Gastric Pathology Flashcards
(130 cards)
1
Q
What is gastritis?
A
Mucosal inflammatory response
2
Q
What causes acute gastritis?
A
Imbalance between mucosal defense and acid environment, if either one is not balanced then inflammation occurs
3
Q
What does acid damage lead to?
A
Superficial inflammation, erosion, ulcers
4
Q
What is the difference between erosion and ulcers?
A
Erosion: loss of superficial epithelium
Ulcers: loss of mucosal layer
5
Q
What does the presence of neutrophils indicate?
A
Acute gastritis
If there is no neutrophils –> gatsropathy
6
Q
What happens if acute gastritis is left untreated?
A
It can lead to bleeding –> acute erosive hemorrhagic gastritis and perforation
7
Q
What are the symptoms of acute gastritis?
A
Usually asymptomatic disease
Mild epigastric pain, nausea, vomiting, or coffee-ground hematemesis & melena in severe cases
8
Q
What are the protective factors of the stomach?
A
Surface mucus secretion
Bicarbonate secretion into mucus
Mucosal blood flow
Epithelial regenerative capacity
Elaboration of prostaglandins
9
Q
What are the risk factors for gastritis?
A
H. pylori infections
NSAIDs
Tobacco
Alcohol
Gastric hyperacidity
Duodenal-gastric reflux
Ischemia
Shock
Bile reflux
Uremic patients
Chemotherapy and radiation
Old age
10
Q
How are ureic patients more vulnerable to gastritis?
A
Inhibition of gastric bicarbonate transporters by ammonium ions, cannot neutralise
11
Q
How is old age a risk for gastritis?
A
Decrease in mucin and bicarbonate secretion which are factors that explain the increaser susceptibility of older adults
12
Q
How is ingestion of harsh chemicals, acids and bases a risk factor for gastritis?
A
Severe gastric mucosal damage due to direct injury
13
Q
What is stress-related mucosal disease?
A
Extensive burn –> curling ulcers (in the proximal duodenum)
14
Q
What does the increase in intracranial pressure and brain injury cause?
A
Cushing ulcers (in the stomach, duodenum and esophagus)
15
Q
How do shock and sepsis contribute to stress-related mucosal disease?
A
It leads to the formation of stress ulcers (local ischemia caused by systemic hypotension or decreased blood flow resulting from stress-induced splanchnic vasoconstriction
16
Q
What is the range of the severity of the stress-related mucosal disease?
A
Range from shallow erosions to multiple deep, penetrating ulcers (perforation & bleeding)
17
Q
How do you end stress-related mucosal disease?
A
Complete reepithelization and healing
18
Q
What are ICU patients given in stress-related mucosal disease?
A
Prophylactic PPI in order to reduce HCl
19
Q
What is the pathology of acute gastritis?
A
Diffusely hyperaemic gastric mucosa, hemorrhagic inflammation
20
Q
What is the pathology of gastropathy?
A
Gastropathy with erosions superficial mucosa is eroded away
21
Q
What is chronic gastritis?
A
Chronic inflammation of the stomach
22
Q
What are the main causes of chronic gastritis?
A
H. pylori gastritis or chronic autoimmune gastritis
23
Q
What other factors could cause chronic gastritis?
A
NSAIDs
Radiation
Bile reflux
System diseases
24
Q
What are examples of systemic diseases that cause chronic gastritis?
A
Crohn disease, amyloidosis, graft vs host disease
25
What are the symptoms of chronic gastritis like compared to acute gastritis?
Less severe but more persistent
26
What are the symptoms of chronic gastritis?
Nausea & upper abdominal pain (typical)
Vomiting and hematemesis (rare)
27
What is the most common cause of gastritis?
H. pylori chronic gastritis, causes about 90% of the cases
28
Which part of the stomach is mainly affected in h. pylori gastritis?
The antrum of the stomach
29
What is the pathogenesis of H. pylori chronic gastritis?
H. pylori secretes creases and proteases with inflammation which will weaken the mucosal defence --> ulceration
30
What is the patients' main complain with H. pylori chronic gastritis?
Epigastric abdominal pain and later peptic ulcer disease and complications
31
What is the pathogenesis of H. pylori chronic gastritis in the body or fundus?
Body or fundus gastritis --> multiform atrophic gastritis with patchy mucosal atrophy --> reduced parietal cells & decrease secretion of acid
32
What does reduced parietal cell mass and decreased acid secretion lead to in h. pylori of the fundus/body?
