Gastrointestinal System Flashcards
GI Tract/Alimentary Tract
Function: Movement of food, Secretion of digestive juices & digestion of food, Absorption of H2O, electrolytes, vitamins and digestive products, Circulation of blood through GI organs to carry away absorbed substances, Local, nervous system and hormonal control of processes
GI Tract/Alimentary Tract Parts
i. Mouth (Oropharynx)
ii. Esophagus
iii. Stomach
iv. Small Intestine
v. Large Intestine
vi. Rectum
vii. Anus
GI Tract/Alimentary Tract Accessory Organs
i. Liver
ii. Gallbladder
iii. Exocrine Pancreas
GI Tract Structure
i. Structure holds throughout entire tract with minor variations
ii. Four layers
1. Mucosa
a. Epithelium w/ mucus secreting cells
i. Folds/plica/rugae
ii. Villi containing lacteals
b. Lamina propria
c. Muscularis mucosa
2. Submusoca – connective tissue
3. Muscularis
a. Longitudinal
b. Circular (thicker, inside)
c. Oblique (in stomach only)
4. Serosa (Adventitia, continuous with mesentery. Fold of serous membrane)
Enteric Nervous System
Two plexuses of intrinsic nerves, embedded within the GI tract walls, forming the Enteric Nervous System, a main branch of the ANS. These circuits regulate motility, blood flow and secretions
Enteric Nervous System : Plexuses of intrinsic nerves
- Submucosal (Meissner Plexus) in submucosa
a. Senses environment within the lumen, regulating blood flow, directing epithelial cell function - Myenteric (Auerbach Plexus) in muscle layers
a. Digestive tract motility
Enteric Nervous System Control - PNS
PNS mediates secretion, motility, pain sensation, intestinal reflexes (i.e., LES relaxation). Increases activity of enteric system. Everything except chewing, swallowing and defecation. Nerve endings secrete ACh.
Enteric Nervous System Control - SNS
SNS inhibits motility, produces vasoconstriction. Nerve endings secrete norepinephrine and a little epinephrine
Nervous System Control - Enteric plexuses
local stimulation with the GI walls; intrinsic.
- Myenteric responsible for GI movement
a. Increased tonicity, intensity, rate, velocity of conduction
b. Inhibits sphincter tone (pylorus and ileocecal valve) - Meissner (submucosal) responsible for GI secretion and local blood flow
a. Very small segment of GI wall, leads to various degrees of unfolding of wall - Both stimulated by PNS/SNS, but can also function alone.
Enteric Nervous System Control
iv. Swallowing center in medulla and pons mediate involuntary swallowing
v. Main neurotransmitters
1. ACh – excites GI activity
2. Norepinephrine – inhibits GI activity (also epinephrine from adrenal medulla)
3. Others provide mix of excitatory and inhibitory (ATP, serotonin, dopamine, CCK, etc.)
GI Electrical Activity
i. Smooth muscle is single unit – when AP is received, contraction travels in all directions, distance determined by excitability of the muscle
ii. Rhythmic Slow waves – in smooth muscle, slow, undulating changes in resting membrane potential. Varying intensity. Do not cause contraction
iii. Increasing positive charge of slow waves excite appearance of spike potentials, which excite muscle contraction. True AP.
1. Nerve fibers: AP caused by rapid Na+ entry. Fast. But only sodium, so no contraction
2. GI tract: channels allow lots of Ca++ to enter with Na+. Slower, leading to long duration of AP. Ca++ enters, and contraction occurs.
