Term
| how does the stomach empty? |
|
Definition
Peristaltic contraction at upper
fundus towards pyloric sphincter
– Greater strength at antrum – propels
chyme forward
– Small amounts of chyme pushed
through partially open sphincter |
|
|
Term
|
Definition
Contraction at closed sphincter – no
emptying
– Chyme “tossed” back |
|
|
Term
| what is the time course of gastric emptying? |
|
Definition
2-6 hrs for gastic emptying
– chyme ejected every 20 s |
|
|
Term
| what are the triggers for gastric emptying? |
|
Definition
excitatory - Chyme in stomach
– Inhibitory (duodenum)
•Fat
• Acid –prior to neutralization
• Hypertonicity
• Distension/chyme |
|
|
Term
| what are the mechanisms for gastric emptying? |
|
Definition
Neural (short and long reflexes
– Hormonal – enterogastrones
(secretin, cholecystokinin-CCK)
– Emotions/pain/aggression |
|
|
Term
| acid triggers secretin release. fat triggers cholecystokinin. |
|
Definition
|
|
Term
| what are the long reflexes of gastric motility? |
|
Definition
“cephalic” / Autonomic
– vagal reflexes or supraspinal
(limbic) centers |
|
|
Term
| what are the short reflexes of gastric motility? |
|
Definition
Myenteric (Auerbach’s) plexus
– Submucosal (Meissner’s) plexus
– Pathways
• Sensory afferents – Meissner’s
(pH, distension, osmolarity,
chyme)
• Afferent to “interneurons” to
efferent (Meissner’s or
Auberbach’s)
• Efferent – muscular or glands |
|
|
Term
| what is the pathway of GI long and short reflexes? |
|
Definition
Long - external stimuli --> sensory receptors --> cephalic brain --> neurons of the submucosal and myenteric plexuses --> smooth muscles or secretory cells --> muscle contraction or relaxtion, exocrine, secretion, defecation, etc.
Short reflexes - LOCAL stimuli --> sensory receptors and neurons --> interneurons --> neurons of the submucosal and myenteric plexuses --> smooth muscles or secretory cells --> muscle contraction or relaxtion, exocrine, secretion, defecation, etc. |
|
|
Term
| how does the endocrine system regulate gastric motility? |
|
Definition
– Secreted into the blood
– Act on accessory organs, other GI parts or the brain |
|
|
Term
| how does the paracrine system regulate gastric motility? |
|
Definition
lumen or ECF
– Lumenal signals bind to apical epithelial receptors
– ECF signals act in the immediate vicinity of secretion |
|
|
Term
| what is the effect of endocrine and paracrine regulation of gastric motility |
|
Definition
Peptides alter secretion and motility
– Alter behavior related to eating |
|
|
Term
| what are the gastrin familiy of hormones? |
|
Definition
stomach - gastrin (important)
intestine - cholecystokinin (important) |
|
|
Term
| what is the secretin family? |
|
Definition
secretin (important)
glucagon like peptide 1 |
|
|
Term
| what is the peptide family? |
|
Definition
motilin
gastric inhibitory peptide |
|
|
Term
|
Definition
| peptides and amino acids trigger its release. it targets ECL cells and parietal cells. it stimulates gastric acid secretion and mucosal growth |
|
|
Term
|
Definition
| it is triggered to be released by acid in the small intestine. it targets cells in the pancrease and stomach. it stimulates bicarb secretion and inhibits gastric emptying and acid secretion. |
|
|
Term
| how does cholecystokinin work? |
|
Definition
| fatty acids and some amino acids trigger it. it targets cells in the gallbladder, pancrease, and stomach. it stimulates gallbladder contraction and pancreatic enzyme secretion. inhibits gastric emptying and acid secretion |
|
|
Term
| what are the two areas of gastric mucosa? |
|
Definition
Oxyntic mucosa - Lines body and fundus
– Pyloric gland area (PGA) - Lines antrum |
|
|
Term
| what are the secretory cells of the stomach? |
|
Definition
Chief cells - pepsinogen
– Parietal (oxyntic) cells - HCl and intrinsic factor
– Mucous cells – line pit/gland entrance |
|
|
Term
|
Definition
release pepsinogen)
– Stimuli- vagal (Ach), gastrin
– Function- precursor to pepsin (activated by HCL) to breakdown proteins. |
|
|
Term
| how do parietal cells work? |
|
Definition
release HCL and intrinsic factor.
