LCCW Gastro Phys - Exam 1
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| What does the GI tract do for us? | transportation, digestions, absorption, excretion, defensive role
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| What stimulates the stretch receptors? | The bolus
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| Control of swallowing comes from where? | The swallowing center in medulla and lower pons
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| What pulls medially to form a slit so that large pieces can't pass? | Palatopharyngeal Fold
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| A series of wave-like muscle contractions that moves food to different processing stations in the digestive tract? | Peristalsis
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| Nervous control - Afferent : | Sensory from mouth travels CN V and IX to medulla oblongata
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| Nervous control - Efferent: | From swallowing center in medulla impulses travel thru CN V, IX, X, and XII, and some upper cervical Nerves
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| Primary Peristalsis: | Transports food from pharynx to stomach (8-10 sec)
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| When does secondary peristalsis occur? | if the whole bolus doesn't enter stomach. Occurs until esophagus is empty.
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| Peristalsis is initiated where? | In the Myentaric system back through glossopharengeal and vagal efferent.
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| Stomach transports the bolus through contractions called what? | Peristalsis and Pyloric pump
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| Pyloric Pump? | Vigorous contractions designed to empty the stomach
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| Segmentations: | Transportation of content in the small intestine
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| Haulstrations: | Transportation of content in the Large Intestine
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| Digestion involves what? | The Breakdown of the food we eat into nutrients that are readily absorbed
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| Ingestion: | Bringing food into the mouth
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| Mechanical digestion: | Physical process prepares food for chemical digestion
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| Chemical Digestion: | Enzymes breakdown food into basic elements
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| Absorption: | from lumen of GI tract into blood or lymph
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| Where does most absorption happen? | In the small intestine
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| Where does absorption of water and electrolytes happen? | In the large intestine
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| Defecation? | elimination of indigestibile substances from the body
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| Which part of the GI is responsible for defecation? | The Large Intestine
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| Salivary glands produce how much per day? | 800-1500 mL/day
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| Parotid Produces what and is where? | Serious Secretion as well as a majority of the saliva. Vestibule - next to the second upper molar.
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| The Submandibular gland produces what and is where? | More Serous >> Mucous. Lingual Frenulum.
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| The Sublingual gland produces what and is where? | More Mucous >> Serous. 10-12 ducts. Open into the floor of mouth.
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| The Ebner's Glands produces what and is where? | Serous only - Circumvallate Papillae (lipase)
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| What is Saliva good for? | cleanses mouth. Dissolves food chemicals (allows us to taste). Moistens food and aids in form bolus. Contains enzymes. contains factors that destroy bacteria. Contain protein antibodies.
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| What destroys bacteria (via saliva)? | Thiocyanate ions, and lysozyme
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| What destroys oral bacterial? | The Protein antibodies in the saliva
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| Parotid gland is stimulated by: | CN IX --> Sup and Inf salivary nuclei --> CN IX ---> 1 ganglion --> parotid gland
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| Sibmandibular and sublingual glands are stimulated by: | taste and tactile receptors on tongue --> CN VII --> sup and inf salivatory nuclei --> CN VII --> Submandibular ganglion --> submandibular and sublingual gland
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| Deciduous teeth: | 20 baby teeth (6 months --> 2 years)
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| Each quarter in baby teeth: | 2 incisors, 1 canine, 2 molars
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| Permanent teeth come in at what age? | 6 years old and take up until 20 years of age to completely erupt
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| Incisor: | Chisel cutting or nipping
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| Canine: | Conical tear or pierce
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| Premolar and molar: | crowns with rounded cusps grinding
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| Enamel: | The white stuff that we see - it's the hardest structure on our bodies.
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| Dentin: | Very Porous. like bone.
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| Pulp/Root Canal: | Space within the tooth
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| Cementum: | Material that binds tooth to the jaw. Adheres to the peridontal ligament.
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| Dental carries: | (Cavities) - caused by dental plaques
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| Dental plaques: | Film of debris (bacteria and sugar)
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| What metabolizes sugars into acids? | Bacteria. Ut de-mineralizes the enamel
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| Bacteria are usually what? | Streptococcus mutans
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| Calculus (tartar): | formed by accumulation of plaque can lead to gingivitis
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| Gingivitis: | Inflammation of tooth/gum interface
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| If Gingivitis is left untreated, it progresses to what? | Periodontal disease
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| What happens that leads up to tooth loss? | Pockets are created on surface of tooth, then bacterial enzymes dissolve the dentin, which leads to tooth loss
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| Xerostomia: | "dry mouth" - absence of saliva production
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| Leukoplakia: | White patches on the surface of mucous membranes
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| Hyperkeratosis: | abnormal thickening of the outer layer of the skin.
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| Xerostomia is caused by what? | mumphs, sjorgens disease, Sarcoidosis and some meds
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| Erythroplakia: | flat red patch or erosions on floor of mouth, tongue or soft palate
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| Erythroplakia is associated with what? | Dysplasia and is precancerous
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| Upper 1/3 of esophagus? | Striated muscles (= voluntary)
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| Lower 1/3 of esophagus? | Smooth muscle (= involuntary)
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| middle of esophagus? | smooth and striated muscles
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| Primary peristalsis is a continuation of what? | The pharyngeal stage
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| What happens to the bolus if it's still present after primary peristalsis? | secondary peristalsis occurs from the distension of esophagus
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| Esophageal stage of swallowing is stimulated by what? | The myenteric n.s. and by reflexes traveling from the vagal afferent fibers (which initiate contraction)
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| LES: | lower esophageal sphincter - is the last 3 cm of esophagus
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| LES's AKA? | Gastroesophageal sphincter
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| LES is normally ________ to prevent reflex | Constricted
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| Atresia: | Absence of a normal opening (pre stomach). Discovered right away
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| Fistula: | Abnormal connection from esophagus to trachea.
