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GI II Exam 1 EH > Chapter 19: The Pancreas > Flashcards

Chapter 19: The Pancreas Flashcards

1
Q

What is the most common congenital anomaly of the pancreas?

What occurs embryologically?

A
  • Pancreas Divisum
  • Failure of fusion of fetal duct system of the dorsal and ventral pancreatic primordia
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2
Q

In Pancreas Divisum the bulk of the pancreas (formed by dorsal primordium) drains through where?

A

Through the small-caliber minor papilla

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3
Q

Annular pancreas is caused by what?

Can lead to what complication?

A
  • A band-like ring of normal pancreatic tissue completely encircles the 2nd portion of the duodenum
  • Can produce duodenal obstruction
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4
Q

Very rarely the pancreas fails to develop (agenesis) and sometimes is due to germline mutation involving which gene?

A

PDX1

*‘P’ for pancreas!

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5
Q

In Western countries which 2 factors account for the majority of acute pancreatitis?

A
  1. Biliary tract disease
  2. Alcoholism
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6
Q

Pancreatic duct obstruction leading to acute pancreatitis is most commonly due to?

What are 4 other risk factors that cause obstruction?

A
  • Gallstones = most common
  • Periampullary neoplasms
  • Choledochoceles
  • Parasites —> Ascaris lumbricoides + Clonorchis sinensis
  • Possible pancreas divisum
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7
Q

Local fat necrosis in acute pancreatitis is caused by what?

A

Lipase is produced in an active form –> local fat necrosis

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8
Q

Which ion plays a key role in regulating trypsin activation?

A

Ca2+

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9
Q

How do low Ca2+ levels vs. high Ca2+ levels have an affect on trypsin?

A
  • High Ca2+ –> loss of autoinhibition = trypsin activation
  • Low Ca2+ –> trypsin cleaves and inactivates itself = inactivation
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10
Q

How does primary acinar cell injury play a role in the pathogenesis of acute pancreatitis?

i.e., role of oxidative stress, what’s activated and which TF’s expressed

A
  • Oxidative stress may generate free radicals –> membrane lipid oxidation + activation of TF’s such as AP1 and NF-kB
  • Increased Ca2+ flux leads to increased Trypsin
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11
Q

Alcohol consumption causes a transient increase in the contraction of what?

A

Sphincter of Oddi

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12
Q

Which 3 metabolic disorders are implicated in the development of acute pancreatitis?

A
  1. Hypertriglyceridemia
  2. Hypercalcemic states
  3. Hyperparathyroidism –> increased Ca2+
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13
Q

Which virus has been linked to pancreatitis?

A

Mumps - Paramyxovirus - ssRNA virus

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14
Q

Hereditary pancreatitis due to a trypsinogen mutation has what type of inheritance pattern?

Which gene is mutated and is it a loss or gain of function?

A
  • Autosomal Dominant
  • Gain-of-function in PRSS1 (chromosome 7) –> Trypsinogen gene
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15
Q

Hereditary pancreatitis can also be caused by a loss-of-function mutation in which gene?

Inheritance pattern of this mutation?

A
  • SPINK1 (chromosome 5) –> encodes a trypsin inhibitor
  • Autosomal recessive
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16
Q

How do mutations in the CFTR gene lead to potential duct obstruction and the development of pancreatitis?

A

Decreased HCO3- secretion by ductal cells –> promotes protein plugging + duct obstruction

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17
Q

In the milder form, acute interstitial pancreatitis, what are the 3 histologic alterations seen?

A
  • Mild inflammation
  • Interstitial edema
  • Focal areas of fat necrosis (due to lipase)
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18
Q

In the more severe form, acute necrotizing pancreatitis, what are some of the characteristic histological changes?

Which cells are necrosed?

A
  • Necrosis of acinar and ductal tissues + islets of Langerhans
  • Vascular injury –> hemorrhage into pancreatic parenchyma
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19
Q

What is the cardinal clinical symptom of acute pancreatitis?

Where does this pain refer to and how is it characterized?

A
  • Abdominal pain
  • Constant + intense –> referred to upper back or left shoulder
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20
Q

Elevated plasma levels of what support the diagnosis of acute pancreatitis?

Describe the timeline of these elevations (first 24 hours to 96 hours)?

A
  • Elevation of amylase during the first 24 hours
  • Rising lipase level by 72 to 96 hours
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21
Q

Full-blown acute pancreatitis is a medical emergency and how does it typically manifest clinically?

