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Pathology 1 > GI 2 > Flashcards

GI 2 Flashcards

1
Q

Congenital Pyloric stenosis EPIDIOMIOLOGY + CAUSES

A

M > F
-Genetic predisposition for children from affected parents
-Acquired pyloric obstruction, as a result of
chronic duodenal ulcer with scarring

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2
Q

Congenital Pyloric Stenosis PATHOPHYSIOLOGY + CLINICAL FINDINGS

A

Progressive hypertrophy of the circular muscular layer in the pyloric sphincter

Clinical findings:
 Projectile vomiting; not bile stained fluid  Palpable mass (“OLIVE”); epigastrium (70% cases)
 Obvious hyperperistalsis

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3
Q

GASTROPARESIS definitions

A

Decreased stomach motility, due to:
 Autonomic neuropathy (e.g. Diabetes Mellitus)
 Previous vagotomy

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4
Q

GASTROPARESIS clinical findings + treatments

A

Clinical findings:
 Early satiety and bloating
 Vomiting of undigested food

Treatment:
 Frequent, small meals
 Metoclopramide

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5
Q

Acute Gastritis CLINICAL FEATURES

A

Asymptomatic disease, or
Variable degrees of epigastric pain, nausea
and vomiting, or
More severe cases: Mucosal erosion,
ulceration, haemorrhage, haematemesis,
melena, or massive blood loss (rarely)

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6
Q

Microscopic findings:
Mild Acute Gastritis:
Moderate oedema and slight vascular
congestion in the lamina propria Intact surface epithelium Scattered neutrophils, intraepithelial

More severe mucosal damage:
Erosion or loss of superficial epithelium
Formation of mucosal neutrophilic infiltrates
and purulent exudates Occurrence of haemorrhages
Acute Erosive Haemorrhagic Gastritis: Con-
current presence of erosion and haemorrhage

A

Acute Gastritis:
 Microscopic findings:

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7
Q

Acute Erosive Haemorrhagic Gastritis:
Causes + Clinical findings

A

Causes: NSAID, alcohol, H. Pylori, smoking,
severe burn (Curling ulcer), CNS injury
(Cushing ulcer)

Clinical findings:
Haematemesis Melena Iron deficiency

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8
Q

Type A Chronic Atrophic Gastritis =
Autoimmune Gastritis:
Definition +localisation +complications

A

‘Abs to parietal cells (produce HCl and
intrinsic factor) and intrinsic factor (necessary for the absorption of Vit. B12 [Cobalamin])
Development of Pernicious anaemia
Localisation: Body and fundus

Association/Complications:
 Achlorhydria with Hypergastrinaemia
 Vit. B12 deficiency => Macrocytic anaemia
 ↑ Risk for gastric Adeno-Ca

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9
Q

Type B Chronic Atrophic Gastritis =
H. Pylori (causes) associated Gastritis:

CLINICAL FINDINGS + COMPLICATIONS/ ASSOCIATIONS + localisation

A

-Localisation: Antrum and pylorus
Clinical findings: Increased gastric acid
secretion
Complications/Associations: Gastric and
duodenal peptic ulcers, gastric Adeno-
Carcinoma and Lymphoma (MALT-type)

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10
Q

Type B Chronic Atrophic Gastritis =
H. Pylori associated Gastritis:

Pathophysiology:

A

Production of urease, protease
 Conversion of amino groups in proteins to
ammonia, by Urease
 Development of Chronic Gastritis and peptic
ulcer by the action of secretion products
Colonisation of mucous layer lining without
invasion of the wall
 Attachment to blood group O receptors on
mucosal cells

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11
Q

Microscopic findings:
Chronic inflammatory infiltrate in the
lamina propria
Intestinal metaplasia (similar to Barrett
Oesophagus) => Progression to Adeno-Ca

A

Type B Chronic Atrophic Gastritis =
H. Pylori associated Gastritis:

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12
Q

ACUTE PEPTIC ULCER
Cause

A

Complication of therapy with NSAIDs or
due to severe physiologic stress

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13
Q

ACUTE PEPTIC ULCER
Types of Ulcer (associated with stress factors):

A

. Stress Ulcers: Critically ill patients with shock,
sepsis or severe trauma
. Curling Ulcers: Proximal duodenum; Severe
burns or trauma
.Cushing Ulcers: Stomach, duodenum, or
oesophagus; Individuals with intracranial
disease; Increased rate of perforation

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14
Q

Pathogenesis
. NSAID-induced ulcers:
Direct chemical irritation + Cyclooxygenase
inhi-bition =>Prevention of Prostaglandin
synthesis => Elimination of Prostaglandin‟s
protective effect
Prostaglandin’s protective effect: Enhanced
bicarbonate secretion and ↑ vascular perfusion

Ulcers associated with brain injury:
Direct stimulation of vagal nuclei =>Gastric
acid hypersecretion

Ulcers associated with critically ill patients:
Systemic acidosis =>Decrease in intracellular
pH of mucosal cells =>Mucosal injury

A

ACUTE PEPTIC ULCER
Pathogenesis:

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15
Q

Macroscopic features:
 Acute Ulcers:
Round; Size: <1cm Ulcer base: Brown to black
 Acute Stress Ulcers:
Sharply demarcated Normal adjacent mucosa

 Microscopic findings:
Layers of Ulcer:
-Necrotic debris
-Mainly, neutrophilic infiltration

A

’, ACUTE PEPTIC ULCER

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16
Q

ACUTE PEPTIC ULCER
Clinical features + complications + treatment

A

Clinical features:
 Nausea
 omiting
 Haematemesis

Complications:Perforation

Treatment:
 Proton pump inhibitors
 Histamine H2 receptor antagonists

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17
Q

Peptic. Ulcer. Disease
CAUSES + epidemiology

A

‘ Causes: H. pylori infection (most common);
NSAID use
Epidemiology: Lifetime risk for development of an ulcer: 10% for Males and 4% for Females

