3-4 Cephalic / Oral / Esophageal Phases Flashcards
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A: Cephalic Phase = “preparedness” and is activation of GI tract for meal readiness WITHOUT food ingestion present. It can be activated by
- Idea of Food
- Olfaction
- Visual Stimuli
- Auditory Stimuli
B: Sensory Afferent Inputs—> [Cortex & hypOthalamus]—>[Vagus n. cell bodies in Lower Pons/Upper Medulla]—> [Parasympathetic Vagus Stimulation]—->stimulates..
1) Salivary Secretion (via CN7 and CN9)
2) Gastric Secretion
3) Pancreatic Secretion
4) Gallbladder Contraction
5) Oddi’s Sphincter relaxation
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A: Oral Phase:
*Similar to Cephalic EXCEPT FOOD IS ACTUALLY IN MOUTH
*Leads to MORE activation of GI sensory inputs due to [taste buds] & mechanical receptors of mouth & [upper pharynx]
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B: Chewing:
*Enhances GI Activation and Breaks food into smaller pieces—> mechanical disruption that allows food mixing with [salivary amylases] and [lingual lipase]–> mild digestion only
*Also allows Food mixing with Salivary [Mucin glycoprotein] which helps chewing & swallowing
C: [Dry mouth Xerostomia]= impaired salivary secretion that can be congenital or autoimmune. —> DEC pH in oral cavity—> tooth decay / esophageal erosions / dysphagia
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A: Muscles of Mastication “When chewing TAKE MANY LIL MINIS!”
- TEMPORALIS (MOST IMP)
- Medial Pterygoids
- Lateral Pterygoids
- Masseter
B: These are innervated by [CN5 B3-Mandibular division] and elevate, protract and Retract jaws
C: Pterygoids ALSO have the ability to move mandible Laterally back-and-forth
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A: GI Secretions come from
- glands associated with tract= Salivary / pancreas / Liver
- Gut Wall Glands = [Duodenal Brunner Gland]
- Intestinal Mucosa
B: secretions are full of water / electrolytes / protein & humoral agents …and are initiated by [secretagogue signals] which act on secretory cells as endocrine, paracrine or NEUROCRINE modulators
D: 2 Types of Glandular Secretions
1) Serous = water / electrolytes / enzymes
E: (Mixxed SubMandibular) salivary glands have [Serous Demilune] which allows them to be Mixxed
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F: These are all contained within a [Tubuloalveolar Structure]
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A: Salivary Glands have 2 main structures
1) Acinus = Blind end of the duct system and is lined with [acinar cells] that actually do the Secreting. [Acinar Cells] produce [INITIAL isoTonic SALIVA] which travels—> [intercalated duct]—-> [Striated Duct (lined with Ductal cells)] which alters into FHS
2) Network of collecting Ducts is where [Final HypOtonic Saliva] empties into the gut after having electrolytes altered from Ductal Cells in the Striated Duct
B: [MyoEpithelial Cells] wrap AROUND the [Acinus] and [intercalated duct]. They contain actin & myosin which allows contraction when stimulated neurally–>expels saliva forward and Out
C: Salivary Lobule Structures are separated by [Septa Connective Tissue]
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B: {{Nuclei of mucous cells are DARKER than serous cells}} {{BUTTTT [mucous sublingual] gland typically stains LIGHT}} unless converted into Serous producing by Dz which would make it stain Dark
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A: Saliva is made 1L/day {less than 1 mL/min} and job is to:
1) Lubricate ingested food with mucus in order to aid mvmnt in esophagus AND Lubrication helps w/Speech
2) Protect by Diluting and Buffering ingested foods. When vomiting these buffers neutralize gastric acid & pepsin.