What causes the serious systemic complications and what are these complications that may be seen?

A
  • Sudden disasterous onset of “acute abdomen”
  • Release of toxic enzymes, cytokines, and other mediators into circulation —> leukocytosis, DIC, edema, and acute respiratory distress syndrome
  • Shock and acute renal tubular necrosis may occur
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22
Q

What is the key to management of someone who presents with acute pancreatitis?

A

“Resting” the pancreas by total restriction of oral intake and by supportive therapy w/ IV fluids + analgesia

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23
Q

What are 2 ominous complications that can arise with acute pancreatitis?

A
  1. Acute respiratory distress syndrome
  2. Acute renal failure
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24
Q

How does acute vs. chronic pancreatitis differ in the type of injury that occurs to the pancreatic parenchyma (ie., reversible or irreversible)

A
  • Acute is associated with reversible injury
  • Chronic is associated with irreversible injury
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25
Q

Which patient population (age and sex) is most commonly affected by chronic pancreatitis?

What is the most common cause?

A
  • Middle-aged males
  • Long-term alcohol abuse
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26
Q

While many of the cytokines produced during acute and chronic pancreatitis are similar, which type tends to predominate in chronic pancreatitis?

Leads to activation of?

A
  • Fibrogenic –> TGF-β and PDGF
  • Activation and proliferation of periacinar myofibroblasts (pancreatic stellate cells)
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27
Q

The activation of pancreatic stellate cells in chronic pancreatitis results in the deposition of?

A

Collagen and fibrosis

28
Q

Autoimmune pancreatitis is a distinct form of chronic pancreatitis associated with the presence of which cells in the pancreas?

A

IgG4-secreting plasma cells

29
Q

Why is it important to be able to differentiate Autoimmune Pancreatitis from a Pancreatic Carcinoma?

A

Autoimmune pancreatitis RESPONDS to steroid therapy

30
Q

Which type of pancreatitis is characterized by fibrosis, atrophy and dropout of acini, and variable dilation of pancreatic ducts?

A

Chronic pancreatitis

31
Q

Chronic pancreatitis caused by alcohol abuse is characterized by which histologic findings?

A
  • Ductal dilation
  • Intraluminal protein plugs and calcifications
32
Q

Chronic pancreatitis may present in many different ways, such as?

May be precipitated by?

A
  • Following repeat bouts of acute pancreatitis
  • Repeat attacks of mild-moderately severe abdominal pain or persistent abdominal pain
  • Attacks may be precipated by alcohol abuse, overeating, or the use of opioids + other drugs
  • Malabsorption sx’s (steatorrhea) or DM
33
Q

In some patients, chronic pancreatitis may be clinically silent until the development of what?

A
  • Pancreatic insufficiency –> steatorrhea
  • Diabetes mellitus (due to destruction of exocrine and endocrine pancrease)
34
Q

Diagnosis of chronic pancreatitis requires a high degree of suspicion, but which finding on CT and ultrasound can be very helpful?

A

Calcifications with pancreas

35
Q

Which type of pancreatitis is associated with a 40% lifetime risk of developing pancreatic cancer?

A

Hereditary pancreatitis

36
Q

Pseudocysts of the pancreas are localized collections of what?

They are rich in?

Lack?

A
  • Collections of necrotic and hemorrhagic material
  • Rich in pancreatic enzymes
  • Lack and epithelial lining
37
Q

Pseudocysts of the pancreas typically arise following?

May also arise as a result of?

A

- Bout of acute pancreatitis, particularly one superimposed on chronic alcoholic pancreatitis

- Trauma

38
Q

Pseudocysts may be situated within the pancreas but are more commonly found where?

A
  • Lesser omental sac
  • Retroperitoneum btw stomach and transverse colon
  • Or btw stomach and liver
39
Q

When areas of intrapancreatic or peripancreatic hemorrhage are walled off by fibrous tissue and granulation tissue, this forms what?

A

Pseudocysts

40
Q

What is the 5-year survival rate for Pancreatic Carcinoma (aka infiltrating ductal adenocarcinoma)?

A

<5%; poor

41
Q

Invasive pancreatic cancers are believed to arise from which well-defined noninvasive precursor lesions in small ducts?

A

Pancreatic intraepithelial neoplasia (PanIN)

42
Q

Which is the most frequently altered oncogene in pancreatic cancer?

