BSCI202 Digestive

organs of the alimentary canal (continuous tube through which food passes)

mouth, pharynx, esophagus, stomach, small intestine, large intestine, anus

accessory digestive organs

teeth, tongue, salivary glands (parotid, sublingual, submandibular), liver, gallbladder, pancreas

what happens in ingestion and propulsion

-ingestion: taking food into digestive tract via mouth
-propulsion: movement of food through the alimentary canal
-structures: mouth is the site of ingestion, propulsion involves pharynx and esophagus (for swallowing) and the entire GI tract (for peristalsis)

what happens in mechanical breakdown?

-the physical preparation of food for chemical digestion by increasing its surface area
-happens in mouth, stomach, small intestine

what happens in chemical digestion?

-catabolic process where complex food molecules are broken down into their chemical building blocks by enzymes
-stomach, small intestines, pancreas, liver

what happens in absorption?

-passage of digested end products from the lumen of the GI tract through mucosal cells into the blood or lymph
-small and large intestine

the mechanisms of deglutition (swallowing)

1. buccal phase (voluntary): mouth: voluntarily using tongue to press bolus against hard palate, then forcing into oropharynx

2. pharyngeal-esophageal phase (involuntary): bolus stimulates receptors in posterior pharynx to make it involuntary and transports to stomach

how is “right of way” of bolus over airflow accomplished

-nasopharynx is blocked: soft palate and uvula close it off to prevent food from going up into nasal cavity
-larynx is blocked: epiglottis covers larynx to seal off trachea so food doesn’t enter the lungs
*all routes to lungs are temporarily closed during the split second it takes to swallow

how does bolus make it to stomach?

1. bolus clears pharynx

2. upper esophageal sphincter relaxes to allow the food into the esophagus and then quickly contracts again to prevent backflow

3. bolus is moved down esophagus via peristalsis

4. cardioesophageal (lower esophageal) sphincter opens when food presses against it so bolus can enter and then closes to protect esophagus from stomach acid

four layers of the alimentary canal

mucosa, submucosa, muscularis externa, serosa

mucosa: composition, function, structural variations

innermost layer (moist epithelial membrane that lines the lumen)
-composition: lining epithelium, lamina propria (loose areolar connective tissue), and muscularis mucosae (thin layer of smooth muscle)
-function: secretes mucus, digestive enzymes, and hormones, absorbs nutrients, protects against infectious diseases
-variations: mouth/esophagus (stratified squamous epithelium to protect against abrasion), stomach/small intestine (simple columnar epithelium with mucus-secreting cells for secretion and absorption)

submucosa: composition, function, structural variations

second innermost layer
-composition: external areolar connective tissue containing a rich supply of blood, lymphatic vessels, lymphoid follicles, nerve fibers
-functions: abundant elastic fibers allow GI tract to regain shape after stretching
-structural variations: in duodenum, there are specialized duodenal galnds that secrete alkaline mucus to neutralize acidic chyme from stomach

muscularis externa: composition, function, structural variations

-composition: two layers of smooth muscle: inner circular layer and outer longitudinal layer
-function: responsible for segmentation and peristalsis; circular layer also thickens in certain areas to form sphincters that are valves to prevent backflow
-variations: stomac has third (oblique) layer of muscle, esophagus has top third of skeletal (voluntary) muscle

serosa: composition, function, structural variations

outermost layer
-composition: protective outer layer formed of areolar connective tissue covered with mesothelium (single layer of squamous epithelial cells)
-functions: reduces friction between digestive organs and abdominal wall
-variations: in esophagus, serosa is replaced by adventitia (fibrous CT that binds it to surrounding structures)

structure of the gastric mucosa

stomach lining that is dotted with deep gastric pits, which lead into tubular gastric glands that produce gastric juice. the five types of cells that make up these glands are chief, parietal, neck mucous, G (enteroendocrine), and D (enteroendocrine)

parietal cells: secretions and roles

-HCl: makes stomach extremely acidic, which is necessary to activate pepsin, denature proteins, and kill bacteria
-intrinsic factor: glycoprotein required for absorption of vitamin B12 in small intestine, which is important for DNA synthesis and RBC production

chief cells: secretions and roles

-pepsinogen (inactive zymogen): inactive form of pepsin: activated by HCl from parietal cells and pepsin itself through a positive feedback mechanism. pepsin is the main enzyme for protein digestion
-lipases: about 15% of overall GI lipolysis (fat digestion)

mucous neck cells: secretions and roles

produce a thin, acidic mucus to contribute to protective mucosal barrier

G cells: secretions and roles

gastrin: a hormone released into blood (NOT stomach lumen) to stimulate HCl from parietal, pepsinogen from chief, and mucus from mucous neck cells + and increase gastric motility

