GIT Pathology Flashcards

1
Q

What is an ulcer

A

A breach in the continuity of skin, epithelium or mucous membrane caused by sloughing out of inflammed necrotic tissue
In the stomach, when it involves the mucosa and submucosa?

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2
Q

What is an erosion

A

Typically chxd by partial loss of the epithelium with the bm left intact.
Or inflammation that is limited to the mucosa

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3
Q

About GERD

A

also known as reflux oesophagitis
May be erosive or non erosive
Histology shows:
Inflammatory cells in the surface epithelium
Dilated intercellular spaces
Basal cell hyperplasia

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4
Q

Aetiology factors for GERD

A

Dan’s Pc
D- delayed gastric emptying
A-alcohol
N-nasogratric tube
S- sliding hernia
P-pregnancy
C-cigarette smoking

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5
Q

What is GERD

A

An upper Gi chronic disease in which stomach contents continuously flow up into the esophagus resulting in symptoms and or complications

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6
Q

Symptoms and complications of GERD

A

Symptoms
Heartburn
Regurgitation
Odynophagia
Dysphagia
Non cardiac chest pain

Complications
Esophagus
Esophageal stricture
Barrett’s esophagus

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7
Q

What is Barretts esophagus

A

Barrett’s esophagusis a condition in which there is an abnormal (metaplastic) change in themucosalcells lining the lower portion of theesophagus, fromstratified squamous epitheliumtosimple columnar epitheliumwith interspersedgoblet cellsthat are normally present only in thesmall intestineandlarge intestine

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8
Q

Acute hemorrhagic gastritis

A

Also known as erosive gastritis
Basically a focal mucosal erosion with necrosis, hemorrhage and inflammation .
What is erosion?

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9
Q

In acute hemorrhagic gastritis, the margins and base of the erosion are indurated and red from hemorrhage. T/f

A

F….they are NOT indurated

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10
Q

Symptoms of ahg

A

Could be asymptomatic, nausea ,pain, vomiting
Hematemesis

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11
Q

Causes of ahg

A

NSAIDs e.g. aspirin
– steroid therapy
– cancer chemotherapy and radiotherapy
– alcohol abuse
– caffeine
– cigarette smoking
– bacterial infections and sepsis
– extensive burn injury (Curling’s ulcer)
– emotional stress
– shock syndrome
– portal hypertension
– corrosive ingestion
– increased intracranial pressure (Cushing’s ulcer)

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12
Q

What are the stress ulcers

A

Curling ulcer
Cushing’s ulcer

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13
Q

What is curling’s ulcer

A

Curling’s ulceris an acute gastric erosion resulting as a complication from severe burns when reducedplasmavolume leads to ischemia and cell necrosis (sloughing) of thegastric mucosa

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14
Q

What is Cushing’s ulcer

A

The mechanism of development of Cushing ulcers is thought to be due to direct stimulation of vagal nuclei as a result of increasedintracranial pressure. Brain tumors, traumatic head injury, and other intracranial processes including infections, can cause increased intracranial pressure and lead to overstimulation of the vagus nerve.[3]Efferentfibers of thevagus nervethen releaseacetylcholineonto gastricparietal cellM3receptors, causing insertion ofhydrogen potassium ATPasevesicles into the apical plasma membrane. The end result is increased secretion ofgastric acidwith eventual ulceration of the gastric mucosa.

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15
Q

Pathogenesis of ahg

A

Increased acid secretions
Decreased bicarbonate secretions
Decreased gastric emptying
Hypoperfusion of gastric mucosa
Vagal hyperstimulation

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16
Q

Acute hemorrhagic gastritis involves erosion that may coalesce to form ulcers when severe. T/f

A

T

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17
Q

Peptic ulcer disease

A

Affects any organ that becomes lined by gastric mucosa
• Chronic, usually solitary
• Age: 30-60yrs
• Biopsy recommened to r/o malignancy presenting as ulcer

