1
Q
Are the upper and lower oesophageal sphincters true anatomical sphincters?
A
No — they are not well-defined anatomical sphincters, but functionally act as sphincters.
2
Q
What is the primary mechanism that moves the bolus through the oesophagus?
A
Peristalsis — coordinated muscle contractions push the bolus toward the stomach.
3
Q
When is the lower oesophageal sphincter (LES) normally open?
A
Only during swallowing — otherwise it remains closed to prevent reflux.
4
Q
What type of epithelium lines the oesophageal mucosa? What is its function?
A
Stratified squamous epithelium — it resists abrasion from swallowed food.
5
Q
What does the submucosa of the oesophagus contain and what is its function?
A
Oesophageal glands that secrete mucus to lubricate the bolus and protect the epithelium.
6
Q
What are the layers of muscle in the oesophageal muscularis externa?
A
Inner circular layer
Outer longitudinal layer
7
Q
What type of muscle is found in different sections of the oesophagus?
A
Upper 1/3: Skeletal muscle
Middle 1/3: Mixed skeletal and smooth muscle
Lower 1/3: Smooth muscle
8
Q
What is the adventitia of the oesophagus and its function?
A
Connective tissue layer that anchors the oesophagus to the posterior body wall.
9
Q
What is GORD (Gastro-Oesophageal Reflux Disease)?
A
A chronic gastrointestinal disorder where gastric contents regurgitate into the oesophagus, disrupting the oesophagogastric junction barrier.
10
Q
How common is GORD in Western countries?
A
It affects about 20% of adults — it is the most common GIT disorder.
11
Q
What causes tissue damage in GORD?
A
Acidic gastric contents reflux into the oesophagus, causing irritation and possible erosion of the mucosa.
12
Q
What are the two clinical forms of GORD?
A
Non-erosive reflux disease (NERD)
Erosive oesophagitis
13
Q
Which gender is more commonly affected by GORD?
A
Women are more commonly affected than men.
14
Q
Is there a known specific cause for GORD?
A
No — the exact cause is unknown, but several contributing factors and mechanisms are identified.
15
Q
What motor abnormality contributes to GORD?
A
Defective oesophageal peristalsis, which leads to impaired acid clearance.
16
Q
How does the lower oesophageal sphincter (LES) contribute to GORD?
A
Reduced LES tone
Transient LES relaxation
These allow reflux of gastric contents into the oesophagus.
17
Q
How does a hiatal hernia contribute to GORD?
A
It disrupts the oesophagogastric junction, allowing stomach contents to move more easily into the oesophagus.
18
Q
Name one gastric motility issue that contributes to GORD.
A
Delayed gastric emptying — increases stomach pressure and promotes reflux.
19
Q
How does obesity increase the risk of GORD?
A
Increased intra-abdominal pressure forces gastric contents upward.
20
Q
List at least three additional risk factors for GORD.
A
Age ≥ 50 years
Tobacco or alcohol use
Post-meal lying down (supination)
Pregnancy
Connective tissue disorders
Certain medications (NSAIDs, aspirin, nitrates)
21
Q
What is defective oesophageal peristalsis, and how does it contribute to GORD?
A
Impaired oesophageal peristalsis decreases clearance of gastric reflux, leading to severe reflux symptoms and mucosal damage.
22
Q
What percentage of GORD patients have impaired oesophageal peristalsis?
A
21% of GORD patients.
23
Q
What happens when LES function is impaired in GORD?
A
A weakened LES allows gastric contents to reflux into the oesophagus, increasing symptoms and damage.
24
Q
What are TLESRs, and how do they contribute to GORD?
A
LESRs are frequent, transient relaxations of the LES not triggered by swallowing. They allow gastric contents to reflux due to intragastric pressure exceeding LES pressure.
25
Name at least 4 factors that influence LES tone and TLESRs.
Alcohol, smoking, caffeine, pregnancy, nitrates, calcium channel blockers.
26
What is a hiatal hernia, and how does it worsen GORD?
