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Gastroenterology > Pathology > Flashcards

Pathology Flashcards

1
Q

Causes of acute oesophagitis? Is this common or rare?

A

RARE

  • Corrosive following chemical ingestion (child swallows something they shouldn’t)
  • Infective in immunocompromised pts
    e. g. candidiasis, herpes, CMV
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2
Q

Causes of chronic oesophagitis? Is this common or rare?

A

COMMON

Most common cause is reflux oesophagitis

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3
Q

Common complications of reflux?

A

ulceration (bleeding), stricture (heal by fibrosis, contraction in a hollow organ, you’ll get dysphagia) and Barrett’s oesophagus

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4
Q

Define Barretts oesophagus

A

Replacement of stratified squamous epithelium by columnar epithelium

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5
Q

Complications of Barretts oesophagus?

A

This is unstable mucosa and with continuing damage can get dysplasia and therefore carcinoma of the oesophagus

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6
Q

Describe eosinophilic oesophagitis

A

Rarer cause of oesophagitis
The pH probe is negative for reflux and have high eosinophils
Often in atopic individuals

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7
Q

Are benign oesophageal tumours rare or common? What is the most common type?

A

These are all extremely rare

The most common of these rare tumours is a squamous papilloma

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8
Q

Two types of malignant oesophageal tumour?

A

Squamous cell carcinoma and Adenocarcinoma

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9
Q

In adenocarcinoma of the oesophagus what is the key premalignant change?

A

Barretts oesophagus

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10
Q

Causes of acute gastritis?

A 
This is an irritant chemical injury
•	Severe burns
•	Shock
•	Severe trauma
•	Head Injury
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11
Q

Causes of chronic gastritis?

A
  • Autoimmune
    • Bacterial
    • Chemical
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12
Q

Most common type of chronic gastritis is due to …..

A

H. pylori infection

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13
Q

Rarest type of chronic gastritis is ____ in this there are antibodies to ______

A

auto-immune

parietal cells and intrinsic factor

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14
Q

Chemical gastritis is the ____ most common cause of chronic gastritis it can be due to ___________

A

second

Due to NSAIDs, alcohol, bile reflux

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15
Q

Sites of peptic ulceration?

A

Duodenum (Ist. part), Stomach (junction of body and antrum), Oesophago-gastric Junction

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16
Q

What is ulceration?

A

Breach in the mucosa

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17
Q

In peptic ulcers the two things that are unbalanced are

A

acid and mucosal defence

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18
Q

Complications of peptic ulcers?

A

perforation, penetration, haemorrhage, stenosis and intractable pain

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19
Q

Benign gastric tumours?

A
  • Hyperplastic polyps

- Cystic fundic gland polyps

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20
Q

3 malignant gastric tumours?

A

Adenocarcinomas, GISTs and Lymphomas

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21
Q

What is a key factor in developing gastric tumours?

A

H. pylori infection particularly in gastric lymphomas

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22
Q

Describe the two types of gastric adenocarcinomas

A

Intestinal which is exophytic/ polyploid mass

Diffuse type which expands/infiltrates stomach wall, diffuse type whole stomach is swollen.

Diffuse type is worse cause it usually has no margins so can’t take it out without taking out the whole stomach.

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23
Q

Causes of ischaemia of the small bowel?

A
  • May get a mesenteric arterial occlusion
  • Other reasons for ischaemia could be shock, strangulation (loop of small bowel gets stuck somewhere it shouldn’t), drugs and hyper-viscosity of blood
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24
Q

What part of the small bowel wall is most sensitive to hypoxia?

A

The mucosa as this is the most metabolically active

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25
Q

Explain Meckel’s diverticulum

A

Is an outpouching or bulge in the lower part of the small intestine. The bulge is congenital (present at birth) and is a leftover of the umbilical cord. Meckel’s diverticulum is the most common congenital defect of the gastrointestinal tract.

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26
Q

Primary tumours of the small bowel are quite rare

Secondary tumours (metastases) are much more common usually from the _______________

Primary tumours of the small bowel are most commonly ___________

A

colon, ovary or stomach

lymphomas, neuroendocrine tumours and carcinomas

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27
Q

2 conditions associated with increased risk for carcinoma of the small bowel?

A

Crohn’s and Coeliacs

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28
Q

Pathology of appendicitis?