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18
Q

Peptic ulcer disease location

A

-Gastric antrum and first portion of duodenum

-Oesophagus: Result of GOERD, ectopic gastric
mucosa
-Small intestine: Gastric heterotopia within a
Meckel diverticulum

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19
Q

Peptic ulcer disease Pathogenesis

A

 Imbalance btw mucosal defenses and
offensive agents  Chronic Gastritis  Peptic ulcer disease
 H. pylori infection. (Gastric hyperacidity)
 Parietal cell hyperplasia (GH)
 Excessive secretory responses. (GH)
 Impaired inhibition of stimulatory (GH)
mechanisms (e.g. Gastrin release)
 Chronic renal failure and hyperparathyroidism =>↑ Gastrin production (GH)
 Uncontrolled release of Gastrin (Zollinger-Ellison syndrome) => Multiple peptic ulcers

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20
Q

Macroscopic features:
 Lesions: <0.3 cm  Shallow; 0.6 cm  Deep
 Round to oval
 Sharply punched out defect
 Base: Smooth and clean

Microscopic findings:
 Base: Rich vascular granulation tissue
infiltrated with mononuclear leukocytes and a fibrous or collagenous scar
 Possible involvement of the entire thickness
of the wall by scarring

A

PEPTIC ULCER DISEASE

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21
Q

PEPTIC ULCER DISEASE Clinical features

A

Clinical features:
 Epigastric burning or aching pain
 Bloating and belching
 Iron deficiency anaemia
 Frank haemorrhage
 Perforation
 Occurrence of pain: 1-3 hours after meals
(during the day) and worse at night  Relief of pain: Intake of alkali or food

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22
Q

PEPTIC ULCER DISEASE

Treatment

A

-Antibiotics (H. pylori)
-Proton pump inhibitors => Neutralisation of
gastric acid

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23
Q

MENETRIER DISEASE
-Hypertrophic or Hyperplastic
Gastropathy, Giant Hypertrophic Gastritis, and
Giant Hypertrophy of Gastric rugae

CRITERIA for DIAGNOSIS

A

Giant mucosal folds, involving the corpus and possibly antrum
Low acid production, even after stimulation
Mucosal protein loss
Histologic findings of corpus foveolar hyperplasia and glandular atrophy

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24
Q

Macroscopic features:
 Markedly hypertrophic rugae, resembling
cerebral convolutions
 Abrupt transition between normal and diseased
mucosa
 Typical form of the disease: Diffuse involvement
of the fundic portion, with sparing of the antrum
 Localised form of the disease: Well-circum-
scribed cerebroid mass either in the fundus or
the antrum

A

‘MENETRIER DISEASE

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25
Q

: Microscopic findings:
 On the surface of the folds: Gastric foveolae
enormously elongated, sometimes with a corkscrew (tortuous) appearance (foveolar hyperplasia)
 Often, cystic dilation with mucous accumulation
 Extension of cysts into the deeper mucosal
layers and even occasionally the submucosa
 Reduction of the glandular component (corpus
gland atrophy)
 Frequently, presence of non-specific
inflammation in the superficial mucosa

A

MENETRIER DISEASE
.

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26
Q

MENETRIER DISEASE
Clinical features:

A

Hypochlorhydria or achlorhydria and often
impressive hypoproteinaemia

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27
Q

MENETRIER DISEASE
Management

A

 Adults: Fully developed disease is progressive
and requires subtotal gastrectomy
 Paediatric cases of so-called Ménétrier Disease
are of the type that spontaneously resolve
(self-limited disease)

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28
Q

Gastric polyps is what ?

A

Neoplasm of stomach

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29
Q

Gastric polyps.

Pathogenesis: Develop as a result of:

A

-Epithelial or stromal cell hyperplasia
 Inflammation
 Ectopia
 Neoplasia

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30
Q

Gastric polyps definition

A

 Definition: Nodules or masses that project
above the level of the surrounding mucosa

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31
Q

Gastric polyps TYPES

A

Types of polyps:
 Hyperplastic polyps  Inflammatory polyps  Fundic gland polyps  Adenomas

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32
Q

-INFLAMMATORY & HYPERPLASTIC POLYPS
Pathogenesis

A

Chronic gastritis➡️ Injury and reactive hyperplasia
➡️Development of polyp

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33
Q

Macroscopy:
 Ovoid lesions; Size: <1cm; Smooth surface  Microscopy:
 Irregular, cystically dilated and elongated foveolar
glands  Oedematous lamina propria  Acute and chronic inflammation  Surface erosions (may be present)

A

INFLAMMATORY & HYPERPLASTIC POLYPS

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34
Q

FUNDIC GLAND POLYPS

Epidemiology

A

Epidemiology

 Sporadic occurrence
 Persons with Familial Adenomatous Polyposis

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35
Q

FUNDIC GLAND POLYPS
. Cause/Pathogenesis:

A

Cause/Pathogenesis:
 Proton pump inhibitors  Reduced acidity 
Increased Gastrin secretion  Glandular hyperplasia

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36
Q

FUNDIC GLAND POLYPS
Clinical features:

A

‘Clinical features:
 Nausea; Vomiting; Epigastric pain

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37
Q

Macroscopy: Well-circumscribed polyps in the
gastric body and fundus

Microscopy:
 Cystically dilated, irregular glands  Lining of the glands: Flattened parietal and
chief cells
.

