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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
Pathogenesis of Ulcers associated with brain injury
Direct stimulation of vagal nuclei --> Gastric acid hypersecretion
26
Pathogenesis of Ulcers associated with critically ill patients (Stress ulcres)
Systemic acidosis --> Decrease in intracellular pH of mucosal cells --> Mucosal injury
27
Clinical features of Acute peptic ulcers
1) Nausea 2) Vomiting 3) Haematemesis
28
Complications of Acute peptic ulcer
Perforation
29
Treatment of Acute peptic ulcer
1) Proton pump inhibitors 2) Histamine H2 receptor antagonists
30
Causes of Peptic Ulcer disease
1) H. pylori infection (most common) 2)NSAID
31
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
32
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
33
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
33
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
34
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
35
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**
36
Localisation of MENETRIER DISEASE
Centred along the greater curvature
37
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
38
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
39
clinical features of MENETRIER DISEASE
1) Hypochlorhydria or achlorhydria 2) hypoproteinaemia
40
DD of Menetrier disease
Malignant Lymphoma or Carcinoma
41
Management of Menetrier Disease?
* Adults: Fully developed disease is progressive —> requires **subtotal gastrectomy** * Paediatric cases --> **self-limited disease**
42
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
43
Inflammatory infiltrates in Type A and B Chronic Atrophic Gastritis
Type A --> Macrophages, lymphocytes Type B --> Neutrophils, subepithelial plasma cells
44
Round; Size: <1cm Ulcer base: Brown to black Are feautes of what type of ulcer?
Acute ulcer
45
Macro: Sharply demarcated Normal adjacent mucosa Are the features of what type of ulcer?
Acute stress ulcer
46
Microscopic findings: Layers of Ulcer: --> Necrotic debris --> Mainly, neutrophilic infiltration Are what type of ulcer?
Acute peptic ucler
47
epi of INFLAMMATORY & HYPERPLASTIC POLYPS
75% of all gastric polyps; Individuals 50-60 yrs.
48
patho of inflammatory & hyperplastic polyps
Chronic gastritis --> Injury and reactive hyperplasia --> Development of polyp
49
Macroscopy: - Ovoid lesions; Size: <1cm; Smooth surface what type of neoplasm?
INFLAMMATORY & HYPERPLASTIC POLYPS
50
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
51
Epi of Fundic gland polyps
- Sporadic occurrence - Persons with Familial Adenomatous Polyposis
52
casuse/ patho of fundic gland polyps
Proton pump inhibitors --> **Reduced acidity** --> **Increased Gastrin secretion** --> **Glandular hyperplasia**
53
Clinical featurs of Fundic gland poylps
1) Nausea; 2) Vomiting; 3) Epigastric pain
54
Macroscopy: Well-circumscribed polyps in the **gastric body and fundus** feature of what type of gastric neoplasm?
fundic gland polyps
55
Microscopy: - Cystically **dilated, irregular glands** - Lining of the glands: **Flattened parietal and chief cells** features of what type of gastric neoplasm?
Fundic gland polyps
56
Epi of gastric adenoma
-10% of all gastric polyps - Ages: 50-60 yrs.; M:F = 3:1
57
cause/patho of Gastric andenoma
Chronic gastritis --> Atrophy and intestinal metaplasia
58
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
59
location of gastric adenoma
Antrum of the stomach
60
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
61
Cause of Zollinger Ellison Syndrom aka **Gastrinomas**
uncontrolled gastrin secretion (gastrin secreting-tumors)
62
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
63
Clinical manifestaions of Zollinger elisson syndrome
1) Duodenal ulcers 2) Chronic diarrhoea
64
Treatment of Zollinger Ellison syndrom
Blockade of acid hypersecretion: 1) Proton pump inhibitors or 2) High-dose H2 histamine receptor antagonists
65
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
66
epi of Carcinoma of the stomach
1) >50 yrs 2) Men > Women 3) blood group A persons
67
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)
68
**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
69
Cause of Intestinal Type Gastric cancer
Germline mutations in **Adenomatous Polyposis Coli (APC) genes** (patients with FAP) *Familial adenomatous polyposis (FAP)
70
Patient with E-cadherin gene mutations develop what type of cancer?