A

acute inflammation with neutrophils, mucosal ulceration, serosal congestion, exudate, pus in lumen

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29
Q

Coeliacs is strongly associated with

A

childhood diabetes

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30
Q

Definition of Crohn’s disease?

A
  • Chronic inflammatory and ulcerating condition of the GI tract that can affect anywhere from the mouth to the anus
  • Most common in the terminal ileum and colon
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31
Q

Appearance of crohn’s on endoscopy?

A

Ulcerated with mucosal cobblestone appearance

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32
Q

Histological appearance of Crohn’s?

A

Non-caseating granuloma formation, will also be increased inflammatory cells within the lamina propria. Histologically it will all vary throughout the GI tract.

The inflammation is transmural- it extends all the way to the serosa and the disease is discontinuous with skip lesions and normal intervening bowel.

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33
Q

Complications of Crohn’s?

A

Fistula form as the inflammation extends so far through the bowel wall
Intestinal obstruction
Malabsorption of the ileum is involved
Cancer (smaller risk than in ulcerative colitis)

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34
Q

Definition of ulcerative colitis?

A

Chronic inflammatory disorder confined to colon and rectum with inflammation in the mucosa and submucosa nearly always involving the rectum

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35
Q

Histological appearance of ulcerative colitis

A

No granulomas
Ulcers that may be linear
Get swollen curving mucosa forming pseudo-polyps

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36
Q

Complications of ulcerative colitis

A

Toxic megacolon- the inflammation is so severe that the colon becomes greatly dilated and thinned. There is a high risk of perforation with peritonitis.
Dysplasia and Colonic Cancer increased risk

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37
Q

What are the main distinguishing differences between Crohn’s and ulcerative colitis?

A

In ulcerative colitis the lesions are continuous but only in the mucosa. In Crohn’s there are skip lesions that are transmural.

In ulcerative colitis the inflammation tends to begin in the rectum and move up whereas crohn’s has more ill involvement and not always rectal involvement,

Ulcerative colitis has granular, ulcerated mucosa with no fissuring and crowns has discretely ulcerated mucosa with a cobblestone appearance and fissuring.

Ulcerative colitis causes muscular shortening of the colon whereas crohns is fibrous with strictures often forming

In ulcerative colitis, fistulae are rare but malignancy more common. Opposite for crohns

In ulcerative colitis anal lesions are much less common.

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38
Q

What is a polyp?

A

A protrusion above an epithelial surface

39
Q

Why must all adenomas of the colon be removed?

A

They are premalignant

40
Q

Duke’s staging of colorectal carcinomas?

A

Dukes A: Confined by muscularis propria
Dukes B: Through muscularis propria/ externa
Dukes C: Metastatic to lymph nodes

41
Q

Patterns of spread of colorectal cancers?

A

Local invasion: Mesorectum, Peritoneum, Other organs
Lymphatic spread: Mesenteric nodes
Haematogenous: Liver, distant sites

42
Q

Differences between left and right sided colorectal presentations?

A

75% Left sided (rectum, sigmoid, descending)
p/c: Blood PR, Altered bowel habit, Obstruction

25% Right sided (Caecum, Ascending)
p/c: Anaemia, Weight loss

43
Q

Where is diverticular disease most commonly found?

A

The sigmoid colon

44
Q

What is diverticular disease related to?

A

A low fibre diet and increased intraluminal pressure

45
Q

Complications of diverticular disease?

A

inflammation, rupture, abscess, fistula and massive bleeding

46
Q

Histology of ischaemic colitis?

A

withering of crypts, pink smudgy lamina propria and fewer chronic inflammatory cells

47
Q

What is Antibiotic Induced Pseuodomembranous Colitis and what is it treated with?

A

Type of colitis that occurs with patients infected with C difficile due to broad spectrum antibiotics

Treated with vancomycin

48
Q

Explain microscopic colitis and the types

A
  • Two subsets of diseases that are often overlooked due to normal findings on endoscopy
  • Patients present with watery diarrhoea
  • Collagenous colitis results in a thickened basement membrane with a subepithelial collagenous band. Plasma cells are increased in number in the lamina propria
  • Lymphocytic colitis results in a marked increase in intraepithelial lymphocytes akin to those seen in coeliac disease
  • There is no chronic architectural changes to the crypts in either
49
Q

Three main types of jaundice?

