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Pathology Flashcards

1
Q

What is a polyp?

A

A protrusion above an epithelial surface

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2
Q

Classify the vast amount of polyps in the large bowel

A

Benign, epithelial and neoplastic

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3
Q

Differential diagnosis of a colonic polyp

A

Adenoma
Serrated polyp
Polypoid carcinoma
Other

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4
Q

Three macroscopic appearances of removed colonic polyps

A

Pedunculated
Sessile
Flat

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5
Q

Explain adenoma of the colon

A

Benign tumours of the colon. Not yet invasive, and do not metastasise. All dysplastic = must be removed

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6
Q

Adenoma-Carcinoma Sequence

A

Normal epithelium -> mutations to APC -> small adenoma -> further mutation e.g. k-ras -> large adenoma -> chromosomal mutations e.g. p53 -> Invasive adenocarcinoma

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7
Q

Why remove all adenomas?

A

They are premalignant

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8
Q

Removal of adenomas by…?

A

Endoscopy

Surgery

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9
Q

Primary treatment of Adenocarcinoma

A

Surgical removal of colon/rectum for staging

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10
Q

What kind of tumours are majorly found in the large bowel?

A

Malignant Adenocarcinomas

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11
Q

Colorectal Carcinoma - Dukes Staging

A

Dukes A = Confined by muscular propria
Dukes B = Through muscular propria
Dukes C = Metastatic to lymph nodes

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12
Q

Left Sided Colorectal Carcinoma

A

75%
P/R Bleeding
Altered Bowel Habit
Obstruction

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13
Q

Right Sided Colorectal Carcinoma

A

25%
Anaemia
Weight Loss

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14
Q

Colorectal carcinoma - Gross appearance

A

Varied =
Polypoid
Stricturing
Ulcerating

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15
Q

Colorectal carcinoma - Histopathological appearance

A

Typical adenocarcinoma

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16
Q

Colorectal carcinoma - Local invasion

A

Mesorectum, peritoneum, other organs

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17
Q

Colorectal carcinoma - Lymphatic spread

A

Mesenteric nodes

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18
Q

Colorectal carcinoma - Haematogenous spread

A

Liver, distant sites

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19
Q

Inherited Colorectal Carcinoma - HNPCC

A

Late onset (50/60s)

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20
Q

Inherited Colorectal Carcinoma - FAP

A 
Early onset (teens)
>100 polyps
Mutation to FAP gene
Tumours throughout colon
Adenocarcinoma NOS
Desmoid tumours & thyroid carcinomas
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21
Q

Diverticular Disease - Histopathology

A

Out-pouchings of mucosa

These are at increased risk of bursting and releasing septic contents into the abdominal cavity

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22
Q

Diverticular Disease - Complications

A 
Inflammation 
Rupture
Abscess
Fistula
Massive Bleeding
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23
Q

Ischaemia of the Large Bowel - Endoscopic View

A

Diffusely ulcerated and erythematous mucosa

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24
Q

Ischaemia of the Large Bowel - Histopathology

A

Withering of crypts
Smudging of lamina propria
Fewer chronic inflammatory cells

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25
Q

Ischaemia of the Large Bowel - Aetiology

A

CVS disease, A Fib, Embolus, Atherosclerosis (usually IMA), Shock, Vasculitis

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26
Q

Ischaemia of the Large Bowel - Clinical Context

A

Elderly
Left sided
Segmental on endoscopy

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27
Q

Ischaemia of the Large Bowel - Complications

A

Massive Bleeding
Rupture
Stricture

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28
Q

Antibiotic-Induced “Pseudomembranous” Colitis - Endoscopic View and Gross Appearance

A

Speckled, spotted appearance

Patchy, yellow membranous exudate on mucosal surface

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29
Q

Antibiotic-Induced “Pseudomembranous” Colitis - Histopathology

A

Explosive fibrinopurulent exudate on surface (volcano lesions)

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30
Q

Antibiotic-Induced “Pseudomembranous” Colitis - Causes

A

Patients in broad spectrum of antibiotics - C Diff proliferates
Toxins A and B attack endothelium and epithelium, causing mini-infarcts along the membrane

