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