A hiatal hernia occurs when the stomach or abdominal organs push upward through a weakened oesophageal hiatus in the diaphragm, shortening and weakening the LES and increasing reflux.
27
What is the 4 pathophysiology of GORD?
1. Defective oesophageal peristalsis
2. Impaired Lower Oesophageal Sphincter (LES) Function
3. Transient LES Relaxations (TLESRs)
4. Hiatal Hernia
28
What are the signs and symptoms of GORD?
- Heartburn and regurgitation
- Dysphagia
- Odynophagia
- Epigastric
- Naeusea
29
What is grade A in GORD Los Angeles Classification?
1+ mucosal break no longer than 5mm that does not extend between the tops of two mucosal folds
30
What is grade B in GORD Los Angeles Classification?
1+ mucosal break more than 5mm long that does not extend between the tops of 2 mucosal folds
31
What is grade C in GORD Los Angeles Classification?
1+ mucosal break that is continuous between the tops of two or more mucosal folds which involve less than 75% of the circumference
32
What is grade D in GORD Los Angeles Classification?
1+ mucosal break which involves at 75% of the oesophageal circumference
33
What is the Los Angeles classification?
Its a classification system of GORD that describe the endoscopic appearance
34
What are the complications of GORD?
- Oesophagitis
- Ulcerations/bleeding
- Regurgitation of acid into the lungs
- Adult onset asthma
- Stricture
- Barretss oesophagus
35
What causes oesophagitis in GORD?
Acid exposure leads to inflammation, irritation, and swelling of the oesophagus.
36
What complications can result from severe oesophagitis?
Ulcerations, bleeding, tissue erosion, and vascular damage.
37
How does acid regurgitation into the lungs contribute to adult-onset asthma?
Acid aspiration irritates the airways, causing breathing difficulties, cough, and asthma-like symptoms.
38
What is the role of the protective nerve reflex in acid reflux-related respiratory symptoms?
It triggers airway tightening (bronchospasm) to prevent acid entry into the lungs, causing breathing difficulty.
39
What is an oesophageal stricture, and what causes it?
A stricture is abnormal narrowing/tightening of the oesophagus caused by scar formation during healing of oesophageal damage.
40
What cellular change occurs in Barrett’s oesophagus?
Normal squamous epithelium is replaced by columnar epithelium.
41
Why is Barrett’s oesophagus clinically significant?
It is associated with an increased risk of oesophageal adenocarcinoma.
42
What is the GORD investifation?
- History and physical exam
- 24 hours pH monitoring
- Endoscopy
- If suspicious of Barrett's Oesophagus -- biopsy
43
Lifestyle modifications in the treatment of GORD
- Avoiding meals at least 3 hours before bed
- Maintaining good sleep
- Elevation of the head end of the bed
- Diet modification with the elimination of chocolate, caffeine and spicy foods, citrus, and carbonated beverages
44
Medications for GORD treatment
- Antacids = neutralise acids
- Histamine receptor antagonists = decrease acid production
- PPI = decrease acid production
45
Surgical treatment of GORD
- Medically refactory GERD
- Noncompliance
- Experience side effects with medical therapy
- Underlying large hiatal hernia
- Individuals who desire to discontinue long-term medical treatment
46
Endoluminal therapy in the treatment of GORD
Magnetic sphincter augmentation
47
Which cells produce mucus in the stomach, and what is its function?
Mucus surface and mucous neck cells produce mucus, which prevents direct acid contact with the epithelium.
48
What is the role of bicarbonate in gastric protection, and which cells secrete it?
Surface mucous cells secrete bicarbonate, which neutralises acid near the epithelium.
49
How does prostaglandin (PGE2) protect the stomach lining?
PGE2 attenuates acid production, stimulates bicarbonate and mucus secretion, and increases mucosal blood flow.
50
How do tight junctions between epithelial cells protect the stomach lining?
They prevent acid breaches through the epithelium by creating a sealed barrier.
51
Why is rapid epithelial regeneration important for gastric protection?
