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BMS 460 > Pathophysiology of GI Tract > Flashcards

Pathophysiology of GI Tract Flashcards

1
Q

what are the two types of salivary glands and their secretions?

A
  • serous glands (ex: parotid): mostly serous cells, secrete nonviscous saliva with water, electrolytes, and enzymes
  • mixed glands (ex: submandibular, sublingual): serous and mucous cells, secrete a viscous saliva with mucin glycoproteins
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2
Q

how is salivation regulated?

A
  • mostly controlled by the autonomic nervous system
  • both branches of the ANS stimulate salivation, but the parasympathetic nervous system does it more strongly than sympathetic
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3
Q

mumps

A
  • salivary gland disease
  • acute viral illness caused by mumps virus
  • symptoms include fever, headache, muscle aches, etc.
  • frequently affects parotid salivary glands
  • can cause inflammation of brain or tissue covering brain (encephalitis) and spinal cord (meningitis)
  • can also cause orchitis (inflammation of testes)
  • most common cause of aseptic meningitis
  • males past puberty who develop mumps have a 15-20% risk of orchitis
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4
Q

sjogren’s syndrome

A
  • salivary gland disease
  • autoimmune disorder
  • lymphocytic infiltration of exocrine glands
  • mainly affects salivary and lacrimal glands: because inflammation is targeted here, patients get dry mouth and eyes (pulls water out of everywhere else?)
  • people older than 40, 9/10 are women
  • also can affect digestive organs, lungs, kidneys, joints, blood vessels, nerves
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5
Q

warthin tumor

A
  • papillary cystadenoma lymphomatosum, or adenolymphoma
  • benign tumor of the salivary glands
  • strong association with cigarette smoking
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6
Q

what mainly influences gastric secretions?

A

the vagus nerve!

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7
Q

in addition to stimulating parietal cells, what else does vagus nerve stimulate?

A
  • ECL cells to secrete histamine (H)
  • G cells to secrete gastrin (G)
  • delta (D) cells to secrete somatostatin (S)
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8
Q

describe stimulation of gastric secretions

A
  • dilation of the stomach by food initiates vasovagal reflex
  • reflex promotes release of ACh from terminal branches of vagus nerve and parasympathetic autonomic nerves in the stomach
  • ACh stimulates parietal cell to make HCl
  • HCl stimulates chief cell to make pepsinogen, and converts pepsinogen to pepsin
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9
Q

what does gastrin stimulate?

A
  • first of all, gastrin gets secreted by G cells in response to vagus nerve
  • gastrin stimulates parietal cells to secrete HCl. then, HCl stimulates chief cells to secrete pepsin via pepsinogen
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10
Q

what does pepsin do?

A
  • first of all, pepsin is released from chief cells in response to HCl from parietal cells
  • pepsin cleaves proteins to aa’s, and some of these aa’s (tryprophan and phenylalanine), stimulate G cells to release gastrin, which further stimulates HCl production
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11
Q

what happens when gastric pH drops below 3?

A
  • gastrin secretion stops
  • this amount of acidity also inhibits parietal cells producing HCl
  • when it drops below 2, HCl production completely stops
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12
Q

what does somatostatin do?

A
  • inhibits secretion of gastrin (which is from G cells)
  • inhibits secretin of HCl from parietal cells
  • note: somatostatin is an inhibitor of gastric secretion
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13
Q

what happens when food enters the duodenum?

A
  • firstly, note the use of the word FOOD
  • it leads to release of inhibitors of gastric secretion: secretin, CCK, GIP (gastric inhibitory peptide), and somatostatin
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14
Q

what happens when chyme enters the ileum?

A
  • firstly, note the use of the word CHYME
  • leads to release of peptide YY, which inhibits gastric emptying (slow the system down) - CCK also does this
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15
Q

what role does histamine play?

A

histamine potentiates the response to ACh and gastrin, so it stimulates gastrin secretion

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16
Q

what is atrophic gastritis?

