Digestion in STOMACH, Vomiting, Hunger, SATIETY

STOMACH, Vomiting, Hunger

Rodolfo T. Rafael,M.D.

http://www.clinical-updates.blogspot.com 2


AnatomyFunctional ComponentsMusculatureInnervation


Functional Components

funduscorpusantrumantrum and pylorus


Musculature

functional syncytiumFundus- contraction is weakAntrum- contraction is greaterPyloric sphincter


InnervationIntrinsic- myenteric and submucosal plexus directlyresponsible for peristalsis

Myenteric Plexusbetween circular and longitudinal muscle

Submucosal Plexusbetween circular muscle and mucosa

ExtrinsicSympathetic

celiac plexusinhibits motility

Parasympatheticvagus nerve

stimulate motility


MotilityFunctionStorage is Accomplished by Receptive Relaxation and AccommodationPeristalsisRetropulsionGastric EmptyingRegulation of Gastric EmptyingVomiting


FunctionStorage

orad region- enlarge to accomodate the food

Mixingcaudad stomach- presence of food--increases the contractile activity of the stomach

Peristalsis and RetropulsionChyme

Emptyingchyme propelled into the intestine


Receptive Relaxation and Accomodation

Receptive Relaxationpart of peristalsis process

swallowing and esophageal motility

Accommodationinitiated by bolus of food

vagovagal reflexreceptive relaxation

Inhibitory NeurotransmitterVIP or NO

Effects of Vagotomydiminishes receptive relaxation and accommodation

2 liters


Peristalsisinitiated near the fundal-corpus borderMechanics of Peristalsis- produced by periodic changes in membrane potential

initiated by pacemakerslow wave or (BER) consist of upstroke and plateau phaseVelocity 1 cm/sec 3-4 cm/secUpstroke is due to the flow of Na+ and Ca2+

into the cell and that the plateau is dependent primarily on the flow of Ca2+ into the cell

Forces of Peristalsisgastrin and (ACH)

increase the size of the slow wave plateau potentialActivate second messengers


Retropulsion

back- and- forth movement of the chymecaused by the forceful propulsion of food against the closed pyloric sphincter

breaks the chyme


Gastric Emptyingchyme is decomposed into small pieces less than (1mm3) to fit through the pyloric sphincter.

2-7ml escape into the duodenumchyme passing through the pylorus depends on the size of the particlesRate of Gastric Emptying of solids depends on the rate chyme is broken downLiquid empty much faster than solid


Regulation of Gastric EmptyingLocal Reflexes

Excitatory reflexes- initiated by expansion of antrumInhibitory Reflexes-enterogastric reflexes

Purpose- prevent the flow of chymeCause- high osmolarity, low pH, fat and protein digestion products, low osmolality, the caloric content of food, distention of the duodenal wall

HormonesExcitatory Effects

Gastrin- antral distentionInhibitory Effects

CCK- fat or protein digestion productsSecretin- acid, direct inhibitory effect on smooth muscle

Migrating Motor Complex (MMC)begins within the esophagus60-90 minutesmotilin


Vomitingforceful expulsion of the foodInitiation

Vomiting CenterChemoreceptor Trigger zone

Mechanical Sequence of VomitingDeep inspiration closing of glottis pressure wave originating in the intestine propels chyme into the oradstomach increase in abdominal pressure forces the chyme into the esophagus and out of the stomach.Retching may precede vomiting

involves all of the involuntary motions of vomiting but without the production of vomitusthe chyme is not ejected


Gastric SecretionGeneral ConsiderationHCl SecretionGastrin SecretionPepsinogen SecretionIntrinsic Factor


General Consideration

Functionbreakdown of food into small particles2 L/day



PhasesThe Cephalic phase

thought, sight, taste or smell of fooddependent on the integrity of the vagal fibersSecretion

HCl from parietal cellsGastrin from G cellsPepsinogen from peptic cells

Half of the gastric secretion released during meal result from cephalically induced vagalstimulation


General ConsiderationThe Gastric Phase

entry of food into the stomachfood buffers acids, raises pH, and allows other stimuli to release acidDistention of the corpus local and vagovagal reflexes increase in HClDistention of the antrum local and vagovagal reflexes Gastrin is release from antral G cells Gastrin release is inhibited at low pH (<3)Low pH local reflexesPepsinogen SecretionRate of Gastric secretion is less than Cephalic but continues for longer time



The Intestinal PhaseChyme begins to empty from the stomachduodenumlittle gastric secretion


General ConsiderationGastric Secretory Cells

Oxyntic glandslocated in the fundus and corpus of the stomach

The Parietal (oxyntic cells)HClIntrinsic factor absorption of vitB12 by the ileum

Peptic (Chief Cells)- pepsinogenMucous cell- mucus

Pyloric Glandsantrum and pyloric regions

G cellsrelease of gastrin (G17, G34)basolateral surface of G cells circulation oradstomach stimulate parietal cell HCl


HCl Secretion

Function of HCLMechanism of HCl secretionSubstances Affecting HCl secretionRegulation of Gastric Acid secretion