Stimuli – vagal, gastrin, histamine
– Function
• HCl activates pepsin
– protein breakdown/denaturation
– kill microorganisms
• Intrinsic factor – facilitate B12
absorption |
|
|
Term
| how do mucous cells work? |
|
Definition
make alkaline mucus. Stimuli – mechanical
– Function – protect mucosa against
pepsin, HCl |
|
|
Term
| what are the endocrine and paracrine cells of the stomach? |
|
Definition
| G cells, enterochromaffin like cells (ECL), D cells |
|
|
Term
|
Definition
they release gastrin (antrum and duodenum). Stimuli- ACh, protein products
– Function- stimulate parietal, chief,
ECL cells |
|
|
Term
|
Definition
make histamine. Stimuli – Ach, gastrin
– Function – stimulate parietal cells |
|
|
Term
|
Definition
make somatostatin. Stimuli – acid
– Function - inhibit parietal, chief,
ECL cells |
|
|
Term
| how does the gastric mucosal barrier/HCL secretion work? |
|
Definition
Enables stomach to contain acid without injuring itself
• Functions of HCl
– Pepsinogen to pepsin, H+ medium for optimal pepsin activity
– Breakdown tissues /denature proteins
– Kills most microorganisms |
|
|
Term
| What are the phases of gastric secretion? |
|
Definition
| cephalic phase and the gastric phase. |
|
|
Term
| what is the cephalic phase of gastric secretion? |
|
Definition
Deglutition reflex –food from
pharynx to stomach (3.5 L/day)
– Long and short reflexes - HCl,
pepsinogen secretion before
stomach |
|
|
Term
| what is the gastric phase of gastric secretion? |
|
Definition
Storage of food (receptive
relaxation of fundus)
– Digest into chyme
(pepsin/mechanical) – protein
presence increase secretions |
|
|
Term
| what are the steps of the gastric phase? |
|
Definition
1. food/cephalic (vagal) reflex
→gastrin from G-cells
2. Gastrin (Ach/vagal) →
a. parietal cell release of HCl
b. ECL release of histamine
(stimulates parietal cells)
3. HCl →
a. Chief cell release of
pepsinogen
b. Pepsinogen to pepsin
c. D cell release of
somatostatin →turns down
HCl/pepsin activity |
|
|
Term
| what are the parts of the intestinal phase? |
|
Definition
(inhibitory)
– Controlled chyme entry into small intestine
• Feedback: limit gastric secretions
• Feedforward: promote digestion/motility, secretion small intest.
– Secretin –
• slows gastric emptying & gastric acid production
• Stimulates pancreatic HCO
3
-production to buffer acidic chyme
– cholecystokinin (CCK)
• Trigger – lipid; slows gastric motility/HCl secretion
• Acts hormonally on the pancreas, hypothalamus, gallbladder
– Gastric Inhibitory Peptide, Glucagon-like Peptide-1
• Slow gastric acid and emptying
• stimulate insulin release from pancreas |
|
|
Term
| what are plicae circulares? |
|
Definition
Segmentation
• Ring-like contractions – intermittent contraction/relaxation
with alternating neighboring segments
• Purpose: mixes chyme throughout small intestine lumen |
|
|
Term
| how does small intestine motility work? |
|
Definition
initiated by pacemaker cells, produce basic electrical rhythm (BER)
• Circular smooth muscle responsiveness influenced by distension,
gastrin, and extrinsic nerve activity
• Functions
– Mixing chyme with digestive juices
– Exposing chyme to absorptive surfaces |
|
|
Term
| what is the absorptive surface of the small intestine? |
|
Definition
Inner surface = circular folds
– Microscopic villi
– Brush border (microvilli) enterocy |
|
|
Term
| what are the glandular secretions of the pancreas? |
|
Definition
Exocrine function (pancreatic juice) and endocrine (insulin/glucagon)
– HCl in Small Intest. →Secretin secretion →NaHCO3 secretion by
duct cells
– Fat (some protein) →CCK secretion →digestive enzymes
•Proteins
– Trypsinogen →trypsin (by enterokinase/enteropepsidase)
– Chymotrypsinogen →chymotrypsin (by trypsin)
– Procarboxypeptidase →carboxypeptidase (by trypsin)
• Starch/polysaccharides via amylase
• Triglycerides into monoglycerides via lipase (1º GI fat enzyme)
– Enzyme secretion does NOT vary according to meal |
|
|
Term
| what pancreatic enzymes break down proteins, carbs, and fats, respectively? |
|
Definition
Proteins
– Trypsinogen →trypsin (by enterokinase/enteropepsidase)
– Chymotrypsinogen →chymotrypsin (by trypsin)
– Procarboxypeptidase →carboxypeptidase (by trypsin)
• Starch/polysaccharides via amylase
• Triglycerides into monoglycerides via lipase (1º GI fat enzyme) |
|
|
Term
| what are the digestive functions of the liver? |
|
Definition
Storage (glycogen, fats, iron,
copper, vitamins)
– Activates vitamin D
– Removes bacteria and wornout RBCs
– Excretes cholesterol and
bilirubin (from RBCs)
processes major nutrient categories.
