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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
causes of acute pancreatitis
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
acute pancreatitis pathogenesis
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
what are the different types of AP?
- acute interstitial pancreatitis (mild) - acute necrotising pancreatitis - acute haemorrhagic pancreatitis
28
what is the final common pathway in AP?
increased intracellular calcium and inappropriate enzyme activation
29
theories of AP
- 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
signs and symptoms of AP
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
AP diagnosis
- 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
glasgow imrie criteria for AP
PANCREAS
33
what is a good marker for inflammation?
low albumin levels — tissue permeability increases so leak albumin more not nutritional marker
34
AP patietns can develop early what?
acute respiratory distress syndrome due to fluid, protein etc leakage into interstitium — makes it harder to breathe
35
describe the Atlanta Classification to assess the severity of AP
mild = no organ failure, or complication moderate = transient organ failure OR complication severe = persistent organ dysfunction lasting >48 hrs
36
what are possible complications of AP?
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
what can be used to look for gallstones?
USS Magnetic resonance cholangiopancreatography (MRCP) endoscopy ultrasound (EUS) latter 2 if BMI is high
38
how can gallstones be removed?
ERCP = Endoscopic retrograde cholangiopancreatography cholecystectomy (GB removal)
39
chronic pancreatitis key features
- 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
causes of CP
- 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
CP pathogeneis
42
CP : how can lifestyle factors result in cell damage?
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
signs and symptoms of CP
- 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
why is there pain in CP?
- pressure in duct or parenchyma causing pancreatic ischaemia - inflammation and pancreatic fibrosis - abnormal CNS processing - reduced bicarbonate secretion
45
what enzyme levels fall first in CP?
lipase levels fall before protease and amylase
46
fat malabsorption occurs when lipase production is reduce by what percentage?
90%
47
what does malabsorption result in?
- steatorrhoea (lots of fat in faeces - difficult to flush) - weight loss reduced bicarbonate — acidic environment — reduced bile acid secretion
48
CP diagnosis
- 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
CP management
- lifestyle — smoking cessation and alcohol counselling - pain control - treat malabsorption - identify complications such as cysts
50
how is pain managed in CP?
- analgesia — NSAIDs, opiates, neuropathic eg. tricyclic antidepressants - optimise diabetic control - endoscopic therapy — stone disease/strictures - nerve blocks - surgery — decompression versus resection
51
how is malabsorption treated in CP?
- 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
describe pancreatogenic diabetes in CP
- 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
what are possible complications of CP?
- 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
describe pancreatic cancer in CP
- adenocarcinoma more common in CP - 5% develop over 20 year period - increased pain, weight loss, obstructive jaundice - poor prognosis
55
what is responsible for the production of enzymes in the exocrine pancreas?
CCK
56
what is responsible for the production of bicarbonate in the exocrine pancreas?
secretin
57
AP summary
- gallstones and alcohol - multi-organ failure - high mortality - reversible
58
CP summary
- alcohol - chronic symptoms - pain, malabsorption, higher risk of cancer - irreversible

PBL SEM 4 (50 decks)

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