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Pathophysiology Final > GERD > Flashcards

GERD Flashcards

1
Q

What does GERD stand for?

A

Gastroesophageal reflux disease

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2
Q

What is the neurotransmitter responsible for regulating tone of the lower esophageal sphincter?

A

Ach
(therefore we do not want to use anti-cholinergics)
(this could cause a problem for people who also suffer from asthma-> atrovent)

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3
Q

normal physiology of acid in the esophagus

A

1) acid and food reflux into the esophagus
2) peristalsis returns most acid reflux to the stomach
3) after peristalsis, a small amount of acid remains in the esophagus
4) saliva neutralizes the remaining acid in the esophagus

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4
Q

what are the normal defenses mechanisms against acid in the esophagus

A

1) peristalsis

2) saliva that contains bicarbonate in it to neutralize the stomach acid

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5
Q

lower esophageal sphincter (LES)

A
  • 3-4cm of tonically contracted smooth muscle situated at the gastroesophageal junction
  • main function is to protect the esophagus from noxious stomach contents
  • dynamic to protect against reflux in a variety of situations such as swallowing, recumbency, and abdominal straining
  • tone is maintained by Ach
  • pressure is 15-30mmHg above intragastric pressure and varies from person to person-> this downward pressure forces the flap down
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6
Q

Explain how the LES pressure exhibits diurnal variation

A
  • highest at night (otherwise all our stomach contents would come back up)
  • lowest at daytime and postprandially (after you eat)
  • therefore it is weakest right after you eat-> why the flap is slightly delayed in closing- why you experience heartburn after you eat
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7
Q

what else is the LES pressure affected by?

A

-various drugs, foods, and hormones

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8
Q

pyloric sphincter

A

-controls emptying of stomach contents into the duodenum

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9
Q

How does the pyloric sphincter contribute to GERD

A
  • by delaying gastric emptying and therefore increasing intra-abdominal pressure that opens LES
  • as soon as food backs up it creates the intra-abdominal pressure that opens LES
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10
Q

what is the best non-pharm to prevent GERD

A
  • get ACTIVE!

- will increase transport of GI motility (and therefore reduce the intra-abdominal pressure)

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11
Q

duodenum

A
  • first portion of the small intestine
  • continues digestion of chyme
  • pH around 6.5
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12
Q

main components of the stomach

A

-fundus, body, antrum, pyloric sphincter, and stomach lining

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13
Q

what is the pH of the stomach’s gastric juices?

A

1

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14
Q

what does the gastric juices contain

A

-Hcl, electrolytes (Na, K, sulfates, phosphates, Ca, bicarbonate), water, ezymes (pepsin), and organic substances (mucus and proteins)

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15
Q

what protects the stomach walls from the gastric juices?

A

-lipoprotein rich membrane

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16
Q

what influences the ability of the mucosa membrane to withstand injury

A

-age and nutritional status

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17
Q

How can gastric juices contribute to GERD?

A

by too much acid being produced

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18
Q

how can excess acid production be stopped?

A
  • work directly on the parietal cells that produce the acid

- proton pump inhibitors- by inhibiting you reduce the output of acid (this blocks the ultimate effect of histamine)

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19
Q

Gastric acid production

A
  • done by gastric glands deep within stomach lining
  • parietal cells, G cells, and Enterochromaffin-like cells all lead to acid production
  • controlled by 3 regulatory pathways that overlap and are stimulated by the vagus nerve by food (all 3 of these bind to receptors on the parietal cell to increase acid production
    1) Ach- sight, smell, and taste of food; stomach distension
    2) Gastrin- dietary aa stimulate G cells; Ach via stomach distension; elevated pH (lower pH is inhibitory via release of somatostatin from antral D cells)
    3) Histamine (H2)- via Ach and gastrin (HENCE H2 blockers)
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20
Q

which cells within the stomach lining do not contribute to acid production

A

-mucous cells (aka superficial epithelial lining)-> mucus
chief cells-> pepsinogen (chymotrypsin, gastric lipase)-> aka digestive enzymes (while these are not acid, if the mucosal lining is gone these can still do damage)

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21
Q

what does the parietal cells secrete

A

-HCl and intrinsic factor (B12)

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22
Q

what does G cells in the antrum secrete

A

gastrin

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23
Q

what does the Enterochromaffin-like cells secrete?

A

Histamine

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24
Q

how does histamine contribute to acid production?

A

receptors located on the parietal cells and when stimulated by histamine, gastric acid (HCL) secretion occurs. It is the most important gastric acid secretion stimulant and is released from enterochromaffin-like cells by gastric and cholinergic activity.

