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USMLE GI > Pathology part 2 (Cancer, liver, pancreas) > Flashcards

Pathology part 2 (Cancer, liver, pancreas) Flashcards

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USMLE® Step 1 flashcards
1
Q

What is Peutz-Jeghers syndrome?

A
  • Small dark coloured spots on lips, nostrils, anus
  • Develop polyps (hamartomatous) in colon
  • Increased risk of GI cancers and breast
  • Autosomal dominant
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2
Q

What syndromes are associated with hamartomatous polyps in the colon?

A
  • Peutz-Jeghers

- Juvenile polyposis synrdrome

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3
Q

Name the generally nonneoplastic polyps?

A
  • Hamartomatous polyps (peutz-jeghers, juvenile polyposis)
  • Hyperplastic polyps (most common)
  • Inflammatory pseudopolyps (IBD)
  • Mucosal polyps (clinically insignificant)
  • Submucosal polyps (lipomas, leiomyomas, fibromas)
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4
Q

What noneoplastic polyp is associated with IBD?

A

Inflammatory pseudopolyps

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5
Q

What is the most common polyp?

A

Hyperplastic

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6
Q

What are mucosal polyps?

A
  • Small, usually < 5 mm
  • They look similar to normal mucosa
  • Clinically insignificant
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7
Q

What types of growths are submucosal polyps?

A
  • May be lipomas, leiomyomas and other lesions
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8
Q

Where are hyperplastic polyps most commonly found?

A

Rectosigmoid

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9
Q

What can hyperplastic polyps develop into?

A

Serrated polyps and more advanced lesions

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10
Q

Via what pathway do adenomatous polyps arise?

A

Neoplastic, via chromosomal instability pathway with mutations in APC and KRAS

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11
Q

What do adenomatous polyps arise with?

A

Usually asymptomatic, may present with occult bleeding

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12
Q

What has a greater malignant potential tubular or villous histology?

A

Villous more malignant than tubular (tubulovillous in between)
- Villous histology is villainous

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13
Q

How do serrated polyps develop?

A
  • Neoplastic
  • Characterised by CpG island methylator phenotype (CIMP; cytosine base followed by guanine, linked by a phosphodiester bond)
  • Defect may silence MMR gene (DNA mismatch repair) expression
  • Mutations lead to mucrosatellite instability and mutations in BRAF
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14
Q

What do serrated polyps look like on biopsy?

A

‘Saw-tooth’ pattern of crypts on biopsy

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15
Q

What percetage colorectal cancers are caused by serrated polyps?

A

20% of cases of sporadic CRC

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16
Q

FAP is what kind of mutation, on what gene and in what location?

A
  • Autosomal dominant
  • APC tumour suppressor gene
  • Chromosome 5q21-22
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17
Q

When do polyps arise in FAP?

A

Thousands arise all throughout colon after puberty, rectum always involved

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18
Q

How is FAP treated?

A
  • Prophylactic colectomy as 100% progress to CRC
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19
Q

What is Gardner syndrome?

A
  • FAP + osseus and soft tissue tumours (eg osteomas of skull or mandible)
  • Congenital hypertrophy of retinal pigment epithelium
  • Impacted/supernumerary teeth
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20
Q

What is turcot syndrome?

Turcot - Turban

A
  • FAP or Lynch +

- Malignant CNS tumour (medulloblastic, glioma)

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21
Q

What is Juvenile polyposis syndrome?

A
  • Aut dominant
  • Children < 5 years old
  • Numerous hamartomatous polyps
  • Increased risk of CRC
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22
Q

What genes are affected in Lynch syndrome?

A
  • MLH1, MSH2
  • Mismatch repair genes
  • Microsatellite instability
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23
Q

What cancers are assocaited with Lynch syndrome?

A
  • 80% progress to CRC
  • Proximal colon always involved
  • Associated with endometrial, ovarian and skin cancers
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24
Q

What is a useful tumour marker to predict recurrent colorectal cancer?

A

CEA tumor marker (should not be used for screening)

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25
Q

What percentage of colon cancer patients have a FH?

A

25%

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26
Q

Where is colon cancer most common / least common?

A

Rectosigmoid > Ascending > Descending

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27
Q

What is hematochezia?

A

Fresh blood in stools

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28
Q

What bacterial infection is associated with colon cancer?

A

S bovis (gallolyticus) bacteremia/endocarditis or as an acute episode of diverticulitis

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29
Q

What are the signs of colon cancer in the ascending colon?

