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PBL SEM 4 > clinical overview : diseases of the exocrine pancreas > Flashcards

clinical overview : diseases of the exocrine pancreas Flashcards

1
Q

what kind of organ is the pancreas?

A

retroperitoneal

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2
Q

the pancreas anteriorly faces the what?

A

lesser sac

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3
Q

the head of the pancreas borders the confluence of what?

A

superior mesenteric vein and the portal vein

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4
Q

pancreas: body left border of ____ and _____

A

SMV and aorta

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5
Q

pancreas: tail the left border of the _____ to the _______

A

aorta to the splenic hilum

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6
Q

what are the different parts of the pancreas?

A

uncinate process, head, neck, body, tail

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7
Q
A
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8
Q
A
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9
Q

ducts vs acinar cell secretions

A

duct - bicarbonate
acinar - digestive enzymes

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10
Q
A
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11
Q

describe the endocrine function of the pancreas

A
  • 20% by mass
  • Islet cells secrete hormones
  • blood glucose homeostasis
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12
Q

describe the exocrine function of the pancreas

A
  • 80% by mass
  • digestive enzymes
  • acid buffering
  • release into duodenum
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13
Q

what is the gastro-colic reflex initiated by?

A

food ingestion

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14
Q

what is released as a response to food in the stomach? effect?

A

gastrin — HCl and pepsinogen release

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15
Q

what is released from intestinal mucosa and acts on the pancreas? effect?

A

secretin — HCO3 secretion from duct cells and decreases acid release and gastric motility

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16
Q

what does CCK do?

A

acts on pancreas —produces digestive pro enzymes — act on gall bladder (to produce contractions) — help secrete GB contents (bile - to help emulsification of lipids)

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17
Q

control of the exocrine pancreas:

what from the brain/CNS act positively to enhance pancreatic secetions?

A

ACh, VIP (vasoactive intestinal peptide) and GRP (gastrin-releasing peptide)

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18
Q

control of the exocrine pancreas:

what from the duodenum act positively to enhance pancreatic secetions?

A

CCK (produces digestive pro enzymes) and secretin (HCO3 secretion and decreases acid release and gastric motility)

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19
Q

control of the exocrine pancreas:

what acts negatively on the pancreas to reduce pancreatic secretions?

A

somatostatin, pancreatic polypeptides

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20
Q

what are the functions of the exocrine pancreas?

A
  • production of enzymes to facilitate digestion (lipase, proteases, amylase, nucleases)
  • release of enzymes into duodenum
  • NaHCO3 buffering of gastric juices
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21
Q

describe fat digestion

A
  • LIPASE
  • triglyceride molecule too large to be absorbed
  • hydrolysis requires presence of bile acids — emulsification
  • triglyceride broken down into monoglycerides and 2 free fatty acids
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22
Q

describe protein digestion

A
  • pro-enzymes (chymotrypsinogen and trypsinogen)
  • trypsinogen activated by duodenal enterokinase to trypsin (active form)
  • trypsin can itself activate pro-enzymes
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23
Q

describe carbohydrate digestion

A
  • AMYLASE
  • secreted from pancreas and salivary glands
  • digest starch and glycogen
  • produces maltose (disaccharide) and maltriose (trisaccharide)
  • brush border enzymes complete digestion to glucose
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24
Q

acute pancreatitis key things

A
  • sudden onset
  • life threatening
  • reversible (usually)
25
Q

causes of acute pancreatitis

A

I GET SMASHED

I - idiopathic (20%)
G - gallstones (50%) = most common
E - ethanol (25%)
T - trauma/tumour
S - steroids
M - mumps
A - autoimmune
S - scorpion venom
H - hyperlipidaemia
E - ERCP
D - drugs

26
Q

acute pancreatitis pathogenesis

A

inappropriate intra-pancreatic activation of trypsin, leading to acinar auto-digestion and death

mild — pancreatic inflammation and oedema
severe — pancreatic necrosis and multi-organ failure, death

27
Q

what are the different types of AP?

A
  • acute interstitial pancreatitis (mild)
  • acute necrotising pancreatitis
  • acute haemorrhagic pancreatitis
28
Q

what is the final common pathway in AP?

A

increased intracellular calcium and inappropriate enzyme activation

29
Q

theories of AP

A
  • pancreatic ductal obstruction (eg. stone from GB blocks pancreatic duct)
  • abnormal pancreatic secretion (digestive enzymes produced inside instead of outside the pancreas, leading to a cascade of abnormal activation)
  • ductal damage
  • direct toxin effect (alcohol - directly causes pancreatic inflammation , inflammation and membrane destruction, hypertriglycerodaemia, protein deposition)
30
Q

signs and symptoms of AP

A

massive systemic inflammatory response

  • severe abdominal and back pain
  • nausea and vomiting
  • respiratory distress
  • fever
  • haemorrhage
  • shock
  • hypotension
  • tachycardia
  • oliguric
  • cullen’s sign = superficial bruising in the subcutaneous fat around the umbilicus
31
Q

AP diagnosis

A
  • severe abdominal pain
    and
  • enzyme release into bloodstream — amylase (normal in 10%), lipase (more sensitive/specific)
  • CXR - exclude perforation
  • CT - assess for pancreatic necrosis, abscess or fluid collection

ultrasound is sub optimum as transverse mesocolon (often with air in it) overlies the pancreas. can be used to find gall stones

32
Q

glasgow imrie criteria for AP

A

PANCREAS

33
Q

what is a good marker for inflammation?

