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Anatomy and Physiology > digestive ii > Flashcards

digestive ii Flashcards

1
Q

Stomach: nerve and blood supply

A

ANS nerve supply

  • sympathetic from thoracic splanchnic nerves via celiac plexus
  • parasympathetic via vagus nerve

Blood supply:

  • celiac trunk (gastric and splenic branches
  • veins of hepatic portal system
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2
Q

Stomach microscopic anatomy

A 
4 tunics
Muscularis and mucosa modified
Muscularis external
-3 layers of smooth muscle
-inner oblique layer allows stomach to churn, mix, move, and break down food

Mucosal pits for secretion of gastric juices

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3
Q

Stomach mucosa

A
  • simple columnar epithelium composed of mucous cells –> secrete 2-layer coat of alkaline mucus (surface layer traps bicarbonate-rich fluid beneath it)
  • dotted with gastric pits, containing gastric glands, producing gastric juices (mostly in body and fundus)

Parietal cell, chief cell, enteroendocrine cells (G cells), mucous neck cells

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4
Q

Stomach mucosa parietal cell

A

secrete HCL –> ph = 1.5-3.5 –> denatures proteins, activates pepsin, breaks down plant walls, and kills bacteria

secretes intrinsic factor = glycoprotein required for absorption of B12 in small intestine –> only func of stomach that’s critical for life

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5
Q

Chief cells

A

secrete pepsinogen = inactive enzyme –> activated to pepsin by HCl and by pepsin itself (positive feedback mechanism)

secretes lipases –> digest 15% of lipids

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6
Q

Enteroendocrine cells

A

secrete chem messengers into lamina propria (NOT LUMEN)

  • act as paracrines –> serotonin and histamine
  • hormones –> somatostatin (also a paracrine) and gastrin
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7
Q

Mucosal barrier

A

harsh digestive conditions in stomach
has mucosal barrier to protect
-thick layer of bicarbonate-rich mucus
-tight junctions between epithelial cells (prevent juice seeping underneath tissue)
-damaged epithelial cells quickly replaced by division of stem cells (surface cells replaced wvery 3-6 days)

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8
Q

Digestive breakdown process in stomach

A
  • mechanical breakdown
  • denaturation of prots by HCl
  • enzymatic digestion of prots by pepsin (and milk protein by rennin in infants)
  • enzymatic digestion of lipids by both salivary and gastric lipase
  • delivers chyme to small intestine

Lipid soluble stuff, like alcohol and aspirin absorbed into blood

Only stomach fun esential to life is secretion of intrinsic factor for B12 absorption

  • B12 needed –> for RBC maturation
  • lack of intrinsic factor causes pernicious anemia
  • treated with B12 injections
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9
Q

Rgulation of gastric secretions: overview of neural and hormonal

A

Both neural and hormonal mechanisms
Gastric mucosa makes up to 3 L of gastric juices per day
Vagus nerve stimulation increases the secretions
Sympathetic stimulation decreases the secretions

Hormonal control largely gastrin

  • increases enzyme and HCl secretions
  • most small intestine secretions are gastrin antagonists
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10
Q

Regulation of gastric secretions: first 2 of the 3 phases

A
  1. Cephalic (reflex) phase = conditioned reflex triggered by aroma, taste, sight, thought
  2. Gastric phase –> lasts 3-4 hrs; 2/3 gastric juice released
    - stimulated by distension, peptides, low acidity, gastrin (major stimulus)
    - enteroendocrine G cells stimulated by caffein, peptines, and rising pH –> stimulate gastrin
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11
Q

Stimuli of gastric phase

A

Gastrin stimulates enzyme and HCl release
-low pH inhibits gastrin secretion (as between meals)

Buffering action of ingeted proteins –> rising pH stimulates gastrin secretions

3 chems: ACh, histamine, and gastrin stimulate parietal cells through second-messenger system –> all 3 are necessary for max HCl secretion

