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Clin Med II > Acute and chronic Pancreatitis > Flashcards

Acute and chronic Pancreatitis Flashcards

1
Q

Pancreatitis

A

Inflammatory process in which pancreatic enzymes autodigest the gland

Characterized clinically by abdominal pain and elevated levels of serum pancreatic enzymes

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2
Q

Acute pancreatitis

A

Can be mild or severe in nature and treatment is based upon this.

With acute pancreatitis the gland heals without any chronic impairment of function or morphological changes.

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3
Q

Chronic pancreatitis

A

Recurs intermittently

Leads to functional and morphologic loss of the gland

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4
Q

Endocrine function of the pancreas

A

Responsible for insulin production

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5
Q

Exocrine function of the pancreas

A

Acinar cells manufacture, store and secrete digestive enzymes leading to carbohydrate, fat, and protein metabolism

Ductal cells secrete H₂0 and NaHCO3

~80 % of the gross weight of the pancreas supports exocrine function.

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6
Q

Zymogens

A

Name for the vesicle that packs and stores digestive enzymes are produced within the pancreatic acinar cells.

Zymogens prevent the enzymes from “autodigesting” the cells that synthesized them

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7
Q

Production of digestive enzymes in the pancreas

A

manufactured in the rough ER –> Further processing in the Golgi apparatus –> Packaged into zymogens as proenzymes

Hormones stimulate the release of these proenzymes into the pancreatic duct when we eat.

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8
Q

Trypsinogen

A

Precursor form or zymogen of trypsin

Produced by the pancreas

Found in pancreatic juice, along with amylase, lipase, and chymotrypsinogen

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9
Q

Enterokinase

A

Attached to the intestinal surface

Cleaves trypsinogen activating it to trypsin

Trypsin, in turn, converts zymogens including trypsinogen itself to their activated enzyme forms through enzymatic cleavage

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10
Q

Trypsin

A

Trypsin facilitates the conversion of the other proenzymes to their active forms

Feedback mechanism exists to limit pancreatic enzyme activation after appropriate metabolism has occurred

Hypothesized that elevated levels of trypsin

Leads to decreased CCK and secretin levels

Limits further pancreatic secretion

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11
Q

What are the two most common causes of acute pancreatitis?

A

Alcohol consumption
Biliary stone disease

Gallstones are the most common cause of acute pancreatitis.

Alcohol is the most common cause of chronic pancreatitis.

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12
Q

What are 2 initiating events of gallstone pancreatitis?

A

Reflux of bile into the pancreatic duct due to transient obstruction of the ampulla during passage of gallstones

Obstruction at the ampulla secondary to stone(s) or edema resulting from the passage of a stone

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13
Q

Risk of a stone causing pancreatitis is _______ proportional to size

A

inversely

Occult microlithiasis → probably responsible for most cases of idiopathic acute pancreatitis

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14
Q

Treatment of gallstone associated pancreatitis

A

Cholecystectomy and clearing the CBD of stones prevents recurrence

Confirms cause-and-effect relationship

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15
Q

Alcohol use and acute pancreatitis

A

Ethanol leads to intracellular accumulation of digestive enzymes and their premature activation and release

Increases the permeability of ductules:
Allows enzymes to reach the parenchyma and cause pancreatic damage

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16
Q

Ethanol effects of the pancreas

A

Increases the protein content of pancreatic juice

Decreases bicarbonate levels and trypsin inhibitor concentrations

Can lead to the formation of protein plugs that block pancreatic outflow

**Know that this can usually be associated with chronic pancreatitis but can also be due to large binge drinking.

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17
Q

ERCP- acute pancreatitis

A

4% of causes

Can have mechanical injury: due to prolonged manipulation around papillary orifice

or Thermal injury: for electrocautery current

increased risk if:
Endoscopist is inexperienced

Patient is thought to have sphincter of Oddi dysfunction

Manometry(measures pressures in surrounding ducts) is performed on the sphincter of Oddi

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18
Q

Acute pancreatitis: Hypertriglyceridemia

A

Only 1-4% of cases of acute
Serum triglyceride concentrations > 1000 mg/dL

Most believe that the association is caused by the underlying derangement in lipid metabolism rather than by pancreatitis causing hyperlipidemia (controversial).

