Chapter 14b – Digestive system

1. Chewing, Swallowing, and Esophageal Peristalsisa. Chewing

i. Breaking down into small pieces is by teethe and movement or tongue, and saliva which is secreted from salivary glands.

ii. Parotid, sublingual, and submandibular glands are salivary glands which secrete saliva1. 80 to 90% is water

iii. By teeth, tongue, and saliva, we break down food and it is ready for transport.iv. Upper esophageal sphincter opens and receives food content then contracts or closes. Then

we have peristalsis movement in esophagus which carries food to stomachb. Swallowing

i. Controlled by two cranial nerves CN9 (glossopharyngeal) and CN 10 (vagus)1. During this, we have closure of two things

a. Nasopharynx which prevents passage from oral cavity to nasal cavity i. Breathing is inhibited

b. Closure of epiglottis which prevents passage of food into tracheai. Laryngeal muscle contract to close glottis

2. We have relaxation of upper esophageal sphincter which is 1st signal for peristalsis in esophagus.

c. Esophagus i. Structure

1. 25- 30 cm long, propels food into the stomach2. It is about 40cm from the incisor teeth.3. We have 3 narrow parts

a. Upper esophageal sphincter prevents air entering esophagusb. Aortic narrowing surrounded by arch of aortac. Lower esophageal sphincter (diaphragmatic narrowing) connected to

stomach4. Starts at the level of C6 vertebra (cricoid cartilage)5. It lies on the vertebral column6. accompanied by right and left vagus nerves7. passes through esophageal hiatus of diaphragm at the level of T10 and enters

thoracic cavity8. Aorta passes through diaphragm and enters abdominal cavity at T12 9. Inferior vena cava passes through diaphragm and enters ab cavity at T8 levels10. Esophageal hiatus is name of entrance of esophagus

a. Esophagus enters abdominal cavity through esophageal hiatusi. Has lower esophageal sphincter connected to stomach called

cardia which is where esophagus enter stomach ii. Innervation of GI tract

1. Under control of ANS2. Parasympathetic (Ach) by vagus accelerates everything

3. Sympathetic inhibits everything (NE)a. NE has negative affect and Ach has positive affect

iii. Esophageal motility1. Break down food content in oral cavity 2. Upper esophageal sphincter relaxes to permit food to enter the esophagus

a. Sphincter then contracts to prevent food reflux into pharynx.3. Primary peristaltic contraction creates an area of high pressure behind the food

a. Peristaltic contraction moves down and gravity accelerates movement4. Secondary peristaltic contraction clears the esophagus of any remaining food5. Relaxation of lower esophageal sphincter

a. Surrounded by smooth muscle innervated by enteric nervous systemb. Relaxation controlled by vagus and by VIP – vasoactive inhibitory peptide

6. Orad region of stomach receives food from lower esophageal sphincteriv. Clinical problems

1. Gastric refluxa. Could by congenital, manipulation of tissue during surgeryb. Muscle cannot contract well in lower esophageal sphincter which leads to…

i. Gastric reflux in stomach which contains HCl and comes back into esophagus

ii. Burning sensation and feels pain in retrosternal area. iii. You need to differentiate between myocardial infarction and gastric

reflux.2. Achalasia (cardiospasm)

a. Problem is innervation of smooth muscle by enteric nervous system b. This leads to

i. Failure of complete opening of lower esophageal sphincter – called cardia spasm

ii. Food accumulates in upper part of lower esophageal sphincter1. We say increased lower esophageal sphincters pressure –

increased LES pressureiii. This accumulates fluid in upper part of sphincter because that part

cannot relax and normally contract and so it just spasms causes dilated proximal esophagus and aperistalsis

iv. Patient has dysphagia means cannot swallow food content and fluid cannot get into stomach

d. Dorsal view of esophagusi. Esophagus is continuation of Pharynxii. Esophageal plexus – vagus nerve

iii. Gastric nerves – gastric plexusiv. Pharynx has constrictor muscles superior, middle, and inferior muscles