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18
Q

Cross match the blood groups in pud

A

Blood group O-duodenal ulcer
A-Gastric ulcer

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19
Q

Aetiology of pud

A

Genetic: 4X more common in first degree relatives; blood
group O for duodenal
– Medications: NSAIDs, steroids
– Helicobacter pylori chronic gastritis
– Hormonal hypersection: gastrin (Zollinger-Ellison syndrome,
gastrinoma)
– Psychological stress: business executives; medical students
(3rd & 4th yr especially) and medical practioners
– Cigarette smoking (diets like caffeine, alcohol, etc. are
unproven)
– Liver cirrhosis
– α1-antitrypsin deficiency

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20
Q

How does alpha 1- antitrypsin deficiency cause pud

A

So basically yh, alpha anti trypsin is an enzyme that inhibits activation of trypsinogen to trypsin..which is a pancreatic enzyme
So when there is deficiency, activity of trypsin continues uninhibited and thus there’ll be digestion of tissues…including the duodenum leading to duodenal ulcers

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21
Q

Petechial erosion is a feature of

A

Acute hemorrhagic gastritis

22
Q

The commonest site for pud is

A

First part of the duodenum…typically affects the gastroduodenal artery

23
Q

In the stomach, gastric ulcers typically appear where, and affect what artery

A

Lesser curvature, affects the left gastric artery.

24
Q

What part of the esophagus is affected in pud

A

Distal part,related to gerd

25
When puds become multiple in the duodenum and jejenum rather than solitary,then think of?
Zollinger Ellison syndrome or gastrinomas
26
The margins in pud are typically raised or heaped up. T/f
False, they are PUNCHED OUT or less commonly undermined
27
The base of an ulcer in pud consists of
A mixture of fibrin, necrotic tissue, neutrophils and granulation tissue
28
Gastric ulcers occur when
Greater after meals Whereas duodenal ulcers are decreased after meals
29
Typhoid fever triad
Fever Bloody diarrhea Perforation with peritonitis
30
Typhoid fever typically affects?
The terminal ileum with longitudinal ulcers overlying the Peyer's patches
31
Typhoid histiocytes implies that the lesion is rich in neutrophils and poor in macrophages. T/f
F...rather its rich in macrophages and poor in neutrophils
32
The principal cause of acute abdomen is
Appendicitis(right iliac fossa pain)
33
Aetiologic agents of appendicitis
faecoliths, worms, endogenous and exogenous stones and hyperplastic lymphoid tissue in the wall . Basically block the appendiceal neck lumen
34
Distant complications of appendicitis
(a) rupture; (b) peritonitis; (c) septic shock syndrome; (d) portal vein thrombophebitis with pre hepatic ph...death
35
Intestinal obstruction are classified into 3
Intramural Mural Extramural
36
In all cases, the clinical manifestation of intestinal obstruction is
Acute abdomen with pain Fever Vomiting and shock
37
What is a volvulus
A volvulus is when a loop of intestine twists around itself and the mesentery that supports it, resulting in a bowel obstruction
38
What is intussuseption
Occurs when a portion of bowel (intussuscipiens) swallows another length of bowel (intussusceptum) • Usually during first 5 years of life, 50% within first year
39
The point of traction or leading point for intussusception is
A mass lesion
40
Causes of intussusception
– lymphoid hyperplasia (common in children; from viral infections) – tumours like intramural lipoma or leiomyoma or carcinoma – diarrhoea – idiopathic
41
What is a hernia
A protrusion of am organ through an abnormal defect in the wall of the cavity containing it
42
Commonest carcinom in the esophagus and anus
Squamous cell carcinoma
43
Commonest carcinoma in the stomach
Adenocarcinoma
44
Commonest carcinoma in the intestine
Neuroendocrine carcinoma
45
Oesophago-gastro-intestinal tumors could be
Endophytic Endo exophytic Exophytic
46
Oesophago-gastro-intestinal tumors are usually
ulcerated with variable lymph node and distant metastasis
47
In children, volvulus typically occurs in what organ
Midgut
48
In adults, volvulus typically occurs in what organ
Sigmoid-seniors
49
Yellow glassy stones are known as
Pure cholesterol stones
50
Brown multifaceted stones are known as
Mixed cholesterol stones