It allows quick repair of any acid-induced damage to the stomach lining.
52
What is Peptic Ulcer Disease (PUD)?
A condition characterized by a discontinuation (break) in the inner GI lining due to gastric acid secretion or pepsin.
53
What is the common underlying issue for both GERD and PUD?
Excess gastric acid.
54
How deep does a peptic ulcer extend in the gastric epithelium?
It extends into the muscularis mucosae layer.
55
Where does PUD usually occur?
In the stomach and proximal duodenum.
56
How does the incidence of duodenal ulcers compare to gastric ulcers?
Duodenal ulcers are 4 times more common than gastric ulcers.
57
Duodenal ulcers are 4 times more common than gastric ulcers.
Lower oesophagus, distal duodenum, or jejunum.
58
What is the most common infectious cause of PUD?
Helicobacter pylori infection, responsible for 90% of duodenal ulcers and 70–90% of gastric ulcers.
59
What class of drugs is a major non-infectious cause of PUD?
NSAIDs (non-steroidal anti-inflammatory drugs).
60
Name 4 other medications that can cause PUD.
Corticosteroids, bisphosphonates, potassium chloride, fluorouracil.
61
What is Zollinger-Ellison syndrome, and how does it cause PUD?
A rare condition involving a gastrin-secreting tumor (gastrinoma) that causes excessive acid secretion leading to ulcers.
62
Which malignancies are associated with PUD development?
Gastric cancer, lung cancer, lymphomas.
63
How can stress contribute to PUD?
Acute illness, burns, or head injury can cause physiological stress ulcers.
64
List 4 additional rare causes of PUD.
Viral infection, vascular insufficiency, radiation therapy, Crohn disease, and chemotherapy.
65
What is the basic pathophysiological mechanism of H. pylori-associated PUD?
It results from an imbalance between gastric mucosal protective factors and destructive factors caused by H. pylori infection.
66
How does H. pylori survive and colonize the gastric mucosa?
Through virulence factors that help it adhere to mucosa, neutralize acid, cause inflammation, and move toward epithelium.
67
What is the function of urease in H. pylori infection?
Urease breaks down urea into ammonia, neutralizing stomach acid and creating a more hospitable environment for H. pylori.
68
How do CagA and VacA toxins contribute to PUD?
They promote gastric mucosal inflammation and cause host tissue damage.
69
What is the role of H. pylori flagella in PUD pathophysiology?
Flagella provide motility, allowing the bacteria to move toward and adhere to the gastric epithelium.
70
How does prostaglandin normally protect the gastric mucosa?
By stimulating gastric mucus and bicarbonate secretion and maintaining mucosal blood flow.
71
How do NSAIDs contribute to PUD via COX-1 inhibition?
NSAIDs block COX-1, reducing prostaglandin synthesis, leading to decreased mucus/bicarbonate secretion and reduced mucosal blood flow.
72
How can NSAIDs cause direct epithelial damage?
Through topical irritation of the gastric epithelium, leading to mucosal injury.
73
What is the effect of NSAID-induced COX-2 inhibition on gastric mucosa?
It promotes leukocyte adhesion, activates polymorphonuclear neutrophils (PMNs), and inhibits nitric oxide (NO) production, contributing to mucosal injury.
74
How does alcohol contribute to PUD?
Alcohol irritates the gastric mucosa and increases gastric acidity, weakening mucosal defenses.
75
What is Zollinger-Ellison syndrome, and how does it cause PUD?
A condition with a gastrinoma (gastrin-secreting tumor) causing excessive gastrin release, stimulating parietal cells to overproduce HCl.
76
How does cystic fibrosis contribute to PUD?
It creates a hypersecretory gastric environment, increasing acid levels and ulcer risk.
77
How does hyperparathyroidism lead to PUD?
Elevated parathyroid hormone indirectly stimulates gastric acid secretion, contributing to ulcer formation.