1. No smooth musclev. Pathology

1. In week 3 of pregnancy, embryo has 3 layersa. Ectoderm

i. Gives rise to epidermis layer of skin, auricle (external ear), lens of eye, CNS, PNS (peripheral nervous system), adrenal medulla of adrenal gland

b. Mesodermi. Gives rise to dermis layer of skin, connective tissue, muscle (any

muscle like skeletal, smooth, cardiac), bones, ovary and testicles, male and female reproductive tract, kidney and urinary system (renal system), blood vessels

c. Endodermi. Gives rise to entire GI tract except oral cavity and anus. ii. Don’t forget that smooth muscle in GI is from mesoderm. Endocrine

glands are from endoderm. iii. Endoderm gives rise to esophagusiv. Ventral portion (anterior) portion have some cells proliferate and

become trachea and lung bud.v. After formation of these, we have tracheal esophageal membrane

form which separate esophagus from trachea in fetus. vi. 1st 8 weeks of pregnancy we call child embryo, after week 9 until birth

we call then fetus. vii. Esophagus should form tube internally – failure means that instead of

connection to stomach, we have a separation between upper and lower part.

2. Esophageal Atresiaa. Part esophagus membrane is missing closure between proximal and distal

esophagusb. Atresia means lack of tissue 100% or 90%. Means no smooth muscle or tube.

Maybe very thin membrane layer with lack of muscle and nerves. c. Stenosis means diameter is not normal and smaller than average.

i. Stenosis means narrow part of esophagus and can affect peristalsis but patient or newborn could have vomiting but not coughing (since not connected to trachea)

d. Signs and symptomsi. When endoscopy tube cannot reach stomachii. During breast feeding or after, newborn has vomiting, cannot gain

weight, weakness, you have to diagnose in time or child can die. 3. Tracheal esophageal Fistula

a. Opening due to failure of development of tracheal esophageal membrane which leads to abnormal connection between esophagus and trachea.

b. Signs and symptoms in newborn

i. Coughing or vomiting after breast feeding (coughing since esophagus connected to trachea)

ii. In long term, respiratory infection such as bacterial infection because milk gets into trachea and respiratory tract

c. Treatmenti. Close opening by surgeryii. 80-90% fistula is associated with esophageal atresia which is

congenital problem4. Esophageal cancers

a. Hot tea can irritate esophagus and increase risk of esophagitis and cancer5. Hiatal hernia

a. Hernia in esophageal hiatus in diaphragm protrusion of part of stomach through esophageal hiatus of diaphragm

b. Two types of herniasi. Type A

1. When part of lower esophageal sphincter, cardia, and even part of fundus of stomach slide through esophageal hiatus

2. Signs and symptomsa. Retrosternal painb. Gastric refluxc. Esophagitis because of acid refluxd. Sometimes vomitinge. Regurgitation –food comes up to esophagus because

lower esophageal sphincter cannot closeii. Type B

1. Hernia only in fundus in stomach which comes to stomach through hiatus.

2. We have normal position of lower esophageal sphincter.3. Signs and symptoms

a. Pain due to heart burnb. No regurgitation

2. Surgerya. Fundoplication reinforces barrier to reflux that lower esophageal valve normally provides

i. This is to correct gastric refluxii. Upper part of stomach (fundus) is wrapped (plicated) around lower part of esophagus

(hiatus). This closes risk for herniab. Radiofrequency treatment

i. Burn tissue that surround lower esophageal tissue and hiatusii. This thickening prevents hernia by tightening weak valve

3. Stomach

a. Stomach located in left upper quadrant of abdominal cavity. Connected to lower esophageal sphincter.

b. Has different parts and each part secretes a specific hormonec. Parts of stomach 4 parts and 2 curvatures

i. Cardiaii. Fundus

iii. Bodyiv. Pyloric part

1. Has 3 partsa. Pyloric antrumb. Pyloric canalc. Pyloric sphincter

v. We have lesser and greater curvaturevi. Duodenum is connected to pyloric sphinctervii. Orad region upper part that includes fundus and proximal body

