Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
95 Cards in this Set
- Front
- Back
The trachea is (anterior, posterior) to the esophagus.
|
anterior
|
|
A tumor from the esophagus can spread to the trachea and cause the development of a _______
|
tracheo-esophageal fistula.
|
|
Blood supply of esophagus and implciations
|
It steals arterial branches from the inferior thyroid artery, aorta, etc. Therefore, esophageal surgery is very difficult since many blood vessel anomalies can be present.
|
|
What are the 3 functional/physiological phases of swallowing?
|
1) Preparatory phase - conscious effort to ingest food and reflexes in the oral cavity that help prepare bolus to be swallowed
2) Transfer phase - reflex activities in oral and pharyngeal phases 3) Transport phase - transport of food bolus thru LES and stomach |
|
What are the 3 anatomical phases of swallowing?
|
1) Oral
2) Pharyngeal 3) Esophageal |
|
Where is voluntary/striated muscle located re the esophagus?
|
In the upper 1/3.
|
|
What innervates the voluntary/striated muscle of the esophagus?
|
The upper 1/3 of esophague is innervated by lower motor neurons that are <b>all excitatory</b> by release ACh at motor end plates.
Carried by cranial nerves, including Vagus. |
|
Where is involuntary/smooth muscle located re the esophagus?
|
Lower 2/3 and Lower Esophageal Sphincter
|
|
What innervates the involuntary/smooth muscle of the esophagus?
|
Autonomic innervations that consist of extrinsic preganglionic fibers that are carried in teh vagus nerves and intramural postganglionic neurons that are part of the myenteric plexus.
There is <b> excitatory pathway (ACh) and inhibitory pathway (VIP/NO) </b> |
|
What do the excitatory autonomic neurons innervating esophageal smooth muscle release?
|
ACh, just like the voluntary muscle.
|
|
What do the inhibitory autonomic neurons innervating esophageal smooth muscle release?
|
Vasoactive intestinal peptide (VIP) and NO
|
|
Where is the upper esophageal sphincter located?
|
The UES is between pharynx and cervical esophagus.
Made of back of thyroid/cricoid cartilage, hyoid bone, and three muscles: cricopharyngeus, thyropharyngeus, and cranial cervical esophagus. |
|
Between what muscles is there a zone of sparse musculature through which a zenker's diverticulum might emerge?
|
The thyropharyngeus and cricopharnygeus, which are oriented in different directions.
|
|
Major anti-reflux barrier
|
Lower esophageal sphincter (LES)
|
|
Deglutition : defn
|
act/process of swallowing
|
|
Neural mechanism of primary peristalsis
|
Premotor neurons in solitary tract send projections to dorsal motor nucleus of vagus, which inhibits the LES and excites others sequentially.
|
|
Neural mechanism of secondary peristalsis
|
Local intramural reflex that's elicited by distension of the esophagus.
Clears esophagus of food residues. |
|
What is the transient LES relaxation? (TLESR)
|
It's inappropriate relaxation of the LES without the peristaltic stimuli. May be part of belch reflex, implicated as important mech for GERD.
|
|
What are some important Extra-esophageal symptoms of esophageal diseases?
|
Asthma
Halitosis Cough Apnea Hemoptysis Hoarseness Dental erosions |
|
Odynophagia: defn
|
pain with swallowing.
Can be achy or stabbing with radiation. |
|
Pyrosis: defn
|
"heartburn"
Burning discomfort behind breastbone, beginning inferiorly and radiation up to neck |
|
What is water brash?
|
Sudden appearance in mouth of slightly sour or salty fluid secreted from salivary glands in response to intraesophageal acid
|
|
Physiology of heartburn
|
Not well understood. Same symptom can be elicited with distension of esophagus, reflex of bile salts, and others.
|
|
Globus sensation: defn
|
Feeling of tightness or lump in thoat. NOT related to swallowing.
|
|
Hiatal hernia: defn
|
herniation of gastroesophageal junction and/or stomach thru diaphragmatic hiatus. Different types.
|
|
What is the strongest predcitor of the severity of esophagitis?
|
Size of hiatal hernia
|
|
Barrett's esophagus: defn
|
metaplastic columnar epithelium replaces the normal squamous epithelium of the distal esophagus.
|
|
Complications of Barrrett's esophagus
|
Higher risk for esophageal adenocarcinoma
|
|
4 GERD management options
|
1) Lifestyle mods
2) Acid neutralization (antacids) 3) proton pump inhibitors 4) anti-reflux surgery |
|
What is eosinophilis esophagitis?
|
Symptoms of esophageal dysfunction in association with histologic evidence of eosinophilic infiltration of esophageal mucosa
|
|
T/F eosinophilic esophagitis is associated with atopy
|
T.
|
|
T/F There are normally a small amount of eosinophils in the esophagus.
|
F. Unlike the rest of the Gi tract, the esophagus normally doesn't contain eosinophils
|
|
Tx for eosinophilic esophagitis
|
fluticasone (swallowed instead of inhaled)
|
|
What is achalasia cardia?
|
Insufficient lower esophageal sphincter relaxation and loss of esophageal peristalsis.