A

FUNDIC GLAND POLYPS

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38
Q

-Epidemiology:
 10% of all gastric polyps
 Mostly, sessile and growth in tubulo-villous or
pure villous pattern; pure pedunculated tubular lesions are rare
 Ages: 50-60 yrs.; M:F = 3:1

A

‘GASTRIC ADENOMA

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39
Q

GASTRIC ADENOMA

Cause/Pathogenesis:

A

Cause/Pathogenesis:
 Chronic gastritis➡️ Atrophy and intestinal
metaplasia

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40
Q

GASTRIC ADENOMA

Risk for malignant transformation:

A

Risk for malignant transformation:
 Dependent on lesion‟s size (risk elevated with
lesions >2cm)
 Presence of Adeno-CAs in up to 30% of gastric
adenomas

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41
Q

Microscopic features:
 Histologically, two types:
Adenomas with intestinal differentiation
(Goblet cells and/or Paneth cells) Adenomas with gastric differentiation
(Columnar cells containing neutral mucin)
 Epithelial dysplasia, classified as:
Low-grade: Enlargement, elongation and hyper-
chromasia of nuclei, epithelial crowding, pseudo- stratification
High-grade: More severe cytologic atypia and
irregular architecture (glandular budding, gland-within-gland, cribriform pattern)

A

Gastric adenoma

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42
Q

GASTRIC ADENOMA
Localisation:

A

Localisation: Antrum of the stomach

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43
Q

ZOLLINGER ELLISON SYNDROME
Cause

A

Caused by gastrin-secreting tumours, Gastrinomas

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44
Q

ZOLLINGER ELLISON SYNDROME
Localisation:

A

> 80% of Gastrinomas arise within
the triangle defined as the confluence of the cystic
and common bile duct superiorly, the second and
third portions of the duodenum inferiorly, and the
neck and body of the pancreas medially

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45
Q

ZOLLINGER ELLISON SYNDROME
Epidemiology and Genetics:

A

Epidemiology and Genetics:
 75% of patients = Sporadic, solitary tumours;
Surgical resection
 25% of pts. = Association with Multiple
Endocrine Neoplasia type I (MEN type I);
Multiple tumours or metastatic disease;
Somatostatin analogues

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46
Q

ZOLLINGER ELLISON SYNDROME
 Clinical manifestations

A

-Duodenal ulcers or
chronic diarrhoea

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47
Q

ZOLLINGER ELLISON SYNDROME

. Pathological findings within Stomach:

A

‘Pathological findings within Stomach:
 5x increase in number of parietal cells => Doubling of oxyntic mucosal thickness
 Hyperplasia of mucous neck cells, mucin hyperproduction
 Proliferation of endocrine cells => Small dysplastic nodules (sometimes), true
Carcinoid Tumours (rarely)

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48
Q

ZOLLINGER ELLISON SYNDROME
Diagnostic procedures:

A

.. Diagnostic procedures:
 Somatostatin Receptor Scintigraphy
 Endoscopic Ultrasonography

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49
Q

ZOLLINGER ELLISON SYNDROME

Treatment:

A

Treatment: Blockade of acid hypersecretion:
 Proton pump inhibitors or
 High-dose H2 histamine receptor antagonists

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50
Q

ZOLLINGER ELLISON SYNDROME
Progression:

A

Progression:
 In general, slow growing tumours
 60-90% of Gastrinomas are malignant

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51
Q

CARCINOMA OF THE STOMACH
Epidemiology:

A

Epidemiology:
 Most common after 50 yrs.
 Men > Women
 Most frequent occurrence in blood group A persons

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52
Q

CARCINOMA OF THE STOMACH

Aetiologic factors

A

Aetiologic factors: ‘.
-H. pylori
- Nitrosamines from dietary amines and nitrites used in food preservatives. Smoked fish (Japan)
-Excessive salt intake and diet low in fresh fruits and vegetables
-Achlorhydria and Chronic Gastritis +/- Pernicious Anaemia
-Menetrier disease (Giant Hypertrophic Gastritis)  Familial cases associated with mutations to E-Cadherin gene (CDH1):
. -Diffuse infiltrating signet-ring cell CAs
-Patients with these mutations =>. Development of lobular CA of the breast

-Patients with Lynch syndrome (Hereditary Non-Polyposis Colorectal Cancer) => Increased risk for
gastric CA

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53
Q

-CARCINOMA OF THE STOMACH
 Pathogenesis:
Mutations:

A

. Mutations:
Germline mutations in CDHI (encodes E-Cad-
herin); Protein contributing to epithelial inter-
cellular adhesion; Loss of E-Cadherin function
=>Development of diffuse type gastric cancer
Germline mutations in Adenomatous Polyposis
Coli (APC) genes (patients with FAP) =>
Increased risk of intestinal type gastric cancer
Acquired mutations of β-Catenin = Sporadic
intestinal type gastric cancer
TP53 mutations = Majority of sporadic gastric
cancers of both histologic types

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54
Q

CARCINOMA OF THE STOMACH
 Pathogenesis (cont.):

H. pylori:

A

Pathogenesis (cont.):
 H. pylori:

H. pylori induced Chronic Gastritis =>
Increased production of pro-inflammatory
proteins (IL-1β and TNF)
Polymorphisms related to enhanced production
of these cytokines => Intestinal-type gastric CA

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55
Q

CARCINOMA OF THE STOMACH
 Pathogenesis (cont.):
EBV:

A

EBV:
EBV-positive tumours characterised by:

1.Localisation: Proximal stomach
2.Diffuse morphology
3,Marked lymphocytic infiltrate

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56
Q

Characteristics:
 Localisation: Minor curvature of the antrum
or pre-pyloric region => Spread to the adjacent organs, peritoneum, regional lymph nodes and liver

 Distal sites:
Virchow node: Supra-clavicular lymph
nodes with metastasis of gastric CA
Krukenberg tumours: Bilateral involvement
of the ovaries by tumour metastasis;
Tumour consisted of signet ring-cells

A

CARCINOMA OF THE STOMACH
 Characteristics:

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57
Q

Macro-/Microscopic features:
A. Intestinal type:
Association with H. pylori
Polypoid carcinoma; solid mass projecting
into the lumen
Possible, ulceration
DD: Peptic Ulcer (smooth base, non-elevated
punched out margins) vs. CA (Ulcer with
irregular necrotic base and firm raised
margins)

A

:. CARCINOMA OF THE STOMACH

A. Intestinal type:

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58
Q

. Macro-/Microscopic features (cont.):

Synonym: Linitis plastica, leather-bottle
stomach
NO association with H. pylori
Macroscopy: Thickened, rigid stomach wall Microscopy: Diffuse signet-ring cells
infiltrates with accompanying extensive
fibrosis

A

CARCINOMA OF THE STOMACH
Infiltrating or Diffuse CA:

