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Path 2022 > Histopath - Liver & GI > Flashcards

Histopath - Liver & GI Flashcards

1
Q

Granuloma - definition & diseases seen in

A

Organised collection of activated (epithelioid) macrophages

Seen in:

  • TB
  • Leprosy
  • Cat-scratch disease
  • Idiopathic reaction in sarcoid
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2
Q

General features of squamous cell carcinoma

A

Keratin production

Intercellular bridges

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3
Q

General features of Adenocacrcinoma

A

Mucin production

Glands

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4
Q

Histochemical stains

A

Fontana - melanin

Congo Red - ‘apple green birefringence’ (amyloid)

Prussian Blue - Iron (haemochromatosis)

Haematoxylin & Eosin - H stains basic parts purple/blue, E stains acidic parts red/pink

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5
Q

Rhodamine vs Rhodanine stains

A

RhodaMine = TB stain

RhodaNine = Wilson’s disease
- golden brown colour on blue counterstain

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6
Q

Histological features of EtOH liver disease

A

Fatty liver

  • large droplet fatty change
  • ‘large, pale, yellow, greasy’

Alcoholic hepatitis

  • mainly zone 3
  • fatty change
  • ballooning +/- Mallory Denk bodies
  • neutrophil polymorphs
  • pericellular fibrosis
  • megamitochondria
  • ‘large + fibrotic’

Liver failure

  • micro nodules of regenerating hepatocytes
  • surrounding fibrous cuff
  • +/- fatty change if currently drinking
  • ‘shrunken + brown’
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7
Q

Acute & Chronic hepatitis histological features

A

Acute hepatitis

  • spotty necrosis
  • usually concentrated around portal triad

Chronic hepatitis

  • viral = zone 1
  • portal inflammation
  • interface hepatitis ‘piecemeal necrosis’ (even though death is by apoptosis)
  • lobular inflammation (resembles acute spotty necrosis)
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8
Q

Overdose rule?

A 
If PT (in seconds) > number of hours since OD
--> transfer to specialist liver unit for transplant
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9
Q

Pattern of nodule size in liver disease

A

MICROnodulae = alcoholic hepatitis, insulin resistance

MACROnodular = viral hepatitis, Wilson’s, Alpha-1-antitrypsin deficiency

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10
Q

Primary biliary cholangitis diagnostic features

A

Histology:

  • Bile duct loss
  • Chronic inflammation
    • granulomas

Other: Anti-mitochondrial antibodies e.g. anti M2 = gold standard

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11
Q

Primary sclerosing cholangitis diagnostic features

A

Histology:

  • concentric fibrosis
  • ‘onion skinning’

Bile duct imaging e.g. ERCP, MRCP

pANCA Ab detection

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12
Q

Autoimmune hepatitis diagnostic features

A

Histology:

  • extensive inflammatory infiltrate
  • abundant plasma cells
  • pale perinuclear area

Anti-smooth muscle actin Abs
Anti liver-kidney microsomal Ig

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13
Q

Hepatic granulomas - causes?

A

Specific: PBC, drugs
General: TB (caseating), sarcoid (non-caseating)

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14
Q

Normal range of bilirubin

A

5-17

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15
Q

Pre-hepatic causes of raised bilirubin

A

UNconjugated

Haemolytic anaemia

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16
Q

Hepatic causes of raised bilirubin

A

Hepatitis - viral, EtOH

Cirrhosis

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17
Q

Post hepatic causes of high bilirubin

A

Obstruction - gallstones, ca. head of pancreas

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18
Q

Ix needed for pre-hepatic (unconjugated) hyperbilirubinaemia

A

FBC
Blood film

Coomb’s test?

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19
Q

Genetics of Gilbert’s

A

Autosomal recessive

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20
Q

Pathogenesis + presentation of Gilbert’s

A

UDP glucoronyl transferase activity reduced to 30%

Causes slight jaundice
Worse when fasting/stressed
No bilirubin in urine (unconjugated bilirubin highly bound to albumin)

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21
Q

Best measure of liver (synthetic) function?

