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Digestive MBChB 2 > Lecture 23; Pancreatic and gallbladder pathology > Flashcards

Lecture 23; Pancreatic and gallbladder pathology Flashcards

1
Q

Describe the examination of pancreas;

A

“hidden” non palpable organ and symptoms are late onset (Late stage of detection often)

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2
Q

What can the functions of the pancreas be categorised into?

A
  • Exocrine (80-90%)

- Endocrine (10-20%)

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3
Q

Describe the cellular structure of the pancreatic exocrine glands;

A
  • Composed of acinar cells and ducts

- Acinar cells contain zymogen granules

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4
Q

Whats in the zymogen granules?

A

Zymogens = inactive enzyme precursors for trypsin, chymotrypsin, amylase, lipase, nucelase and elastase.

Released as pro-enzymes then activated by trypsin

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5
Q

Describe the cellular structure of the pancreatic endocrine glands;

A

Islets of langerhans

- Secrete insulin, glucagon and other hormones

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6
Q

What are some potential pathologies of the pancreas;

A
  • Congenital/Genetic: Cystic fibrosis
  • Inflammatory/Ineffective: Actue and chronic pancreatitis
  • Malignant: Carcinoma of the pancreas
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7
Q

Describe what acute pancreatitis is and its spectrum;

A

Inflammation of the pancreas - associated with acinar cell injury

  • Spectrum of severity and duration
  • Mild 60-70% cases, low mortality
  • Severe 30-40% cases, 20-30% mortality
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8
Q

What are the four major categories of acute pancreatitis eitiology? and an example for each;

A
  • Metabolic -> ALCOHOL
  • Mechanical -> GALLSTONES, trauma
  • Vascular -> Shock, vasculitis
  • Infection -> Mumps

and drugs.

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9
Q

What is the most common causes of acute pancreatitis?

A

Alcohol and gallstones

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10
Q

What does damage to pancreatic acinar cause?

A

Damage to pancreatic acinar and release of enzymes into immediate environment/ducts. This results in damage to the pancreas (Think POM and how this might cause damage)

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11
Q

What is the pathology of pancreatitis?

A
  • Autodigestion by pancreatic enzymes

- Cell injury response mediated by inflammatory enzymes

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12
Q

What are the consequences of pancreatic enzyme release in the ducts;

A
  • Proteases: Proteolytic destruction acini, ducts, islets
  • Lipases: Fat necrosis- Pancreas and other sites
  • Elastases: Blood vessel destruction leading to interstitial haemorrhage

Cell injury response: Inflammation, oedema, impaired blood flow, ischemia

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13
Q

What are the key events to trigger an acute pancreatic event?

A
  • Obstruction

- Direct injury to acinar cells

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14
Q

Write some notes on obstruction and duct pressures;

A

Pancreatic duct obstruction by gallstones and ductal concretions present in alcoholics

  • Increased intrapancreatic ductal pressure
  • Accumulation of enzyme rich interstitial fluid
  • Fat necrosis as lipases already active
  • promotes oedema and local inflammation
  • Pressure and oedema compromises local blood flow
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15
Q

What are the clinical features of acute pancreatitis?

A
  • Acute pain, epigastric
  • Nausea and vomiting
  • Fever, tachycardia
  • Marked abdominal tenderness
  • may have ileus
  • rarely shock
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16
Q

How is acute pancreatitis diagnosed?

A
  • High white cell count
  • Elevated serum amylase (lipase)
  • CT scan; Oedema, necrosis and psuedocysts
  • Rarely may need laprotomy (but imaging now so good, rare)
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17
Q

How is acute pancreatitis managed?

A

Rest the pancreas

  • IV fluids
  • NG suction (decrease pressure)
  • Analgesia
  • Close monitoring
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18
Q

What are complications of acute pancreatitis at a systemic, metabolic and visceral level?

A
  • Hypotension, shock, renal and respiratory failure due to massive release of pro-inflammatory cytokines
  • Metabolic; Low Ca, hyperglyceamia, jaundice
  • Pancreatic psuedocysts
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19
Q

What is chronic pancreatitis defined as?

A

Defined as repeated bouts of pancreatic inflammation with loss of pancreatic parenchyma and replacement of fibrous tissue

20
Q

What is the eitiology of chronic pancreatitis?

A

60-70% have heavy alcohol intake.
- Intraductal plugs; Proteins, cell debris

Other causes;

  • Previous acute pancreatitis
  • Severe malnutrition
  • Hereditary/CFTR mutations (CF)
21
Q

What is the pathology of chronic pancreatitis?

A
  • Fibrotic organ
  • Atrophy of the exocrine component (relative sparing of islets)
  • Mild chronic inflam infiltrate i.e macrophages
  • Intraductal protein plugs and calcified concretions (seen on imaging)
22
Q

What are the clinical features of chronic pancreatitis?