3) Saliva also maintains healthy oral tissue by washing away bacteria w/Lysozyme–>lyses bacterial cell walls
4) Initially digested starches and lipids but NOT MAJORLY
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A: Saliva composition depends on how fast its made…
1. INorganically= Water/HCO3/Na/K/Ca/Mg/Cl/Fl
- Organically=
º[Salivary amylase: STARTS OFF starch digestion]
º[Lingual Lipase: Lipid digestion]
º[Mucus Glycoprotein from mucin]
º[Lysozyme: lyses bacterial cell walls]
º[Kallikrein: converts plasma protein–>(bradykinin vasoDilator) in order to INC blood flow to salivary glands for better secretion]
B: [FHS Final hypOtonic Saliva] has higher K+ & HCO3(since these are secreted into it) but has [A LOT LOWER Na+ AND Cl- in it]–> hypOtonic
C: Saliva is made in 2 steps
1st-[iiS Initial ISOTONIC saliva] is made by [Acinar cells]
2nd- [Striated Duct DUCTAL CELLS] modify [Initial ISOTONIC Saliva] with 3 Lumen transporters
ºNa/H (Takes Na+ OUT)
ºCl/HCO3 (Takes Cl- OUT)
ºH/K (Takes H+ OUT)
ºThese transporters Secrete K and HCO3 INTO [FHS] but no more than the NaCl Taken out + Ductal cells are NOT permeable to water —> hypOtonic
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B: Saliva composition can change based on how fast its made because if flow is too fast(x > 4mL/min) there is less time for NaCl to be taken out during modification—> [Final Saliva = closer to Plasma/LESS hypOtonic!]
EXCEPTION TO THIS RULE IS HCO3 because it is selectively stimulated during INC salivary production by PARAsympathetics)
**Final Saliva is never isotonic. Only [less hypOtonic] **
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C: Salivary Secretion is ONLY NEURAL and is stimulated by BOTH sympathetic and [PARAsympathetic -more dominant]. When stimulated by NEURAL input –>
-INC Saliva production
-INC HCO3 & Enzyme Secretion
-MyoEpithelial Cell Contraction
D: PARAsympathetics use CN7 and CN9 to release AcH to interact with muscarinic receptors–> [INC IP3 and intracell Ca+] –> INC Saliva Secretion. THIS CAN BE BLOCKED BY ATROPINE and Turned OFF by Dehydration/Fear/Sleep]
D2: Nausea TURNS ON PARAsympathetic salivary secretion
E: sympathetics from T1-T3 have postganglionic neurons release NorEpi which interacts with [Beta-adrenergic receptors]–>INC cAMP–> INC Saliva Secretion
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SWALLOWING REFLEX
A: Swallowing can be initiated voluntarily and then it is almost entirely REFLEX. This Reflex propels food from Mouth–>Pharynx–>Stomach. It inhibits Respiration/Speech/food entrance into trachea
B: Stretch receptors near opening of pharynx are stimulated
–>sends sensory impulses to [Medullary/Lower Pons Swallowing Center]
C: [Medullary/Lower Pons Swallowing Center]–>sends motor impulses to pharynx and upper esophagus via CN7&9 AND THEN remaining esophagus via CN10
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3 Phases of Swallowing
A) [Oral voluntary] = started when tongue forces food bolus back toward pharynx activating stretch receptors and initiating INvoluntary Swallowing REFLEX
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B) [Pharyngeal INvoluntary] = last less than 1 second BUT HAS A LOT GOING ON!
1st: Soft Palate is pulled up and [palatopharyngeal fold] moves inward creating narrow passage and Covers nasopharynx–>Food Moves into pharynx
2nd: Epiglottis then covers larynx AND Respiration is paused via inhibition by the swallowing center
3rd: [Upper Esophagal Sphincter] RELAXES to receive food bolus and Pharynx contracts moving food into esophagus.
4th: Peristaltic Contraction wave is initiated forcing food bolus down and after it crosses UES the [Swallowing REFLEX] closes the UES preventing pharyngeal reflux
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C) [Esophageal INvoluntary] is controlled by REFLEX AND [intrinsic Enteric Nervous System]
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3 Phases of Swallowing
A) [Oral voluntary] = started when tongue forces food bolus back toward pharynx activating stretch receptors and initiating INvoluntary Swallowing REFLEX
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B) [Pharyngeal INvoluntary] = last less than 1 second BUT HAS A LOT GOING ON!