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59
Q

LYMPHOMA OF THE STOMACH

Cytogenetic abnormalities:

A

Cytogenetic abnormalities: (11;18) trans-location;
Involvement of MALT1 and IAP2 genes; High predictive value, since its presence associated with unresponsiveness to: i. Antibiotic treatment and ii. Therapy with oral alkylating agents

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60
Q

Microscopic features:
 Dense infiltrate of small lymphoid cells, often
accompanied by scattered reactive lymphoid follicles  Lymphoid cells: Variable admixture of small lympho-
cytes, centrocyte-like cells, and monocytoid cells  Common finding, focal or extensive plasmacytoid
differentiation  Possible presence of „Dutcher bodies‟ (true intra-
nuclear eosinophilic inclusions made up of immu-
noglobulin)  Great diagnostic significance  Important diagnostic sign: Infiltration of the
glandular epithelium by neoplastic lymphocytes,
resulting in so-called „lympho-epithelial lesions‟

A

EXTRANODAL MARGINAL ZONE LYMPHOMA (MALT)
Microscopic features:

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61
Q

LARGE B-CELL LYMPHOMA

A

-High-grade, aggressive lymphoma
-Usually, in individuals over the age of 50 years

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62
Q

LARGE B-CELL LYMPHOMA
Clinical manifestation:

A

Clinical manifestation:
Large palpable mass (and still excellent physical
condition of the patients)

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63
Q

Macroscopic findings:
with a tendency to spare the pylorus
 Large lobulated (sometimes polypoid) mass
 Commonly, superficial or deep ulceration

A

LARGE B-CELL LYMPHOMA

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64
Q

LARGE B-CELL LYMPHOMA
Preferred (predilection) localisation

A

Site of predilection: Distal half of the stomach,
with a tendency to spare the pylorus

65
Q

Microscopic features:
 Most cases composed of cells resembling
large non-cleaved cells (centroblasts) but with a slightly more abundant cytoplasm, sometimes resulting in a plasmablastic or immunoblastic appearance
 Multinucleated cell forms resembling Reed-
Sternberg cells may be present  The phenotypic features are those of B cells

A

LARGE B-CELL LYMPHOMA

66
Q

Differential diagnosis w/ Undifferentiated CARCINOMA
. Microscopic features favouring Lymphoma:
Lack of continuity between epithelium and
tumour cells
 Lack of suggestion of an acinar pattern
 Preservation of muscularis mucosae fibers

 Immuno-cytochemical evaluation of lymphoid
and epithelial markers in difficult cases

A

LARGE B-CELL LYMPHOMA

67
Q

LARGE B-CELL LYMPHOMA
Prognosis and Progression

A

Prognosis and Progression
 Prognosis for gastric Large B-Cell Lymphoma,
substantially better than for gastric Carcinoma
 The overall 5-year disease-free survival rate:
Approximately 60%

Favourable prognostic features:
Small tumour size Superficial mural invasion Absence of regional lymph node involvement
.

68
Q

CARCINOID TUMOURS
Definition

A

Originate from endocrine organs (e.g. endocrine pan-
creas) and neuroendocrine-differentiated GI epithelia
(e.g. G-cells) as well as tracheo-bronhial tree and lungs

69
Q

CARCINOID TUMOURS
. Gastric Carcinoids are associated with:


A

Gastric Carcinoids are associated with:

 Endocrine cell hyperplasia
 Chronic atrophic gastritis
 Zollinger-Ellison syndrome

70
Q

CARCINOID TUMOURS
. Grading based mainly on:

A

Grading based mainly on:
 Mitotic index
 Ki-67 immuno-positive cells (%)

71
Q

Macroscopic features:
 Intramural or submucosal masses => Small
polypoid lesions
 Yellow or tan in appearance
 Intense Desmoplasia => Kinking of the bowel
and obstruction

Microscopic findings:
 Arrangement of the cells in: i. Islands, ii.
Glands, iii. Trabeculae, iv. Strands, or v. Sheets
 Cells:
Scant, pink granular cytoplasm
Round to oval stippled nucleus

A

CARCINOID TUMOURS

72
Q

CARCINOID TUMOURS

Immunohistochemistry

A

Immunohistochemistry: Neuron-Specific Enolase
(NSE), Chromogranin, Synaptophysin

73
Q

CARCINOID TUMOURS

Clinical features:

A

Clinical features:
 Symptoms depend on hormones produced by the Tm
Carcinoid Syndrome:
Cause: Secretion of vasoactive substances (e.g.
kinins, VIP, angiotensin II, (nor)epinephrine, etc.)

Clinical picture:
Cutaneous flushing Sweating Bronchospasm Colicky abdominal pain Diarrhoea

74
Q

CARCINOID TUMOURS
Prognosis:

A

Prognosis: Depends primarily on tumour‟s location:
Foregut Carcinoid Tumours:
Oesophagus, Stomach, Duodenum
Rarely, metastases
Gastric carcinoids develop as a result of prolonged Gastrin hypersecretion in Zollinger
Ellison syndrome

Midgut Carcinoid Tumours:
Jejunum, Ileum
Multiple and aggressive
Poor outcome: i. Depth of local invasion,
ii. Increased size, iii. Necrosis, and iv. Mitosis

Hindgut Carcinoids:
Appendix vermiformis (benign), Colorectum Incidentalomas
Rectal Carcinoids:
Abdominal pain and weight loss
Occasionally, metastases

75
Q

GASTRO-INTESTINAL STROMAL TUMOUR (GIST)

A

Mesenchymal tumours, derived from pacemaker
(myenteric interstitial) cells of Cajal

Most common mesenchymal tumour of the abdomen

76
Q

GASTRO-INTESTINAL STROMAL TUMOUR (GIST)

Localisation

A

Localisation: Submucosa of stomach, small and
large intestine and extra-gastrointestinal sites

77
Q

GASTRO-INTESTINAL STROMAL TUMOUR (GIST)