Detoxifying/degrading wastes,
hormones, drugs,
– Synthesizes plasma proteins |
|
|
Term
|
Definition
RBCs removed in liver (macrophages)
– Characteristic yellow color
– w/digestive enzymes – feces
becomes brown
it is the yellow breakdown product of normal heme catabolism. Heme is found in hemoglobin, a principal component of red blood cells |
|
|
Term
| how does secretion of bile/bile salts work? |
|
Definition
Formation/secretion by liver, enters duodenum
– Stored/concentrated in gall bladder b/t meals
• Bile salts – cholesterol derivative
– Converts fat micelles into liquid emulsion
– After fat digestion/absorption, most bile reabsorbed in blood
• Others: Cholesterol, lecithin, bilirubin |
|
|
Term
|
Definition
very small fat droplets
– Hydrophobic core surrounded by water-soluble exterior
– Lecithin allows transport of cholesterol (hydrophobic) through H20 |
|
|
Term
| so what the hell happens in the intestine? |
|
Definition
Intestinal mucosal enzymes (brush border enzymes)
– Transport into
• enterocytes (absorptive cells lining gut)
• Blood or lymphatic vessels |
|
|
Term
| how does sugar digestion/absorption work? |
|
Definition
| salivary and pancreatic amylases break sugras down into disaccharides. intestinal mucosal enzymes break di sacharrides to monosacharrides. |
|
|
Term
| how does protein digestion/ absorption work? |
|
Definition
Pancreatic Proteases/Peptidases + HCl, Pepsin
• Intestinal mucosal (brush border) enzymes
• Peptidases – Polypeptides to AAs |
|
|
Term
| how does fat absorption work? |
|
Definition
Pancreatic Lipases
• Bile (stimulated by CCK) - Emulsifies lipids, increase lipase
action
• Bile salts, Triglycerides to FFA and glycerol – micelle absorption
Micelle reformation into TGs
– Exocytosis into chylomicrons (lipoprotein binding)
– Absorb into “lacteals”/lymphatics |
|
|
Term
| what is the function of the large intestine? |
|
Definition
Drying/storage organ (colon, cecum, appendix, rectum)
– Taeniae coli – longitudinal muscle
– Haustra (pouches sacs)
• Allow motility
• Autonomous rhythmicity
• Contents after digestion
– indigestible food residues
– unabsorbed biliary components
– remaining fluid
• Colon
– Extracts H20, salt
– Feces – eliminated |
|
|
Term
| what is the gastrocolic reflex? |
|
Definition
– Stomach to colon by gastrin,
ANS
– Most evident after first meal of
the day
– Followed by urge to defecate |
|
|
Term
| what is the defecation reflex? |
|
Definition
stretch receptors in rectal wall
with distension
– Relaxation of internal anal
sphincter; contraction of rectum,
sigmoid colon
– Voluntary relaxation of anal
sphincter |
|
|
Term
| what happens to macronutrients during the absorptive state? |
|
Definition
Carbohydrate
– glucose to liver, fat, muscle;
main post-fed energy
source
– glycogen (muscle/liver)
– triglycerides (adipose/liver)
•Protein -AAs to liver
(ketoacids/urea), muscle
(protein)
• Triglycerides
– Chylomicrons to adipose
(storage)
– Liver (TGs to VLDL to
adipose) |
|
|
Term
| how does insulin secretion work in the absorptive state? |
|
Definition
Beta cells of Islets of Langerhans
(pancreas)
• Release:
– Increased blood glucose
– Increased AA, GIP
– Increased parasympathetic activity
– decreased sympathetic activity
• Acts on muscle, liver, adipocytes
– Increase glucose uptake
– Stop glucose output (liver) |
|
|
Term
| what happens to macronutrients during the post-absorptive or catabolic state? |
|
Definition
Carbohydrate
– Maintain blood glucose
– Sources
• Liver/muscle glycogen
• Gluconeogenesis is from AAs
•Protein - AAs to liver for
gluconeogenesis
• Triglycerides
– FFAs for muscle/heart |
|
|
Term
| what secretes glucagon, and what does it do? |
|
Definition
alpha cells of the pancreas. Release:
– Decreased blood glucose
– Increased sympathetic
activity
• Acts on muscle, liver,
adipocytes
– Breakdown of liver
glycogen
– Increased
gluconeogenesis
– Increase ketone synthesis |
|
|
Term
| how does cholesterol function/regulation work? |
|
Definition
Sources:
– Dietary (small intestine)
– Synthesis – most cells, increased in liver, endocrine
• Function
– Part of membrane lipid bilayers
– Synthesis of bile salts
– Steroid hormones (aldosterone/cortisol and sex hormones)
– Pathological effects (atherosclerosis)
• Regulation: increase dietary cholesterol increase plasma cholesterol --> decrease liver synthesis |
|
|
Term
| describe the cephalic phase of gastric secretion. |
|
Definition
Taste, smell, sight of food, tactile
sensations in mouth/esophagus
stimulate parasympathetic system
(green arrow).
