GI ll Flashcards
Epi of Congenital Pyloris stenosis
Males > Females
causes of CONGENITAL PYLORIC STENOSIS
- Genetic predisposition for children from affected parents
- Acquired pyloric obstruction, as a result of chronic duodenal ulcer with scarring
Pathophysiology of CONGENITAL PYLORIC STENOSIS
Progressive hypertrophy of the circular muscular layer in the pyloric sphincter
Clinical findings of CONGENITAL PYLORIC STENOSIS
1) Projectile vomiting (not bile stained fluid)
2)Palpable mass (“olive”); epigastrium (70% cases)
3) Obvious hyperperistalsis
Clinical Findings of GASTROPARESIS
1) Early satiety and bloating
2) Vomiting of undigested food
Treatment of GASTROPARESIS
1) Frequent, small meals
2) Metoclopramide
Clinical features of Acute gasterities
1) Asymptomatic disease, or
2) Variable degrees of –> epigastric pain, nausea
and vomiting, or
3) More severe cases: Mucosal erosion,
ulceration, haemorrhage, haematemesis,
melena, or massive blood loss (rarely)
Microscopic findings:
1) Mild features:
* Moderate oedema and slight vascular
congestion in the lamina propria
* Intact surface epithelium
* Scattered neutrophils, intraepithelial
2) More severe mucosal damage:
* Erosion or loss of superficial epithelium
* Formation of mucosal neutrophilic infiltrates
and purulent exudates
* Occurrence of haemorrhages
Are the features of what GI disorder?
Acute Gastritis
Gastric lumen is strongly acidic (pH: ~1) –> potential to damage the gastric mucosa
what protective mechanisms does the GI system take to protect against gastric injury?
1) Secretion of mucin by surface foveolar cells
–> Formation of a thin layer of mucus –>
Prevention of large food particles directly
touching the epithelium
2) Mucous layer –> Promotes formation of a layer of fluid (neutral pH as a result of bicarbonate ion secretion by surface epithelial cells) over the epithelium –> Protection of the mucosa
3) Rich vascular supply to the gastric mucosa
–> Delivery of oxygen, bicarbonate and nutrients and removal of acid
causes Acute Gastritis?
1) Reduced mucin synthesis in the elderly
2) NSAIDs, through their interference with cyto-protection –> normally provided by prostaglandins or reduction of bicarbonate secretion
3) Uraemic patients + H. pylori infection –> Inhibition of gastric bicarbonate transporters by ammonium ions
4) Ingestion of harsh chemicals (acids/bases) –> Direct injury to mucosal epithelial and stromal cells
5) Excessive alcohol consumption, NSAIDs,
radiation therapy, and chemotherapy –>
Direct cellular injury
Causes of Acute Erosive Haemorrhagic Gastritis?
1) NSAID,
2) alcohol,
3) H. Pylori infection,
4) smoking,
5) severe burn (Curling ulcer),
6) CNS injury (Cushing ulcer)
*H.Pylori –> Helicobacter Pylori
Clinical findings of Acute Erosive Haemorrhagic Gastritis
1) Haematemesis (vomiting blood)
2) Melena (black stool)
3) Iron deficiency
The 2 types of Chronic Atrophic Gasteritis and their difference
1) Type A Chronic Atrophic Gastritis = Autoimmune Gastritis
2) Type B Chronic Atrophic Gastritis =
H. Pylori associated Gastritis
Localisation of Type A,B Chronic Atrophic Gastritis
A–>Body and fundus
B–>Antrum and pylorus
cause of Type B Chronic Atrophic Gastritis
H. pylori
Clinical findings of Type B Chronic Atrophic Gastritis
Increased gastric acid
secretion
serology of Autoimmune Gasteritis (Type A)
Abs to parietal cells (H+, K+-
ATPase, intrinsic factor)
[*Intrinsic factors are imporant for the absorption of Vit.B12 ]
Complications of Type A Chronic Atrophic Gastritis (Autoimmune Gastritis)
1) Achlorhydria with Hypergastrinaemia
2) Vit. B12 deficiency –> Macrocytic anaemia
3) ↑ Risk for gastric Adeno-Ca
Commplications/associations of Type B Chronic Atrophic Gastritis (H. Pylori )
1) Gastric ulcer
2) duodenal peptic ulcers
3) Gastric AdenoCarcinoma and
4) Lymphoma (MALT-type)
Pathophysiology of Type B Chronic Atrophic Gastritis
1) 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
2) Colonisation of mucous layer lining without invasion of the wall
*Attachment to blood group O receptors on mucosal cells
Microscopic findings:
-Chronic inflammatory infiltrate in the
lamina propria
-Intestinal metaplasia (similar to Barrett
Oesophagus) –> Progression to Adeno-Ca
Are the features of what GI disorder?
