Pancreatic Pathology Flashcards
Split between exocrine and endocrine pancreas
80% of pancreas is exocrine
- contains acinar cells and secretes proenzymes/ proteases
20% is endocrine
- contains islets of langerhans and secretes glucagon, insulin and somatostatin
Pancreatitis
Inflammatory broad disorder of the pancreas. Can be acute or chronic
Acute = function of the pancreas can return to normal if the underlying cause is removed
Chronic = irreversible damage to the exocrine pancreas
Acute pancreatitis
Usually focal edema, fat necrosis or acute hemorrhages
Common especially within the western world
- incidence = 10-20/100K
Most common cause is impact ion of gallstones within the common bile duct and impeding the flow of pancreatic enzymes Through the ampulla of vater
Second most common is excessive alcohol intake
both alcoholism and gallstones account for 80% of acute pancreatitis cases
Pathogenesis of acute pancreatitis
Appears to be caused by auto digestion of pancreas by inappropriately activated pancreatic enzymes
the primary prematurely activated enzyme is trypsin which unleashes proenzymes which leads to tissue injury and inflammation
What are the 3 pathways that can incite the initial enzyme activation to lead to acute pancreatitis?
1) Pancreatic duct obstruction
2) Primary acinar cell injury
3) Defective intracellular transport of proenzymes within acinar cells
What are the mechanisms behind alcohols consumption on acute pancreatitis?
1) alcohol transiently keeps sphincter of oddi contracted tight and increases pancreatic exocrine secretion
2) has direct toxic effects on acinar cells and induces oxidative stress in acinar cells = membrane damage
3) increases secretion of protein-rich pancreatic fluid which forms “protein plugs” leading to obstruction of small pancreatic ducts
What are the 5 basic alterations in acute pancreatitis?
1) microvascular leakage w/ edema
2) necrosis of fat by lipases
3) acute inflammatory reactions
4) proteolytic destruction of pancreatic parenchyma
5) destruction of blood vessels leading to interstitial hemorrhage
Clinical features of pancreatitis
- marked abdominal pain is the #1 symptom*
- can range from mild to so severe it is incapacitating
Also shows:
- elevated levels of serum amylase and lipase (#1 diagnostic example)
- absence of bowel sounds
- (+/-) hypocalcemia (if present = poor prognosis)
- *full blown acute pancreatitis is a medical emergency**
- pain in this instance will be intense, constant and refer to the upper back
What are diagnostic features of severe acute pancreatitis and complications?
Intestine referred pain and the following
- fat necrosis
- leukocytosis
Complications
- DIC
- shock
- renal failure
Treatment for acute pancreatitis
Supportive therapy
- maintain blood pressure and alleviate pain
- rest the pancreas and restrict oral foods/fluids
- surgery (if necrotic)
In surviving patients: produces sterile or infected pancreatic abscesses or pseudocysts
Chronic pancreatitis
Prolonged inflammation for he pancreas associated with irreversible destruction of exocrine parenchyma, fibrosis.
- late stages = destruction of endocrine parenchyma
By far the most common cause = long-term alcohol abuse
- middle aged men = more likely
Other causes:
- duct obstruction
- hereditary pancreatitis
- autoimmune pancreatitis
What cytokine is seen in chronic pancreatitis but never in acute pancreatitis?
TGF-B and other profibrogenic cytokines
Clinical features of chronic pancreatitis
#1 symptom is repeated bouts of intense jaundice
Symptoms :
- abdominal distention
- indigestion
- Persistent/recurrent abdominal pain that radiates to the back (<10% can be silent with no pain though)
- no onset diabetes
- malabsorption
- DEAK deficiencies
long term outlook is poor with 50% mortality within 20-25 years
What are the most common causes of chronic pancreatitis attacks
Alcohol abuse
Overeating/binge eating
Opiate use/ sympathetic drug use
What is the most feared complication of chronic pancreatitis
Pancreatic cancers
- 5% of adults get this within 20 years of having chronic pancreatitis
- **if develops in children due to hereditary loss of PRSS1 gene function = 40-55% risk of pancreatic cancer (often undoes pancreatectomy to avoid this risk)