HCl Secretion

Function of HCLbreakdown of proteinoptimal pH for the action of pepsinhinders the growth bacteria


HCl SecretionMechanism of HCl secretion

HCl is secreted into the parietal cell canaliculiH+ entering the canaliculi is supplied by dissociation of carbonic acid within the parietal cellMost of the HCl neutralized and reabsorbed within the small intestineActive transport processes require large amount of ATPThe pH of the parietal cell secretion can be as low as 0.8H+-K+-ATPase pump can be irreversibly inhibited by the drug OMEPRAZOLE



HCl is secreted into the parietal cell canaliculi

Active transport begun by the transport of K+ and Cl- into the canaliculi. Cl- transported by a pump or through a channelH+ is then exchanged for K+

by the H+- K+- ATPase pumpWater enters the canaliculidown the osmotic gradient created by the movement of HCl into the canaliculi



H+ entering the canaliculi is supplied by dissociation of carbonic acid within the parietal cell

H2CO3 is formedCO2 + H2O H2CO3 H+ + HCO3

-

H2CO3 from CO2 catalyzed by carbonic anhydrase

HCO3- diffuses back in the plasma


HCl SecretionSubstances Affecting HCl secretion

Stimulation of HCl secretionAch

neurotransmitterHistamine

mast cellsparacrine agentranitidine, cimitidine

GastrinG cellshormone

Inhibition of HCl secretionSomatostatin

inhibit HCl (parietal cell) Gastrin G cellsreleased from interneurons within the enteric nervous system


HCl Secretion

Regulation of Gastric Acid secretionStimulation During the Cephalic PhaseStimulation During the Gastric PhaseInhibition During the Gastric PhaseStimulation During the Intestinal PhaseInhibition During the Intestinal Phase


HCl Secretion

Regulation of Gastric Acid secretionStimulation During the Cephalic Phase

vagus nerve+ Ach- somatostatinenhance secretion of HCl


HCl Secretion

Regulation of Gastric Acid secretionStimulation During the Gastric Phase

amount of ingested proteingood bufferamino acids and peptides parietal cells HCl

Alcohol and Caffeine


HCl Secretion

Regulation of Gastric Acid secretionInhibition During the Gastric Phase

presence of acid in the stomacha low (<pH 2) – HCl and gastrin secretionLow pH release somatostatin


HCl Secretion

Regulation of Gastric Acid secretionStimulation During the Intestinal Phase

protein digestion products within the duodenum increase HCl secretionentero-oxyntinamino acids


HCl Secretion

Regulation of Gastric Acid secretionInhibition During the Intestinal Phase

food enters the duodenumH+, fatty acids, and increased osmolarityenterogastrones (GIP) inhibits gastrin release and parietal cell secretion of HCl


Gastrin Secretion

Function of GastrinSubstances Affecting Gastrin SecretionRegulation of Gastrin Secretion


Gastrin Secretion

Function of Gastrinstimulates HCl secretionincrease gastric and intestinal motilityincrease pancreatic secretionproper growth of GI mucosa


Gastrin Secretion

Substances Affecting Gastrin SecretionStimulation

Bombesin [gastrin-releasing peptide (GRP)]vagus nerve increase release during cephalic phase

InhibitionSomatostatin

vagus nerve inhibit the release during cephalic phase


Gastrin Secretion

Regulation of Gastrin Secretionvagal stimulation, pH, enterogastronesprotein digestion product, alcohol, and coffee


Pepsinogen SecretionFunction

pepsinproteolytic enzyme

RegulationCephalic Phase

vagally stimulated cholinergic neurons within the enteric nervous system chief cells

Gastric Phaselow pHACh

Intestinal Phasesecretin


Intrinsic Factor

Definitionglycoprotein secreted by parietal cells of the gastric mucosa

Functionabsorption of Vit B12


Gastric Mucosal BarrierAutodigestionRate of RepairUlcer Therapy


Gastric Mucosal BarrierAutodigestion is prevented by:

Mucus, which contains HCO3-A high Blood FlowHigh Turnover rate

5 x 105 mucosal cells are shed / minutereplacing the entire mucosa 1-3 days

Prostaglandinsmaintain the gastric mucosal barrier


Gastric Mucosal BarrierRate of Repair

48 hours3-5 months

depends on the extent of injury


Gastric Mucosal BarrierUlcer Therapy

drugs that neutralize gastric acid (antacid)prevent acid release (PPI, H2 antagonistAntibiotics for H. pylori


Gastric Digestion and Absorption

DigestionAbsorption



DigestionCHO

salivary amylase CHON

10%gastric pepsin

Fatminimal due to restriction of gastric lipase activity to triglycerides short chain fatty acidsAcid and Pepsin break emulsion



AbsorptionNutrients

very little absorptionSubstance absorbed

highly lipid- soluble substancesAspirin- un-ionized and fat soluble ionizes intracellularly damaging mucosal cells bleedingEthanol absorbed in proportion to its concentration.