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C) [Esophageal INvoluntary] is controlled by REFLEX AND [intrinsic Enteric Nervous System]
ºThe UES / LES and Esophagus propel food from pharynx
—>Stomach AND sphincters protect airway from swallowed material or esophagus from acid reflux
1st: [Swallowing Reflex] coordinates [Primary Peristaltic contraction]–>moves food down
2nd: [intrinsic Enteric Nervous System] coordinates [secondary peristaltic contraction] which clears esophagus of bolus. This is INITIATED by Esophageal Distention from the bolus
3rd: As [secondary peristaltic wave] approaches LES it relaxes along with the [proximal orad stomach] = [Receptive Relaxation].
3rdB: The [proximal orad stomach] relaxes because mechanoreceptors detach stomach distension –> activate [vasovagal reflex]–>CNS sends efferent relaxation signals using [Peptidergic vagal fiber NTS VIP]
4th: As soon as food bolus enters [proximal orad stomach] LES Contracts to its high resting tone. At resting tone pressure at sphincter is HIGHER than esophagus OR [proximal orad stomach]
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A: Because of esophagus location, Abd Pressure is HIGHER which leads to 2 maintenance problems:
1) Air has to be kept out Upper Esophagus by UES
2) Gastric Content has to be kept out of Lower Esophagus by LES
A2: INC [intraabdominal pressure] (like from pregnancy or obesity)—> [Gastroesophageal reflux ]
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B:
ºUpper Esophagus is mostly Skeletal muscle [(Outer Longitudinal) vs. (inner circular)]
ºMid Esophagus HAS BOTH SKELETAL AND SMOOTH M.
ºLower Esophagus mostly Smooth m.
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C: In Esophagus Mucosa is covered by a THICK layer of [Stratified Squamous Epithelium] to protect it from abrasion & friction during bolus mvmnt
D: Stomach Mucosa is covered by [Simple Columnar Epithelium]
E: Chronic GERD will Convert [Esophageal Stratified Squamous Epithelium] —> [Stomach Simple Columnar epithelium] = METAPLASIA! If this condition Worsens even further it’ll be converted into [Intestinal Goblet Cells] which secrete MUCUS! = [Barretts Esophagus Intestinal Metaplasia]
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A:GERD is treated with either
1) [H2 receptor ANTagonist = ranitidine–> DEC Gastric Acid Secretion
or
2) [Proton Pump inhibitors] = Omeprazole
B: (H+ Protons) and Pepsin are EQUALLY DESTRUCTIVE to Esophagus. Duodenum is protected by [Pancreatic HCO3 secretions] but during Pancreatic Dz or if gastric emptying occurs too fast —> Damaged Duodenum
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C: [Hiatal Hernia] occurs when upper stomach protrudes thru the [Esophageal Hiatus] on the diaphragm into the Chest. This will weaken the muscle allowing MORE herniation upward or even trapping stomach ABOVE the diaphragm!
C2: [Hiatal Hernia] major sx = Acid Reflux and eventually the LES no longer works properly. **60% of people over 60 y/o will develop some [Hiatal Hernia]
C3: HH is caused by
- Age (60% of people over 60)
- Weight Lifting
- Obesity
- Genetic Predisposition
- Constipation
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A: Achalasia = Esophageal motility dz in which [Peristaltic Contractions] are NOT normal AND LES does not Relax during [Swallowing Reflex]
B: Achalasia Sx = Dysphagia / Regurgitation / [chest pain]
C: Tx= ºSurgical myotomy along esophagus to remove the [myenteric plexus] causing disruptive [Peristaltic Contraction] ºCa+ channel blockers ºBOTOX injection in the LES ºmuscle relaxants