A

Pro-thrombin time (PT)

Also:
albumin, PTTK, Bilirubin
Enzymes (GGT, ALP, ALT, AST) only show location of damage not degree.

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22
Q

Clinical features of Chronic stable liver disease

A

Palmar erythema
Spider naevi (>5)
Dupuytren’s contracture
Gynaecomastia

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23
Q

Clinical features of portal HTN

A

Porto-systemic anastomoses

  • caput medusae
  • oesophageal varices
  • rectal varices

Splenomegaly
Scrotal oedema
Shifting dullness (ascites)

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24
Q

Clinical feature of decompensated liver failure

A

Hyperammonaemia

  • Flapping tremor
  • confusion

Jaundice (accumulation of bile salts)

Hepatic coma, death

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25
Q

Role of Stellate cells in liver?

A

Store vitamin A

Differentiate into myofibrobasts when there is damage to liver –> make collagen, form scars

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26
Q

Inflammatory adaptations in liver

A

Loss of microvilli
Stellate cells activate
Deposition of collagen (scar matrix) in space of Disse
Loss of fenestrae - endothelial cells become continuous

Result = blood does not interact with hepatocytes

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27
Q

Most important RF for hepatocellular carcinoma

A

Cirrhosis

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28
Q

Classification of chronic hepatitis

A 
Grade = severity of inflammation
Stage = severity of fibrosis

Stage more important than grade for prognosis.

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29
Q

What are mallory denk bodies?

A

Collapsed cytoskeleton in swollen hepatocytes

Present in EtOH hepatitis

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30
Q

Haemochromatosis pathogenesis

A

Mutation om Chr6 (HFe)

Increased GI iron absorption (with no way to excrete it)

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31
Q

Wilson’s disease pathogenesis

A

Mutation on Chr 13
Often >1 mutation

Failure of excretion of copper into bile by hepatocytes –> accumulation in liver, CNS

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32
Q

Tx for Wilson’s disease

A

Zinc

Trientine

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33
Q

Histological Ix for Wilson’ disease

A

Rhodanine stain - copper in hepatocytes (brown on blue counterstain)

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34
Q

Histology of alpha anti-trypsin 1 deficiency

A

Intra-cytoplasmic inclusions (misfiled protein)
Macronodular hepatitis
Cirrhosis

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35
Q

Macroscopic appearance of liver adenoma

A

Sharp demarcation

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36
Q

Most common type of liver malignancy?

A

Metastatic

Receives blood from pancreas, stomach, large bowel etc. via portal circulation

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37
Q

Tumour marker for primary hepatocellular carcinoma?

A

Alpha foeto protein (AFP)

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38
Q

Associations with Primary cholangiocarcinoma

A

Primary sclerosis cholangitis (PSC)
Worm infections (North Thailand)
Cirrhosis

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39
Q

Cause of nutmeg liver?

A

Congestive heart failure

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40
Q

Hirschsprung’s disease pathogenesis

A

Absence of ganglion cells from Auerbach (mesenteric) and Meissner (submucosal) plexus of rectum and distal colon.

Uncoordinated peristalsis causes functional obstruction

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41
Q

Diagnostic Ix for Hirschsprung’s

A

Full thickness rectal biopsy

- Hypertrophied nerve fibres but no ganglia

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42
Q

Locations of volvulus

A 
Small bowel (infants)
Sigmoid colon (elderly)
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43
Q

Definition of volvulus?

A

Complete twisting of loop of bowel
at mesenteric base
around vascular pedicle

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44
Q

Pathogenesis of diverticular disease

A

High intra-luminal pressure forces mucosa through ‘weak points’ of bowel

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45
Q

Most common location for diverticular disease

A

Left colon (90%)

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46
Q

Histology of pseudomembranous colitis

A

Macroscopic:

  • erytemaotus
  • ‘wet cornflake’ lesions (pseudomembranes)
47
Q

most common vascular disorder of intestinal tract?