Type B Chronic Atrophic Gastritis =
H. Pylori associated Gastritis
causes of Acute Peptic Ulcer
1)NSAIDs
2)Sever physiologic stress
Types of Ulcers (associated with stress factors)?
1) Stress Ulcers: Critically ill patients with shock, sepsis or severe trauma
2) Curling Ulcers: Proximal duodenum; Severe burns or trauma
3) Cushing Ulcers: Stomach, duodenum, or oesophagus; Individuals with intracranial disease; Increased rate of perforation
Pathogenesis of NSAID-induced ulcers
*Direct chemical irritation + Cyclooxygenase
inhi-bition –> Prevention of Prostaglandin
synthesis –> Elimination of Prostaglandin‟s
protective effect
* Protaglandin’s protective effect: Enhanced
bicarbonate secretion and ↑ vascular perfusion
Pathogenesis of Ulcers associated with brain injury
Direct stimulation of vagal nuclei –> Gastric acid hypersecretion
Pathogenesis of Ulcers associated with critically ill patients (Stress ulcres)
Systemic acidosis –> Decrease in intracellular
pH of mucosal cells –> Mucosal injury
Clinical features of Acute peptic ulcers
1) Nausea
2) Vomiting
3) Haematemesis
Complications of Acute peptic ulcer
Perforation
Treatment of Acute peptic ulcer
1) Proton pump inhibitors
2) Histamine H2 receptor antagonists
Causes of Peptic Ulcer disease
1) H. pylori infection (most common)
2)NSAID
Location of Peptic ulcer disease
1) Gastric antrum and first portion of duodenum
2) Oesophagus: Result of GOERD, ectopic gastric
mucosa
3) Small intestine: Gastric heterotopia within a
Meckel diverticulum
Macroscopic features:
- Lesions: <0.3 cm –> Shallow; 0.6 cm –> Deep
- Round to oval
- Sharply punched out defect
- Base: Smooth and clean
Are the features of what GI disorder?
PEPTIC ULCER DISEASE
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
Are the features of what GI disorder?
PEPTIC ULCER DISEASE
Clinical feature of peptic ulcer disease?
1) Epigastric burning or aching pain
2) Bloating and belching
3) Iron deficiency anaemia
4) Frank haemorrhage
5) Perforation
*Occurrence of pain: 1-3 hours after meals
(during the day) and worse at night
what can be taken to relife the pain of peptic ulcer disease
1) Antibiotics (H. pylori)
2) Alkali : Proton pump inhibitors -> Neutralisation of gastric acid
3) food
Criteria for the Diagnosis of Menetrier Disease
- 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
Localisation of MENETRIER DISEASE
Centred along the greater curvature
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-circumscribed cerebroid mass either in the fundus or the antrum
Are the features of what GI disorder?
MENETRIER DISEASE
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
Are the features of what GI disorder?
MENETRIER DISEASE
clinical features of MENETRIER DISEASE
1) Hypochlorhydria or achlorhydria
2) hypoproteinaemia
DD of Menetrier disease
Malignant Lymphoma or Carcinoma
Management of Menetrier Disease?
