Lecom - Physiology 66: Physiology Of Gi Disorders

Front 1

Damage to what nerves cause paralysis of significant portions of the swallowing mechanism?

Back 1

CN 5, CN 9, CN 10

Front 2

What diseases can damage the swallow center of the brain stem?

Back 2

Poliomyelitis or Encephalitis

Front 3

What diseases can effect the swallowing muscles?

Back 3

Muscle Dystrophy, Myasthenia Gravis, Botulism

Front 4

Abnormalities that can occur when swallowing mechanisms are partially or totally paralyzed are:

Back 4

1. Complete abrogation of the Swallow act so that swallowing cannot occur 2. Failure of teh glottis to close so that food passes into the lungs instead of the esophagus 3. failure of the soft palate and uvula to close the posterior nares so that food refluxes into the nose during swallowing

Front 5

Deep Anesthesia Paralysis

Back 5

Paralysis of swallowing mechanism occuring during deep anestheia can lead to patients choking to death on vomit rather than swallowing it

Front 6

Achlasia

Back 6

condition in which the lower esophageal sphincter fails to relax during swallowing

Front 7

Achlasia Pathology

Back 7

Myenteric Plexus of lower 2/3 of esophagus is damaged, as a result musculature of the lower esophagus remains spastically contracted

Front 8

Achlasia Treatment

Back 8

Considerable benefit can be achieved by stretching lower end of esophagus by means of a balloon inflated on end of a swallowed esophageal tube, antispasmotic drugs that relax smooth muscle can also be helpful

Front 9

Inflammation of gastritis

Back 9

May be only superficial and not very harmful or it can penetrate deeply into gastric mucosa, in many cases causing complete atrophy of gastric mucosa

Front 10

Cause of Gastritis

Back 10

Much of gastritis is caused by chronic bacterial infection of gastric mucosa

Front 11

Common ingested irritant substances that can cause Gastritis?

Back 11

Alcohol and Aspirin

Front 12

Low Levels of Stomach Absorption

Back 12

Mainly due to two specific features of gastric mucosa, these are known as "Gastric Barrier" 1. lined with highly resistant mucous cells that secrete viscid and adherent mucus 2. has tight junctions between the adjacent epithelial cells

Front 13

Achlorydia

Back 13

(low acid) fails to secrete HCL when ph of gastric secretions fails to decrease belos 6.5 after stimulationàwhen acid is not secreted pepcid is usually inhibited as well need acid environment

Front 14

Pernicious anemia

Back 14

Normal gastric secretion contain intrinsic factor –must be present for adequate absorption of vitamin B12 from ileum...Often with gastric removal or cancer of terminal ileum

Front 15

Intrinsic factor

Back 15

binds with B12 and protects it until it reaches the terminal ileum, where factor binds with factorsàallows B12 to be absorbed. W/OUT this only about 1/150 of B12 is absorbed...W/out B12 young new RBC fail to mature while they are still forming in the bone marrow

Front 16

Peptic Ulcer

Back 16

Excoriated area of mucosa caused by digestive actions of gastric juices affected by rate of action of secretion and protection of mucous imbalance. Freq first part of duodenum, lower end of esophagus, or in surgery at those sites

Front 17

How is Duodenum protected from acidic stomach contents

Back 17

Duodenum is protected by alkalinity of small intestines especially pancreatic bicarb to neutralize HCL levels of bicarb at brunners gland and from bile from liver...If exceass acid enter the duodenum it causes stomach to slow down dumping of contents by hormones and reflex

Front 18

What role does acid play in the small intestine?

Back 18

Acid in small intestine liberates secretin from intestinal mucosa and this tells pancreas to spit out a bunch of basic stuff

Front 19

Helicobacter pylori

Back 19

Breaks down gastroduodenal Mucosal barrier by digging and can liquefy the barrier

Front 20

Cause of Peptic Ulcers

Back 20

Smoking, increased nervous stimulation, alcohol, aspirin, stress can break barrier as well and cause ulcers

Front 21

Peptic Ulcer Treatment

Back 21

Antibiotics and acid suppressor drug, ranitidine, antihistamine that blocks receptors

Front 22

Abnormal digestion due to pancreatic secretion problems caused by removal:

Back 22

Head of the pancreas has been removed from cancer- causes no enzymes to be produced and 60% of fat entering small intestine can not be absorbed and 1/3 carbs and proteins fatty poo

Front 23

Pancreatitis

Back 23

most common cause is alcohol and then blockage of ampulla of vater by a gallstone. Causes the enzymes to get damned up and get activated and eat pancreasàso much tripsongen overcomes trypsin inhibitor and a small amount of trypsinogen becomes activated to trypsin and sets off all the others

Front 24

Nontropical Sprue

Back 24

Idiopathic sprue, or celiac disease (kids), glutten enteropathy toxic effects of gluten found in wheat and rye, glutten has direct destructive effect on enterocytes.

