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GI Phases
- ▪ Cephalic
- ▪ Oral
- ▪ Pharyngeal
- ▪ Esophageal
- ▪ UGI
- ▪ LGI
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Cephalic Phase
▪ Role of the brain
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LIMBIC SYSTEM
▪ Responsible for basic urges (Controls)
▪ Hippocampus – long term memory
▪ Amygdala- reward and fear, mating
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Cerebrum
• Can overcome limbic system (cortex)
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• Can enhance the limbic system
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Pineal Gland
- • Measures circadian rhythms in response to light
- • Low Melatonin with light
- • High Melatonin with dark
- • Melatonin (tryptophan) milk and turkey
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Pineal Gland (Rhythms of the day)
- • 1st 8 hours:
- • Catabolism in the morning
- • Take vitamins
- • Exercise in the A.M. to burn most fat
- • 2nd 8 hours
- • Mixture of catabolism and anabolism
- • 3rd 8 hours: (Night time)
- • Catabolism is off
- • Anabolism is on
- • Getting ready to fall asleep.
- • Explains “Jet lag”, gain weight if eat in evening…
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Hypothalamus (Hunger Center)
• Hunger Center (lateral nucleus of hypoth)
• Controlled by low glucose
- • Low glucose (Hypoglycemia) ↑Firing of hunger center
- • This center can be stimulated by the sight of food: therefore can always feel hungry
- • Stimulated 20% of the time
- • Lesion:
- • anorexia → because no longer have “hunger signal”
- • Could be associated with Anorexia Nervosa/Body dysmorphic
- • Anorexics feel they are not thin enough
- • Patient trying to please the mom – look for executive mom type- hard to please.
- • Treat with SSRI to get at hunger center
- Selective serotonin reuptake inhibitors
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Hypothalamus (Satiety Center)
• Satiety Center (medial nucleus of hypoth)
• ↑Glucose (Hyperglycemia) ↑firing of satiety center
- • Stimulated 80% of the time
- • Lesions/Abnormalities:
- • Die of Hyperphagia = overeating.
- • Could be associated with Bulimia
- • Girl trying please boyfriend.
- • Signs to look for:
- • Abrasion of knuckles
- • Loss of enamel on teeth
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Hypothalamus (Functions)
- • Controls MENSES
- • progesterone stimulates hunger system
• Pregnancy due to corpus lutetium
- • Controls TEMPERATURE:
- • ANTERIOR Hypothalamus: cools (inhibits NE)
- • Lesion anterior- die from: hyperthermia
- • POSTERIOR Hypothalamus: warms
- • Lesion posterior- die from hypothermia
- • Acetaminophen: for use with fever
- (stimulate anterior hypothalamus- cools), then it
- blocks posterior so you do not go back up again
- • Toxicity- microsteatosis (small fat cells in liver)
- • Reye syndrome in children
- • Tx: N-acetylcystine-reducing agent
- • 4 hour level will determine if you use it
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Ideal Body Weight
- • Men: 5 feet = 106 lbs
- • Women: 5 feet= 100 lbs
• Add 5 lbs for per inch past that…
- • Small frame: add 15 lbs
- • Large frame: add 30 lbs
• (i.e. male 5’10”: 106 + 50 +30 = 186 lbs)
• Obesity is considered 20% over ideal body weight
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Neurotransmitters
- • Neurotransmitters in the hypothalamus are NE and Serotonin
- • NE & Serotonin can contribute to both centers
• Amphetamines will cause ↑release of preformed catecholamines so NE and Serotonin levels will go up and hit satiety center: won’t be hungry.
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Prader-Willi
• Lesion of the satiety center (Ventromedial)
• Trinucleotide repeats
- • Genomic imprinting
- • Uniparental disomy (one parent genes, both chromo)
• Chromosome 15
- • Huge Appetite
- • Die due to over eating
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Stress Response (Sympathetic)
- • Anytime the body senses stress, sets off the same reflex
- • 1st Parasympathetic then 2nd Sympathetic discharge
- • Sympathetic ↑vasoconstriction in GI and skin
- • Stress ulcer (GI doesn’t have blood supply to protect itself)
- • Ex. Hospital protocol- Patients in the ICU need to be on H2 blockers.
• Sympathetic for Ejaculation.
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Stress Response (Parasympathetic)
• 1st Parasympathetic then 2nd Sympathetic discharge
- • “You scared the crap out of me!!!”