A

Pre hepatic, hepatic and post hepatic

50
Q

Describe pre-hepatic jaundice

A

This is due to increased red blood cell destruction, this may be caused by haemolytic anaemia. The increase is in unconjugated bilirubin.

51
Q

Describe hepatic jaundice

A

This is due to liver failure e.g. hepatitis meaning you cannot conjugate bilirubin- the rise is therefore in unconjugated bilirubin.

52
Q

Describe post hepatic jaundice

A

This is caused by failure to excrete conjugated bilirubin. e.g. if a stone was obstructing the common bile duct or there was a carcinoma at the head of the pancreas. The rise is therefore in conjugated bilirubin.

53
Q

Hepatocytes in what zone of the liver acinus are most susceptible to injury?

A

Zone 3

54
Q

Examples of other viruses that can affect the liver but also affect other tissues?

A

Yellow fever
Herpes viruses- Epstein Barr, cytomegalovirus, herpes simplex.
Cosackie A and B
Lassa Fever

55
Q

What is fulminant hepatitis?

A

Rare syndrome of massive necrosis of liver parenchyma and a decrease in liver size (acute yellow atrophy) that usually occurs after infection with certain hepatitis viruses, exposure to toxic agents, or drug-induced injury.

56
Q

What is acute yellow atrophy of the liver?

A

Loss of substance in liver with remaining liver tissue turning an opaque yellowish colour without markings and largely necrotic. There is bile duct hyperplasia

57
Q

What is the definition of chronic hepatitis?

A

Inflammation of the liver which lasts for more than 6 months

58
Q

What are the four main causes of chronic hepatitis?

A

1) Persistent viral infection- B, D or C
2) Auto-immune hepatitis- especially in young women
3) Drugs
4) Metabolic disorders- AAT deficiency and Wilsons

59
Q

What is cirrhosis defined as?

A

A diffuse process (ie the whole liver is affected) characterised by fibrosis and conversion of the liver architecture into abnormal nodules.

60
Q

Cellular mechanism of liver fibrosis?

A

Hepatic stellate/ Ito cells (fat storing) found in the space of Disse are activated and transformed into myofibroblasq-like cells under the influence of cytokines such as TGF-alpha, PDGF and TGF-beta. These activated cells synthesis collagen leading to fibrosis.

61
Q

3 major complications of cirrhosis?

A

Hepatocellular failure
Portal hypertension
Hepatocellular carcinoma

62
Q

3 main forms of alcoholic liver disease? Which are reversible?

A 
Fatty liver (most individuals and is reversible on withdrawal)
Alcoholic Hepatitis (mainly reversible)
Alcoholic Cirrhosis (irreversible)
63
Q

Describe alcoholic fatty liver

A

This occurs in most heavy drinkers even after a single episode of heavy intake. Fat accumulates in hepatocytes due to abnormalities in the intermediate metabolism of lipids and carbohydrates. Known as steatosis (abnormal retention of lipids).

64
Q

Describe alcoholic hepatitis

A

This happens in heavy drinkers and get liver swelling, liver cell necrosis, neutrophil polymorph infiltration, pericellular fibrosis.

65
Q

Describe Non-alcoholic fatty liver disease (NAFLD)?

A

This is a fatty liver condition that develops in patients who do not drink alcohol. The liver may show steatosis, steatohepatitis or cirrhosis, the changes are often less marked than those seen with alcohol. It is associated with metabolic syndromes of obesity, insulin resistance, dyslipidaemia or hypertension.

66
Q

Difference between NASH and NAFLD?

A

NAFLD is fatty liver but NASH has inflammation and liver cell damage

67
Q

3 examples of autoimmune liver diseases?

A

Primary biliary cirrhosis
Primary sclerosis cholangitis
Autoimmune hepatitis

68
Q

What is primary biliary cirrhosis?

A

A chronic autoimmune disorder than mainly affects middle-aged women. There is destruction of intra-hepatic bile ducts leading to scarring and eventually cirrhosis. Most patients have anti-mitochondrial antibodies in their serum and there can be an overlap with chronic auto-immune hepatitis.

69
Q

What is primary sclerosing cholangitis?

A

This is an autoimmune disease that attacks the bile ducts, both intra and extra hepatic. It is usually men that are affected and there is a strong association with ulcerative colitis.

70
Q

What is chronic auto-immune hepatitis?

