Mod 7 - GIT

• 1) series of hollow organs
• 2) separated by sphincters
• 3) specialized secretions
• 4) characteristic layered structure
• 5) dibgestion consists of mechanical and chemical processes

• 1) energy replenishment
• 2) building blocks for metabolism (essential AA, fatty acids, minerals, vitamins)

hunger/satiety: regulates energy intake

appetite: regulates specific nutrient intake

stimulatory: ghrelin (released by stomach during fasting)

• inhibitory:
• stomach stretch receptors;
• CCK, insulin, and PYY (gastro-intestinal hormones)
• leptin (released by growing fat cells)

• 1) food motility
• 2) secretion of enzymes
• 3) acidity

Vagus: esophagus, stomach, pancreas, a little to SI and LI, stimulates ENS

Sacral nerves: distal half of LI, anus, defecation reflexes

celiac ganglion and the meseteric ganglion

innervate all parts

release norepinephrine which inhibits peristalsis and increases sphincter tone

gastrin: released by stomach (releases HCL, increase intestine movement, release of pepsinogen)

Secretin: released by SI, pancrease secretes alkaline, pro-enzyme, stimulates intestinal motility

CCK: secreted by SI, secretion of proenzymes and bile

Gastric Inhibitory Peptide: insulin secretion, inhibits gastric secretion and motility

1) celiac: you know food is coming, increased salivation and blood flow, stomach motility inhibited, initiates secretions

2) Gastric phase: food is in stomach, increases blood flow, increases SM stimulation, secretion of bile, panc juices, intestinal juices, intestinal mobility

3) Intestinal phase: chyme in duodenum, inhibits stomach to prevent overloading, secretion of bile, panc juices, intest. juices, increase blood flow to intest., gallbladder constriction and relaxation of sphincter of Oddi

Superficial to deep: Rectus abdominus, external oblique, internal oblique, transverse

• Superficial to deep:
• skin, Camper's fascia, external oblique, internal oblique, transverse abdominal, transversalis fascia, parietal peritoneium

semilunar line that marks the border of the rectus abdominus

skin, camper's fascia, external oblique apon., internal oblique apon., rectus abd., internal oblique apon., transvers abd. apon., transversalis fascia, parietal perit.

• inguinal ligament
• inguinal canal
• spermatic cord (round ligament in females)

• Vas def.
• testicular a (off aorta)
• testicular v
• lymphatics
• Cremaster muscle (raise and lower testes based on temp)
• sympathetic fibres
• genital branch of genitofemoral n

indirect: enters deep inquinal ring, exits superficial inguinal ring, can cause strangulation

direct: inters in Hasselbach's triangle and exits superficial inguinal ring, more common in old men, less serious

• parotid: watery, little mucus, amylase-rich
• submadibular: high in lysozyme
• lingual: mixed

• lubrication
• amylase (breaks down starch)
• protective functions (mucins coat, acts as a buffer, control of water intake (dry mouth), antimicrobial, drug absorption

• 1) liquid comes from capillary
• 2) acinar cells add mucin, amylase, etc
• 3) primary secretion is isotonic with plasma
• 4) duct cells remove Na and add K (more K is added therefore secretion becomes more hypotonic)
• 5) add bicarbonate and remove CL AND Vice versa

• 1) voluntary phase: tongue moves bolus to back of mouth
• 2) pharyngeal phase: bolus activates pressure sensors, triggers reflexes in teh swallowing centers of the brain stem. close epiglottis, esophagal sphincter opens
• 3) esophagal phase: peristaltic wave. Primary wave is goes from pharynx to stomach, secondary waves continue in esophagus (if necessary) until food is all in stomach

• 1) parietal cells (acid and intrinsic factor)
• 2) chief cells (pepsinogen)
• 3) mucous cells (secrete mucus, bicarbonate, sodium)
• 4) enterochromaffin-like (ECL) cells secrete histamine

• 1) cheif cells (pepsinogen)
• 2) endocrine cells (gastrin, somatostatin)

