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Pathology Term 2 > Week 4 - HEPATOBILIARY > Flashcards

Week 4 - HEPATOBILIARY Flashcards

Cholecystitis, Cholelithiasis + Cancer, Pancreatitis, Pancreatic Cancer

1
Q

What is commonest cause of cholecystitis?

A

Cholelithiasis - 95%

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2
Q

What is the pathogenesis of cholecystitis?

A
  1. obstruction
  2. stasis (of bile)
  3. increased pressure in gall bladder
  4. ischaemia
  5. mucosal damage by bile salts (detergent) –> therefore inflammation + secondary infections (e.g. E. coli)
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3
Q

What are the complications of cholecystitis?

A
  • cholangitis (inflammation spreads to biliary tree –> secondary biliary cirrhosis)
  • empyema
  • rupture
  • peritonitis
  • gall stone ileus
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4
Q

What are the clinical features of acute cholecystitis?

A
  • biliary pain –> steady, progressive, RUQ to R shoulder radiation
  • obstructive jaundice (20% cases) –> when total obstruction of CBD occurs
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5
Q

What is morphology of acute cholecystitis?

A

Acute inflammation
-neutrophils, oedema, vasodilation
Haemorrhage

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6
Q

What disorder is suspected if serum amylase is increased?

A

Acute pancreatitis

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7
Q

What is gall stone ileus?

A
  • complication of acute cholecystitis

- one of the gall stones enters GIT + causes obstruction

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8
Q

What is a key difference between acute and chronic cholecystitis?

A
  • markedly thicker and more concentrated bile in chronic –> BILIARY GRAVEL
  • also.. pts. with chronic cholecystitis typically present with nausea/vomiting + intolerance for fatty food
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9
Q

What is the microscopy of chronic cholecystitis?

A
  • chronic inflammation
  • thick fibrotic wall
  • aschoff-rokitansky sinuses –> excess luminal pressure pushes glands through muscular layer (herniation)
  • atrophy of mucosa + muscle hypertrophy
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10
Q

What are aschoff-rokitansky sinuses?

A

-herniation of mucosal glands through the mucosa seen in chronic cholecystitis

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11
Q

What is acalculous cholecystitis?

A
  • cholecystitis without gall stones
  • seen in pts. with sepsis, burns, hypotension, trauma, diabetes
  • secondary to wall ischaemia –> decreased protection and movement –> stasis
  • mild biliary symptoms (as primary disease is prominent)
  • increased risk of gangrene or perforation
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12
Q

What is cholesterolosis?

A
  • type of chronic cholecystitis
  • increased cholesterol accumulates within the folds of the mucosa causing hundreds of small polyps
  • STRAWBERRY GALL BLADDER –> as multiple polyps cause characteristic gross feature
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13
Q

What are risk factors for cholecystitis/cholelithiasis?

A

FFFF

  • female
  • fat
  • forty
  • fertile
  • fair-skinned
  • oral contraceptives
  • disorders of bile metabolism
  • hyperlipidaemia
  • diabetes
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14
Q

What are the 2 major types of gall stones?

A
  1. Mixed cholesterol stones (80%)
    - stones with calcium, bile, blood and increased cholesterol
  2. Pigment stones (20%)
    - black –> hemoglobin (hemolytic anemia)
    - brown –> calcium increased (infections/IBD)
    - yellow –> pure cholesterol (familial hyperlipidaemia)
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15
Q

What are the 3 triad features of cholelithiasis?

A
  1. RUQ steady pain
  2. fever
  3. leukocytosis
  • progressive –> R shoulder/back radiation of pain
  • steady NOT colicky pain
  • *BUT 70-80% of pts. are asymptomatic
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16
Q

What is the typical chronic presentation of cholelithiasis?

A

Fat intolerance
-indigestion, stomach upsets, flatulence following fatty foods

*clay stools (fat in stools due to lack of bile digesting fats) –> foul-smelling, sticky, pale

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17
Q

What is cholecystokinin?

A

Hormone released in response to fat food ingestion causing gall bladder contraction –> bile secretion

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18
Q

What is bile composed of and how is cholesterol made soluble?

A
  1. cholesterol
  2. bile salts
  3. bile pigment

*cholesterol made soluble by bile salts + lecithins (detergents) –> therefore, increased cholesterol or decreased bile salts = GALL STONES

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19
Q

What are the 4 pathogenetic factors of cholelithiasis?

A
  1. increased cholesterol/decreased bile salts
  2. stasis of bile
  3. pancreatic enzyme reflux into gall bladder
  4. infection

*deposition of cholesterol crystals leading to stone formation

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20
Q

What are the 4 etiological factors for cholelithiasis?

A
  1. Age/Sex: - female, fair, fat, forty, fertile
  2. Enironmental: - increased estrogen, OCP, pregnancy, obesity, rapid wt. loss
  3. Acquired: - hemolysis, infection, bile stasis
  4. Hereditary: - ABCG8 gene mutation (sterol transporter –> therefore increased cholesterol)
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21
Q

True or False?