Breakdown of triglycerides into toxic free fatty acids by pancreatic lipases → cause of lipotoxicity during acute pancreatitis

Tends to be more severe than alcohol- or gallstone-induced disease

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19
Q

Acute pancreatitis: Trauma

A

Blunt or penetrating trauma can damage the pancreas

Uncommon injuries due to retroperitoneal location

Pancreatic injury occurs more often in penetrating injuries than in blunt abdominal trauma.

Healing of pancreatic ductal injuries can lead to scarring and stricture of the main pancreatic duct

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20
Q

Amylase and lipase levels in abdominal trauma

A

Abdominal trauma causes an elevation of amylase and lipase levels in 17% of cases and clinical pancreatitis in 5% of cases.

Be aware of this when working up a patient with abdominal trauma.

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21
Q

Acute pancreatitis: Drugs

A

Relatively rare occurrence (accounting for approximately 2% of cases)

Probably related to an unknown predisposition

Hypersensitivity reaction

Generation of a toxic metabolite. This is usually a more mild form.

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22
Q

Acute pancreatitis: infection

A

> 1% of pancreatitis cases

Viral causes: mumps, coxsackie, cytomegalovirus (CMV), hepatitis, Epstein-Barr virus (EBV), echovirus, varicella-zoster virus (VZV), measles, and rubella

Bacterial causes: Mycoplasma pneumoniae, Salmonella, Campylobacter, and Mycobacterium tuberculosis

Roundworm (ascaris) much less common especially in the US.

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23
Q

Acute pancreatitis: Hereditary (PRSSI)

A

Autosomal dominant disorder related to mutations of the cationic trypsinogen gene (PRSS1).

Causes premature activation of trypsinogen to trypsin.

Can trigger the entire zymogen activation cascade in the pancreas instead of the intestine.

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24
Q

Acute pancreatitis: Cystic fibrosis

A

CFTR (cystic fibrosis transmembrane conductance regulator) mutation plays a role in predisposing patients to acute pancreatitis

Causes abnormalities of ductal secretion

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25
Q

Acute pancreatitis: Hypercalcemia

A

Hypercalcemia from any cause(hyperparathyroidism, TPN, excessive vitamin D intake) can lead to acute pancreatitis

Proposed mechanisms:

  1. Deposition of calcium in the pancreatic duct
  2. Calcium activation of trypsinogen within the pancreatic parenchyma
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26
Q

Acute pancreatitis: Tumors

A

Obstruction of the pancreatic ductal system by a tumor.

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27
Q

Acute pancreatitis: Toxins

A

Exposure to organophosphate insecticide can cause acute pancreatitis.

Scorpion and snake bites

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28
Q

Acute pancreatitis: postsurgical

A

May occur in the postoperative period of various surgical procedures (e.g., abdominal or cardiopulmonary bypass surgery).

Mechanism is unclear
May damage the gland by causing ischemia

Often with higher complication rate.

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29
Q

Risk factors for postsurgical pancreatitis

A

Preoperative renal insufficiency
Postoperative hypotension
Perioperative administration of calcium chloride

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30
Q

Vascular pancreatitis

A

Vasculitis can predispose patients to pancreatic ischemia.

Uncommon cause of clinically significant pancreatitis

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31
Q

Acute pancreatitis: Autoimmune

A

Super rare!

Usually in young people (approximately 40 years) who also suffer from inflammatory bowel disease

Pathogenesis is unclear.

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32
Q

Remembering causes of pancreatitis: GET SMASHED

A

G: Gallstones
E: Ethanol- Alcohol
T: Trauma

S: Steroids
M: Mumps (infectious)
A: Autoimmune
S: Scorpion bite
H: Hyperlipidemia
E: ERCP
D: Drugs
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33
Q

Acute pancreatitis: History

A

Cardinal symptom: Upper abdominal pain that is dull, boring, and steady.

Sudden in onset and gradually intensifies in severity to constant ache that can be severe.