A
  • Commoner in females
  • Associated with other AI diseases
  • Chronic hepatitis pattern
  • Numerous plasma cells
  • Autoantibodies to smooth muscle, nuclear or LKM, raised IgG
  • May have triggers, including some drugs
71
Q

3 liver storage diseases?

A

1) Haemochromatosis- too much iron
2) Wilson’s disease- too much copper
3) AAT deficiency- protease inbalance- destruction of liver and lung tissue

72
Q

Someone presents with diabetes and funny bronze colour to skin think?

A

Haemochromatosis

73
Q

Child presents with liver disease and gold ring around eye think?

A

Wilsons disease

74
Q

Someone presents with emphysema and liver disease think?

A

AAT Deficiency

75
Q

The most common tumours of the liver are?

A

Secondary metastases commonly from GI tract, lung and breast.

76
Q

What is the most common primary malignancy of the liver? What is it associated with?

A

Hepatocellular carcinoma

Viral Hepatitis and Cirrhosis

77
Q

What is Cholecystitis?

A

inflammation of the gallbladder, it is usually associated with gall stones

78
Q

What is Cholangitis?

A

inflammation of the bile duct system

79
Q

What is colic?

A

Severe pain in the abdomen caused by wind or obstruction

80
Q

What is Cholelithiasis?

A

The formation of gall stones

81
Q

Gallstones form when there is an imbalance between the ________1_____________
Cholesterol stones are associated with _____2______ in the bile- associated with ____________3____________
Bile pigment stones are associated with _______________4________________
Most gall stones are ______5_______

A

1) ratio of cholesterol to bile salts disrupting micelle formation
2) excessive cholesterol
3) diabetes, obesity, females and genetic factors
4) chronic haemolysis with excess bilirubin production- the excess bilirubin cannot be dissolved into the bile salts
5) a mixture of both

82
Q

Describe acute cholecystitis

A
  • Occurs when gallstones are obstructing outflow of bile
  • The gall bladder Initially sterile, then becomes infected
  • May cause empyema, rupture, peritonitis
83
Q

Describe chronic cholecystitis

A
  • May develop insidiously or after bouts of acute cholecystitis
  • In the majority of cases the symptoms are of vague indigestion, intolerance of fatty foods and vague right hypochondrial pain
  • The gallbladder is packed with gall stones and the wall is thickened and fibrosed
84
Q

What happens when there are stones in the common bile duct?

A

This is a complication of gall stones and this can cause obstructive jaundice as well as ascending infection (cholangitis) and acute pancreatitis

85
Q

What is gallstone ileus?

A

Rare form of small bowel obstruction- a stone may ulcerate through the gallbladder into the intestine and cause obstruction

86
Q

Describe carcinoma of the gallbladder? What is it associated with?

A
  • This is rare but almost always associated with gallstones

* Most cases are adenocarcinomas which spread directly to the liver

87
Q

What is cholangiocarcinoma? What is it associated with?

A

Carcinoma of the bile ducts. This is associated with ulcerative colitis and primary sclerosing cholangitis and presents with obstructive jaundice

88
Q

What does acute pancreatitis present with? What is it associated with?

A
  • This presents with sudden acute onset of abdominal pain, patients may be severely shocked and will have elevated serum amylase
  • Main causes are gall stones and alcohol
89
Q

Initiating event of acute pancreatitis caused by gall stones?

A

Bile reflux is the initiating event, stones can pass down the bile duct and block the ampulla of vater causing reflux of bile along the pancreatic duct

90
Q

What happens in acute pancreatitis?

A
  • The loss of the protective sphincter also autodigestion of the pancreatic acini.
  • There is release of lytic pancreatic enzymes proteases and lipases
  • Intra- and peripancreatic fat necrosis by lipases
  • Tissue destruction and haemorrhage by proteases
91
Q

Main complications of acute pancreatitis?

A

Shock and pancreatic pseuodcyst

92
Q

Who does chronic pancreatitis predominantly effect? What happens?

A
  • This predominantly affects alcoholics.

* There is replacement of pancreas by chronic inflammation and scar tissue and destruction of exocrine acini and islets

93
Q

Where do the majority of carcinomas of the pancreas occur?

A

In the head of the pancreas

94
Q

What will carcinomas of the head of the pancreas often present with? Why?

A

Carcinomas in the head will often obstruct the bile duct and therefore present with jaundice.

Gastroenterology (28 decks)

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