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Pathology > GI ll > Flashcards

GI ll Flashcards

1
Q

Epi of Congenital Pyloris stenosis

A

Males > Females

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2
Q

causes of CONGENITAL PYLORIC STENOSIS

A
  • Genetic predisposition for children from affected parents
  • Acquired pyloric obstruction, as a result of chronic duodenal ulcer with scarring
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3
Q

Pathophysiology of CONGENITAL PYLORIC STENOSIS

A

Progressive hypertrophy of the circular muscular layer in the pyloric sphincter

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4
Q

Clinical findings of CONGENITAL PYLORIC STENOSIS

A

1) Projectile vomiting (not bile stained fluid)
2)Palpable mass (“olive”); epigastrium (70% cases)
3) Obvious hyperperistalsis

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5
Q

Clinical Findings of GASTROPARESIS

A

1) Early satiety and bloating
2) Vomiting of undigested food

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6
Q

Treatment of GASTROPARESIS

A

1) Frequent, small meals
2) Metoclopramide

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7
Q

Clinical features of Acute gasterities

A

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)

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8
Q

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?

A

Acute Gastritis

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9
Q

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?

A

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

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10
Q

causes Acute Gastritis?

A

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

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11
Q

Causes of Acute Erosive Haemorrhagic Gastritis?

A

1) NSAID,
2) alcohol,
3) H. Pylori infection,
4) smoking,
5) severe burn (Curling ulcer),
6) CNS injury (Cushing ulcer)

*H.Pylori –> Helicobacter Pylori

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12
Q

Clinical findings of Acute Erosive Haemorrhagic Gastritis

A

1) Haematemesis (vomiting blood)
2) Melena (black stool)
3) Iron deficiency

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13
Q

The 2 types of Chronic Atrophic Gasteritis and their difference

A

1) Type A Chronic Atrophic Gastritis = Autoimmune Gastritis
2) Type B Chronic Atrophic Gastritis =
H. Pylori associated Gastritis

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14
Q

Localisation of Type A,B Chronic Atrophic Gastritis

A

A–>Body and fundus
B–>Antrum and pylorus

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15
Q

cause of Type B Chronic Atrophic Gastritis

A

H. pylori

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16
Q

Clinical findings of Type B Chronic Atrophic Gastritis

A

Increased gastric acid
secretion

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17
Q

serology of Autoimmune Gasteritis (Type A)

A

Abs to parietal cells (H+, K+-
ATPase, intrinsic factor)

[*Intrinsic factors are imporant for the absorption of Vit.B12 ]

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18
Q

Complications of Type A Chronic Atrophic Gastritis (Autoimmune Gastritis)

A

1) Achlorhydria with Hypergastrinaemia
2) Vit. B12 deficiency –> Macrocytic anaemia
3) ↑ Risk for gastric Adeno-Ca

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19
Q

Commplications/associations of Type B Chronic Atrophic Gastritis (H. Pylori )

A

1) Gastric ulcer
2) duodenal peptic ulcers
3) Gastric AdenoCarcinoma and
4) Lymphoma (MALT-type)

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20
Q

Pathophysiology of Type B Chronic Atrophic Gastritis

A

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

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21
Q

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?

A

Type B Chronic Atrophic Gastritis =
H. Pylori associated Gastritis

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22
Q

causes of Acute Peptic Ulcer

A

1)NSAIDs
2)Sever physiologic stress

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23
Q

Types of Ulcers (associated with stress factors)?

A

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

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24
Q

Pathogenesis of NSAID-induced ulcers

A

*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

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25
Q

Pathogenesis of Ulcers associated with brain injury

A

Direct stimulation of vagal nuclei –> Gastric acid hypersecretion

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26
Q

Pathogenesis of Ulcers associated with critically ill patients (Stress ulcres)

A

Systemic acidosis –> Decrease in intracellular
pH of mucosal cells –> Mucosal injury

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27
Q

Clinical features of Acute peptic ulcers

A

1) Nausea
2) Vomiting
3) Haematemesis

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28
Q

Complications of Acute peptic ulcer

A

Perforation

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29
Q

Treatment of Acute peptic ulcer

A

1) Proton pump inhibitors
2) Histamine H2 receptor antagonists

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30
Q

Causes of Peptic Ulcer disease

A

1) H. pylori infection (most common)
2)NSAID

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31
Q

Location of Peptic ulcer disease

A

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

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32
Q

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?

