Alimentary Pathology Flashcards

1
Q

What is the aetiology of Reflux Oesophagitis

A
  • Frequent relaxations of the LOS
  • Low LOS pressure
  • Increased Abdominal Pressure (ie. during Pregnancy)
  • Hiatus Hernia
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2
Q

What are the epithelial changes in Reflux Oesophagitis?

A
  • Thickening of squamous epithelium

- Ulceration of oesophageal epithelium when severe reflux

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3
Q

What are the complications of Reflux Oesophagitis?

A
  • Healing by FibrosisStricture FormationImpaired Oesophageal motilityOesophageal Obstruction
  • Barrett’s Oesophagus
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4
Q

What is Barrett’s Oesophagus?

A
  • Type of metaplasia
  • Response in some patients to Oesophageal reflux
  • Pre-malignant condition
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5
Q

What type of metaplasia occurs in Barrett’s Oeseophagus?

A

Transformation from non-keratinised stratified squamous epithelium to simple columnar epithelium
(ie. looks like intestinal mucosa -> “intestinal metaplasia”)

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6
Q

What malignancy does Barrett’s Oesophagus cause?

A

Oesophageal Adenocarcinoma

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7
Q

What are the risk factors for Oesophageal Squamous cell carcinoma

A
  • Smoking
  • Alcohol
  • Dietary Carcinogens
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8
Q

What are the risk factors for Oesophageal Adenocarcinoma

A
  • Barrett’s Metaplasia

- Obesity (Hiatus Hernia -> effects on LOS)

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9
Q

What is the most common place for Oesophageal cancer metastasis?

A

Liver!

(Portal venous system!)

(need to assess Liver with CT scanning in pts with oesophageal cancer to assess for mets)

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10
Q

Does oesophageal cancer have a poor prognosis?

A

Yes!

<15% survival rate at 5 yrs

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11
Q

What are the 3 aetiological types of Gastritis?

A

(ABC!)

  • Autoimmune (Type A)
  • Bacterial (Type B)
  • Chemical injury (Type C)
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12
Q

What is the pathophysiology of Type A (Autoimmune) Gastritis?

A
  • Organ-specific autoimmune disease

- Autoantibodies to parietal cells -> causes loss of intrinsic factor and decreased gastric acid secretion

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13
Q

What is the commonest clinical presentation of patients with Type A (Autoimmune) Gastritis?

A
  • Vitamin B12-deficiency (Pernicious anaemia)

due to damage to gastric parietal cells -> causes loss of intrinsic factor

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14
Q

What is the commonest type of Gastritis?

What is it caused by?

A
  • Type B: Bacterial Gastritis

- H. Pylori

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15
Q

What are the most common causes of Type C (Chemical injury) Gastritis?

A
  • Drugs: NSAIDs
    (reduced gastric mucus production -> more harmful effects of gastric acid on gastric mucosa)
  • Alcohol
  • Bile reflux
    (from Duodenum into stomach -> due to problems with pyloric valve due to ie. surgery, or obstruction (DU, or scar tissue))
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16
Q

What is the usual cause of Peptic Ulceration?

A

Usually H. Pylori-related

increases gastric acid production

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17
Q

What are the complications of Peptic Ulceration?

A
  • Bleeding
  • Haemorrhage (= acute)
  • Anaemia (= chronic)
  • Perforation (peritonitis)
  • Healing by Fibrosis (obstruction)
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18
Q

What is the most common cause of stomach cancer?

A

PREVIOUS H. Pylori infection

not current!

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19
Q

What is the most common type of stomach cancer?

A

Adenocarcinoma

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20
Q

Where does stomach cancer usually metastasise to

A

Liver

nb. portal venous system!

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21
Q

Does stomach cancer have a poor prognosis?

A

Yes!

<20% survival rate at 5 yrs

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22
Q

What are the main causes of Acute Liver Injury?

A
  • Hepatitis

- Bile duct obstruction

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23
Q

What are the 3 main causes of Hepatitis?

A
  • Viruses
  • Alcohol
  • Drugs (prescribed + recreational)
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24
Q

What are the 4 most common viruses causing viral hepatitis?

A

Hepatitis…

  • A
  • B
  • C
  • E
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25
Q

What type/s of viral hepatitis most commonly progress to chronic hepatitis and cirrhosis?

A
  • Hepatitis B (most common)

- Hepatitis C

26
Q

Which is the No. 1 cause of Chronic Liver disease (+ Cirrhosis) globally?

A

Chronic alcohol consumption

27
Q

Which is the No. 1 cause of acute Hepatitis globally?

A

Hepatitis B

28
Q

What causes Jaundice?

A
  • Increased circulating Bilirubin

- Caused by altered metabolism of Bilirubin

29
Q

What is the most common cause of Pre-Hepatic Jaundice?

A
  • caused by excessive Hb breakdown in Spleen due to excessive RBC breakdown (haemolysis) -> causes excessive bilirubin conversion from haem *
  • Haemolytic anaemia
30
Q

What are the most common causes of Intra-hepatic Jaundice?

A
  • damage to the liver -> cholestasis, intrahepatic bile duct obstruction *
  • Alcoholic Liver disease
  • Viral Hepatitis
  • Iatrogenic, e.g. medication
  • Hereditary Haemochromatosis
  • Autoimmune Hepatitis
  • Primary Biliary Cirrhosis or Primary Sclerosing Cholangitis
  • Hepatocellular Carcinoma
31
Q

What are the most common causes of Post-Hepatic Jaundice?