Intestinal metaplasia (increase in goblet cells) which increases the risk of adenocarcinoma
33
What determines H. pylori pathogenesis?
Virulence factors and host factors
34
What are some examples of the virulence factors of h. pylori?
Flagella
Urease
Adhesion (LPS, O-antigens)
Toxins
35
What are some examples of host factors regarding H. pylori?
Increased expression of proinflammatory cytokines
Decreased expression of the anti-inflammatory cytokine which is associated with the development of pan-gastritis & cancer
Iron deficiency
36
What are examples of proinflammatory cytokines?
TNF
IL-1β
37
What is an example of an anti-inflammatory cytokine?
IL-10
38
What are the different diagnostic techniques for h. pylori?
Non-invasive serologic test for antibodies
Fecal bacterial antigene detection
Urea breath test
Gastric biopsy
Bacterial culture
Bacterial DNA detection by PCR
Biopsy
39
What is one of the limitations of the non-invasive serologic test?
Detects active & prior infections, so in the case that you have previously been exposed to h. pylori but you are infected now as well the test will not be able to show the results
40
What is the urea breath test?
A test that depends on the generation of ammonia by the bacterial urease, the more the ammonia --> positive test
41
Why is it important to perform biopsies for h. pylori infections?
To check for progression, especially because of the increased risk of adenocarcinoma
42
What colour cells are neutrophils?
Pale pink
43
What are the pathological features of h. pylori?
1. Intraepithelial and lamina propria neutrophils infiltration
2. Lymphoid aggregates with germinal centres & subepithelial plasma cells within lamina propria
3. Represent an indued form of MALT, that has the potential to transform into lymphoma
4. Spiral-shaped H. pylori highlighted by the WS silver stain
44
Are lymphoid cells commonly found in the stomach?
No, under healthy conditions, there is no lymphoid cells in the stomach
45
Where are the h. pylori micro-organisms abundant?
Within surface mucus
46
What is chronic autoimmune gastritis?
Autoimmune destructon of gastric parietal cells, type IV hypersensitivity reaction in body and fundus
47
What kind of cells is type IV hypersensitivity reaction mediated by?
CD4+ and T-lymphocytes
48
What % of patients are affected by chronic autoimmune gastritis?
Less than 10% of chronic gastritis
49
What do the auto-antibodies attack in autoimmune gastritis?
Parietal cells and intrinsic factor
50
What happens during chronic autoimmune gastritis?
Defective acid secretion
Reduced serum pepsinogen I concentration
Megaloblastic anemia
Atrophy of mucosa with intestinal metaplasia
51
What is the most common cause of diffuse atrophic gastritis?
Chronic autoimmune gastritis
52
What does defective acid secretion in chronic autoimmune gastritis lead to?
Achlorhydia --> due to increased gastrin levels because of astral G-cell hyperplasia which can lead to endocrine cell hyperplasia (tumor)
53
Why does gastrin increase in chronic autoimmune gastritis?
Because there is defective acid secretion, so gastric increases in order to stimulate the acid-producing cells (parietal)
54
What causes the reduced serum pepsinogen I concentration?
The chief cell destruction, which also get affected because they are next to the parietal cells
55
What does the atrophy of mucosa with intestinal metaplasia lead to?
Increased risk of gastric adenocarcinoma
56
What are the complications of chronic gastritis?
Peptic ulcer disease
Mucosal atrophy & intestinal metaplasia --> dysplasia & adenocarcinoma
Lymphoma (MALT)
57
Which sections of the stomach/ small intestine are involved in peptic ulcer disease?
Proximal duodenum (90% of the cases)
Distal stomach (10%))
58
What cause PUD ?
Decreased mucosal protection against gastric acid or Increased gastric acid secretion
59
What are some risk factors of PUD?
H. pylori
Smoking, Alcohol, Drugs
COPD
NSAIDs
Stress
Endocrine cell hyperplasia
Zollinger-Ellison Syndrome
Viral infection
60
How is COPD a risk factor of PUD?
Due to chronic hypoxia there is an increase of gastric acid secretion
61
Why is Zollinger-Ellison syndrome a risk factor of PUD?
It causes the secretion of gastrin
62
What is the main cause of duodenal ulcer?
H. pylori for > 95% of the cases
Rarely to ZE syndrome
63
What is the main characteristic symptom of duodenal ulcer?
Presents with epigastric pain that decreases with meals
64
Why does the epigastric pain decrease with meals in duodenal ulcers?
