pancreas and gallbladder Flashcards by mohamed nascer

what are congenital anomalies of pancreas ?

1- Agenesis ( not formed )

2- Pancreatic divisum —> ( single pancreatic duct is not formed but rather remains 2 distinct dorsal and ventral duct )

3- Annular pancreas —> Second part of the duodenum is surrounded by a ring of pancreatic tissue continuous with the head of pancreas

4- Heterotopic pancreas ( pan tissue any where but normal position )

5- Cysts ( True congenital, acquired ( pseudocyst ), neoplastic )

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what is pancreatitis ?

Inflammatory disorder of pancreas

range from mild self limited disease to life threating

Widely destructive process

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compare acute pancreatitis and chronic in case of reversibility ?

Acute —> function can return to normal if underlying cause is removed

Chronic —->Irreversible destruction of EXOCRINE pancreatic parenchyma

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how does pancreatitis become life threating ?

Enzymes get activated either :

Digestive
or
Coagulation

Digestive will digest the pancreatic tissue = very severe

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describe acute pancreatitis ?

Group of reversible lesions characterized by inflammation of pancreas

ranging from :

Edema and fat necrosis TO parenchymal necrosis with severe hemorrhage

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what causes acute pancreatitis ?

Approx 80% of cases are attributable to either :

Biliary tract stones OR alcoholism

others are : I GET SMASHED

I—> idiopathic

G —-> gall stones

E—> ETHANOL

T—> Trauma

S —> Steroids

M—-> mumps

A —> autoimmune

S —-> scorpion venom

H—-> Hyperlipidemia

E—> EMBOLI or ERCP

D—> Drugs

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what is the pathogenesis of pancreatitis ?

Autodigestion of pancreatic substances by inappropriately activated enzymes

Pancreatic enzymes must be enzymatically cleaved to be activated

TRYPSIN —> Important for activation of the enzymes

So ACTIVATION OF TRYPSIN IS CRITICAL TRIGGERING EVENT IN ACUTE PANCREATITIS

If trypsin is inappropriately generated from its proenzyme trypsinogen —> IT CAN ACTIVATE ITSELF AS WELL AS OTHER PROENZYMES :

Phospholipases and elastases

which can partake in the autodigestion

Trypsin also CONVERTS PREKALLIKERIN to its activated form thus sparking kinin system and by activation of factor XII ( hageman factor ) —-> also sets in motion the clotting and complement systems —> intravascular coagulation —> very dangerous

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why do we have hemorrhage in acute pancreatitis ?

elastase destroys blood vessels

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what are the importer blood markers for acute pancreatitis ?

Amylase – > sensitive

Lipase —> longer and specific

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how does obstruction cause acute pancreatitis ?

Obstruction lead to :

1- Edema

2- Impairment in blood flow

3- ischemia

4- Injury to pancreatic and acinar cells

5- activation and release of enzymes irritation by some substances ( alcohol, drugs, virus )

6- Release of proenzymes and lysosomal hydrolases

7- activations of enzymes

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how does defect in intracellular transport result in acute pancreatitis?

Defect in transport —>

1- accumulation of materials inside the cell

2- delivery of proenzymes to lysosomes to destroy material

3- activation of enzymes

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what are the investigations of acute pancreatitis ?

1- Serum amylase and lipase —> diagnostic

Serum lipase remains elevated longer than amylase and its more specific BUT LESS SENSITIVE

2- CRP elevation , full blood count , LFT, serum glucose

3- CT ( shows pancreatic edema, hemorrhage and necrosis )

4- Ultrasound scan must be done within 48 hours of admission to identify gallstones in bile duct

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what is the morphology of acute pancreatitis ?

range from :

Trivial inflammation
to
Severe and extensive edema and hemorrhage

alteration include :

1- Microvascular leakage causing edema

2- Necrosis of fat by lipolytic enzymes

3- Acute inflammatory reaction

4- Proteolytic destruction of pancreatic parenchyma

5- Destruction of blood vessels with subsequent interstitial HEMORRHAGE

MOST IMPOTANT FEATURES :

1- INFLAMMATION
2- FAT NECROSIS-> large clear circles without nucleus
3- HEMORRHAGE–> Black reddish areas

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grossly features of acute pancreatitis?

chalky fat necrosis due to lipase enzyme

whitish necrosis area compared to normal yellow pancreatic parenchyma

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microscopic features of acute pancreatitis ?

Fat necrosis

Blood vessels very thin cuz of elastase –> leak hemorrhage

Reddish area to hemorrhage

Inflammatory infiltrate

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what are the complication acute pancreatitis ?