A
  • chronic inflammation and thinning of the gastric wall
  • one of the causes of B12 deficiency, or pernicious anemia
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17
Q

relate atrophic gastritis to achlorhydria

A
  • in atrophic gastritis, many of the glands containing acid-secreting parietal cells are destroyed, limiting the amount of gastric acid secreted. this is achlorhydria
  • lack of acid production causes a loss of feedback inhibition of gastrin secretion (no inhibition, so get hypergastremia and ECL hyperplasia)
  • protein digestion and iron absorption are also impaired. basically can’t digest things like normal
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18
Q

where is histamine released from and what does it do?

A
  • released from ECL cells
  • stimulates gastric acid secretion from parietal cells by stimulating H2 receptors
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19
Q

how does the H+/K+ pump get inserted into the membrane of parietal cells?

A
  • parietal cell has excitatory receptors for gastrin, histamine, ACh. when these bind, second messengers cause insertion of the pump into the plasma membrane of parietal cells
  • parietal cells also have receptor for somatostatin, which inhibits this process
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20
Q

describe the zones of the stomach mucosa in order of increasing pH from lumen to bloodstream)

A
  • gastric lumen: H+ rich zone
  • mucus gel neutralization zone
  • HCO3- rich zone (mucus gel)
  • gastric epithelium
  • note: this is in gastric pit, above the location of HCl production (see slide 21)
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21
Q

what do prostaglandins do in maintaining the integrity of the GI wall?

A

prostaglandins stimulate mucous production by stimulating blood flow within the mucosa. it makes sense that this would stimulate mucus production because some prostaglandins lead to vasodilation and increased capillary permeability

22
Q

what do anti-inflammatory drugs do to impair mucosal blood flow?

A
  • inhibit prostaglandin synthesis!
  • because they impair mucosal blood flow, they will compromise mucous production, which makes the mucous layer less protective
23
Q

corticosteroids

A
  • anti-inflammatory drug
  • inhibit phospholipase A2, thus inhibiting the synthesis of arachadonic acid from membrane phospholipids
  • this means that prostaglandins can’t be made, so mucosal blood flow may be impaired
24
Q

aspirin and NSAIDs

A
  • inhibit COX
  • this stops prostaglandin production from arachadonic acid
  • this means that mucosal blood flow will be impaired
25
Q

how exactly do decreased prostaglandins affect the GI wall?

A
  • compromises protective abilities of the mucosa, such as secretion of mucus and bicarbonate
  • lack of prostaglandins can cause irritation of the mucosa (gastritis) or ulceration (PUD)
    –> I think this is all because not enough prostaglandins so not enough blood flow to mucosa so not enough mucous production!!
26
Q

describe the gastric pit (see pic on slide 20)

A
  • gastric pit has epithelial cells covered by protective gastric mucus blanket
  • below gastric pit (below mucous neck cells), there are parietal cells (secreting bicarbonate into bloodstream and HCl into the gastric pit), and chief cells (secreting gastrin)
  • bicarbonate that enters the bloodstream can go up into gastric epithelial cells and then get into the protective mucous layer
27
Q

describe the protective mucous gastric blanket

A
  • gastric epithelium gets sodium and bicarbonate from the bloodstream (which was put there by the parietal cells) (remember these are fenestrated capillaries)
  • this bicarbonate gets secreted from the gastric epithelial cells into the mucous gel, which is a bicarbonate rich zone
  • above that, there is a mucus gel neutralization zone
  • above that is the gastric lumen, which is a H+ rich zone
28
Q

GERD (gastro-esophageal reflux disease)

A
  • weakened LES closure strength, resulting in reflux
  • this reflux causes ulcerations mediated by pepsin and HCl
  • normally, the LES is supposed to prevent this reflux
  • symptoms include heartburn and esophagitis
  • treatment includes surgical repair of LES and gastric acid inhibitors to decrease gastric acid
29
Q

what are some things that can weaken LES closure in GERD?