A

PEPTIC ULCER DISEASE

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33
Q

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?

A

PEPTIC ULCER DISEASE

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33
Q

Clinical feature of peptic ulcer disease?

A

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

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34
Q

what can be taken to relife the pain of peptic ulcer disease

A

1) Antibiotics (H. pylori)
2) Alkali : Proton pump inhibitors -> Neutralisation of gastric acid
3) food

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35
Q

Criteria for the Diagnosis of Menetrier Disease

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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36
Q

Localisation of MENETRIER DISEASE

A

Centred along the greater curvature

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37
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-circumscribed cerebroid mass either in the fundus or the antrum

Are the features of what GI disorder?

A

MENETRIER DISEASE

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38
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

Are the features of what GI disorder?

A

MENETRIER DISEASE

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39
Q

clinical features of MENETRIER DISEASE

A

1) Hypochlorhydria or achlorhydria
2) hypoproteinaemia

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40
Q

DD of Menetrier disease

A

Malignant Lymphoma or Carcinoma

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41
Q

Management of Menetrier Disease?

A
  • Adults: Fully developed disease is progressive —> requires subtotal gastrectomy
  • Paediatric cases –> self-limited disease
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42
Q

Pathogensis of Peptic ulcer disease

A

*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

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43
Q

Inflammatory infiltrates in Type A and B Chronic Atrophic Gastritis

A

Type A –> Macrophages, lymphocytes
Type B –> Neutrophils, subepithelial plasma cells

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44
Q

Round; Size: <1cm
Ulcer base: Brown to black
Are feautes of what type of ulcer?

A

Acute ulcer

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45
Q

Macro:
Sharply demarcated
Normal adjacent mucosa

Are the features of what type of ulcer?

A

Acute stress ulcer

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46
Q

Microscopic findings:
Layers of Ulcer:
–> Necrotic debris
–> Mainly, neutrophilic infiltration

Are what type of ulcer?

A

Acute peptic ucler

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47
Q

epi of INFLAMMATORY &
HYPERPLASTIC POLYPS

A

75% of all gastric polyps; Individuals 50-60 yrs.

48
Q

patho of inflammatory & hyperplastic polyps

A

Chronic gastritis –> Injury and reactive hyperplasia
–> Development of polyp

49
Q

Macroscopy:
- Ovoid lesions; Size: <1cm; Smooth surface

what type of neoplasm?

A

INFLAMMATORY &
HYPERPLASTIC POLYPS

50
Q

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?

A

INFLAMMATORY &
HYPERPLASTIC POLYPS

51
Q

Epi of Fundic gland polyps

A
  • Sporadic occurrence
  • Persons with Familial Adenomatous Polyposis
52
Q

casuse/ patho of fundic gland polyps

A

Proton pump inhibitors –> Reduced acidity –>
Increased Gastrin secretion –> Glandular
hyperplasia

53
Q

Clinical featurs of Fundic gland poylps

A

1) Nausea;
2) Vomiting;
3) Epigastric pain

54
Q

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

feature of what type of gastric neoplasm?

A

fundic gland polyps

55
Q

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

features of what type of gastric neoplasm?

A

Fundic gland polyps

56
Q

Epi of gastric adenoma

A

-10% of all gastric polyps
- Ages: 50-60 yrs.; M:F = 3:1

57
Q

cause/patho of Gastric andenoma

A

Chronic gastritis –> Atrophy and intestinal metaplasia

58
Q

Risk for malignant transofromation of gastric adenoma

A

1) Dependent on lesion‟s size (risk elevated with
lesions >2cm)
2) Presence of Adeno-CAs in up to 30% of gastric
adenomas

59
Q

location of gastric adenoma

A

Antrum of the stomach

60
Q

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?

