PANCREAS ENDOCRINE Most imp disease Diabetes mellitus tumors EXOCRINE Pancreatitis Carcinomas Functions of pancreas Endocrine portion constitute what portion B cells secrete Endocrine cells are called ID: 935386
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Slide1
PANKREAS
DR.RUTH SHIFA
Slide2PANCREASENDOCRINE
Most imp disease- Diabetes mellitustumors
EXOCRINE
Pancreatitis
Carcinomas
Slide3Functions of pancreas
Endocrine portion constitute what portion?????
B cells secrete : ?
Endocrine cells are called: ?
How many I of L cells are present: ?
Slide4Pancreatic
acini
-exocrine
acinar
cells.
synthesis and packaging of digestive enzymes for secretion into a central lumen
.
Slide5Inflammation of the Pancreas
Pancreatitis
acute
chronic
Slide6Clinical Situation
Pt. X-
a 32 year,
divorced,
business executive
brought to the emergency department
C/O- abdominal & back pain and vomiting x 2 days.
6
Slide7O/E
- trying to sit up, continuously movement on the bed. is alert ; able to answer questions, but refuses to let anyone touch his abdomen or his back.
He rates his pain at 10/10
Slide8His skin is hot, dry and flushed with
turgor
and he complains of extreme thirst.
VS: BP 100/60,
T-100°F, P-120, R- 28 shallow, O
2
sats-90%
Slide9Acute Pancreatitis
Laboratory tests
Serum amylase- hallmark test
Serum lipase – also elevated
Blood glucose
Serum calcium- Decreased
Triglycerides
Slide10CAUSES
GET SMASHED
Slide11Acute Pancreatitis
Etiology and
Pathophysiology
Pancreatic Ducts become obstructed
Hypersecretion of the exocrine
enzymes of pancreas
These enzymes enter the bile duct, where they are activated and with bile back up into the pancreatic duct
Pancreatitis
Slide12Progression of Disease
Autodigestion
Acute Inflammation of Pancreas
Necrosis of Pancreas
Digestion of vascular walls
Thrombus and Hemorrhage
Death
Slide13Acute Severe Pancreatitis
Pathophysiology
13
Injury or disruption of pancreatic ducts
leakage of active pancreatic enzymes
autodigestion
Breakdown of cell membranes
edema vascular damage, hemorrhage, necrosis inflammatory mediators Shock, MODS, …..
Slide14P
Q
R
S
T
None stated – comes on when recumbent
Deep, piercing (knife-like), continuous, twisting
LUQ or mid-
epigastrium
radiating to back
Patient may flex spine to get relief
Aggravated by eating & alcohol
Unrelieved by vomiting
Aggravated by supine position or walking
Relieved by sitting up & leaning forward
Severe “10”/10
Sudden onset
14
CLINICAL FEATURES
Slide15Slide16Morphology-Gross & M/E.
Mild inflammation and edema to severe extensive necrosis and hemorrhage
.
Edema
Fat necrosis
An acute inflammatory reaction
Proteolytic
destruction of pancreatic parenchyma
Destruction of blood vessels with interstitial hemorrhage.
Slide17Diagnostic Tests & Procedures
Abdominal and chest filmsCT scanUltrasound
Aspiration biopsy
Peritoneal
lavage
Endoscopic Retrograde
Cholangio-pancreatography
(ERCP)
17
Slide18Chronic pancreatitis
Slide19COMPLICATIONS
Slide20Pancreatic neoplasms
Slide21Serous cystadenoma
Slide22Pancreatic CA
Risk factors
:
Smoking/alcohol
diets high in fat, beef, pork & processed meats
diabetes
chemical exposure
chronic pancreatitis
CM’s
:
abdominal pain,
anorexia, nausea,
jaundice, diarrhea
Metastasis by time of diagnosis
Diagnosis
–
tumor markers- CA19-9, CEA
CT with biopsy, ERCP with biopsy
Staging by TNM (Tumor, nodes,
mets
)
22
Slide23Adenocarcinoma
Slide24Questions-
1. Pancreatitis-acute/chronic2.
Adenocarcinoma
3.
Pathophysiology
of pancreatitis