78
Signs and symptoms of PUD
- Epigastric abdominal pain
- Bloating
- Abdominal fullness
- Nausea and vomiting
- Weight loss/weight gain
- Hematemesis
- Melena
79
How to diagnose PUD?
- Barium x-ray or upper GI series
- Laboratory testing
- Urea breath tests
- Serology
- Biopsy
- Endoscopic diagnosis
80
How does PUD cause upper GI bleeding?
Ulcer erosion damages small blood vessels, leading to chronic blood loss.
81
What are the consequences of chronic blood loss in PUD?
Depletion of iron stores and reduced hemoglobin (Hb), resulting in anemia.
82
How does PUD cause gastric outlet obstruction?
Healing ulcers form scar tissue, which constricts the pylorus and obstructs gastric emptying.
83
What symptoms are commonly associated with gastric outlet obstruction?
Abdominal bloating and a feeling of fullness.
84
What happens in PUD perforation?
The ulcer penetrates through the full thickness of the gastric or duodenal wall, leading to leakage of gastric contents into the peritoneum.
85
What is ulcer penetration in PUD?
The ulcer extends into adjacent organs (e.g., pancreas or liver) without free perforation.
86
How is PUD linked to gastric cancer?
Chronic ulceration, particularly in association with H. pylori infection or Barrett’s changes, can increase the risk of gastric malignancy.
87
What are the main goals of PUD management?
Relieve symptoms, heal ulcers, prevent recurrences, and prevent complications.
88
How do antacids work in PUD management?
They neutralize gastric acid.
89
What is the mechanism of Histamine H2-receptor antagonists?
They reduce gastric acid production by blocking H2 receptors in the stomach.
90
How do proton pump inhibitors (PPIs) reduce acid secretion?
They inactivate the hydrogen-potassium ATPase pump on parietal cells, blocking final acid secretion.
91
What is the mechanism of sucralfate in PUD treatment?
It forms a protective barrier over the ulcer crater, stimulates prostaglandin synthesis, and binds noxious agents like bile salts.
92
What is misoprostol, and how does it help in PUD?
Misoprostol is a prostaglandin E1 analog that increases mucosal resistance and inhibits acid secretion.
93
What is the standard therapy to eradicate H. pylori?
2 weeks of triple therapy: bismuth + tetracycline or amoxicillin + metronidazole.
94
What dietary changes are recommended for managing PUD?
Avoid spicy foods and late-night meals; eat a healthy balanced diet low in cholesterol; drink plenty of water and fresh juices.
95
How do omega-3 polyunsaturated fatty acids help in PUD?
They have anti-inflammatory effects and help protect the stomach from ulcers.
96
What is vagotomy, and why is it used in PUD?
Vagotomy is surgical cutting of the vagus nerve to reduce acid secretion.
97
What does vagotomy with antrectomy involve?
Removal of the gastric antrum along with cutting the vagus nerve to reduce acid production and gastrin stimulation.
98
What is a subtotal gastrectomy in PUD management?
Surgical removal of a large part of the stomach to reduce acid secretion and remove ulcerated tissue.
99
Large vs. Small Intestine
100
What are the two main types of Inflammatory Bowel Disease (IBD)?
Crohn disease (CD) and Ulcerative colitis (UC).
101
What part of the digestive tract can Crohn disease affect?
Any part of the digestive tract from the mouth to the anus.
102
What is the depth of inflammation in Crohn disease?
Full thickness (transmural) inflammation of the bowel wall.
103
Which part of the bowel does ulcerative colitis primarily affect?
The inner lining (mucosa) of the colon and rectum.
104
What is proctitis in UC?
Inflammation limited to the rectum.
105
What is proctosigmoiditis in UC?
Inflammation extending from the rectum into the sigmoid colon.
106
What is pancolitis in UC?
Inflammation involving the entire colon up to the cecum.
107
How are Crohn disease and ulcerative colitis histologically differentiated?
By the depth of bowel wall involvement: CD is transmural, while UC is mucosal (inner lining only).
108
What is the underlying immune mechanism of IBD?