A

Gastric adenoma

61
Q

Cause of Zollinger Ellison Syndrom
aka Gastrinomas

A

uncontrolled gastrin secretion
(gastrin secreting-tumors)

62
Q

Location of Zollinger Ellison Syndrome

A

1) third and second portion of the duodenum (inferiorly)
2) common bile duct superiorly
3) neck and body of the pancerease medially

63
Q

Clinical manifestaions of Zollinger elisson syndrome

A

1) Duodenal ulcers
2) Chronic diarrhoea

64
Q

Treatment of Zollinger Ellison syndrom

A

Blockade of acid hypersecretion:
1) Proton pump inhibitors or
2) High-dose H2 histamine receptor antagonists

65
Q

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?

A

Gastrinoma –> Zollinger Ellison Syndrom

66
Q

epi of Carcinoma of the stomach

A

1) >50 yrs
2) Men > Women
3) blood group A persons

67
Q

causes of Stomach Carcinomas

A

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)

68
Q

Singet ring cell Adenocarinoma is the characteristic Histopathology findings of what type of disorder? state the casue of this condition

A

Diffuse type Gastric Carcinoma
Cause –> mutations in CDHI( E-Cadherine gene), which results in loss of E-Cadherine function

69
Q

Cause of Intestinal Type Gastric cancer

A

Germline mutations in Adenomatous Polyposis
Coli (APC) genes (patients with FAP)

*Familial adenomatous polyposis (FAP)

70
Q

Patient with E-cadherin gene mutations develop what type of cancer?

A

1) Diffuse Gastric carnimoa
2) Lobular CA of the breast

71
Q

Pathogens causing gastric carcinoma + their complications

A

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

72
Q

location of Gastric carcinoma

A

Minor curvature of the antrum
or pre-pyloric region –> Spread to the
adjacent organs, peritoneum, regional lymph
nodes and liver

73
Q

Macro-/Microscopic features:
–> Association with H. pylori
–> Polypoid carcinoma; solid mass projecting
into the lumen
–> Possible, ulceration
Features of what type of Gastric carcinoma?

A

Intestinal gastric carcinoma

74
Q

State the Histopathological differences between Peptic cancer and peptic ulcer

A

1) Peptic Ulcer (smooth base, non-elevated
punched out margins) vs.
2) Peptic CA (Ulcer with irregular necrotic base and firm raised
margins)

75
Q

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?

A

Diffuse gastric carcinoma (aka Linitis plastica/ Leather-bottle stomach)

76
Q

most common type of Lymphoma of the stomach

A

Extranodal Marginal Zone B-cell Lymphoma (MALT)

77
Q

MALT - Extranodal Marginal Zone B-cell Lymphoma is associated with?

A

1) H.pylori infection
2) Possible regressing after antibiotic treatment
3) Therapy with oral Alkylating agents

78
Q

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?

A

Extranodal Marginal Zone B-cell Lymphoma (MALT)

79
Q

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

A

1) Reactivity (+)
2) Negativity (-)

80
Q

Epi of Large B-cell Lymphoma

A

> 50 yrs

81
Q

Clinical manifestations of Large B-cell Lymphoma

A

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

82
Q

Macroscopic findings:
* Large lobulated (sometimes polypoid) mass
* Commonly, superficial or deep CENTRAL ulceration

Features of what type of gastric carcinoma?

A

LARGE B-CELL LYMPHOMA

83
Q

loc. of LARGE B-CELL LYMPHOMA

A

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

84
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 ReedSternberg cells may be present
- The phenotypic features are those of B cells

Are the features of what Type of Gastric Carcinoma?

A

Large B-cell Lymphoma

85
Q

Gastric Carcinoids are associated with?

A

1) Endocrine cell hyperplasia
2) Chronic atrophic gastritis
3) Zollinger-Ellison syndrome

86
Q

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?

A

Cacinoid tumours

87
Q

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?

A

Carcinoid tumours

88
Q

Immunohistochemistry of Carcinoid tumours

A

1) Neuron-Specific Enolase
(NSE),
2) Chromogranin,
3) Synaptophysin

89
Q

clincial features of Carcinoid tumours

A

1)Cutaneous flushing
2) Sweating
3) Bronchospasm
4) Colicky abdominal pain
5) Diarrhoea

90
Q

location of GASTRO-INTESTINAL STROMAL TUMOUR (GIST)

A

1) Submucosa of stomach,
2) small and large intestine and
3) extra-gastrointestinal sites

91
Q

Patho of GIST

A

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

92
Q

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?