D cells: secretions and roles

somatostatin (hormone) that acts as a “brake” to inhibit gastric secretion and motility, helping regulate digestive processes when stomach is emptying or environment becomes too acidic

surface mucous cells: secretion

thick, alkaline, neutralizing & protective bicarbonate-mucus

peristalsis vs. segmentation

-peristalsis: visceral smooth muscle (pacemaker cells) alternate waves of contraction and relaxation to move the bolus in distal one-way movement: esophagus, LI, some in stomach and SI
-segmentation: churns, mixes, and fragments bolus to mix food with digestive juices in forward and backward movement + increases absorption by repeatedly pushing food against mucosa: stomach, SI

relationship between stomach and pernicious anemia

-intrinsic factor secreted by parietal cells of the stomach binds to vitamin B12, allowing it to be absorbed in the bloodstream where it is used to synthesize RBCs.
-pernicious anemia occurs when there is a lack of intrinsic factor - usually when body’s immune system destroyed its own gastric mucosa → no B12 means RBCs can’t mature properly

gross anatomy of the small intestine

-three sections: duodenum, jejunum (where intense chemical digestion + absorption happen), ileum
-muscular tube
-extends from pyloric sphincter (at base of stomach) to the ileocecal valve (entry to large intestine)

histology of the small intestine

*massive surface area to maximize nutrient uptake
-circular folds (plicae circulares): deep, permanent folds of the mucosa/submucosa that force chyme to spiral through the lumen, slowing its movements to allow more time for absorption
-villi: finger-like projections of the mucosa - each villus contains capillary bed and wide lymphatic capillary for absorbing nutrients and fats
-microvilli: tiny projections on the plasma membrane of absorptive cells that form a brush border and contain enzymes that complete carbohydrate and protein digestion

secretions of small intestine

-enterocytes: absorptive cells that make up bulk of epithelium - absorb nutrients and electrolytes in villi
-goblet cells: produce mucus to lubricate passage of chyme
-enteroendocrine cells: produce hormones like enterogastrones that regulate release of bile and pancreatic juice
-paneth cells: located deep in intestinal crypts to secrete antimicrobial agents to destroy bacteria
-stem cells: continuously divide to replace epithelium every 3-5 days
-duodenal (brunner’s) glands: secrete alkaline mucus in duodenum to neutralize acidic chyme coming from stomach

how does chemical and mechanical digestion happen in small intestine

-chemical: relies on combination of pancreatic juice, bile form liver (fat emulsifier), and its own brush border enzymes
-mechanical: segmentation to mix chyme with digestive juices and push against mucosa for absorption

gross anatomy of large intestine (8)

-cecum: first part: sac-like structure lying below the ileocecal valve
-appendix: blind-ended tube containing masses of lymphoid tissue: bacterial “storehouse”
-ascending colon: travels up right side of abdominal cavity to level of right kidney
-transverse colon: passes horizontally across abdominal cavity
-descending colon: travels down left side of posterior abdominal wall
-sigmoid colon: S-shaped portion that enters pelvis
-rectum: located in pelvis and has three rectal valves that allow gas without feces to pass
-anal canal: last part: opens to exterior at anus: has internal and external sphincters

histology of large intestine

-no villi or circular folds because most nutrient absorption already finished
-goblet cells: produce mucus to ease passage of feces and protect intestinal wall from irritating acids and gases produced by resident bacteria
-teniae coli: longitudinal layer of muscularis externa is redced to three bands of smooth muscle, which causes the wall to pucker inpocket-like sacs called haustra - helps mix fecal matter, slowly propel stool forward, and bowel can expand as it fills