NO PARIETAL CELLS AND THEREFORE NO ACID

• 1) basal state: low rate, huge variation between individuals, low pH (no buffers)
• 2) Cephalic phase (food is coming): stimulates vagus nerve, stimulates H+ and gastrin, inhibits somatostatin (30% of secretion)
• 3) Gastric phase: distension of stomach stimulates vagus, dig protein activates antral G cells (gastrin) (50-60% of secretion)
• 4) Intestinal phase: intestinal cells and absorbed AA's cause small amount of secretion (5-10%)

• water/saline: leaves quickly
• acid meal: takes longer
• presence of lipids: takes even longer

Makes sure the duodenum doesn't get overloaded.

• B12 deficiency
• can't convert Fe3 to Fe2
• need to regulate food intake

• 1) tubulovesicles have H+ pumps
• 2) t. vesicles move to the basilar membrane when duct cell is activated
• 3) pump H+ into the blood and HCO3- into the cell and ultimately into the duct.

• proteins: trypsin, chymotrypsin, carboxypolypeptidase
• carbs: pancreatic amylase
• fat: pancreatic lipase, phospholipase, others

-secretory: oversecretion of water, absorption cant cope, caused by bacterial toxins or overstim. of ENS

-defective ion transport: fat malapsorption, bile acids, diabetes, inflammatory mediators like histamine

-osmotic diarrhoea: hyperosmotic fluid in lumen, fermentation can cause hyperosmotic

-hypermotility of intestines: bacterial toxins

Increase motility: CCK, secretin, gastrin,

Increase peristalsis: motilin (hormone relseased after chyme turns alkaline)

Decrease peristalsis: enteroglucagon (when glucose and fat in chyme)

• -fluidity of contents promotes emptying
• -pressure and chem irritation in ilium increase peristalsis and relaxes sphincter
• -pressure or chem irritation in cecum inhibits peristalsis and excites sphincter

• 1)Sent to liver
• 2) liver converts fructose and galactose to glucose
• 3) glucose released back into blood
•   -enters cells for glycolysis and citric acid cycle
•   -liver converts to glycogen (skeletal muscle) and TAG (adipose tissue)
•   -

• glucose
• very LDL's (from liver)
• chylomicrons

All stored as TAGs

stomach, spleen, small intestine, pancreas, large intestine

lots of bilirubin in the blood (bile reflux into blood). Urine is dark because of conjugate bilirubin excretion.

Cholesterol stones: cholesterol precipitates in gall bladder. Due to chronically high bile acid : lecithin (phospholipid) ratio. Increased risk in women. low bile salts.

Pigment stones: overload of unconjugated bilirubin

1) lining (red) flexible: over loosely fibrous LP, not many dermal papillae. Found: soft palate, inside lips and cheeks, ventral tongue, over alveolar bone (except where it is gingiva)

2) Masticatory (pink) immobile: in contact with food, keratinized or para keratinized, found: gingiva, hard palate

3) Specialized: aterior 2/3 of dorsum of tongue, may be keratinized has papillae.

1) filliform: heavily keratinized, no taste buds, why we brush our teeth.

2) Circuvallate papillae: taste buds flushed by von Ibner's glands, may be keratinized

3) fungiform papillae: not keratinized, taste buds on surface, 

4) foliate papillae: no keratinized, taste buds on lateral wall

Serous (red, look like pizza slice): secretes watery or albuminous fluid

Mucous (look like adipocyte): secrete mucus

• 1) centroacinar cells: beginning of duct
• 2) intercalated duct: secrete sodium and bicarbonate, stimulated by secreting
• 3) intralobular
• 4) interlobular
• 5) pancreatic duct

-Hepatocytes: 80% of liver vol, many microvilli facing blood plasma (in space of Disse), cell surface of adjacent cells form microscopic channels called bile canaliculi, lots of breakdown (therefore lots of RER)

