Pancreas Flashcards
Pancreas Anatomy
95% made up of ACINAR TISSUE –> makes DIGESTIVE ENZYMES (trypsin, chymotrypsin, lipase)
Ducts lined by flat, cuboidal epithelium carry these digestive enzymes
Acini + Ducts = EXOCRINE compartment
2% of the parenchyma is made of islet cells –> INSULIN and GLUCAGON = ENDOCRINE compartment
Pancreatic Agenesis
Absence of the pancreas via a germline mutation of PDX1, a transcription factor responsible for pancreas formation; not really compatible with life
Heterotopic or Ectopic pancreas
More common than agenesis; could be asymptomatic
Pancreatic tissue outside of where it should be, usually within the GI tract
Acini and glands may or may not have islets
Acinar cells are functional –> auto-digestion can occur –> pain or mucosal bleeding
Pancreas DIVISUM
Failure of FUSION OF THE DUCTAL SYSTEMS
In the adult the pancreas is a single structure –> during embryonic development there are TWO different buds (dorsal facing backward, ventral forward)
VENTRAL pancreatic bud rotates and joins dorsal bud, and the VENTRAL persists, becoming the main drainage of the whole organ
In PANCREAS DIVISUM, there are two systems draining into the duodenum –> NARROW DORSAL duct (normally not involved) now has to carry a lot of secretions –> narrow with lots of secretions = buildup/backup
Enzyme leakage occurs –> Pancreatic damage –> RECURRENT ACUTE INFLAMMATION (Pancreatitis)
ANNULAR PANCREAS
Constriction that occurs when the ROTATION OF THE VENTRAL PANCREAS IS INCOMPLETE
Constricts the SECOND part of the DUODENUM
Child will present with intestinal obstruction soon after birth because the constriction won’t allow food material to pass beyond the stomach
Main difference between acute and chronic pancreatitis?
ACUTE –> glands will usually return to normal if the underlying cause of inflammation is removed
Chronic –> IRREVERSIBLE destruction of the pancreatic parenchyma
Two most important causes of Pancreatitis?
ALCOHOL –> direct cytotoxicity in the US; also causes constriction of the ampulla of Vater, causing a function obstruction in the outflow tract
BILIARY TRACT DISEASE –> gallstones leave the gallbladder and can get impacted in the ampulla of Vater and thus prevent flow of the pancreatic enzymes –> back-leak of enzymes into the pancreas –> destruction!
Other causes –> pancreas divisum, parasites, meds, trauma to the ducts, infections (mumps, Coxsackie), genetics
Genetic Causes of Pancreatitis
Most common – Mutation tot he PROTEIN CATIONIC TRIPSINOGEN (PRSS1) gene
Children have recurrent attacks with this mutation; this gene normally breaks down proteins –> no breakdown of trypsin –> parenchymal damage; INCREASED risk of pancreatic cancer
Mutation of SPINK1 –> normally a trypsin inhibitor; loss of function mutation –> too much trypsin –> damage to the parenchyma; not as common as PRSS1
Mutation in CFTR gene –> same gene as CF; may or may not have other classic CF symptoms (can be solely pancreatic)
Two types of ACUTE pancreatitis?
Interstitial –> Inflammation that often responds well to conservative therapy (adequate HYDRATION)
Necrotic/Hemorrhagic –> MUCH more severe; surgical emergency; blood leaks through pancreatic tissue and settles outside of the abdominal muscles –> bruising in the LATERAL FLANK REGION
How do acute pancreatitis patients present?
SEVERE ABDOMINAL PAIN; dull and constant, gradually starts out and reaches a steady peak; RADIATION TO THE BACK in about half of cases; N/V
Complications of Pancreatitis?
SHOCK –> decreased BP with all the fluid leaking out of damaged vessels
DIC – activation of the coagulation cascade; particularly bad in END ORGANS
ARDS – from breakdown of surfactant in the lungs and collapse of the alveoli
RENAL FAILURE - either from microthrombi or from shock
PANCREATIC ABSCESS – infection; life threatening
PANCREATIC PSEUDOCYST – LATE complication, particularly in alcohol induced pancreatitis –> SYMPTOMATIC CYSTIC LESION –> pseudo b/c it is NOT lined by epithelium, but instead lined by FIBROUS GRANULATION TISSUE with ragged edges and enzyme rich fluid –> aspiration shows ridiculously high amounts of pancreatic enzymes –> the fear with these is that they can grow so large and compress other structures, or perforate and secrete all their contents
Chronic Pancreatitis
IRREVERSIBLE destruction of the pancreatic parenchyma!!!
Enzyme production impaired –> patients usually on supplements; EXOCRINE (digestive) INSUFFICIENCY OCCURS EARLY
ENDOCRINE (insulin, glucagon) INSUFFICIENCY OCCURS LATER
Most common cause? CHRONIC ALCOHOL ABUSE
Others? Recurrent acute pancreatitis, pancreas divisor, hereditary pancreatitis
Not acutely life threatening, but 20 yr mortality is 50%
Five Features of CHRONIC pancreatitis?
Loss of ACINI
Fibrosis
Dilated DUCTS
Enlarged Islets (acini are gone, so they seem more apparent)
Chronic inflammation
Clinical Manifestations of Chronic Pancreatitis
Lose EXOCRINE long before ENDOCRINE, so there is less trypsin/lipase –> POOR BREAKDOWN/ABSORPTION OF FAT
Fat soluble ADEK vitamins are not absorbed either; deficiencies of these vitamins can have serious complications –> blindness, clotting problems, etc
Lack of PROTEIN ABSORPTION –> HYPOproteinemia and thus a loss of fluid into the pleural/abdominal cavity = PLEURAL EFFUSIONS, ASCITES
Stones/calcifications of the pancreas
PAIN –> Pancreas is very NERVE-RICH structure, and fibrosis can impinge on the nerves
SEVERE pain radiating to the BACK –> make sure to rule out PANCREATIC CANCER when this symptom presents
Most prevalent pancreatic tumors?
90% are DUCTAL ADENOCARCINOMAS
