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3A week 4 - HPB, malabsoprtion and EDs > acute and chronic pancreatitis > Flashcards

acute and chronic pancreatitis Flashcards

1
Q

what is acute pancreatitis

A

Acute inflammation of the pancreas - surgical emergency

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2
Q

What are the different types of acute pancreatitis? (2)

A
  1. Acute interstitial oedematous pancreatitis (IEP) - no pancreatic tissue death (80% of cases - majority do well - <1% mortality);
  2. Necrotizing pancreatitis - Pancreatic cell death (Pts don’t do well - 20% mortality)
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3
Q

What is the general progression
for IEP?

A

IEP -> Acute pancreatic fluid collections [fluid collection around pancreas <4 weeks] -> Pseudocysts [fluid collections around pancreas >4 weeks]

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4
Q

what is IEP (pancreas)

A

Exocrine Pancreatic Insufficiency - when your pancreas doesn’t make enough digestive enzymes

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5
Q

What is the general progression
for necrotising pancreatitis?

A

Necrotising pancreatitis -> Acute necrotic collections [collection of cell death around the pancreas] -> Walled off
necrosis (WON) [Necrosis forms a wall with dead tissue within]

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6
Q

Which age group
are more at risk of developing acute pancreatitis?

A

older

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7
Q

In which scenarios could acute
pancreatitis present in under
14-15 (4)

A
  1. Hereditary;
  2. traumatic;
  3. anatomic anomaly;
  4. (perhaps drugs)
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8
Q

What are the general groups of causes of acute pancreatitis? (2)

A
  1. Anything which increases pressure in the pancreatic duct
  2. Anything which changes the intracellular calcium in Acinar cells
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9
Q

Which other infections can
cause acute pancreatitis? (3)

A
  1. mumps
  2. coxsackievirus
  3. Hep E
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10
Q

What causes acute pancreatitis? (11)

A

I GET SMASHED
I - idiopathic/ischaemia (e.g., after cardiac surgery)
G - Gallstones
E - Ethanol (Alcohol)
T - Trauma (seatbelt after RTA) + Triglycerides high (>11.1)
S - Steroids
M - Mumps / Malignancy - mechanical blockagefrom pancreatic cancer
A - Autoimmune disease (SLE / Sjogren’s)
S - Scorpion venom (rare and unlikely cause)
H - Hypercalcaemia
E - Endoscopic retrograde cholangio-pancreatography (ERCP - camera up the bile duct)
D - Drugs (Azathioprine, NSAIDs, Diuretics, sodium valproate)

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11
Q

Which drug classes can cause acute hepatitis (7)

A
  1. AIDs drugs [didanosine, pentamidine]
  2. Antimicrobial [metronidazole, sulfonamides, tetracycline, nitrofurantoin]
  3. Diuretics [Furosemide, thiazides]
  4. Immunosuppressive [azathioprine]
  5. Neuropsychiatric [sodium valproate]
  6. Anti inflammatory [Sulfasalazine]
  7. Others [calcium, oestrogen, accutane, propofol, vit A (through raised triglycerides), exenatide]
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12
Q

What genetic condition can cause acute pancreatitis?

A

Autosomal dominant mutation in the tripsinogen gene (PRSS1 gene) - autoactivates in the pancreas (where it normally should do so in the bowel) into tripsin (enzyme
which breaks down protein)

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13
Q

What can mumps cause? (7)

A
  1. Orchitis (testes),
  2. oophoritis (ovaries),
  3. mastitis (breast),
  4. meningitis,
  5. encephalitis,
  6. pancreatitis,
  7. hearing loss
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14
Q

What do acinar cells do in the
pancreas?

A

make enzymes

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15
Q

What is the pathophysiology of acute
pancreatitis? (4)

A
  1. Cause triggers a premature and exaggerated activation of the digestive enzymes within the pancreas;
  2. The resulting pancreatic inflammatory response causes an increase in
    vascular permeability and subsequent fluid shifts (aka “third spacing”);
  3. Enzymes are released from the pancreas into the systemic circulation, causing autodigestion of fats (resulting
    in ‘fat necrosis’) and blood vessels (sometimes leading to haemorrhage in the retroperitoneal space);
  4. Fat necrosis can cause the release of free fatty acids, reacting with serum calcium to form chalky deposits in fatty tissue,
    resulting in hypocalcaemia
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16
Q

What does severe end-stage pancreatitis eventually result in?

A

Partial or complete necrosis of the pancreas

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17
Q

How does acute pancreatitis tend
to present? (7)

A
  1. Sudden onset severe epigastric pain (can radiate to back better leaning forward);
  2. N&V;
  3. Cullen’s sign;
  4. Grey Turner’s sign [retroperitoneal haemorrhage];
  5. Tetany [hypocalcaemia]
  6. Can be jaundiced if cholestasis is the cause
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18
Q

What do you find on examination for acute pancreatitis?