- • ↑GI motility
- • ↑GI acid output
- • Parasympathetic ALWAYS precedes SYMPATHETIC
- • Ex. Point and Shoot:
• Parasympathetic for erection
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Oral
• Put food into mouth- salivary glands respond
- • SALIVARY GLANDS
- • Parotid [ in front of ear ](serous)-water - CN 9
- • Lingual [ on tongue ] (most serous) CN 7
- • Sublingual [under tongue] (most mucus) CN 7
- • Submandibular [jaw] (mucus) CN 7
- • Saliva in your mouth has to be HYPOTONIC (cracker)
- • Food on your cheek- food will get stuck (gummy bear)
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Why Saliva is made
- • Saliva needs to be basic for 3 reasons:
- • Acidic Food
- • Bacteria fermenting glucose to lactic acid
- • reflux
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Saliva Mechanisms
- • Isotonic Plasma
- • 1° saliva
- • Saliva needs to be BASIC ↑↑↑ HCO3 Production
- • Exchange
- • 3 Na out
- • 1 Cl out
- • 2 K in
- • HCO in
- • 2° Saliva = hypotonic
- • Saliva has more Na and Bicarb → Very Alkalotic
- • Reflux → Normal phenomenon
- • GERD –with symptoms
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Saliva Syndromes
- • Esophagitis
- • What you see on a scope
- • look for T cells, macrophages in raw spots
- • BARRETT’S ESOPHAGUS
- • short to long columnar
- • MALORY WEIS SYNDROME
- • tears in submucosa (ETOH, vomiting)
- • BOORHAAVE’S SYNDROME
- • Rupture of esophagus
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Saliva also contains
• IgA
• Lipase- little fat break down
• Amylase: breaks alpha 1,4 bonds
• Lysozyme: a detergent
- • HCO3: three sources of acid
- • From food (drinks)
- • Produced by bacteria ( strep mutans)
- • Reflux
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Parasympathetic stimulation in saliva
• will produce more saliva
- • this saliva will have ↑osmolarity, (more salt)
- • No more than 300 mOsm
- • Can’t be hypertonic (Because saliva goes through very fast)
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Drugs that simulates saliva
• same as parasympathetic stimulation
- • Acetylcholine
- • CNS: excitatory
- • PNS: activates muscles
- • Methacholine
- • dx asthma (old)
- • beta 2 agonist to bring you out
- • Pilocarpine
- • sweat test ( > 60)
- • open angle glaucoma (chronic)
- • Carbachol-
- • post op urinary retention (stimulate bladder emptying)
- • Bethanechol
- • post op urinary retention
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Sympathetic stimulation in saliva
• Vasoconstriction = ↓ salivary production because blood is being shunted away, however, the blood will be thick and ↑ Na concentration
• NE → α>β
- • Epi → β>α
- • Pseudoephedrine → stress incontinence
- • Phenylephrine → tx: for neurogenic shock
- • vasoconstricts arteries
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Saliva secretions
- • Saliva also secretes IgA
- • Used to coat bacteria in the mouth from food you eat → provides protection
- • Also secretes Lysozyme
- • Acts as a detergent
- • Prevents adhesion to the teeth
- • Lipase
- • Fat digestion begins in mouth, but that is negligible
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Salivary Amylase
- • Start Carbohydrate digestion
- • Lactase
- • Most common SECONDARY dissacharidase deficiency.
- • 1st enzyme to disappear with diarrhea.