A
  • progesterone
  • fatty foods
  • caffeine
  • ethanol
  • smoking
30
Q

hiatal hernia

A
  • defect in the diaphragm, allowing part of the stomach to pass through the hiatus in to the thorax
  • symptoms and treatment similar to GERD
31
Q

predisposing factors for hiatal hernia

A

increased intra-abdominal pressure due to pregnancy, obesity, chronic straining/coughing, ascites (fluid buildup in the abdomen, can be part of liver disease)

32
Q

describe nerve supply to heart vs. esophagus

A
  • afferent visceral sensory pain fibers from both the esophagus and the heart end without synapse in the first four segments of the thoracic spinal cord
  • 1% of patients who attend a hospital for heartburn have non-GERD heartburn, which means there may be relation to ischemic heart disease
33
Q

how to inhibit parietal cell activity

A
  • antihistamines and anticholinergics
  • antihistamines stop the histamine from the ECL cells from binding H2 receptor on parietal cell, which would lead to cAMP increase and insertion of the H+/K+ pump into the parietal cell membrane
  • anticholinergics stop ACh from vagus nerve from binding M3 receptors on parietal cells, which has the same effect
34
Q

what is the final common pathway of acid secretion in parietal cells

A
  • the H+/K+ pump itself!
  • inhibited by proton pump inhibitors
35
Q

two ways to target the H+/K+ pump

A
  1. inhibit insertion of the pump: H2 receptor blockers (antihistamines) and M3 receptor blockers (anticholinergics)
  2. inhibit inserted pump: proton pump inhibitors
36
Q

barrett’s esophagus

A
  • in GERD, the mucosal epithelium of the esophagus starts to look like the gastric mucosal epithelium
  • it goes from stratified squamous epithelium to a columnar epithelium (this is metaplasia!)
  • this increases the risk for esophageal adenocarcinoma, which usually occurs in the distal 1/3 of the esophagus
  • this means there will be gastric secretions in the esopahgus?
  • columnar metaplasia in the lower esophagus is what we refer to as “barrett’s esophagus”
37
Q

carcinoma of the esophagus

A
  • squamous cell carcinoma starts as an in situ lesion, referred to as squamous dysplasia
  • half of squamous cell carcinomas are in the middle 1/3 of the esophagus
  • because there is no serosa on most of the esophagus, esophageal cancers tend to spread locally before they are detected
38
Q

what is a peptic ulcer?

A
  • erosion in the lining of the stomach or duodenum (there can be both gastric and duodenal ulcers)
  • can be caused by both HCl and pepsin
  • epithelial layer and alkaline mucous (in stomach) are broken down
  • this breakdown can be caused by aspirin, NSAIDS, alcohol, and bile acids
  • can also be caused by H. pylori infection
  • H. pylori thrives in acidic conditions, so can be treated with antibiotics or inhibitors of gastric secretion
39
Q

excessive gastrin production

A
  • this can be caused by increase in basal (baseline) activity of the vagus nerve, leading to increased gastrin release which increases HCl release
  • this can cause G-cell neoplasia (gastrinoma)
  • in G-cell neoplasia, excessive gastrin is produced, which can lead to hyperplasia of ECL cells, causing too much histamine secretion
  • both of these factors ultimately result in chronic overstimulation of parietal cells, resulting in excess HCl which leads to peptic ulcers
  • this means that a peptic ulcer can be the result of a gastric cancer!
40
Q

what kind of conditions cause complications like GI bleeding?

A
  • GI bleeding can be caused by peptic ulcer disease (PUD) or malignant conditions
  • in cases of GI bleeding, malignant conditions like gastrinoma (which can occur in ZES), need to be ruled out because GI bleeding can occur in both these issues as well as PUD, which can be a benign condition
  • basically, we need to rule out whether cancer is involved in GI bleeding
  • note: finding a duodenal ulcer indicates a high probability of H. pylori and low probability of malignancy
  • overall: do not assume bleeding/other gastric symptoms are just because there is too much acid!!!
41
Q

zoellinger-ellison syndrome

A

triad: when symptoms of PUD occur alongside hypersecretion of gastric acid and the presence of gastrinoma
- 20-30% of multiple endocrine neoplasia-1 cases exhibit ZES

