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Medicine year 1 semester 2 > Case 11- Pathology > Flashcards

Case 11- Pathology Flashcards

1
Q

Oesophagitis

A

Inflammation of the oesophageal mucosa

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2
Q

Causes of Oesophagitis

A

CRAMPS V

Chemical injury by acidic/alkaline solutions
Radiation therapy
Alcohol abuse
Medications
Physical injury
Surgery
Vomiting

Most important cause is reflux of gastric contents in to the lower oesophagus i.e. GORD

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3
Q

Gastro-oesophageal reflux (GOR)

A

When the stomach contents move back up the oesophagus. Having GOR once in a while is common

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4
Q

Gastro-oesophageal reflux disease (GORD)

A

Symptoms or mucosal damage produced by the abdominal reflux of gastric contents into the oesophagus. Often chronic and relapsing. Acid reflux from the stomach.

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5
Q

Symptoms of GORD and Oesophagitis

A

Regular heartburn, a painful burning sensation in the middle of your chest behind the sternum (breastbone) and in the middle of the abdomen. Taste of food or acid in the back of your mouth.

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6
Q

Common GORD symptoms

A

Bad breath, nausea, pain in your chest or the upper part of your abdomen, problems swallowing or painful swallowing, respiratory problems and vomiting.

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7
Q

Causes of GORD

A

RETCH

Resistance= mucosal resistance is reduced, junctional complexes break down and allow acid to enter the mucosa. Reduced bicarbonate

Emptying= decrease in gastric emptying increases the likelihood and frequency of reflux

Tone= Lower oesophageal sphincter tone is reduced, due to pregnancy, obesity and medication

Clearance= oesophageal clearance is reduced, reduction in salivary flow and production. Seen in smokers, the elderly, alcohol

Hernia= loose hiatus muscles in the diaphragm, allows contents from the stomach to enter the oesophagus

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8
Q

Two main symptoms of GORD

A

Symptoms:
Heartburn- aggravated by fatty/spicy/acidic foods. Most common nocturnally
Acid regurgitation- bitter taste in mouth. Bad breath, nausea, dysphagia, vomiting

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9
Q

Diagnosis of GORD/ oesophagitis

A
  • Clinical- symptoms of heartburn
  • Endoscopic- red/congested mucosa
  • Manometric- decreased sphincter pressure
  • pH- below 4
  • Pathological- microscopic evidence of oesophagitis i.e. the presence of acidification and necrotic cells
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10
Q

Complications of GORD

A

Oesophageal stricture- damage to cells cause scar tissue formation and narrowing of the oesophagus leading to dysphagia
Oesophageal bleeding- can cause ulceration which can haemorrhage
Oesophageal ulcers - where mucosal erosion extends to the submucosa and beyond
Barrett’s Oesophagus

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11
Q

Gastritis

A

Inflammation of the stomach lining

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12
Q

Gastritis symptoms

A

Vomiting, bloating, abdominal pain, nausea, burning and anorexia

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13
Q

Gastritis risk factors

A

Unhealthy food, drug induced (NSAID), H-pylori/ infection, alcohol, spicy food, smoking, reflux

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14
Q

How NSAIDs cause gastritis

A

NSAIDs inhibit gastroduodenal prostaglandin synthesis, resulting in reduced secretion of mucus and bicarbonate and decreased mucosal blood flow. These factors are normally protective of the mucosa and the balance of mucosal protection/acidic attack can be upset, promoting ulcer formation.

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15
Q

Acute gastritis

A

Associated with neutrophil infiltration
Surface erosion causing severe mucosal damage
Haemorrhage development
Erosion of the epithelium doesn’t cross the muscularis mucosa, unlike in peptic ulcers

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16
Q

Acute gastritis- aggressive factors and protective factors

A

Due to an imbalance in aggressive factors and protective factors.
Aggressive factors- increased acid secretion with back diffusion.
Protective factors- decreased production of a bicarbonate buffer. Reduced blood flow and disruption of the adherent mucus layer. Direct damage to the epithelium.