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31
Q

Antibiotic-Induced “Pseudomembranous” Colitis - Symptoms

A

Massive diarrhoea and bleeding

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32
Q

Antibiotic-Induced “Pseudomembranous” Colitis - Treatment

A

Flagyl/Vancomycin
May need colectomy
May be fatal

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33
Q

Collagenous Colitis - Appearance

A 
Endoscope = Normal 
Histology = Increase in thickness of sub epithelial collagen
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34
Q

Collagenous Colitis - Clinically

A

Watery diarrhoea
Normal endoscopy
History of causative drugs

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35
Q

Lymphocytic Colitis - Appearance

A 
Endoscope = Normal 
Histology = Normal architecture, but massive increase in intraepithelial lymphocytes
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36
Q

Lymphocytic Colitis - Clinically

A

Watery diarrhoea
Normal endoscopy
Raise possibility of Coeliac disease

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37
Q

Radiation Colitis - Endoscopy Appearance

A

Red, angry bowel

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38
Q

Radiation Colitis - Histology

A

Bizarre stream cells

Bizzarre vessels

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39
Q

Radiation Colitis - Cause

A

History of cervical/prostate cancer

Radiation therapy damaged cells

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40
Q

Acute (infective) Colitis _ Endoscopy Appearance

A

Very red
Very ulcerated
Very inflamed

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41
Q

Acute (infective) Colitis - Histology

A

Busy epithelium but not crypt irregularity

Florid diffuse acute cryptitis

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42
Q

Acute (infective) Colitis - Causes

A

Infection

Rarely: Drugs, ischaemia, endoscopy prep.

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43
Q

Acute (infective) Colitis - Diagnosis

A

Stool sample culture

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44
Q

Normal Appearance of the Liver

A

Light, tan in colour

Smooth regular surface

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45
Q

Pathogenesis of Liver Disease

A

Insult to hepatocytes
Inflammation
Fibrosis
Cirrhosis

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46
Q

Causes of Acute Onset of Jaundice

A

Viruses
Alcohol
Drugs
Bile duct obstruction

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47
Q

Histological Appearance of Paracetamol Poisoning

A

Confluent necrosis produce massive acute necrosis and liver failure
(lots of hepatocyte death)

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48
Q

Consequences of Acute Liver Failure

A

Complete recovery
Chronic liver disease
Death from liver failure

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49
Q

Pre-Hepatic Jaundice

A

Too much harm to break down
Haemolysis of any cause
Haemolytic anaemias
Unconjugated billrubin

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50
Q

Hepatic Jaundice

A 
Liver cells injured or dead
Acute liver failure 
Alcoholic hepatitis 
Cirrhosis (decompensated)
Bile duct loss
Pregnancy 
Conjugated jaundice
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51
Q

Post-Hepatic Jaundice

A 
Biel cannot escape into the bowel 
Congenital biliary atresia 
Gallstones blocking CBD
Strictures of CBD
Tumours
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52
Q

Appearance of a Cirrhotic Liver

A

Nodular, craggy, scarred

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53
Q

Histological Appearance of Cirrhosis

A

Bands of fibrosis separating regenerative nodules of hepatocytes
Loss of function of hepatocytes due to alteration of hepatic microvasculature

54
Q

Complications of Cirrhosis

A

Portal hypertension =
Oesophageal varices
Caput medusa
Rectal varices

Ascites

Liver Failure

55
Q

Alcoholic Liver Disease - Pathology Influenced By

A

Extent of the alcohol abuse

Individual factors

56
Q

Pathogenesis of Alcoholic Liver Disease

A

Increased peripheral release of fatty acids
Increased synthesis of fatty acids within the liver cells
Acetaldehyde, a product of alcohol metabolism, is probably responsible for liver cell injury (manifested by the formation of Mallory’s hyalin)
Increased collagen synthesis by fibroblasts

57
Q

Appearance of Alcoholic Fatty Liver - Days

A

Yellow

Greasy

58
Q

Histological Appearance of Alcoholic Fatty Liver - Days

A

Fat vacuoles appear clear in hepatocytes

59
Q

Histological Appearance of Alcoholic Fatty Liver - Heavy Drinking Weeks to Months

A

Accumulation of bile
Hepatocytes with thick dark pink cytoplasm
Accumulation of neutrophils

60
Q

Histological Appearance of Alcoholic Fatty Liver - Heavy Drinking Months to Years