- Adults: Fully developed disease is progressive —> requires subtotal gastrectomy
- Paediatric cases –> self-limited disease
Pathogensis of Peptic ulcer disease
*Imbalance btw mucosal defenses and offensive agents –> Chronic Gastritis
—> Peptic ulcer disease
Gastric hyperacidity:
^ H. pylori infection
^ Parietal cell hyperplasia
^ Excessive secretory responses —> increased gastric acid
^ Impaired inhibition of stimulatory mechanisms (e.g. Gastrin release)
^ Chronic renal failure and hyperparathyroidism –> ↑ Gastrin production
*Uncontrolled release of Gastrin (Zollinger-Ellison syndrome) –> Multiple peptic ulcers
Inflammatory infiltrates in Type A and B Chronic Atrophic Gastritis
Type A –> Macrophages, lymphocytes
Type B –> Neutrophils, subepithelial plasma cells
Round; Size: <1cm
Ulcer base: Brown to black
Are feautes of what type of ulcer?
Acute ulcer
Macro:
Sharply demarcated
Normal adjacent mucosa
Are the features of what type of ulcer?
Acute stress ulcer
Microscopic findings:
Layers of Ulcer:
–> Necrotic debris
–> Mainly, neutrophilic infiltration
Are what type of ulcer?
Acute peptic ucler
epi of INFLAMMATORY &
HYPERPLASTIC POLYPS
75% of all gastric polyps; Individuals 50-60 yrs.
patho of inflammatory & hyperplastic polyps
Chronic gastritis –> Injury and reactive hyperplasia
–> Development of polyp
Macroscopy:
- Ovoid lesions; Size: <1cm; Smooth surface
what type of neoplasm?
INFLAMMATORY &
HYPERPLASTIC POLYPS
Microscopy:
- Irregular, cystically dilated and elongated foveolar
glands
- Oedematous lamina propria (Excess of laminia propria)
- Acute and chronic inflammation
- Surface erosions(may be present)
Features of what type of neoplasm?
INFLAMMATORY &
HYPERPLASTIC POLYPS
Epi of Fundic gland polyps
- Sporadic occurrence
- Persons with Familial Adenomatous Polyposis
casuse/ patho of fundic gland polyps
Proton pump inhibitors –> Reduced acidity –>
Increased Gastrin secretion –> Glandular
hyperplasia
Clinical featurs of Fundic gland poylps
1) Nausea;
2) Vomiting;
3) Epigastric pain
Macroscopy: Well-circumscribed polyps in the gastric body and fundus
feature of what type of gastric neoplasm?
fundic gland polyps
Microscopy:
- Cystically dilated, irregular glands
- Lining of the glands: Flattened parietal and
chief cells
features of what type of gastric neoplasm?
Fundic gland polyps
Epi of gastric adenoma
-10% of all gastric polyps
- Ages: 50-60 yrs.; M:F = 3:1
cause/patho of Gastric andenoma
Chronic gastritis –> Atrophy and intestinal metaplasia
Risk for malignant transofromation of gastric adenoma
1) Dependent on lesion‟s size (risk elevated with
lesions >2cm)
2) Presence of Adeno-CAs in up to 30% of gastric
adenomas
location of gastric adenoma
Antrum of the stomach
Microscopic features:
- Histologically, two types:
1) Adenomas with intestinal differentiation
(Goblet cells and/or Paneth cells)
2) Adenomas with gastric differentiation
(Columnar cells containing neutral mucin)
Are the features of what type of gastric neoplasm?
Gastric adenoma
Cause of Zollinger Ellison Syndrom
aka Gastrinomas
uncontrolled gastrin secretion
(gastrin secreting-tumors)
Location of Zollinger Ellison Syndrome
1) third and second portion of the duodenum (inferiorly)
2) common bile duct superiorly
3) neck and body of the pancerease medially
Clinical manifestaions of Zollinger elisson syndrome
1) Duodenal ulcers
2) Chronic diarrhoea
Treatment of Zollinger Ellison syndrom
Blockade of acid hypersecretion:
1) Proton pump inhibitors or
2) High-dose H2 histamine receptor antagonists
Pathological findigs findings within the stomach:
1) 5x increase in number of parietal cells [parietal cell hyperplasia]
–> Doubling of oxyntic mucosal thickness
2) Hyperplasia of mucous neck cells, mucin
hyperproduction
3) Proliferation of endocrine cells –> Small
dysplastic nodules (sometimes), true
Carcinoid Tumours (rarely)
Are the features of what gastric condition?