• -Ito cells: may form part of sinusoid wall, make vit A, make most of liver's CT, can diff into myofibroblasts
• -Kupffer cells: macrophage, also form wall of sinusoid, degrade old RBCs, filter the lumen

-sinusoidal epithelial cells: form a fenestrated epithelium, line the sinusoid, BM forms outer wall of the space of Disse 

-pit cells: NK cells,

• -Mucosa:
•   -3 layers (epithelium, lamina prop (BV's and lymphocytes), muscularis mucosae(gentle agitation));
•   -4 types (protective, secreting, absorptive, absorptive/protective)

-Submucosa: strongest layer in gut; Meissner's plexus, glands in esophagus and upper duodenum

-muscularis externa: long and circular muscle, myenteric nerve plexus

-serosa, adventitia:

• 1) entry of enzymes into blood (leakage, production)
• 2) efflux of enzymes from damaged cells
• 3) clearance of enzymes

HC disease: elevated AST, ALT, LD

BT disease: elevated ALK, GGT, 5'NT

Observe relative increase over Upper Limit of Normal (ULN)

viral hepatitis (acute): cell damage causes release of cytoplasmic AST and ALT (ALT>=AST)

Necrosis of hepatocytes: release of both cytoplasmic and mitochondrial AST and ALT (AST>ALT)

chronic alcoholism: AST>ALT (>2:1)

Recall that there is lots of AST in the mitochondria, not so much for ALT

• All three hepatitises
• Alcoholic hepatitis
• toxic injury
• ischemic injury

Sources: liver, bone, placenta, ilium

Check and see if GGT or 5'NT are also elevated

• -riboflavin, thiamin, B12, K are made
• -fermentation of cellulose
• -recirculation of bile salts
• -prevent growth of harmful bacteria

• -surface and neck mucous cells
• -stem cells
• -Chief cells (pepsinogen and lipase) - apical granules
• -Parietal cells (HCl and intrinsic factor) - proton pumps in tubulovesicles (bigger than chief)
• -enteroendocrine cells: secretes hormones into lamina propria

• surface cells
• fenestrated capillaries that pick it up from the basal side of parietal cells

• -enterocyte: absorptive cell, glycocalyx on microvilli
• -goblet cells: mucous
• -enteroendocrine cells: secerete gastrin, somatostatin, CCK, secretin, others
• -paneth cells: at base of cells, innate immune system
• -M cells: antigen-presenting cells
• -stem cells (in crypts): make other cells

duodenum: brunner's glands, sphincter of Oddi,  intestinal glands (=crypts)

Jejunum: long and finger-like with well-developed lacteals

Ilium: Peyer's patches (lymphoid tiss., capped by M cells), shorter villi

• genes
• lifestyle
• abnormal feeding
• childhood overnutrition

• amphetamines: inhibit feeding centres
• Sibutramine: inhibit feeding centres and increase metabolism
•   -both of these overexcite the CNS
• Orlistat: lipase inhibitor (you will just poop out lipids)
• Gastric bypass surgery: decrease amount of food being eaten.

• Inanition: extreme weight loss
• anorexia: diminished appetite
• a. nervosa: abnormal psychic state with aversion to food
• cachexia: abnormally high metabolism
• bulemia nervosa: highly irregular feeding pattern with NO extreme weight loss
• Ednos: extreme preoccupation with weight.

• Right
• Left
• quadrate (anterior)
• Caudate (posterior)

• 1st 2 separated by the falciform lig
• last 2 on inferior surface of liver

• esophageal
• peri-umbilical
• colic
• rectal

out-pouchings of intestinal mucosa

-usually asymptomatic: can rupture causing BRB to be in stool, other minor GI symptoms

-may also become infected like an appendix

symptoms: abdom. pain, change in stool habits, weight loss, anorexia, fatigue, occult bleeding, BRB, may be palpable

treatment: combination of surgery and medical care

• males: prostate, deep lymph nodes, 
• females: internal genitalia, pelvic bones, deep LNs

both: rectal tumors, occult blood