A

GIST- gastrointestinal stromal tumour

93
Q

Microscopic features:
- Thin, elongated spindle cells or
- Plumper epithelioid cells
- c-KIT (CD117) immuno-positivity

Are the features of what gastric Neoplasm

A

GASTRO-INTESTINAL STROMAL
TUMOUR (GIST)

94
Q

Prognosis of GIST

A

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

95
Q

Causes of Acute arterial obstruction

A

1) Severe atherosclerosis
2) Aortic aneurysm
3) Hypercoagulable states
4) Oral contraceptives
5) Embolisation of cardiac vegetations or aortic
atheromas

96
Q

causes of Intestinal Hypoperfusion

A

1) Cardiac failure
2) Shock
3) Vasculitides (PAN, Henoch-Schönlein purpura,
Wegener granulomatosis, etc.)

97
Q

The 2 phases of Isheamic bowel disease
(intestinal respose to Iscaemia)

A

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

98
Q

Clinical features of Ischeamic Bowel disease

A

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

99
Q

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?

A

Ischeamic bowel disease

100
Q

Malabsorption results from disturbance in at
least one of the four phases of nutrient
absorption. State/Explain each phase.

A

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

101
Q

calssification of Diarrhoea

A
  1. Secretory diarrhoea
  2. Osmotic diarrhoea
  3. Malabsorbative Diarrhoea
  4. Exudative Diarrhoea
102
Q

loction of coeliac disease

A

Second portion of duodenum or
proximal jejunum

103
Q

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?

A

Coeliac disease

104
Q

Coeliac disesae results in what kind of Defects?

A

1) Terminal Digestion
2) Trans-epithelial transport

105
Q

clincial features of silent vs Latent Coeliac disease

A

Silent coeliac disease:
- Positive serology
- Villous atrophy
- Absence of symptoms
Latent coeliac disease:
- Positive serology
- Absent villous atrophy

106
Q

Classic symptoms of Pediatric coeliac disease

A

1) Irritability
2) Abdominal distention
3) Anorexia
4) Diarrhoea
5) Failure to thrive
6) Weight loss or muscle wasting

107
Q

Non-classic symptoms of Coeliac disease

A

1) Abdominal pain
2) Nausea
3) Vomiting
4) Bloating or constipation
5) Pruritic blistering skin lesion (Dermatitis
herpetiformis or Duhring’s disease)

108
Q

Pseudomemebranous colitis is aka ?

A

Antibiotic-associated diarrhoea

109
Q

casue of pseudomembranous colitis

A

Clostridium difficile

110
Q

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?

A

PSEUDOMEMBRANOUS COLITIS

111
Q

Clinical features of Pseudomembranous colitis

A

1) Fever
2) Leukocytosis
3) Abdominal pain
4) Cramps
5) Hypo-albuminaemia
6) Watery diarrhoea
7) Dehydration
8) Faecal leukocytes
9) Occult blood

112
Q

Treatment of Pseudomembranous colits

A

Vancomycin / Metroindazole

113
Q

Causative agent of Whipple disease

A

: Tropheryma whippelii
(Gram [+] actinomycete

114
Q

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?

A

Whipple disease

115
Q

Main Clinical symptom of Whipple disease

A

Malabsorbative Diarrhoea –> casued by Impaired Lymphatic transport

116
Q

Patho of Whipple disease ?

A

Accumulation of bacteria-laden macrophages–> in the Synovial membranes of affected joints, cardiac valves, brain and Mesenteric lymph nodes

117
Q

Clinical presentaions of Whipple disease

A

Triad of:
1) Diarrhoea
2) Weight loss
3) Malabsorption

118
Q

Complications of Ischeamic bowel disease

A

Break down of mucosal barrier –> Bacteria enter the circulation –> Sepsis

Pathology (11 decks)

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