42
Q

define gastrinoma

A

gastrin-secreting malignant tumor of non-beta islet cells of pancreas or other organs

43
Q

achalasia of the esophagus

A
  • achalasia is a degenerative esophageal disease culminating in aperistalsis of the esophageal body and abnormal relaxation of LES
  • it is usually idiopathic, but can sometimes be caused by chagas disease
  • underlying cause of achalasia this is T-cell mediated destruction and fibrous replacement of esophageal myenteric plexus (cause of this is unknown)
  • destruction of myenteric plexus messes up esophageal smooth muscle activity
  • this leads to decreased or absent peristaltic activity in the distal esophagus, impaired LES relaxation, and increased LES pressure
44
Q

what issues can dysregulation of myenteric plexus in achalasia of the esophagus cause?

A
  • food can’t easily pass through the stomach
  • may have dysphagia
  • chest pain from esophageal distention
  • frequent bouts of pneumonia because contents of the esophagus can frequently be aspirated
  • neural function cannot be restored! this means that treatment is palliative, prioritizes symptom control, and tries to preserve the esophagus as a passive conduit
  • overall, try to reduce LES pressure and minimize reflux
45
Q

congenital form of megacolon

A

hirschsprung disease
- congenital disorder of large intestine: autonomic ganglia in smooth muscle are absent or reduced
- both myenteric and submucosal plexuses are involved!!
- also called congenital aganglionic megacolon
- basically, results when normal migration of neural crest cells from cecum to rectum is prematurely arrested, or ganglion cells undergo premature death
- we don’t know the mechanism behind defective neural crest cell migration, but there is almost always a genetic component involved
- the manifestation is that coordinated peristaltic contractions are absent, causing functional obstruction, resulting in dilation proximal to the affected segment (megacolon)
- Hirschsprung often coexists with other anomalies, down syndrome particular

46
Q

describe pathophysiology of hirschsprung disease

A
  • remember, this is the congenital form of megacolon
  • heterozygous loss-of-function mutations in the proto-oncogene RET (encodes a tyrosine kinase receptor) account for majority of familial hirschsprung cases, and 15% of sporadic cases
  • there are also mutations in at least 7 other genes that code for proteins involved in enteric neurodevelopment, including:
    –> RET ligand glial-derived neurotrophic factor
    –> endothelin
    –> endothelin receptor
  • all of the above mutations only account for 30% of cases (or fewer), suggesting there are other causes that have not yet been discovered
47
Q

where do cells of the myenteric and submucosal plexuses originate?

A
  • mostly from the vagal segment (see pic on slide 28)
  • plexuses form during 12-16 weeks development
  • the earlier the arrest in development of these cells, the longer the aganglionic section
48
Q

acquired form of megacolon

A
  • chagas disease
  • caused by trypanosoma cruzi, an intracellular protozoan
  • T. cruzi requires brief exposure to acidic phagolysosome to stimulate development of intracellular stage of the parasite
  • parasites reproduce in the cytoplasm of host cells and then develop flagella
  • now they lyse host cells, enter the bloodstream, and penetrate smooth, skeletal, and heart muscles
  • this can destroy the myenteric plexus, causing toxic megacolon
  • overall, chagas disease can damage myenteric plexus (causing megacolon and esophagus dilation) or damage to myocardial cells and conductance pathways (causing dilated cardiomyopathy and cardiac arrhythmias)
49
Q

differentiate chagas and hirschsprung disease

A

hirschsprung: congenital, absent or too few ganglia in smooth muscle
chagas: LOSS of ganglia

50
Q

describe myocarditis in chronic chagas disease

A
  • trypanosomes (virus-infected cells) parasitize scattered myofibers
  • this is accompanied by infiltrate of neutrophils, lymphocytes, macrophages, and some eosinophils
  • this causes myocarditis
  • chronic chagas cardiomyopathy is often treated with heart transplant
  • in chronic chagas, the mechanism of cardiac and digestive damage is controversial, but we think it is part of immune response incited by T. cruzi parasites

BMS 460 (34 decks)

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