Pain can radiate into the back in half of the patients.

Pain is worse with movement and made better by sitting and leaning forward.

Associated N/V

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34
Q

Clinical presentation of severe pancreatits

A

Typically presents with weakness, sweating, and anxiety.

Dyspnea due to diaphragmatic inflammation secondary to pancreatitis

Hx of alcohol intake or a heavy meal immediately preceding sxs
Hx of biliary colic in the past? Recent operative or other invasive procedures (e.g., ERCP)
? family hx of hypertriglyceridemia

Patients frequently have a history of previous biliary colic and binge alcohol consumption

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35
Q

Acute pancreatitis physical exam

A

Fever, abdominal tenderness with guarding in upper abdomen, abdominal distention, Tachycardia, Hypotension, diminished bowel sounds

Less common Jaundice, dyspnea

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36
Q

Uncommon physical exam findings with severe necrotizing pancreatitis

A

Cullen sign: Bluish discoloration around the umbilicus resulting from hemoperitoneum

Grey-Turner sign: Reddish-brown discoloration along the flanks resulting from retroperitoneal blood dissecting along tissue planes

These signs are associated with a poor prognosis

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37
Q

Acute pancreatitis differential diagnosis

A 
Perforated viscus (PUD)
Acute cholecystitis
Acute bowel obstruction
Mesenteric ischemia
Renal colic
AMI
Dissecting AAA
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38
Q

Acute pancreatitis labs: serum amylase

A

Elevation > three times the upper limit of normal has a sensitivity for the diagnosis of acute pancreatitis of 67 to 83 percent and a specificity of 85 to 98 percent.

Rises within 6 to 12 hours of the onset of acute pancreatitis

Short half-life (≈10 hours) and in uncomplicated attacks returns to normal within three to five days

Dx may be missed in patients who present >24 hours after the onset of pancreatitis

39
Q

Acute pancreatitis labs: Lipase

A

Elevation > three times the upper limit of normal has a sensitivity and specificity for acute pancreatitis ranging from 82 to 100 percent

Rises within 4 to 8 hours of the onset of symptoms

Peaks at 24 hours
Returns to normal within 8 to 14 days.

40
Q

Acute pancreatitis labs: Amylase vs lipase

A

Lipase elevations occur earlier and last longer than elevations in amylase.

Lipase is more sensitive as compared with amylase in patients with pancreatitis secondary to alcohol.

Lipase is the most important test to pay attention to because amylase can be seen in other conditions.

41
Q

Acute pancreatitis labs: Liver enzymes

A

Determine ALP, total bilirubin, AST and ALT levels.

An ALT level >150 U/L suggests gallstone pancreatitis and a more fulminant disease course.

42
Q

Acute pancreatitis: electolytes

A

Electrolytes: Disturbance in the electrolyte balance is usually found secondary to third spacing of fluids
Fluids may “leak out” into the peritoneal cavity, causing depletion of the intracellular, interstitial or vascular compartments.

43
Q

Acute pancreatitis labs: Hypo and hypercalcemia

A

Hypocalcemia: Due to sequestration of ionized calcium in the damaged tissue

Hypercalcemia: ?etiology of pancreatitis

44
Q

Acute pancreatitis labs: Elelvated HCT

A

Hemoconcentration due to extravasation of intravascular fluid into third spaces

Admission Hct >47% → sensitive measure of more severe disease

45
Q

Acute pancreatitis labs: Blood glucose

A

may be elevated from beta-cell injury (make insulin)

46
Q

Acute pancreatitis labs: cholesterol and triglyceride levels

A

Search for an etiology of pancreatitis

47
Q

Acute pancreatitis labs: CRP

A

Obtain 24-48 hours after presentation
Higher levels correlate with a propensity toward organ failure
≥ 10 mg/dL strongly indicates severe pancreatitis

48
Q

Acute pancreatitis: Prognosis labs

A 
Lactic dehydrogenase (LDH), BUN, and bicarbonate. 
Measure at admission and at 48 hours in order to help determine the Ranson criteria.

