Upload
others
View
1
Download
0
Embed Size (px)
Citation preview
STOMACH, Vomiting, Hunger
Rodolfo T. Rafael,M.D.
http://www.clinical-updates.blogspot.com 2
http://www.clinical-updates.blogspot.com 3
AnatomyFunctional ComponentsMusculatureInnervation
http://www.clinical-updates.blogspot.com 4
Functional Components
funduscorpusantrumantrum and pylorus
http://www.clinical-updates.blogspot.com 5
Musculature
functional syncytiumFundus- contraction is weakAntrum- contraction is greaterPyloric sphincter
http://www.clinical-updates.blogspot.com 6
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
http://www.clinical-updates.blogspot.com 7
MotilityFunctionStorage is Accomplished by Receptive Relaxation and AccommodationPeristalsisRetropulsionGastric EmptyingRegulation of Gastric EmptyingVomiting
http://www.clinical-updates.blogspot.com 8
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
http://www.clinical-updates.blogspot.com 9
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
http://www.clinical-updates.blogspot.com 10
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
http://www.clinical-updates.blogspot.com 11
Retropulsion
back- and- forth movement of the chymecaused by the forceful propulsion of food against the closed pyloric sphincter
breaks the chyme
http://www.clinical-updates.blogspot.com 12
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
http://www.clinical-updates.blogspot.com 13
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
http://www.clinical-updates.blogspot.com 14
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
http://www.clinical-updates.blogspot.com 15
Gastric SecretionGeneral ConsiderationHCl SecretionGastrin SecretionPepsinogen SecretionIntrinsic Factor
http://www.clinical-updates.blogspot.com 16
General Consideration
Functionbreakdown of food into small particles2 L/day
http://www.clinical-updates.blogspot.com 17
General Consideration
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
http://www.clinical-updates.blogspot.com 18
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
http://www.clinical-updates.blogspot.com 19
General Consideration
The Intestinal PhaseChyme begins to empty from the stomachduodenumlittle gastric secretion
http://www.clinical-updates.blogspot.com 20
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
http://www.clinical-updates.blogspot.com 21
HCl Secretion
Function of HCLMechanism of HCl secretionSubstances Affecting HCl secretionRegulation of Gastric Acid secretion
http://www.clinical-updates.blogspot.com 22
HCl Secretion
Function of HCLbreakdown of proteinoptimal pH for the action of pepsinhinders the growth bacteria
http://www.clinical-updates.blogspot.com 23
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
http://www.clinical-updates.blogspot.com 24
HCl SecretionMechanism of HCl secretion
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
http://www.clinical-updates.blogspot.com 25
HCl SecretionMechanism of HCl secretion
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
http://www.clinical-updates.blogspot.com 26
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
http://www.clinical-updates.blogspot.com 27
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
http://www.clinical-updates.blogspot.com 28
HCl Secretion
Regulation of Gastric Acid secretionStimulation During the Cephalic Phase
vagus nerve+ Ach- somatostatinenhance secretion of HCl
http://www.clinical-updates.blogspot.com 29
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
http://www.clinical-updates.blogspot.com 30
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
http://www.clinical-updates.blogspot.com 31
HCl Secretion
Regulation of Gastric Acid secretionStimulation During the Intestinal Phase
protein digestion products within the duodenum increase HCl secretionentero-oxyntinamino acids
http://www.clinical-updates.blogspot.com 32
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
http://www.clinical-updates.blogspot.com 33
Gastrin Secretion
Function of GastrinSubstances Affecting Gastrin SecretionRegulation of Gastrin Secretion
http://www.clinical-updates.blogspot.com 34
Gastrin Secretion
Function of Gastrinstimulates HCl secretionincrease gastric and intestinal motilityincrease pancreatic secretionproper growth of GI mucosa
http://www.clinical-updates.blogspot.com 35
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
http://www.clinical-updates.blogspot.com 36
Gastrin Secretion
Regulation of Gastrin Secretionvagal stimulation, pH, enterogastronesprotein digestion product, alcohol, and coffee
http://www.clinical-updates.blogspot.com 37
Pepsinogen SecretionFunction
pepsinproteolytic enzyme
RegulationCephalic Phase
vagally stimulated cholinergic neurons within the enteric nervous system chief cells
Gastric Phaselow pHACh
Intestinal Phasesecretin
http://www.clinical-updates.blogspot.com 38
Intrinsic Factor
Definitionglycoprotein secreted by parietal cells of the gastric mucosa
Functionabsorption of Vit B12
http://www.clinical-updates.blogspot.com 39
Gastric Mucosal BarrierAutodigestionRate of RepairUlcer Therapy
http://www.clinical-updates.blogspot.com 40
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
http://www.clinical-updates.blogspot.com 41
Gastric Mucosal BarrierRate of Repair
48 hours3-5 months
depends on the extent of injury
http://www.clinical-updates.blogspot.com 42
Gastric Mucosal BarrierUlcer Therapy
drugs that neutralize gastric acid (antacid)prevent acid release (PPI, H2 antagonistAntibiotics for H. pylori
http://www.clinical-updates.blogspot.com 43
Gastric Digestion and Absorption
DigestionAbsorption
http://www.clinical-updates.blogspot.com 44
Gastric Digestion and Absorption
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
http://www.clinical-updates.blogspot.com 45
Gastric Digestion and Absorption
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
http://www.clinical-updates.blogspot.com 47
http://www.clinical-updates.blogspot.com 48
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.
http://www.clinical-updates.blogspot.com 49
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
http://www.clinical-updates.blogspot.com 50
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.
http://www.clinical-updates.blogspot.com 51
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.
http://www.clinical-updates.blogspot.com 52
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.
http://www.clinical-updates.blogspot.com 53
Peripheral Mechanisms Operating to Signal the Neural Centers Regulating Food Intake
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.
http://www.clinical-updates.blogspot.com 54
Peripheral Mechanisms Operating to Signal the Neural Centers Regulating Food Intake
B. Nutritional or Metabolic Regulation (long-term regulation).
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.
http://www.clinical-updates.blogspot.com 55
Peripheral Mechanisms Operating to Signal the Neural Centers Regulating Food Intake
B. Nutritional or Metabolic Regulation (long-term regulation).
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.
http://www.clinical-updates.blogspot.com 56
Peripheral Mechanisms Operating to Signal the Neural Centers Regulating Food Intake
B. Nutritional or Metabolic Regulation (long-term regulation).
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).
http://www.clinical-updates.blogspot.com 57
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
Thank You!
For Yawning!