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25
Q

How does gastrin contribute to acid production?

A
  • is a peptide hormone that is the most potent in stimulating secretion of gastric acid (HCl) by the parietal cells of the stomach and aids in gastric motility
  • Gastrin binds to cholecystokinin B receptors to stimulate the release of histamines in enterochromaffin-like cells, and it induces the insertion of K+/H+ ATPase pumps into the apical membrane of parietal cells (which in turn increases H+ release into the stomach cavity). Its release is stimulated by peptides in the lumen of the stomach.
  • May impact lower esophageal sphincter (LES) tone, causing it to contract
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26
Q

What is so dangerous about gastric acid?

A
  • Has HCl pH 1-2: denatures and hydrolyze protein, TG, and carbohydrates
  • Has pepsin and other proteases rapidly hydrolyzes protein
  • If there is an imbalance between gastric acid and mucosal defenses can result in inflammation, and damage to stomach lining leading to ulcerations
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27
Q

how many acid pumps do each parietal cell have

A

-1 million (hence the use of proton pump inhibitors)

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28
Q

H-K-ATPase proton

A
  • exchange H ions from the cytosol for K in the canaliculi using energy from ATP
  • there is passive movement of K and Cl ions into the canaliculus
  • when H ins are transported out they meet up with Cl ions to form HCl
  • by acting on these pumps we can decrease acid production (and also help prevent stomach cancers in people with hyper-active parietal cells)
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29
Q

Is there a standard definition for GERD

A
  • no

- it is about the clinical presentation and clinical history

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30
Q

What is GERD

A

-chronic disorder related to the retrograde flow of gastro-duodenal contents into the esophagus and/or adjacent organs, resulting in a spectrum of symptoms, with or without tissue damage

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31
Q

How long is GERD a chronic disorder until?

A

-until you do something to change it (i.e. change your lifestyle- diet, exercise, quit smoking, etc)

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32
Q

Why is it important to have both symptoms and pathophysiological changes in the definition?

A
  • because most people experience some reflux every hour without symptoms or changes
  • pathological reflux (i.e. the damaging of tissues) results in the true definition of GERD vs heartburn which is an unpleasant/ burning sensation below sternum
  • these changes can lead to a host of other issues
  • pathological reflux is also more frequent and in longer duration occurring both day and night disrupting patient’s life
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33
Q

Epidemiology

A
  • 44% of american pop suffer GERD symptoms monthly and 20% weekly
  • prevalence is higher in Western countries and increases with adults over 40
  • no real gender differences (except in pregnancy-> this increases intra-abdominal pressure)
  • mortality rate is 1 in 100000 (but the repeated wearing away of the esophageal lining can turn into ulcer/tumor)
  • true incidence is hard to know (b/c many don’t seek medical treatment and there is no standard definition for diagnosis)
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34
Q

What are the areas of the body in which signs/ symptoms of GERD can occur?

A
  • chest
  • pulmonary
  • oral
  • throat
  • ear
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35
Q

What symptoms occur in the chest area?

A
  • heartburn
  • regurgitation
  • chest pain
  • dysphagia/ odynophagia
  • belching
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36
Q

what symptoms occur in the pulmonary area?

A
  • non-allergic asthma
  • cough
  • aspiration
  • hoarseness
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37
Q

What symptoms occur in the oral area?

A
  • tooth decay

- gingivitis

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38
Q

What symptoms occur in throat area?

A
  • globus sensation
  • hoarseness
  • laryngitis
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39
Q

what symptom can eventually occur in the ear?

A
  • ear ache

- by the time it gets here that means the condition has gotten a lot worse (symptoms becoming more symptomatic)

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40
Q

What is the hallmark symptom of GERD?

A

heartburn-> most common sign

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41
Q

At what time does heartburn usually occur?