Pathogenesis

A

Pathogenesis:
 75-80% of GISTs: Oncogenic, gain-of-function
mutations of the gene encoding the tyrosine kinase
c-KIT
 8% of GISTs: Activating mutations of PDGFRA

78
Q

Macroscopic features:
 Primary lesions: Solitary, well circumscribed,
fleshy submucosal masses
 Metastases: Multiple small serosal nodules or
fewer nodules in the liver

Microscopic features:
 Thin, elongated spindle cells or
 Plumper epithelioid cells
 c-KIT (CD117) immuno-positivity in 95% of
GISTs

A

GASTRO-INTESTINAL STROMAL TUMOUR (GIST)

79
Q

GASTRO-INTESTINAL STROMAL TUMOUR (GIST)
Clinical features:

A

Clinical features:

   Symptoms are related to: Mass effect Mucosal ulceration
80
Q

GASTRO-INTESTINAL STROMAL TUMOUR (GIST)

Prognosis

A

Prognosis, correlates with:
 Tumour size
 Mitotic Index (MI)
 Location
 Gastric GISTs less aggressive than small-
intestine GISTs
 Gastric GISTs:
Recurrence or metastasis: <5cm tumours 
Rare; >10cm and high MI <=> Common

81
Q

HERNIATION
Definition

A

Definition: Any weakness or defect in the wall
of the peritoneal cavity may permit protrusion
of a serosa-lined pouch of peritoneum called
hernia sac

82
Q

HERNIATION.

Localisation

A

Lo’calisation: Occurrence of acquired hernias
most commonly anteriorly (inguinal and
femoral canals or umbilicus, or at sites of
surgical scars)

83
Q

HERNIATION

Complications:

A

Complications:
 Visceral protrusion (external herniation)

 Inguinal hernias (mostly with narrow orifices and large sacs): Entrapment of small bowel loops or portions of omentum => Pressure at the neck of the pouch => Impairment of venous drainage of the entrapped viscous => Stasis and oedema=> Increase in the bulk of the herniated loop => Permanent entrapment or incarceration => Over time, arterial and venous compromise (strangulation) => Infarction

84
Q

ADHESIONS
Causes

A

. Causes:
 Congenital
 Acquired: Surgical procedures, infection or
other causes of peritoneal inflammation, such
as endometriosis
‘

85
Q

ADHESIONS

Complications

A

Complications: Development of closed loops
through which other viscera may slide =>
Entrapment => Internal herniation =>
Obstruction and strangulation

86
Q

‘VOLVULUS
Definition + clinical presentation

A

Complete twisting of a loop of bowel about its
mesenteric base of attachment, which produces
both luminal and vascular compromise
 Clinical presentation: Features of obstruction
and infarction

87
Q

VOLVULUS

Localisation

A

-Localisation: Large redundant loops of sigmoid
colon (most often), caecum, small bowel, stomach,
or transverse colon (rarely)

88
Q

INTUSSUSCEPTION

A

Condition by which a segment of the intestine,
constricted by a wave of peristalsis, telescopes
into the immediately distal segment

89
Q

INTUSSUSCEPTION
,. Progression:

A

‘Progression: Once trapped, the invaginated
segment is propelled by peristalsis and pulls the
mesentery along

90
Q

INTUSSUSCEPTION
Causes

A

Causes:
 Infants and children: In some cases,
association with Rotavirus infection
 Older children and adults: Intraluminal mass
or tumour (serves as the point of traction)

91
Q

INTUSSUSCEPTION
Complications:

A

Complications: Untreated intussusception may
progress to intestinal obstruction, compression of
mesenteric vessels and infarction

92
Q

INTUSSUSCEPTION
, Management

A

Management:
 Infants and young children: Barium enema
(effectively reduces the intussusception)
 Older patients: Surgical interventio

93
Q

ISCHAEMIC BOWEL DISEASE
Classification of ischaemic damage to bowel:

A

Classification of ischaemic damage to bowel:
 Mucosal infarction: Up to muscularis mucosae
 Mural infarction of mucosa and submucosa
 Trans-mural infarction: All three layers of the
wall

94
Q

ISCHAEMIC BOWEL DISEASE
. Causes

A

Causes:
 Acute or chronic hypo-perfusion => Mucosal or
mural infarctions
 Acute vascular obstruction => Trans-mural
infarction

95
Q

ISCHAEMIC BOWEL DISEASE
Causes of acute arterial obstruction:

A

Causes of acute arterial obstruction:
 Severe atherosclerosis
 Aortic aneurysm
 Hypercoagulable states
 Oral contraceptives
 Embolisation of cardiac vegetations or aortic
atheromas

96
Q

ISCHAEMIC BOWEL DISEASE

Causes of intestinal hypoperfusion:

A

Causes of intestinal hypoperfusion:
 Cardiac failure  Shock  Vasculitides (PAN, Henoch-Schönlein purpura,
Wegener granulomatosis, etc.)

97
Q

ISCHAEMIC BOWEL DISEASE
Pathogenesis:

A

Pathogenesis:

Phases of intestinal responses to ischaemia:
First phase: Occurrence of initial hypoxic
injury at the onset of vascular compromise
.
Second phase: Reperfusion injury;Due to
increased permeability of capillaries and
arterioles => Increase of diffusion and fluid
filtration across the tissues, free radical
production, neutrophil infiltration and
release of inflammatory mediators

Severity of ischaemic bowel disease depends on:
-Time frame for its development
-Severity of vascular compromise
-Affected vessels

Intestinal vascular anatomy contributes
to distribution of ischaemic damage:
1. Watershed zones: Intestinal segments
particularly susceptible to ischaemia;
These are: Splenic flexure, Sigmoid
colon and Rectum
2. Morphologic configuration of intestinal
capillaries allows good blood supply
of crypts but leaves epithelial cells
vulnerable to ischaemia

98
Q

Macroscopic features:
 Distribution of lesions: Segmental and
irregular
 Haemorrhagic and ulcerated mucosa
 Oedema induced thickening of the wall
 Severe disease (e.g. Acute arterial
thrombosis => Transmural infarction):
Extensive mucosal and submucosal
haemorrhage and necrosis; Coagulative
necrosis of muscularis propria (1-4 days)
=> Purulent serositis => Perforation

