigment Greasy and floating: presence of abnormally large quantities of unabsorbed fat *Bile is not properly secreted?

Answer 27

Gallstones can cause jaundice, leading to yellowing of the sclera (whites of the eyes) and darkening of urine, because a gallstone can block the bile duct, preventing bile, which contains bilirubin, from flowing into the intestines, causing (conjugated) bilirubin to build up in the bloodstream and be excreted in the urine - Bilirubin is not very water soluble - Hepatocytes conjugate bilirubin secreted into intestines → most will be secreted in feces - Intestinal bacteria modify bilirubin → deconjugated bilirubin can re-enter circulation (very small amounts) → converted to Urobilinogen (colourless)

Answer 28

jaundice = yellowing of skin, sclera and mucous membranes Plasma bilirubin > 34 uM/L *Bilirubin is not very water soluble

Answer 29

Last form of bilirubin modified by bacteria in the SI → ready to go into the feces

Answer 30

The gallbladder concentrates the bile, but does not produce it → no problem as long as the patient does not have a very fatty meal in 1 sitting because the body will not be able to process all the fat