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17
Q

Pathogenesis of acute gastritis

A

Triggers lead to increase in acid secretion and decrease in protective factors
Decreased bicarbonate production
Direct damage to epithelium

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18
Q

Acute gastritis symptoms

A

Abdominal pain
Haematemesis
Nausea
Heartburn

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19
Q

Chronic gastritis

A

Associated with lymphocytes and plasma cells. The presence of chronic mucosal inflammatory changes leading eventually to mucosal atrophy and intestinal metaplasia. Mucosal atrophy is loss of gastric glandular cells. Loss of gastric glandular cells
Intestinal metaplasia = surface, glandular and foveolar epithelia are replaced by intestinal epithelium

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20
Q

Causes of chronic gastritis

A
  • Autoimmune
  • Bacterial- H.pylori (90%)
  • Chemical- bile and bicarbonate, pyloric bypass operations, gallstones and disorganised motility
  • Drugs- Aspirin, NSAID
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21
Q

Symptoms of chronic gastritis

A

Often asymptomatic. Associated with epigastric pain, nausea and vomiting

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22
Q

Peptic ulcer disease

A

Tissue necrosis of the mucosa of the alimentary tract (stomach, lower oesophagus or small intestine) which extends through the muscularis mucosa into the submucosa or deeper. It is an open sore in the lining of the stomach and duodenum.

23
Q

Symptoms of peptic ulcer disease

A

Vomiting, bloating, abdominal pain, nausea, burning pain in the abdomen and anorexia

24
Q

Risk factors for peptic ulcer disease

A

Family history, unhealthy food, drug induced (NSAID), H.Pylori/infection and stress.

25
Q

Peptic ulcer vs Peptic erosion

A

Erosion= a defect occurring above the muscularis mucosa, doesnt transverse this layer

Ulcer= breaches through the muscularis mucosa in to the submucosa, can even go deeper to where the blood vessels are. Slower to heal

26
Q

Acute ulcers and chronic ulcers

A

Acute ulcers = normally due to severe stress or chemical injury
Chronic ulcers = normally due to H.pylori infection

27
Q

What causes an ulcer

A

It results from the loss of balance between the mucosal defence and the acid attack. These normal gastric defence are damaged by exposure to injurious agents. This then leads to destruction and erosion of the mucosa.

28
Q

Mechanisms of normal gastric defence

A
  • Surface mucus secretion.
  • Bicarbonate secretion into the mucus.
  • Mucosal blood flow
  • Membrane transport within the apical surface
  • Epithelial regenerative capacity
  • Prostaglandin synthesis
29
Q

Parts of an ulcer

A

An ulcer is split into the exudate and necrotic tissue on top, the granulation tissue in the middle and fibrous tissue at the bottom.

30
Q

Major complications of Peptic ulcers

A

1) Haemorrhage- may be fatal or cause Iron deficient anaemia
2) Perforation of the GI tract- stomach contents spill into abdominal cavity, leads to acute peritonitis
3) Penetration- ulcer perforates into nearby organs
4) Cancer- Increased risk when H.pylori caused the ulcer
5) Fibrosis- obstructs pylorus, patients will have an hourglass stomach
6) Gastric outlet obstruction — this may result from strictures and stenosis of the pylorus and/or duodenum due to chronic inflammation and scarring.

31
Q

Gastric ulcer

A

Pain 1-2 hours after food intake. Presents with Hematemesis (coffee ground blood in vomit), weight loss, equal in both sexes. Melena (sticky dark faeces). Heartburn, chest discomfort and early satiety are commonly seen. Can cause gastric carcinoma. Occurs in the stomach at the lesser curvature and Antrum. Not associated with nocturnal wakening

32
Q

Duodenal ulcer

A

Pain 2-5 hours after food intake (relieved by food). There is Melena (digested blood in stool). You get weight gain and night waking. It is more common in males. Occurs in the first part of the duodenum. Heartburn and chest discomfort are less common but can be seen. The pain may keep the patient up at night.

33
Q

Gastric mucosal protection- diffusion barrier

A

Lubricates and protects the stomach from its contents.
• Anatomical barrier- resistant epithelium (apical membrane and tight junctions between cells in gastric glands are relatively impermeable to H+).
• Physiological barrier- mucus gel layer and bicarbonate.

34
Q

Features that warrant a gastroenterology referral

A
  • Bleeding or anemia
  • Early satiety
  • Unexplained weight loss
  • Progressive dysphagia or odynophagia
  • Recurrent vomiting
  • Family history of gastrointestinal cancer
35
Q

Barrett’s Oesophagus

A

A pre-cancerous state caused by long-standing GORD. Can progress to adenocarcinoma

Chronic damage due to acid exposure as a result of the malfunction of the lower oesophageal sphincter. Promotes inflammatory response
Ultimately leading to epithelial necrosis
Believed to promote metaplasia of the stratified squamous epithelia to simple columnar epithelia

36
Q

Progression of Barrett’s Oesophagus

A

Normal oesophageal epithelium –> Barrett oesophagus –> Dysplastic Barrett oesophagus –> Oesophageal adenocarcinoma

37
Q

Diagnosing Barrett’s Oesophagus

A

Barrett’s oesophagus on a OGD (Esophagogastroduodenoscopy) in combination with histological changes. Instead of the oesophagus being lined with normal stratified squamous cells it is lined by simple columnar epithelium with interspersed goblet cells. There will also be increased immune cells.