3. Baseline voltage of resting membrane can also change.
4. Tonic & rhythmic contractions possible.
Splanchnic Flow
i. Blood flow with nutrients from the gut, spleen, and pancreas all travels to the liver via the portal vein
ii. Except fats which do not go through the portal vein, but instead travel through the lymphatic system, bypassing the liver.
iii. In the liver, blood passes through sinusoids to hepatic veins and then to vena cava
iv. Allows reticuloendothelial cells in liver sinusoids to remove bacteria and particles, preventing transport to the rest of the body
Oropharynx : Function
Chew, mix with saliva, and swallow
Oropharynx : Anatomy
a. Salivary Glands
i. Parotids – serous
1. Ptyalin (salivary amylase, enzyme for digesting starches)
ii. Sublingual – serous and mucus
iii. Submandibular – serous and mucus
b. Tongue
i. Skeletal muscle (hyoid bone!) with thousands of taste buds.
ii. Pushes food into a bolus, propels posteriorly and upward
c. Teeth
i. Mastication, mediated by reflexes
d. Constrictor muscles of the pharynx
i. Open and close entry to the nasopharynx
Saliva
1L per day of water, mucus, bicarbonate, potassium, salivary amylase, lingual lipase, chloride, sodium, IgA
i. Hypotonic
ii. Maintains pH 6.0-7.0, favoring amylase digestive activity (carbohydrates)
iii. Lingual lipase needs pH 4.5 – 5.4 to digest fats (seen in stomach)
iv. Neutralizes bacterial acids, prevents tooth decay
v. IgA helps prevent infection
Oropharynx : Stimulation
a. PNS & SNS both stimulate salivation
b. No hormonal regulation
c. Cephalic phase stimulation begins
i. Sour, smooth excite
ii. Food contacts epithelium
iii. Irritation/nausea – saliva increases, removes irritant, dilutes, neutralizes
iv. Also by insulin secretion in hyperglycemic environment (not if normoglycemic)
v. Aggression
Oropharynx : Inhibition
a. Anxiety, fear, dehydration, rage
b. Rough texture inhibits cephalic phase
Oropharynx : Process
a. Voluntary/Involuntary components
b. Food enters mouth
i. Carbohydrates (sucrose/cane sugar, lactose/milk products and starches/non-animal such as potatoes, grains) and cellulose which is indigestible
ii. Proteins
iii. Fats
c. Mixed with saliva, segmented into bolus by tongue and propelled back and upward
i. Some carbohydrate digestion occurs (5%)
d. Pharynx muscles contract and raise soft palate to prevent entry of bolus into nasopharynx
e. Respiration inhibited by the medulla swallowing center
f. Laryngeal muscles elevate the larynx and glottis to enlarge opening to the esophagus
g. Epiglottis slides back to close off the larynx and trachea
h. (Upper Esophageal Sphincter relaxes and food enters esophagus)
i. Process takes < 1 second
Oropharynx : Pathophysiology
Apthous ulcers – disruption to the mucosal surface from trauma, infection or inflammation
Esophagus : Function
Passage of food, liquid and saliva from the oropharynx to the stomach through peristalsis
Esophagus : Anatomy
a. C6 to T10-T11, 25 cm long
b. Behind trachea, in front of erector muscles, passes through the diaphragm and ends at the cardia
c. Upper Esophageal sphincter (functional, not anatomic)
i. Voluntary with swallow, mediated by swallowing center
ii. Maintains basic tonicity to prevent air entry into esophagus during respiration
d. Lower Esophageal sphincter (functional, not anatomic)
i. Involuntary
ii. Maintains basic tonicity to prevent backflow from stomach
e. Mucosa
i. Epithelium w/ mucus secreting cells
ii. Lamina propria
iii. Muscularis mucosa
f. Submucosa
i. Loose connective tissue,
ii. Blood vessels
iii. Lymphatics & lymphoid follicles
iv. Meissner plexus
v. Mucus-secreting glands
g. Muscularis Propria
i. Inner circular layer – ring contractions
ii. Auerbach plexus (aka Myenteric)
iii. Outer longitudinal layer – shortening contractions
iv. Muscularis Propria muscle
1. Proximal 1/3 skeletal
2. Middle 1/3 smooth & skeletal
3. Distal 1/3 smooth
h. Adventitia
i. Connective tissue fascial layer surrounding esophagus (retroperitoneal)
Esophagus : Stimulation
a. Meissner plexus
b. Auerbach plexus
c. Vagus nerve (along adventitia)
Esophagus : Inhibition
a. LES sphincter tone relaxes with non-adrenergic, non-cholinergic vagal impulses
b. LES sphincter tone relaxes with progesterone, secretin and glucagon
Esophagus : Process
a. (Epiglottis slides back to close off the larynx and trachea)
b. UES relaxes with swallowing
c. Primary peristalsis
i. Coordinated contractions to propel bolus down esophagus
ii. Each wave of contraction preceded by wave of relaxation
iii. Gravity-assisted
d. If bolus gets stuck, stretch receptors signal swallowing center to contract in secondary waves of peristalsis until esophagus is cleared.