A

Collagen played down around cells

Collagen appears blue

61
Q

Appearance of Alcoholic Cirrhosis

A

Micro-nodular cirrhosis with abundant white scarring

62
Q

Histological Appearance of Alcoholic Cirrhosis

A

Bands of fibrosis separating regenerative nodules

63
Q

Alcoholic Liver Disease - Outcome

A 
Cirrhosis 
Portal hypertension 
Malnutrition 
Hepatocellular carcinoma 
Social disintegration
64
Q

Non-Alcoholic Steatohepatitis

A

Non-drinkers
Pathologically identical to alcoholic liver disease
Occurs in patients with diabetes, obesity, hyperlipidaemia
May lead to fibrosis and cirrhosis
Increasing incidence

65
Q

Common causes of viral hepatitis

A

Hep A, B, C, E

66
Q

Rarer causes of viral hepatitis

A 
Hep D 
Epstein-Barr virus 
Yellow fever virus 
Herpes Simplex virus
Cytomegalovirus
67
Q

Hepatitis A - Histological Appearance

A

Death of hepatocytes
Directly cytopathic
No immunological phase

68
Q

Chronic Viral Hepatitis -Histological Appearance

A

Visible immune cells are damaging the liver
Dense portal chronic inflammation (erodes the border)
Interface hepatitis (piecemeal necrosis)
Fibrosis forms bridges between different portal areas (bridges filled with collagen)
Cirrhosis
Not distinguishable from other chronic hepatitis causes

69
Q

Hepatits B - Outcomes

A 
Fulminant acute infection (death)
Chronic hepatitis 
Cirrhosis 
Hepatocellular carcinoma
Asymptomatic (carrier)
70
Q

Hepatitis C - Outcomes

A

Chronic hepatitis

Cirrhosis

71
Q

Causes of Chronic Hepatitis

A

Viruses = Hep B and C

Drug induced

Autoimmune =
Primary biliary cirrhosis/cholangitis
Autoimmune hepatitis
Primary sclerosing cholangitis

72
Q

Primary Biliary Cirrhosis - Aetiology and Clinical

A

Rare autoimmune disease, unknown aetiology
Associated with autoantibodies to mitochondria
Females (90%)
Biopsy is to stage disease or diagnose uncertain cases
Outcome is unpredictable

73
Q

Primary Biliary Cirrhosis - Histological Appearance

A

Chronic portal inflammation
Inflamed bile ducts
Granulomas around bile ducts
Cirrhosis

74
Q

Primary Biliary Cholangitis - Pathogenesis

A

If untreated, bile duct loss leads to cholestasis liver injury, inflammation, fibrosis and cirrhosis

75
Q

Autoimmune Hepatitis - Clinical

A

Commoner in females
Associated with other AI
Chronic hepatitis pattern
May have triggers, including some drugs

76
Q

Autoimmune Hepatitis - Histological Appearance

A

Numerous plasma cells
Autoantibodies to smooth muscle, nuclear or LKM
Raised IgG

77
Q

Chronic Drug-Induced Hepatitis - Clinical

A

Similar features to all other types of chronic hepatitis
May trigger an autoimmune hepatitis
Chronic active process
Many causes

78
Q

General Points about Drugs and the Liver

A

Innumerable drugs can damage the liver
May be dose related or idiosyncratic
Can cause hepatitis, granulomas, fibrosis, necrosis, failure, cholestasis or cirrhosis
Can mimic any liver disease

79
Q

Primary Sclerosing Cholangitis - Clinical

A

Chronic inflammatory process affecting intra- and extra-hepatic bile ducts
Leads to pericardial fibrosis, duct destruction, jaundice and fibrosis
Associated with UC
More common in males
Increased risk of malignancy in bile ducts and colon

80
Q

Primary Sclerosing Cholangitis - Histological Appearance

A

Periductal onion-skinning fibrosis

Loss/damage of bile ducts

81
Q

Storage Disease - Types

A

Haemochromatosis
Wilsons Disease
Alpha-1-Antitrypsin Deficiency

82
Q

What is haemochromatosis?