importance of microbiota for large intestine

-over 1000 types of bacteria
-necessary for fermentation: ferment indigestible carbohydrates to produce flatus
-synthesize B complex citamins and vitamin K, which liver needs to produce clotting proteins
-immunity: help keep pathogenic bacteria in check

defecation reflex in large intestine

parasympathetic reflex
1. stimulus: distension of rectal wall by mass movement of feces
2. reflex: stretching sends signals to spinal cord, which triggers parasympathetic motor efferents to cause sigmoid colon and rectum to contract and the internal anal sphincter to relax
3. fecse being forced into anal canal sends message to brain. we make a conscious decision to either keep the external anal sphincter closed or relax it to allow defecation.

salivary glands: functions and secretions

-three main pairs: parotid, submandibular, sublingual
-main functions: clean mouth, dissolve food chemical so can be tasted, moistens food and helps compact into bolus for swallowing
-secretions: saliva: salivary amylase begins starch chemical breakdown

liver: functions and secretions

-heaviest gland in body
-produces and secretes bile
-bile salt emulsifies fats (breaks large fat globules into smaller droplets) to provide more surface area for digestive enzymes
-bilirubin: pigment formed from heme that’s broken down by intestinal bacteria to give feces brown color

gallbladder: functions and secretions

-stores bile not immediately needs for digestion
-concentrates bile by absorbing water and ions
-when fatty chyme enters duodenum, the hormone CCK (expressed by SI) causes gallbladder to contract and expels bile into bile duct

pancreas: functions and secretions

*has both endocrine and exocrine functions
-function: produce pancreatic juice with many enzymes that can break down all categories of food
-secretions: bicarbonate (neutralizes highly acidic chyme coming from stomach), proteases (secreted as inactive zymogens to prevent pancreas from digesting itself and then activated in duodenum), amylases, lipases, and nucleases

how do accessory structures connect to the alimentary canal

-salivary glands open into different areas of mouth
-duodenum entry point: hepatopancreatic ampulla: bile duct (bile leaves liver through common hepatic duct + gallbladder connects via cystic duct) + main pancreatic duct. entry is controlled by sphincter of oddi (hepatopancreatic sphincter), which stays closed until fatty chyme enters duodenum

hormonal control of alimentary canal + accessory organs

-CCK is released by small intestine when fat is detected so gallbladder contracts and hepatopancreatic sphincter relaxes, so that bile and pancreatic juice can enter canal
-secretin is released by small intestine in response to acidic chyme to tell pancreas to release bicarbonate to neutralize the acid

process of absorption of sugars: location, cells, mechanisms

-location: small intestine (lumen to enterocyte (absorptive cells of intestinal mucosa) to blood)
-pancreatic amylase and brush border enzymes break down carbohydrates into monosaccharides
1. glucose and galactose are transported into enterocyte via seconadry active transport with Na+ ions via DGLT cotransporter
2. fructose moves into cell by faciliated diffusion
3. glucose, galactose, and fructose move out of the cell via faciliated diffusion(GLUT2 sugar transporter)
*maintained by Na/K ATPase pump on basolateral membrane that creates massive vacuum of sodium inside

process of absorption of proteins: location, cells, mechanisms

-location: small intestine
1. proteins have been broken down into amino acids by pancreatic proteases, brush border enzymes, or enterocytes
2. amino acids enter cell using active transport into enterocytes and move to their opposite side
3. amino acids leave enterocytes by facilitated diffusion and enter capillary via endothelial intercellular clefts

process of absorption of lipids: location, cells, mechanisms

1. bile salts wrap around fatty acids and monoglycerides to get through watery fluid → forms micelle (tiny sphere)

2. fatty acids and monoglycerides dissolve straight through lipid cell membrane of enterocyte via simple diffusion

3. the pieces are put back together into full triglycerides in ER

4. wrapped into water-soluble transport sphere called chylomicron (massive)

5. chylomicrons packed into vesicles and ejected via exocytosis

6. slip into wide, open-ended lymphatic capillairs (lacteals) and travel through lymph system before being dumped int main bloodstream later

three phases of gastric secretion

1. cephalic phase: the sight/smell/taste/thought of food sends sensory inputs to hypothalamus, which stimulates vagus nerve to send signals to gastric glands to secrete gastric juices