Gastrinoma –> Zollinger Ellison Syndrom
epi of Carcinoma of the stomach
1) >50 yrs
2) Men > Women
3) blood group A persons
causes of Stomach Carcinomas
1) H.Pylori infection
2) A diet hight in smoked fish (Nitrosamin)
3) diet high salt intake and low in fresh fruits and vegetables
3) Penicious aneamia (Low RBC)
4) Chronic gasteritis
5) Family histroy of mutations of CDH1 (E-Cadherin gene)
6) Menetrier disease (Giant Hypertrophy gastritis)
Singet ring cell Adenocarinoma is the characteristic Histopathology findings of what type of disorder? state the casue of this condition
Diffuse type Gastric Carcinoma
Cause –> mutations in CDHI( E-Cadherine gene), which results in loss of E-Cadherine function
Cause of Intestinal Type Gastric cancer
Germline mutations in Adenomatous Polyposis
Coli (APC) genes (patients with FAP)
*Familial adenomatous polyposis (FAP)
Patient with E-cadherin gene mutations develop what type of cancer?
1) Diffuse Gastric carnimoa
2) Lobular CA of the breast
Pathogens causing gastric carcinoma + their complications
1) 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
2) EBV-Epstein–Barr virus –> positive tumours
Localisation: Proximal stomach
- Diffuse morphology
- Marked lymphocytic infiltrate
location of Gastric carcinoma
Minor curvature of the antrum
or pre-pyloric region –> Spread to the
adjacent organs, peritoneum, regional lymph
nodes and liver
Macro-/Microscopic features:
–> Association with H. pylori
–> Polypoid carcinoma; solid mass projecting
into the lumen
–> Possible, ulceration
Features of what type of Gastric carcinoma?
Intestinal gastric carcinoma
State the Histopathological differences between Peptic cancer and peptic ulcer
1) Peptic Ulcer (smooth base, non-elevated
punched out margins) vs.
2) Peptic CA (Ulcer with irregular necrotic base and firm raised
margins)
Macro-/Microscopic features:
–> NO association with H. pylori
–> Macroscopy: Thickened, rigid stomach wall
–> Microscopy: Diffuse signet-ring cells
infiltrates with accompanying extensive
fibrosis
Are the features of what type of gastric carcinoma?
Diffuse gastric carcinoma (aka Linitis plastica/ Leather-bottle stomach)
most common type of Lymphoma of the stomach
Extranodal Marginal Zone B-cell Lymphoma (MALT)
MALT - Extranodal Marginal Zone B-cell Lymphoma is associated with?
1) H.pylori infection
2) Possible regressing after antibiotic treatment
3) Therapy with oral Alkylating agents
Microscopic features:
- Dense infiltrate of small lymphoid cells, often
accompanied by scattered reactive lymphoid follicles
- Lymphoid cells: Variable admixture of small lymphocytes, centrocyte-like cells, and monocytoid cells
- Common finding, focal or extensive plasmacytoid
differentiation
- Possible presence of “Dutcher bodies‟
- Important diagnostic sign: Infiltration of the
glandular epithelium by neoplastic lymphocytes,
resulting in so-called “lympho-epithelial lesions”
Are the features of what type of Gastric cancer?
