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Pathology Post Midterm > Module 2: GI: Pancreatic Lesions > Flashcards

Module 2: GI: Pancreatic Lesions Flashcards

1
Q

Moving onto the Pancreatic lesions, first lets start with the inflammatory lesions. What is the etiology for acute pancreatitis?

A

Gallstones and alcohol are the most common causes

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2
Q

What is the pathogenesis for acute pancreatitis?

A

Pancreatic Injury — release of tyrpsin then amylase and lipase — released FAs combine with Ca2+ —- saponification (chalky white deposits on surface of pancreas )

  • –can lead to hypocalcemia and tetany
  • -Liquefactive necrosis of the exocrine pancreas
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3
Q

What is the presentation for acute pancreatitis?

A

Excruciating and sudden onset epigastric pain
Fever
Nause
Vomiting

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4
Q

Explain the elevation in the enzymes with acute pancreatitis?

A

Amylase elevated initially
—first 24 hours is more sensitive
Lipase elevated 72-96 hours
–more specific

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5
Q

What is the definitive diagnosis of acute pancreatitis?

A

CT/MRI

  • -fat in the peripancreatic space and liquefactive in the exocrine pancreas also called pancreatic acini necrosis
  • -spares the islets of langerhans
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6
Q

what is the most important prognostic factor for acute pancreatitis?

A

Decreased calcium levels

–lower the worse the prognosis

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7
Q

What are complications of acute pancreatitis?

A

Septic Shock (recurrent bacterial infections)
Hypovolemic Shock
Acute tubular necrosis
Hypocalcemia
–cardiac arrhythmias and tetany
ARDS
–enzymes damage lung (diffuse alveolar damage due to damage to the type II pneumocytes)
DIC
–Enzymes activate both clotting pathways

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8
Q

In acute pancreatitis is the endocrine or exocrine pancreas destroyed?

A

Exocrine pancreas destroyed first

  • -islets spread
  • -liquefactive necrosis
  • -fat necrosis
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9
Q

Next moving onto chronic pancreatitis, what is the etiology?

A

Chronic alcoholism most common cause
–recurrent acute pancreatitis
Cystic Fibrosis (due to mucus plugs)
Malabsorption: intraluminal hydrolysis of
-fat, fat soluble vitamins, and B12 is defective

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10
Q

In chronic pancreatitis is the endocrine or exocrine pancreas destroyed?

A

Starts in exocrine and affects islets

then progresses to endocrine

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11
Q

What investigations are done for chronic pancreatitis?

A

CT scan most accurate

–dystrophic calcification and fibrosis of the pancreas

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12
Q

What is the most important prognostic indicator for chronic pancreatitis?

A

Dystrophic Calcification with low Calcium

–causes malabsorption of Vit D

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13
Q

What are complications of chronic pancreatitis?

A
  1. Malabsorption
  2. DM type I (insulin for life)
  3. Pancreatic Adenocarcinoma
  4. Pancreatic pseudocysts (lined by fibrous scar/granulation tissue, due to atrophy of the epithelium) (susceptible to infection) (seen on histology)
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14
Q

Moving on to Autoimmune pancreatitis (lymphoplasmacytic sclerosing pancreatitis/ duct-destructive pancreatitis). There are two types, describe type I

A

Type 1: Lymphoplasmacytic infiltrate centered around large and medium sized interlobular duct

  • -periductal and perivenular fibrosis
  • -obliterative phlebitis (arteries are spared)
  • -Increased IgG4 plasma cells
  • -male predominance
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15
Q

Describe type 2 autoimmune pancreatitis

A

Type 2: Lymphoplasmacytic Infiltrate centered around ducts

  • -granulocytic epithelial lesions with partial/complete duct obstruction/obliteration
  • -Ig4 plasma cells are usually absent
  • -affects genders equally
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16
Q

What is the presentation for autoimmune pancreatitis?