e. Just before bolus arrives at LES, LES relaxes with relaxation wave to allow passage of bolus to stomach
Esophagus : Pathophysiology
a. Esophageal spasms
i. Greater stretch of esophagus leads to greater contractions. Tx: Antispasmodics, dietary changes.
b. Esophageal strictures
i. Narrowing of esophagus from scar tissue. Associated with GERD.
c. Esophageal rings
i. Bands of esophageal muscle tissue forming in the lower esophagus. Associated with GERD. Tx: Dietary changes, esophageal dilation
ii. Achalasia
1. LES fails to relax, prohibiting food from entering the stomach. Esophageal swelling, infection, ulceration. Tx: Antispasmodics for smooth muscle, balloon placement
Stomach : Function
a. Stores food (Food stacks vertically, fluids to antrum)
b. Secretes digestive juices
c. Mixes food and digestive juices via peristalsis
d. Propels partially digested food (chyme) into the duodenum
Stomach : Anatomy : General
a. Bounded by Lower Esophageal Sphincter (LES), Greater and Lesser Curvatures, and Pyloric Sphincter
b. At rest, small (50 mL)
c. Peritoneum – serous membrane with visceral and parietal surfaces
d. Peritoneal cavity – space between peritoneal membranes – lubricates, prevents friction
Stomach : Anatomy : Mesentery and Fundus
e. Mesentery – fold of the peritoneum attaching the stomach, small intestine, pancreas and spleen t the posterior wall of the abdomen. Ffacilitates intestinal motility, houses blood vessels, nerves and lymphatics
f. Fundus (upper), Body (middle) and Pylorus/ Antrum (lower)
i. Fundus stores food pre-processing
ii. Muscle layers thicken distally
Stomach : Anatomy : Mucosa -
Glandular Epithelium (except at lesser curvature), folded into rugae
1. Rugae expand and fold
a. Increase volume without increasing pressure
b. Increase surface area utilized for digestion
Stomach : Anatomy : Mucosa - Oxyntic Glands
Oxyntic Glands (fundus and body)
a. Parietal cells secrete HCl and Intrinsic Factor (needed to absorb Vitamin B12) b. Chief cells (aka peptic cells) secrete pepsinogen, which requires HCl to split to pepsin, a digestive enzyme active at pH 1.8-3.5, but inactive at pH > 5. c. ECL cells secrete histamine (stimulates gastric acid secretion) d. D cells secrete somatostatin (inhibits gastrin-gastric acid pathway) e. G cells secrete gastrin (stimulates gastric acid secretion) f. Mucous neck cells secrete mucus (Goblet cells)
Stomach : Anatomy : Mucosa - Pyloric Glands
Pyloric Glands (antrum)
a. G cells secrete gastrin (stimulates gastric acid secretion) b. D cells secrete somatostatin c. Mucous neck cells secrete mucus (Goblet cells)
Stomach : Anatomy : Mucosa - Surface Mucous Cells
Surface Mucous Cells
a. Between the glands, special mucous cells secrete an abundance of viscid mucus. Protective, coats 1 mm thick. Very alkaline. Increases with proximity of food to epithelium
ii. Lamina propria
iii. Muscularis mucosa
Stomach : Anatomy : Submucosa
i. Loose connective tissue,
ii. Blood vessels
iii. Lymphatics & lymphoid follicles
iv. Meissner’ s plexus
v. Mucus-secreting glands
Stomach : Anatomy : Muscularis Propria
i. Inner oblique layer – churning