Which chromosome is it on?

A

KRAS - Cr. 12p

43
Q

Mutations in KRAS signaling associated w/ pancreatic cancer most notably leads to activation of which 2 pathways?

A

MAPK and PI3K/AKT-pathways

44
Q

What is the most frequently inactivated tumor suppressor gene in pancreatic cancers?

Which chromosome is it on?

A
  • CDKN2A/p16
  • Cr. 9p
45
Q

Which tumor suppressor gene is inactivated in 55% of pancreatic cancers and encodes a protein essential for TGF-β signaling?

A

SMAD4 on Cr. 18q

46
Q

Hypermethylation of the promoter of which tumor suppressor gene has been implicated in pancreatic cancer?

A

CDKN2A

47
Q

What is the typical age range for the onset of pancreatic cancer?

More commonly seen in which ethnicities?

A
  • Age 60-80 yo
  • More common in blacks and Ashkenazi Jews (BRCA2)
48
Q

What is the strongest enviornmental risk factor for the development of pancreatic cancer?

A

Cigarette smoking doubles the risk

*Consumption of diet rich in fats also been implicated

49
Q

What are 2 risk factors for pancreatic cancer, which may also be complications of the development of cancer?

A
  1. Chronic pancreatitis
  2. Diabetes mellitus
50
Q

New-onset DM in an older patient (60-80 yo) may be the first sign that they have?

A

Pancreatic cancer

51
Q

Germline mutations in which gene is associated with familial atypical multiple-mole melanoma syndrome and almost always the development of pancreatic cancer?

A

CDKN2A

52
Q

The majority of pancreatic cancers arise in which part of the pancreas?

A

Head (60%) > Body (15%) > Tail (5%)

53
Q

The vast majority of pancreatic cancers take the form of?

A

Ductal adenocarinomas

54
Q

What are 2 features characteristic of pancreatic cancer (i.e., behavior and reaction elicited)?

A
  1. Highly invasive (even “early” invasive pancreatic cancers extensively invade peripancreatic tissue)
  2. Elicits an intense host reaction in the form of dense fibrosis (“desmoplastic response”)
55
Q

Majority of the carcinomas of the head of the pancreas obstruct what?

Leads to which clinical signs and symptoms?

A
  • Distal common bile duct
  • Marked distention of biliary tree + Obstructive Jaundice
56
Q

Why do pancreatic cancers of the body and tail often remain silent for some time?

A

Do not impinge on the biliary tract like those of the head

57
Q

Pancreatic cancers often grow along whicn structures and can directly invade into which organs/structures?

A
  • Often along blood vessels and nerves
  • Directly into: spleen, adrenals, transverse colon, and stomach
58
Q

Which 2 sites are the primary sites for distant metastases by pancreatic cancer?

A
  • Liver
  • Lungs
59
Q

Which disorder is associated with the highest increased risk (130-fold) for the development of pancreatic cancer?

What is the associated gene?

A
  • Peutz-Jegher syndrome
  • STK11
60
Q

Which colorectal cancer is associated with an increased risk for pancreatic cancer?

Associated genes?

A
  • HNPCC
  • MLH1, MSH2
61
Q

Carcinomas of the pancreas typically remain silent until what occurs; producing what initial symptom?

Symptoms of advanced disease?

A
  • Until invasion occurs
  • Pain is usually the 1st symptom, but by this time the cancer is usually beyond cure
  • Weight loss, anorexia, and generalized malaise = cachexia = advanced disease
62
Q

Which “sign” is seen in a small % of patients with pancreatic cancer?

A

Migratory thrombophlebitis or the Trousseau sign

63
Q

Which elevated serum markers associated with pancreatic cancer can be used to assess a pts response to treatment?

Are they specific and sensitive?

A
  • Carcinoembryonic antigen
  • CA19-9 antigen

*Non-specific and lack sensitivity needed to be used as tests to screen the wider population

64
Q

Which rare pancreatic tumor occurs in children and what are its distinct microscopic findings?

A
  • Pancreatoblastoma
  • Squamous islands admixed with acinar cells

*Metastatic but better prognosis than pancreatic ductal cell carcinomas

65
Q

What is the hallmark of pancreatic cancer?

A

Intense desmoplastc rxn w/ dense stromal fibrosis

GI II Exam 1 EH (12 decks)

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