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Applied Pathophysiology > Peptic Ulcers & GERD > Flashcards

Peptic Ulcers & GERD Flashcards

1
Q

Where does stomach acid come from?

A
  1. Surface epithelium: protective mucous
  2. Chief cells: Pepsinogen and Lipase
  3. Parietal cells: HCl, Intrinsic factor

Enteroendocrine /Enterochromafin cells (ECL): 1. G cells:Gastrin
2. Histamine
3. D-cells:somatostatin

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2
Q

What is acid secretion by?

A

Parietal cells:
H+ and Cl– are released by the actions of two separate pumps (& then in the stomach they’ll mix together).

H+ may be as much as 3 million times as great in the lumen (as low as pH 2) as in the blood.

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3
Q

What are the 2 Pumps?

A

Pump #1) HCO3—Cl- exchanger

Pump #2) H+–K+ ATPase active-transport (proton pump)

Proton pump (H+/K+ exchanger) inhibitors are important in decreasing acid secretion. (Omeprazole, Lansoprazole, Rabeprazole and Pantoprazole)

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4
Q

How do you control Acid Secretion?

A

1) Gastrin from blood (acting on gastrin/CCK-B receptor),

2) Acetylcholine (nerve control) (M3 receptor),

3) histamine (ECL cells)(H2 receptor)

4) presence of food in the lumen

5) lumen pH, regulate Acid production by Parietal cells.

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5
Q

What is the schematic model for physiologic control of hydrogen ion (acid) secretion by the parietal cells of the gastric fundic glands?

A

Parietal cells are stimulated to secrete acid (H+) by
1) gastrin,
2) acetylcholine (M3 receptor), and
3) histamine (H2 receptor).

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6
Q

How is acid secreted by H+/K+/ATPase proton pump into the stomach?

A

When there is food (peptides) in the lumen (small intestine) GASTRIN is secreted by ANTRAL G CELLS into blood vessels. Within the stomach, gastrin passes from the blood vessels into the submucosal tissue and binds to gastrin-CCK-B receptors on parietal cells and enterochromaffin-like (ECL) cells.

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7
Q

What do the Vagus nerve stimulate?

A

The Vagus nerve stimulates postganglionic neurons of the enteric nervous system to release ACETYLACHOLINE (ACh), which binds to M3 receptors on parietal cells and ECL cells. Stimulation of ECL cells by gastrin (CCK-B receptor) or acetylcholine (M3 receptor) stimulates release of HISTAMINE. Within the gastric antrum, Vagal stimulation of postganglionic enteric neurons enhances gastrin release directly by stimulation of antral G cells (through gastrin-releasing peptide, GRP) and indirectly by inhibition of somatostatin secretion from antral D cells.

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8
Q

What controls the inhibition of acid secretion?

A

ANTRAL D CELLS are stimulated to release SOMATOSTATIN by the rise in intraluminal H+ concentration and by CCK that is released into the bloodstream by duodenal I CELLS in response to proteins and fats (not shown).

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9
Q

How is the mucosa protected ? (Three levels)

A

1) Pre-epithelial (Mucous layer): A physical barrier against pepsin ( other proteases), enriched in HCO3- to neutralize acid (H+). pH is from 7- ~2

  • 2) Superficial epithelial (Mucous cells): rapid renewal
    – mucus and bicarbonate production
    – Presence of Stem cells for repair
  • 3) Mucosal blood flow: supplies the HCO3-
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10
Q

What is the importance of Stomach Acid?

A

is one of your body’s first defenses to NEUTRALIZE PATHOGENS.

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11
Q

What denatures proteins, making it easier for digestion?

A

Stomach acid

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12
Q

What activates pepsin, necessary to metabolize protein?

A

Stomach acid

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13
Q

What also activates intrinsic factor, a protein that helps your body absorb vitamin B12?

A

Stomach acid

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14
Q

What stimulates bile secretion for fat/lipid digestion and absorption?

A

Stomach acid

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15
Q

What are Peptic Ulcers?