LDH (50-200 U/L)→ marker of tissue breakdown (cell damage)
Present in virtually all tissues and not very specific

Marked increase LDH >500 U/L suggests a poor prognosis

49
Q

Acute pancreatitis diagnosis

A

Diagnosis of acute pancreatitis requires two of the following three criteria:
1. Characteristic acute onset of epigastric or vague abdominal pain that may radiate to the back.

  1. Serum amylase or lipase levels greater than or equal to 3 times the upper limit of normal.
  2. Imaging study with characteristic changes
    CT, MRI, abdominal ultrasound or endoscopic ultrasound
50
Q

Acute pancreatitis: When should we NOT order imaging

A

Characteristic abdominal pain + elevation in serum lipase or amylase to 3X or greater than the upper limit of normal =
No imaging is required to establish the diagnosis of acute pancreatitis

51
Q

Acute pancreatitis: When should be order imaging?

A

When the diagnosis is in doubt

When severe pancreatitis is present

When a given imaging study might provide specific information needed to answer a clinical question(biliary pancreatitis)

52
Q

Acute pancreatitis: Abdominal US

A

Most useful initial test in determining the etiology of pancreatitis (esp. if concern of biliary issues)

Can also be helping in detecting gallstones.

53
Q

Acute pancreatitis: AXR

A

Helpful in ruling out other etiologies for acute abdominal pain.

KUB with the pt upright detects free air in the abdomen –> Perforated viscus

Pancreatic calcifications may be seen in chronic pancreatitis

54
Q

Acute pancreatitis: Abdominal CT with IV contrast

A

Imaging study of choice for assessing complications.

Always indicated in patients with severe acute pancreatitis

Seldom needed within the first 72 hrs after symptom onset unless the diagnosis is uncertain. Inflammatory changes are often not radiographically present until 72 hrs.

55
Q

Acute pancreatitis prognosis

A

Overall mortality in acute pancreatitis is 10-15%.

Mortality in severe acute pancreatitis (20% of presentations) ≈30%
Multiorgan system failure → major cause of mortality.

56
Q

Systemic manifestations of acute severe pancreatitis

A

Acute respiratory distress syndrome (ARDS)
Acute renal failure
Cardiac depression
Hemorrhage and hypotensive shock.

57
Q

Mild acute pancreatitis

A

Absence of organ failure and local or systemic complications

58
Q

Moderately severe acute pancreatitis

A

no organ failure or transient(<48 hours) organ failure and/or local complication

59
Q

Severe acute pancreatitis

A

Persistent organ failure (>48 hours) that may involve one or multiple organs(cardiovascular, respiratory, or renal)

Can be determined based on patients presentation, labs, and imaging. Important to treat aggressively.

60
Q

Rating severity of pancreatitis: Atlanta classification

A

Based on CT imaging:
Interstitial edematous acute pancreatitis (mild) → acute inflammation of the pancreatic parenchyma and peripancreatic tissues but without recognizable tissue necrosis.

Necrotizing acute pancreatitis (severe) → inflammation associated with pancreatic parenchymal necrosis and/or peripancreatic necrosis

61
Q

Clinical predictors of severe acute pancreatitis:

A 
Older age (>55 yo)
Alcoholic pancreatitis
Short onset of symptoms to hospital admission (<24hrs)
Obesity (BMI>30)
Comorbid disease.
62
Q

Clinical predictors: Ranson criteria

A

Calculated on admission and at 48 hours

Score of 0-2 → minimal mortality
Admitted to the med/surg for medical therapy and support
Score of 3-5 → 10-20% mortality rate
Admitted to ICU
Score higher than 5 after 48 hours → mortality >50% and associated with more systemic complications

63
Q

Drawbacks of Ranson criteria

A

Score is valid only at 48 hours after onset and not at any later time during the disease
Sensitivity is only 73% and the specificity is 77% for predicting mortality

64
Q

Clinical predictors: Apache II

A

Acute Physiology And Chronic Health Examination (APACHE) II score.

Advantage of being able to assess the patient at any point during the illness.

Recommended test from american gastroenterological association.