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12
Q

HCl formation

A

Parietal cells pump H+ from carbonic acid breakdown into stomach lumen

  • K+ goes into cells to balance charge
  • HCO3- is made from carbonic acid breakdown
  • HCO3- enters blood through Cl- and HCO3- antiporter –> blood leaving the stomach is more alkaline (called alkaline tide)
  • Cl- follows the H+ to make HCl
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13
Q

Third phase of gastric secretion

  • stimulatory component
  • inhibitory component
  • override
A

Intestinal phase:

Stimulatory component
-partially digested food enters small intestine –> brief intestinal gastrin release

Inhibitory effects (enterogastric reflex and enterogastrones)

  • chyme with H+, fats, peptides, irritating substances –> inhibit gastrin
  • enterogastrones = secretin, cholecystokinin (CCK), vasoactive intestinal peptide (VIP) –> all inhibit gastrin

If small intestine is pushed to accept more chyme = “dumping system”

  • naesea and vomiting
  • common in gastric reduction for weight loss
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14
Q

Enterogastric reflex

A

3 reflexes act to:

  • inhibit vagal nuclei in medulla
  • inhibit local reflexes
  • activate sympathetic fibers –> tightening of pyloric sphincter –> no more food entry to small intestine

These lead to decreased gastric activity and protects the small intestine from excessive acidity

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15
Q

Response of stomach to filling

A

stretches to accommodate incoming food

  • pressure constant until 1.5 L food ingested
  • reflex-mediated receptive relaxation
  • coordinated by swallowing center of brainstem

gastric accommodation –> plasticity (stress-relaxation response) of smooth muscle –> basically is capable of establishing a new set point of stretch

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16
Q

Gastric contractile activity

A

Peristaltic waves move toward pylorus at rate of 3 per minute

  • basic electrical rhythm (BER) set by enteric pacemaker cells (formerly interstitial cells of Cajal)
  • pacemaker cells linked by gap junctions –> entire muscularis contracts

Distension and gastrin increase force of contraction

Most vigorous near pylorus

Chyme is either

  • delivered in 3 ml spurts to duadenum or
  • forced backward into stomach (retropulsion)
17
Q

Regulation of Gastric emptying

A

as chyme enters duadenum

  • receptors respond to stretch and chem signals
  • enterogastric reflex and enterogastrones inhibit gastric secretions and duodenal filling

Carb-rich chyme moves quickly through duodenum

Fatty chyme remains in duodenum 6+ hrs

18
Q

Jejunum and Ileum

A

Jejunum extends from duodenum to ileum and is about 2.5 m long

Ileum joins large intestine at ileocecal valve and is about 3.6 m long

19
Q

Liver and Gallbladder

A

Liver
-biggest gland in body
-4 lobes –> right, left, caudate, and quadrate
-many funcs: only digestive func is bile production (bile = fat emulsifier)
BILE IS NOT AN ENZYME

Gallbladder

  • chief function = bile storage (w/o water from liver)
  • DOES NOT MAKE BILE, JUST STORES IT
20
Q

Liver Associated Structures

A
  • lesser omentum anchors liver to stomach
  • hepatic artery and vein enter at porta hepatis

bile ducts

  • common hepatic duct leaves liver
  • cystic duct connects to gallbladder
  • bile duct formed by union of common hepatic and cystic ducts
21
Q

Liver microscopic anatomy

A

Liver lobules

  • hexagonal structural and functional units
  • composed of plates of hepatocytes (liver cells) –> filter and process nutrient rich blood
  • central vein in longitudinal axis

Portal triad at each corner of lobule

  • Branch of hepatic artery supplies oxygen
  • branch of hepatic portal vein brings nutrient-rich blood
  • bile duct receives bile from bile canaliculi and takes it to GI tract

Liver sinusoids = leaky capillaries bt hepatic plates

Stellate macrophages (hepatic macrophages/ Kupffer cells) in liver sinusoids remove debris and old RBCs