Watermoves in both directiondoes not follow osmotic gradientWater soluble substance

Na, K+, Glucose, and Amino acids absorbed in insignificant amounts

Hunger and

Satiety



Introduction

The regulation of feeding is the regulation of energy intake which involves not only the quantitative adjustment of energy intake to match metabolic needs, but also the qualitative selection of nutrients required for healthy sustenance. Small errors in matching intake with utilization can over time lead to gross changes in body weight and in nutritional status.


IntroductionDefinitions and Terminology

1. Hunger: Awareness of the need to eat. Can be accompanied by a number of symptoms such as hunger pangs, salivation in anticipation, restlessness and food-seeking behavior. Hunger reflects a physiological need. 2. Appetite: This is the desire to eat and is not necessarily accompanied by need to eat. Appetite is more a process of choice or selection, and is generally a learned behavior.3. Satiety: Satiety is the lack of desire to continue feeding and is accompanied by a vague feeling of fullness. It is associated with a lack of need.4. Obesity: increased body weight beyond the limits of skeletal and physical requirements as result of excessive accumulation of body fat.

Phagia (to eat)polyphagia - nondiscriminatory eating hyperphagia - excessive eatinghypophagia - inadequate eating


Neural Regulatory Centers for the Control of Food Intake

A. Hypothalamus - Location of the feeding centers.1. Ventromedial Nucleus (VMN): Neurons in this nucleus provide satiety signals.

a. Stimulation of the VMN causes experimental animals to behave as if satiated.b. Lesioning the VMN causes hyperphagia and obesity (hypothalamic obesity).

2. Lateral nucleus (LN): This nucleus serves as the hunger center.a. Stimulation of the LN causes pronounced hyperphagia.b. Lesioning the LN causes experimental animals to stop eating.

3. Interactions between the VMN and LNSignals associated with satiety reach the VMN and activate specific neurons. The VMN is then thought to inhibit the LN via interconnecting neural pathways. As a result, hunger is suppressed. When satietysignals decrease the inhibition on the LN is removed and hunger is experienced. Recent evidence suggests the neurons whose cell bodies are located in the Paraventricular Nucleus (PVN) may also provide input to the LN which initiate satiety.


Neural Regulatory Centers for the Control of Food Intake

B. Limbic System: The amygdaloid nucleus and the limbic system are involved in emotional responses which relate to preservation.

1. Lesions in the amygdala generally cause experimental animals to become hyperphagic, polyphagic and obese. These changes are associated with apparent loss of "appetite memory" and loss of discrimination between foods. 2. Amygdala has inputs from olfactory bulb indicating a connection between emotional response and primary sensory stimulation.3. All stimuli from the limbic system "pass through" the hypothalamus.


Peripheral Mechanisms Operating to Signal the Neural Centers Regulating Food Intake

A. Alimentary Regulation: Signals originating from the Alimentary Canal itself (short-term regulation). 1. Important in feeding activity during a "digestive" period.2. Anatomical components of alimentary regulation

a. Role of mouth and pharynx Sensory input from this region can modulate activity of hypothalamic feeding centers. Experimental evidence:i. effect of an esophageal fistula: food entering the mouth but not reaching the stomach reduces hunger temporarily.ii. effect of the destruction of taste sensation: reduces effect offood in mouth.

b. Role of stomach and intestine.i. stomach and intestine empty (hunger contractions).ii. stomach and intestine filled produce satiety.



B. Nutritional or Metabolic Regulation (long-term regulation).

1. Thermostatic regulation: (Specific Dynamic Action or Effect)2. Blood metabolite regulation: GlucostaticHypothesis3. Hormonal Regulation: Leptin, Insulin, CCK.




1. Thermostatic regulation: (Specific Dynamic Action or Effect)After eating the body's metabolic rate increases which is accompanied by an increase in heat production. The increase in heat production is thought to provide a satiety signal to the hypothalamus.




2. Blood metabolite regulation: GlucostaticHypothesisAccording to this theory the level of blood metabolites act as the satiety signal. For example, evidence exists for glucose, free fatty acid and specific amino acids acting as regulators. However, only glucose appears to act directly at the level of the hypothalamus. When blood glucose decreases, activity in neurons of the VMN and PVN also decreases and hunger is stimulated.




3. Hormonal Regulation: Leptin, Insulin, CCK.Recent studies have demonstrated the existence of a peptide hormone produced by adipose tissue which may regulate feeding and nutrient deposition. This peptide is called Leptin.

Receptors for Leptin and insulin have been localized to the hypothalamus suggesting a hormonal basis for regulating long term feeding behavior.

In addition, receptors for the hormone cholecystokinin(CCK) are found in several hypothalamic regions suggesting direct input during the course of digesting a meal when CCK levels are high.

Loss of sensitivity to these signals may be involved in the development of pathological states (e.g., diabetes, obesity).


Factors that Affect Food Intake

A. Psychological State: (Limbic inputs)1. Learned eating behavior2. Emotionally induced eating or not eating

B. Pharmacology (Drugs):1. Stimulants tend to suppress eating2. Depressants stimulate eating

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Digestion in STOMACH, Vomiting, Hunger, SATIETY