GI physiology Flashcards by Alex Alanis

Steps in smooth muscle contraction

voltage-gated Ca entry, SR Ca release –> increased intracellular Ca –> binds calmodulin –> activates MLCK –> myosin phosphorylation by ATP –> crossbridge cycling –> contraction

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resting membrane potential of circular smooth muscle cells

-60 mV

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slow waves/ basic electric rhythm

spontaneous rhythmic waves of depolarization. magnitude = 10-15 mV

Does not cause contraction

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Effect of Ach on smooth muscle

causes action potentials to fire at each slow wave peak –> voltage-gated channel opening –> contraction at the frequency of BER (12/min)

more action potentials –> greater force of contraction

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predominant motor activity in the intestines

segmentation = isolated, uncoordinated smooth muscle contraction/relaxation –> mixing without net propulsion –> ensures proper digestion and absorption

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coordinated (via vagal input) contractions of adjacent segments in a proximal to distal manner

peristalsis

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intestinal relaxation distal to food bolus, produced by pressure of the proximal bolus

receptive relaxation

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effect of cutting the vagus nerve

BERs remain, but are disorganized –> abolished peristalsis

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phases of swallowing

voluntary = tongue moves food back to pharynx –> soft palate pushed upward, closed nasopharynx via upper constrictor muscle contraction

pharyngeal = respiration inhibited for 1-2 seconds, larynx raises and glottis closes

esophageal = UES relaxation, peristalsis –> food descends esophagus –> LES relaxation

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Phases of gastric motility

after eating, contractions start in mid-stomach at frequency of 3/min –> stronger, faster contractions in antrum –> transient opening of pylorus –> smaller particles and chyme leave the stomach, most content reflected back (retropulsion)

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what increases rate of gastric emptying?

combination of gastric distension and gastrin

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control of gastric emptying

duodenal distention and irritation (acidity and high osmolarity) –> reflex inhibition of gastric peristalsis, increased pyloric tone

fats in duodenum –> CCK secreted by enteric endocrine cells –> decreased gastric motility

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transit time of chyme in intestines

3-5h

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Purpose of myoelectric motor complexes

every 90 minutes –> removes bacteria and indigestible material

only occurs during fasting

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Normal fecal fluid loss

100-200ml

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mass movements

colonic forward propulsion. giant migrating contractions

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primary stimulator of colonic contractions

distention

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gastrocolic reflex

stimulates mass movements, pushing feces into the rectum

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defecation reflex

spinal reflex, mediated by the pelvic nerves –> relaxation of internal anal sphincter

sufficient to empty lower bowel in babies and pts with damaged spinal cords

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Parietal cells

secrete HCl via ATP consumption –> luminal pH of 2

secrete intrinsic factor –> B12 absorption

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Mechanism of acid secretion by parietal cells

CO2 diffuses into the cell from blood –> combines with OH- from H2O (produces H+, which is pumped to lumen via H/K ATPase) –> HCO3-, via carbonic anhydrase –> exchanged for Cl- in blood via Cl/HCO3 exchanger –> Cl to lumen via luminal Cl channel

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Stimulation of acid secretion

Direct path: Ach from vagus nerve –> M3 receptors –> parietal cell acid secretion

Gastrin –> increased intracellular Ca –> direct and/or indirect path –> H+ secretion

Indirect path: Ach from vagus nerve –> ECL M3 receptors –> Histamine release –> parietal cell H2 receptor binding –> Gs –> adenylate cyclase –> Ca and cAMP –> kinase activation –> phosphorylation of H/K ATPase

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4 phases of gastric acid secretion

basal (inter-digestive) phase,

3 phases associated with eating: cephalic phase, gastric phase, intestinal phase

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Circadian rhythm –> rate of acid secretion in lowest in the morning before awakening and highest in the evening. resting pH = 3-7

basal (inter-digestive) phase

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initiated by smell, sight, taste and swallowing of food

cephalic phase

Vagal mediation of cephalic phase

stimulation of vagus --> release of Ach, triggering of histamine release from ECL cells, release of gastrin-releasing peptide (GRP) from the vagal and enteric neurons, and inhibition of somatostatin release from delta cells in the stomach

How much acid secretion is accounted for by the cephalic phase?

30% of total acid secretion

initiated by entry of food into the stomach

gastric phase

components of the gastric phase

food distends the gastric mucosa --> vagovagal and ENS reflexes partially digested proteins --> antral gastrin (G) cell stimulation --> gastrin secretion

How much acid secretion is accounted for by the gastric phase?