A

are defects in the GASTRIC or DUODENAL MUCOSA that extend through the MUSCULARIS MUCOSA (1st thin layer, under endothelium).

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16
Q

What is the incidence of Peptic Ulcers?

A
  • Duodenum (80%)!!!!
  • Stomach (19%)
  • Stomach-Duodenum (4%)
  • GE junction (1%)
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17
Q

What is the epidemiology of Peptic Ulcers?

A
  • In the United States, peptic ulcer disease (PUD) affects approximately 4.5 million people annually.
  • Approximately 10% of the US population has evidence of a duodenal ulcer at some time.
  • Overall the PUD is on DECLINE over the past 3-4 decades. But hospitalization rate is approximately 30 patients per 100,000
  • Lifetime prevalence is approximately 11-14% in men (GREATER IN MALES) and 8-11% in women. Global prevalence varies in different regions.
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18
Q

What are the stages of Ulcer Formation (Mucosal Damage)?

A
  1. Irritation and inflammation (Gastritis) of the stomach lining
  2. Erosion
  3. Ulcer
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19
Q
  1. Irritation and inflammation (Gastritis) of the stomach lining:
A

lining is red & swollen

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20
Q
  1. Erosion:
A

superficial injury or of the gastrointestinal (GI) mucosa caused by decrease in mucosal defenses or increase in gastric acid

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21
Q
  1. Ulcer:
A

complete erosion through the GI Mucosa extends through the muscularis mucosa into the submucosa or deeper resulting in a GI BLEEDING.

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22
Q

What are the main etiologies/causes of PUD?

A
  1. Helicobacter pylori (H pylori) MOST COMMON (90% of Duodenal and 75% of gastric ulcers)
  2. NSAID induced (most common non- H pylori) (non-steroidal anti-inflammatory drugs)
    ex: Aspirin is major 1
  3. Stress induced (uncommon)
  4. Smoking
  5. Cocaine/Amphetamine
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23
Q

Why can NSAIDs cause PUD?

A
  • INHBITIS PROSTAGLANDIN SYNTHESIS by the mucosa (suppresses Cox-1)

Prostaglandins importance:
* Stimulate bicarbonate secretion
* mucus secretion
* Stimulate mucosal cell growth
* Decrease acid production

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24
Q

What are NSAIDs?

A

are WEAK ACIDS but can decrease the hydrophobicity of mucous layer (allowing acid penetration)

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25
Q

How can stress cause PUD?

A

May result from increased Vagal stimulation (worry, anxiety, alcohol, increased Parietal cell mass) Gastrinoma is a tumor of G-Cells (increase gastrin)

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26
Q

How can smoking cause PUD?

A

increases gastric acid production, decreases gastroduodenal prostaglandin and HCO3 production, increases Duodenogastric reflux.

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27
Q

How can Cocaine/Amphetamine cause PUD?

A

Reduces blood flow to gastric mucosa, decrease HCO3-

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28
Q

What is H. pylori?

A

a gram-negative bacterium found on the luminal surface of the gastric epithelium

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29
Q

What does H. pylori induce?

A

It induces CHRONIC INFLAMMATION of the underlying mucosa. The infection is usually contracted in the first few years of life and tends to persist indefinitely unless treated.

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30
Q

What is H. pylori’s prevalence?

A

Its prevalence INCREASES WITH OLDER AGE & with LOWER SOCIOECONOMIC STATUS during childhood and thus varies robustly around the world.

At least 50% of the world’s human population has H. pylori infection.

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31
Q

Where can H. pylori survive?

A

The organism can survive in the ACIDIC environment of the stomach partly owing to its HIGH UREASE ACTIVITY; urease converts the urea present in gastric juice to alkaline ammonia and carbon dioxide.

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32
Q

Infection with H. pylori is a _____

A

cofactor in the development of duodenal or gastric ulcers.

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33
Q

The great majority of patients with H. pylori infection will _______

A

NOT have any clinically significant complications.