65
Q

Other clinical predictors:

A

SIRS: Systemic inflammatory response syndrome
BISAP: Bedside index of severity in Acute pancreatitis score
HAPS: Harmless Acute pancreatitis score

66
Q

Acute pancreatitis treatment

A

Supportive care with fluid resuscitation, pain control and nutritional support.

NPO
IV fluid hydration
Analgesics

*Antibiotics generally are not indicated.

67
Q

Acute pancreatitis treatment: Aggressive hydration

A

Aggressive hydration at a rate of 5 to 10 mL/kg per hour using NS or LR.

Severe volume depletion: 20 mL/kg over 30 minutes and 3 mL/kg/hr for next 8-12 hours.

Reassess fluid requirements at frequent intervals in the first six hours of admission and for the next 24 to 48 hours.

68
Q

Fluids and hypercalcemis

A

Avoid located ringer’s because it contains 3 mEq/L calcium.

69
Q

Acute pancreatitis: Analgesia

A

Treat abdominal pain

Opioids are safe and effective at providing pain control in patients with acute pancreatitis:
IV hydromorphone or fentanyl

Remember**Adequate fluid resuscitation should be the first priority

70
Q

Acute pancreatitis treatment: Monitoring

A

Monitor vital signs, urine output, electrolytes (esp. due to fluid resuscitation), magnesium, serum glucose (for severe).

71
Q

When to progress to solid diet after NPO?

A

Mild pancreatitis → in the absence of ileus (NBS) and N/V
As soon as the pain is decreasing(without IV analgesia), inflammatory markers are improving, and appetite returns (usually around 24- 48 hours) attempt clear liquid to solid food diet as tolerated.

Moderately severe/severe: Enteral feeding rather than parenteral nutrition is recommended.

72
Q

Extrapancreatic infection

A

Ex: septicemia, pneumonia, and urinary tract infections

Extrapancreatic infections associated with an increase in mortality→ Treat them accordingly!

73
Q

Pancreatitis complications: Pseudocyste

A

Peripancreatic fluid collection containing high concentrations of pancreatic enzymes within a defined fibrous wall and lacking an epithelial lining(thus the “pseudo”).

Acutely fluid is not well defined but over 4 weeks fluid collection is much more organized

74
Q

Pancreatitis complications:

A

At 4 weeks:
Walled-off pancreatic necrosis (WOPN)
Collection is defined by a fibrotic and inflammatory wall

Infected necrosis:
Bacterial invasion of necrotic pancreatic tissue
Mortality rate >20%
Related to sepsis and multiorgan failure

75
Q

Necrotizing pancreatitis pathyphysiology

A

Premature intra-acinar activation of digestive zymogens into their active forms (e.g., trypsinogen to trypsin) –> causes autodigestion –> fluid collection –> Injury to the pancreatic duct or its branches leads to leakage of pancreatic enzymes

76
Q

Acute pancreatitis necrotizing pancreatitis: Treatment

A 
Endoscopic drainage
CT-guided or  endoscopic ultrasonography guided needle aspirations
Surgical drainage (procedure for cure)
77
Q

When to consult for complications of pancreatitis?

A

Consult a surgeon, gastroenterologist, and/or interventional radiology with any complications of pancreatitis:

Severe acute pancreatitis (SAP)
Associated pancreatic abscess
Necrotizing pancreatitis
Pancreatic pseudocyst (especially if symptomatic)
Impacted gallstone
Cholecystits
Small bowel obstruction
78
Q

Chronic pancreatitis

A

Continuing, chronic, inflammatory process of the pancreas, characterized by irreversible morphologic changes.

79
Q

Chronic pancreatitis: Presentation

A

May be asymptomatic over long periods of time.
Can present with a fibrotic mass
Symptoms of pancreatic insufficiency without pain.

Most commonly there is chronic abdominal pain and normal or mildly elevated pancreatic enzyme levels

DM and steatorrhea due to lose of endocrine and exocrine function

Diarrhea and weight loss

80
Q

Amylase and lapse in chronic pancreatitis

A

Tend to be normal in chronic pancreatitis.