The food stimulates acid, and thus more bicarbonate which helps neutralise the pH and cause relief of symptoms
65
What are the symptoms of more severe cases of duodenal ulcers?
May be complicated by rupture bleeding, acute pancreatitis or pyloric channel and duodenal obstruction.
66
Where are duodenal ulcers found?
Usually on the anterior wall, few cm from pyloric valve
67
How does H. pylori cause duodenal ulcers?
Due to the destruction of somatostatin producing cells in the antrum
Increase gastrin effect leading to an increase in acid secretion
Releases cytotoxins that inhibit duodenal bicarbonate production
68
What are the main causes of gastric ulcers?
H. pylori
NSAIDs and bile reflux
69
What is the main characteristic symptom of gastric ulcer?
Present with gastric pain that gets greater with meals
70
Why does pain get greater with meals in gastric ulcers?
Food stimulates gastric secretion so if the ulcer is in the stomach, more acid will mean more pain
71
Where are gastric ulcers usually located?
Lesser curvature of antrum
72
What may be the more severe symptoms of gastric ulcers?
Rupture with bleeding or increased risk of cancer
(perforation & bleeding)
73
How does H. pylori relate to gastric ulcers?
H. pylori in the body --> gastric ulcer
74
What causes the gastric ulcer in the body of the stomach?
Multifocal atrophic gastritis due to parietal cell destruction
75
What are gastrin and HCl levels like in gastric ulcers caused by H. pylorus?
HCl: normal or low
Gatsrin: normal
76
What causes the formation of the gastric ulcer (H. pylori)?
Bacterial products (ammonia & cytotoxic( and inflammatory response
77
What are the gross features of peptic ulcers?
Usually oval, sharply punched out defect
Less than -.3cm in diameter tend to be shallow
78
What are the 4 distinct zones of peptic ulcers' morphology?
Necrotic debris
Inflammation
Granulation Tissue
Fibrosis
79
What are the main complications of PUD?
Bleeding
Perforation
Obstruction
80
How does a pneumoperitoneum occur?
Anterior duodenal ulcers can perforate into the anterior abdominal cavity --> pneumoperitoneum (free air under the diaphragm)
81
What is a common symptom of pneumoperitoneum?
Pain referred to the shoulder via irritation of phrenic nerve
82
What are the different types of benign gastric tumors?
Inflammatory hyperplastic polyps, fundic gland polyps, adenomatous polyps
83
What are the different kind of primary malignant gastric tumors?
Adenocarcinoma
Carcinoid
Gastrointestinal stromal tunour
Lymphoma
84
What about secondary malignant gastric tumours?
They are very uncommon
85
Where are the different types of benign gastric tumors located?
Inflammatory and hyperplastic polyps: Antrum
Fundic Gland Polyps: body and fundus
Gastric adenomas: Antrum
86
What is the predominant cell type of each benign gastric tumor?
Inflammatory and hyperplastic polyps: Mucous
Fundic Gland Polyps: parietal and chief
Gastric adenomas: Dysplastic, intestinal
87
What are the inflammatory infiltrates for each kind of benign gastric tumor?
Inflammatory and hyperplastic polyps: neutrophils and lymphocytes
Fundic Gland Polyps: none
Gastric adenomas: variable
88
What are the symptoms of each kind of benign tumor?
Inflammatory and hyperplastic polyps: similar to chronic gastritis
Fundic Gland Polyps: none or nausea
Gastric adenomas: similar to chronic gastritis
89
What are the risk factors for each of the kinds of benign gastric tumor?
Inflammatory and hyperplastic polyps: chronic gastritis, h. pylori
Fundic Gland Polyps: PPIs, FAP
Gastric adenomas: chronic gastritis, atrophy, intestinal metaplasia
90
What is each benign gastric tumours association with adenocarcinoma?
Inflammatory and hyperplastic polyps: Occasional
Fundic Gland Polyps: syndromic (FAP) only
Gastric adenomas: Frequent
91
What are the risk factors of gastric cancers?
Environmental factors: h. pylori infection, EBV, smoking and alcohol, diet (high-salt), obesity and previous gastric bypass
Host related factors: familial predisposition, hereditary gastric cancer, association with other inherited cancers
Other: pernicious anemia
92
What is the function of CDH1 gene?
Codes for e-cadherin which sticks epithelium together
93
What is the most common type of gastric malignancy?
Gastric adenocarcinoma
94
What are the subdivisions of gastric adenocarcinoma?
Intestinal and diffuse
95
What are the patient presentations in gastric adenocarcinoma?