It involves repetitive episodes of gastrointestinal inflammation caused by an abnormal immune response to gut microflora.
109
What is the suspected cause of IBD?
The exact cause is unknown, but it occurs in genetically susceptible individuals after an inappropriate immune response to intestinal flora.
110
How does smoking affect Crohn disease and ulcerative colitis?
Smoking increases the risk of Crohn disease but appears to protect against ulcerative colitis.
111
What is the typical age of onset for IBD?
Most cases occur between ages 15–30, with up to 25% developing IBD by adolescence.
112
What is the second peak incidence of IBD?
A smaller peak occurs after age 60 (10–15% of cases).
113
Is there a gender difference in Crohn disease and ulcerative colitis?
Crohn disease is slightly more common in females, while ulcerative colitis affects males and females equally.
114
Inflammatory Bowl Disease Pathophysiology
115
Histopathology of Chron's Disease
* The entire intestinal wall is involved
* Lymphocytic infiltrate
* Granulomas may be seen
116
Histopathology of Ulcerative Colitis
* Inflammation of only the mucosa and submucosa with the formation of cryptic abscesses and mucosal ulcer
* Neutrophilic infiltrate along with crypt distortion and crypt abscesses
* No granuloma
117
Endoscopy of Chron's Disease
Due to linear ulcers between the normal mucosa leading to cobblestone appearance
118
Endoscopy of Ulcerative Colitis
The colon becomes more rigid and short with a loss of the haustral markings leading to a lead-pipe appearance on a barium enema
119
What segment of GI tract is affected in Chron's disease?
- Any segment of GI tract
- Typically spares the rectum
120
What segment of GI tract does ulcerative colitis affect?
- Rectum and progresses in an uninterrupted fashion to the proximal colon
121
What are the signs and symptoms of ulcerative colitis?
* Bloody diarrhea with or without mucus
* Tenesmus, a sensation of incomplete evacuation
* Abdominal pain; predominantly left lower or left upper quadrant abdominal pain
122
What are the signs and symptoms of Crohn disease?
* Vary considerably depending on the region of gastrointestinal involvement
* Fistula formation, or stricture formation
* Non-bloody diarrhea
* Weight loss
* Abdominal pain; right lower quadrant pain
123
Ulcerative Colitis vs. Chrons Disease
124
How do you diagnose inflammatory bowl disease?
- Clinical findings
- Inflammatory laboratory markers
- Imaging findings
- Endoscopic biopsies
125
Treatment/management of chron's disease?
- Depends of the portion of GI tract involved
- Budesonide (steroid with significant metabolisation)
- Moderate to severe = anti-TNF or surgical treatment
126
Treatment/management of ulceratrive colitis
- Mild to moderate = aminosalicylate agents
- Or oral glucocorticords or immunomodulators
127
What is coeliac disease?
* Also known as gluten-sensitive
enteropathy
* Is a chronic autoimmune disease with strong genetic link (HLA DQ2 and HLA DQ8)
* Characterised by damage of enterocytes in the small intestine and and villi atrophy
128
What is the pathophysiology of coeliac disease?
A peptide derived from gluten gliadin causes damage to the small intestine
- Local inflammation
- Destruction of SI Villi
- Decreased functionality of the intestinal surface and malabsorption
129
What is the histopathology of coeliac disease?
- Only involves the mucosa of the small intestine
- Villi may be absent or atrophic and the crypt hyperplasia is present
130
What are the signs and symptoms of coeliac disease
- Diarrhea
- Abdominal distension
- Discomfort or pain
- Vomiting and constipation
- Lethargy
- Aphthous ulcers in the mouth
- CHronic headaches
- Delayed menarche
131
How ro diagnose for Coeliac Disease?
- Gluten challenge diet
- Serological tests to determine antibodies
- Test for HLA
- Endoscopy
- Imaging
132
How to treat/manage coeliac disease?
- Gluten-free diet
- Corticosteroids (only benefit small percentage)
Systemic Pathology
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