A

Ischaemic colitis / infarction

48
Q

Usual location of ischaemic colitis / infarction

A

Watershed zones (where previous and next blood supply poorly overlap –> area with poor supply vulnerable to ischaemia)

Splenic flexure - SMA, IMA
Rectosigmoid - IMA, internal iliac artery

48
Q

Usual location of ischaemic colitis / infarction

A

Watershed zones (where previous and next blood supply poorly overlap –> area with poor supply vulnerable to ischaemia)

Splenic flexure - SMA, IMA
Rectosigmoid - IMA, internal iliac artery

49
Q

Causes of ischaemic colitis / infarction

A

Arterial occlusion - atheroma, thrombosis, embolism

Venous occlusion - thrombus, hyper coagulable state

Small vessel disease - DM, cholesterol emboli, vasculitis

Low flow states - CCF, haemorrhage, shock

Obstruction - hernia, intussusception, volvulus, adhesions

50
Q

Key histological features of Crohn’s

A 
Mouth - anus
Skip lesions
Transmural inflammation
Non caseating granulomas
Sinus / fistula common
51
Q

Key histological features of UC

A 
Rectum + colon
\+/- mild 'backwash ileitis' and appendiceal involvement
Continuous
Mucosal inflammation only
Shallow ulcers
Bowel wall normal thickness
52
Q

Complications of UC

A

Toxic megacolon
Adenocarcinoma - 20-30x risk
Severe haemorrhage

53
Q

Complications of Crohn’s

A

Fat wrapping

Thick ‘rubber hose’ bowel wall, narrow lumen

Linear ulcers, fissures
Abscesses

Adenocarcinoma (less than UC)

54
Q

Derm manifestations of UC & Crohn’s

A

Crohn’s: Pyoderma gangrenosum, erythema multiforme, erythema nodosum

UC: Pydoerma gangrenosum, erythema nodosum

55
Q

Non Neo-plastic polyps

A

Hyperplastic - very common, no progression (for exam purposes)

Inflammatory ‘pseudopolyps’ - areas of regenerating mucosa which project into lumen, seen in UC

Hamartomatous - juvenile, Peutz-Jeghers

56
Q

Neoplastic polyps

A

Tubular

Tubulovillous

Villous

57
Q

Risk factors for cancer (from polyp)

A

Size - >4cm approx 45% invasive malignancy

Proportion of villous component

Degree of dysplastic change

58
Q

Familial adenomatous polyposis - genetics & pathogenesis

A

Autosomal dominant
Chromosome 5q21 - APC tumour suppressor gene
Minimum 100 polyps (usually colorectal adenomatous)

Virtually 100% develop ca. within 10-15 yrs

59
Q

Garnder’s syndrome - key features

A

Subtype of Familial adenomatous polyposis

Distinct extra-intestinal features

  • multiple oestomas of skull, mandible
  • epidermoid cysts
  • desmoid tumours
  • dental caries, unerupted supernumerary death
  • post surgical mesenteric fibromatoses
60
Q

Hereditary non polyposis colon cancer - genetics, pathogenesis

A

Autosomal dominant, uncommon
Involves 1 of 4 DNA mismatch repair genes –> DNA replication errors

Onset of colorectal ca. at early age

61
Q

Type & distribution of cancer in HNPCC (Lynch syndrome)

A

high % proximal to splenic flexure
Poorly differentiated + mutinous carcinoma more common

+ extracolonic cancer: endometrial, prostate, breast, stomach

62
Q

Most common type of lower GI cancer

A

Adenocarcinoma - 98%

63
Q

RF for Lower GI cancer

A

Diet - low fibre, high fat
Lack of exercise, obesity
Familial
Chronic IBD

64
Q

Tumour marker for lower GI cancer

A

Carcinoembryonic antigen (CEA)

65
Q

Staging system for lower GI cancer

A

Duke’s

A = limited to mucosa

B1 = extending into muscular propria
B2 = transmural invasion, no LN
C1 = extending into muscular propria, LN involvement
C2 = transmural invasion, LN involvement

D = distant mets

66
Q

Layers of normal oesophagus

A

Epithelium
Submucosa
Muscular extra

67
Q

Normal stomach - features of body

A

Lined by gastric mucosa columnar epithelium - foveolar, mucin secreting

Specialised glands in lamina propria - produce acid, IF.

