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Pathology > Histopathology Part 2- (p149-166- GI, Pancreatic + Liver) > Flashcards

Histopathology Part 2- (p149-166- GI, Pancreatic + Liver) Flashcards

1
Q

What is the epithelial cytology of the oesophagus?

A

Squamous epithelium for proximal 2/3
Columnar epithelium for distal 1/3
Joined by Z line/squamo-columnar junction

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2
Q

What is the commonest cause of oesophagitis?

A

GORD

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3
Q

What are the complications of GORD?

A

Ulceration, haemorrhage->haematemesis or melaena, Barret’s oesophagus, stricture, perforation

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4
Q

How is GORD treated?

A

Lifestyle- stop smoking, weight loss

PPI/H2 receptor antagonists

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5
Q

What is Barrett’s oesophagus?

A

Intestinal metaplasia of squamous mucosa -> columnar epithelium -> upwards migration of z line
Can lead to adenocarcinoma

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6
Q

Risk factors for squamous cell oesophageal carcinoma?

A 
ETOH
Smoking
Achalasia of cardia
Plummer-Vinson syndrome
Nutritional deficiencies
Nitrosamines
HPV
6x more common in Afro-carribeans
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7
Q

How does squamous cell oesophageal carcinoma present?

A 
Progressive dysphagia (solids -> fluids)
Odynophagia (pain)
Anorexia
Severe weight loss
Rapid growth and early spread to LN, liver and to proximal strictures
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8
Q

What are varices?

A

Engorged dilated veins usually due to portal HTN

Pt vomits units of blood

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9
Q

How do you treat varices?

A

Emergency endoscopy -> sclerotherapy/banding

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10
Q

How do gastric ulcers present clinically?

A

Epigastric pain +/- weight loss

Worse with food, relieved by antacids

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11
Q

RFs for gastric ulcer?

A

H. pylori, smoking, NSAIDs, stress, delayed gastric emptying, elderly

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12
Q

Histology of gastric ulcer?

A

Breach through muscularis mucosa into submucosa

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13
Q

What causes gastric lymphoma?

A

H. pylori- chronic antigen stimulation

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14
Q

How do you treat gastric lymphoma?

A

Remove H.pylori using triple therapy- PPI, clarithromycin + amoxicillin or metro

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15
Q

How does duodenal ulcer present clinically?

A

4x more common than GU
Epigastric pain worse at night
Relieved by food and milk
Younger adults

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16
Q

RFs for duodenal ulcers?

A 
H. pylori
Drugs
Aspirin
NSAIDs
Steroids
Smoking
Drugs
Acid secretion
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17
Q

What is the pathophysiology of coeliac disease?

A

T cell mediated autoimmune disease (DQ2 or DQ8), gluten intolerance results in villous atrophy and malabsorption

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18
Q

How does coeliac disease present?

A 
Young children and Irish women- EMQ
Steatorrhoea
Abdo pain
Bloating
N+V
Weight loss
Fatigue
IDA
Failure to thrive
Rash
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19
Q

Serological tests for coeliac disease?

A

Anti-endomysial ab, anti-tissue transglutaminase, anti-gliadin

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20
Q

Gold standard Ix for coeliac disease?

A

Upper GI endoscopy and duodenal biopsy

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21
Q

Treatment of coeliac?

A

Gluten free diet

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22
Q

What is Hirschsprung’s disease and how does it present clinically?

A

Absence of ganglion cells in the myenteric plexus (Genetics- RET proto-oncogene Cr10+)
Presents with symptoms and signs of obstruction in young babies, mainly males

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23
Q

How is Hirschsprung’s treated?

A

Resection of affected segment

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24
Q

Causes of bowel obstruction?

A

Constipation
Diverticular disease
Adhesions
Herniation
External mass e.g. fetus, aneurysm, foreign body
Volvulus- complete twisting of bowel loop at mesenteric base around vascular pedicle, small bowel
Intussusception

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25
Q

Epidemiology of Crohn’s?