ii. Middle circular layer
iii. Auerbach’ s plexus
iv. Outer longitudinal layer – shortening contractions
Stomach : Anatomy : Serosa
i. Connective tissue continuous with the peritoneum (intraperitoneal)
Stomach : Anatomy : Pyloric Sphincter
Separating stomach from duodenum. Tonic contraction, allows fluids to pass. Widens with repeated peristaltic contractions
Stomach : Stimulation
a. Secretions lowest in the morning, highest in the afternoon and evening
b. Secretions increase with aggression or hostility
c. Cephalic phase stimulates secretions before food arrives in stomach (sight, smell, taste, thought)
d. Gastric phase secretions
i. PNS - Stimulation of digestive secretions, contractions, relaxation of sphincters
ii. Enteric – communicates with PNS and SNS
Stomach : Inhibition
a. SNS - Inhibition of GI secretion, contraction of sphincters and blood vessels
b. Secretion inhibited by bad tastes, rage, fear, pain
Stomach : Process
a. PNS stimulation causes release of digestive secretions (HCl, Intrinsic Factor, histamine, mucus), contractions, and relaxation of sphincters
i. Swallowing causes fundus to relax (receptive relaxation, Vagovagal reflex), and food passes through LES
1. Allows for increased volume without increased pressure
ii. HCl and Pepsin break down food fibers and protein, producing Chyme – liquid, undigested particles
iii. Stomach distends & pH rises due to arrive of acidic food bolus
iv. If contents contain carbohydrates, digestion by salivary amylase continues (40%)
v. If contents contain protein, gastrin is released from G cells in the antrum, stimulating gastric acid and histamine secretion. Protein digestion products buffer the acid, increasing the pH. Pepsinogen is released from Chief cells and uses HCl to split to pepsin. Pepsin and HCl begin to digest proteins.
vi. If contents contain fat, swallowed lingual lipase begins digestion
5. Emulsification & lipolysis – Mechanical action in the stomach and small intestine break triglycerides into tiny particles. Process is continued in duodenum.
Stomach : Process : Peristalsis in the Stomach
i. Pace mediated by cells of Cajal (pacemakers for slow waves)
ii. Contractions stimulated by Auerbach plexus at any point by distension, chemical or irritant, also from strong PNS signal
iii. Each contraction begins 2-3 cm back (pinching off more food), pushing 5-10 cm before dying out. Downstream relaxation.
1. Greater volume (distension) results in faster contractions (emptying)
a. Stretch receptors activate myenteric reflex, increase pump rate and decrease pyloric tone
iv. Velocity increases with downward progression
1. Retropulsion – propulsion back from sphincter, results in more mixing
Stomach : Process : Reflexes
a. If gastric motility and secretion increase, the gastroileal reflex increases ileal motility , emptying the ileum in preparation for more chyme
b. Gastroenteric reflex – distension of the stomach triggers peristalsis
Stomach : Pathophysiology
Gastritis – Permeability of mucus layer allows digestive enzymes to attack mucosa. Helicobacter Pylori decreases mucosal barrier and increases acid secretions.
