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imed3004 > Cholelithiasis, Cholecystitis and Pancreatitis > Flashcards

Cholelithiasis, Cholecystitis and Pancreatitis Flashcards

1
Q

What is the function of the gall bladder?

A

Stores and concetrates bile

Releases bile into the duodenum after food is ingested (Cholecystokinin)

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2
Q

What are the parts of the gallbladder?

A

Has a fundus, body, and neck

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3
Q

Where is the gallbladder located?

A

Lies in GB fossa on the inferior surface of the right hepatic lobe.

It is 7 - 10cm long

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4
Q

Where does bile go when being released into the duodenum?

A

Cystic duct which joins the common hepatic duct

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5
Q

What is contained in bile?

A

Water

bile acids

Bile salts

Bilirubin

Cholesterol

Phospholipids

Excreted drugs or hormones

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6
Q

What percentage of the population gets cholelithiasis?

A

Gallstones are present in 10 - 20% of the adult population

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7
Q

What are gallstones made of?

A

Cholesterol

Bilirubin

Calcium salts

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8
Q

What percentage of people with cholelithiasis will develop complications or biliary colic?

A

20%

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9
Q

How are gallstones classified?

A

Based on amount of cholesterol in the stones:

Cholesterol (>50% crystalline cholesterol monohydrate)

Pigment (Bilirubin and calcium salts)

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10
Q

Where in the world are gallstones more yellow in colour and why?

A

Western countries are more yellow due to higher cholesterol content in the stones.

African and Asian populations more often have black gallstones

Asian countries more often than the others have large brown gallstones.

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11
Q

What causes cholesterol stones? (pathogenesis)

A

Bile salts and phospholipids render cholesterol soluble in bile.

When bile cholesterol concentration exceeds solubilising capacity of bile = supersaturation, cholesterol nucleates into solid cholesterol monohydrate crystals.

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12
Q

What 4 conditions contribute to cholesterol GS formation?

A

Supersaturation

Hypomotility of GB

Cholesterol nucleation

Hypersecretion of mucous traps nucleated crystals leading to aggregation causing formation of biliary sludge.

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13
Q

What causes black pigmentation stones?

A

Disorders that lead to elevated levels of unconjugated bilirubin in bile. Unconjugated bilirubin combines with calcium to form calcium bilirubinate.

Disorders leading to elevated levels of unconjugated bilirubin include:

Haemolytic syndromes

Severe ileal dysfunction

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14
Q

What causes brown pigmentation stones?

A

Tend to form in bile ducts.

They contain bacterial degradation products of biliary lipids, calcium salts of fatty acids, unconjugated bilirubin, and precipitated cholesterol possibly due to bacterial infection.

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15
Q

What are possible complications of cholelithiasis?

A

Cholecystitis

Empyema

Perforation

Fistula

Cholangitis

Obstructive cholestasis

Pancreatitis

Gallstone ileus

Increased risk of carcinoma

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16
Q

What is acute calculous cholecystitis?

A

Acute inflammation of GB precipitated in vast majority of cases by GS obstruction of neck or cystic duct.

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17
Q

What causes obstruction in acute calculous CS?

A

Chemical irritation

Mechanical irritation

Ischaemia

Superimposed infection

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18
Q

What causes acute acalculous CS?

A

2 - 15% of patietns whtat undergo cholecystectomy get this

Associated with trauma, non-biliary surgery, sepsis, burns, parenteral nutrition, mechanical ventilation, multiple blood transfusions, prior use of narcotics, or AB

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19
Q

What causes acute acalculous CS?

A

Bile stasis and increase viscosity resulting in obstruction

Mucosal ischaemia

Infection

External obstruction of biliary tree

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20
Q

What are the clinical symptoms of acute acalculous CS?

A

Similar to acute calculous CS but masked by precipitating and associated conditions.

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21
Q

What is more likely to happen in acute acalculous CS compared to calculous CS?

A

Incidence of gangrene and perforation is higher.

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22
Q

What are the histological differences between calculous and acalculous CS?

A

Only the presence of stones are different.

Specific histological differences between acute calculous and acalculous cholecystitis are lacking

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23
Q

What is the clinical presentation of acute calculous CS?

A

Acute biliary or abdominal pain and tenderness (RUQ)

Mild presentation which may resolve without intervention.

Guarding

Nausea & Vomiting

Persistence of symptoms beyond 24 hours

Leukocytosis

Hyperbilirubinaemia.