A

Excess iron within the liver

83
Q

Primary Haemochromatosis - Causes

A 
Genetic condition
Inherited autosomal recessive condition 
Gene defect very complex
Exces absorption of iron from intestine, abnormal iron metabolism 
Worse in homozygotes, men
84
Q

Primary Haemochromatosis - Histological Appearance

A

Iron accumulates in hepatocytes

Iron confirmed by Perls Stain

85
Q

Primary Haemochromatosis - Clinical

A

Iron deposited in liver, assymptomatic for years
Eventually deposited in portal connective tissue and stimulates fibrosis
Cirrhosis if not treated
Predisposes to carcinoma
Also causes diabetes, cardiac failure and impotence

86
Q

Secondary Haemochromatosis - Causes

A

Iron overload from diet
Transfusions
Iron therapy

87
Q

Haemochromatosis - Outcomes

A

Depends on genetics, therapy (venesection), cofactors like alcohol
Cirrhosis
Hepatocellular carcinoma

88
Q

Wilson’s Disease

A

Inherited autosomal recessive disorder of copper metabolism
Copper accumulates in liver and brain (basal ganglia)
Kayser-Fleischer rings at corneal limbus
Low serum caeruloplasmin
Causes chronic hepatitis and neurological deterioration

89
Q

Alpha-1-Antitrypsin Deficiency

A

Inherited autosomal recessive disorder of production of an enzyme inhibitor
Causes empysema and cirrhosis
Cytoplasmic globules of unsecreted globules of protein in liver cells

90
Q

Tumours of the Liver

A

Primary (rare)
Hepatocellular adenoma
Hepatocellular carcinoma (Hepatoma)

Secondary (common)
Multiple
Metastases from colon, pancreas, stomach, breast, lung and others

91
Q

Hepatocellular Adenoma

A

Benign
Females
May become large - can rupture or bleed
Most remain asymptomatic

92
Q

Hepatocellular Carcinoma

A

Rare in Europe
Associated with Hep B, Hep C, Cirrhosis, PBC, PSC
Usually presents as mass, pain, obstruction
usually advanced unless discovered incidentally
Poor prognosis

93
Q

Hepatocellular Carcinoma - Histopathological Types

A 
Hepatocyte = Malignant tumour of liver cells
Cholangio = Malignant tumour of bile ducts
94
Q

What is Cholelithiasis?

A

Gallstones

Defined as hard stone-like or gravel-like material formed within the biliary system most commonly the gallbladder

95
Q

What is normal bile made from?

A

Micelles of cholesterol, phospholipid, bile salts and bilirubin

96
Q

Where is normal bile stored and how is it released?

A

Stored and concentrated in gallbladder, released by common cystic duct into the 2nd part of the duodenum through common bile duct and Ampulla of Vater

97
Q

Pathogenesis of Cholesterol Gallstones

A

Gallstones form when there is an imbalance between the ratio of cholesterol to bile salts, disrupting micelle formation
Free crystallisation on micelle surface

98
Q

Risk Factors for Cholesterol Gallstones

A 
Cholesterol excess in bile 
Female
Obesity 
Diabetics
Genetic
99
Q

Pathogenesis of Pigment Gallstones

A

Excess bilirubin cannot be solubilised in bile salts

Tend to be black

100
Q

Risk Factors for Pigment Gallstones

A

Excess bilirubin
Due to excess haemolysis
e.g. Haemolytic anaemia

101
Q

Pathogenesis of Gallstones

A

Gallbladder pH and mucosal glycoproteins may be contributory factors
Infection and inflammation of biliary lining
Most gallstones are a mixture (mixed stones)
Pure cholesterol and pure pigment stones do occur
Calcium carbonate stones do occur

102
Q

Pathology of Gallstones

A 
Acute Cholecystitis
Chronic Cholecystitis
Mucocoele
Empyema
Carcinoma
Ascending Cholangitis
Obstructive Jaundice
Gallstone Ileus
Acute Pancreatitis
Chronic Pancreatitis
103
Q

What is cholecystitis?

A

Inflammation of gallbladder
Usually associated with gallstones
Acute or chronic
Common

104
Q

Acute Cholecystitis

A

Gallstones obstructing outflow of bile
Initially sterile, then becomes infected
May cause empyema, rupture, peritonitis
Causes intense adhesions within 2-3 days

105
Q

Acute Cholecystitis - Appearance

A 
Gross = Red, haemorrhage, mixed gallstones embedded in pus 
Histology = Acute inflammation indicated by neutrophils
106
Q

Chronic Cholecystitis

A

Associated with Gallstones
May develop insidiously or after bouts of acute cholecystitis
Galbladder wall is thickened but not distended

107
Q

Chronic Cholecystitis - Appearance

A 
Gross = Mixed stones and thickened gallbladder wall due to fibrosis
Histology = Chronic inflammation and Rokitansky-Aschoff sinuses
108
Q

What do stones in the common bile duct cause?