1. Receives ingested foodviii. Caudad region includes antrum (pyloric) and distal body

1. Mises food and propels it into duodenum

d. Arteries for GI tracti. Celiac artery branch of abdominal aorta which gives three branches to abdominal cavity

1. Gives branches to different organsa. Left gastric artery

b. Common hepatic arteryc. Duodenum artery Superior part of duodenumd. Splenic arterye. Head of pancreas or pancreatic artery

ii. Superior mesenteric arteryiii. Inferior mesenteric artery

e. Nerve supply to stomachi. By enteric nervous system under control of ANSii. Parasympathetic has positive affect

iii. Sympathetic has negative affect on GI tractf. Muscles

i. 3 types1. Longitudinal outer layer2. Circular inner layer3. Oblique 3rd layer that is missing in pyloric and lesser curvature

ii. Size of stomach depends on size of body which is normalg. Motor functions of stomach

i. Storage of foodii. Chyme

1. Is mixed food with gastric enzymes and mucus which is ready for digestion and absorption by epithelial cell, mostly small intestine and large intestine

2. 10% of digestion and absorption in stomach3. 90% of digestion and absorption occurs in small intestine4. Fluid absorption occurs mostly in large intestine

iii. Controlled rate of passage and quality of digestion of food to duodenum

4. Gastric mucosaa. Has numerous gastric folds and pits gastric glands open into pitsb. Mucosa and pits covered by columnar epitheliumc. Epithelial cells produce mucus which protects the epithelium against auto-digestiond. Gastric gland cells

i. 1st Parietal cell (fundus/body)1. Secretes two things

a. HClb. IF – intrinsic factor

2. Functiona. HCl is required for conversion of pepsinogen into pepsinb. Pepsin is important for digestion of proteinc. IF uptakes vitamin B12 and carries it to ileum which is last part of small

intestine and ileum absorbs vitamin B12ii. 2nd Chief (zymogenic) cells (fundus/body)

1. Secretes pepsinogen a. This is inactive form which needs HCl to becomes pepsin which digests

proteiniii. 3rd Goblet cells

1. Secrete mucus iv. 4th Enterochromaffin-like (ECL) cells (stomach/intestine)

1. Secrete paracrine hormones such as…a. Serotonin Controls gastric acid secretionb. Somatostatin Inhibits other gastric hormone secretion

i. Is secreted by D cellsc. Histamine Increases gastric acid secretion

v. 5th G cells (pyloric antrum)1. Secrete gastrin has direct effect on parietal cell and it increases acid secretion2. Tumor in G cells

a. Causes gastritis because level of gastrin increases, and this stimulates parietal cells

b. Stimulating parietal cells increases gastric acid which irritates layer of stomach leading to gastritis and gastric ulcer.

c. Also have hypertrophy and hyperplasia of gastric mucosa3. Zollinger-Ellison syndrome gastrin secretion by non-beta cells of pancreas

(multiple ulcers in stomach)4. Factors that Increase Gastrin secretion

a. Small peptides and amino acids in lumen of stomach

i. Phenylalanine and tryptophan has strongest stimulating effectb. Distention of stomachc. Vagal stimulation mediated by gastrin-releasing peptides (GRP)

5. Factors that inhibit Gastrin secretiona. Too much H+ in lumen of stomach

vi. 6th I cell (duodenum)1. Secrete CCK cholecystokinin

a. Functioni. Has effect on gall bladder

1. It contracts gall bladder for releasing of bile into bile ductii. Increases pancreatic enzymes and pancreatic bicarbonate secretion

1. Amylase, lipase, and protease are pancreatic enzymesiii. Relaxes sphincter Oddi

1. Located in second part of duodenum which receives bile from common bile duct for emulsification of fat in duodenum and it receives pancreatic enzymes from enzymes for digestion of carbs, lipids, and proteins.