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24
Q

How is acute calculous CS investigated?

A

Bloodwork

Chest X ray

US - GB wall thickening, pericholecystic fluid, GS

Tc-HIDA nuclear medicine scan - radioactive tracer excreted into bile.

CT scan

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25
Q

What are the morphological changes that occur in patients with acute calculous CS?

A

Enlarged and tense

Red, blotchy appearance

Green black discolouration

Fibrin over serosa

Suppurative exudate in severe cases

Obstructing stone

Lumen containing turbid fluid or pus

Thick and oedematous wall

Necrosis

Emphysematous

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26
Q

What are the histological changes that occur in patients with acute calculous CS?

A

Reactive epithelium/erosion

Inflammatory cells in the wall.

Muscles become thicker

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27
Q

How is acute cholecystitis treated?

A

Observe vital signs, nul by mouth and pain relief

Surgery: Open or laparoscopic operation. Either acutely or after the attack has settled down. Should be performed within 2 - 3 days of onset of symptoms.

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28
Q

What could go wrong if surgery is not done on acute CS?

A

After this period, development of adhesions and transmural inflammation increases risk of complications.

29
Q

What causes chronic cholecystitis?

A

Calculous (90%) and acalculous

Supersaturation of bile leading to chronic inflammation and stone formation.

30
Q

What are the symptoms of chronic cholecystitis?

A

Most common symptom is episodic abdominal pain in the epigastrum or RUQ which can be precipitated by food.

Mild to moderate tenderness can be elicited by palpation

31
Q

What are the histological features of chronic cholecystitis?

A

Loss of epithelium of gall bladder. Metaplastic changes

Thick muscular and fibrous tissue. (fibrosis)

Inflammation changes from neutrophils to macrophages and lymphocytes

32
Q

What are the macroscopic features of chronic cholecystitis?

A

Serosa may be dulled, fibrous adhesions, shrunken and fibrotic, wall thin or thick, attenuated and trabeculated mucosa.

33
Q

What are the most important causes of pancreatitis?

A

Gallstones

Alcoholism

34
Q

How does the pancreas form?

A

Outpouching of the duodenum formed by fusion of ventral and dorsal bud; fusion of ventral and distal portion of the dorsal duct forms the MPD

The proximal portion of the dorsal duct can persist to form the accessory duct of Santorini

35
Q

What are the parts of the pancreas?

A

Head

Uncinate

Neck

Body

Tail

36
Q

What are the 2 components of the pancreas histologically?

A

Endocrine and exocrine (80 - 85%)

37
Q

What is a pancreas divisum deformity? What is a possible consequence of this?

A

No division between dorsal and ventral ducts so accessory pancreatic duct is the only present duct which is smaller.

The result is that the pancreas is more likely to be obstructed in this deformity and so acute pancreatitis is more likely in people with this deformity.

38
Q

What is acute pancreatitis?

A

Reversible pancreatic injury associated with inflammation.

39
Q

What causes acute pancreatitis?

A

Several factors:

Genetic: mutations in cationic trypsinogen, trypsin inhibitor, and CF transmembrane conductance inhibitor.

Metabolic: Alcohol consumption, hyperlipoproteinaemia, hypercalcaemia, and drugs

Mechanical: Pancreatic tumours, trauma, iatrogenic, pancreatic dividum, parasites

Vascular

Infectious

40
Q

What are the genetic mutations associated with acute pancreatitis?

A

Cationic trypsinogen (PPSS1)

Trypsin inhibitor genes (SPINK1)

CFTR gene

VITAMIN C

41
Q

What are the metabolic causes of acute pancreatitis?

A

Alcohol

Hyperlipoproteinaemia

Hypercalcaemia

Drugs

VITAMIN C

42
Q

What are the mechanical causes of acute pancreatitis?

A

Gallstones

Pancreatic tumours

Trauma

Iatrogenic

Pancreatic dividum

Parasites

VITAMIN C

43
Q

What are the vascular causes of acute pancreatitis?

A

Shock

Atheroembolism

Vasculitis

VITAMIN C

44
Q

What are the infectious causes of acute pancreatitis?

A

Mumps

VITAMIN C

45
Q

What are the mechanisms of injury to the pancreas?

A

Pancreatic duct obstruction

Primary acinar cell injury

Defective intracellular transport of proenzymes within acinar cells.