Poor esophageal emptying of barium, dilation esophagus |
|
Goal for achalasia tx
|
Relief of sx and improved esophageal emptying.
|
|
What is achalasia tx?
|
pneumatic dilation and surgical myotomy
Also injection of LES with botulinum, or tx with CCBs or nitrates |
|
What is Zenker's diverticulum?
|
Outpouching of mucosa thru Killians triangle, area of muscular weakness between oblique fibers of inferior pharyngeal constrictor and transverse fibers of cricopharyngeus
|
|
area of muscular weakness between oblique fibers of inferior pharyngeal constrictor and transverse fibers of cricopharyngeus thru which a Zenker's diverticulum can occur
|
Killian's triangle
|
|
sx of Zenker's diverticulum
|
Dysphagia, foul breath, gurgling in throat, pulmoanry aspiration
|
|
Typical Zenker's diverticulum patient
|
male 6-8th decade
|
|
chronic abdominal pain and altered bowel habits in absence of organic cause
|
irritable bowel syndrome
|
|
What are the Rome III diagnostic criteria for irritable bowel syndrome?
|
Recurrent abdominal pain or discomfort at least 3 days/month in last 3 months associated with 2 or more of the following
1) Improvement with defecation 2) Onset associated with a change in frequency of stool 3) Onset associated with a change in the form (appearance) of stool |
|
hematochezia: defn
|
passage of fresh blood per anus, usually in or with stools (contrast with melena).
|
|
What are IBS "alarm" features for which to consider an alternative dx?
|
1) hematochezia
2) Weight loss >10 lbs 3) Family hx of colon cancer 4) recurring fever 5) Anemia 6) Chronic severe diarrhea |
|
borborygmus: defn
|
stomach growling, rumbling, gurgling
|
|
Most common type of hiatal hernia (95%)
|
Sliding
|
|
Which esophageal cancer:
almost always in upper and middle third of esophagus (smoking, alcohol, achalasia) |
squamous cell
|
|
Which esophageal cancer:
almost always in lower third of esophagus |
adenocarcinoma
|
|
What is considered to be the gold standard for the diagnosis of GERD?
|
Nothing. All of the methods (upper endoscopy, impedance testing, barium esophagram) have their problems.
|
|
Converts pepsinogen --> pepsin (pepsin is the proteolytic enzyme)
|
Gastric acid
|
|
The proton pump inhibitors end in what?
|
-azole
|
|
What does gastric acid facilitate absorption of?
|
iron, B12, calcium
|
|
2 functional areas of stomach
|
oxyntic(parietal) areas - secrete acid - 80%
pyloric gland areas - secrete gastrin - 20% |
|
The cardia, fundus, and body are the ______ area, while the antrum is the _____ area.
|
oxyntic ; pyloric gland
|
|
Where are the pepsinogen-secreting chief cells found in the stomach?
|
At the base of the oxyntic gland
|
|
In the oxyntic gland, Somatostatin cells are structurally and functionally coupled to the parietal and histamine-containing Enterochromaffin-like cells (ECL)s and inhibit the secretion of __ and ___
|
acid and histamine
|
|
In the pyloric gland, Somatostatin cells are structurally and functionally coupled to ____ cells and inhibit secretion of _______.
|
G cells; gastrin
|
|
two main complexes of the enteric nervous system
|
1) Myenteric plexus
2) Submucosal plexus |
|
What does the myenteric plexus innervate and do?
|
Innervates circular and longitudinal muscle layers, regulates motility.
|
|
What does the submucosal plexus innervate and do?
|
innervates the mucosa, regulates secretion.
|
|
The efferent fibers of the vagus are (pre, post) ganglionic, release ______.
|
pre; ACh
|
|
How does H pylori stimulate gastrin and acid secretion?
|
It inhibits antral somatostatin secretion, thus stimulating gastrin and acid secretion.
|
|
Release of acid into stomach lumen (stimulates, inhibits) somatostatin secretion
|
stimulates
|
|
The H/K/ATPase reabsorbs ___ in exchange for ____
|
K; H
|
|
What is the structure of the H/K/ATPase?
|
Heterodimer, consisting of an α catalytic portion and a β subunit.
|
|
How do the -azoles interact with the H/K/ATPase?
|
They inhibit the activity of the α subunit
|
|
What causes the H/K/ATPase to become active?
|
Stimulation causes it to be translocated to the membrane
|
|
What types of things increase gastrin release?
|
Presence of proteins, amino acids, amines.