A
  • Repeated attacks of abdominal pain-often bought on by alcohol
  • Can be more persistent pain

If ongoing

  • Loss of exocrine function (metabolic implications)
  • Psuedocysts
  • Rarely diabetes mellitus
23
Q

How is chronic pancreatitis diagnosed?

A
  • Clinical suspicion
  • Serum amylase - but may not be elevated
  • CT imaging
24
Q

Whats often the outcome of pancreatic cancer?

A
  • Survival is very poor as relies on pain or obstruction of pancreas. So if it occurs in tail then can be quite progressed.
  • Whipples procedure if operation occurs.
25
Q

What are the risk factors of pancreatic carcinoma?

A

Theyre associations

  • Smokers
  • Rare hereditary cases
  • Alcohol and coffee are suggested
26
Q

Whats the pathology of adenocarcinoma;

A

Head; Biliary obstruction
Tail; Often silent, spreads to nodes of adjacent organs

Think location and what it will do

27
Q

Whats the clinical features of adenocarcinoma;

A
  • Obstructive jaundice
  • Pain
  • Weight loss
  • Pancreatitis and obstruction
  • Thrombophlebitis (venous thrombosis)

Confirmed on imaging and biopsy

28
Q

What may pancreatic endocrine tumours result in?

A

Islet cell tumor

  • Rare
  • May elaborate pancreatic hormones
  • Hypoglycemia
  • Most benign
  • Treat with resection
29
Q

What are pancreatic pathologies?

A
  • Acute pancreatitis
  • Chronic pancreatitis
  • Carcinoma of the pancreas
    Other; CF or endocrine tumours
30
Q

What are gall bladder pathologies?

A
  • Gallstones
  • Cholecystitis
  • Carcinoma of the gallbladder
31
Q

What is cholelithiasis?

A

Gallstones, 80% are ‘Silent’

32
Q

What are the types of gallstones?

A 
Cholesterol stones (80%); Cholesterol monohydrate
Pigment stones; Bilirubin and calcium salts
33
Q

Whats the pathogenesis of cholesterol stones?

A
  • Bile supersaturated with cholesterol
  • Conditions favouring crystal formation
  • Cholesterol crystals remain in gall bladder long enough for stones to form i.e stasis
34
Q

What are the risk factors for cholelithiasis?

A
  • Age and gender (F)
  • Estrogenic influence (contraception, pregnancy), obesity and rapid weight loss
  • Gallbladder stasis
  • Family history

Rare in underdeveloped or developing countries.

35
Q

What are the risk factors for a pigment stone?

A

Disorders that favour the formation of bilirubin stones are;

  • chronic heamolytic conditions
  • bacterial infection of the biliary tree

predom in non-western pops

36
Q

What are the potential clinical consequences of gallstones?

A

May be asymptomatic
- 70-80%

Symptomatic; 1-3% per year

  • Cholecystisis (acute/chronic)
  • Biliary colic- due to choledocholithiasis

Complications of above;
- Cholangitis, obstructive cholestasis, pancreatitis

37
Q

What is acute cholecystisis?

A
  • Mostly gallstones
  • Obstruction of the neck of gallbladder or cystic duct
  • Chemical irritation appears to be the major factor with bacterial infection later
38
Q

What are the clinical presentation and laboratory results of cholecystisis?

A
  • RUQ pain and tenderness
  • Febrile
    Laboratory
  • Neutrophil leucocytosis
  • Raised bilirubin, ALP and GGT if stone common bile duct
  • Imaging = ultrasound of gall bladder
39
Q

How is acute or chronic cholecystisis managed?

A

Initial acute event;

  • Conservative therapy; IV fluid, pain releif
  • Up to 25% may require acute surgical intervention

Chronic
- Cholecystectomy

40
Q

What is choledocholithiasis? and complications?

A

Presence of stones within the biliary tree

Complications

  • Biliary obstruction; colicky abdominal pain or obstructive jaundice
  • Pancreatitis
  • Cholangitis (inflam of bile duct system)
41
Q

What are the potential cancers of the biliary system?

A
  • Carcinoma of the gall bladder

- Carcinoma of the extrahepatic ducts

42
Q

Describe the presentation of the gall bladder carcinoma;

A

Presents

  • Later in life
  • F>M
  • Poor prognosis
  • Increased with gallstones and chronic infections
43
Q

Describe the pathology of gall bladder carcinoma;

A

Pathology

  • Most are adenocarcinomas
  • Rarely squamous or mixed
  • Most have invaded the liver by the time of diagnosis.
44
Q

Write some notes on carcinoma of the extrahepatic bile ducts;

A
  • Uncommon
  • May involve the ampullary region
  • Frequently present with slowly progressive obstruction of bile duct i.e jaundice, pale stools, weight loss, nausea
45
Q

Whats important to remember if theres any obstruction in the cysto-hepato-pancreatic network?

A 
Think about its location (name)
- Which organs itll obstruct
i.e
Pancreas -> pancreatitis
Liver -> Jaundice (hyperbilirubinemia)
Gall bladder -> Steatorhoea

Or all?

Digestive MBChB 2 (31 decks)

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