A
  • usually after a meal
  • aggravated by bending over
  • > 2x per week suggests GERD
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42
Q

What is almost certain if heartburn occurs with regurgitation

A

90% certainty of GERD diagnosis

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43
Q

extraesophageal symptoms

A

-laryngitis, pharyngitis, chronic sinusitis, dental erosions, asthma, and chronic cough

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44
Q

difference between heartburn, regurgitation, and dyspepsia

A

heartburn- burning pain that can move up from stomach to the middle of the chest and maybe into thought (can include regurgitation)
regurgitation- symptom of acid reflux; contents of stomach move into the esophagus and maybe into throat (sour taste in mouth)
dyspepsia- aka indigestion; mostly stomach discomfort (burping, nausea, bloating, upper abdominal pain)
-all are used to describe symptoms of GERD, but each can happen independently of GERD too

45
Q

true or false: there is only one cause of GERD

A 
false- it is multifactorial and hard to know what is the exact mech sometimes
when things go wrong:
-decreased salivation
-impaired esophageal acid clearance
-impaired tissue resistance
-transient LES relaxation
-decreased resting tone of LES
-delayed gastric emptying
-hiatus hernia
-too much acid prouced
46
Q

what is the key factor in the causation of GERD

A

-the retrograde movement of acid or duodenal contents from the stomach into the esophagus

47
Q

what characteristics of the reflux are important

A

the content and the volume

  • these substances> protective mechs of the esophagus
  • it comes down to the aggressive mechs that are harmful to the esophagus that overwhelm protective mechs such as peristalsis, mucous production and salivation
48
Q

What can the content of the reflux include?

A

acid, pepsin, bile, and pancreatic enzymes

49
Q

dysfunction in the LES pressure

A

1) spontaneous LES relaxation
2) increases in intra-abdominal pressure
3) sphincter is atonic

  • exact mech is not known- lasts 10-35 seconds, but esophageal distension, vomiting, belching, and retching can cause a lower LESP
  • while these things happen to everyone, it comes down to the protective measures
  • may occur with straining, bending over, eating or coughing
  • allos gastric contents to move freely between sphincter and esophagus- usually associated with severe esophagitis
50
Q

spontaneous LES relaxation

A
  • not associated with swallowing= transient LES relaxation (TLESR)
  • most common causative mech
  • unrelated to swallowing or peristalsis
51
Q

what are some causes of increases of intra-abdominal pressure

A

-thigh clothing, obesity, pregnancy

52
Q

spincter is atonic

A
  • no tone-> may need surgical intervention

- factors that can lower LES tone include endogenous hormones, meds, and food

53
Q

true or false: TLSER can occur in anyone- some may have it and not lead to GERD

A

true- all depends on their protective mechs, as well as the potency and time exposed to the gastric contents

54
Q

mechanisms of GERD in normal volunteers vs patients with GERD (% comparisons)

A

Tone LES: 94% vs 65%
Transient increase in intra-ab pressure: 5% vs 17%
atonic sphincter: 1% vs 18%

55
Q

Food that increases LES pressure

A

protein (good!!!)

56
Q

food that decreases LES pressure

A

fat, chocolate, ethanol, peppermint, garlic, onions

57
Q

hormones that increases LES pressure

A

gastrin, motilin, Sub P

58
Q

hormones that decrease LES pressure

A

glucagon, progesterone, estrogen (therefore be careful with females on birth control)

59
Q

What process do medications that increase LES pressure undergo?

A

speed up GI mobility (aka they are GI mobility agonists)

60
Q

What is a major medication that can decrease LES pressure?

A

-anticholinergics (also nicotine, caffeine, nitrates, DA, narcs,)

61
Q

esophagus is cleared mainly by:

A

1) primary peristalsis due to swallowing (secondary peristalsis due to esophageal distension or gravity)
2) swallowing increases salivary flow (contains bicarbonate that buffers acidic content)

62
Q

impaired acid clearance

A

-decreased peristalsis, decreased salivation, and increased frequency of reflux leads to increased time the mucosa is exposed to gastric contents

63
Q

true or false: production of saliva naturally decreases as we age

A

true (especially if they have Sjorgen’s)

64
Q

true or false saliva production increases as we sleep

A

false- decreases therefore making nocturnal GERD an issue for many patients

65
Q

whats an easy non-pharm to help patients with GERD, especially elderly

A

-suck on a sugarless candy to increase salivation

66
Q

what does severity of GERD depend on?

A
  • duration of acid exposure
  • composition of the reflux
  • delay of gastric emptying
67
Q

what is the primary cause of symptoms and tissue damage

A
  • the duration of acid exposure -threshold seems to be a pH of 4
  • the more time exposed to reflux under pH of 4 the more severe symptoms and longer recovery (only so many defence mechanisms)
  • a pH of 4 is the threshold between erosive and non-erosive reflux in a 24 hour period and improved healing rates after 8 weeks (if pH can be maintained above 4, most patients will remain symptom free and eventually lead to healing
68
Q

what are the most notable compositions of the reflux

A
  • pH of 2, pepsin, and acid (at pH 2, pepsinogen is activated)
  • bile or alkaline pancreatic secretions (bile acids are also a direct irritant)
69
Q

what does the delay of gastric emptying lead to

A

-increase in gastric volume= increased frequency and volume to be refluxed (fatty meals and smoking contribute)

70
Q

true or false: the most important thing to try and prevent is regurgitation of the stomach

A

true-> it is more acidic

71
Q

true or false: more pain is felt at lower pH levels

A

true (eventually weans off at pH 4)

72
Q

is there a gold standard to diagnosing GERD?

