Acute pancreatitis Flashcards

1
Q

What is the mortality rate of severe pancreatitis?

A

up to 10% to 30%

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2
Q

mortality in pancreatitis has a bimodal distribution.

describe it and what is the most common cause of death?

A

EARLY PHASE - multiorgan dysfunction syndrome (most common). LATE PHASE - SEPTIC COMPLICATIONS
The most common cause of death is multiorgan dysfunction syndrome.
in the first 2 weeks (early phase), the multiorgan dysfunction syndrome is the final result of
an intense inflammatory cascade triggered initially by pancreatic inflammation.
Mortality after 2 weeks (late period), is often caused by septic complications.

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3
Q

which pprotease is responsible for cell death (and which cell) in acute pancreatitis?

A

The cytosolic cathepsin B induces apoptosis or necrosis, leading to acinar cell death.

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4
Q

what is the most common cause of pancreatitis?

how many cases in the U.S?

A

Gallstone pancreatitis.

40% of U.S. cases.

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5
Q

what is the incidence for a patient with gallstones to develop pancreatitis?

A

3 - 8 %

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6
Q

what are the two theories of pancreatitis mechanism?

A

Obstructive theory, pancreatic injury is the result of
excessive pressure inside the pancreatic duct. This increased intraductal pressure is the result of continuous secretion of pancreatic juice in the presence of pancreatic duct obstruction.
Reflux, theory proposes that stones become impacted in the ampulla of Vater and form a common channel that allows bile salt reflux into the pancreas. Animal models have shown that bile salts cause direct acinar cell necrosis because they increase the concentration
of calcium in the cytoplasm; however, this has never been proven in humans

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7
Q

what are the factors that contribute to ethanol-induced pancreatitis?

A

heavy ethanol abuse (>100 g/day for at least 5 years), smoking, and genetic predisposition.

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8
Q

what is the second most common cause

of pancreatitis worldwide. What percentage of cases?

A

Excessive ethanol consumption.

35% of cases

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9
Q

what type of anatomic obstruction can cause abnormal flow of pancreatic juice into the duodenum and pancreatic injury?

A

pancreatic tumors, parasites, and congenital defects

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10
Q

name an anatomic variation that can cause pancreatitis (controversial). what percentage of the population has this variation? what is the treatment?

A

Pancreas divisum. annular pancreas (less common).
present in 10% of the population.
5% to 10% lifetime risk for pancratitis
ERCP with minor papillotomy and stenting may be beneficial for such patients.

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11
Q

which parasite can cause pancreatitis?

A

Ascaris lumbricoides

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12
Q

What is the most common complication after ERCP. percentage?

A

Pancreatitis. up to 5% of patients!

90-95% mild pancreatitis

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13
Q

Up to 2% of acute pancreatitis cases are caused by medications. What are the most common agents?

A

sulfonamides, metronidazole, erythromycin,

tetracyclines, thiazides, furosemide, statins, acetaminophen and more…

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14
Q

Which metabolic factors can cause pancreatitis?

A

Hypertriglyceridemia and hypercalcemia

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15
Q

level of triglyceride that can cause pancreatitits?

A

> 1000 mg/dL - suspected

>2000 mg/dL - confirms the diagnosis

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16
Q

what are the cardinal symptoms of acute pancreatitis?

A

epigastric or periumbilical CONSTANT pain that radiates to the back. Up to 90% of patients have nausea or vomiting that typically does not relieve the pain

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17
Q

describe two rare findings of pancreatitis?

what causes them?

A

flank and periumbilical ecchymosis (Grey Turner and Cullen signs, respectively). Both are indicative
of retroperitoneal bleeding associated with severe pancreatitis.

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18
Q

possible physical examination findings of the lung on acute pancreatitis

A

Dullness to percussion and decreased breathing sounds in the left or, less commonly, in the right hemithorax suggest pleural effusion secondary to AP.

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19
Q

which of the two - amylase or lipase is more indicative for acute pancreatitis 24 - 48 hours after the onset and why?

A

lipase levels is a more sensitive indicator to
establish the diagnosis. Lipase is also a more specific marker of AP.
The serum half-life of amylase is shorter than that of lipase.