1) **Diffuse** Gastric carnimoa 2) **Lobular CA** of the breast
71
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
72
location of Gastric carcinoma
**Minor curvature of the antrum or pre-pyloric region** --> Spread to the adjacent organs, peritoneum, regional lymph nodes and liver
73
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
74
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**)
75
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)
76
most common type of Lymphoma of the stomach
Extranodal Marginal Zone B-cell Lymphoma (MALT)
77
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
78
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)
79
**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 (-)
80
Epi of Large B-cell Lymphoma
>50 yrs
81
Clinical manifestations of Large B-cell Lymphoma
**Large palpable mass** (and still excellent physical condition of the patients)
82
Macroscopic findings: * **Large lobulated** (sometimes polypoid) mass * Commonly, **superficial or deep CENTRAL ulceration** Features of what type of gastric carcinoma?
LARGE B-CELL LYMPHOMA
83
loc. of LARGE B-CELL LYMPHOMA
Distal half of the stomach, with a tendency to spare the pylorus
84
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
85
Gastric Carcinoids are associated with?
1) Endocrine cell hyperplasia 2) Chronic atrophic gastritis 3) Zollinger-Ellison syndrome
86
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
87
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
88
Immunohistochemistry of Carcinoid tumours
1) Neuron-Specific Enolase (NSE), 2) Chromogranin, 3) Synaptophysin
89
clincial features of Carcinoid tumours
1)Cutaneous flushing 2) Sweating 3) Bronchospasm 4) Colicky abdominal pain 5) Diarrhoea
90
location of **GASTRO-INTESTINAL STROMAL TUMOUR (GIST)**
1) Submucosa of stomach, 2) small and large intestine and 3) extra-gastrointestinal sites
91
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**
92
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
93
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)
94
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
95
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
96
causes of Intestinal Hypoperfusion
1) Cardiac failure 2) Shock 3) Vasculitides (PAN, Henoch-Schönlein purpura, Wegener granulomatosis, etc.)
97
The 2 phases of Isheamic bowel disease (intestinal respose to Iscaemia)
1) **First phase** : Occurrence of initial **hypoxic injury**at 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
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
99
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
100
**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
101
calssification of Diarrhoea
1. Secretory diarrhoea 2. Osmotic diarrhoea 3. Malabsorbative Diarrhoea 4. Exudative Diarrhoea
102
loction of coeliac disease
Second portion of duodenum or proximal jejunum
103
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
104
Coeliac disesae results in what kind of Defects?
1) Terminal Digestion 2) Trans-epithelial transport
105
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**
106
**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
107
**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)
108
Pseudomemebranous colitis is aka ?
Antibiotic-associated diarrhoea
109
casue of pseudomembranous colitis
Clostridium difficile
110
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
111
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
112
Treatment of Pseudomembranous colits
Vancomycin / Metroindazole
113
Causative agent of Whipple disease
: Tropheryma whippelii (Gram [+] actinomycete
114
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
115
Main Clinical symptom of Whipple disease
Malabsorbative Diarrhoea --> casued by **Impaired Lymphatic transport**
116
Patho of Whipple disease ?
**Accumulation of bacteria-laden macrophages**--> in the Synovial membranes of affected joints, cardiac valves, brain and Mesenteric lymph nodes
117
Clinical presentaions of Whipple disease
Triad of: 1) Diarrhoea 2) Weight loss 3) Malabsorption
118
Complications of Ischeamic bowel disease
Break down of mucosal barrier --> Bacteria enter the circulation --> **Sepsis**

Pathology (11 decks)

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