Distension. Neutralization of the lumen (antisecretory drugs), atrophy. Massive small bowel resection. H pylori |
|
What are indications for measurement of gastric acid secretion in humans?
|
Recurrent ulcer, especially after acid-reducing surgery, to r/o ZES and to test completeness of vagotomy.
|
|
Defn of peptic ulcer disease
|
Benign ulcerative lesion of the stomach and/or duodenum extending thru muscularis mucosa
|
|
T/F Gastric acid is central to the pathogenesis of the peptic ulcer diseases
|
T
|
|
Clinical features of peptic ulcer disease
|
1) Abdominal pain
2) Nausea/vomiting - unusual unless there's an obstruction 3) Complications of bleeding, obstruction, perforation, pancreatitis |
|
tx for peptic ulcer disease
|
Antisecretory drugs: H2 blockers or PPIs
Eliminate inciting factor (H pylori) or NSAIDS. If not eliminated, then it will recur. Surgery (highly selective vagotomy or antrectomy) |
|
What type of bacteria is H pylori?
|
Spiral shaped gram-negative with flagella
|
|
How to dx H pylori?
|
Histologic stains
Rapid urease test (H pylori has urease and metabolizes urea to NH3 and CO2) Urea breath test Serology Culture |
|
What are the two enzymes that nonselective NSAIDs inhibit?
|
COX1 (constitutive) and COX2 (induced by inflammatory stimuli)
|
|
Which COX provides GI cytoprotection as well as platelet activity?
|
COX1
|
|
T/F There is direct AND indirect damage done to gastric mucosa by aspirin and ibuprofen
|
T
|
|
What is the indirect damage done to the gastric mucosa by NSAIDs?
|
Decreased mucosal blood flow
Decrease mucus secretion Decrease bicarb secretion Increase acid secretion Leukocyte adherence to vasculature Increase TNFα |
|
Side effects / toxicity of NSAIDs
|
1) Ulcers (pain, bleeding, perforation, obstruction)
2) Elevated transaminases 3) Inhibition of platelet aggregation 4) Kidney: fluid retention, hyperkalemia, ARF, HBP |
|
How is the NSAID-induced ulcer prevented?
|
Discontinue or change the NSAID
Misoprostol H2R Antagonists - high dose PPIs use a COX2 selective NSAID (there is concern for CV problems) |
|
Zollinger-Ellison Syndrome: Defn
|
Gastrin secreting tumor causing gastric acid hypersecretion
|
|
Where are the gastrinomas located?
|
>95% in pancreas and duodenum
|
|
20% of Zollinger-Ellison syndrome patients hve what disease?
|
MEN1: multiple endocrine neoplasia type 1
|
|
Symptoms of Zollinger-Ellison syndrome
|
Pain, Diarrhea, Dysphagia/heartburn
|
|
Tx of Zollinger-Ellison
|
Control acid hypersecretion (PPIs)
Localie and remove tumor. If no liver metastases then evaluate whether patient has MEN1 |
|
_____ cell releases somatostatin which inhibits the ECL cell from releasing histamine and the parietal cell from releasing H+
|
D
|
|
What are the effects of the vagus' release of ACh onto the D cell?
|
They INHIBIT the D cell (inhibits the release of somatostatin (which promotes release of gastrin))
|
|
What are the effects of the vagus' release of ACh onto the G cell?
|
Stimulates G cell
|
|
What are the effects of the vagus' release of ACh onto the parietal cell?
|
stimulates release of H+
|
|
When is the best time to take PPIs?
|
Before meals
|
|
What are potential side effects of PPIs?
|
"addiction" - rebound acid hypersecretion
Drug-drug interactions Increased susceptibility to C. difficile infections Osteoporosis/fracture Hypomagnesemia |
|
What is the mechanism behind the physiological addiction to PPIs?
|
Normally H+ inhibits the release of gastrin by stimulating SST. However, when there is less H+, there is MORE GASTRIN. It takes awhile for this effect to balance out.
|
|
An ulcer is A TRANSMUCOSAL hole that occurs in the esophagus, stomach,
duodenum, or intestine due to a combination of ____ and _____. |
ACID and PEPSIN
|
|
Best diagnostic tests for H pylori
|
Urea breath test
Rapid urease test |