- • Will stop producing at age 4
- • lactose intolerance
- • Sucrase
- • The most common PRIMARY (congenital) dissacharidase deficiency
- • Maltase
- • α- dextranase
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Salivary Amylase Break down products
• Lactose = glu and gal
• Sucrose = glu and fru
• Maltose = 2 glucose and α 1,4 linkages
• α– dextrins = 2 glucose w/ α 1,6 linkage
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Cystic Fibrosis
- • MCC: of malabsorption in children
- • meconium ileus (bowel obstruction)
• Autosomal recessive inheritance
• CFTR gene on chromosome 7
- • Defective CHLORIDE transport
- • Chloride traps sodium, increasing the salt
- content and thickness of secretions
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Cystic Fibrosis bacterial enemies
• Staph Aureus and Pseudomonas Aeruginosa
• MUST cover Staph Aureus with one antibiotic and Pseudomonas Aeruginosa with two antibiotics
- • Dx: Pilocarpine
- • Cl sweat test
- • < 40 Normal
- • 40 – 60 Heterozygous
- • > 60 CF
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Cystic Fibrosis (Presents with)
• Meconium ileus: first presentation in neonate
• Predispose to Oxalate kidney stones
• lungs (thick mucus)
• Steatorrhea = fatty stools/ oily diarrhea
- • Malabsorption develops as pancreatic ducts
- become clogged
• sweat glands and epididymis (men infertil)
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Reflux
• A normal phenomenon: GERD
- • ESOPHAGITIS-
- • tissue inflammation (T-cell/Mac)
- • BARRETT’S ESOPHAGUS-
- • short to long columnar
- • MALORY WEIS SYNDROME-
- • tears in submucosa (ETOH, vomiting)
- • BOORHAAVE’S SYNDROME-
- • Rupture of esophagus
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Muscles of Mastication
- • Masseter- (cheek) closes
- • Temporalis- (closes) moves jaw forward and back
- • Medial Pterygoids (closes)
- • Lateral Pterygoids- (opens) lowers jaw
- • Innervated by cranial nerve 5 (Trigeminal)-
- mandibular V3
• Develop from first branchial arch
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Swallowing
- • Tip of tongue rises
- • Sides of tongue rise and fold medially
- • Tip of tongue rises to hard palate
- • Gravity begins bolus rolling
- • When bolus approaches trachea, epiglottis
- • Closes off glottis
- • Bolus rolls over epiglottis/touches the pharynx
- • CN 9, 10 sense the bolus
- • UES opens relaxes
- • Bolus drops into esophagus
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Esophagus
- • Upper 1/3 has skeletal muscle
- • Voluntary activity
- • made up of 4 muscles
- • Superior and middle pharyngeal constrictors
- • Gag reflex controlled by CN IX and X
• Smooth muscle bottom 2/3
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Esophageal Peristalsis
• Nucleus Ambiguus: innervates the UES efferent vagus (motor CN 10)
• Dorsal motor nucleus: innervates the rest of GI – efferent vagus (motor CN 10)
• Primary peristalsis: requires vagus nerve and Auerbach’s plexus; begins just distal to the UES only
• Secondary peristalsis: intrinsic to smooth muscle; can begin anywhere in GI
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Esophageal Pathology Diverticuli
• They are small, bulging pouches that can form in the lining of your digestive system
- • Zencker's
- • Above UES = Congential
- • Traction
- • Below UES and below LES → traction
- • Presentation:
- • Coughing up undigested food.
- • Malodorous halitosis
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Esophageal Pathology: Esophageal atresia with distal TE fistula
- • Esophageal atresia with distal TE fistula
- • Blind pouch at top of esophagus.
- • M/C congential esophageal problem
- • Presentation:
- • vomiting with first feeding
- • Look for big gastric bubble on X-Ray
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Esophageal Pathology: Choanale atresia
• membrane that connects to pharynx does not dissolve
• Choanale- space between nostrils and pharynx
- • Presentation
- • turn blue when they feed
- • turn pink when they cry
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Esophageal Pathology: Achalasia
• Lack of aurebachs plexus (ganglia) in lower esophagus
• GI tract will contract but won’t relax
- • Presentation:
- • Will start chocking and gagging when start on cereal (but ok with milk)
- • Look for Bird’s beak on Barium Swallow
- • Diagnosis
- • Monometry: ↑ pressure across the LES
- • Treatment:
- • Bougie used to dialate esophagus
- • partial Vagotomy (the nerve causes the narrowing)
- • Myotomy (to split tightened muscle fibers)
- • Sudden loss of Ganglia in adult causing Achalasia
- • indicates Chagas disease (6 months trip from S. America)
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Esophageal Pathology: Hirschsprungs
• Same diseases in the rectum → loss of both Auerbach’s and Meissener’s
• Rectum won’t be able to relax
- • Presentation:
- • Constipation
• Diagnose with Barium
• Treatment: remove part of the rectum that’s affected.
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Esophageal Pathology:Esophageal Webs
• Strips of mucosa going across esophagus (congenital)
- • They can start bleeding after burns hot liquids
- • Fe deficiency anemia:Plummer-Vinson
• Diagnose with Barium swallow
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GERD
• Gastroesophageal reflux disease (GERD) occurs when stomach acid repeatedly flows back into the tube connecting your mouth and stomach (esophagus).
• This backwash (acid reflux) can irritate the lining of your esophagus.
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Bernstein test
• is a method to reproduce symptoms of heartburn. (GERD)
• A nasogastric (NG) tube is passed through one side of your nose and into your esophagus. Mild hydrochloric acid will be sent down the tube, followed by salt water (saline) solution.
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