Small Intestine : Function
Absorption and propulsive peristalsis
Small Intestine : Anatomy
a. 5 meters, 3 sections
i. Duodenum
1. From pylorus to suspensory ligament (Treitz ligament)
2. Retroperitoneal
ii. Jejunum
1. Ends at ileum
2. Hangs from mesentery with ileum
3. Intraperitoneal
iii. Ileum – ends at ileocecal valve (sphincter)
1. Hangs from mesentery with jejunum
2. Intraperitoneal
b. Peritoneum
c. Peritoneal cavity
d. Mesentery
Small Intestine : Anatomy : Mucosa - Epithelium
- Circular folds/Valves of Kerckring/plicae circulares
a. Two folds of mucous membrane, do not change shape
b. Increase absorptive area, slow the passage of food
c. Covered with villi - Villi increase surface area for digestion and absorption
- Villi secrete digestive enzymes and absorb nutrients
a. Absorptive columnar cells (tight junctions) to absorb water and electrolytes
i. Microvilli create a brush border, further increase absorptive surface
ii. Brush border has thick “unstirred” layer of fluid to absorb other substances
iii. Goblet cells secrete mucus
b. Lacteal with lymphatic channel to absorb and transport fat molecules then drain to thoracic duct
Small Intestine : Anatomy : Mucosa - Epithelium/Brunner’s Glands
a. Mucous glands at top of duodenum
b. Secrete alkaline mucus (bicarbonate) for protection, neutralization of acid
Small Intestine : Anatomy : Mucosa - Epithelium/Crypts of Leiberkuhn
Secrete digestive juices, hold undifferentiated cells to replace epithelial population every 4-7 days
Small Intestine : Anatomy : Mucosa - Epithelium/I-cells
(duodenum and jejunum)
Secrete Cholecystokinin which slows gastric emptying and increases bile ejection
Small Intestine : Anatomy : Mucosa
ii. Lamina propria
1. Peyer’s Patches (only in ileum)
iii. Muscularis mucosa
Small Intestine : Anatomy : Submucosa
i. Brunner’s glands (only in duodenum)
ii. Meissner’ s plexus
Small Intestine : Anatomy : Muscularis Propria
i. Inner circular layer – ring contractions
ii. Auerbach plexus (aka Myenteric)
iii. Outer longitudinal layer – shortening contractions
Small Intestine : Anatomy : Serosa/Adventitia
Serosa/Adventitia
Small Intestine : Anatomy : Ileocecal sphincter
i. When cecum is distended, both cecum contraction and ileal peristalsis increase to move contents downward
ii. When cecum is irritated (i.e., inflamed appendix), sphincter spasms causing partial paralysis of ileum, preventing movement of contents downward
Small Intestine : Anatomy : Ileocecal valve
i. Valve protrudes into cecum
ii. Forcefully closes with buildup in cecum. Lips reverse into ileum to prevent backflow
Small Intestine : Stimulation
a. Intestinal phase: Peristalsis triggered by stretch of duodenum from entrance of chyme
b. Hormones gastrin, CCK, insulin, motilin, serotonin enhance peristalsis
Small Intestine : Inhibition
a. Distention, irritant, acidity, CCK, GIP and Secretin delay emptying
b. Presence of acid, fat, protein breakdown products, hyperosmotic or hypo-osmotic fluids, or irritants in duodenum stimulate release of CCK and GIP into circulation
i. CCK stimulates release of bile from the gallbladder and enzymes from the pancreas. Inhibits Chief/Parietal/Peristalsis
ii. GIP (Gastric Inhibitory Polypeptide, or Glucose-dependent Insullinotropic Peptide) stimulates release of insulin from the pancreas. Inhibits Chief/Parietal/Peristalsis.
iii. Decrease in pH stimulates release of Secretin into circulation (inhibits Chief/Parietal/Peristalsis)
Small Intestine : Process : 1. Segmentation
Mix and cut – chain of sausages
Small Intestine : Process : 2. Peristalsis
Movement through intestine
Small Intestine : Process : 3. Interdigestive contractions
Slow waves propel residual contents into colon
Small Intestine : Process : 4. Digestion & absorption of carbohydrates, proteins and fats
i. Addition of small intestine sucrase, maltase and lactase, and addition of pancreatic amylase, facilitate digestion of carbohydrates
1. Absorbed and transported to villus capillaries then liver
ii. Addition of pancreatic enzymes trypsinogen, chymotrypsin facilitates digestion of proteins
1. Most protein absorbed in small intestine
2. 5-10% eliminated in feces
3. Absorbed and transported to villus capillaries then liver
iii. Addition of bile salts from the liver and lipase from the pancreas facilitate digestion of fats
1. Partially digested fats (from lingual lipase action in stomach) bathed with bile (bile salts & Lecithin)
a. Prevent fat reformation, increase surface area
2. Pancreatic lipase splits fats into free fatty acids through lipolysis
a. Absorbed through unstirred layer of brush border
3. Micelle formation using the bile salts for efficient absorption
a. Bile stays behind for enterohepatic circulation recycling
b. Fat breakdown products to lacteals then liver
4. Resynthesis of triglycerides and phospholipids in the cell to chylomicrons. Enter intercellular space, lacteals, lymphatic channels and systemic circulation
Small Intestine : Absorption of Vitamins, Minerals : Calcium
i. Absorbed via passive , active and carrier proteins
ii. Absorption enhanced by bile salts, which also facilitate absorption of Vitamin D
iii. Special: Increased demand leads to increased uptake
Small Intestine : Absorption of Vitamins, Minerals : Vitamin B12
i. Released from animal proteins, liver & kidney by gastric and pancreatic enzymes
ii. Binds to Intrinsic factor, making it resistant to digestion
iii. Absorption in terminal ileum. Necessary for normal erythrocyte maturation.
