G & E EXAM 3

passage way and stop gastric reflux and regurgitation

function of esophagus

reflux

gastric contents flow back into the esophagus

regurgitation

gastric contents flow back into mouth or airway

stops reflux

lower esophageal sphincter (LES) function

stops regurgitation

upper esophageal sphincter (UES) function

relay neurons between vagus and smooth muscle

role of enteric nervous system

modulate enteric nervous system

role of vagus

striated

what type of muscle is the UES

smooth

what type of muscle is the LES

upper

which esophageal sphincter can be voluntarily controlled?

acetylcholine

neurotransmitter release by Auerback’s plexus, promotes SMOOTH muscle CONTRACTION in esophagus

nitric oxide

cause SMOOTH muscle RELAXATION in esophagus

LES fails to relax, and peristalsis impaired

effect of destroying Auerbach’s plexus on the relaxation of the LES?

Auerbach’s (myenteric) plexus

a network of neurons located in the gastrointestinal tract, responsible for regulating the mobility and contractions of the smooth muscles.

enteric nervous system

can independently control gut motility, without input from the vagus nerve (“second brain of gut”)

primary peristalsis

contraction initiated by SWALLOW

secondary peristalsis

contraction initiated by STRETCH or REFLUX

reflux prevention and neutralization

mechanisms broken down by GERD

lubrication, buffering, antimicrobial

role of salivary secretions in esophagus

tLERs

reflex stimulated by gastric distension to relax LES and allow venting of air from stomach

more acid reflux during episodes

how are tLESRs different in patients with GERD

no swallowing or salivary secretions

effect of sleep on salivary secretions and esophageal peristalsis

hiatal hernia

part of the stomach pushes through diaphragm into the chest cavity

vagus

what mediates tLESR

during sleep

when is clearance of acid reflux the most impaired in GERD patients

dysphagia

common symptom of esophageal MOTOR disorders (scleroderma and achalasia)

scleroderma

autoimmune destruction of smooth muscle

achalasia

destruction of enteric nervous system in esophagus, no peristalsis and failure of LES to relax

odynophagia

acute pain during swallowing

ulceration

most common cause of ODYNDOPHAGIA

dysphagia

difficulty swallowing

dysmotility or obstruction (cancer)

most common cause of DYSPHAGIA

heartburn

a burning sensation in the chest unrelated to swallowing

reflux

most common cause of heartburn

esophageal carcinoma

41 year old patient presents with NEW onset DYSPHAGIA what is the likely diagnosis?

endoscopy

if ESOPHAGEAL CARCINOMA is suspect what is the NEXT STEP?

mucosa, submucosa, muscularis propria, adventitia/serosa

main layers of the gut wall

no serosa layer

why are cancers of the esophagus less contained?

epithelium lamina propria, muscularis mucosa

what resides in the mucosa

glands and nerves

what resides in submucosa

muscle and nerves

what resides in muscularis propria

nerve, blood vessels, lymphatic, loose connective tissue

what resides in serosa

non-keratinized stratified squamous epithelium

type of mucosa is in the esophagus

muscularis propria (of GI tract)

Where is Auerbach’s Plexus

CREST (calcinosis, raynauds, esophageal dysmotility, skin thickening, telangiectasia)

symptoms of scleroderma

schatzkis ring

muscular or mucosal ring in distal esophagus associated with hiatal hernia

dysphagia

most common symptom of schatzkis ring

Mallory Weiss tear

tears in esophageal mucosa due to rapid increase in intraluminal pressure 

excessive vomiting and retching

cause of mallory weiss tear

vomiting bright red blood

presentation of mallory weiss tear

Boerhaave Syndrome

full-thickness esophageal rupture

esophageal varices

dilated submucosal veins in esophagus caused by hypertension

esophageal varices

patient with alcohol misuse starts vomiting bright red blood what is the likely diagnosis

level of aortic arch

Where do pills often get stuck in the esophagus?

immunosuppression (ex: steroid)

What underlying condition allows for Candida, Herpes, and CMV 

esophagitis that causes ODYNOPHAGIA?

medication, alcohol, tobacco, obesity, diabetic neuropathy

common causes of GERD

Barrett’s esophagus

normal squamous epithelium replaced by columnar epithelium goblet cells

barretts esophagus

what can GERD lead to?

adenocarcinoma

what can BARRETTS ESOPHAGUS lead to?

squamous cell carcinoma

cancer found in upper(proximal) and middle esophagus

adenocarcinoma

cancer found in lower(distal) esophagus

LES

which esophageal sphincter opens first

store, mix, grind, meter, sterilize, intrinsic factor, reduce Fe+++

jobs of stomach

fundic and antral

two areas of the stomach

storage and acid

function of fundic portion of stomach

grind, mix, and meter

function of antral portion of stomach

parietal, chief, ECL, D cells

cells of FUNDIC portion of stomach

g cells and d cells

cells of ANTRAL portion of stomach

acid and intrinsic factor

what do PARIETAL cells PRODUCE?

pepsinogen and gastric lipase

what do CHIEF cells PRODUCE?

histamine and cytokines

what do ECL cells PRODUCE?

somatostatin

what do D cells PRODUCE?

gastrin

what do G cells PRODUCE?

inhibits secretion from other cells (ex: parietal)

FUNCTION of SOMATOSTATIN

stimulate parietal cells

FUNCTION of HISTAMINE

somatostatin

inhibits parietal cell fom producing gastric acid

H⁺, K⁺ ATPase pump

actively transports hydrogen ions out of cells, crucial for acid secretion from PARIETAL cells

H+ and bicarb

two key molecules produced inside parietal cells in production of GASTRIC ACID

alkaline tide

rise in pH (alkaline) following gastric acid secretion in the stomach due to HCO₃⁻ (bicarbonate) byproduct

incorporated into mucus secretions of stomach

what happens to bicarb as it is released into the bloodstream during acid secretion.

protects stomach

Why is gastric mucous so important?

receptive relaxation

vagus mediates smooth muscle relaxation via vagovagal reflex (NO) in response to stretch in esophagus

antral grinding

vagus stimulates muscular contraction via ACh

receptive relaxation

expansion of stomach without increasing pressure

early satiety 

What happens to receptive relaxation in a vagatomy (vagus nerve cut)?

somatostatin

downregulates ECL and parietal secretion in response to H+

histamine

most potent STIMULATOR of GASTRIC ACID production

gastrin

ENDOCRINE hormone that causes ECL to release histamine

Histamine

Biogenic amine (not a classic hormone) that STIMULATES PARIETAL cells

H pylori (most common) and NSAIDs 

2 common causes of peptic ulcer

decrease somatostatin and increase gastrin

how does H pylori cause ulcer

decrease prostaglandins

how do NSAIDs cause peptic ulcers

increase blood flow, mucus production, cytoprotection, accelerate healing

how do prostaglandins protect the gastric mucosa

bicarb delivery to mucus

Why is mucous and gastric mucosal blood flow important to protect against peptic ulcers?

decrease blood flow and mucus production

how can smoking lead to ulcers

haptocorrin

binds vitamin B₁₂ in the mouth and stomach to protect it from acid degradation

Intrinsic factor

binds vitamin B₁₂ in the intestine and is ESSENTIAL for its absorption

lack of haptocorrin or intrinsic factor

What leads to B₁₂ deficiency?

I cells

intestinal cells that produce cholecystokinin (CCK)

mucus, bicarb, blood flow, regeneration, prostaglandin

gastric DEFENSIVE forces