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pancreas and liver > Pancreatitis > Flashcards

Pancreatitis Flashcards

1
Q

What are the two components of pancreatic juice?

A

viscous, enzyme rich juice in low volume

watery, HCO3- rich juice in high volume

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2
Q

What cells produce the enzyme rich juice?

A

Acinar cells

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3
Q

What cells produce the HCO3- juice?

A

Duct and centroacinar cells

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4
Q

How are enzymes stored in the pancreas

A

as zymogens

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5
Q

why are enzymes released as zymogens?

A

to prevent autodigestion of acini and ducts

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6
Q

where are pancreatic enzymes activated?

A

duodenum

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7
Q

what protective inhibitor is also present in the pancreas?

A

trypsin inhibitor (prevent trypsin activation)

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8
Q

what converts trypsinogen - trypsin

A

enterokinase

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9
Q

what does trypsin do in the duodenum other than act as a digestive enzyme?

A

activated all other proteolytic enzymes, some lipolytic

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10
Q

where is enterokinase found

A

brush border of duodenum

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11
Q

what is acute pancreatitis?

A

rapid onset inflammation of the pancreas

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12
Q

what is chronic pancreatitis?

A

long-standing inflammation of the pancreas

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13
Q

what are the causes of pancreatitis? GETSMASHED

A 
Gallstones
Ethanol
Trauma
Steroids
Mumps +other viruses e.g EBV
Autoimmune
Scorpion/snake bite
Hypercalcaemia, hypertriglyceridaemia, hypothermia
ERCP (complications)
Drugs (Steroids/sulfonamides, azothiopire, NSAIDs, diuretics)
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14
Q

name a few pathophysiological causes of acute pancreatitis

A

pressure increases
bile reflux
reflux of duodenal contents
enzyme diffusion, protein precipitation (alcohol)
premature intracellular enzyme activation
increased permeability of pancreatic duct

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15
Q

how does alcohol cause pancreatitis?

A

precipitates proteins in ducts, causes a plug, increasing upstream pressure leading to pancreatitis

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16
Q

how can pancreatic enzymes be activated intracellularly?

A

zymogens and lysosomal proteases incorporated to same vesicles may activate trypsin

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17
Q

what are the consequences of trypsin activation?

A

autocatalysis, activation of prothrombin, complement, phospolipase A2, elastase, kallikrein.

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18
Q

what are the symptoms associated with the consequences of trypsin activation?

A

hypocalcaemia, hyperglycaemia, pancreatic gangrene, pain, shock, hypoxia and anuria

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19
Q

what is oedematous pancreatitis

A

AP where fat necrosis and oedema occur first

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20
Q

what is hemorrhagic pancreatitis

A

AP where mass bleeding predominates (enzymes break down tissue)

21
Q

what is necrotic pancreatitis

A

AP sometimes + infection

dead tissue

22
Q

what are grey turners and cullens sign associated with?

A

haemorrhagic pancreatitis

23
Q

what are the main symptoms of acute pancreatitis?

A

epigastric pain (radiate to back), relieved by sitting forward
nausea and vomiting +++
fever

24
Q

what are some differential diagnoses for acute pancreatitis?

A

gallstone disease, peptic ulcer, leaking/ruptured AAA, raised amylase

25
Q

what blood test is performed for acute pancreatitis?

A

amylase/lipase (should be increased)

26
Q

what X rays may be performed for acute pancreatitis?

A

erect chest, plain abdo

27
Q

why may you use ultrasound for someone with AP?

A

investigate gallstones as a cause

28
Q

when may you perform a CT for AP

A

patients not settling w conservative treatment & 48-72hrs after onset

29
Q

when may you perform MRCP for AP?

A

if gallstones are suspected with abnormal LFTs

30
Q

when may you perform ERCP for AP

A

to remove CBD gallstones

31
Q

how is the severity of AP assessed?

A

modified glasgow criteria

32
Q

what is included in the Modified glasgow criteria? PANCREAS

A 
Po2
Age (>55)
Neutrophil/WBC
Calcium (low)
Renal (urea increased)
Enzymes AST, LDH
Albumin low
Sugar high
33
Q

what score suggests severe pancreatitis?

A

3+

34
Q

what other than modified glasgow can suggest severe pancreatitis?

A

CRP >200

35
Q

how do you manage AP?

A 
ABC 
Fluid resuscitation (iv fluids, monitoring)
Analgesia
Pancreatic rest (NJ feeding, TPN)
Determine underlying cause
36
Q

what is rarely required for AP?

A

surgery

37
Q

what are the systemic complications of AP?

A 
hypocalcaemia
hyperglycaemia possible diabetes
systemic inflammatory response syndrome
acute renal failure
adult respiratory distress syndrome
disseminated intravascular coagulation
multi organ failure
death
38
Q

what is the causation behind hypocalcaemia?

A

lipase - free fatty acids - chelate Ca2+ salts - decreased serum Ca2+ (saponification)

39
Q

what are the local complications of AP?

A 
necrosis
abcess
psuedocyst
hemorrhage
thrombosis
chronic pancreatitis
40
Q

what is a pancreatic psuedocyst?

A

peri-pancreatic fluid collection
increased pancreatic enzymes within fibrous capsule
presents >6 weeks after AP

41
Q

when may pseudocysts need drained?

A

pain
it causes obstruction of CBD etc
infected (abcess)

42
Q

where may thrombosis appear in AP

A

splenic vein, superior mesenteric vein, portal vein

43
Q

what are the main symptoms of chronic pancreatitis?

A 
pain
weight loss (malabsorption)
diabetes mellitus (type1)
diarrhoea
steatorrhoea
obstructive jaundice
44
Q

what are some causes of CP

A

tumours, alcohol abuse, papillary stenosis

45
Q

how can tumours cause CP

A

cause main pancreatic duct occlusion, duct distension activating chronic inflammation

46
Q

how can alcohol cause CP

A

decrease HCO3- increasing proenzyme conc. leads to activation and a protein plug
decrease citrate, lithostatin. leads to calcium precipitation and deposition. also helps activate enzymes

47
Q

how is CP managed

A

no intervention unless in pain

48
Q

how may surgery help CP

A

drainage, attach small bowel to head of pancreas, total pancreatectomy

49
Q

how may stones be removed for CP

A

endoscopically - lithotripsy, possible stent

pancreas and liver (3 decks)

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