A

Western population
Peak onset 20s, F>M
White 2-5x>non-white
Smoking worsens symptoms

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26
Q

Epidemiology of UC?

A

Slightly more common
White>non-whites
Peak age 20-25

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27
Q

Aetiology of Crohns?

A

Unknown
MZ twin concordance 50%
Hygiene hypothesis

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28
Q

Aetiology of UC?

A

Unknown

MZ twin concordance 15%

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29
Q

Pathophysiology of crohn’s?

A

Whole GI tract (mouth to anus)- most common terminal ileum and caecum
Patchy distribution -> ‘skip lesions’
Healthy mucosa lies above diseased mucosa -> cobblestone appearance
Aphthous ulcers (rosethorn)
Non caseating granulomas seen
Transmural inflammation
Fistulas and fissures common

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30
Q

Pathophysiology of UC?

A

Extends proximally from rectum
Continuous involvement of mucosa
Small bowel not affected normally
Extensive superficial broad ulcers
Inflammation confined to mucosa
No granulomas/fissures/fistulae/strictures
Islands of regenerating mucosa bulge into lumen -> pseudopolyps

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31
Q

Clinical features of crohn’s?

A

Intermittent diarrhoea
Pain
Fever

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32
Q

Clinical features of UC?

A

Associated more with bloody diarrhoea, mucus

Crampy abdo pain relieved by defecation

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33
Q

Extra GI manifestations of IBD?

A 
A PIE SAC
Aphthous ulcers 
Pyoderma gangrenosum 
Iritis 
Erythema nodosum 
Sclerosing cholangitis 
Arthritis 
Clubbing of fingertips
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34
Q

Complications of Crohn’s?

A

Strictures (requiring bowel resection)
Fistulae
Abscess formation
Perforation

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35
Q

Complications of UC?

A

Severe haemorrhage
Toxic megacolon -> perforation
30% require colectomy within 3y
Adenocarcinoma (20-30x risk)

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36
Q

Ix for Crohn’s?

A

Systemic markers of inflammation e.g. ESR, CRP, Barium contrast, endoscopy

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37
Q

Ix for UC?

A

Rectal biopsy
Flexi sig/colonoscopy
AXR
Stool culture

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38
Q

Management of Crohn’s?

A

Mild- Prednisolone
Severe- IV hydrocortisone, metronidazole

Additional- azathioprine, methotrexate, infliximab

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39
Q

Management of UC?

A

Mild- pred + mesalazine
Mod- Pred + Mes + steroid enema bd
Severe- Admit, nbm, IV fluids and IV hydrocortisone, rectal steroids
Remission- Mes + azathioprine (2nd line)

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40
Q

What is the pathophysiology of c difficile infection?

A

Use of abx e.g. cipro or ceph’s kill off commensals allowing c.diff to flourish. It’s exotoxins cause pseudomembranous colitis

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41
Q

How do you investigate c diff infection?

A

Stool culture

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42
Q

How do you treat c difficile infection?

A

Metronidazole (covers anaerobic) or vancomycin (2’ line)

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43
Q

What is probably responsible for the high incidence of diverticular disease in the west?

A

A low fibre diet

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44
Q

What is the pathophysiology of diverticular disease?

A

High intraluminal pressure results in outpouchings at weak points in the bowel wall (can be seen on barium enema CT or endoscopy)- 90% occur in left colon- often asymptomatic but sometimes PR bleed

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45
Q

Complications of diverticular disease?

A

Diverticulitis- fever and peritonism, gross perforation, fistula, obstruction (due to fibrosis)

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46
Q

What is carcinoid syndrome?

A

Diverse group of tumours of enterochromaffin cell origin which produce 5-HT (serotonin)
Commonly found in bowel and usually slow growing
Presents with bronchoconstriction, flushing and diarrhoea
Can lead to carcinoid crisis

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47
Q

How do you investigate carcinoid syndrome?

