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					     PANCREAS
 Exocrine and endocrine function
 Extends from c-loop to the hilum
of spleen
 Main pancreatic duct (Wirsung)
drains into papilla of vater
 Accessory duct (Santorini)----
minor papilla.
    Exocrine-----80-85% of pancreas.
    Endocrine----about 1 million clusters of
     islets of langerhans.
    Islets-----insulin, glucagon, &
     somatostatin
    EXOCRINE COMPONENTS :
    1) Acinar cells—enzymes
    2) Ductules & ducts ---to convey
        secretion
Normal Pancreas
                  Normal

- Gross & Micro
   Secretes 2 – 2.5 liters of bicarbonate rich
    fluid containing enzymes & proenzymes
   Exocrine products are inert---- prevent self
    digestion
   Present as proenzymes - trypsinogen,
    chymotrypsinogen, procarboxypeptidase,
    proelastase,etc.
   These require activation (duodenum)
   Enteropeptidase in duodenum- cleaves
    trypsinogen trypsinactivates other
    proenzymes.
    SELF DIGESTION IS PREVENTED
     BY :
1.      enzymes in inactive form
2.      requires active trypsin
3.      trypsin inhibitor
Acute pancreatitis
   Is inflammation of the pancreas
   Can be acute/chronic
   It can be a life-threatening illness
    with severe complications. Each
    year, about 210,000 people in the
    United States are admitted to the
    hospital with acute pancreatitis.
       Acute pancreatitis
   2 types
   Milder- acute edematous
    pancreatitis
   Severe- acute
    hemorrhagic necrotizing
    pancreatitis
  Etiology : Get Smashed!
G allstones
E thanol
T rauma
S teroids
Mumps
A utoimmune
S corpion venom
Hyperlipidaemia / hypercalcaemia / hypothermia
E RCP ( surgery)
Drugs (azathioprines)
Etiology
ETIOLOGIC FACTORS




Alcohol and gall stones : 2 most
important cause accounting for
90% of cases
   Pathogenesis
  Pancreatic enzymes escape into the surrounding tissue
  Trypsin causes premature activation of enzymes

Release of kallikrein     Elastase     Phospholipases   Phospholipase
and chymotrypsin                       Proteases        Lipase




                        Destroys the   Destroys          Breaksdown
Increases capillary
                        elastin in     membrane          fat
permeability
                        vessel walls   phospholipids
                                       And proteins


Interstitial edema      Haemorrhage     Pancreatic        Fat
                                        necrosis          necrosis
  Acute Pancreatitis -                         Normal
         Gross




“Chalky” fat necrosis




                        Parenchymal necrosis
Acute pancreatitis
Acute haemorrhagic necrotizing
     Pancreatitis - Gross
Acute Pancreatitis   Normal
     – Micro
 (autodigestion)
Acute Pancreatitis –
Micro (fat necrosis)
             Clinical Features:
 History:
 Abdominal pain:
  severe, usually after eating a large meal or
 consuming alcohol,rddiates to the back or to
 the shoulder

 Shock   in severe case.

 Abdominal   Examination:
 Tenderness in epigastric & guarding of
  abdominal muscles.
 In severe advanced case:
1. Grey turners sign.
2. Cullen’s sign.
    Cullen’s sign




Grey Turner’s sign
       LAB FINDINGS
 Raised Serum. amylase—first 24
  hrs.
 Raised Serum lipase levels-72 to 96
  hrs
 Hypocalcemia-poor prognostic sign

 Hyperglycemia and glycosuria in
  some cases
    Acute pancreatitis
   Laboratory finding
   Amylase and lipase (elevations of amylase are
    more sensitive but less specific than lipase in the
    diagnosis of acute pancreatitis )
   500
   400                                        Lipase
   300
                              Amylase
   200
   100
   0
      0   1H 24H             48H          5DAY
     SYSTEMIC COMPLICATIONS:
1.   Shock & renal failure:(pancreatic necrosis is
     association with leakage of fluid in the
     pancreatic bed
2.   Hypo Calcemia: sequestration of Ca in fat
     necrosis.(saponification)
3.   Hypoalbuminemia: Capillary permeability.
4.   Hyperglucemia: due to disruption of
     pancreatic islets.
5.   Respiratory distress: phospholipases
     destroy surfactant
             LOCALISED
           COMPLICATION
   Pancreatic pseudocyst
         Chronic Pancreatitis
   Recurrent bouts of inflammation leads
    to loss of pancreatic parenchyma and
    replacement by fibrosis
   Primary causes:
     Alcohol abuse
     Hypercalcemia
     Hyperlipoproteinemia
     Hereditary pancreatitis
Chronic Pancreatitis - Gross
          White areas of fibrosis


 Normal
                Normal
   Chronic
 Pancreatitis
- Microscopy
           Clinical features
   Repeated attacks of pain
              - severe/mild
              - back pain
              - diabetes

   Pancreatic malabsorption-Fat malabsorption-
    Steatorrhoea
   Impaired absorption of fat soluble vitamins A, D,
    E, K-vitamin deficiencies
       Pancreatic Pseudocysts
    Localized collections
    of pancreatic
     secretions (within or
    adjacent to pancreas)
    Virtually all arise
    after a bout of
    acute
     or chronic
    pancreatitis

Pancreatic Pseudocyst - Micro




               Lack a true epithelial lining
                  Lined by macrophages,
                  fibrosis
    CARCINOMA-PANCREAS

 Increasing incidence
 Risk factors

1. Cigarette smoking,

2. Obesity

3. High caloric food

4. Chronic pancreatitis

5. Diabetes mellitus
       Ductal Adenocarcinoma
         - Clinical Features
   Painless jaundice
    Abdominal pain
                                 TROUSSEAU

                                    SIGN
   Weight loss
   Migratory thrombophlebitis
        Ductal Adenocarcinoma
               - Gross
   Most occur in the
    head of the pancreas
    (60%)
   Poorly
    circumscribed, grey-
    white, firm masses
   Can infiltrate
    outside the pancreas
    into other organs
   Spreads through
    lymphatics – lymph
    nodes
   Blood stream
Adenocarcinoma

				
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posted:12/1/2011
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