Muscular mucosae

No goblet cells!

68
Q

Normal stomach - features of antrum

A

Lined by gastric mucosa columnar epithelium - foveolar, mucin secreting

Non specialised glands in lamina propria - gastric pits

Muscular mucosae

69
Q

Normal duodenum features

A

Glandular epithelium with goblet cells - ‘intestinal type’

Villous architecture - villous:crypt ratio of >2:1

70
Q

Features of acute oesophagitis

A

Neutrophils

71
Q

Most common cause of acute oesophagitis

A

GORD / reflux

72
Q

Barrett’s oesophagus types

A

Without goblet cells - gastric type metaplasia

With goblet cells - intestinal type metaplasia, more likely to progress to ca.

73
Q

Barrett’s oesophagus - basic process/pathogenesis

A

Squamous epithelium replaced by metaplastic columnar epithelium

74
Q

Most common oesophageal ca.?

A

Adenocarcinoma (in ‘developed’ countries)

Squamous cell carcinoma (in ‘developing’ countries)

75
Q

Adenocarcinoma of oesophagus - key features

A

Associated with reflux

Lower oesophagus

Gland formation + mucin production (hallmarks of adenocarcinoma)

76
Q

Squamous cell carcinoma of oeseophagus - key features

A

Associated with EtOH & smoking

mid-lower oesophagus

Keratin production (+ intercellular bridges)

77
Q

Causes of oesophageal varices

A

Cirrhosis - most common

+ portal vein thrombosis

78
Q

Causes of acute gastritis

A

Chemical - aspirin, NSAIDs, alcohol, corrosives

Infection - Helicobacter pylori

79
Q

Causes of chronic gastritis

A

Autoimmune - anti-parietal Abs, mainly affects body of stmach

Bacterial - H. pylori, affects antrum

Chemical - NSAIDs, reflux, affects antrum

80
Q

Biopsy finding in H. pylori infection

A

Gastric ulcer

Chronic gastritis +/- acute activity

81
Q

Complications of H. pylori infection

A

CLO-IM dysplasia

Adenocarcinoma

Lymphoma (MALToma)

82
Q

Definition of ulcer

A

Defect through muscularis propria

83
Q

Most common type of gastric cancer?

A

Adenocarcinoma (95%)

84
Q

Morphological categories of gastric adenocarcinoma

A

Intestinal - well differentiated

Diffuse - poorly differentiated (linitis plastica), includes signet ring cell carcinoma!

85
Q

Other (non adenocarcinoma) gastric cancer types

A

Squamous cell carcinoma

Lymphoma - MALToma

Gastrointestinal stromal tumour (GIST)

Neuroendocrine tumour

86
Q

Pathogenesis of duodenitis

A

Increased acid production in stomach
Spills over into duodeum
Chronic inflammation, gastric metaplasia

NOTE: once gastric type cells present, duodenum is vulnerable to H. Pylori

87
Q

Causative organism of Whipple’s disease

A

tropheryma whipellii

Rare bacterial infection seen in duodenum

88
Q

Biopsy evidence of coeliac disease

A

Villous atrophy

Crypt hyperplasia

Increased intraepithelial lymphocytes (normal <20 per 100 enterocytes)

NOTE: will only show this if currently eating gluten

89
Q

Coeliac-associated cancer

A

In duodenum

T cell origin ‘enteropathy associated T cell lymphoma’ (EATL)

90
Q

Functional cells of pancreas?