A
  • Occult bleeding
  • Exophytic mass
  • iron deficiency anemia
  • Weight loss
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30
Q

What are the signs of colon cancer in the descending colon?

A
  • Infiltrating mass
  • Partial obstruction
  • Colicky pain
  • Hematochezia
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31
Q

What are risk factors for colon cancer?

A
  • Adenomatous and serrated polyps
  • Familial cancer syndromes
  • IBD
  • Tobacco
  • Processed meat + low fiber diet
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32
Q

Mutations in APC and FAP (chromosomal instability pathway)cause cancer via what sequence?

A

Adenoma-carcinoma sequence

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33
Q

What causes CRC via the serrated polyp pathway?

A

Microsatellite instability pathway

- Mutations or methylation of mismatch repair genes (eg MLH1/Lynch)

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34
Q

The serrated polyp (Lynch) CRC pathway usually leads to CRC where?

A
  • Right-sided CRC
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35
Q

How can NSAIDs be chemopreventive?

A

Overexpression of COX-2 has been linked to CRC

36
Q

Molecular pathway

A

LEARN

37
Q

What patients may experience spontaneous bacterial peritonitis?

A

Patients with cirrhosis and ascites

38
Q

What organisms may cause spontaneous bacterial peritonitis?

A
  • E. coli, Klebsiella (gram -ves most common)

- Streptococcus

39
Q

What is Reye syndrome?

A
  • Childhood hepatic encephalopathy
  • VZV or influenza treated with aspirin

Reye of sunSHINE

  • Steatosis of liver/hepatocytes
  • Hypoglycemia
  • Hepatomegaly
  • Infection
  • Not awake (coma)
  • Encephalopathy
    • Vomitting
40
Q

Describe how aspirin actually causes on a microscopic level Reye syndrome?

A
  • Aspirin metabolites decrease Beta-oxidation by reversible inhibition of mitochondrial enzymes (changes to mitochondrial abnormalities)
41
Q

What are 3 main stages of alcoholic liver disease?

A
  • Hepatic steatosis
  • Alcoholic hepatitis
  • Alcoholic cirrhosis
42
Q

What can be seen in hepatic steatosis?

A

Macrovesicular fatty change that may be reversible with alcohol cessation

43
Q

What can be seen in alcoholic hepatitis?

A
  • Swollen and necrotic hepatocytes with neutrophilic infiltration
  • Mallory bodies (intracytoplasmic eosinophilic inclusions of damaged keratin filaments)
44
Q

What can be seen in alcoholic cirrhosis?

A
  • Sclerosis around central vein may be seen in early disease
  • Regenerative nodules surrounded by fibrous bands in response to chronic liver injury -> portal hypertension, end-stage liver disease
45
Q

What may be associated with autoimmune hepatitis?

A
  • Positive antinuclear, anti-SM and anti-liver/kidney microsomal antibodies
46
Q

What can be seen on histology in autoimmune hepatitis?

A

Portal and periportal lymphoplasmacytic infiltrate

47
Q

What may trigger hepatic encephalopathy?

A
  • Increased NH3 production and absorption (due to GI bleed, constipation, infection)
  • Decreased NH3 removal (due to renal failure, diuretics, nypassed hepatic blood flow post-TIPS)
48
Q

How is hepatic encephalopathy treated?

A
  • Lactulose (Increased NH4+ generation)

- Rifaximin (Decreased NH3-producing gut bacteria)

49
Q

What are the different types of liver tumour?

A
  • Hepatic hemangioma (most common)
  • Focal nodular hyperplasia (asymptomatic)
  • Hepatocellular carcinoma (primary malignant tumour)
  • Hepatic angiosarcoma (rare malignant tumour of endothelial origin)
  • Metastases
50
Q

What are the signs of focal nodular hyperplasia?

A
  • Females 35-50
  • Hyperplastic reaction of hepatocytes to an abherrant dystrophic artery
  • Marked by central stellate scar
  • Asymptomatic usually
51
Q

What bug may lead to hepatocellular carcinoma?

A

Aspergillus’ aflatoxin

52
Q

What may be the signs of hepatocellular carcinoma?

A
  • Anorexia, jaundice, tender hepatomegaly, decompensation of previously stable cirrhosis
  • Budd-Chiari syndrome
53
Q

How can hepatocellular carcinoma spread?

A

Hematogenously

54
Q

How is hepatocellular carcinoma diagnosed?

A
  • Increased alpha-fetoprotein
  • US or contrast CT/MRI
  • Biopsy
55
Q

What is hepatic adenoma linked to?