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20
Q

acute pancreatitis - lab results?

A

Typically hyperglycemic,
Leukocytosis
Liver enzyme elevation.

The elevation of alanine aminotransferase levels in the serum in the context of AP confirmed by high pancreatic enzyme levels has a positive predictive value of 95% in the diagnosis of acute biliary pancreatitis.

Combined with the presence of gallstones on ultrasound have an even higher sensitivity (97%) and specificity (100%) for diagnosing acute biliary pancreatitis.

21
Q

Which findings can be found on simple abdominal radiograph of acute pancreatitis?
why should it be performed?

A

Althoughnot useful for diagnosis, they can help rule out other conditions, such as perforated ulcer disease. Nonspecific findings:
air-fluid levels suggestive of ileus, cutoff colon sign as
a result of colonic spasm at the splenic flexure, and widening of the duodenal C loop caused by severe pancreatic head edema.

22
Q

the rule of US in acute pancreatitis

A

this test should always be ordered in patients with AP because of its high sensitivity (95%) in diagnosing gallstones.

The usefulness for diagnosis is limited by intra-abdominal fat and increased intestinal gas as a result of ileus.

23
Q

What is the best modality for evaluation of the pancreatitis?

A

Contrast-enhanced computed tomography.

Noncontrast CT scanning may also be of value in the setting of renal failure by identifying fluid collections or extraluminal air

24
Q

which phase of CT is the most valuable to evaluate pancreatitis?

A

portal venous phase
(65 to 70 seconds after injection of contrast material), which allows evaluation of the viability of the pancreatic parenchyma, amount of peripancreatic inflammation, and presence of intra-abdominal free air or fluid collections.

25
Q

MRCP is not indicated in acute pancreatitis, what is its important role?
which additional act can improve its findings?

A

evaluation unexplained or recurrent pancreatitis.
it allows complete visualization of the biliary and pancreatic duct anatomy.

intravenous (IV) administration of secretin increases pancreatic duct secretion, which causes a transient distention of the pancreatic duct.

26
Q

secretin MRCP is useful to demontrate…

A

pancreas divisum, intraductal papillary mucinous neoplasm (IPMN), or a small tumor in the pancreatic duct.

27
Q

evaluation method of persistent choledocholithiasis in AP?

A

Endoscopic ultrasound (EUS).

EUS has been proven to be sensitive for identifying choledocholithiasis; it allows examination of the biliary tree and pancreas with no risk of worsening of the pancreatitis.

28
Q

when ERCP is indicated for acute pancreatitis?

A
  1. severe acute biliary pancreatitis
  2. patients who develop cholangitis
  3. persistent bile duct obstruction demonstrated by other imaging modalities, such as EUS.
  4. older patients with poor performance status or severe comorbidities that preclude surgery, ERCP with sphincterotomy is a safe alternative to prevent recurrent biliary pancreatitis

Routine ERCP for suspected gallstone pancreatitis reveals no evidence of persistent obstruction in most cases and may actually worsen symptoms because of manipulation of the gland.

29
Q

describe the Ranson criteria,
What are the disadvantages of this criteria?
what is its main use and why?

A

predicts the severity of the disease on the basis of 11 parameters obtained at the time of admission or 48 hours later.

mortality rate correlates with number of positive parameters.
Severe pancreatitis is diagnosed if three or more of the Ranson criteria are fulfilled.

The main disadvantage is that it does not
predict the severity of disease at the time of the admission because six parameters are assessed only after 48 hours of admission.

mainly used to rule out severe pancreatitis or to predict the risk of mortality.
Low positive predictive value (50%) and high
negative predictive value (90%).

30
Q

signs that can indicate severe pancreatitis?

A

local pancreatic complications (necrosis, abscess, or pseudocyst)
any evidence of organ failure.

