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General Surgery > Pancreas Pathology > Flashcards

Pancreas Pathology Flashcards

1
Q

what are the causes of acute pancreatitis? (GET SMASHED)

A
  • Gallstones
  • Ethanol
  • Trauma – post op
  • Steroids
  • Mumps = Infection – also CMV, coxsackie
  • Autoimmune
  • Scorpion bites
  • Hypercalcaemia, hypothermia, hyperlipidaemia
  • ERCP
  • Drugs = sodium valproate, azathioprine
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2
Q

what is the pathophysiology of acute pancreatitis?

A

Sudden inflammation and haemorrhaging of the pancreatitis due to destruction by its own digestive enzymes – autodigestion

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3
Q

what role does acinar cells play in pancreatitis?

A

if inactive proenzyme or zymogen is activated early can cause damage to pancreas (eats itself?)

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4
Q

how can alcohol cause pancreatitis?

A
  • increase zymogen production by altering membrane causing early activation
  • secretion decreases fluid and bicarbonate production in ducts causing pancreatic juices to become thick,
    causes blockage, build up, distension
  • stimulate immune response in acinar cells
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5
Q

how can gallstones cause pancreatitis?

A

gallstone can occur at sphincter of odi causing pancreatic blockage
leads to build up, enzyme activation and distension

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6
Q

What are the clinical symptoms of acute pancreatitis?

A
  • Upper abdominal pain - begins in epigastrium, become intensity as spreads in peritoneal cavity, back pain
  • Nausea/vomiting
  • Tachycardia, hypotension, oliguric
  • Tenderness, guarding
  • Reduced/absent bowel sounds
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7
Q

what are the clinical signs of acute pancreatitis?

A
  • Cullen’s Sign – periumbilical bruising

* Grey Turner sign – flank bruising

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8
Q

how does Duodenopancreatic reflux cause pancreatitis?

A

trauma, surgery, duodenal fluid contains enterokinase that activates pancreatic proenzymes

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9
Q

what causes pancreatic tissue destruction in acute pancreatitis?

A

from proteases & inflammatory response of the body – raised intracellular calcium can cause this activation

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10
Q

what follows pancreatic tissue destruction in acute pancreatitis pathophysiology?

A
  • Blood vessels become leaky and rupture y proteases digesting the walls of the blood vessel – amylase is released
  • edema causes capsule of pancrease to swell
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11
Q

what causes skin discolouration in acute pancreatitis?

A

• lipases destroy peripancreatic fat as well as abdomen and subcutaneous tissue – discolouration of the skin

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12
Q

what are the consequences of pancreatic tissue destruction in acute pancreatitis?

A 
Hypocalcaemia
•	Liquefactive haemorrhagic necrosis
•	Pancreatic pseudocyst 
•	Destruction of islets cells = hyperglycaemia = type II diabetes
•	Pulmonary failure
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13
Q

how does pancreatitis lead to pulmonary failure?

A

circulating activated digestive enzyme leads to loss of surfacrnt, atelectasis and irritation leading to ARDS

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14
Q

what investigations should be done in acute pancreatitis?

A 
Bloods
CXR
Contrast enhanced spiral CT 
ECG
MRI/MRCP
ERCP
Operative biopsies or needle aspiration cytology
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15
Q

what will blood results show in acute pancreatitis?

A
  • Raised amylase
  • Raised lipase
  • Raised blood glucose
  • Moderate leucocytosis and anaemia in severe cases
  • Serum bilirubin is often raised
  • Hypoxia in extreme cases
  • Low serum calcium
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16
Q

what scoring system is used in pancreatitis?

A

Glasgow Score – Acronym Pancreas

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17
Q

what are the criteria of the glasgow scoring system for pancreatitis?

A 
o	PO2 Oxygen < 60mmHg or 7.9kPa
o	Age > 55
o	Neutrophilia White blood cells > 15
o	Calcium < 2 mmol/L
o	Renal Urea > 16 mmol/L
o	Enzymes Lactate dehydrogenase (LDH) > 600iu/L Aspartate transaminase (AST) > 200iu/L
o	Albumin < 32g/L
o	Sugar Glucose > 10 mmol/L
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18
Q

what is the management of acute pancreatitis?