A

24h urine 5-HIAA (main metabolite of serotonin)

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48
Q

How do you treat carcinoid syndrome?

A

Octreotide- somatostatin analogue

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49
Q

What is an adenoma?

A

Benign dysplastic lesions that are the precursor to most adenocarcinomas
Found in 50% >50y in western world

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50
Q

Most important risk factor for malignancy in adenomas?

A

Large size, in addition to dysplasia and increased villous component

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51
Q

What types of non-neoplastic polyps are there?

A

Hamartomatous polyp
Hyperplastic polyp
Inflammatory- pseudopolyp

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52
Q

What is the second most common cause of cancer death in UK?

A

Colorectal

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53
Q

What percentage of colorectal cancers are adenocarcinoma?

A

98%

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54
Q

Aetiology of colorectal cancer?

A

Diet (low fibre, high fat), lack of exercise, obesity, familial syndromes, chronic IBD

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55
Q

Investigations in colorectal cancer?

A 
Protoscopy
Sigmoidoscopy
Colonoscopy
Barium enema
Bloods e.g. FBC
CT/MRI
Carcinoembryonic antigen (CEA)- monitor disease
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56
Q

With which system and how is colorectal cancer staged?

A 
Duke's staging- helps decide treatment
A- confined to mucosa 
B1- extending into muscularis propria
B2- transmural invasion, no LN involved
C1- Extending into muscularis propria, with LN metastases
C2- transmural invasion with LN mets
D- distant mets
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57
Q

How is colorectal cancer managed?

A

Surgery
Radiotherapy- post-op to decrease local recurrence
Chemo in palliation- 5-FU

58
Q

What mutations are responsible for familial adenomatous polyposis (FAP)?

A

70% AD mutation in APC gene (C5q1)

30% AR mutation in DNA mismatch repair genes

59
Q

How does FAP present?

A

Around 10-15y, >100 adenomatous polyps- ALL will progress to adenocarcinoma if not treated by 30 so prophylactic colectomy

60
Q

What mutations are responsible for hereditary non-polyposis colorectal cancer (HNPCC)?

A

AD mutations in DNA mismatch

61
Q

What is the role of the pancreas?

A

Produces 2L a day of enzymic HCO3- rich fluid, stimulated by secretin and CCK

62
Q

Where is secretin produced and what does it do?

A

Produced by s-cells of duodenum, controls gastric acid secretion and buffering with HCO3-

63
Q

Where is cholecystokinin (CCK) produced and what does it do?

A

Made by I-cells in duodenum.

Responsible for stimulating digestion of fat and protein by causing release of digestive enzymes

64
Q

What are the exocrine functions of the pancreas?

A

Secretes digestive enzymes into ducts- proteases, lipases and amylase

65
Q

What are the endocrine functions of the pancreas?

A

Secretes products e.g. hormones into blood stream
Alpha cells- glucagon
Beta cells- insulin
Delta- Somatostatin regulates above cells
D1- Vasoactive peptide, stimulates secretion of H2O into pancreatic system

66
Q

How do you diagnose DM?

A

Fasting plasma glucose>7

or random plasma glucose >11.1

67
Q

What is the pathophysiology of T1DM?

A

Autoimmune destruction of beta cells by CD4+ and CD8+ T lymphocytes, may present with DKA

68
Q

Pathophysiology of T2DM?

A

Linked to obesity and insulin resistance

69
Q

Complications of diabetes?

A

Macrovascular- cardiac, renal, cerebral
Microvascular- retinopathy, PVS
Other- polydipsia, polyuria and recurrent infections

70
Q

What score is used to assess acute pancreatitis?

A

GLASGOW- 3 or more leads to ITU referral

71
Q

Causes of acute pancreatitis?

A 
I GET SMASHED
Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion venom
Hyperlipidaemia
ERCP
Drugs e.g. thiazides
72
Q

Presentation of acute pancreatitis?

