Pancreatitis Flashcards

(49 cards)

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
what blood test is performed for acute pancreatitis?
amylase/lipase (should be increased)
26
what X rays may be performed for acute pancreatitis?
erect chest, plain abdo
27
why may you use ultrasound for someone with AP?
investigate gallstones as a cause
28
when may you perform a CT for AP
patients not settling w conservative treatment & 48-72hrs after onset
29
when may you perform MRCP for AP?
if gallstones are suspected with abnormal LFTs
30
when may you perform ERCP for AP
to remove CBD gallstones
31
how is the severity of AP assessed?
modified glasgow criteria
32
what is included in the Modified glasgow criteria? PANCREAS
``` Po2 Age (>55) Neutrophil/WBC Calcium (low) Renal (urea increased) Enzymes AST, LDH Albumin low Sugar high ```
33
what score suggests severe pancreatitis?
3+
34
what other than modified glasgow can suggest severe pancreatitis?
CRP >200
35
how do you manage AP?
``` ABC Fluid resuscitation (iv fluids, monitoring) Analgesia Pancreatic rest (NJ feeding, TPN) Determine underlying cause ```
36
what is rarely required for AP?
surgery
37
what are the systemic complications of AP?
``` hypocalcaemia hyperglycaemia possible diabetes systemic inflammatory response syndrome acute renal failure adult respiratory distress syndrome disseminated intravascular coagulation multi organ failure death ```
38
what is the causation behind hypocalcaemia?
lipase - free fatty acids - chelate Ca2+ salts - decreased serum Ca2+ (saponification)
39
what are the local complications of AP?
``` necrosis abcess psuedocyst hemorrhage thrombosis chronic pancreatitis ```
40
what is a pancreatic psuedocyst?
peri-pancreatic fluid collection increased pancreatic enzymes within fibrous capsule presents >6 weeks after AP
41
when may pseudocysts need drained?
pain it causes obstruction of CBD etc infected (abcess)
42
where may thrombosis appear in AP
splenic vein, superior mesenteric vein, portal vein
43
what are the main symptoms of chronic pancreatitis?
``` pain weight loss (malabsorption) diabetes mellitus (type1) diarrhoea steatorrhoea obstructive jaundice ```
44
what are some causes of CP
tumours, alcohol abuse, papillary stenosis
45
how can tumours cause CP
cause main pancreatic duct occlusion, duct distension activating chronic inflammation
46
how can alcohol cause CP
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
how is CP managed
no intervention unless in pain
48
how may surgery help CP
drainage, attach small bowel to head of pancreas, total pancreatectomy
49
how may stones be removed for CP
endoscopically - lithotripsy, possible stent