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Pancreatitis Flashcards

(41 cards)

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1
Q

What is pancreatitis?

A

inflammation of the pancreas

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2
Q

What is acute pancreatitis?

A

A disorder of the exocrine pancreas associated with acinar cell injury with local and systemic inflammatory response

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3
Q

What is chronic pancreatitis?

A

involves longer-term inflammation and symptoms with a progressive and permanent deterioration in pancreatic function.

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4
Q

3 key causes of pancreatitis?

A

Gallstones
Alcohol
Post-ERCP (endoscopic retrograde cholangio pancreatograph)

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5
Q

What is gallstone pancreatitis?

A

gallstones getting trapped at the end of the biliary system (ampulla of Vater)> blocks the flow of bile and pancreatic juice into the duodenum > Reflux of bile into the pancreatic duct> prevents pancreatic juice containing enzymes from being secreted, results in inflammation in the pancreas.

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6
Q

What is gallstone pancreatitis more common in?

A

Women and older patients

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7
Q

Alcohol and pancreatitis?

A

Alcohol is directly toxic to pancreatic cells, resulting in inflammation.

Alcohol-induced pancreatitis is more common in men and younger patients.

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8
Q

Pneumonic for causes of pancreatitis?

A

I GET SMASHED

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9
Q

I GET SMASHED

A

I – Idiopathic
G – Gallstones
E – Ethanol (alcohol consumption)
T – Trauma
S – Steroids
M – Mumps
A – Autoimmune
S – Scorpion sting (the one everyone remembers)
H – Hyperlipidaemia
E – ERCP
D – Drugs (furosemide, thiazide diuretics and azathioprine)

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10
Q

Presentation of acute pancreatitis

A

Severe epigastric pain
Radiating through to the back
Associated vomiting
Abdominal tenderness
Systemically unwell (e.g., low-grade fever and tachycardia)
Anorexia
Jaundice
hypotension
Dehydration

Acute pancreatitis is a clinical diagnosis, based mainly on the presenting features and the amylase level.

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11
Q

Initial investigations for any acute abdomen:

A

FBC (for white cell count)
U&E (for urea)
LFT (for transaminases and albumin)
Calcium
ABG (for PaO2 and blood glucose)

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12
Q

What is raised in acute pancreatitis

A

Amylase is raised more than 3 times the upper limit of normal in acute pancreatitis.

Lipase is also raised in acute pancreatitis. It is considered more sensitive and specific than amylase.

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13
Q

What is the Glasgow score

A

The Glasgow score is used to assess the severity of pancreatitis. It gives a numerical score based on how many of the key criteria are present:

0 or 1 – mild pancreatitis
2 – moderate pancreatitis
3 or more – severe pancreatitis

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14
Q

How can the criteria for the Glasgow score be remembered?

A

PANCREAS Pnemonic

P – Pa02 < 8 KPa
A – Age > 55
N – Neutrophils (WBC > 15)
C – Calcium < 2
R – uRea >16
E – Enzymes (LDH > 600 or AST/ALT >200)
A – Albumin < 32
S – Sugar (Glucose >10)

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15
Q

Management of acute pancreatitis

A

Require admission to supportive management - moderate or severe cases should be considered for high dependency unit or ICU
Management involves:
-Initial resuscitation (ABCDE approach)
-IV fluids
-Nil by mouth
-Analgesia
-Careful monitoring
-Treatment of gallstones in gallstone pancreatitis (ERCP / cholecystectomy)
-Antibiotics if there is evidence of a specific infection (e.g., abscess or infected necrotic area)
-Treatment of complications (e.g., endoscopic or percutaneous drainage of large collections)

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16
Q

Ho long does it take to for patients with acute pancreatitis to improve

A

3-7 days

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17
Q

Complications of acute pancreatitis

Study These Flashcards
A
  • Necrosis of the pancreas
  • Infection in a necrotic area
  • Abscess formation
  • Acute peripancreatic fluid collections
  • Pseudocysts (collections of pancreatic juice) can develop - 4 weeks after acute pancreatitis
  • Chronic pancreatitis
18
Q

What is chronic pancreatitis?

Study These Flashcards
A

refers to chronic inflammation in the pancreas. It results in fibrosis and reduced function of the pancreatic tissue and loss of exocirne pancreatic tissue

19
Q

Most common cause of chronic pancreatitis?

Study These Flashcards
A

Alcohol is the most common cause. It presents with similar symptoms to acute pancreatitis, but generally less intense and longer-lasting.

20
Q

Key complications for chronic pancreatitis

Study These Flashcards
A
  • chronic epigastric pain
  • Loss of exocrine function, resulting in a lack of pancreatic enzymes (particularly lipase) secreted into the GI tract
  • Loss of endocrine function, resulting in a lack of insulin, leading to diabetes
  • Damage and strictures to the duct system, resulting in obstruction in the excretion of pancreatic juice and bile
  • Formation of pseudocysts or abscesses
21
Q

What is the management of chronic pancreatitis

Study These Flashcards
A
  • Abstinence from alcohol and smoking is important in managing symptoms and complications.
  • Analgesia - manage the pain
  • Replacement pancreatic enzymes (Creon) - requires if there is a loss of pancreatic enzymes
  • Subcutaneous insulin regimes
  • ERCP with stenting
  • Surgery
22
Q

What is the epidemiology of acute pancreatitis?