22
Q

Hepatocytes

A

increased rough and smooth ER, golgi, peroxisomes, and mitochondria

func:

  • process bloodborne nutrients
  • store fat-soluble vitamins
  • perform detoxification
  • makes 900 ml bile per day —–> KNOW THIS
23
Q

Liver regenerative capacity

A
  • restores full size in 6-12 months after 80%

- injury –> hepatocytes –> growth factors –> endothelial cell production

24
Q

Bile

A

yellow-green alkaline solution containing:

  • bile salts = cholesterol derivatives that function in fat emulsification and absorption
  • bilirubin = pigment formed from heme –> bacteria break down in intestine to stercobilin –> brown color of feces
  • cholesterol, triglycerides, phospholipids, and electrolytes

BILES ISN’T A DIGESTIVE ENZYME –> it doesn’t break chem bonds –> it emulsifies, turning big fat globules into little fat globules

25
Q

Enterohepatic circulation

A

-recycles bile salts

bile salts –> duodenum –> reabsorbed from ileum –> hepatic portal blood –> liver –> secreted into bile

26
Q

Gallbladder

A
  • Thin-walled muscular sac on ventral surface of liver
  • stores and concentrates bile by absorbing water and ions
  • muscular contractions release bile via cystic duct which flows into bile duct. –> contractions are stimulated by CCK from small intestine
27
Q

Pancreas

A

Location

  • mostly retroperitoneal, deep to greater curvature of stomach
  • head encircled by duodenum –> tail abuts spleen

Endocrine func: pancreatic islets secrete insulin and glucagon

Exocrine func:

  • acini (clusters of secretory cells) secrete pancreatic juice to duodenum via main pancreatic duct
  • zymogen granules of acini cells contain proenzymes
28
Q

Pancreatic juice

A

1200-1500 ml/day

  • watery alkaline solution (ph 8) neutralizes chyme
  • electrolytes (mostly HCO3-) actually secreted by cells lining ducts, not acinar cells

Enzymes

  • amylase, lipases, nucleases secreted in active form but require ions or bile for optimal activity
  • proteases secreted in inactive form
29
Q

Protease activation in duodenum

A
  • trypsinogen activated to trypsin by brush border enzyme enteropeptidase (enterokinase)
  • Procarboxypeptidase, proelastase, and chymotrypsinogen activated by tripsin
30
Q

Regulation of Bile Secretion

A

Bile secretion stimulated by

  • bile salts in enterohepatic circulation
  • Secretin from intestinal cells exposed to HCl and fatty chyme

Hepatopancreatic sphyncter closed unless digestion active –> bile stored in gallbladder
-released to small intestine usually only with contraction

Gallbladder contraction stimulated by

  • cholecytokinin (CCK) from intestinal cells exposed to acidic, fatty chyme
  • vagal stimulation (minor stimulus)
  • CCK also causes secretion of pancreatic juice and hepatopancreatic sphincter to relax
31
Q

Regulation of Pancreatic Secretion

A

CCK induces secretion of enzyme rich pancreatic juice by acini

  • secretin causes secretion of bicarbonate-rich pancreatic juice by duct cells
  • vagal stimulation also causes release of pancreatic juice (minor stimulus)
32
Q

Steps for release of bile and pancreatic juice

A
  1. chyme entering duodenum causes duodenal enteroendocrine cells to release cholecystokinin (CCK) and secretin
  2. CCK and secretin enter bloodstream
  3. CCK induces secretion of enzyme-rich pancreatic juice. Secretin causes secretion of HCO3- rich pancreatic juice
  4. Bile salts and, to a lesser extent, secretin transported via bloodstream stimulate liver to produce bile more rapidly
  5. CCK (via blood stream) causes gallbladder to contract and Hepatopancreatic Sphincter to relax. Bile enters duodenu
  6. During cephalic and gastric phases, vagal nerce stimulates gallbladder to contract weakly

Anatomy and Physiology (50 decks)

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