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Morbid Anatomy > GIT Pathology > Flashcards

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
Q

When puds become multiple in the duodenum and jejenum rather than solitary,then think of?

A

Zollinger Ellison syndrome or gastrinomas

26
Q

The margins in pud are typically raised or heaped up. T/f

A

False, they are PUNCHED OUT or less commonly undermined

27
Q

The base of an ulcer in pud consists of

A

A mixture of fibrin, necrotic tissue,
neutrophils and granulation tissue

28
Q

Gastric ulcers occur when

A

Greater after meals
Whereas duodenal ulcers are decreased after meals

29
Q

Typhoid fever triad

A

Fever
Bloody diarrhea
Perforation with peritonitis

30
Q

Typhoid fever typically affects?

A

The terminal ileum with longitudinal ulcers overlying the Peyer’s patches

31
Q

Typhoid histiocytes implies that the lesion is rich in neutrophils and poor in macrophages. T/f

A

F…rather its rich in macrophages and poor in neutrophils

32
Q

The principal cause of acute abdomen is

A

Appendicitis(right iliac fossa pain)

33
Q

Aetiologic agents of appendicitis

A

faecoliths, worms,
endogenous and exogenous stones and hyperplastic lymphoid
tissue in the wall
.
Basically block the appendiceal neck lumen

34
Q

Distant complications of appendicitis

A

(a) rupture; (b) peritonitis; (c) septic
shock syndrome; (d) portal vein thrombophebitis with pre hepatic ph…death

35
Q

Intestinal obstruction are classified into 3

A

Intramural
Mural
Extramural

36
Q

In all cases, the clinical manifestation of intestinal obstruction is

A

Acute abdomen with pain
Fever
Vomiting and shock

37
Q

What is a volvulus

A

Avolvulusis when a loop ofintestinetwists around itself and themesenterythat supports it, resulting in abowel obstruction

38
Q

What is intussuseption

A

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
Q

The point of traction or leading point for intussusception is

A

A mass lesion

40
Q

Causes of intussusception

A

– lymphoid hyperplasia (common in children; from viral
infections)
– tumours like intramural lipoma or leiomyoma or carcinoma
– diarrhoea
– idiopathic

41
Q

What is a hernia

A

A protrusion of am organ through an abnormal defect in the wall of the cavity containing it

42
Q

Commonest carcinom in the esophagus and anus

A

Squamous cell carcinoma

43
Q

Commonest carcinoma in the stomach

A

Adenocarcinoma

44
Q

Commonest carcinoma in the intestine

A

Neuroendocrine carcinoma

45
Q

Oesophago-gastro-intestinal tumors could be

A

Endophytic
Endo exophytic
Exophytic

46
Q

Oesophago-gastro-intestinal tumors are usually

A

ulcerated with variable lymph node and
distant metastasis

47
Q

In children, volvulus typically occurs in what organ

A

Midgut

48
Q

In adults, volvulus typically occurs in what organ

A

Sigmoid-seniors

49
Q

Yellow glassy stones are known as

A

Pure cholesterol stones

50
Q

Brown multifaceted stones are known as

A

Mixed cholesterol stones

Morbid Anatomy (6 decks)

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