A

Severe epigastric pain radiating to back, relieved by sitting forward
Vomiting prominent
Amylase only transiently increased, serum lipase is more sensitive
Can lead to pseudocyst formation

73
Q

Histology of acute pancreatitis?

A

Coagulative necrosis

74
Q

Causes of chronic pancreatitis?

A 
Alcoholism
Cystic fibrosis
Hereditary
Pancreatic duct obstruction e.g. stones/tumour
Autoimmune- IgG4 sclerosin
75
Q

Presentation of chronic pancreatitis?

A

Epigastric pain radiating to back, malabsorption due to lack of enzymes to digest food

76
Q

Histology of chronic pancreatitis?

A

V similar to Ca pancreas- fibrosis and loss of exocrine tissue, duct dilatation with thick secretions, calcification

77
Q

Presentation of acinar cell carcinoma?

A

Non-specific sx, abdo pain, wt loss, nausea and diarrhoea

78
Q

Histopathology of acinar cell carcinoma?

A

Neoplastic epithelial cells with eosinophilic granular cytoplasm. Positive immunoreactivity for lipase, trypsin and chymotrypsin

79
Q

Prognosis of acinar cell carcinoma?

A

Median survival 18m from diagnosis. 5y survival <10%

80
Q

Most common pancreatic malignancy?

A

Ductal adenocarcinoma of pancreas (85% of all pancreatic malignancies)
M>F

81
Q

RF for pancreatic carcinoma?

A

Smoking
Diet
Genetic e.g. FAP, HNPCC

82
Q

Clinical features of pancreatic carcinoma?

A 
Weight loss and anorexia
Upper abdo and back pain
Jaundice (PAINLESS), pruritis, steatorrhoea
DM
Trousseau's syndrome (25%)- recurrent superficial thrombophlebitis
Ascites
Abdo mass
Virchow's node
Courvoisier's sign
83
Q

Ix in pancreatic carcinoma?

A

Bloods- low Hb, raised Bili + Ca2+
CT/MRI/ERCP
Ca19-9 >70IU/mL

84
Q

Management of pancreatic carcinoma?

A

Chemotherapy is palliative (5-FU)
Surgery- Whipple’s procedure
Prognosis v poor- <5% 5y survival

85
Q

What are the different types of multiple endocrine neoplasia (MEN)?

A

MEN1- PPP- Parathyroid hyplasia, pancreatic endocrine tumour (often phaeo), pituitary adenoma

MEN2A- Parathyroid, thyroid, phaeo

MEN2B- Medullary thyroid, phaeo, neuroma, marfanoid phenotype

86
Q

What are the 5 main functions of the liver?

A

Metabolism- glycolysis, glycogen storage, glucose, amino acid and fatty acid synthesis, hormone, lipoprotein and drug metabolism

Protein synthesis- makes all circulating proteins except gamma globulins

Storage- glycogen, vit A, D, B12, K, folate, iron + copper

Bile synthesis- 600-1000ml daily

Immune function- antigens from gut reach liver via portal circulation. Phagocytosed by Kupffer cells

87
Q

What benign liver tumours are there?

A

Hepatic adenoma

Haemangioma

88
Q

What malignant liver tumours are there?

A 
Hepatocellular carcinoma
Angiosarcoma
Hepatoblastoma
Cholangiocarcinoma
Metastases from other primary tumours
89
Q

What drug is hepatic adenoma associated with?

A

OCP

90
Q

Causes of hepatocellular carcinoma?

A

Hep B+C, alcoholic cirrhosis, haemochromatosis, NAFLD, aflatoxin, androgenic steroids

91
Q

Investigations for hepatocellular carcinoma?

A

Alpha-fetoprotein

USS

92
Q

Causes of cholangiocarcinoma?

A 
PSC
Parasitic liver disease
Chronic liver disease
Congenital liver abnormalities
Lynch syndrome type II
93
Q

Most common malignant liver lesion?