A

low albumin levels — tissue permeability increases so leak albumin more

not nutritional marker

34
Q

AP patietns can develop early what?

A

acute respiratory distress syndrome due to fluid, protein etc leakage into interstitium — makes it harder to breathe

35
Q

describe the Atlanta Classification to assess the severity of AP

A

mild = no organ failure, or complication
moderate = transient organ failure OR complication
severe = persistent organ dysfunction lasting >48 hrs

36
Q

what are possible complications of AP?

A
  1. acute fluid collection — common, usually self resolving
  2. pseudocysts — organised fluid collections lined by granulation tissue, may self resolve, no infection, symptoms due to mass effect (can press against something), symptoms due to infection
  3. Walled Off pancreatic Necrosis (WON) — dying/non-viable pancreatic tissue, requires drainage, has infection
37
Q

what can be used to look for gallstones?

A

USS

Magnetic resonance cholangiopancreatography (MRCP)

endoscopy ultrasound (EUS)

latter 2 if BMI is high

38
Q

how can gallstones be removed?

A

ERCP = Endoscopic retrograde cholangiopancreatography

cholecystectomy (GB removal)

39
Q

chronic pancreatitis key features

A
  • chronic, continuous inflammation
  • fibrotic changes, loss of tissue and acinar to ductal metaplasia (loss of functional unit)
  • impairment of pancreatic function (exocrine - digestive enzymes, endocrine - insulin)
  • chronic pain
40
Q

causes of CP

A
  • idiopathic (20-30%)
  • alcohol (60-70%) - but dont assume
  • genetic eg. cystic fibrosis (CFTR), SPINK1, PRSS1
  • autoimmune eg. IgG4
  • hyperlipidaemia - hypertriglceriaemia

can occur after AP
can occur without overt preceding illness
can have acute flairs of chronic pancreatitis

41
Q

CP pathogeneis

A
42
Q

CP : how can lifestyle factors result in cell damage?

A
  1. tobacco smoke and alcohol metabolism
  2. pancreatic oxidative stress (alcohol dehydrogenase)
  3. cytochrome P450 non-oxidative pathway
  4. reactive oxygen species
  5. cell damage
43
Q

signs and symptoms of CP

A
  • pain - epigastric to back, episodic (relating to ongoing damage)
  • malabsorption — weight loss, steatorrhoea - fat malabsorption
  • diabetes type 3 (due to endocrine part)
  • jaundice - due to bile duct obstruction
44
Q

why is there pain in CP?

A
  • pressure in duct or parenchyma causing pancreatic ischaemia
  • inflammation and pancreatic fibrosis
  • abnormal CNS processing
  • reduced bicarbonate secretion
45
Q

what enzyme levels fall first in CP?

A

lipase levels fall before protease and amylase

46
Q

fat malabsorption occurs when lipase production is reduce by what percentage?

A

90%

47
Q

what does malabsorption result in?

A
  • steatorrhoea (lots of fat in faeces - difficult to flush)
  • weight loss

reduced bicarbonate — acidic environment — reduced bile acid secretion

48
Q

CP diagnosis

A
  • faecal elastase — assesses pancreas function, measure of fat in stool
  • endoscopic ultrasound — look for changes eg. atrophy, calcification
  • CT/MRI

possible:
- 14CO2 breath test
- PABA (para-amino Benzoic acid) - urine collection, increasingly uncommon
- direct hormonal stimulation (research)

49
Q

CP management

A
  • lifestyle — smoking cessation and alcohol counselling
  • pain control
  • treat malabsorption
  • identify complications such as cysts
50
Q

how is pain managed in CP?

A
  • analgesia — NSAIDs, opiates, neuropathic eg. tricyclic antidepressants
  • optimise diabetic control
  • endoscopic therapy — stone disease/strictures
  • nerve blocks
  • surgery — decompression versus resection
51
Q

how is malabsorption treated in CP?

A
  • replacement of pancreatic enzymes — Creon/pancreatin = combination of protease, lipase and amylase

capsules/granules taken before and during meals/snacks
mimick normal secretion
titration to symptom

52
Q

describe pancreatogenic diabetes in CP

A
  • type 3c
  • 5-10% of all diabetes
  • independent predictor of mortality
  • pancreas dysfunction due to destruction of beta cells from recurrent fibrosis and inflammation
  • difficult to manage — patient characteristics, risk of hypoglycaemia
  • usually low insulin requirements
  • insulin pumps can be useful
53
Q

what are possible complications of CP?

A
  • pseudocysts — localised fluid collection, can be massive - obstruction, can become infected
  • bleeding — variceal (due to underlying cause - ALD) ( splenic vein thrombosis), pseudocysts, pseudo aneurysm
  • obstruction - mass effect - bile duct, duodenal
54
Q

describe pancreatic cancer in CP

A
  • adenocarcinoma more common in CP
  • 5% develop over 20 year period
  • increased pain, weight loss, obstructive jaundice
  • poor prognosis
55
Q

what is responsible for the production of enzymes in the exocrine pancreas?

A

CCK

56
Q

what is responsible for the production of bicarbonate in the exocrine pancreas?

A

secretin

57
Q

AP summary

A
  • gallstones and alcohol
  • multi-organ failure
  • high mortality
  • reversible
58
Q

CP summary

A
  • alcohol
  • chronic symptoms - pain, malabsorption, higher risk of cancer
  • irreversible

PBL SEM 4 (50 decks)

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