A
  • Replace fluids
  • Nasogastric suction
  • Prophylactic antibiotics – broad spectrum – not given so routinely
  • Analgesia
  • Enteral nutrition
  • With multiorgan failure – ventilation and renal support
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19
Q

what are th complications of acute pancreatitis?

A
  • Hypovolemic Shock
  • DIC
  • ARDS
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20
Q

What are the causes of chronic pancreatitis?

A
  • Alcohol
  • Genetic - associated with aminoaciduria or hyperparathyroidism or cystic fibrosis
  • Obstruction – benign or malignant
  • Congenital abnormalities – pancreas divisum
  • Hypercalaemia
  • Malnutrition
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21
Q

what is the pathophysiology of chronic pancreatitis?

A

Persistent inflammation leads to: - fibrosis of the ducts leading to narrowing

  • calcification deposist on protein plugs
  • pancreatic atrophy
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22
Q

what is the consequence of chronic pancreatitis of pancreas function?

A

Pancreatic insufficiency - fewer enzymes produced by acinar cells
damage to alpha and beta cells

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23
Q

what are the clinical consequences of chronic pancreatitis?

A

Problems absorbing fat (weight loss, fatty stools)
Diabetes
Pancreatic pseudocysts
pancreatic cancer

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24
Q

what are the clinical features of chronic pancreatitis?

A
  • Pain in epigastric region – may radiate to back, linked to eating meals, lasts several houses
  • Pancreatic Insufficiency – weight loss, deficient in vitamins, fatty stools
  • Jaundice attributed to common duct blockage
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25
Q

what investigations can be done for chronic pancreatitis?

A 
Bloods
Xray, CT
ERCP
Faecal elastase levels
PABA and pancteolauryl tests
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26
Q

what will blood results in chronic pancreatitis show?

A

Lipase and Amylase may or may not be raised

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27
Q

what will ERCP in chronic pancreatitis show?

A

chain of lakes appearance – stenosis and dilatation

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28
Q

What is the management of chronic pancreatitis?

A 
Pain relief – NSAIDs and opiates. Tricyclic antidepressants e.g. amitriptyline for chronic pain
PPI 
Replace digestive enzymes
Vitamins
Diabetic management
Manage risk factors
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29
Q

what are the modifiable risk factors associated with pancreatic carcinoma?

A

o Smoking
o Obesity
o Diet high in red meat
o Alcohol Abuse

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30
Q

what are the non-modifiable risk factors associated with pancreatic carcinoma?

A

o Male
o African American
o >65

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31
Q

what diseases are risk factors for pancreatic carcinoma?

A 
o	Diabetes
o	Pylori infection
o	Chronic pancreatitis
o	Partial Gastrectomy   
o	Liver cirrhosis
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32
Q

what are the genes associated with pancreatic carcinoma?

A

o BRAC2

o PALB2

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33
Q

the pancreas is made up of which two cell types?

A

Endocrine

Exocrine

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34
Q

which cell type do pancreatic carcinomas commonly occur in?

A

exocrine

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35
Q

what are the different types of exocrine pancreatic carcinomas?

A

Adenocarcinoma (epithelial cells lining ducts)
Exocrine Tumours of Acinar Cells
Cystadenocarcinoma
Undifferentiated

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36
Q

where to pancreatic adenocarcinomas commonly occur?

A

60% occur in head, 25% in body, 15% in tail

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37
Q

where do pancreatic head adenocarcinomas arise from?

A

1/3 are periampullary, arising from the ampulla of Vater, the duodenal mucosa or the lower end of the common bile duct

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38
Q

what is the microscopic appearance of pancreatic adenocarcinomas?

A

tumours arising in the epithelial cells lining pancreatic ducts

39
Q

what is the macroscopic appearance of pancreatic adenocarcinomas?

A

infiltrating, hard, irregular

40
Q

where to pancreatic adenocarcinomas commonly invade into?