Gall stones are typically visible on an X-ray

A

False

  • typically radioluscent (not seen on X-ray)
  • ONLY visible if calcium concentration in stone is markedly increased
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22
Q

Why are gall stones faceted in appearance?

A
  • stones present for many yrs

- rubbing of stones against each other causes faceting –> joint like surfaces

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23
Q

What is the morphology of mixed cholesterol gallstones (commonest)?

A
  • yellowish, golden, grey-brown stones
  • shiny, faceted stones
  • varying colour based on contents
  • biliary gravel –> stasis
  • chol. >50% + bile + cells + blood + calcium (10%)
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24
Q

What is the morphology of pure cholesterol gall stones?

A
  • round
  • yellow
  • spiky surface –> bleeding

*marked hypercholesterolemia (usually familial)

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25
Q

What is the morphology of pigment stones in hemolytic anemia?

A
  • dark/black
  • friable soft stone (can crush in hand - powdery)
  • increased bilirubin (from hemolytic anemias)
  • thick wall; neck obstruction
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26
Q

What is choledocholithiasis?

A

gall stones present in the CBD

27
Q

What are complications of cholelithiasis?

A
  • acute cholecystitis –> COMMONEST
  • choledocholithiasis
  • pancreatitis (stone obstructs distal CBD causing bile reflux into pancreas
  • acute/chonic cholangitis
  • gall stone ileus
  • gall bladder cancer
  • cholangiocarcinoma
28
Q

What is the commonest tumour of gall bladder?

A

adenocarcinoma

-tumours are v. rare

29
Q

What are the 2 types of gall bladder tumours?

A
  1. adenocarcinoma
    - increase F
    - abdo. pain, anorexia, increased ALP
    - late Dx./poor prognosis
  2. cholangiocarcinoma
    - bile duct adenocarcinoma
    - early obstruction
    - treated early/better prognosis
    - irregular dysplastic glands
30
Q

What is Klatskin tumour?

A

-bile duct adenocarcinoma occuring at the hilum junction

31
Q

True or False?

Pancreas is predominantly en endocrine organ

A

False

  • predominantly exocrine (digestive juices/enzymes)
  • endocrine 1-2%
32
Q

What is meant by pancreatic enzymes being proenzymes?

A

Enzymes are lytic but inactive

33
Q

What activates the pancreas and what protective mechanism is in place to prevent overactivation?

A
  • activated by trypsin in duodenum

- acini secrete trypsin inhibitors

34
Q

What are the 3 congenital pancreas disorders and briefly describe the commonest one?

A
  1. Pancreas divisum (commonest - 3%)
    - no wirsung duct (duct that joins minor + major ducts)–> leads to obstruction –> chronic pancreatitis
  2. Annular pancreas
    - pancreas encircles duodenum
  3. Ectopic pancreas
    - pancreatic tissue in other organs (commonly stomach/duodenal wall)`
35
Q

What is the key diagnostic test for pancreatitis?

A
  • serum amylase (<24hrs)

- serum lipase (>72hrs)

36
Q

What is contraindicated in terms of investigations of pancreatitis?

A

BIOPSY

  • hazardous
  • don’t ouch the pancreas
  • can activate and cause increase enzyme secretion
37
Q

Where is the pancreas located?

A

behind the stomach

-it is a retroperitoneal organ

38
Q

Outline microscopy of a normal pancreas

A

Acini (exocrine)
-digestive proenzymes released to duodenum (activated here)

Islets of langerhans (endocrine)
-clusters of endocrine cells (alpha, beta, delta)

39
Q

What is acute pancreatitis?

A
  • acute, reversible inflammation of the pancreas due to spreading enzymatic autodigestion - “eating itself”
  • causes haemorrhage + fat necrosis –> shock and multi-organ failure
  • activation/defective inactivation of trypsin
40
Q

What is the etiology of acute pancreatitis? and specify the commonest.

A

COMMONEST –> alcohol (M) + gall stones (F) - 80%

  • obstruction to outflow; acinar cell injury; defective intracellular transport
  • shock, immune, mumps, hypercalcemia, drugs, surgery, ERCP (DON’T touch the pancreas)
41
Q

What enzymes are released in pancreatic damage and what do each result in?

A
  • lipase –> fat necrosis (inflammation)
  • protease –> BV injury (bleeding)
  • amylase –> diagnostic test
42
Q

Outline pathogenesis of acute pancreatitis

A

-alcohol and gallstones result in ductal obstruction, acinar cell injury and defective intracellular transport

Therefore:

  • release/activation of pancreatic enzymes
  • damage to pancreas occurs (inflammation)
  • increased serum amylase
  • increased lipase –> fat necrosis
  • increased proteases –> BV injury (bleeding)
43
Q

Why does pancreatitis epigastric pain radiate to the back?

A

It is a retroperitoneal organ located at the back (behind the stomach)

44
Q

What are the clinical features of acute pancreatitis?