Extranodal Marginal Zone B-cell Lymphoma (MALT)
Extranodal Marginal Zone B-cell Lymphoma (MALT)
Characteristic combination of immunohistochemical markers:
1) ————- ((+/-) immuni-staining) immuno-staining) for CD20, CD79a, CD21, CD35, BCL2 and
Immunoglobulins (mainly surface, but also
cytoplasmic)
2) postivity/Negativity( [+/-] immuno-staining) for CD5, CD10, CD23, and cyclin D1
1) Reactivity (+)
2) Negativity (-)
Epi of Large B-cell Lymphoma
> 50 yrs
Clinical manifestations of Large B-cell Lymphoma
Large palpable mass (and still excellent physical
condition of the patients)
Macroscopic findings:
* Large lobulated (sometimes polypoid) mass
* Commonly, superficial or deep CENTRAL ulceration
Features of what type of gastric carcinoma?
LARGE B-CELL LYMPHOMA
loc. of LARGE B-CELL LYMPHOMA
Distal half of the stomach,
with a tendency to spare the pylorus
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 ReedSternberg cells may be present
- The phenotypic features are those of B cells
Are the features of what Type of Gastric Carcinoma?
Large B-cell Lymphoma
Gastric Carcinoids are associated with?
1) Endocrine cell hyperplasia
2) Chronic atrophic gastritis
3) Zollinger-Ellison syndrome
Macroscopic features:
- Intramural or submucosal masses –> Small
polypoid lesions
- Yellow or tan in appearance
- Intense Desmoplasia –> Kinking of the bowel
and obstruction
Are the features of what type of Gastric carcinoma?
Cacinoid tumours
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
Are the features of what type of Gastric cancer?
Carcinoid tumours
Immunohistochemistry of Carcinoid tumours
1) Neuron-Specific Enolase
(NSE),
2) Chromogranin,
3) Synaptophysin
clincial features of Carcinoid tumours
1)Cutaneous flushing
2) Sweating
3) Bronchospasm
4) Colicky abdominal pain
5) Diarrhoea
location of GASTRO-INTESTINAL STROMAL TUMOUR (GIST)
1) Submucosa of stomach,
2) small and large intestine and
3) extra-gastrointestinal sites
Patho of GIST
1) 75-80% of GISTs: Oncogenic, gain-of-function mutations of the gene encoding the tyrosine kinase c-KIT
2) 8% of GISTs: Activating mutations of PDGFRA
Macroscopic features:
- Primary lesions: Solitary, well circumscribed,
fleshy submucosal masses
- Metastases: Multiple small serosal nodules or
fewer nodules in the liver
Are the features of what gastric neoplasm?
GIST- gastrointestinal stromal tumour
Microscopic features:
- Thin, elongated spindle cells or
- Plumper epithelioid cells
- c-KIT (CD117) immuno-positivity
Are the features of what gastric Neoplasm
GASTRO-INTESTINAL STROMAL
TUMOUR (GIST)
Prognosis of GIST
1) Tumour size
2) Mitotic Index (MI)
3) Location
4) Gastric GISTs less aggressive than small intestine GISTs
–> Gastric GISTs:
-Recurrence or metastasis: <5cm tumours <>
Rare; >10cm and high MI <> Common
Causes of Acute arterial obstruction
1) Severe atherosclerosis
2) Aortic aneurysm
3) Hypercoagulable states
4) Oral contraceptives
5) Embolisation of cardiac vegetations or aortic
atheromas
causes of Intestinal Hypoperfusion
1) Cardiac failure
2) Shock
3) Vasculitides (PAN, Henoch-Schönlein purpura,
Wegener granulomatosis, etc.)
The 2 phases of Isheamic bowel disease
(intestinal respose to Iscaemia)
1) First phase : Occurrence of initial hypoxic
injuryat the onset of vascular compromise
2) 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
Clinical features of Ischeamic Bowel disease
1) Sudden, severe abdominal pain
2) Tenderness
3) Nausea and Vomiting
4) Bloody diarrhoea or melaena (“tarry” feces)
–> Vascular collapse and shock (due to blood loss)
5) Decline or disappearance of peristaltic sounds
6) Muscular spasm –> Board-like rigidity of the
abdominal wall
micro/macro:
- Necrosis of the superficial epithelium
- Haemorrhage in the lamina propria
- Preservation of the colonic crypts’ base
Are the features of of what gastric condition?