A
  • Intra-luminal causes: ie. gallstones
  • Mural causes: ie. cholangiocarcinoma, strictures (ie. PSC (NOT PBC)), or drug-induced cholestasis
  • Extra-mural causes: ie. pancreatic cancer, abdominal masses (e.g. lymphomas)
32
Q

How is PBC diagnosed?

A
  • A persistent elevation of serum alkaline phosphatase (ALP)
  • The presence of Anti-Mitochondrial auto-Antibodies (AMA)
  • (mainly females)
33
Q

What condition is PSC associated with?

A
  • IBD

80% of PSC pts have IBD

34
Q

How is PSC diagnosed?

A
  • MRI of bile ducts
35
Q

What are the main causes of Hepatic Cirrhosis?

A
  • Alcohol
  • Hepatitis B, C
  • Immune-mediated Liver Disease: auto-immune hepatitis, PBC
  • Metabolic Disorders: primary haemachromatosis, Wilson’s disease
  • Obesity: DM
36
Q

What types of Viral Hepatitis cause Hepatic Cirrhosis?

A
  • Hepatitis B + C
37
Q

What types of Viral Hepatitis have a vaccine?

A
  • Hepatitis A + B
38
Q

What is the most common type of Liver cancer?

A
  • Metastatic tumour -> common site of metastasis! (esp. from GIT tumours)

(secondary liver cancer is more common than primary liver cancer!!)

39
Q

What are the effects of CBD obstruction?

A
  • Jaundice
  • No bile excreted into Duodenum
  • Ascending Cholangitis -> due to infection of bile proximal to the obstruction
  • Secondary Biliary Cirrhosis (if obstruction is prolonged)
40
Q

Where is Meissner’s Plexus?

A

Submucosa

41
Q

Where is Auerbach’s (Myenteric) Plexus?

A

Muscularis Externa: between the inner circular and outer longitudinal layer

42
Q

What are the common causes of Common Bile duct Obstruction?

A
  • Gallstones
  • Bile duct Tumours (ie. Cholangiocarcinoma)
  • Benign Stricture (PSC, not PBC bc extra-hepatic!)
  • External compression ie. Tumours (nb. head of the pancreas tumours!)
43
Q

What parts of the Small Intestine are retroperitoneal?

A
  • Most of the Duodenum !!

except from the Duodenal Cap! (Proximal D1)

44
Q

Which parts of the Colon are intraperitoneal?

A
  • Caecum
  • Transverse Colon
  • Sigmoid Colon
45
Q

What are the different types of Inflammatory Bowel Diseases?

A
  • UC
  • Crohn’s
  • Ischaemic Colitis
  • Radiation Colitis
  • Appendicitis
46
Q

Which auto-antibody is positive in the majority (75%) of UC?

A

p- ANCA

47
Q

Which gene mutation is associated with Crohn’s?

A

NOD2

48
Q

What causes IBD?

A

Exaggerated immune response against normal flora with defects in the epithelial barrier function in genetically susceptible individuals

49
Q

What is the typical age of diagnosis of UC and Crohn’s?

A

20-40yrs

50
Q

Pathology of UC?

A
  • Large bowel only
  • Continuous pattern of inflammation
  • Rectum to proximal
  • Pseudopolyps
  • Ulceration
  • Limited to the Mucosa + Submucosa (not Transmural)
51
Q

Pathology of Crohn’s?

A
  • Affects any level of GIT from mouth to anus
  • “Skip lesions” -> sharp demarcations of disease segments from adjacent normal tissue
  • “Cobblestone” ulceration
52
Q

Histology of UC?

A
  • Inflammation limited to Mucosa + Submucosa
  • Architectural disarray of Crypts
  • Mucosal Atrophy
  • Pseudopolyps - (ulceration into submucosa)
  • NO GRANULOMAS
53
Q

Histology of Crohn’s?

A
  • Crypt abscesses (!!!)
  • Deep ulceration
  • Transmural inflammation (!!!) -> “chain of pearls”
  • NON-CASEATING GRANULOMAS (!!!)
54
Q

Complications of UC?

A

Acute:

  • Haemorrhage
  • Toxic dilatation
  • Perforation
  • Venous Thromboembolism

Chronic:
- Colon cancer -> risk if Pancolitis >10 yrs

55
Q

Complications of Crohn’s?

A
  • Malnutrition
  • Strictures
  • Fistulae
  • Abscesses
  • Colon cancer (5x inc. risk)
56
Q

What part of the GIT is most susceptible to Ischaemic Enteritis?

A

Splenic Flexure (LUQ)

-> “Watershed” area

57
Q

Where does Radiation Colitis typically occur?

A
  • Usually Rectum

post-pelvic RT

58
Q

Clinical Features of Radiation Colitis

A
  • Anorexia
  • Abdominal cramps
  • Diarrhoea
  • Malabsorption
  • Chronic -> mimics IBD
59
Q

What are the main causes of Appendicitis?

A
  • Obstruction

ie. Faecolith or RTI causing LN enlargement

60
Q

What is the most common type of CRC?

A

Adenocarcinoma (98%)

61
Q

What are the main risk factors for development of Colorectal Adenocarcinoma?

A

• Lifestyle - diet, alcohol intake, insufficient fruit and veg

• FH
- genetics + lifestyle

• IBD
- UC & Crohn’s Disease

• Genetics:

  • FAP
  • HNPCC
  • Peutz-Jeghers
62
Q

Which inherited syndromes most commonly cause CRC?

A

o FAP → (defect in APC gene → tumour suppressor)

o HNPCC → (defect in MSH2 → mis-match repair (MMR) protein)

o Peutz-Jeghers → (defect in STK11/LKB1 → tumour suppressor)