Download Physiology Ch 66 p799-805 [4-25

Physiology Ch 66 p799-805
Physiology of Gastrointestinal Disorders
Disorders of Swallowing and Esophagus:
1. Paralysis of Swallowing Mechanism – damage to 5th, 9th, and 10th cranial nerve will damage
swallowing mechanism. Poliomyelitis and encephalitis will also prevent normal swallowing by
damaging swallowing center in brain
-muscle dystrophy or myasthenia gravis can prevent it as well
-abnormalities include complete abrogation of swallowing act, failure of glottis to close, failure
of soft palate and uvula to close so food refluxes into nose
-under deep anesthesia, patients can vomit materials from stomach, which do not get
swallowed down and instead get sucked into trachea
2. Achalasia and Megaesophagus – achalasia is when lower esophageal sphincter fails to relax
during swallowing, and food fails to pass into stomach (damage to myenteric plexus)
-if achalasia becomes severe, esophagus cannot empty food for many hours, distending it until it
can hold 1L of food, which becomes infected and can cause ulceration
Disorders of the Stomach
1. Gastritis – Inflammation of Gastric Mucosa – can be superficial/benign or penetrating deeply
and causing complete atrophy of gastric mucosa and causing ulceration by peptic secretions
-gastritis is often caused by bacterial infection of mucosa which can be treated
-several irritants can cause damage leading to gastritis, such as alcohol and aspirin
-absorption from stomach directly into blood is low, but the low level is due to two features of
mucosa:
a. it is lined with resistant mucous cells that secrete mucus
b. it has tight junctions between adjacent epithelial cells forming gastric barrier
-gastric barrier normally resistant to diffusion
-in gastritis, permeability of stomach increases and H+ ions diffuse into epithelium, can ulcerate
-Chronic gastritis can lead to gastric atrophy and loss of stomach secretions – loss of glandular
secretions leads to achlorhydria and potentially pernicious anemia
-Achlorhydria is when stomach fails to secrete HCl and pH fails to fall below 6.5
-Hypochlorhydria is diminished HCl secretino, causing pepsin not to be secreted
-Gastric atrophy may cause pernicious anemia – pernicious anemia is common with gastric
atrophy and achlorhydria
-intrinsic factor is normal gastric secretion by parietal cells that secrete HCl, and IF must
be present for binding Vit. B12 in stomach and absorption of the complex in the ileum
-without IF, only 1/50th of B12 is absorbed and causes failure of RBC maturation
2. Peptic Ulcer – excoriated area of stomach or intestinal mucosa caused by digestion by gastric
juice or duodenal secretions. Most frequent areas are near pylorus, along lesser curvature near
antrum, or lower end of esophagus
-a marginal ulcer can occur where surgical cut has been made between stomach and jejunum
-ulceration occurs due to imbalance between rate of secretion of gastric juice and the degree of
protection given by mucosal barrier and neutralization of gastric acid by duodenal juices
-duodenum is protected by alkalinity of small intestinal secretions, important is
pancreatic secretion which contains high HCO3 that can neutralize HCl and inactivate
pepsin to prevent digestion of mucosa
-HCO3 also provided by Brunners glands and in bile coming from liver
-2 feedback mechanisms ensure that the neutralization of gastric juices is complete:
1. acid entering duodenum inhibits gastric secretion and peristalsis of stomach by
nervous reflexes and hormonal feedback
2. acid in small intestine liberates secretin from intestinal mucosa which goes to
pancreas to promote secretion of pancreatic HCO3 and pancreatic juice
-peptic ulcer can be caused by excess secretion of pepsin or diminished ability of GI to protect
Specific Causes of Peptic Ulcer: H. Pylori breaks down GI mucosal membrane and stimulates
gastric acid secretion
-peptic ulcers in first part of duodenum is found where gastric acid secretion is greater than
normal, and any increase in gastric acid secetion can cause ulceration
-smoking, alcohol, and aspirin increase peptic ulcer risk
Treatment of Peptic Ulcers – use of antibiotics to kill bacteria, acid-suppression drugs
(ranitidine, an antihistaminic that blocks stimulatory effecto f histamine on gastric glands to
reduce gastric acid secretion)
Disorders of the Small Intestine:
1. Abnormal Digestion of Food – Pancreatic Failure – if pancreas fails to secrete juice into
duodenum, bad stuff happens. It occurs in pancreatitis, when pancreatic duct is blocked, after
head of pancreas is removed due to malignancy
-loss of trypsin, chymotrypsin, carboxypeptidase, amylase, lipase and others, and fatty
feces are excreted
-Pancreatitis – most common cause is drinking excess alcohol, and second most common is
blockage of papilla of Vater by a gallstone (both = 90% of all cases)
-eventually, enzymes overcome amount of trypsin inhibitor and activated trypsin,
chymotrypsin, and carboxypeptidase destroy the pancreas
2. Malabsorption by the Small Intestine – Sprue – malabsorption is called sprue
-nontropical sprue called idiopathic sprue, celiac disease, or gluten enteropathy results from
toxic effects of gluten present in certain types of grains, wheat and rye
-gluten destroys enterocytes, causing villi to disappear in severe forms to reduce
absorptive area of the gut
-tropical sprue occurs in tropics and can be treated with antibacterial agents, inflammatory
-malabsorption in sprue – intestinal absorption of fat is more impaired than other digestive
products, and appears in stool, called steatorrhea
-malabsorption causes impaired absorption of proteins carbs, Ca, Vit K, folic acid, Vit
B12, causing nutritional deficiency, osteomalacia, inadequate blood coagulation,
macrocytic anemia