A
  • constant, severe epigastric pain radiating to the back
  • abdominal distension, guarding, rigidity
  • diminished or absent bowel sounds (functional intestinal obstruction)
  • mild jaundice (CBD obstruction)
  • fever
  • vomiting
  • DIC, shock, fat necrosis, haemorrhage (proteases)
  • respiratory/circulatory failure
  • hypocalcemia
  • increased amylase/lipase
45
Q

What is the pathogenesis of hypocalcemia in acute pancreatitis?

A
  • lipase released from damaged/activated cells
  • fat necrosis
  • increased fatty acids
  • fatty acids bind calcium
  • increased calcium is dragged down and excreted with fatty acids –> hypocalcemia + calcium soaps
46
Q

True or False?

Only lipase is increased in chronic pancreatitis

A

True

  • amylase (<24hrs)
  • lipase (>72hrs)
47
Q

What are the 3 causes of acute pancreatitis in an alcoholic?

A
  1. duct obstruction
  2. acinar cell injury
  3. defective intracellular transport
48
Q

What is Grey Turner’s and Cullen’s sign?

A

Grey Turner’s
-discolouration of flanks/posterior portion of abdomen due to seepage of blood from proteases causing haemorrhage

Cullen’s

  • tracking of leaked blood to umbilicus
  • periumbilical ecchymosis
49
Q

What are gross features of acute pancreatitis?

A
  • oedema + inflammation
  • haemorrhage
  • fat necrosis (calcium soaps –> white spots indicating fatty acid release)
50
Q

What are the microscopic features of acute pancreatitis?

A
  • fat necrosis (opaque fat cells)
  • inflammatory cells increased
  • haemorrhage
51
Q

What are laboratory diagnostic findings in acute pancreatitis?

A
  • FBC –> increased neutrophils/leukocytes
  • increased serum amylase/lipase
  • decreased albumin when severe
  • hypocalcemia (fat necrosis)
  • BSLs –> hyperglycemia if loss of endocrine part
  • ALP/bilirubin –> mild increase if CBD obstruction due to gall stones
52
Q

What is chronic pancreatitis?

A
  • recurrent acute pancreatitis –> + fibrosis, scarring and atrophy of acini & ducts with calcification
  • loss of pancreatic function
  • malabsorption, decreased albumin, wt. loss (improper digestion)
  • pleural effusions ?
53
Q

What are complications of chronic pancreatitis?

A
  • pseudocyst
  • T1DM (endocrine cell damage)
  • cancer
  • steatorrhea/malabsorption –> pale stools
54
Q

What is a pancreatic pseudocyst?

A
  • a collection of fluid around the pancreas. The fluid in the cyst is usually pancreatic juice that has leaked out of a damaged pancreatic duct
  • it has no epithelial lining
  • complication of chronic pancreatitis
55
Q

What are microscopic features of chronic pancreatitis?

A
  • extensive fibrosis
  • acinar cell atrophy
  • dilated ducts
  • plenty of inflammation
56
Q

What is the commonest and most clinically significant pancreatic tumour?

A

Adenocarcinoma

  • commonly arises in head of pancreas
  • 4th common cancer (next to colon)
  • late age (>60yrs)
  • increased in males
  • highest mortality (5yr survival <5%) - :(
57
Q

What are the risk factors for pancreatic cancer?

A
  • smoking
  • diet (increased calorie, fat, meat, salt, fried/refined foods)
  • chronic pancreatitis
  • diabetes
  • MEN
  • colon cancer
58
Q

What are the gene mutations associated with pancreatic cancer and which is the most common?

A 
CDK2NA = most common
Also:
-K-ras
-BRCA1/2
-MLH1/MSH2
-SPINK1 --> hereditary pancreatitis
59
Q

What is the gene mutation for herditary pancreatitis?

A

SPINK1

60
Q

What is the pathogenesis of pancreatic cancer?

A

Risk factors –> genetic mutations (K-ras) –> PanIN (pancreatic in situ neoplasia) –> invasive carcinoma

61
Q

What are the clinical features of pancreatic carcinoma?

A
  • epigastric pain –> radiates to the back
  • significant weight loss
  • depression*
  • jaundice (CBD obstruction)
  • Courvoisier’s sign –> palpable gall bladder + jaundice
  • Trousseau’s sign –> migratory thrombophlebitis
  • T1DM –> beta cell destruction
62
Q

What are the gross and microscopic features of pancreatic cancer?

A

Gross:

  • near head of pancreas
  • involves pancreatic duct + CBD
  • hard, irregular white tissue

Micro:

  • irregular dysplastic glands in dense stroma (fibrous tissue)
  • fibrosis
  • irregular nuclei
63
Q

Outline pancreatic cancer staging (T1 –> T4)

A

T1: - <2cm, no ductal incolvement
T2: - >2cm, with ductal involvement
T3: - invades duodenum, bile duct, major veins, or peripancreatic tissues
T4: - invades stomach, spleen, colon or larger arteries

64
Q

What is the pathogenesis of pedal oedema in chronic pancreatitis?

A

Lack of absorption/protein digestion –> hypoalbuminemia –> decreased oncotic pressure –> PEDAL OEDEMA (leaky capillaries)

Pathology Term 2 (6 decks)

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