2. CCK relaxes this sphincter and duodenum receives all these things

vii. 7th S cells (duodenum)1. Secrete secretin

a. Controls gastric acid secretion and it controls pancreatic enzymes and pancreatic bicarbonate secretion.

viii. 8th Cells in duodenum1. Secrete GIP gastric intestinal peptide

a. Sensitive to oral glucose (eating chocolate)b. Oral sugars increase GIP from duodenum and jejunum which leads to

stimulation of pancreas for secretion of insulin from pancreas. c. Insulin takes glucose into cell for ATP production.

e. Secretion of gastric juices 2 phasesi. Nervous secretion by vagus nerve, activated by taste, smell and sight (even if stomach is

empty)ii. Gastric (digestive) phase secretion stimulated by food ingestion

5. Other Important hormonesa. VIP – vasoactive intestinal peptide

i. Acts as neurohormoneii. Source of secretion is from neuron of mucus layer and smooth muscle layer

iii. Function1. Relaxation of smooth muscle 2. Increases intestinal secretion3. Increases pancreatic and gastrin secretion

b. GRP – gastrin releasing peptidei. Secreted by neurons ii. Function

1. Increases gastrin secretionc. Enkephalin

i. Secreted by neuron ii. Function

1. Controls contraction of smooth muscle2. Decreases intestinal secretion

d. Neural peptide Yi. Secreted by neuronii. Function

1. Relaxation of smooth muscle2. Decreases intestinal secretion

e. Substance Pi. Secreted by neuron or co-secreted with AChii. Function

1. Controls contraction of smooth muscle2. Increases salivary secretion

f. Secretini. By S cells in duodenumii. Function

1. Controls the acid media (H+) in duodenum2. Increases pancreatic bicarbonate secretion3. Increases biliary bicarbonate (from bile)4. Decreases gastric acid secretion

g. GIPi. Sensitive to oral sugarii. Function

1. Stimulates insulin secretion

6. Gastric motilitya. Means peristalsisb. Before peristalsis in stomach, we have slow wave which receives food content and forms chime c. Mixing of food content with gastric enzymes (formation of chyme) is controlled by contraction and

relaxation of smooth muscle which is controlled by enteric systemd. Vagus nerve and ACh accelerate this processe. Slow wave is converted into spike wavef. Every 90 minutes, we have strong contraction which clears GI of residual food migrating

myoelectric complexg. 10% of digestion and absorption occurs in stomach

7. Gastric emptyinga. The caudad region of the stomach contracts to propel food into the duodenumb. The rate of gastric emptying is fastest when the stomach contents are isotonicc. Fat inhibits gastric emptying (increases gastric emptying time) by release of CCK

i. When duodenum has fat chyme then CCK inhibits early emptying of stomach (it stops stomach) since it needs time to digest fat.

ii. Inhibits early gastric emptying since it requires longer time for digestion. d. H+ in duodenum also inhibits gastric emptyinge. Peristaltic waves create a gradient of food in stomach selecting the most digested chyme to atrum

i. More intense waves can force chyme through pylorus in waves of jets called peristaltic pump

8. Innervation of stomacha. Parasympathetic

i. Vagus nerve is main nerve of parasympathetic and increases everything in stomach, peristalsis and secretion of endocrine hormones

ii. Vagus nerve innervates parietal cell for gastric acid secretioniii. Over secretion of acid leads to gastritisiv. Vagotomy remove branches of vagus nerve

1. Sometimes medication doesn’t work and control gastric acid secretion and in severe conditions they have to surgically remove some branches of vagus nerve which innervate fundus of stomach. This controls gastric acid secretion

b. Sympathetici. Coming from splanchnic nerves (u8pper lumbar) which synapse in Celiac ganglionii. Postganglionic fibers innervate stomach

iii. Inhibit peristalsis and gastric secretioniv. Cause pyloric contractionv. Convey pain