A 
CBD
Duodenum
Portal Vein
Superior Mesenteric Artery 
Inferior Vena Cava
41
Q

what lymph nodes do pancreatic adenocarcinomas spread to?

A

To adjacent lymph nodes and nodes in the porta hepatis

42
Q

what is pancreatic adenocarcinoma trans coelomic spread?

A

With peritoneal seeding and ascites

43
Q

what are the clinical features of pancreatic adenocarcinoma?

A

Nausea, vomiting, fatigue, Weight loss
Mid-epigastric pain
o Radiates to mid/lower back
o Worse when lying flat

44
Q

what are the symptoms of advanced pancreatic carcinomas?

A

o Trousseau = Blood clots felt as small lumps under skin
o Courvoisier
 Gallbladder enlarged and palpable, non tender
o Pulmonary Emboli – SOB, chest pain
o Diabetes – polyuria, polydipsia
o Ascites

45
Q

what are the tumour location affects of pancreatic carcinomas?

A

o Head – obstruction of common bile duct = obstructive jaundice
 Loss of appetite, darker urine, lighter stools, pruritis, yellowing
o Endocrine = New onset diabetes

46
Q

what will blood tests in pancreatic carcinoma show?

A

o Nonspecific - Serum amylase and lipase elevated, Ca 19-9 antigen increased, CEA increased
o Obstructive jaundice - Raised alkaline phosphate, transaminase
o Anaemia
o Hyperglycaemia
o Hypokalaemia
o Hypercalcaemia

47
Q

what imaging can be used for pancreatic adenocarcinoma?

A

o US
o CXR
o Endoscopic US or biopsy – endoscopy can help diagnosis, histology not required for formal diagnosis
o CT/PET

48
Q

what are the stages of pancreatic carcinoma?

A
  1. Less than 2cm
  2. Greater than 2cm
  3. Growing into neighbouring tissue 4. Metastatic
49
Q

what are the management options for pancreatic carcinoma?

A
  • Chemotherapy = Neoadjuvant, adjuvant or in non-surgical treatment
  • Radiotherapy – reserved for adjuvant usage in potentially curable
  • Whipple Procedure
50
Q

what is a whipple procedure?

A

Due to shared blood supply – removal of gall bladder, jejunum and stomach

51
Q

What are the pancreatic islet cells?

A 
Beta
Alpha
Delta
Pancreatic Polypeptide cells
Enterochromaffin cells
D1 cells
G cells
52
Q

what do beta cells in the pancreas do?

A

Secrete insulin

53
Q

what do alpha cells in the pancreas do?

A

Secrete glucagon

54
Q

what do delta cells in the pancreas do?

A

secrete somatostatin

55
Q

what do pancreatic polypeptide cells cells in the pancreas do?

A

secrete pancreatic polypeptide

56
Q

what do enterochromaffin cells in the pancreas do?

A

secrete serotonin

57
Q

what do D1 cells in the pancreas do?

A

secrete vasoactive intestinal peptide (VIPP)

58
Q

what do G cells in the pancreas do?

A

secrete gastrin

59
Q

how does insulin work?

A

Lowers blood glucose by transporting glucose into the cell and pushes potassium into the cell – decreases blood potassium

60
Q

how does glucagon work?

A
  • Raises blood glucose levels

* Gets liver to generate glucose from amino acids + lipids and break down glycogen into glucose

61
Q

how does somatostatin work?

A

• Decreases release of insulin, glucagon and serotonin

62
Q

how does pancreatic polypeptide work?

A

• Stimulates release of digestive enzymes from stomach + small intestines – slows down intestinal movement

63
Q

what effect does serotonin have on the GI tract?

A

increases motility of GI tract

64
Q

how does VIPP work?

A

 Relaxes small intestine, stimulates digestive enzymes, inhibits hydrochloric acid

65
Q

how does gastrin work?

A

 stimulates parietal cells to produce hydrochloric acid

 stimulates glands in the epithelium layer

66
Q

what is the cause of pancreatic Pancreatic Neuroendocrine Tumours ?