Disorders of the Large Intestine –
1. Constipation – slow movement of feces through large intestine, associated with hard/dry
feces in descending colon because of overabsorption of fluid caused by tumors, adhesions,
ulcers, or irregular bowel habits
-not allowing defecation to occur when reflexes are excited causes less strong reflexes
over the years, and colon becomes atonic
-can also be caused by spasm of small segment of sigmoid colon, only a slight degree of spasm is
capable of causing serious constipation
Megacolon (Hirschsprung’s Disease) – if constipation is so severe that bowel movements occur
very infrequently, lots of fecal matter accumulates in colon causing colon to distend, causing
hirschprung’s diseases
-frequent cause is lack of ganglion cells in myenteric plexus in segment of sigmoid colon
Diarrhea – results from rapid movement of fecal matter in large intestine
-Enteritis – inflammation of GI tract caused by virus or bacteria, and most extensive in the large
intestine where mucosa is irritated and enhances rate of secretion. Motility of increased also
increased, so lots of fluid is available for washing infectious agent toward anus
-cholera bacterium that causes diarrhea, directly stimulates excessive secretions from
the crypts of lieberkuhn in distal ilem and colon, causing fluid loss and death
-most important therapy is fluid and electrolyte replacement
-Psychogenic Diarrhea – during extreme stress, excessive parasympathetic stimulation increases
motility and excess secretion of mucus in distal colon
-Ulcerative Colitis – extensive areas of walls of large intestine become inflamed and ulcerated,
causing mass movements to occur throughout much of the day instead of 10-30 minutes,
causing repeated diarrhea
-can be autoimmune or infectious in nature
Paralysis of Defecation in Spinal Cord Injuries – defecation is normally initiated by accumulation
of feces in rectum to cause a defecation reflex passing from rectum to conus medullaris of spinal
cord to colon, sigmoid, rectum and anus
-When spinal cord is injured between conus medullaris and brain, voluntary portion of
defecation is blocked while basic defecation is intact, but small enema will fix
Vomiting – upper GI tract gets rid of contents due to irritation, over distention, and overly
excitable. Distention of duodenum is especially strong for vomiting
-sensory signals from pharynx, esophagus, stomach, and duodenum send nerve signals
by vagal and sympathetics to nuclei in brain called vomiting center
-motor impulses are transmitted for vomiting by CN 5, 7, 9, 10, 12 to upper GI tract,
through vagal and sympathetics to lower GI tract, and through spinal nerves to
diaphragm and abdomen
-Antiperistalsis begins minutes before vomiting, meaning peristalsis UP the GI tract, and may
begin in the ileum, at a rate of 2-3cm/s and can push small intestine contents back through
stomach in 3-5 min
-this causes distention of upper GI, giving signal to begin vomiting act
-strong intrinsic contractions occur in stomach and duodenum with relaxation of esophageal
sphincter to allow vomitus to move up, and abdominal muscles take over to expel vomitus
-the vomiting center has been stimulated, and the sequence of events are
1. Deep breath
2. Raising of hyoid bone and larynx to pull upper esophageal sphincter open
3. closing of glottis to prevent vomitus to flow into lungs
4. lifting of soft palate to close posterior nares
5. strong downward contraction of diaphragm and abdominal wall muscles to build
intragastric pressure up
6. lower esophageal sphincter relaxes allowing vomitus to flow through esophagus
Chemoreceptor trigger zone in brain medulla for initiation of vomiting by drugs or motion
sickness – bilaterally near fourth ventricle is a zone called chemoreceptor trigger zone for
vomiting, and electrical stimulation can initiate vomiting, but drugs like apomorphine,
morphine, and digitalis derivatives can stimulate vomiting
-change of motion can cause vomiting through vestibular labyrinth in inner ear transmitting
signal to vestibular nuclei into cerebellum and then to chemoreceptor trigger zone
Nausea – conscious recognition of subconscious excitation in an area of excitation in part of
medulla associated with vomiting, and can be caused by:
-irritative impulses coming form GI tract, impulses originating in lower brain with motion
sickness, or impulses from cerebral cortex to initiate vomiting
Gastrointestinal Obstruction – can become obstructed due to cancer, fibrotic constriction
resulting from ulceration or from peritoneal adhesions, spasm of a segment of gut, and paralysis
of gut
-if obstruction occurs near pylorus (fibrotic constriction after peptic ulceration), persistent
vomiting occurs and depresses bodily nutrition, can cause whole body metabolic alkalosis
-if obstruction is beyond the stomach, antiperistaltic reflux from small intestine causes juices to
flow backward into stomach and the juices are vomited along with stomach secretions, causing
dehydration
-if obstruction is near distal end of large intestine, feces accumulate in colon for a week or more
and patient gets constipation. Vomiting occurs after a long time
Gases in GI tract: Flatus
-gases called flatus, enter GI tract from swallowed air, gases formed from gut as a result of
bacterial action, or gases that diffuse from blood into GI tract
-most gases are mixes of N2 and O2 from air, and expelled by belching
-in large intestine, most gases arise from bacterial action including CO2, methane, H2, can be
explosive
-Certain foods can cause greater expulsion of flatus through anus than others: beans, cabbage,
onion, cauliflower, corn, and vinegar
-average amount of gas expelled is 0.6L, but 7-10L build up each day, and the remainder is
absorbed through blood and expelled through lungs