C-reactive protein (CRP) > 150 mg/ml
(peaks 48 to 72 hours after the onset of pancreatitis and correlates with the severity of the disease)

31
Q

Ranson Prognostic Criteria for Gallstone Pancreatitis

11 points

A

At presentation
• Age >70 years
• Blood glucose level >220 mg/dL
• White blood cell count >18,000 cells/mm3
• Lactate dehydrogenase level >400 IU/liter
• Aspartate aminotransferase level >250 IU/liter
After 48 hours of admission
• Hematocrit*: decrease >10%
• Serum calcium level <8 mg/dL
• Base deficit >5 mEq/L
• Blood urea nitrogen level: increase >2 mg/dL
• Fluid requirement >4 liters
• PaO2: Not available

32
Q

Treatment of acute pancreatitis

A

fluids, O2, analgestics, pulse oximeter:

aggressive fluid resuscitation with isotonic crystalloid solution. may need catheter.

PULSE OXIMETRY because one of the most common
systemic complications of AP is hypoxemia caused by the acute lung injury associated with this disease.

supplementary oxyge - saturation > 95%.
analgesia.

33
Q

which patients with biliary pancreatitis should be operated? which operation?

A

With the exception of older patients and those with poor performance status, laparoscopic cholecystectomy
is indicated for all patients with mild acute biliary pancreatitis.

34
Q

when patients with biliary pancreatitis should be operated?

A

Studies have shown that early laparoscopic cholecystectomy, defined as laparoscopic cholecystectomy during the initial admission to the hospital, is a safe procedure that decreases recurrence of the disease.
For patients with severe pancreatitis, early surgery may increase the morbidity and length of stay

35
Q

when should patients with severe biliary pancreatitis should be operated?

A

conservative treatment for at least 6 weeks before laparoscopic cholecystectomy

36
Q

what is the percentage of acute abdominal fluid during an episode of acute pancreatitis?

A

30% to 57% of patients.

37
Q

does luid collections due to pancreatitis are surrounded or encased by epithelium or fibrotic capsule?
if not, who does?

A

no.

pseudocysts and cystic neoplasias of the pancreas do.

38
Q

what is the treatment for fluid collections due to pancreatitis?

A

supportive because most fluid collections will be spontaneously reabsorbed by the peritoneum.

39
Q

what are the signs of fluid collection infection in pancreatitis?
how can it be confirmed?
what is the treatment?

A

Fever, elevated, white blood cell count, and abdominal pain suggest infection of this fluid, and percutaneous aspiration is confirmatory. Percutaneous drainage and IV administration of antibiotics should be instituted
if infection is present.

40
Q

how many patients with AP will develop pancreatic necrosis?

A

Up to 20%

41
Q

It is important to identify and to provide proper treatment for pancreatic necrosis because most
patients who develop multiorgan failure have necrotizing pancreatitis;
how many people who died from AP had pancreatic necrosis?

A

it has been documented in up to 80% of the autopsies of patients who died after an episode of AP.

42
Q

what is the main complication of pancreatic necrosis? what is the risk for this complication?

A

Infection.
Therisk is directly related to the amount of necrosis;
pancreatic necrosis involving - risk of infection:
<30% of the gland - risk 22%.
30-50% - 37% risk
>70% of the gland - 46% risk

43
Q

modified Marshall scoring system?

Respiratory

A

Respiratory (PaO2/FiO2)

0) >400
1) 301-400
2) 201-300
3) 101-200
4) ≤101

44
Q

modified Marshall scoring system?

Renal

A

creatintine (for non CRF)

0) <1.4
1) 1.4-1.8
2) 1.9-3.6
3) 3.6-4.9
4) >4.9

45
Q

modified Marshall scoring system?

Cardiovascular

A

(systolic blood pressure, mmHg)

0) >90
1) <90, fluid responsive
2) <90, not fluid responsive
3) <90, pH <7.3
4) <90, pH <7.2

46
Q

CT finding that confirms infected pancreatic necrosis

A

Evidence of air within the pancreatic necrosis.

rare finding.

47
Q

what is the treatment for infected pancreatic necrosis?

A

IV antibiotics
Because of their penetration into the pancreas and spectrum coverage, carbapenems are the first option of treatment.
Alternative therapy includes quinolones, metronidazole, third generation cephalosporins, and piperacillin

48
Q

Pancreatic Pseudocysts p 1530

A

Pancreatic Pseudocysts p 1530