Study These Flashcards
A
  • Increases with advancing age
  • Afro-Caribbean ethnicity: risk is 2-3 fold higher in black populations than white
  • Sex: alcohol-related pancreatitis is more common in males, whilst gallstone-related pancreatitis is more common in females
  • Gallstone pancreatitis is more common in white women >60 years of age, especially among patients with microlithiasis.
23
Q

In its most severe form what is the mortality of acute pancreatitis?

Study These Flashcards
A

40-80%
Can cause:
* Extensive pancreatic and peripancreatic necrosis
* Haemorrhage

24
Q

Pathophysiology of acute pancreatitis?

Study These Flashcards
A
  • pancreatic enzymes are activated early
  • causing self perpetuating pancreatic inflammation
  • via enzyme mediated AUTO DIGESTION
25
Pathophysiology of gallstone pancreatitis
* build up of enzyme rich fluid within the pancrease which is blocked due to obstruction from a stone in the ampulla of vater * Intracellular Ca2+ increases and causes the early activation of trypsinogen * trypsinogen is cleaved (by cathepsin B) to trypsin, and trypsin degradation (by chymotrypsin C) is impaired and overwhelmed leading to a buildup of trypsin and thus increased enzymatic digestion of the pancreas and inflammation leading to extensive acinar damage
26
Pathophysiology of alcohol-induced pancreatitis
- increase in release of ca2+ which causes early release of pancreatic enyzmes - ampulla of vater contracts - the pancreatic enzymes cause leaky vessels as they eat through the vessel wall - this causes OEDEMA, INFLAMMATION and HYPOVOLAEMIA
27
What does destruction of the blood vessels by ezymes in pancreatitis cause?
haemorrhage - Destruction of the adjacent islets of Langerhans can result in hyperglycaemia as beta cells will be destroyed resulting in less insulin
28
What do lipolytic enzymes cause?
at necrosis, which can result, if extensive and involving the anterior abdominal wall, in skin discolouration (Grey Turner’s sign) * released fatty acids bind to Ca2+ ions, forming white precipitates in the necrotic fat * If this is very severe, it can result in hypocalcaemia - presenting with tetany
29
Erect Chest x ray
Essential to exclude gastroduodenal perforation - which also raises serum amylase
30
What can an abdominal ultrasound diagnose?
Gallstone pancreatitis
31
Pancreatic scoring systems
* Used as a predictor of severity and prognostic tool * Glasgow & Ranson scoring systems: - Use various factors such as; age, neutrophils, calcium and blood glucose etc to predict a severe attack (80% sensitive), although only after 48 hours from presentation
32
Treatment for acute pancreatitis
-Nil by mouth - nasogastric tube for DIETARY SUPPLEMENTS (as less pancreatic enzymes are released so need to support patients nutritionally!) to decrease pancreatic stimulation - Urinary catheter - ANALGESIA - e.g. IM PETHIDINE or IV MORPHINE - Drainage of collections may be required - Prophylactic antibiotics like beta-lactams
33
Epidemiology of chronic pancreatitis
- Worldwide prevalence is around 4-5% - MALES affected more than females - Median age of presentation is 51
34
Main causes of chronic pancreatitis
* COMMONEST CAUSE in the developed world is long-term alcohol excess (60-70%) * Chronic kidney disease * Hereditary: - Defects in the trypsinogen gene - Cystic fibrosis * Autoimmune pancreatitis - raised IgG4 (seen in many autoimmune disorders) trigger pancreatitis * Idiopathic * Trauma * Recurrent acute pancreatitis
35
Pathophysiology of chronic pancreatitis
Obstruction or reduction in bicarbonate secretion, which produces an alkaline pH which in turn stabilises trypsinogen, leads to the activation of trypsinogen as pH rises making it more unstable and causing its activation into trypsin which leads to pancreatic tissue necrosis with eventual fibrosis
36
Clinical presentation of chronic pancreatitis
- Epigastric pain that ‘bores’ through to the back - Nausea and vomiting - Decreased appetite - Exocrine dysfunction
37
Diagnosis for chronic pancreatitis
- Serum amylase and lipase: * May be elevated, but in advanced disease, there may not be sufficient residual acinar cells to produce elevation - Faecal elastase will be abnormal in majority patients with moderate-severe disease - Abdominal ultrasound and contrast-enhance CT - MRI with MRCP to identify more subtle abnormalities
38
Treatment for chronic pancreatitis
- Alcohol cessation - Abdominal pain: * NSAIDs * Opiate e.g. ORAL TRAMADOL * Tricyclic antidepressants e.g. AMITRYPTYLINE - Duct drainage - Shock wave lithotripsy to fragment gallstones in the head of pancreas
39
How does stenosis occur in pancreatitis
- ductal dilatation - stellate cells lay down fibrotic tissue - narrowiing - stenosis
40
role of trypsin
activated from trypsinogen by enteropeptidases in the duodenum - trypsin activates pancreatic zymogens to active enzymes +
41
What medications cause acute pancreatitis
azathioprine, mesalazine*, didanosine, bendroflumethiazide, furosemide, pentamidine, steroids, sodium valproate

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