A

Acinar cells

  • produce enzymes
  • have abundant rough ER + Golgi
91
Q

Definition of acute pancreatitis

A

Acute inflammation of pancreas

caused by aberrant release of pancreatic enzymes

92
Q

Causes of acute pancreatitis

A

Duct obstruction

  • Gallstones - 50%
  • Trauma - fibrotic scarring, narrowing
  • Tumours
    • EtOH

Metabolic/toxic

  • Alcohol - 33%
  • Drugs e.g. thiazides
  • Hypercalcaemia
  • Hyperlipidaemia

Poor blood supply - shock, hypothermia

Infection - mumps

Autoimmune

Idiopathic - 15%

93
Q

Pathophysiology of acute pancreatitis (from gallstones)

A

Gallstone stuck distal to where common bile duct + pancreatic duct join

Reflux up pancreatic duct

Damage to acini + release of pro-enzymes which become activated

Activated enzymes cause acinar necrosis –> further enzyme release

94
Q

Histology of fat necrosis in acute pancreatitis

A

Macroscopic:
Necrosis forms free fatty acids
Ca2+ ions bind to free fatty acids, forming soaps
Seen as yellow/white foci

Microscopic
Blue = histological correlates of white/yellow foci

95
Q

Pathophysiology of acute pancreatitis (due to EtOH)

A

Spasm/oedema of Sphincter of Oddi + formation of protein-rich pancreatic fluid

Fluid obstructs pancreatic ducts

96
Q

Patterns of injury in acute pancreatitis

A

Periductal - necrosis of acinar cells near ducts (obstruction)

Perilobular - necrosis at edges of lobules (ischaemia)

Panlobular - progressive periductal + perilobular damage

97
Q

Causes of chronic pancreatitis

A

Metabolic/toxic

  • alcohol 80%
  • haemochromatosis

Duct obstruction

  • gallstones
  • abnormal pancreatic duct
  • CF ‘mucoviscoidosis’

Tumours

Autoimmune

98
Q

Complications of chronic pancreatitis

A

Malabsorption
Diabetes mellitus (late - neuroendocrine cells survive relatively well)
Pseudocysts
Increased risk of ca. of pancreas

99
Q

Pancreatic pseudocyst - key features

A

Lined by fibrous tissue - not epithelial lining
Contain fluid rich in pancreatic enzymes OR necrotic material
Usually connect with pancreatic ducts

100
Q

Possible outcomes of pancreatic pseudocyst

A

Perforate
Become infected
Compress adjacent structures
Resolve

101
Q

Key features of Autoimmune pancreatitis

A

Large no. of IgG4 + plasma cells

Involves pancreas, bile ducts + almost any other body part

102
Q

Most common pancreatic neoplasm?

A

Ductal carcinoma - 85%

103
Q

Risk factors for pancreatic ductal carcinoma

A

Smoking
BMI, dietary factors
Diabetes
Chronic pancreatitis

104
Q

Pathogenesis of pancreatic ductal carcinoma

A

Arise from dysplastic lesions

  • pancreatic intraductal neoplasms (PanIN)
  • intraductal mucinous papillary neoplasm

K-Ras mutation in 95%

105
Q

Tumour marker for pancreatic ductal carcinoma

A

Carbohydrate antigen 19-9 (CA19-9)

106
Q

Distribution of pancreatic ductal carcinoma

A

Head 60% - may present earlier due to obstruction of biliary tree
Body
Tail
Diffuse

107
Q

Histology of pancreatic ductal carcinoma

A

Adenocarcinoma so mucin production + glands

Set in desmoplastic stroma (storm that arises in response to cancer - fibrous reaction)

Perineural invasion - characteristic

108
Q

Pancreatic endocrine neoplasms - key features

A

Usually NON secretory
But can release glucagon, insulin etc.

Difficult to predict behaviour.
May be associated with MEN 1

109
Q

Most common secretory tumour

A

Insulinoma

110
Q

Risk factors for gallstones (cholelithiasis)

A

Increase age ‘forty’
Female

Ethnicity & geography - Native American
Hereditary disorders of bile metabolism
Drugs - COCP
Acquired disorders - rapid weight loss (increased excretion of lipids)

111
Q

Pigment gallstones - characteristics

A

Contain calcium salts of unconjugated bilirubin
Multiple
Mostly radio-opaque

112
Q

features of chronic cholecystitis

A

Chronic inflammation - lymphocytes
Fibrosis
Thickened wall (normal <2mm)
Diverticula e.g. Rokitansky-Aschoff sinuses

90% associated with gallstones

113
Q

Most common cause of gallbladder ca.

A

Gallstones - 90% associated

Path 2022 (12 decks)

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