A

ISCHAEMIC BOWEL DISEASE

99
Q

Microscopic findings:
 Atrophy or sloughing of surface epithelium
 Hyper-proliferative crypts
 Recruitment of neutrophils within hours of
reperfusion
 Acute phases of ischaemia: Bacterial super-
infection and enterotoxin release => Pseudo-
membrane formation
 Chronic ischaemia: Fibrous scarring of the
lamina propria, and less common stricture

A

ISCHAEMIC BOWEL DISEASE

100
Q

ISCHAEMIC BOWEL DISEASE

Clinical Features

A

Clinical Features:
 Sudden, severe abdominal pain
 Tenderness
 Nausea and Vomiting
 Bloody diarrhoea or melaena (“tarry” feces) =>
Vascular collapse and shock (due to blood loss)
 Decline or disappearance of peristaltic sounds
 Muscular spasm =>Board-like rigidity of the
abdominal wall

101
Q

ISCHAEMIC BOWEL DISEASE

DD

A

DD: Acute appendicitis, perforated ulcer, acute
cholecystitis

102
Q

ISCHAEMIC BOWEL DISEASE
. Complications

A

Complications: Break down of mucosal barrier
=> Bacteria enter the circulation => Sepsis

103
Q

ANGIODYSPLASIA

A

Characterised by malformed submucosal and
mucosal blood vessels

104
Q

ANGIODYSPLASIA

Localisation

A

Localisation: Caecum or right Colon

105
Q

ANGIODYSPLASIA

Pathogenesis

A

Pathogenesis:
 Normal bowel distention and contraction
=> Occlusion of the submucosal veins (penetrate through the muscularis propria) => Focal dilation and tortuosity of overlying submucosal and mucosal vessels
 Caecum: Largest diameter of any colonic
segment => Greatest wall tension => Development of angiodysplasias (preferable locus)
 Age related degenerative vascular changes
 Angiodysplasia has also been linked to
aortic stenosis and Meckel diverticulum (congenital anomaly?)

106
Q

Microscopic findings:
 Ectatic nests of tortuous veins, venules,
and capillaries  Separation of the vascular channels from
the intestinal lumen, by only the vascular
wall and a layer of attenuated epithelial
cells; As a result of this: Limited injury of
the vessel => Significant haemorrhage

A

ANGIODYSPLASIA

107
Q

Malabsorption

A

Malabsorption: Characterised by defective
absorption of fats, fat- and water-soluble
vitamins, proteins, carbohydrates,
electrolytes and minerals, and water

108
Q

! MALABSORPTION
Pathogenesis:

A

Pathogenesis:
Malabsorption results from disturbance in at
least one of the four phases of nutrient
absorption:
1. Intraluminal digestion, in which proteins,
carbohydrates, and fats are broken down into
forms suitable for absorption
2. Terminal digestion, which involves the
hydrolysis of carbohydrates and peptides by
disaccharidases and peptidases, respectively,
in the brush-border of the small intestinal
mucosa
3. Transepithelial transport, in which
nutrients, fluid and electrolytes are transported across and processed within the small intestinal epithelium
4. Lymphatic transport of absorbed lipids

109
Q

MALABSORPTION
Clinical features:

A

Clinical features:
 Chronic malabsorption: Chronic diarrhoea,
weight loss, anorexia, abdominal distention, borborygmi*, and muscle wasting
 Hallmark of malabsorption <=> Steatorrhoea
(excessive faecal fat and bulky, frothy, greasy, yellow or clay-coloured stools)
* Borborygmus: A rumbling or gurgling noise made by the movement of fluid and gas in the intestines

110
Q

MALABSORPTION SYNDROMES
Similarities among the various Malabsorption
Syndromes

A

General symptoms:
 Diarrhoea  Flatus  Abdominal pain  Weight loss

  • Inadequate absorption of Vitamins and
    Minerals:
    Pyridoxine, folate, or Vitamin B12 deficiency
    => Anaemia and Mucositis
    Vitamin K deficiency => Bleeding
    Calcium, Magnesium, or Vitamin D
    deficiencies => Osteopenia and Tetany
    Vitamin A or B12 deficiencies => Peripheral
    Neuropathy
111
Q

DIARRHOEA
Definition:

A

‘Definition: Increase in stool mass, frequency, or
fluidity, typically greater than 200gr per day

112
Q

DIARRHOEA

Dysentery

A

‘Dysentery: Painful, bloody, small-volume
diarrhoea

113
Q

Classification of diarrhoea

A

’. 1. Secretory diarrhoea:
 Characterised by isotonic (with plasma) stool
 Persists during fasting

  1. Osmotic diarrhoea:
     Typical in lactase deficiency
     Due to the excessive osmotic forces exerted
    by unabsorbed luminal solutes
     >50 mOsm more concentrated than plasma
     Abates with fasting
  2. Malabsorptive diarrhoea:
     Result of generalised failures of nutrient
    absorption
     Associated with steatorrhoea
     Relieved by fasting
  3. Exudative diarrhoea:
     Due to inflammatory disease
     Characterised by purulent, bloody stools
     Continues during fasting
114
Q

COELIAC DISEASE
. Synonyms

A

Synonyms: Coeliac Sprue or Gluten-sensitive
Enteropathy

115
Q

COELIAC DISEASE
. Causes

A

Causes: Immune-mediated enteropathy,
triggered by the ingestion of Gluten-containing
cereals (e.g. wheat, rye, barley) in genetically
predisposed individuals

116
Q

COELIAC DISEASE
Predisposing factors:

A

Predisposing factors:
 Class II HLA-DQ2 or HLA-DQ8 alleles
 Association with: Type I Diabetes Mellitus,
Thyroiditis, Sjögren syndrome, IgA nephro-
pathy, Down syndrome and Turner syndrome

117
Q

COELIAC DISEASE
Pathogenesis:

A

Pathogenesis:
 Digestion of Gluten into amino acids and
peptides (Gliadin peptide; resistant to degradation by gastric, pancreatic and small intestinal proteases)
 Deamidation of Gliadin by tissue trans-
glutaminase
 Interaction of deamidated Gliadin with APCs
 Presentation of the former to the CD4+ T cells
-Production of cytokines (IFNγ) by the latter
(CD4+ T) => Tissue damage
 B cell response: Production of the following
Antibodies:
Anti tissue trans-glutaminase (anti-tTG)
Anti-deamidated Gliadin
- Anti-endomysial
-Deamidated Gliadin peptides induce
epithelial cell to produce IL15
 IL15 triggers activation and proliferation of
CD8+ T cells
 CD8+ T cells express NKG2D (MIC-A
receptor) and become cytotoxic, thus kill
enterocytes that express MIC-A
 Tissue damage favours the movement of
Gliadin across the epithelium =>
Perpetuation of the disease‟s cycle

118
Q

COELIAC DISEASE

Localisation

A

Localisation: Second portion of duodenum or
proximal jejunum

119
Q

‘Microscopic findings:
 Increased numbers of intraepithelial CD8+ T
cells
 Intraepithelial lymphocytosis
 Crypt hyperplasia (Increased crypt mitotic
activity => Limitation in differentiation
ability of absorptive enterocytes => Defects in
terminal digestion and trans-epithelial
transport)
 Villous atrophy (Loss of mucosal and brush-
border surface area => Malabsorption)
 Fully developed disease: Increased numbers
of plasma cells, mast cells and eosinophils,
within upper part of the lamina propria

A

COELIAC DISEASE

120
Q

COELIAC DISEASE
 Clinical Features:
Silent coeliac disease + Latent coeliac disease

A

-Silent coeliac disease:
Positive serology
Villous atrophy
Absence of symptoms

  • Latent coeliac disease:
    Positive serology
    Absent villous atrophy
121
Q

COELIAC DISEASE
Clinical Features (cont.):
 Symptomatic adult coeliac disease:

A

Symptomatic adult coeliac disease:
Anaemia (Iron, Vitamin B12 and folate
deficiency)
Diarrhoea
Bloating
Fatigue

122
Q

COELIAC DISEASE
Clinical features
Pediatric coeliac disease:

Classic symptoms;

A

Classic symptoms; 6-24 months
Irritability
Abdominal distention
Anorexia
Diarrhoea
Failure to thrive
Weight loss or muscle wasting

123
Q

. Clinical Features (cont.):
 Pediatric coeliac disease:
Non-Classic symptoms (older children)

A

Abdominal pain
Nausea
Vomiting
Bloating or constipation
Pruritic blistering skin lesion (Dermatitis
herpetiformis or Duhring’s disease)

124
Q

COELIAC DISEASE
 Laboratory Findings:

A

Laboratory Findings:
 IgA Abs to tissue trans-glutaminase
 IgA or IgG Abs to deamidated Gliadin
 Absence of HLA-DQ2 or HLA-DQ8 (high
negative predictive value)

125
Q

Coeliac-disease associated malignancies:
.

A

Coeliac-disease associated malignancies:
 Enteropathy-associated T Cell Lymphoma
 Small intestinal Adenocarcinoma

126
Q

TROPICAL SPRUE
+ epidemiology

A

Malabsorption syndrome

Epidemiology:
 Occurrence, almost exclusively in people living
in or visiting the tropics
 Generally endemic; although epidemics have
been reported

127
Q

-TROPICAL SPRUE

Causes

A

Causes:
 No definite causal organism
 Overgrowth of aerobic enteric bacteria has been documented
 Proposed aetiologic factors: Various infections,
including Cyclospora or enterotoxigenic bacteria

128
Q

. TROPICAL SPRUE

Histologic findings

A

Histologic findings:
 Similar to Coeliac disease, but:
 Total villous atrophy <=> Uncommon in tropical
sprue
 Tropical Sprue involves the distal small bowel
 Enlarged (megaloblastic) nuclei within epithelial
cells (reminiscent of those seen in pernicious
anaemia)

129
Q

TROPICAL SPRUE

Clinical features

A

Clinical features:
 Malabasorption usually manifested within days
or a few weeks of an acute diarrhoeal enteric infection
 High frequency of folate or Vit. B12 deficiencies

130
Q

AUTOIMMUNE ENTEROPATHY

A

X-linked disorder characterised by severe
persistent diarrhoea and autoimmune disease
MOSTLY IN YOUNG CHILDREN

131
Q

AUTOIMMUNE ENTEROPATHY
IPEX: Severe familial form

A

-Acronym for:

Immune dysregulation
Polyendocrinopathy ‘
Enteropathy
X-linkage

132
Q

AUTOIMMUNE ENTEROPATHY

Causes

A

Causes: Germline mutation in the FOXP3 gene
(located on the X chromosome)

133
Q

AUTOIMMUNE ENTEROPATHY
 Pathogenesis:

A

Pathogenesis:
 FOXP3: Transcription factor expressed in
CD4+ regulatory T cells
 Individuals with IPEX and FOXP3 mutations
=> Defective T-regulatory function
 Link between less severe forms of autoimmune
enteropathy and other defects in regulatory T
cell function

134
Q

Microscopic findings:
 Increased numbers of intraepithelial
lymphocytes within the small intestine
 Often, presence of neutrophils
 Autoantibodies to enterocytes and goblet cells
(common), antibodies to parietal or islet cells
(in some cases)

A

. AUTOIMMUNE ENTEROPATHY

135
Q

AUTOIMMUNE ENTEROPATHY

Treatment

A

-Treatment:
 Immunosuppressive medications (e.g. cyclo-
sporine)
 Bone marrow transplantation (in rare cases)

136
Q

LACTASE (DISSACHARIDASE) DEFICIENCY

Dissacharidases

A

. Dissacharidases: Located in the apical
brush-border membrane of the villus
absorptive epithelial cells
.Biochemical defect  Unremarkable biopsy
histology

137
Q

Two types of lactase deficiency:
1. Congenital lactase deficiency:
Cause + clinical + management