Front 25

Nontropical Sprue effect on Enterocytes:

Back 25

Microvilli destroyed- decrease absorbtive surface 2x more sever conditions the villi themselves become blunted or disappear all together reducing even more surface area

Front 26

Nontropical Sprue Treatment

Back 26

Cure is to remove wheat and rye from diet! Gluten free nigga

Front 27

Tropical Sprue

Back 27

Usually caused by inflammation of intestinal mucosa from unidentified infectious agent, usually found in tropics

Front 28

Symptoms of Tropical Sprue

Back 28

Malabsorption in sprue- fat is more impaired in early sprue excess fat in stool, even though it is digested it is not absorbed! Idiopathic steatorhea. in severe cases- proteins, carbs, vitamin K, folic acid, viatamin B12 and other stuff is not absorbed. Suffers: nutritional deficiency, wasting of body, osteomalacia (demineralized of bone), inadequate blood coagulation (lack of vitamin K), macrocytic anemia of pernicious anemia type (lack of vitamin B12 and folic acid absorption)

Front 29

COSTIPATION

Back 29

slow movement of feces through the large intestineàassoc. with large quantities of dry hard feces in descending colon that accumulate necaue of the long time available for absorption of fluids. Any path of intestine that obstructs movement of intestinal contents (tumors, adhesions, ulcers can cause constipation). reflexes become weakened if not used enough (use laxatives too long) and become atonic and don’t work anymore or muscle spasm of colon

Front 30

Reflexes responsible for movement of feces in the large intestines?

Back 30

gastrocolic and duodenocolic reflexes cause mass movement of feces in large intestine

Front 31

MEGACOLON

Back 31

Lack or deficiency of ganglion cells in myenteric plexus in a segment of sigmoid colon. No reflexes or stimuli can make it work. Sigmoid closes off and poo builds

Front 32

DIARRHEA

Back 32

Rapid movement of poo

Front 33

Enteritis

Back 33

Infection cause by virus or bacteria in intestine tract, mucosa gets irritated and secretion increases a whole lot, so large quantities of fluid are available to wash out cholera- directly stimulates excess secretion of electrolytes and fluid from crypts of luberkuhn in distal ileum and colon 10-12L a day so replace or you will die

Front 34

Psychogenic Diarrhea

Back 34

Excess stimulation of parasympathetic nervous system which greatly excites motility and secretion f mucus in the distal colon

Front 35

Ulcerative colitis

Back 35

Extensive area of walls of large intestine become inflamed and ulcerated. Mass movements constantly vs. every 30-1hr. the ulcer keeps getting infected with bacteria unless ileostomy gives time to heal.

Front 36

Defecation

Back 36

Usually initiated by movement of feces into rectum, which causes a spinal cord mediated defecation reflex passing from the rectum to the spinal cord and then back to the descending colon, rectum, sigmoid, anus

Front 37

Destruction of conus medullaris

Back 37

Can destroy distal segments of cord where the cord reflex is integrated, and thus paralyzing defecation all together (need large enemas, and support measures)
If injured higher up in spinal cord- the voluntary portion of defecation is blocked, but cord reflex is can still occur→small enema is sufficient

Front 38

VOMITING

Back 38

Upper GI tract rids itself of contents, when any part is irritated excess distension of duodenum, or irritation can cause puke

Front 39

Sensory Impulses for Vomiting

Back 39

Impulses are transmitted by vagal and sympathetic afferents to bilateral vomiting center of Medulla

Front 40

Motor Impulses for Vomiting

Back 40

Motor impulses- are transmitted from vomit center through the 5,7,9 10, 12 nerves to upper GI tract and through spinal nerves to diaphragm and ab muscles

Front 41

ANTIPERISTALSIS PRELUDE TO VOMIT

Back 41

Early stage of excess GI irritation or overdistension, antiperistalsis begins to occur many mins before vomiting, this pushes stuff down and it irritates to the dudodenum and that rebounds

Front 42

HOW TO VOMIT

Back 42

A deep breath, then raising of hyoid bone and the larynx to pull the upper esophageal sphincter opens, closing of glottis, lifting of softe palate to close posterior nares, then diaphragm pulls down and abs contract to create pressure, the lower sphincter opens and out comes puke explosively

Front 43

CHEMORECEPTOR TRIGGER OF VOMIT

Back 43

On floor of 4th ventricle is the chemoreceptor trigger zone for vomitingà electric stimulation of this initiates vomiting (morphine, apomorphine, can stimulate) vestibular nerve triggers when moving fast and goes to the cerebellum then through Target zone..Gross images or smalles stimulate certain areas of hypothalamus to cause puke

Front 44

GI OBSTRUCTION

Back 44

Cancer, fibrotic constriction resulting from ulceration or from peritoneal adhesions, spasm of a segment or paralysis of a segment of the gut; Can cause excess vomiting and lead to alkalosis

Front 45

What will happen in GI system above obstruction

Back 45

Parts above the obstruction will secrete tons of fluid and this can cause excess loss of fluids, proteins don’t get absorbed so plasma decreases and circulatory shock happens.

Front 46

Symptoms of long term colon obstruction

Back 46

Obstruction of large intestine for long times can cause it to burst and dehydration and circulatory shock occur

Front 47

FLATUS

Back 47

gas being pushed through anus, rarely onto another person's face

Front 48

How gas enters the GI

Back 48

From swallowed air, bacteria actions, gases tha diffuse from the blood into the GI

Front 49

Make up of Flatus

Back 49

Most are mix of nitrogen and O2, burping. CO2 accumulates because reaction b/w acidic gastric juice and basic pancreatic juice

Front 50

Large intestines contribution to Flatus

Back 50

In large intestine mostly from bacteria carbon dioxide, methane and hydrogen, these can mix and explode

Front 51

Food Effect on Flatus

Back 51

FOODS- are a suitable medium for gas-forming bacteria (unfermented sugars are a good substrate for colonic bacteria)

Front 52

Cause of Flatus action

Back 52

Irritation of large intestine which promotes rapid peristaltic expulsion of gases before they can be absorbed most gas is absorbed into blood through the intestinal mucosa.