A
  • Rare, benign tumour
  • Linked to OCP and anabolic steroid use
  • May regress or spontaneously rupture (abdo pain + shock)
56
Q

What are some of the sources of malignant liver tumours?

A
  • GI
  • Breast
  • Lungs
    Rarely solitary metastases
57
Q

What may cause nutmeg liver (mottled appearence)?

A

Budd-Chiari syndrome

58
Q

What can alpha1 antitrypsin deficiency cause in liver on histology?

A

Misfolded gene product protein aggregates in hepatocellular ER -> cirrhosis with PAS positive globules in liver

59
Q

What may cause neonatal jaundice?

A
  • Lower activity of UDP gluconyltransferase (physiological clears up by itself)
  • Biliary atresia (pediatric liver transplantation)
60
Q

What causes biliary atresia?

A
  • Fibro-obliterative destruction of bile ducts -> cholestasis
61
Q

What are the 4 hereditary hyperbilirubinemia syndromes?

A
  • Gilbert syndrome
  • Crigler-Najjar syndrome type 1
  • Dubin-Johnson syndrome
  • Rotor syndrome
    All autosomal recessive
62
Q

What enzyme is decreased in Gilbert syndrome?

A

UDP-gluconyltransferase

63
Q

What causes Crigler-Najjar syndrome?

A

Absent UDP-gluconyltransferase

64
Q

How is Crigler-Najjar syndrome treated?

A
  • Plasmapheresis, phototherapy

- Liver transplant is curative

65
Q

Type 2 crigler-Najjar syndrome which is less severe can be treated with what?

A

Phenobarbital which increases liver enzyme synthesis

66
Q

What causes Dubin-Johnson syndrome?

A
  • Conjugated hyperbilirubinemia due to defective liver excretion
  • Dark/black liver due to impaired excretion of epinephrine metabolites, benign
67
Q

What causes causes Rotor syndrome?

A
  • Similar to Dubin-Johnson but milder
  • Liver looks Regular (not black)
  • Impaired hepatic storage of conjugated bilirubin
68
Q

What is th defect in Wilson disease?

A
  • Hepatocyte copper-transporting ATPase

- ATP7B gene, chromosome 13

69
Q

What is Wilson disease treated with?

A
  • Chelation with penicillamine or trientine
  • Oral zinc
  • Liver transplant in acute liver failure
70
Q

Hamosiderin (iron) can be identified with what?

A
  • Prussian blue stain on biopsy

- Liver MRI

71
Q

How is Haemochromatosis treated?

A
  • Phlebotomy
  • Iron chelation with:
  • Deferasirox, deferoxamine, deferipone
72
Q

How is PBC (primary biliary cholangitis) treated?

A

Ursodiol

73
Q

What disease is associated with primary sclerosing cholangitis?

A
  • Ulcerative colitis

- Increases risk of cirrhosis, cholangiocarcinoma and gallbladder cancer

74
Q

PSC has what signs?

A
  • Onion skin bile duct fibrosis

- Alternating strictures and dilation with beading of intra and extrahepatic bile ducts on ERCP, MRCP

75
Q

What antibodies can be increased in PSC?

A
  • Positive for MPO-ANCA/p-ANCA

- Increased IgM

76
Q

PBC has what signs in the blood?

A
  • Anti-mitochondrial antibody

- Increased IgM

77
Q

Describe pigment stones and what they are made from?

A
  • Black: Ca2+, bilirubinate, hemolysis, radiopaque

- Brown: Radiolucent, infection

78
Q

What is choledocholithiasis?

A

Presence of gallstone(s) in the common bile duct

79
Q

What is acalculous cholecystitis caused by?

A

Gallbladder stasis, hypoperfusion, CMV infection, critically ill patients

80
Q

What is Charcot triad?

A
  • Jaundice
  • Fever
  • RUQ pain
81
Q

What is Reynolds pentad?

A
  • Jaundice
  • Fever
  • RUQ pain
  • Altered mental status
  • Shock
82
Q

What is Porcelain gallbladder?

A

Calcified gallbladder due to chronic cholecystitis, usually found incidentally on imaging

83
Q

What can porcelain gallbladder predispose to?

A 
Gallbladder cancer (likely adenocarcinoma)
- Prophylactic cholecystectomy recommended
84
Q

What cacn be seen on histology of cholangiocarcinoma?

A

Infiltrating neoplastic glands associated with desmoplastic stroma

85
Q

What tumour marker is associated with pancreatic adenocarcinoma?

A

CA 19-9 tumor marker (also CEA, less specific)

USMLE GI (4 decks)

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