A

Mets from other primary tumours- GI tract, breast or bronchus

94
Q

Define cirrhosis?

A

Diffuse abnormality of liver architecture that interferes with blood flow and liver function- hepatocyte necrosis, fibrosis, nodules, portal HTN

95
Q

7 major causes of cirrhosis?

A 
Alcoholic  liver disease
Non-alcoholic fatty liver disease
Chronic viral hepatitis
Autoimmune hepatitis
Biliary- PBC + PSC
Genetic- haemochromatosis, Wilson's, alpha-1 antitrypsin deficiency etc
Drugs- e.g. methotrexate
96
Q

How is cirrhosis classified?

A

According to nodule size:
Micronodular <3mm- uniform liver involvement- caused by alcoholic hepatitis or biliary tract disease
Macronodular >3mm- variable nodule size- caused by viral hep, Wilson’s or alpha-1 antitrypsin def

97
Q

What is used to indicate prognosis in liver cirrhosis?

A

Modified Child’s Pugh Score

98
Q

What is the pathophysiology of portal HTN?

A

Increased portal pressure secondary to increased vascular resistance in liver, hyperdynamic circulation, sodium retention and plasma volume expansion

Leads to venous system dilating and collateral vessels forming

99
Q

Causes of portal HTN?

A

Prehepatic- portal vein thrombosis (e.g. Factor V Leiden)

Hepatic- pre-sinusoidal- schistosomiasis, PBC, sarcoid, sinusoidal- cirrhosis, post-sinusoidal- veno-occlusive

Post-hepatic- Budd-Chiari syndrome (occlusion of hepatic vein)

100
Q

What are the macroscopic characteristics of hepatic steatosis (fatty liver)?

A

Large, pale, yellow and greasy liver

101
Q

What are the microscopic characteristics of hepatic steatosis (fatty liver)?

A

Steatosis- accumulation of fat droplets in hepatocytes

Chronic exposure -> fibrosis

102
Q

How can hepatic steatosis be reversed?

A

Fully reversible if alcohol avoided

103
Q

What are the macroscopic characteristics of alcoholic hepatitis?

A

Large fibrotic liver

104
Q

What are the microscopic characteristics of alcoholic hepatitis?

A

Hepatocyte ballooning and necrosis due to accumulation of fat, water and proteins
Mallory bodies
Fibrosis

105
Q

What are the macroscopic characteristics of alcoholic cirrhosis?

A

Yellow-tan, fatty, enlarged

Transforms into shrunken non-fatty brown organ

106
Q

What are the microscopic characteristics of alcoholic cirrhosis?

A

Micronodular cirrhosis- small nodules + bands of fibrous tissue

107
Q

What is most common cause of chronic liver disease in west?

A

Non-alcoholic fatty liver disease

108
Q

Who does Non-alcoholic fatty liver disease commonly occur in?

A

Mainly in obese individuals with hyperlipidaemia/metabolic syndrome
Diabetes also a RF

109
Q

When does autoimmune hepatitis commonly occur?

A

Common with other autoimmune diseases e.g. coeliac, SLE, RA, thyroiditis, sjogrens, UC

110
Q

What are the 2 different types of autoimmune hepatitis?

A

Type 1- ANA (antinuclear Ig), anti-SMA, anti-actin Ig, anti-soluble liver antigen Ig
Type 2- Anti-LKM Ig

111
Q

How do you treat autoimmune hepatitis?

A

Immune suppression until transplant, but disease returns in upto 40%

112
Q

What is the pathology of Primary Biliary Cirrhosis (PBC)?

A

Autoimmune inflammatory destruction of medium sized intrahepatic bile ducts -> cholestasis -> SLOW development of cirrhosis

113
Q

What is the F:M ratio of PBC?

A

10:1

PSC is M>F

114
Q

What would blood tests show in PBC?