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| What is the most common fistula? | The lower esophageal fistula (near where the trachea "Y"s)
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| What are the 2 S/S of Atresia? | Regurgitation and excessive secretions
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| What is the least common fistula? | H-Type fistula
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| S/S of H-type fistula? | Cyanosis (turning blue) and distended abdomen
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| S/S of Fistula? | Choking, Cyanosis, aspertation pnemonia
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| Diverticula (of esophagus): | Is an outpouching of the wall of the esophagus
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| Diverticula is caused by what? | motor disturbance
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| Zenker Diverticulum? | Uncommon. HIGH on esophagus.
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| S/S of Zenker Diverticulum? | Regurgitation of food eaten a few days prior
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| Traction Diverticulum? | Outpouchings occuring at MIDPOINTS of the esophagus. Usually Asymptomatic.
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| Epiphrenic diveritculum? | Occurs LOW on the esophagus.
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| Achalasia: | Failure of LES to relax in response to swallowing, and absence of peristalsis
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| What is associated with Achalasia? | Associated with a loss of inhibitory ganglion cells in the myenteric plexus of esophagus
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| Achalasia is a compluication of what disease? | Chagas disease - Ganglion cells destroyed by Trypansoma cruzi
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| S/S of Achalasia? | Dysphasia, Odynophagia, and regurgitation.
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| Dysphasia: | Difficulty swallowing
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| Odynophagia: | Painful swallowing
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| Reflux Esophagitis: | Inflamation of esophagis. MOST COMMON ESOPHAGITIS (GERD)
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| GERD = ? | Gastro Esophageal Reflex disorder
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| What is GERD in conjunction with? | Sliding hiatal hernia
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| Factors that lead to LES? (<-- is that supposed to be GERD? Pg 8) | Alcohol, caffeine, chocolate (stimulate gastric secretion), Fatty Foods (slow down gastric emptyin) and Nicotine, CNS depressants, pregnancy and estrogen therapy ( decrease LES activity)
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| S/S of Reflux esophagitis? | Dysphasia, odynophagia, dypepsia, pyrosis, and excessive salivation
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| Pyrosis = | Heart burn
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| What is GERD diagnosed to (if it worsens)? | Barrett Esophagus
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| Barrett Esophagus: | Squamous Epithelium of esophagus is replaced with pseudocolumnar epithelium as a result of chronic reflux
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| Where does Barrett Esophagus occur? | In the lower 3rd of esophagus
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| Barrett Esophagus is increased risk with what? | Smoking
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| Chemical Esophagitis: | Accidental poisoning of children, or attempted suicide in adults
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| Chemical esophagitis can happen due to what? | Alkaline agents (lye), strong acids (sulfuric or hydrochloric) found in cleaners
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| Chemical esophagitis will cause what? | Inflammation and cell death
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| Esophageal Varices: | Dialated Veins beneath the mucousa. Pron to rupture and hemorrhage. In the lower 3rd of esophagus
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| Esophageal Varices is due to what? | Hepatic portal hypertension from cirrhosis of liver
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| S/S of esophageal varices? | Blood in vomit, black tarry stool, and shock
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| Hiatal Hernia: | Herniation of the stomach through an enlarged esophageal hiatus in diaphragm - usually asymptomatic
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| S/S of Hiatal Hernia? | Heartburn and regurgitation
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| Causes of hiatal hernia? | Relacation of LES when stomach full. Tight Clothing around mid and upper abdomen. Lying down after a big meal. Large amount of abdominal adipose tissue.
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| Sliding Hernia: | MOST COMMON (75-95%). The Hiatal laxity allows cardia of stomach and LES to pass above the diaphragm. Most often asymptomatic
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| Paraesophageal (rolling) Hernia: | Portion of the gastric fundus above the diaphragm. Can continually enlarge and in extreme cases stomach herniates into thorax.
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| Which type of hernia NEEDS surgical intervention? | Paraesophageal (rolling) hernia
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| Scleroderma: | Systeic sclerosis is the type that can affect the esophagus
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| Scleroderma is caused by what? | Fibrosis (hardening) in many organs and an abnormality of esophageal mm fixation
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| Scleroderma is primarily where? | The lower third and LES
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| Plummer Vinson syndrome, AKA? | Paterson-kelly syndrome
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| Plummer Vinson syndrome Characterised by what? | Cervical esophageal web (thickening on upper esophagus) causes dysphagia, mucosal lesions of mouth and pharynx and iron deficiency anemia.
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| What can be a complication of plummer-vinson syndrome? | Carcinoma of oropharync and upper ...... upper what?
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| 90% of plummer-vinson syndrome happen in which gender? | Women
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| Mallory-Weiss Syndrome: | Lacerations of the lower esophagus and upper stomach
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| Mallory-Weiss Syndrome is caused by what? | Severe retching, often associated with alcoholism. Pt can also vomit blood.
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| Mallory-Weiss Sydrome can lead to what? | Could also lead to peritonitis or pleurisy due to contents leaking out
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