38
Q

Mechanism of action of cancer formation in the Oesophagus

A

1) Normal stratified squamous epithelium lining of the oesophagus.
2) There is exposure to causative risk factors leading to metaplasia. This is the replacement of normal stratified squamous epithelium lining of the oesophagus with simple columnar epithelium with or without goblet cells.
3) Further dysplasia- abnormal cell growth and cell differentiation
4) Transformation and oesophageal Adenocarcinoma formation (oesophageal cancer).
5) Adenocarcinoma local invasion and secondary site metastasis (spread)

39
Q

Upper GI neoplasm

A
  • Squamous cell carcinomas- usually upper or mid oesophagus. Often detected when malignant, so have reached the basement membrane.
  • Adenocarcinomas- lower oesophagus, stomach and small intestine. The stomach is glandular in structure hence why there is a lot of adenocarcinomas. Often detected when malignant, so have reached the basement membrane.
  • Rare- gastrointestinal stromal tumours (GIST) and Lymphoma (lymphocytes change and grow out of control)
40
Q

When to consider an OGD endoscopy

A 
DOC ALARM
• Dysphagia (difficulty swallowing)
• Odynophagia (pain swallowing)
• Choking
• Anaemia
• Loss of weight
• Age (over 55)
• Recent onset or progressive symptoms
• Melaena / haematemesis
41
Q

Risk factors for upper GI neoplasms

A

Smoking, alcohol, Barrett’s Oesophagus, Asbestos

42
Q

Oesophageal cancer

A

Most Oesophageal cancers are malignant, fewer then 1% are benign

43
Q

Oesophagus- Squamous cell carcinoma

A

90% of oesophageal cancer worldwide. Squamous cells line the oesophagus. Tend to be found in the upper and middle oesophagus

44
Q

Oesophagus- Adenocarcinomas

A

Arises from the superficial and deep glands of the oesophagus, mainly in the lower third of the oesophagus, especially near the gastroesophageal junction. Is a progression of Barrett’s Oesophagus.

45
Q

Epidemiology Oesophageal cancer

A

The rate is three times higher in men than women. The highest rate are found within the Middle East, South Africa, northern China, southern Russia and India. More likely to get it when older.

46
Q

Risk factors for Oesophageal cancer

A 
Alcohol
Smoking
Poor diet
Genetics e.g. peutz-jeghers syndrome
Predisposing conditions e.g. Barretts Oesophagus, diverticula
47
Q

Symptoms of Oesophageal cancer

A
  • Dysphagia- difficulty swallowing
  • Odynophagia- pain when swallowing
  • Weight loss
  • Acid reflux / substernal heart burn
  • Dyspnoea, cough, hoarseness and pain in the retro-sternal, back or right upper abdomen.
48
Q

Types of Gastric Neoplasia

A
  • Adenocarcinomas- more then 90% of stomach cancers develop in the cells of the glandular stomach lining. Derived from columnar glandular epithelium cells.
  • Gastric lymphoma and MALToma- develop in the lymphatic tissue which is beneath the epithelium.
  • Gastrointestinal stromal tumours (GISTs)- develop in the muscle or connective tissue of the stomach wall.
49
Q

Aetiology of Gastric cancer

A

Genetic factors- pernicious anaemia, family history, BRCA 1/2 mutation, type A blood
Precursor lesions- Mentrier’s disease, dysplasia, chronic strophic gastritis
Environmental factors- H.pylori, low vit A and C, smoking, radiation exposure, poor drinking water

50
Q

Clinical presentation of gastric cancer

A 
Weight loss
Abdominal pain
Anaemia
Dysphagia
Nausea and vomiting
Bloating and indigestion
51
Q

Where in the stomach do gastric cancers arise

A

They mostly arise in the antrum (50%), the gastric body (30%), the fundus or cardia (20%).

52
Q

Diffuse gastric adenocarcinoma

A

The tumour consists of discohesive cells i.e. loose intracellular connection infiltrating through all the layers of the stomach wall. It is accompanied by extensive fibrosis and inflammation. Many tumour cells have large intracytoplasmic vacuoles that push the nucleus to the peripheries creating a signet ring appearance. No know precursor for diffuse type. Discohesive cells dont express E-cadherin which connects cells together

53
Q

Intestinal gastric carcinoma

A

A type of adenocarcinoma of the stomach showing papillary growth patterns. Intestinal type tumours follows a step wise progression from chronic gastritis to intestinal metaplasia, dysplasia, carcinoma in situ and invasive carcinoma.

Medicine year 1 semester 2 (61 decks)

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