A

Increased serum ALP, cholesterol, IgM, AMA in 90% and hyperbilirubinaemia

115
Q

What would a US scan show in PBC?

A

No bile duct dilatation

116
Q

What would histology of PBC show?

A

Bile duct loss with granulomas

117
Q

How does PBC present?

A

Fatigue, pruritus, abdo discomfort, skin pigmentation, xanthelasma, steatorrhoea, vit D malabsorption, inflammatory arthropathy

118
Q

How do you treat PBC?

A

Ursodeoxycholic acid in early phase

119
Q

What is the pathology of primary sclerosing cholangitis (PSC)?

A

Inflammation and obliterative fibrosis of extrahepatic and intrahepatic bile ducts -> multi-focal stricture formation with dilation of preserved segments

120
Q

What condition is PSC associated with and which condition does it increase your risk of?

A

IBD (especially UC)

Risk- Cholangiocarcinoma

121
Q

What would blood tests show for PSC?

A

Increased serum ALP, several auto-Ig especially p-ANCA

122
Q

What would a US scan show for PSC?

A

Bile duct dilatation

123
Q

What would an ERCP show for PSC?

A

Beading of bile ducts due to multifocal strictures

124
Q

What are the 3 genetic causes of cirrhosis?

A

Haemochromatosis
Wilson’s disease
Alpha1 antitrypsin deficiency

125
Q

Inheritance pattern of haemochromatosis?

A

Autosomal recessive

126
Q

What is the pathology of haemochromatosis?

A

Mutated HFE gene at 6p21.3 -> increased Fe gut absorption which deposits in liver, heart, pancreas, adrenals, pituitary, joints, skin -> fibrosis

127
Q

What is the histology of haemochromatosis (and what stain would be used)?

A

Fe deposits in liver- stains with Prussian blue stain

128
Q

Signs and symptoms of haemochromatosis?

A 
Skin bronzing (melanin deposition)
Diabetes
Hepatomegaly with micronodular cirrhosis
Cardiomyopathy
Hypogonadism
Pseudogout
129
Q

What investigation findings would you see in haemochromatosis?

A

Increased iron and ferritin
Transferrin saturation >45%
Decreased TIBC

130
Q

How do you treat haemochromatosis?

A

Venesection

Desferrioxamine

131
Q

What age does Wilson’s disease present?

A

11-14yo

132
Q

Inheritance pattern of Wilson’s disease?

A

Autosomal recessive

133
Q

Pathology of Wilson’s disease?

A

Mutated gene ATP7B- encodes copper transporting ATPase expressed on canalicular membrane -> decreased biliary Cu excretion and deposition in liver, CNS, iris

134
Q

What does copper stain with?

A

Rhodanine

135
Q

Signs and symptoms of Wilson’s?

A

Liver disease- acute hepatitis, fulminant liver failure or cirrhosis
Neuro disease- parkinsonism, psychosis, dementia
Kayser Fleischer rings- copper deposits in Desemet’s membrane in cornea

136
Q

Investigation findings in Wilson’s disease?

A

Decreased caeruloplasmin and serum copper

Increased urinary copper

137
Q

Treatment for Wilson’s disease?

A

Lifelong penicillamine

138
Q

What is the inheritance pattern for Alpha1 antitrypsin deficiency?

A

Autosomal dominant

139
Q

What is the pathology of A1AT deficiency?

A

A1AT accumulates in hepatocytes -> intracytoplasmic inclusions -> hepatitis
Lack of A1AT in lungs -> emphysema

140
Q

Histology of A1AT deficiency?

A

Intracytoplasmic inclusions of A1AT which stain with Periodic acid Schiff

141
Q

Signs and symptoms of A1AT deficiency?

A

Neonatal jaundice in kids

Emphysema and chronic liver disease in adults

142
Q

Investigation findings in A1AT deficiency?

A

Decreased A1AT

Absent alpha-globulin band on electrophoresis

Pathology (13 decks)

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