A

no

73
Q

what are some tests that are included?

A
  • endoscopy
  • 24 hour pH monitoring
  • proton pump administering
  • manometry
74
Q

what is the most important tool

A

-looking at clinical history

75
Q

endoscopy

A

-looks at scar tissue in lower esophageal tissue-> look at and possibly biopsy the condition of the mucosa (esophagitis and Barrett’s esophagitis)

76
Q

24 hour pH monitoring

A
  • involves having patient write diary of symptoms and at the same time a pH probe is placed 5cm above the LES and measurements are compared to diary
  • in addition, probe monitors the % of time the pH was low, the frequency and severity of reflux
77
Q

Proton pump admin

A
  • useful, especially hen endoscopy has ruled out other complications such as Barrett’s esophagus, ulcers, or cancer
  • no standard treatment regiment (aka no specific dose with set timeline)
78
Q

Manometry

A

-looks at motility issues by measuring the pressure differences across the stomach, LES, esophagus and pharynx

79
Q

differential diagnosis: heartburn vs cardiac chest pain

A

heartburn- burning substernal pain

  • may spread to neck or throat
  • pain doesn’t change upon exertion (except bending)
  • increasing symptoms when lying down or eating

cardiac chest pain- crushing chest pain (elephant)

  • radiating pain into left arm, neck, back and shoulder
  • pain increases with exertion
  • increasing symptoms till treatment or death
80
Q

clinical complications of GERD

A
  • esophagitis
  • bleeding (can lead to death)
  • esophageal erosions and ulcerations
  • stricture formaton (scar tissue)
  • barrett’s esophagus (normal tissue lining of esophagus change to tissue that resembles lining of intestine- becomes darker in colour)
  • adenocarcinoma of the esophagus
  • THEREFORE NEED TO TREAT/ CHANGE LIFESTYLE ASAP*
81
Q

esophagitis

A

inflammation of esophagus- usually the first sign leading towards GERD

82
Q

what can injury to tissue result in?

A

tissue destruction and the development of erosions and ulcerations

83
Q

how does stricture formation occur?

A

-protective mechs against ulcerations involving the deposition of fibrous tissue leads to stricture formation

84
Q

what does stricture formation cause

A
  • this leads to dysphagia as it always feels like there is something stuck in the throat
  • weight loss in uncommon as most patients will change their diet to suit their needs and avoid pain
85
Q

how does barrett’s esophagus form

A

-when all the other complication s occur and then intestinal-type columnar epithelium cells replace normal but ulcerated squamous epithelial cells, Barrett’s esophagus develops-> severe complication indicating a long-term assault of reflux on the esophagus and is linked to developing cancer

86
Q

factors that trigger GERD

A

-certain foods, obesity, pregnancy, medications, smoking, hiatial hernia

87
Q

explain how food can trigger GERD

A
  • large meals induce TLESRs
  • meals within 2-3 hours of bedtime or with alcohol increase acid production and increase nocturnal GERD (remember that LESP decreases at night)
  • high fatty meals impairs gastric emptying
  • aggravating foods include: raw onions, caffeine, chocolate, alcohol, tomato products, spicy foods, citrus, peppermint, carbonated drinks, coffee, and tea
88
Q

explain how obesity can trigger GERD

A
  • there are conflicting results, but generally recognized that exercise and weight loss with decrease symptoms
  • thought to increase intra-abdominal pressure thereby opening LES
  • weightloss is generally recommended as a first line therapy for treating GERD
89
Q

