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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

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

A

pancreas and salivary glands

24
Q

what does amylase digest

A

starch and glycogen

25
Q

what does this digestion produce

A

Produces maltose (disaccharide) and maltriose (trisaccharide)

26
Q

what do the brush border enzymes do

A

complete digestion to glucose

27
Q

what are the causes of acute pancreatitis

A

idiopathic - 20%
Gallstones - 50%
Microlithasis
Ethanol - 25%
Trauma/tumor
Steroids
Mumps
Autoimmune
Scorpion venom
Hyperlipidaemia
ERCP
Drugs

28
Q

what is the pathogenesis of acute pancreatitis

A

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

29
Q

what is mild acute pancreatitis

A

pancreatic inflammation and oedema

30
Q

what is severe acute pancreatitis

A

pancreatic necrosis and multi organ failure and death

31
Q

what are the signs and symptoms of acute pancreatitis

A

severe abdominal and back pain
Nausea and vomiting
Respiratory distress
Fever
Haemorrhage
Shock
Hypotension
Tachycardia
Oliguric
Cullen’s sign

32
Q

how is acute pancreatitis diagnosed

A

severe abdominal pain and enxyme released into bloodstream

CXR - exclude perforation
+
CT - assess for pancreatic necrosis, abscess or fluid collection

33
Q

what enzymes are released into the bloodstream

A

amylase (normal in 10%)
Lipase (more sensitive/specific)

34
Q

what is the Glasgow Imrie criteria for acute pancreatitis

A

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
Q

what is the altanta classification for acute pancreatitis

A

Mild - no organ failure, or complication
Moderate - transient organ failure OR complication
Severe - persistent organ dysfunction lasting >48 hours

36
Q

what are the complications of AP

A

acute fluid collection
pseudocysts
WON

37
Q

what are these pseuodcysts

A

Organised fluid collections line by granulation tissue
Symptoms due to mass effect
May self resolve
Symptoms due to infection

38
Q

what is WON

A

waled off pancreatic necrosis (WON)
Dying/non-viable pancreatic tissue
Requires drainage

39
Q

what poses a risk for pancreatitis

A

ERCP

40
Q

what is chronic pancreatitis

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

41
Q

what are the causes of chronic pancreatitis

A

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
Q

what is the pathogenesis of chronic pancreatitis

A

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
Q

what does increased cytochrome P450 non-oxidative pathways lead to

A

reactive oxygen species
cell damage

44
Q

what are the signs and symptoms of CP

A

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
Q

what kind of pain is there in chronic pancreatitis

A

pressure in duct or parenchyma causing pancreatic ischaemia
Inflammation and pancreatic fibrosis
Abnormal CNS pain processing
Reduced bicarbonate secretion

46
Q

what is the malabsorption due to chronic pancreatitis

A

lipase levels fall before protease and amylase
Fat malabsorption occurs when lipase production is reduced by 90%

47
Q

what does this result in

A

steatorrhea (7g faecal/100g diet)
Weight loss

Reduced bicarbonate - acidic environment - reduced bile acid secretion

48
Q

how is chronic pancreatitis diagnoses

A

faecal elastase
Endoscopic ultrasound
CT/MRI

49
Q

what are the possible diagnosis techniques in diagnosing chronic pancreatitis

A

14CO2 breath test - in use, not in Manchester
PABA (para-amino benzoic acid)
Urine collection
Increasingly uncommon
direct hormonal stimulation (research)

50
Q

what type of pain management is given to chronic pancreatitis patients

A

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
Q

how do we treat the malabsoprtion of CP

A

replacement of pancreatic enzymes - Creon/pancreatin
Combination of protease, lipase and amylase

Capsules/granules taken before and during meals/snacks
Mimicking normal secretion

52
Q

what is pancreatogenic diabetes - type 3c

A

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
Q

what is the survival rate for CP

A

70% survival 10 years
40% survival 20 years

54
Q

what is the common type of cancer in chronic pancreatitis

A

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
Q

give a summary of the exocrine pancreas

A

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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