34
Q

Progression from Ulcer to _______

A

potentially cancer

35
Q

What are the stages for the potential progression of cancer from ulcers?

A

This process is very slow, taking decades, and may stop at any step: DOESN’T ALWAYS LEAD TO CANCER

Stage 1:
Normal stomach lining (mucosa)

Stage 2:
Inflammation of the stomach lining (chronic gastritis)

Stage 3:
Loss of stomach cells and impaired digestive system (atrophic gastritis)

Stage 4:
Transformation of the stomach lining to intestinal (metaplasia)

Stage 5:
Beginning stages of stomach cancer (dysplasia)

Stage 6:
Stomach cancer (gastric adenocarcinoma)

36
Q

H. pylori infection:

A
  • common precursor of Gastritis & Peptic Ulcers
  • risk factor for Gastric Carcinoma
  • Curved gram - rod
  • Orgamisms synthesize urease, which produces ammonia that damages the gastric mucosa
  • ammonia also neutralizes acid pH, which allows the organism to live in the stomach
  • treatment: Omeprazole, Clarithromycin & Amoxicillin (1 PPI/antacide & 2 antibiotics)
37
Q

What is the most popular diagnosis of invasive/non-invasive methods?

A

Invasive:
- Histology (biopsy)
- require’s expert pathologist

Non-invasive:
- Urea breath test
- expensive, reliable test to evaluate success of treatment for H. pylori

38
Q

What is the Gastritis classification?

A

Acute, Chronic

39
Q

Acute Gastritis:

A

Acute: Erosive or hemorrhagic

  • Acute mucosal injury with patchy erosion (necrosis) often results from local contact with toxic agents.
    (therapeutic, accidental or suicidal) Aspirin, NSAIDS, strong Acid/Alkali, Ethanol.
40
Q

Acute Gastritis symptoms:

A

Epigastric pain, bleeding, sometimes hematemesis
* Aspirin: in low pH, acetylsalicylic acid is non-ionized, lipid soluble and penetrates the surface epithelium, destroys the local barrier. Acid then causes erosion. ASA impairs the platelets function and promotes bleeding.

41
Q

Chronic Gastritis:

A

A) Autoimmune gastritis

B) Chronic gastritis: Helicobacter pylori infection

42
Q

Chronic Gastritis

A) Autoimmune gastritis:

A

– is a chronic inflammatory disease with auto-antibodies against PARIETAL CELLS OF THE CORPUS & FUNDUS of the stomach.

– The known consequence is low gastric acid levels (HYPOCHLOROHYDRIA - b/c don’t have enough parietal cells) and vitamin B12 deficiency (b/c won’t be able to absorb Vit B12 properly)
causing PERNICIOUS ANEMIA (low red blood cells).

– Surface mucosa and gastric glands are normal=normal gastrin level, however achlorohydria leads
to antral-G cell hyperplasia leading to HYPERGASTRINEMIA.

*– IMMUNE SUPPRESSION can result IN PARTIAL REGENERATION of Parietal cells.

43
Q

Chronic gastritis:

B) Helicobacter pylori infection

A

-is caused by the presence of H. pylori infection

-Inflammatory cells are actively present in the mucosal layer

-Infection STARTS in ANTRUM and LEADS to DUODENAL peptic ulcers

-Chronic infection can LEAD TO GASTRIC MUCOSAL ATROPHY and predispose to Gastric carcinoma and
lymphoma.

44
Q

Having H. pylori infection ≠

A

having ulcers or stomach cancer.

45
Q

What are the symptoms like for Ulcers?

A

-MOST people infected with the bacteria NEVER HAVE SYMPTOMS or problems such as ulcers.

-It’s not clear why some infected people develop ulcers and others don’t.

***-H. pylori does NOT cause symptoms: they are usually either symptoms of gastritis or peptic ulcer disease.

Other symptoms may include:
* Weight loss, Loss of appetite, Bloating, Burping, Nausea, Vomiting (vomit may be bloody
or look like coffee grounds), Black, tarry stools

46
Q

What are complications of ulcers?