A

Epigastric tenderness (w/ or w/o guarding); If severe, haemodynamically unstable

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19
Q

What are some complications of
acute pancreatitis? (local -6, systemic -6)

A

LOCAL:
1. Pancreatic necrosis
2. Pancreatic pseudocyst
3. Abscess
4. Fistulae
5. Thrombosis
6. Haemorrhage
SYSTEMIC:
1. Multiorgan failure and sepsis
2. Acute kidney injury
3. ARDs
4. DIC
5. Hypocalcaemia
6. Hyperglycaemia

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20
Q

How can acute pancreatitis lead
to hyperglycaemia?

A

Secondary to destruction of islets of Langerhans and subsequent disturbances to insulin metabolism

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21
Q

How can acute pancreatitis lead to hypocalcaemia?

A

Fat necrosis from released lipases, results in the release of free fatty acids, which react with serum calcium to form chalky deposits in fatty tissue

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22
Q

When should you suspect pancreatic necrosis in a patient with acute pancreatitis?

A

When pts have evidence of persistent systemic inflammation for more than 7-10 days after onset of pancreatitis

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23
Q

How do you confirm pancreatic necrosis

A

CT imaging

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24
Q

whats the mgx of pancreatic necrosis

A

Pancreatic necrosectomy (open or endoscopic) - [note: intervention tends to be delayed until walled-off necrosis has developed, usually 3-5 weeks after
symptom onset]

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25
Q

What is a pancreatic pseudocyst?

A

Collection of fluid containing pancreatic enzymes, blood and necrotic tissue - they occur anywhere within or adjacent to the pancreas;
Don’t have an epithelial lining, instead they
have a vascular and fibrotic wall surrounding the collection;
Prone to haemorrhage, rupture and infection

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26
Q

When do pancreatic pseudocysts
tend to form?

A

weeks after initial episode

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27
Q

How do pseudocysts present (2)

A
  1. Incidental finding
  2. symptoms of mass effect (biliary obstruction or gastric outlet obstruction).
28
Q

how are pseudocysts managed (3)

A
  1. 50% spontaneously resolve so conservative mx usually inital tx;
    When present for >6 weeks, unlikely to resolve themselves =>
  2. surgical debridement;
  3. endoscopic drainage, often into stomach;
29
Q

when should you suspect infect pancreatic necrosis (4)

A
  1. clinical deterioration
  2. raised infection markers
  3. +ve blood cultures
  4. changes of low density on CT
30
Q

How do you confirm infected pancreatic necrosis

A

Fine needle aspiration of the necrosis

31
Q

What do the bloods show in acute pancreatitis?

A
  1. Serum amylase / serum lipase - diagnostic if >3x upper limit of normal;
  2. Serum lipase better for acute pancreatitis as stays higher for longer and amylase can be high in other pathologies;
  3. LFTs - to assess for cholestatic cause of acute pancreatitis (ALT >150 U/L strongly suggestive)
32
Q

In which other pathologies can serum amylase
also be raised? (5)

A
  1. Bowel perforation;
  2. Ectopic pregnancy;
  3. DKA
  4. renal insufficency
  5. salivary inflammation etc.
33
Q

What imaging can you do for gallstones (3)

A
  1. US scan within 24 hours - to find cause (gallstones)
  2. MRCP
  3. endoscopic US (looking for microlithiasis)
34
Q

Although not routinely used
for acute pancreatitis, what could
you see on AXR in acute pancreatitis?

A

Sentinal loop sign - dilated proximal bowel loop adjacent to the pancreas -> due to localised inflammation

35
Q

What other types of imaging can
be used for acute pancreatitis?

A
  1. CXR - to look for pleural effusion or signs of ARDs
  2. Contrast-enhanced CT - if initial assessment and investigations are inconclusive -> pancreatic oedema and swelling
    or any non-enhancing areas - pancreatic necrosis
36
Q

What is something to note
about CT scans and acute appendicitis?

A

Any CT scan used to assess severity of disease should be 6-10 days after admission in pts w/ features of persistent inflammatory response or organ failure as prior to this
time frame, CT-based severity scoring systems have been shown to be = to clinical scoring systems in predicting severity

37
Q

If someone has unexplained pancreatitis, what
should happen for them and why

A

Must have CT scan within 6 weeks to exclude malignant ductal obstruction

38
Q

Which scoring system is used
to assess the severity of acute
pancreatitis and when can you do
the score?

A

The modified Glasgow criteria - If >3 (incl 3) = severe pancreatitis - HDU referral

done within the first 48 hours.

39
Q

How can you remember the
modified Glasgow scoring system?

A

PANCREAS:
P - pO2 <8kPa.
A - Age >55yrs,
N - Neutrophils (/WCC) >15×109/L.
C - Calcium <2mmol/L.
R - Renal function (Urea) >16mmol/L.
E - Enzymes LDH>600U/L or AST>200U/L.
A - Albumin <32g/L.
S - Sugar (blood glucose) >10mmol/L.

40
Q

What are some other risk stratification scores which can be used for pancreatitis?

A
  1. APACHE II score
  2. The Ranson criteria
  3. Balthazar score (CT scoring system)
  4. BISAP [1st 24 hours]
41
Q

What is the management for acute pancreatitis?