A

Obstructive jaundice

109
Q

Carcinoma of the Gallbladder

A 
Rare
Adenocarcinoma
Associated with gallstones
Local invasion of liver
Poor prognosis
110
Q

Carcinoma of Bile Ducts (Cholangiocarcinoma)

A

Rare
Associated with Ulcerative Colitis and Primary Sclerosing Cholangitis
Presents with obstructive jaundice
Adenocarcinoma

111
Q

What is a Klatskin Tumour?

A

Cholangiocarcinoma at bifurcation of hepatic ducts

112
Q

Cholangiocarcinoma - Histology Appearance

A

Densely packed call glands in a fibrous stroma

113
Q

What is Pancreatitis?

A

Inflammation of the pancreas

May be acute or chronic (overlap exists between the two)

114
Q

Acute Pancreatitis - Clinical

A

Adults (rare in children)
Sudden onset severe abdominal pain
Patients may be severely shocked
Elevated serum amylase

115
Q

Acute Pancreatitis - Aetiology

A 
Alcohol
Cholelithiasis
Shock
Mumps
Hyperparathyroidism
Hypothermia
Trauma
Iatrogenic (post ERCP)
116
Q

Acute Pancreatitis - Pathogenesis

A

Bile reflux, duct obstruction due to stone damage to sphincter of Oddi all cause pancreatic duct epithelial injury
Loss of protective barrier allows autodigestion of pancreatic acini
Release of lytic pancreatic enzymes proteases and lipases
Intra- and peripancreatic fat necrosis (lipases)
Tissue destruction and haemorrhage (proteases)

117
Q

Appearance of Acute, Mild Pancreatitis

A

Focal areas of necrosis

118
Q

Appearance of Acute, Moderate Pancreatitis

A

Intrapancreatic fat necrosis (may bind large amounts of calcium)

119
Q

Appearance of Acute, Severe Pancreatitis

A

Complete pancreatic destruction with haemorrhage and fat necrosis

120
Q

What is a Pancreatic Pseudocyst?

A

Fleshy pseudocyst complicating pancreatitis

121
Q

Acute Pancreatitis - Histological Appearance

A

Large areas of pancreas and fat necrosis

122
Q

Acute Pancreatitis - Complications

A 
Death
Shock
Pseudocyst formation
Abscess formation
Hypocalcemia
Hyperglycaemia
123
Q

What is Chronic Pancreatitis?

A

Relapsing disorder may develop insidiously or following bouts of acute pancreatitis

124
Q

Chronic Pancreatitis - Aetiology

A 
Alcohol
Cholelithiasis
Cystic fibrosis
Hyperparathyroidism
Familial
125
Q

Chronic Pancreatitis - Pathology

A

Replacement of pancreas by chronic inflammation and scar tissue
Destruction of exocrine acini and islets

126
Q

Gross Appearance of Chronic Pancreatitis

A

Fibrotic and necrotic

Inflammation and fibrosis can mimick a tumour in the head of the pancreas

127
Q

Chronic Pancreatitis - Histological Appearance

A

Exocrine pancreas is replaced by chronic inflammation and fibrosis (first)

128
Q

Carcinoma of Pancreas

A

Adenocarcinoma
Aetiology Unknown
Weak associated with smoking, diabetes, familial pancreatitis
Poor prognosis (pancreas is intimately related to many important structures. Also, resistant to most forms of chemo)

129
Q

Gross Appearance of Adenocarcinoma of Head of Pancreas

A

Can invade duodenal wall

Can constrict the common bile duct

130
Q

How can Carcinoma of the Tail of the Pancreas spread?

A

By direct invasion of the spleen

131
Q

Adenocarcinoma of Pancreas - Histological Appearance

A

Irregular abortive glands in a dense stroma

132
Q

Adenocarcinoma of Pancreas - Spread

A

Direct spread to other organs e.g. duodenum, stomach, spleen
Spread to local lymph nodes
Haematogenous spread to the liver

GI (24 decks)

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