A

• Mutation in the tumour suppressor Gene
o PTEN
o MEN1

67
Q

MEN1 causes tumour formation in what organs?

A

parathyroid, pituitary, pancreas

68
Q

what are the two kinds of pancreatic neuroendocrine tumours?

A

non functional and functional

69
Q

what are the features of non functional pancreatic neuroendocrine tumour?

A

More common
Asymptomatic until they grow larger and metastases
Compress surrounding structures

70
Q

what are the types of functional pancreatic neuroendocrine tumours?

A 
	Insulinoma
	Gastrinoma
	VIPoma
	Glucagonoma
	Somatostatinoma
	Pancreatic polypeptide cells and extrachromaffin cells rare
71
Q

what is cell type forms an insulinoma?

A

beta cells

72
Q

what is the pathophysiology of beta cells?

A

o Benign, solitary tumours

o High production of insulin

73
Q

what are the clincial features of insulinoma?

A

Symptoms appear during hunger or exercise exercise and relieved by eating
CNS phenomena – weakness, sweating, trembling, epilepsy, confusion, hemiplegia and eventually coma
GI phenomena – hunger, abdo pain, diarrhoea
Excess appetite and weight gain

74
Q

how are insulinomas diagnosed?

A

Whipple Triad
insulin levels
C-peptide levels
Imaging - CT, MR< EUS, selective angiography

75
Q

what is whipples triad?

A

 Attacks induced by startvation or exercise
 During the attack hypoglycaemia is presrnt
 Symptoms are relieved by sugar given orally or IV

76
Q

what are the insulin levels in insulinoma?

A

raised in the presence of hypoglycaemia

77
Q

what are the C-Peptide levels in insulinoma?

A

high with insulinoma, low the exogenous insulin administration

78
Q

what is the management of insulinomas?

A

Tumour excision (+/- whipple)

79
Q

what cell type makes up gastinoma?

A

G cells

80
Q

what is the pathophysiology of gastrinomas?

A

o Secrete large amounts of gastrin = Excess hydrocholirc acid

81
Q

what is the consequence of excess hyaluronic acid in gastrinomas?

A

Zollinger Ellison -Formation of peptic ulcers in stomach, dudoden, jejunum
Hydrocholirc acid also inactivates pancreatic digestive enzymes - Food passes through undigested = steatorrhea

82
Q

how are gastrinomas diagnosed?

A

o Serum gastrin concentration x10 normal
o Basal acid output is high
o Localisation: as for insulinoma

83
Q

what is the management of gastrinomas?

A

o Excision
o PPIs
o Symptoms relapse after cessation of treatment

84
Q

what cell type form VIPomas?

A

D1 cells

85
Q

what is the pathophysiology of VIPomas?

A

Excess vasoactive intestinal peptide

86
Q

What are the clinical features of VIPomas?

A

WDHA syndrome
 Watery diarrhoea – increased fluid secreted by small + large intestine
 Hypokalaemia – low potassium in blood, due to losses in intestinal fluid
 Achlorhydria – absence of hydrochloric acid

87
Q

what cell type do glucagonomas arise from?

A

alpha cells

88
Q

what are the clinical symptoms of glucagonoma?

A

Diabetes

necrolytic migratory ecthyma (rash affecting mouth and limbs)

89
Q

what is the pathophysiology of glucagonoma?

A

Excess blood glucose – diabetes

Loss of lipids and proteins

90
Q

what cell type do somatostatinomas form from?

A

delta cells

91
Q

what is the pathophysiology of somatostatinomas?

A

o Excess somatostatin

 Inhibits release of other pancreatic hormones (insulin, gastrin, VIP)

92
Q

how can neuroendocrine pancreatic tumours be diagnosed?

A

Measure pancreatic hormone level

• CT/MRI

93
Q

what are the clinical features of somatostatinoma?

A

steatorrhea, hypochlorhydria

94
Q

how can neuroendocrine pancreatic tumours be treated?

A

Functional (except somatostatinomas)
o Somatostatin-like medications
o Gastrinomas – medications block gastric acid secretion
• Large tumours = surgery

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