Ischeamic bowel disease
Malabsorption results from disturbance in at
least one of the four phases of nutrient
absorption. State/Explain each phase.
1.Intraluminal digestion –> proteins,
carbohydrates, and fats are broken down into
forms suitable for absorption
2.Terminal digestion –> hydrolysis of carbohydrates and peptides (by disaccharidases and peptidases, respectively, in the brush-border of the small intestinal mucosa)
3.Transepithelial transport –> nutrients, fluid and electrolytes are transported across and processed within the small intestinal epithelium
4.Lymphatic transport of absorbed lipids
calssification of Diarrhoea
- Secretory diarrhoea
- Osmotic diarrhoea
- Malabsorbative Diarrhoea
- Exudative Diarrhoea
loction of coeliac disease
Second portion of duodenum or
proximal jejunum
Microscopic findings:
1) Increased numbers of intraepithelial CD8+ T
cells
2) Intraepithelial lymphocytosis
3) Crypt hyperplasia (Increased crypt mitotic
activity –> Limitation in differentiation
ability of absorptive enterocytes –> Defects in
terminal digestion and trans-epithelial
transport
4) Villous atrophy (Malabsorption)
Fully developed disease –> Increased numbers
of plasma cells, mast cells and eosinophils,
within upper part of the lamina propria
Are the features of what gastric disease?
Coeliac disease
Coeliac disesae results in what kind of Defects?
1) Terminal Digestion
2) Trans-epithelial transport
clincial features of silent vs Latent Coeliac disease
Silent coeliac disease:
- Positive serology
- Villous atrophy
- Absence of symptoms
Latent coeliac disease:
- Positive serology
- Absent villous atrophy
Classic symptoms of Pediatric coeliac disease
1) Irritability
2) Abdominal distention
3) Anorexia
4) Diarrhoea
5) Failure to thrive
6) Weight loss or muscle wasting
Non-classic symptoms of Coeliac disease
1) Abdominal pain
2) Nausea
3) Vomiting
4) Bloating or constipation
5) Pruritic blistering skin lesion (Dermatitis
herpetiformis or Duhring’s disease)
Pseudomemebranous colitis is aka ?
Antibiotic-associated diarrhoea
casue of pseudomembranous colitis
Clostridium difficile
Macro-/Microscopic features:
1) Pseudo-membranes, consisting of an adherent
layer of inflammatory cells and debris
2) Stripped surface epithelium
3) Lamina propria, with:
- Dense infiltrate of neutrophils
- Occasional fibrin thrombi within capillaries
- Dilation of damaged crypts by a mucopurulent exudate –> “Eruption” to the surface, in a fashion reminiscent of a volcano
Are the features of what gastric condition?
PSEUDOMEMBRANOUS COLITIS
Clinical features of Pseudomembranous colitis
1) Fever
2) Leukocytosis
3) Abdominal pain
4) Cramps
5) Hypo-albuminaemia
6) Watery diarrhoea
7) Dehydration
8) Faecal leukocytes
9) Occult blood
Treatment of Pseudomembranous colits
Vancomycin / Metroindazole
Causative agent of Whipple disease
: Tropheryma whippelii
(Gram [+] actinomycete
Macro/micro:
- Marked macrophage infiltrates in lamina propria (of the small intestine)
- Scattered fat vacuoles (White-yellow mucousal plaques)
- Intra-cytoplasmic PAS-positive material within macrophages
*PAS- periodic Acid-Schiff
Are the features of Gastric condition?
Whipple disease
Main Clinical symptom of Whipple disease
Malabsorbative Diarrhoea –> casued by Impaired Lymphatic transport
Patho of Whipple disease ?
Accumulation of bacteria-laden macrophages–> in the Synovial membranes of affected joints, cardiac valves, brain and Mesenteric lymph nodes
Clinical presentaions of Whipple disease
Triad of:
1) Diarrhoea
2) Weight loss
3) Malabsorption
Complications of Ischeamic bowel disease
Break down of mucosal barrier –> Bacteria enter the circulation –> Sepsis
