Digestive System

Mouth

Chewing, tasting

Saliva

Lubrication, protection, digestion, neutralizes acid

Esophagus

Muscular tube that transports food from the pharynx to stomach, lined with epithelial cells

Liver

Metabolism, detoxification, bile

Gallbladder

Bile storage

Small intestine

Digestion, absorption

Cecum

Storage

Stomach

Storage, grinding, mixing food with acid and digestive enzymes, digestion, acid secretion

Large intestines

Fluid and electrolyte absorption

Pancrease

Enzymes, HCO3- buffer

Rectum

Storage, excretion

Amaylase

Enzyme in saliva that breaks down starches into glucose

What happens in the oral/buccal cavity?

Digestion begins, amylase, chewing, and swallowing

Peristalsis

Waves of muscular contractions that move the contents of the digestive tract, controlled by somatic nerves and ANS, triggered by stretch in esophagus sensed by mechanoreceptors

Upper esophageal spincter

tops food and liquids from entering the throat

Lower espohageal spincter

Stops stomach contents from refluxing into the esophagus, intrinsic sphincter, a ring of smooth muscle that is normally closed, controlled by nicotinic ACh receptors

When is the esophagus relaxed?

When inhibited

When is the esophagus contracted?

When excited

What triggers the lower esophageal sphincter to relax?

Food bolus gets near, allows it to open and bolus to enter the stomach

GERD

Gastroesophageal reflux disease, caused by poor muscle tone/frequent relaxation of the lower esophageal sphincter

Fundus

Upper region of the stomach, made of parietal cells, chief cells, and enterochromaffin cells

Parietal cells

Produce acid (H+)

Chief cells

Produce pepsinogen

Pepsinogen

Digestive pre-enzyme of pepsin, break down proteins

Corpus

Body of the stomach, made of parietal, chief, and enterochormaffin cells

Antrum

Lower region of the stomach, has G-cells ,mucus cells, and D-cells

G cells

Secrete gastrin into the blood, stimulates the production of H+, parietal cells, and ECL cells

D-cells

Produce somatostatin, inhibits H+ production

Gastric rugae

Folds of tissue that are exposed when the stomach expands

What causes lactose intolerance?

The body lacks enzymes that break down lactose so it does not get absorbed and feeds the bacteria in the gut. This leads to upset stomach

Esophageal mucosa

Protects from sharp food objects, irritants, and pathogens

3 phases of swallowing

1. Oral (chewing and moving food to the throat conscious)

2. Pharyngeal (controlled by reflexes, moves food from throat to esophagus)

3. Esophageal (Peristalsis moves food from esophagus to stomach)

Mucous neck cells

Secrete mucus and bicarbonate buffer

Enterochromaffin-like cells

Release histamine, stimulate acid production, ECL cells

Mucus layer

Protects epithelial lining from acid, pathogens, and digestive enzymes, contains bicarbonate buffer. Loss of this layer can cause an ulcer

Prostglandins

Stimulate the production of mucus and bicarbonate

Carbonic anhydrase

Makes bicarbonate

How is acid produced by parietal cells?

H+/K+ ATPase pumps H+ into the stomach. Stimulated by histamine, ACh, and gastrin

What receptors does histamine bind to?

H2 (Gs coupled protein)

What receptors does ACh bind to?

M3 (Gq coupled protein)

What receptors does gastrin bind to?

CCK B receptors (Gq coupled protein)

Cephalic phase

Triggered by sight, smell, taste, and swallowing. ACh is released by the vagus nerve and stimulates parietal cells, ECL cells, and G cells, inhibits D cells. The stomach is acidified before food intake

Gastric phase

vagus nerve senses stomach distention, releases ACh to promote H+ secretion and stimulate G cells, D cells activated if pH gets below 3

Intestional phase

Starts when chyme enters small intestines, inhibition of acid from parietal cells and histamine from ECL is triggered by distention of duodenum and fats/ acids

What produces acetylcholine?

Neurons

How does the circulatory system influence GERD?

An increase of blood delivers HCO3- and removes H+

What are the symptoms of GERD?

Inflammation, burning sensation, heartburn, regurgitation

How do NSAIDs influence GERD?

Inhibit prostaglandins, indirectly inhibits mucus and bicarbonate buffer production, the lining of the stomach breaks down and can lead to ulcers and stomach bleeding

What are the contributing factors to GERD?

Diet (coffee, large meals) and positioning after meals (laying down after meals)

What are the general treatments of GERD?

Neutralize HCl with basic salts of Ca/Al, protect the luminal lining using bismuth subsaicylate, and preventing acid release using H2-receptor blocking and proton pump inhibitors

How do H2-receptor blockers work?

They reversible block the H2 receptors in parietal cells to reduce acid secretion

How do proton pump inhibitors work?

They irreversibly block proton pumps