A

No curative management - supportive is the mainstay + treat the underlying cause

42
Q

What kinds of supportive treatment can be given to patients with acute pancreatitis? (4)

A

1.IV fluid resus, and O2 therapy (balanced crystalloid should be used)
2. NG tube + antiemetics if the pt is vomiting profusely, if the patient able to eat, oral intake can be encouraged as tolerated
3. Catheterisation to accurately monitor urine output and start a fluid balance chart (due to the potential for rapid third space losses) - Aim for a urine output of at least >0.5ml/kg/hr
4. Opioid analgesia

43
Q

When would you give IV abx in acute pancreatitis? (2)

A
  1. If the patient also has acute cholangitis as a result of the acute pancreatitis
  2. infected pancreatic necrosis
44
Q

If a pt has gallstones which
caused the acute pancreatitis, how could they be managed?

A

Early laparoscopic cholecystectomy

45
Q

How should a patient be managed
if they have severe acute pancreatitis?

A

HDU referral

46
Q

what is acute cholangitis

A

infection of the biliary tree

47
Q

What can cause pancreatic duct obstruction? (4)

A
  1. Pancreatic cancers
  2. Ampullary cancers (tumours blocking the ampulla of vater)
  3. Duodenal cancers
  4. Worm blocking (3rd world country)
48
Q

What thing can predict mortality
in patients with acute pancreatitis and why?

A

Haematocrit (and serum urea) - shows dehydration -> fluid leaking inside the body

49
Q

What is chronic pancreatitis?

A

Chronically inflamed pancreas which leads to fibrosis and destruction of endocrine (won’t make insulin - T3DM) and exocrine
tissue (can’t make pancreatic enzymes, will malabsorb protein and lipids)

50
Q

How do those with chronic pancreatits present

A
  1. Chronic epigastric pain which radiates to the back and can be relieved by leaning forward.
  2. N&V + diarrhoea.
  3. Steatorrhoea - fatty stool
51
Q

What does chronic pancreatitis look like
histologically?

A

Fibrous tissue surrounding the pancreatic acinar

52
Q

What are some risk factors for chronic pancreatitis? (6)

A
  1. Alcohol
  2. Smoking
  3. Hypercalcaemia
  4. High triglycerides
  5. Autoimmune
  6. Obstructive (CF - sticky secretions in airways, bile ducts and pancreatic ducts - causes inflammation)
  7. Hereditary
    (+ Chronic renal failure)
53
Q

How do you investigate chronic
pancreatitis? (2)

A

Early:
Endoscopic US

Late:
CT best 1st test. - Look for damaged ducts + pancreatic parencrinal calcium
deposition + pancreatic gland atrophy (Can form stones in pancreatic duct)

54
Q

how is chronic pancreatitis managed

A
  1. Manage Diabetes
  2. Manage failure to make enzymes - give PERT (pancreatic replacement therapy - creon is an example brand, degrade at high temps so must keep away from heat)
  3. Manage vitamin malabsorption effects
  4. Endoscopic procedures
55
Q

Which vitamins aren’t absorbed
due to chronic pancreatitis?

A

fat soluble vitamins - A, D, E, K

56
Q

What does vitamin malabsorption result in (chronic pancreatitis)

A

Vitamin A - night blindness.
Vitamin E ?
Vitamin D - Osteoporosis -> give bisphosphonates.
Vitamin K - Increased PTT

57
Q

How can we stage the function of the pancreas?

A
58
Q

Which kinds of endoscopic procedures can be
done?

A

Peustow procedure - pancreatic duct and jejunum opened and anastamosis made between them
[+ Frey’s procedure]

59
Q

What are some complications of
chronic pancreatitis? (3)

A
  1. DM
  2. Progressive malnutrition
  3. Pancreatic cancer
60
Q

examples of substrates that can bind to acinar cells can cause increased Ca2+ levels

A

CCK; bile acid; alcohol

61
Q

what happens to the acinar cells when Ca2+ level are too high

A
  1. necrosis to to mt. MPTP opening
  2. premature tryspinogen activation
  3. impaired autophagy
  4. activation of NF-kB pathway
62
Q

fundamental pathophysiology pathway of acute pancreatitis (6)

A
  1. early trypsinogen -> tripsin activation
  2. cascade of enzyme activation (+ve feedback causing more tripsin activation)
  3. pancreatic damage/autodigestion
  4. systemic inflammatory response syndrome
  5. fluid loss and vascular alterations
  6. organ failure
63
Q

3 key factors for diagnosis acute pancreatitis

A
  1. typical pancreatic type pain (severe, rapid, radiating to back, non undulatory)
  2. radio graphic findings of acute pancreatitis
  3. elevations in blood chemistries (amylase and/or lipase x3 upper limit)
64
Q

whatis the bimodal distribution of acute pancreatitis deaths

A
  1. early (1-2 weeks, often within 72hrs) - MOS, DIC, hypoglycaemia, shock, cholangitis, haemorrhagic pancreatitis etc.
  2. later - acute necrotic collections, secomdary biliary obstruction, hopsital acquired aspiraiton, MRSA etc, PE etc.
65
Q
A

3A week 4 - HPB, malabsoprtion and EDs (3 decks)

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