2. gastric phase: food reaches stomach: stimuli is mechano-sretch-chemo- receptors in wall of stomach. triggers ENS (enteric nervous system - neurons embedded in walls of GI tract) and PSNS to stimulate gastric secretion

3. intestinal phase: chyme starts leaking into duodenum of small intestine - has a brief stimulatory effect followed by a long inhibitory effect

hormonal regulation of gastric secretion

-gastric phase: triggers gastrin (secreted by G cells) to travel through blood to stimulate parietal cells to ramp up HCl production
-intestinal phase: SI releases enterogastrones like secretin and CCK to inhibit gastric secretion and decrease gastric motility - “brake” system to slow the stomach down

neural regulation of gastric secretion

-cephalic: vagus nerve stimulates gastric juice secretion
-gastric: stimulation of stretch receptors triggers local and long reflexes that increase section; negative feedback inhibits gastrin secretion to prevent too acidic
-intestinal: enterogastric reflex in the inhibitory component inhibits the vagus nerve and tightens pyloric sphincter to prevent more food from entering SI

secretin vs CCK vs somatostatin

-secretin: released by duodenum when it tastes the highly acidic chyme form stomach - targets pancreas to secret bicarbonate, liver to increase bile production, stomach to slow HCl production
-CCK: released by duodenum when it detects fats and proteins: targets gallbladder to squeeze out bile, pancreas to release pancreatic juice, hepatopancreatic sphincter to allow bile/pancreatic juice to enter duodenum, and stomach to inhibit activity to give SI time to deal with fat
-somatostatin: produced by D cells to brake entire digetive system: triggered by drop in pH or sympathetic nervous system: secretes almost everything else (gastrin, HCl, pancreatic juices)

metabolism vs anabolism vs catabolism

-metabolism: sum total of all chemical reactions in a living organism
-anabolism: type of metabolism that builds complex molecules from simpler ones (endergonic)
-catabolism: type of metabolism that breaks down complex molecules (exergonic - used to synthesize ATP)

absorptive state: glucose/glycogen catabolism/anabolism

during/shortly after eating, when blood is flooded with nutrients and the goal is to build and store

-hormone in charge: insulin
-glucose catabolism: glycolysis: cells use freshly absorbed glucose to produce ATP immediately
-glycogen anabolism: glycogenesis: liver and skeletal muscles take excess glucose and string it together into glycogen for storage
-lipid/protein anabolism: excess glucose converted into triglycerides and amino acids built into proteins

**anabolism - building reserves while burning the new fuel

postabsorptive state: glucose/glycogen catabolism/anabolism

when GI tract is empty (between meals/overnight), blood glucose levels begin to drop and the goal is to maintain blood glucose levels within homeostatic range

-hormone in charge: glucagon
-glycogen catabolism: glycogenolysis: liver breaks down stored glycogen back into glucose and releases into blood
-lipid catabolism: adipose tissues break down fats into glycerol and fatty acids to be used as alternative fuel
-gluconeogenesis: if glycogen runs low, liver creates “new” glucose from non-carbohydrate sources like amino acids or glycerol

**time to catabolism - tearing down savings to keep blood sugar steady

short-term regulars of appetite

-ghrelin: by parietal cells: empty stomach → hunger
-peptide YY: by ileum and colon: meal terminator: rise after eating and remain high for a few hours to keep you from eating again too soon
-CCK: duodenum and jejunum: short-term satiety signal to terminate meal, stimulates enterogastric reflex (inhibits gastric secretion, gastric motility, constricts pyloric sphincter)

long-term regulators of appetite

-insulin: by pancreatic beta cells: glucose and AA uptake from blood to tissue cells; chronic insulin levels cross into hypothalamus to act as long-term suppressant to signal body is consistently well-fed
-leptin: by adipocytes: amount of leptin in blood is directly proportional to how much body fat you have. leptin stimulates lipolysis (fat breakdown) to promote a high-energy, active metabolic state. travels to hypothalamus to inform it that your long-term fat reserves are full.