Small Intestine : Absorption of Vitamins, Minerals : Iron
i. Released from heme (hemoglobin and myoglobin) in animal proteins. Also from inorganic sources readily absorbed (fruit, cereals, eggs, vegetables)
ii. Special: amount absorbed = amount required. Absorbed more rapidly if deficiency exists.
iii. Absorption facilitated by Vitamin C (changes iron ferrin to iron ferrous)
iv. Absorption reduced when it binds to Ca++, phosphoproteins (milk antacids) and tea
Small Intestine : Absorption of Fluids & Electrolytes
a. 80-95% absorbed in small intestine, remainder absorbed in colon
b. Sodium enters cell in exchange for hydrogen
c. Chloride enters cell in exchange for bicarbonate
d. Potassium moves passively by diffusion across its gradient
Small Intestine : Reflexes
a. If ileum is distended, the ileogastric reflex inhibits gastric motility into the small intestine
b. If any segment of the small intestine is over-distended, the Intestinointestinal reflex inhibits intestinal motility
c. The gastrocolic reflex initiates propulsion through the colon to the sigmoid and rectum, stimulating defecation
Small Intestine : Pathophysiology
a. Peristaltic rush – in response to irritant, pushes contents rapidly through the intestine and colon, resulting in diarrhea
b. Prolonged diarrhea – hypokalemia, metabolic acidosis
Large Intestine : Function
a. Absorb water and electrolytes (proximal half, 5-8 L daily, over 8-15 hours)
b. Store feces (distal half)
Large Intestine : Anatomy 1 of 3
a. 3-6 feet long, sluggish (speed not required)
b. Peritoneum
c. Peritoneal cavity
d. Mesentery – drapes over the front
e. Ileocecal valve between ileum of the small intestine and the cecum
f. Cecum – pouch receives chyme from small intestine
i. Tenaie coli present
g. Vermiform appendix – attached, little or no physiologic function
Large Intestine : Anatomy 2 of 3
h. Ascending colon, Transverse colon, Descending colon
i. Mucosa
1. Rugae
2. Many Crypts of Leiberkuhn
a. Secretion of bicarbonate
b. Secretion of mucus
c. Absorption of chloride ions
ii. Submucosa with Auerbach’s plexus
iii. Muscularis two layers of muscle plus Meissner’s plexus
iv. Serosa
v. Circular segmentations and tenaie coli form Haustra
Large Intestine : Anatomy 3 of 3
i. Sigmoid colon
i. Contains entirely waste/feces/excrement
1. Food residue, unabsorbed GI secretions, shed epithelial cells, bacteria
j. O’Beirne sphincter – controls movement of waste from sigmoid colon to rectum
k. Rectum
l. Anal canal
i. Internal (smooth muscle) sphincter
ii. External (striated muscle, voluntary control) sphincter
Large Intestine : Stimulation
a. PNS increases peristalsis
b. Irritant stimulates increased secretion of H2O and electrolytes in addition to normal viscid alkaline mucus in order to dilute the irritant. Diarrhea
c. Intrinsic (myenteric plexus) and extrinsic (vagus) innervation
i. External sphincter innervated from sacral division of spinal cord
Large Intestine : Process Step 1
Ileocecal valve opens in response to last few peristaltic contractions. Closes when proximal colon is distended.