A
  1. Congenital lactase deficiency:
     Epidemiology & Genetics: Rare, autosomal
    recessive disorder
     Cause: Mutation in the gene encoding lactase
     Clinic: Explosive diarrhoea with watery, frothy
    stools and abdominal distention upon milk
    ingestion
     Management: Termination of milk/milk
    products consumption, thus remove of the
    osmotically active, but unabsorbable lactose
    from the lumen
138
Q

Acquired lactase deficiency:
Cause + clinical

A
  1. Acquired lactase deficiency:
     Cause: Down-regulation of lactase gene
    expression
     Disease presents after childhood
     Onset of disease, sometimes associated with
    enteric viral or bacterial infections
     Clinic: Abdominal fullness, diarrhoea, and
    flatulence, due to fermentation of the
    unabsorbed sugars by colonic bacteria;
    triggered by ingestion of lactose-containing
    dairy products
139
Q

ABETALIPOPROTEINAEMIA

A

Rare autosomal recessive disease,
characterised by an inability to secrete
triglyceride-rich lipoproteins

140
Q

‘ABETALIPOPROTEINAEMIA

Causes

A

Causes: Mutation in the Microsomal
Triglyceride Transfer Protein (MTP) that
catalyses transport of triglycerides,
cholesterol esters, and phospholipids

141
Q

-ABETALIPOPROTEINAEMIA

Pathogenesis

A

Pathogenesis: MTP-deficient enterocytes
unable to export lipoproteins and free fatty
acids => Mono-glycerides cannot be assembled
into chylomicrons => Buildup of triglycerides
within the epithelial cells

142
Q

ABETALIPOPROTEINAEMIA

Microscopic findings + Histochemistry

A

Microscopic findings: Lipid accumulation
in small intestinal epithelial cells

Histochemistry: Oil red-O (demonstration
of lipids)

143
Q

ABETALIPOPROTEINAEMIA
Clinical features:

A

Clinical features:
Presentation in infancy:
 Failure to thrive
 Diarrhoea
 Steatorrhoea

144
Q

ABETALIPOPROTEINAEMIA
Laboratory findings:

A

Laboratory findings:
 Complete absence of all plasma lipoproteins
containing apolipoprotein B
 Failure to absorb essential fatty acids =>
Deficiencies of fat-soluble vitamins
 Presence of acanthocytic red cells (burr cells) in
peripheral blood smears, due to lipid membrane
defects

145
Q

‘PSEUDOMEMBRANOUS COLITIS

Synonym: Antibiotic-associated diarrhoea
Cause

A

Cause: Clostridium difficile; 20% present in
hospitalised adults

146
Q

-PSEUDOMEMBRANOUS COLITIS

Pathogenesis

A

Pathogenesis:
 Prolonged intake of antibiotics => Disruption of the normal colonic microbiota => Overgrowth of C.
difficile => Release of toxins => Ribosylation of
small GTP-ases (Rho) =>
=> Disruption of the epithelial cytoskeleton
=> Loss of tight junction barrier
=> Release of cytokines
=> Apoptosis

147
Q

Macro-/Microscopic features:
 Pseudo-membranes, consisting of an adherent
layer of inflammatory cells and debris
 Stripped surface epithelium

 Lamina propria, with:
Dense infiltrate of neutrophils
Occasional fibrin thrombi within capillaries

 Distention of damaged crypts by a mucopurulent exudate => “Eruption” to the surface, in a fashion reminiscent of a volcano

A

PSEUDOMEMBRANOUS COLITIS

148
Q

PSEUDOMEMBRANOUS COLITIS
Clinical Features:

A

. Clinical Features:
 Fever
 Leukocytosis
 Abdominal pain
 Cramps
 Hypo-albuminaemia
 Watery diarrhoea
 Dehydration
 Faecal leukocytes
 Occult blood

149
Q

‘PSEUDOMEMBRANOUS COLITIS

Diagnosis + Treatment

A

Diagnosis: Detection of C. difficile toxin

Treatment: Metronidazole or Vancomycin

150
Q

WHIPPLE DISEASE + cause

A

Rare, multi-visceral chronic disease

Causative agent: Tropheryma whippelii
(Gram [+] actinomycete)

151
Q

WHIPPLE DISEASE

Localisation

A

Localisation: Mesenteric lymph nodes,
synovial membranes of affected joints, cardiac
valves, brain, and other sites <=> Accumulation
of bacteria-laden macrophages

152
Q

Macroscopic features:
 Shaggy gross appearance to the mucosal
surface, due to villous expansion caused by the dense macrophage infiltrate
 White to yellow mucosal plaques, due to
lymphatic dilatation and mucosal lipid deposition

A

WHIPPLE DISEASE

153
Q

Microscopic findings: Dense accumulation
of distended, foamy macrophages in the small
intestinal lamina propria

A

WHIPPLE DISEASE

154
Q

Histochemistry: Periodic Acid-Schiff (PAS)-
positive, diastase-resistant granules (represent
lysosomes stuffed with partially digested bacteria),
within macrophages

A

WHIPPLE DISEASE

155
Q

WHIPPLE DISEASE

Differential Diagnosis

A

Differential Diagnosis:
 Intestinal Tbc (PAS [+] and acid-fast stain [+])
 Whipple disease (PAS [+] but acid-fast stain [-]

156
Q

WHIPPLE DISEASE

Clinical symptoms:

A

Clinical symptoms: Accumulation of organism-
laden macrophages within the small intestinal
lamina propria and mesenteric lymph nodes =>
Lymphatic obstruction (impaired lymphatic
transport) => Malabsorptive diarrhoea

157
Q

WHIPPLE DISEASE
Clinical presentation: Triad of:

A

 Diarrhoea
 Weight loss
 Malabsorption

158
Q

WHIPPLE DISEASE
Extra-intestinal symptoms:

A

Extra-intestinal symptoms:

 Arthritis and arthralgia
 Fever
 Lymphadenopathy
 Neurologic, cardiac, or pulmonary
disease

Pathology 1 (4 decks)

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