Explain how pregnancy can trigger GERD

A
  • most typically have heartburn symptoms and usually subside after delivery
  • thought to increase intra-abdominal pressure thereby opening up LES
  • also from the excess estrogen and progesterone
90
Q

explain how some meds can trigger GERD

A
  • anticholinergic meds that affect LESP and LES tone and reduces salivation and slow intestinal mobility causing delays in gastric emptying
  • increased risk for NSAID users
91
Q

explain how smoking can trigger GERD

A
  • the nicotene decreases LESP
  • promotes the movement of bile from the intestine to the stomach which changes the content of the reflux
  • smoking also inhibits saliva secretion thereby stopping a natural defence mech
92
Q

hiatal hernia

A
  • the proximal stomach is dislocatedthrough the hiatus of the diaphragm into the chest and the crural diaphragm becomes separated from the LES
  • pulls open LES-> it stretches and opens the sphincter and leaves the esophagus exposed
  • these are found in more than 90% of patients with severe erosive esophagitis; most often found in patients with Barrett’s esophagus and may contribute to its development
93
Q

what are some recommendations that we can give to treat GERD

A

-eat smaller meals, less fatty meals, at least 3-6 hours before sleeping, sleep on an incline, lose weight, exercise, decrease alcohol and coffee consumption

94
Q

hallmark clinical characteristics of GERD (aka red flags)

A
  • chest pain typical of cardiac event
  • recurring vomiting
  • blood loss in vomit or stool
  • dysphagia (difficulty swallowing); especially with solids like rice
  • odynophagia (pain on swallowing)
  • unexplained weight loss >5%
  • family history of gastric cancer/ tumour
  • unexplained cough, hoarseness, or dyspnea

HINT: VBAD

  • persistent Vomiting
  • Bleeding
  • Abdominal weight loss
  • Dyphagia
95
Q

what are the typical ages of GERD

A

under 18 or over 50

96
Q

within lifestyle modifications, what should patients avoid?

A
  • foods that trigger
  • lying down right after meals
  • smoking
  • excessive bending
  • tight fitting clothes
97
Q

within lifestyle modifications what should patients do

A
  • exercise
  • maintain healthy body weight
  • reduce alcohol intake
  • reduce caffeine intake
  • eat smaller, more frequent meals
  • reduce stress
  • sleep with the head elevated higher than pelvis
98
Q

what is the first line treatment for non-complicated mild to mod GERD

A

-lifestyle modifications with or without addition of antacids or H2 blockers

99
Q

OTC options

A
  • antacids (Tums)

- alginic acid (gaviscon)

100
Q

antacids

A
  • lack efficacy data over placebo
  • provide symptomatic relief by raising by raising pH over 4 which decreases conversion of pepsinogen to pepsin
  • neutralizes acidic contents
  • contains Ca, Mg, and Al
101
Q

Alginic acid

A
  • creates a viscous barrier at the top of the stomach contents
  • decreases reflux episodes
  • efficacy is lacking on healing
102
Q

Rx treatment options

A
  • H2 receptor antagonists
  • proton pump inhibitors
  • prokinetics
  • mucosal protectants
103
Q

explain H2 receptor antagonists

A
  • block the action of histamine at the histamine H2 receptors of the parietal cells in the stomach-> decreases production of stomach acid
  • provide immediate relief of symptoms (12 week therapy at BID)
  • all options have similar efficacy-> choice based on kinetic profie and side effects
  • common adverse effects include diarrhea, headache, dizziness, rash and tiredness
104
Q

Proton pump inhibitors

A
  • superior to all other pharm treatments for all types of patients (esp daytime)- most potent inhibitors of acid production
  • newer agents have fewer drug interactions
  • maintains pH above 4 for grater period of time allowing healing
  • best to take 30 mins before breakfast b/c they only work on actively secreting pump
  • side effects are mild and reversible (headache, diarrhea, nausea, abdominal pain, constipation, dizziness, and rash)
  • if symptoms are greater than 2 times a week, these are considered first line
105
Q

prokinetics

A
  • help move contents of stomach faster therefore reducing intra-abdominal pressure
  • signigicant drug interactions and side effects
106
Q

mucosal protectants

A
  • only used in minor GERD; or if patient is at risk and becomes hospitalized (therefore sedentary)
  • protects stomach and esophageal tisue lining (chalk-like coating)
  • not used often
107
Q

alternative off-label treatment options

A
  • baclofen (improves tone of LES and increases gastric emptying- works at antrum)
  • surgical (laparoscopal sphuncter augmentation-device comprised of string of magnetized beads)
  • trazodone and SSRIs (improve esophageal pain on swallowing- analgesics)
  • cholestyramine (from patients who fail PPI therapy and have bile reflux; binds fats and cholesterol and through to increase speed of gastric emptying- evidence is lacking)
  • acupuncture (helps control regurgitation and heartburn- evidence is lacking)
108
Q

overall cause of GERD

A
  • lower esophageal flap loosening
  • slow motility of GI
  • overproduction of acid
  • hiatal hernia

Pathophysiology Final (10 decks)

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