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Semester 4 > Case 3 - clinical overview of disease of the pancreas > Flashcards

Case 3 - clinical overview of disease of the pancreas Flashcards

(55 cards)

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1
Q

what are non specific symptoms of GI discomfort

A

indigestion
fullness
bloating
nausea
pain

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2
Q

what are the intermittent severe indigestion differentials

A

gastro-oesophageal reflux disease
Peptic ulceration
Biliary stone disease
Inflammatory bowel disease
Pancreatic disease

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3
Q

what are the dimensions of the pancreas

A

14-20cm and weighs 100g

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4
Q

how does the pancreas sit in the body

A

anteriorly faces the lesser sac

the head borders the confluence of SMV and PV

body left border of SMV and the aorta

tail the left border of the aorta to the splenic hilum

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5
Q

what is the SMV

A

superior mesenteric vein

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6
Q

what is the PV

A

portal vein

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7
Q

what is the endocrine function of the pancreas

A

20% by mass
islet cells secrete hormones
blood glucose homeostasis

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8
Q

what is the exocrine function of the pancreas

A

80% by mass
digestive enzymes
acid buffering
released into duodenum

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9
Q

what reflex is initiated by food ingestion

A

gastro-colic reflex

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10
Q

what is released into the stomach as a response to food

A

gastrin leads to HCL and pepsinogen

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11
Q

what is released to act on the pancreas

A

secretin is released from intestinal mucosa to act on the pancreas

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12
Q

what does secretin do

A

decreases acid release and gastric motility

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13
Q

what does CCK do

A

acts on pancreas –> lipase and acts on GB for contractions

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14
Q

what are the positive feedback controls of the exocrine pancreas

A

ach
VIP
GRP
CCK
secretin

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15
Q

what are the negative feedback controls of the exocrine pancreas

A

somatostatin
pancreatic polypeptides

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16
Q

what enzymes does the exocrine pancreas produce to facilitate digestion

A

Lipase
Proteases
Amylase
Nucleases

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17
Q

where are these enzymes released

A

into the duodenum

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18
Q

what does hydrolysis require presence of

A

bile acids for emulsification

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19
Q

what does pancreatic lipase do

A

turns triglyceride into monoglyceride and free fatty acids

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20
Q

what is the pro enzyme involved in protein digestion and where is it stored

A

chymo-tripsin

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21
Q

what happens to trypsinogen

A

activated by duodenal enterokinase to trypsin

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22
Q

what does trypsin do

A

activates pro enzymes

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23
Q

where is amylase secreted from

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A

pancreas and salivary glands

24
Q

what does amylase digest

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A

starch and glycogen

25
what does this digestion produce
Produces maltose (disaccharide) and maltriose (trisaccharide)
26
what do the brush border enzymes do
complete digestion to glucose
27
what are the causes of acute pancreatitis
idiopathic - 20% Gallstones - 50% Microlithasis Ethanol - 25% Trauma/tumor Steroids Mumps Autoimmune Scorpion venom Hyperlipidaemia ERCP Drugs
28
what is the pathogenesis of acute pancreatitis
inappropriate intra-pancreatic activation of trpysin leading to acinar auto-digestion and death
29
what is mild acute pancreatitis
pancreatic inflammation and oedema
30
what is severe acute pancreatitis
pancreatic necrosis and multi organ failure and death
31
what are the signs and symptoms of acute pancreatitis