81
Q

Etiologies of chronic pancreatitis

A

Intraductal plugging and obstruction (ethanol (ETOH) abuse, stones, tumors).

Direct toxins and toxic metabolites (ETOH, tobacco, hypercalcemia, hyperlipidemia).

Excessive alcohol consumption is the most common cause of chronic pancreatitis, accounting for about 60% of all cases

Autoimmune (SLE, IBD, Sjögren syndrome)

Idiopathic (30% of cases)

Genetic (CF, hereditary pancreatitis)

82
Q

Chronic pancreatitis: Pancreatic insufficiency

A

Severe exocrine dysfunction

Protein and fat deficiencies do not occur until >90% of pancreatic function is lost

Steatorrhea (from fat malabsorption) usually occurs prior to protein deficiencies
Loose, greasy, foul smelling stools that are difficult to flush

Malabsorption of the fat soluble vitamins (A, D, E, K) and vitamin B12 may also occur.

83
Q

Pancreatic diabetes

A

Glucose intolerance occurs and overt DM usually occurs late in the course of the disease.

Classic triad of calcifications, steatorrhea, and DM usually occurs in late, advanced disease

84
Q

Chronic pancreatitis diagnosis

A

Lipase and amylayse may be elevated(slightly) or normal

Elevated fecal fat excretion of more than 7g of fat per day is diagnostic of malabsorption
72hr fecal fat determination is gold standard.

Assays of fecal chymotrypsin and human pancreatic elastase
Useful in confirming advanced chronic pancreatitis with exocrine insufficiency but have the same limitation as fecal fat analysis.

85
Q

Chronic pancreatitis imaging: ABD plain films

A

1st initial imaging study:

Pancreatic calcifications considered pathognomonic of chronic pancreatitis

86
Q

Chronic pancreatitis imaging: CT scan

A

Indicated to look for complications.
Useful in planning surgical or endoscopic intervention.
Depicts morphologic changes of advanced chronic pancreatitis. Subtle abnormalities of early to moderate chronic pancreatitis are beyond CT resolution

87
Q

Chronic pancreatitis imaging: MRCP

A

Benefits of CT but without the radiation and IV contrast risks.

88
Q

Chronic pancreatitis imaging: ERCP

A

Test of choice for the diagnosis of chronic pancreatitis when calcifications are not present on a plain film of the abdomen and there is no evidence of steatorrhea!

Visualizes the ducts
Often used with therapeutic intent.

89
Q

Chronic pancreatitis goals treatment

A

Goals → pain management, correction of pancreatic insufficiency, and management of complications.

90
Q

Chronic pancreatitis treatment: pain management

A

1st step → recognize and treat the underlying etiology to reduce progressive pancreatic damage

Remove any stones with ERCP

Cessation of smoking — Smoking may accelerate the progress of chronic pancreatitis and may increase the risk of pancreatic cancer

Alcohol abstinence

Judicious use of analgesics
Risk of opioid dependency

91
Q

Chronic pancreatitis treatment: Pancreatic enzyme supplement

A

Suppress pancreatic exocrine secretion and relieve pain in some patients.

Exogenous pancreatic enzymes are taken with a meal
CCK-releasing factors are degraded and CCK release in response to a meal is reduced

Limited to nonalcoholic patients with early chronic pancreatitis and requires the use of uncoated preparations.

Also treat with acid suppression (either with an H2 blocker or PPI) to reduce inactivation of the enzymes from gastric acid

92
Q

Chronic pancreatic complications

A

DM
Pseudocyst
Bile duct obstruction or duodenal obstruction
Due to pseudocyst, stricture, inflammation or fibrosis in the pancreatic head
Pancreatic cancer
Chronic pancreatitis is associated with pancreatic adenocarcinoma (develops in ≈4% of patients within 20 yrs of diagnosis of chronic pancreatitis

93
Q

Chronic pancreatitis: prognosis factors

A 
Age at diagnosis
Smoking
Continued use of alcohol
Presence of liver cirrhosis
Survival rate is 70% at 10 years and 45% at 20 years

Clin Med II (7 decks)

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