2. Vagal output to enteric plexus (pink
arrow), Ach from vagal/enteric triggers
secretions from parietal (HCl) and
chief (pepsinogen) cells in body, AND
gastrin secretion from G-cells in
antrum
5.Gastrin through circulation stimulates
parietal/chief cells, enterochromaffinlike (ECL) cell (facilitate HCl secretion)
(purple arrow) |
|
|
Term
| describe the gastric phase of gastric secretion. |
|
Definition
Stomach distension activates
parasympathetic reflexes
(green).
2. Vagal/Ach output to enteric
plexus for stomach
secretions/motility (pink).
3. Local distension causes local
enteric plexuses to faciltiate
more secretions/motility (HCl,
pepsinogen, gastrin), stretch
causes depolarization |
|
|
Term
| describe the intestinal phase of hastric secretion. |
|
Definition
Chyme, lipids, pH < 2 in
duodenum feedback to
CNS/parasympathetic (green,
pink) – decrease gastric motility
2. D cells (antrum, duodenum)
release somatostatin to inhibit G,
parietal, ECL cells (orange-ish)
3. Secretin (S cells), CCK (I cells),
GIP inhibits gastric motility (gold)
4. Secretin and CCK stimulate
pancreatic secretion of NaCO3-and pancreatic enzymes,
respectively (blue)
5. Bile salts in duodenum trigger
bile secretion from liver (red)
6. CCK initiates gall bladder wall
contraction, sphincter relaxation |
|
|
Term
| what are some inflammatory oral conditions? |
|
Definition
– Herpes simplex virus (cold sores) – younger adults, cold,
wind, sunlight, allergy interactions
– Aphithous ulcers (canker sores) – superficial, local Tx
– Oral candidiasis (thrush) – normal bacterial infection present
with immunocompromise
– Glossitis (tongue); parotitis (parotids) |
|
|
Term
|
Definition
| (dry mouth) – salivary disorders, Sjogren syndrome |
|
|
Term
| what is aphagia/dysphagia? |
|
Definition
|
|
Term
|
Definition
Reflux esophagitis - gastric contents
(“heart-burn”)
• Decreased LES smooth muscle activity (tone)
• CNS depression
• Increased gastric contents/delayed opening of
pylorus
– Barrett Esophagus – squamous to columnar
transformation |
|
|
Term
| what are some esophageal motor dysfunctions? |
|
Definition
Achalasia - incomplete relaxation of LES
– Also non-motor blockage/narrowing |
|
|
Term
| what are some effects of acute and chronic gastritis? |
|
Definition
Acute – NSAIDS/aspirin, EtOH, smoking, severe physical stress (surgery,
burns, ischemia)
• Epigastric pain, nausea, vomiting, severe – hemorrhage
• Inflammation – not erosion
– Chronic – chronic irritants, H. Pylori (90%)
• Atrophy, metaplastia, lymphoid and PMN aggregates
• Nausea, vomiting |
|
|
Term
| what is peptic ulcer disease? |
|
Definition
10% males; 4% females
– Remitting-relapsing,
chronic, solitary lesion
– Imbalance of acid-pepsin
vs defense mechanisms
– also H. Pylori |
|
|
Term
| what is enterocolitis caused by? what is it? |
|
Definition
Microbiological agents (E. coli, salmonella,
cholera toxins)
– Inflammatory disorders (amoebic
dysentery) |
|
|
Term
| what are some malabsorptive disorders? |
|
Definition
intraluminal digestion
– cystic fibrosis/pancreatitis
– bile duct /liver dysfunction (stearrhea)
– nutrient modification by bacterial
overgrowth
• terminal digestion
– disaccharidase deficiency
– bacterial overgrowth/brush border
damage
• transepithelial transport
(abetalipoproteinemia) |
|
|
Term
|
Definition
formation of granulomas
– transmural “skip” lesions; noncontinuous tract
– primarily autoimmune? |
|
|
Term
| what is ulcerative colitis? |
|
Definition
no granulomas
– usually damage to
mucosal/submucosal layers
– continuous lesions start at rectum,
work “up”
– immune dysfunction, possible
bacterial trigger?? |
|
|
Term
| what are some hepatic conditions that we discussed? |
|
Definition
Degeneration/intracellular
accumulation
• toxic/immunological insult
• foamy/edematous appearance –
steatosis
• Necrosis/apoptosis – zonal distribution
• Inflammation – hepatitis
– viral – A-E, Epstein Barr, Herpes
Simplex, Measles
– following chronic injury (toxins,
autoimmune)
• Regeneration/proliferation
• Fibrosis – irreversible hepatic damage
(scarring = cirrhosis) |
|
|