Large Intestine : Process Step 2
Absorption of sodium and chloride ions creates osmotic gradient across the mucosa, causing absorption of water. Minimal sodium and chloride ions left in feces.
Large Intestine : Process Step 3
Contractions
i. Segmentation contractions
1. mix and expose to rugae
ii. Peristaltic contractions
1. slow waves from longitudinal muscle
2. trigger relaxation distally
iii. Giant migrating contractions (mass movements)
1. Push contents toward rectum
2. Force develops over 30 seconds, then relaxes 2-3 minutes. Series lasts 10-30 minutes, ceases, then returns ½ day later.
iv. Mass collects in rectum, triggers desire for defecation
Large Intestine : Process Step 4
Defecation
i. Defecation reflex (rectal reflex) stimulated by rectal wall stretching from movement into the rectum. Inhibited by pain or fear of pain.
1. Internal sphincter relaxes, causing urge to defecate
2. Can be overridden by voluntary external sphincter and muscles of pelvic floor. Rectal wall gradually relaxes and urge passes.
3. Retrograde contraction can displace feces
ii. Facilitated by squatting, sitting or Valsalva
1. Squatting/Sitting straightens angle between rectum and anal canal
2. Sitting/Valsalva Increase intra-abdominal pressure (efficiency of straining)
Large Intestine : Pathophysiology
a. Diarrhea: Increased irritant (i.e., bacterial infection), excess fluid in large intestine exceeding capacity (cholera)
b. Ropy, mucousy feces result from increased PNS stimulation and peristalsis
c. External sphincter paralysis can result from lower spinal cord destruction
d. Peritonitis – Inflammation of the peritoneum. Can be caused by perforation of large intestine or after abdominal surgery. Loops of bowel become plastered together with yellowish fibrinous exudate containing a large number of neutrophils. When this process heals, adhesions may develop, leading to colonic obstruction.
Bacteria in the Gastrointestinal Tract
I. Bacteria increases as tract descends
II. Stomach - sterile due to amount of acid
III. Intestinal tract sterile at birth but becomes colonized with E. coli, Clostridium welchii and Streptococcus after a few hours
i. Normal flora developed by 3-4 weeks old
ii. No digestive or absorptive functions within normal flora, but does help with metabolism of bile salts, hormones, lipids, etc.
Bacteria in the Gastrointestinal Tract : Duodenum
Bacterial growth suppressed by bile acid secretion, intestinal motility and antibody production
Bacteria in the Gastrointestinal Tract : Duodenum and Jejunum
Low concentration of aerobes
i. Primarily streptococci, lactobacilli, staphylococci, enterobacteria, and bacteroides ii. No anerobes proximal to ileum
Bacteria in the Gastrointestinal Tract : Ileum
Anerobes found in ileocecal valve
i. Contains 95% of fecal flora found in 1/3 of solid bulk
1. Bacterioides, clostridia, anaerobic lactobacilli, coliform from ileum to cecum
Accessory Organs
Liver, Gallbladder, Exocrine Pancreas all secrete ezymes for digestion, delivered to the duodenum through ducts
Accessory Organs : Liver
i. Produces bile for digestion of fats and absorption
ii. Receives nutrients absorbed by small intestine and metabolizes/synthesizes them into absorbable forms. Absorbable nutrients released into blood stream or stored
Accessory Organs : Gallbladder
i. Stores and concentrates bile between meals
ii. Ejects bile into ducts for release into the duodenum
Accessory Organs : Exocrine Pancreas
i. Produces enzymes for digestion of carbohydrates, proteins and fats
ii. Produces alkaline fluid to neutralize chyme, creating a duodenal pH to support enzymatic action
Accessory Organs : Liver : Anatomy
a. Largest organ in body, good blood supply
i. Hepatic artery from abdominal aorta with oxygenated blood
ii. Hepatic portal vein from interior/superior mesenteric vein & splenic vein, with a little O2 and many nutrients from the digestive tract
b. Two lobes (right/left) unless viewed from undersurface then include caudate and quadrate
Accessory Organs : Liver : Ligaments
i. Falciform separates right/left lobes, attaches liver to anterior abdominal wall
ii. Roun ligament at free edge of falciform. Remnant.