A
  • Acute or chronic GI tract bleeding (Vomiting of blood/rectal ) may lead to massive blood loss: resulting in hypotension, tachycardia, fainting
  • Gastric cancers
47
Q

What is the pathogenesis of Gastric (stomach) ulcers?

A
  1. H. Pylori infection spreads to most of stomach’s body
  2. Inflammation stimulates increased release of gastrin (Antrum)
  3. Gastrin induces increased acid secretion from body of stomach at first (Body)
  4. Increased acid and inflammation damages the gastric mucosa, causing ulceration
  5. Infection and inflammation causes loss of parietal and chief cells called atrophy, H+ decreases (low acid levels)
48
Q

What is the pathogenesis of Duodenal ulcer? (80% of ulcers here)

A
  1. ANTRAL H. Pylori infection
  2. ANTRAL inflammation stimulates increased
    release of Gastrin (A)
  3. Gastrin induces acid secretion from body of stomach (B)
  4. Increased acid damages the duodenal mucosa, causing ulceration
  5. Duodenal cells change into gastric-like cells (METAPLASIA)
  6. H. pylori spreads to the Metaplastic duodenum

(produce more parietal cells - therefore more acid)

49
Q

Duodenal vs Gastric Ulcers

A

chart add

50
Q

What is Gastroesophageal Reflux Disease (GERD)

A

includes all consequences of reflux of acid or other irritants from the stomach into the esophagus.

51
Q

What happens during NONpathologic reflux?

A
  1. Acid & 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 (bicarb) neutralizes the remaining acid in the esophagus
52
Q

When is it normal (Physiologic Reflux)?

A
  • Postprandial (Occurring after a meal)
  • Short lived
  • No symptoms
  • No night time symptoms (not when lying down)
53
Q

When do you call it GERD (Pathology)?

A
  • Commonly occurs
  • Mucosal injury
  • Nocturnal symptoms
54
Q

What is the epidemiology of GERD?

A
  • The prevalence of GERD in the Western world is estimated to range from 10% to 25%, while the prevalence in Asia is reported to be <5%.
  • Evidence suggests an increase in GERD prevalence since 1995 (p<0.0001), particularly in North America and East Asia.
  • Can happen in all ages, but more common in people older than 40 years
  • In UK and USA, 20-28% have weekly symptoms.
  • 7% have daily occurrence.
  • Except for in pregnancy and NERD (non-erosive reflux disease) no sex dependency is
    reported.
  • Both white and black individuals have a high prevalence of GERD, with black patients having a lower prevalence & persistently lower risk of developing esophagitis
  • Barrett’s esophagus is more common in white males.
55
Q

Barrett’s esophagus is more common in…

A

white males

56
Q

Heartburn:

A

Burning pain that can move up from the stomach to the middle of the chest and maybe into the throat. Can include regurgitation!

57
Q

Regurgitation:

A

A symptom of acid reflux.
Contents of the stomach move into the esophagus and maybe into the throat (sour taste in mouth).

58
Q

Dyspepsia:

A

AKA indigestion
Mostly STOMACH DISCOMFORT and can include; Burping, Nausea, Bloating, Upper abdominal pain.

59
Q

All these terms are used to describe symptoms of GERD however each can happen _______ of GERD.

A

independently

60
Q

NERD: Non-erosive reflux disease:

A

1) patient has no visible lesions in endoscopy , but
2) has the symptoms of the acidic reflux.

61
Q

What are the typical signs/symptoms of GERD?

A
  • Heartburn is the hallmark and the most common sign of GERD
  • Usually occurs AFTER a MEAL
  • Aggravated by bending over (b/c putting more pressure on stomach, which could move acid up)
  • > 2x per week suggests GERD
  • If it occurs with REGURGITATION, there is 90% certainty of GERD diagnosis
62
Q

What is the mech of GERD?