Patients present late with weight loss, abdominal pain, anemia and early satiety & metastasis
96
What are other presentations of gastric adenocarcinoma?
Acanthuses nigricans
Leser-Trelat sign (Seborrheic kreatosis)
97
Which subtype of gastric adenocarcinoma is more common?
Intestinal Type
98
What is the step-up progression of intestinal adenocarcinoma?
Chronic gastritis --> intestinal metaplasia --> dysplasia --> carcinoma insitu --> invasive carcinoma
99
What is intestinal adenocarcinoma seen like in endoscopy?
Large ulcer which is involved in the lesser curvature of antrum
100
What is a limitation to endoscopy when it comes to gastric ulcer vs gastric adenocarcinoma?
We cannot differentiate between them, biopsy is further required
101
What does a benign ulcer look like under a microscope?
Small < 3cm, sharply demarcated surrounded by radiating fold of mucosa
102
What does a malignant ulcer look like under a microscope?
Large, irregular with heaped up margins
103
What is the microscopy of gastric intestinal adenocarcinoma?
Intestinal morphology, composed of columnar gland forming cells infiltrating through desmoplastic stroma.
104
Which kind of adenocarcinoma is not associated with H. pylori?
Diffuse type gastric adenocarcinoma
105
What is diffuse type adenocarcinoma shown as through endoscopy?
Thickening in the stomach wall (linitis plastica)
Stiffening of gastric wall, diffuse regal flattening
Leather bottle appearance
106
What is diffuse type adenocarcinoma shown as through microscopy?
Diffuse infiltration of signet ring cells with desmoplastic reaction
107
What is the prognosis/outcome of diffuse adenocarcinoma like?
Worse outcome than intestinal type
108
What kind of gene mutation can diffuse type adenocarcinoma be associated with?
CDH1 gene mutation
109
How are signet ring cells recognised?
Large cytoplasmic mucin vacuoles, crescente shaped nuclei. They do NOT from glands
110
What is the spread and metastasis of adenocarcinoma like?
May involve the supraclavicular lymph node (Virchow) or axillary node (Irish)
111
Which are the common sites of metastasis of adenocarcinoma?
Liver
Periumbilical region (Mary Joseph nodule); intestinal type
Ovaries (krukenberg); diffuse type
Blumer's shelf
112
What % of malignancies does primary gastric lymphoma form?
5%
113
What is the treatment of primary gastric lymphoma?
Antibiotics, that is different because of the fact that lymphomas are usually treated with chemotherapy
114
What is MALT lymphoma a result of?
Chronic gastritis
115
What is the connection between H. pylori and MALToma?
H. pylori most common inducer in the stomach, found in association with most cases go gastric MALToma
116
What is primary gastric lymphoma shown as grossly?
Mass +/- ulcer, thickened gastric wall, polypoid lesions
117
What is primary gastric lymphoma shown as trough microscopy?
Monomorphous infiltrate of B-cell type lymphoid cells (CD19&20)
118
What is the recurrence rate of MALToma?
Low
119
What is the most common mesenchymal tumor of the abdomen?
Gastric Gatrointestinal Stromal Tumor (GIST)
120
Where does GIST arise from?
Interstitial cells of Cajal, pacemaker cells, of muscularis propria
121
What is the mutation of GISTS?
75 to 80% of them have oncogenic, function-gaining mutation in the receptor tyrosine kinase KIT
8% have mutations in platelet-derived growth factor receptor a
122
What is the treatment of GIST?
Most cases they are given TKI (imatinib)
123
What is the gross morphology of GIST?
Flashy mass covered by intact mucosa & projecting inside the stomach
124
What is the microscopy of GIST?
Composed of bundles, or fascicles of spindle-shaped tumor cells
125
Where do gastric carcinoid tumors arise from?
Diffuse components of the endocrine system and are referred to as well-differentiated neuroendocrine tumors
126
What are the association of gastric carcinoid tumors?
Endocrine cell hyperplasia
Autoimmune chronic atrophic gastritis
MEN-I
ZE syndrome
127
What is the gastric endocrine cell hyperplasia associated with?
PPI therapy
128
What is the gross morphology of carcinoid tumours?
Submucosal tumor nodule
129
What is the microscopy of carcinoid tumors?
Nest of tumor cells embedded in dense fibrous tissue, with bland cytology. The chromatin texture, fine and coarse "salt and paper" pattern
130
How does burn cause ulcers?
Hypovolemia --> mucosal ischemia