iii. Coronary ligament
Accessory Organs : Liver : Glisson fibroelastic capsule
i. Covers liver
ii. Contains blood vessels, lymphatics an nerves
iii. Distension causes pain
Accessory Organs : Liver : Hepatocyte – functional cell
i. Join into plates, to liver lobules, to liver lobes
ii. Regenerative capacity
iii. Forms bile by conjugating bile acids to bile salts which are used in emulsification and absorption of fats
1. Leftover bile salts returned to liver for recycling (enterohepatic circulation)
iv. Metabolizes amino acids to carbohydrate and glucose
v. Synthesizes fat, phospholipids, cholesterol, plasma proteins, non-essential amino acids, serum enzymes (AST, ALT, LDH and Alk Phos)
vi. Store of fat, glycogen, iron, copper, and Vitamins B12, A, D and E
Accessory Organs : Liver : Bile canaliculi
Carry bile from hepatocytes to bile ducts, then to CBD (for release to duodenum through Sphincter of Oddi) or to cystic duct for storage in the gallbladder
Accessory Organs : Liver : Sinusoids
Small capillaries next to hepatocytes
Accessory Organs : Gallbladder : Anatomy
Mucosal tissue absorbs water and electrolytes, leaving bile salts, bile pigments and cholesterol
Accessory Organs : Gallbladder : Function
a. Concentrates and stores bile
i. Mucosa absorbs water and electrolytes leaving bile salts, bile pigments and cholesterol
b. Ejects bile approx. 30 minutes after eating
i. Mediated by vagus nerve, CCK from I cells of the small intestine in response to fat, and protein digestion
ii. Bile flows to cystic duct, common bile duct and to Sphincter of Oddi at the Ampula of Vater at the junction with the duodenum. Sphincter opens and bile is forced into the duodenum.
c. Interdigestive
i. Bile flows from hepatocytes though Right or Left hepatic ducts. Encounters closed Sphincter of Oddi, returns via common bile duct to cystic duct, and into the gallbladder.
Accessory Organs : Pancreas : Anatomy
Exocrine pancreas
i. Acinar glands ii. Acinar cells which secrete enzyme portion of fluid iii. Centroacinar cells secrete bicarbonate portion of the fluid
Accessory Organs : Pancreas : Function
a. Secretes aqueous portion: isotonic, K+, Na+ HCO3-, Cl
b. Secretes alkaline portion: neutralizes acidic chyme, improves digestive environment
c. Secretes enzymes for digestion
i. Tryptin, chymotrypsin, carboxypeptidase (inactive for protection)
ii. Alpha amylase (active for carb digestion)
iii. Lipases (for fat hydrolysis)
d. Secretions drain through duct system to pancreatic duct, to CBD at Ampulla of Vater
e. (Inactive enzymes activated by enterokinase in duodenum)
Acute Pancreatitis
Upper abdomen sudden onset of pain. Sudden inflammation of the pancreas. May be due to blockage of a duct, trauma, penetrating ulcers, carcinoma, etc. Tx: IV fluids, pain medications. If gallstones blocking, may require surgery.
Cholera
Bacterial infection (Vibrio cholera) of the small intestine with profuse watery diarrhea and vomiting. Transmitted via food and water by contact with an infected person’s feces. Diarrhea, vomiting, bluish-grey sin. Tx: Oral rehydration and antibiotics. Current epidemic in Haiti.
Acute Cholecystitis
Pain in the middle to upper right quadrant. Trapping of bile in the gallbladder, often by blockage of the bile duct. Leads to pain, inflammation, irritation, pressure, swelling. Fluids, possibly antibiotics. If stones, may require surgery.
Diverticulitis
Feces get trapped in diverticula, leading to inflammation and infection. LLQ belly pain, multiple symptoms. Tx: Liquid diet, antibiotics. Diverticulosis is similar but lesser pathology, often asymptomatic.