A 
Jaundice
Abdominal Pain 
Mass-like lesion (Differentiates it from chronic pancreatitis)
Recent onset of DM 
Weight Loss
17
Q

What investigations are done for autoimmune pancreatitis/

A

Increased pancreatic enzymes and hypergammaglobulinemia (IgG4)
Autoantibodies: ANA, anti-lactoferrin (ALF), anti-carbonic anhydrase II (ACA-II) and Rheumatoid Factor (Rh)

18
Q

Moving on to carcinoma of the pancreas, what is the most common location?

A

Head/Neck of the pancreas

19
Q

What are the predisposing factors for carcinoma of the pancreas?

A

Smoking (number one)
chronic pancreatitis
KRAS mutations
p53 mutations

20
Q

Is carcinoma of the pancreas exocrine or endocrine?

A

Exocrine is more common and more dangerous

–endocrine is less common and less dangerous

21
Q

What is the presentation of pancreatic cancer?

A 
Obstructive Jaundice (Esp if its in the head) due to compression of the ampulla vader that is initially painless 
Pain (lots ,esp at night)
---retroperitoneal invasion of sacral nerve plexus 
Abdominal Mass 
Intestinal Obstruction 
Pruritus because of bile salts 
Virchows Node 
Sister Mary Joseph Nodule
22
Q

What investigations are done for pancreatic cancer?

A

Biopsy is most accurate
–ductal adenocarcinoma or dysplastic glands invading the pancreas
CA19-9 most accurate tumor marker
–CEA is also elevated
IHC stain of SMAD4 :allows differentiation between benign and malignant

23
Q

What are the complications of pancreatic cancer?

A 
Metastasis: 
--Regional lymph nodes, liver and lungs 
Invasion: 
--bowel, colon and stomach 
Diabetes 
--Damage to islets 
Lots of Mucin production 
--Trousseau's Syndrome (Recurrent migratory thrombophlebitis) in superficial veins 
--DVT (renal vein) 
NBTE
--Marantic Endocarditis: sterile vegetations on valves (fibrin only)
24
Q

What is the treatment and prognosis?

A

Whipple’s Procedure + chemo for Treatment:
–Head and neck, gallbladder (All bile is backing up and gallbladder is inflamed) and proximal duodenum removed
Terrible prognosis

25
Q

What is an insulinoma?

A

Benign, solitary tumor that arise from B cells

–increase insulin

26
Q

What are the clinical manifestations of insulinoma?

A

Whipple’s Triad:

  • -Signs and symptoms of hypoglycemia
  • -hypoglycemia relieved by intake of glucose
  • -low blood glucose levels
27
Q

How do patients with insulinomas present?

A 
Confusion 
Blurred vision 
Muscle Weakness
 Sweating 
Palpitations 
--mostly all due to the hypoglycemia
28
Q

Now finally there are three main pancreatic neoplasms to be touched on really quick. What is a acinar cell carcinoma?

A

Subcutaneous Fat Necrosis & Panniculitis due to lipase

–affects white more and is super rare

29
Q

What is an intra-ductal papillary mucinous neoplasm (IPMN)?

A

Duct is dilated and filled with mucin

  • -Majority in head of pancreas
  • -Lacks ovarian type stroma
30
Q

Finally what is a mucinous cystic neoplasm?

A

Tall columnar mucin secreting cells with surrounding ovarian type stroma

  • -majority in tail of pancreas (not connected to the ductal system)
  • -Exclusively in women
31
Q

What does histological slide for chronic pancreatitis look like?

A

All the pink is collagen

  • -exocrine is the dilated or distended ducts
  • -endocrine is your islets (Which are atrophied and to the left of the pic)
32
Q

Patients can develop something called pseudocysts in chronic pancreatitis, what is this?

A

Collection of serous fluid in the pancreas lined by fibrous scars

33
Q

In regards to pancreatic cancer, explain the spreading via seeding and then metastasis.

A

Spreading: duodenum first, pylorus then colon
Metastasis: regional lymph nodes, liver, lung

Pathology Post Midterm (50 decks)

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