50-60%

stimulation of the intestinal phase

presence of amino acid and partially digested peptides in the proximal portion of the small intestine --> duodenal gastrin (G) cell stimulation --> gastrin secretion --> acid secretion in stomach

Function of mucosal barrier

protect mucosa from acid, prevent diffusional dissipation of the pH gradient

fat absorption

fat digestive products --> lacteal --> --> thoracic duct --> blood stream

total absorptive area of the intestinal surface

200-400 square meters

secreted by the salivary glands, digests starch, in the mouth product = polysaccharides

Amylase

secreted by serous glands of the tongue, digests fat, in mouth and stomach Products: monoglycerides, fatty acids

lingual lipase

secreted by the stomach, digests protein product: polypeptides

pepsin

secreted by the pancreas, digests proteins and polypeptides, located in the duodenum and jejunum Product: small peptides and amino acids

trypsin, chymotrypsin, elastase, carboxypeptidases

secreted by the pancreas, digests starch, located in the duodenum and jejunum Product = maltose, maltotriose, and alpha-limit dextran

amylase

Secreted by the pancreas, digests fat, located in the duodenum and jejunum products = monoglycerides, fatty acids, cholesterol

lipase and colipase, phospholipase A2, cholesterol ester hydrolase (non-specific lipase)

Secreted by the liver, emulsify and dissolve fats, located in the duodenum and jejunum

bile salts

secreted by the stomach, kills bacteria and denatures proteins, located in the stomach

HCl

Ubiquitous secretion, buffers pH

NaHCO3

Ubiquitous secretion, lubricates and protects mucosal surfaces

mucus

Specificity of amylase digestion

catalyzes the hydrolysis of a-1,4 linkages (amylopectins) will never digest cellulose (dietary fiber, a-1,6 linkages), will NEVER PRODUCE free glucose (products converted to glucose by brush-border enzymes)

transports glucose and galactose from intestinal lumen into the cytosol

Na-dependent glucose transporter (SGLT1) in the brush border or apical membrane of enterocytes

transports fructose from the lumen into the cytosol

GLUT5 (Na-independent fructose transporter)

transports fructose, glucose and galactose from cytosol to the blood

GLUT2 (Na-independent fructose transporter)

causes lactose intolerance

absence of lactase (brush-border enzyme)

lactose intolerance

unabsorbed lactose --> osmotic diarrhea; gut bacteria metabolize lactose --> gas

causes glucose-galactose intolerance

genetic absence of SGLT1 (Na/glucose cotransporter) --> potentially fatal in neonates lack of Na and glucose absorption, --> lack of fluid absorption, osmotic fluid secretion --> diarrhea

treatment associated with glucose-galactose malabsorption

replace dietary glucose with fructose (uses different transporter)

two classes of peptidases

endopeptidases (hydrolyze interior peptide bonds) and exopeptidases (hydrolyze one amino acid at a time from the C terminus of proteins and peptides)

Pepsin, trypsin, chymotrypsin, elastase

endopeptidases

Carboxypeptidases A and B

exopeptidases

converts dipeptides to amino acids

Dipeptidase

removes dipeptides from the N terminus

Dipeptidyl aminopeptidase

removes one amino acid at a time from the N terminus

Aminopeptidase

What is the status of pepsinogen at pH 1-3

activated to pepsin

What is the status of pepsinogen at a pH above 5

inactive; remains pepsinogen

Patients with their stomach removed can't secrete HCl or pepsin. Does this mean that they can't digest protein?

No! neither pepsin, nor HCl are essential for protein digestion

Steps of small intestinal protein digestion

activation of trypsinogen to trypsin by enterokinase (brush border) --> activation of all other precursors by trypsin --> hydrolysis of proteins to amino acids and di-, tri-, oligopeptides via trypsin, chymotrypsin, elastase, carboxypeptidase A and B --> brush border proteases hydrolyze oligopeptides to amino acids --> pancreatic proteases digest themselves and each other

Which two amino acids require a specialized carrier for efficient absorption?

proline and glycine

patients lack the Na-amino acid transporters (genetic) --> lack capacity for renal or intestinal absorption of cysteine, lysine, arginine and ornithine excretion of amino acid in the feces/urine

Cysteinuria

genetic absence/defect of the neutral amino acid transporter

Hartnup disease

genetic absence/defect in the Cl channel CFTR

Cystic fibrosis

digests triglycerides --> 2-monoglyceride and two free fatty acids, which can be absorbed

pancreatic lipase

solubilizes 2'-monoglycerides and fatty acids

bile-salt micelles

process of triglyceride absorption

pancreatic lipase digestion --> bile salt micelle solubilization --> entry into enterocyte --> triglycerides resynthesized --> packaged into chylomicrons with cholesterol and apolipoproteins --> golgi --> incorporated into secretory vesicles --> exocytosis to interstitial space --> lacteals (too large for capillaries)

What other nutrients are absorbed via the same route as fats and cholesterol?

Vitamin A, D, E, and K. All are fat-soluble

fat malabsorption disorders

Liver disease c bile salt deficiency Pancreatic insufficiency (lack pancreatic lipase) Weight loss medication use --| lipase activity --> anal leakage

Two important principles for water absorption

water readily moves across the intestinal epithelium --> chyme in duodenum rapidly brought to isotonic equilibrium with the blood water absorption follows the absorption of solutes (absorbed isotonically)

important mechanism for colonic absorption of Na

epithelial sodium channels (ENaC)

Significance of K secretion in colon

increased Na absorption --> increased K secretion net K secretion when lumenal [Na] drops below 25 mM severe diarrhea --> significant fluid loss --> hypokalemia

How is B12 absorbed?

in complex with intrinsic factor in the distal ileum

Result of impaired absorption of B12

pernicious anemia