These lead to autodigestion of pancreas by digestive enzymes

Fat necrosis, interstitial inflammation, vascular damage and haemorrhage, and parenchymal necrosis.

Fat necrosis is release of fatty acids which bind calcium and magnesium ions to form insoluble soaps.

46
Q

What are the histological features of acute pancreatitis?

A

Inflammatory cells (neutrophils predominant)

Necrotic fat with blue calcification surrounding it

Vascular damage and thrombosis and necrosis

47
Q

How does acute pancreatitis present clinically?

A

80% of cases are mild and 20% are severe

48
Q

How do patients present in severe cases of acute pancreatitis?

A

Shock with multiorgan failure due to release of toxic enzymes, cytokines, and other inflammatory mediators into circulation.

49
Q

What are the criteria of diagnosing acute pancreatitis according to revised Atlanta classification of acute pancreatitis?

A

2 of the following 3:

Abdominal pain consistent with AP (acute onset, persistent, severe, epigastric pain that often radiates to the back)

Serum lipase/amylase test at least 3 times greater than upper limit of normal

Characteristic findings on US, CT or less commonly MRI

50
Q

What are the investigations conducted for acute pancreatitis?

A

Biochemical

US

CT

ERCP

51
Q

How is acute pancreatitis treated?

A

Nil by mouth

Supportive

+/- AB

Relieve obstruction

Manage complications.

52
Q

What is an ERCP?

A

Edoscopic Retrograde Cholangio-Pancreatography

ERCP is a procedure where the physician examines the pancreatic and bile ducts using an endoscope which is placed through the mouth and into the stomach and first part of the small intestine (duodenum).

53
Q

What are the local complications that can arise from acute pancreatitis?

A

Peripancreatic fluid collection

Pseudocyst formation

Necrotic collection

Gastric outlet dysfunction

Splenic and portal vein thrombosis

54
Q

What are the systemic complications that can arise form acute pancreatitis?

A

Exacerbation of pre-existing co-morbidity

Organ failure

55
Q

What is chronic pancreatitis?

A

Fibroinflammatory disorder in which acinar compartment is replaced by fibrosis leading to exocrine insufficiency and in late stages destruction of endocrine parenchyma

56
Q

What kind of inflammation is seen in chronic pancreatitis?

A

Fibrous inflammation

57
Q

What is the prevalence of chronic pancreatitis?

A

0.04 - 5%

58
Q

How does alcohol lead to chronic pancreatitis? (ductal obstruction theory)

A

Alcohol increases protein concentration in the pancreatic fluid which plug the pancreatic ducts leading to ductal obstruction.

59
Q

What is the toxic metabolic theory of chronic pancreatitis development?

A

Alcohol has a direct toxic effect on acinar cells (pancreas is involved in hte metabolism of alcohol)

60
Q

What is the necrosis-fibrosis theory of chronic pacreatitis pathogenesis?

A

CP is a consequence of repeated episodes of Acute Pancreatitis. Pancreatic stellate cells activated by cytokines or direct effects of alcohol and metabolites - fibrosis.

61
Q

What are the histological and morphological features of chronic pancreatitis?

A

Shrunken, hard, pale pancreas (due to calcification)

Histology

Stellate cells and patches instead of acinar cells

Loss of exocrine glands

62
Q

What are the clinical symptoms of chronic pancreatitis?

A

Acute or recurrent episodes of Acute Pancreatitis

Constant pain (epigastric pain radiates to back and can be partially relieved by sitting up and leaning forward)

Symptoms related to local complications

Endocrine or exocrine insufficiency

63
Q

What percentage of AP have no known associated process?

A

20%

64
Q

What are the characteristics of hereditary pancreatitis?

A

Recurrent bouts of pancreatitis beginning in childhood

Germline mutations either result in enhanced activation of trypsin or inhibit its activation

Cumulative risk of pancreatic carcinoma at 50 years is 8 - 11% and at 75 years 49 - 55%

65
Q

What is the typical presentation of autoimmune pancreatitis?

A

Mass forming inflammatory lesion of the pancreas (may mimic cancer)

66
Q

What are the clinicopathological subtypes of autoimmune pancreatitis?

A

AIP type 1 - IgG4 related disease

AIP type 2 - Not IgG4 related

67
Q

How is autoimmune pancreatitis treated?

A

Steroids

68
Q

What are the possible causes of autoimmune pancreatitis?

A

Genetic factors

Bacterial infection

Autoimmunity

imed3004 (50 decks)

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