severe abdominal and back pain Nausea and vomiting Respiratory distress Fever Haemorrhage Shock Hypotension Tachycardia Oliguric Cullen’s sign
32
how is acute pancreatitis diagnosed
severe abdominal pain and enxyme released into bloodstream CXR - exclude perforation + CT - assess for pancreatic necrosis, abscess or fluid collection
33
what enzymes are released into the bloodstream
amylase (normal in 10%) Lipase (more sensitive/specific)
34
what is the Glasgow Imrie criteria for acute pancreatitis
3 or more of the below in the first 48 hrs indicates a severe attack PaCO2 <8kPa Age >55 years Neutrophils >15x10 to the power of 9 /L Calcium <2mmol/L Renal Function urea>16mmol/L Enzymes LDH <600iU/L / AST>2000iU/L Albumin <32g/L Sugar. glucose >10mmol/L
35
what is the altanta classification for acute pancreatitis
Mild - no organ failure, or complication Moderate - transient organ failure OR complication Severe - persistent organ dysfunction lasting >48 hours
36
what are the complications of AP
acute fluid collection pseudocysts WON
37
what are these pseuodcysts
Organised fluid collections line by granulation tissue Symptoms due to mass effect May self resolve Symptoms due to infection
38
what is WON
waled off pancreatic necrosis (WON) Dying/non-viable pancreatic tissue Requires drainage
39
what poses a risk for pancreatitis
ERCP
40
what is chronic pancreatitis
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
41
what are the causes of chronic pancreatitis
idiopathic - 20-30% Alcohol - 60-70% - but don’t assume genetic: e.g cystic fibrosis (CFTR), SPINK1, PRSS1 Autoimmune: e.g IgG4 Hyperlipidaemia - hypertriglyceriaemia
42
what is the pathogenesis of chronic pancreatitis
Increased acinar protein secreted leads to increased viscosity pancreatic duct plugging Leads to increased acinar atrophy and fibrosis reduction in NaHCO3 + fluids Leads to increased viscosity pancreatic duct plugging Lead to increased acinar atrophy and fibrosis
43
what does increased cytochrome P450 non-oxidative pathways lead to
reactive oxygen species cell damage
44
what are the signs and symptoms of CP
Pain: epigastric to back Episodic (relating to ongoing damage) Malabsorption: weight loss Steatorrhoea - fat malabsorption Diabetes - type 3 Jaundice - due to bile duct obstruction
45
what kind of pain is there in chronic pancreatitis
pressure in duct or parenchyma causing pancreatic ischaemia Inflammation and pancreatic fibrosis Abnormal CNS pain processing Reduced bicarbonate secretion
46
what is the malabsorption due to chronic pancreatitis
lipase levels fall before protease and amylase Fat malabsorption occurs when lipase production is reduced by 90%
47
what does this result in
steatorrhea (7g faecal/100g diet) Weight loss Reduced bicarbonate - acidic environment - reduced bile acid secretion
48
how is chronic pancreatitis diagnoses
faecal elastase Endoscopic ultrasound CT/MRI
49
what are the possible diagnosis techniques in diagnosing chronic pancreatitis
14CO2 breath test - in use, not in Manchester PABA (para-amino benzoic acid) Urine collection Increasingly uncommon direct hormonal stimulation (research)
50
what type of pain management is given to chronic pancreatitis patients
Analgesia: non steroidal anti inflammatory drugs Opiates Neuropathic e.g tricyclic antidepressants optimise diabetic control endoscopic therapy Stone disease/strictures nerve blocks surgery - decompression verus resection
51
how do we treat the malabsoprtion of CP
replacement of pancreatic enzymes - Creon/pancreatin Combination of protease, lipase and amylase Capsules/granules taken before and during meals/snacks Mimicking normal secretion
52
what is pancreatogenic diabetes - type 3c
5-10% of all diabetes Independent predictor of mortality Difficult to manage - Patient characteristics Risk of hypoglycaemia usually low insulin requirements - but brittle Insulin pumps can be useful
53
what is the survival rate for CP
70% survival 10 years 40% survival 20 years
54
what is the common type of cancer in chronic pancreatitis
Adenocarcinoma more common in chronic pancreatitis 5% develop over 20 year period Increased pain Weight loss Obstructive jaundice Poor prognosis: surgical management Chemotherapy Palliative
55
give a summary of the exocrine pancreas
vital role in protein, fat and carbohydrate digestion Cephalic, gastric, intestinal control Production of enzymes - CCK Production of bicarbonate - secretin Release into duodenum

Semester 4 (80 decks)

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