A
  • MULTIFACTORIAL and hard to know what is the exact mechanism.
    – Motor anomalies
    – Anatomical Anomalies
    – Impaired mucosal resistance

** Key factor is the retrograde movement of acid or duodenal contents from the stomach into the esophagus

63
Q

Two structures comprise
the main (primary) anti-
reflux barrier:

A

A- the intrinsic muscular sphincter known as the lower esophageal sphincter (LES): composed of 1) inner circular smooth muscles of the lower esophagus, 2) sling/clasp fibers of the stomach.

B- diaphragm that functions as an external sphincter-like mechanism.

64
Q

Barrett’s Gastroesophageal junction:

A

Intestinal metaplasia
- could be precursor to cancer

65
Q

What are the factors affecting the integrity of the LES that results in GERD?

A
  1. Spontaneous LES relaxation: The LES is tonically closed at rest, maintaining an average pressure of about 15-30 mmHg higher than intragastric pressure in resting conditions, and thus
    prevents gastroesophageal reflux (Vagus nerve excitatory function). Patient with GERD have decreased resting tonicity than normal.
  • After swallowing: To allow passage of a bolus, LES pressure falls within 1.5 to 2.5 seconds of a swallow and remains low for 6 to 8 seconds as the peristaltic contraction passes through the esophageal body.
  • Relaxation of the LES (after a swallow) occurs when tonic vagal cholinergic excitation to the LES is turned off .
  1. Transient increase in intra-abdominal pressure (gastric pressure):
    * Obesity
    * Pregnancy (progesterone decreases LES pressure)
    * Factors delaying stomach emptying (fatty meals)
    * Tight clothing,
    * BARRET’s ESOPHAGUS, metaplasia of epithelial tissue in esophagus is replaced by intestinal lining (metaplasia).
    * Barrett’s esophagus is often diagnosed in people who have long-term GERD, and obese people)
    * Only a small percentage of people with GERD will develop Barrett’s esophagus.
    * Barrett’s esophagus is associated with an increased risk of developing
    esophageal cancer.
  2. Atonic LES
    * Lack of tonicity due to damage to enteric nervous plexus resulting in APERISTALSIS (no peristalsis contractions) and dilation of esophagus. This is more common in patients with GERD. e.g. n Scleroderma.
66
Q

Transient LES Relaxation (TLESR):

A

is a SPONTANEOUS RELAXATION OF LES (WITHOUT SWALLOWING) that is needed for venting gas from stomach (a protective mechanism by preventing the accumulation of excess gas in the stomach or gas from entering the duodenum). Increased in patients with GERD.

(goes away)

67
Q

______ is the dominant irritant to the esophagus in the development and progression of GERD, although the ________ may contribute to the “reflux burden” when combined with the acid or on their own.

A

Reflux of acid

presence of bile and other compounds in gastric juice

68
Q

Gastric acid level:

A
  • ESOPHAGITIS is not always associated with increased level of acid secretion.
  • Gastric acid secretion is INCREASED IN BARRETT’s ESOPHAGUS but otherwise esophagitis can be seen in low as well as normal acid levels.

This indicates other factors may be involved:
* Duration of Reflux
* Composition of the reflux
* Gastric emptying delay

69
Q

Esophageal mucosa consists of…

A

of partially keratinized stratified squamous epithelium.

70
Q

Major esophageal defenses against injury:

A
  • A SURFACE MUCUS and a WATER LAYER CONTAINING BICARBONATE ions providing an alkaline microenvironment. This MUCUS IN ESOPHAGUS IS WEAK RELATIVE TO THAT OF STOMACH & DUODENUM.
  • The EPITHELIAL CELLS ARE TIGHTLY PACKED BY JUNCTIONAL COMPLEX TO LIMIT THE DIFFUSION OF H+ from lumen to cell and intercellular space. IN ESOPHAGITIS, THE JUNCTIONAL COMPLEXES ARE DAMAGED, LEADING TO INCREASED H+ DIFFUSION INTO THE INTERCELLULAR SPACES.
  • A HCO3- REACH BARRIER IS PRESENT IN THE CELLS AND WITHIN THE INTRACELLULAR SPACE. Blood supply is essential for the delivery of HCO3-. A Na+-DEPENDENT Cl-/HCO3-EXCHANGER ON THE BASOLATERAL MEMBRANE OF SQUAMOUS CELLS provide a route for blood-derived HCO3- to enter the cell cytosol
  • STEL CELLS IN THE EPITHELIUM REPAIR THE DAMAGED EPITHELIUM. Epidermal growth factor (EGF) is a major promoter of cell replication and this can begin as early as 30 minutes after acid injury.
71
Q

What are the clinical complications of GERD?

A
  • Esophagitis
  • Bleeding
  • Esophageal erosions and ulcerations
  • Stricture formation (Formation of scar tissue)
  • Barrett’s esophagus
  • Adenocarcinoma of the esophagus
72
Q

What are the factors that trigger GERD?

A
  • Food
  • Obesity
  • Pregnancy
  • Medications
  • Smoking
73
Q

How does food trigger GERD?

A
  • Large meals induce TLESRs
  • Meals within 2-3 hours of bedtime or with alcohol increase acid production (increase gastric pressure) and increase nocturnal GERD (remember that the LESP decreases at night!)
  • High fatty meals impairs gastric emptying
  • Aggravating foods: raw onions, caffeine, chocolate, alcohol, tomato products, spicy foods, citrus, peppermint, carbonated beverages, coffee, and tea
74
Q

How does obesity trigger GERD?

A

There are conflicting results, but generally recognized that exercise and weight loss will decrease symptoms – thought to increase intra-abdominal pressure thereby opening up LES

75
Q

How does pregnancy trigger GERD?

A

Most typically have heartburn symptoms and usually subside after delivery-
thought to increase intra-abdominal pressure thereby opening up LES

76
Q

How do medications trigger GERD?

A
  • Anticholinergic medications that affect LESP and LES tone and reduces salivation and slow intestinal mobility causing delays in gastric emptying.
  • Increased risk for NSAID users
77
Q

How does smoking trigger GERD?

A

Decreases LESP (nicotine)

78
Q

Hiatus hernia:

A

is a type of hernia in which abdominal organs (typically the stomach) slip through the diaphragm into the middle compartment of the chest.

This may result in gastroesophageal reflux disease (GERD). (b/c esophagus is always exposed to acid this way)

79
Q

How can you diagnose GERD?

A
  • There is NO GOLD STANDARD METHOD:
  • Tests that have been used include:
    – ENDOSCOPY
    – AMBULATORY ACID PROBE TEST: using a probe placed in esophagus that measures the frequency and duration of acid reflux.
    – MANOMETRY (Test of esophageal function: test is used to measure the function (strength) of the lower esophageal sphincter)
    *– Most important tool is a THOROUGH CLINICAL HISTORY.
80
Q

Heartburn

A
  • Burning substernal pain
  • May spread to neck or throat
  • Pain does not change upon exertion (except bending)
  • Regurgitation
  • Increasing symptoms when lying down or eating
81
Q

What are lifestyle modifications for GERD?

A
  • Maintain a Healthy weight
  • Stop Smoking
  • Elevate the head of your bed
  • Don’t lie down after meal
  • Eat slowly and chew well
  • Common triggers include fatty or fried foods, tomato sauce, alcohol, chocolate, mint, garlic,
    onion, and caffeine.
  • Avoid tight-fitting clothing
82
Q

What are the OTC/alternative drugs for GERD?

A
  • Antacids
  • H2-Receptor blockers: Decrease acid production:
  • cimetidine (Tagamet HB), famotidine (Pepcid AC), nizatidine (Axid AR) and ranitidine (Zantac)
  • Proton pump-inhibitor: Block acid and allow healing esophagus:
  • Lansoprazole, Omeperazole

Applied Pathophysiology (34 decks)

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