Systemic :

Shock –> hypovolemia
Organ failure –> due to ischemia

Disseminated intravascular coagulation (DIC)
Pancreatic abscesses
Pseudocysts
Duodenal obstructions

Early ones :

ACUTE RENAL FAILURE, DIC, HYPOCALCEMIA

Late ones :

Abscess or pseudo abscess, fat necrosis, hemorrhage

EALY IS MORE SEVERE and deadly

what chronic pancreatitis ?

Characterized by long standing :

Inflammation

Fibrosis

Destruction of exocrine pancreas

at late stage = Endocrine parenchyma is lost

Distinction between acute and chronic parenreatitis is that in chronic its irreversible

what is the cause of chronic pancreatitis ?

MOST COMMON —> Long term alcohol abuse

Others causes :

Long standing pancreatic duct obstruction ( by pseudocyst calculi, neoplasm , pancreas divisum )

Tropical pancreatitis

Hereditary pancreatitis due to mutation ( in trypsinogen gene PRRS1or SPINK1 gene

what are the grossly features of chronic pancreatitis ?

Loss of lobular appearance

Irregularly distributed fibrosis

Reduced size of pancreas

More firm, More whitish in color due to extensive fibrosis

shrunk due to destruction

what are the microscopic features of chronic pancreatitis ?

Extensive fibrosis

Inflammation

Destruction of ducts –> ductal dilatation

Pseudocysts —> 25% of cases ( dilated ducts that look like cysts but are not cysts )

describe pancreatic carcinomas?

60% of cancers of pancrease ARISE FROM THE HEAD

15% -> body

5%–> Tail

20% —> DIFFUSELY FROM THE WHOLE GLAND

most carcinomas are ductal adenocarcinomas

what are the 2 characteristics features of pancreatic cancer?

1- Highly invasive –> even in early stage

2- Elicits an INTENSE NON NEOPLASTIC HOST REACTION composed of fibroblast, lymphocyte, extracellular matrix —> DESMOPLASTIC RESPONSE

Poor prognosis cuz high invasive

what causes pancreatic cancer?

no one knows

risk factors :

Smoking
Obesity
Diabetes type 2
Chronic pancreatitis
Liver cirrhosis
Other infections
Environmental toxins

what are the grossly features of ductal adenocarcinoma?

Yellow lobular part

Firm white —> tumor—> no lobules, hard ( due to severe desmoplastic reaction and extensive fibrosis )

Invades into fat surrounding the tissue

What are the histological features of adenocarcinoma?

Arise from : DUCTUAL GLANDULAR epithelium Typically Moderately to poorly differentiated adenocarcinoma Perineural and angiolymphatic invasion common ( HIGHLY INVASIVE ) Poorly formed glands are present in densely fibrotic stroma within the pancreatic substance; there are some inflammatory cells Cuz highly invasive u wont see ordinary glands Marked DESMOPLASTIC REACTION ---> fibrosis ---> Pinkish area Almost always associated with chronic pancreatitis

what are famous extra hepatic bile duct and gall bladder problems ?

Anomalies Stones Inflammation ( cholecystitis, cholangitis ) Cyst Neoplasm

describe gall bladder?

Pear shaped organ 4 parts : Fundus Body Neck Infundibulum

what are congenital anomalies of gallbladder?

Congenitally absent gallbladder Duct duplications Bilobed gallbladder Phrygian cap Hypoplasia/agenesis

what cholelithiasis ?

Gallstones 4 types : cholesterol stones --> yellow /green color Pigment stones --> bilirubin = hemolytic anemia Mixed stones Stones with calcium content

what are risk factors of cholelithiasis ?

Cholesterol stones : Imbalance bile composition or improper gallbladder emptying , increases production of cholesterol Yellow/green in color Pigment stones : Black/dark brown in color Due to a lot of bilirubin --> Hemolytic anemia Other causes : Bile supersaturated with cholesterol Hypomotility Cholesterol seeds in bile like crystals Excess mucous gallbladder

describe cholesterol stones ?

Due to increased cholesterol in bile exceeding the capacity of bile to get rid of cholesterol to keep it soluble RadioLUCENT ( no calcium ) Yellow Risk factors : 4 Fs --> fat, fertile, female ,forty age Estrogen --> increase HDL, increase lipoprotein R on hepatocyte Clofibrate (Antilipidemic agent ): ---> Inc-HMG-Coa Reductase activity , Decrease conversion of cholesterol to bile acids , less soluble so precipitates Crohn disease --> Diseased ileum fails to absorb bile salts as a result, cholesterol builds up Cirrhosis : Decrease bile salt production , so cholesterol is less soluble

describe bilirubin salts?

Radiopaque --> seen on x ray Black in color Risk factors : Extravascular hemolysis Biliary tact infection : Deconjugate bilirubin increase risk of it precipitating E.coli Ascaris lumbricoides Clonorchis sinessis , chines liver fluke, obstruction

Symptoms of gallstones?

Fever Jaundice Abdominal pain Nausea vomiting

complications of gall stone ?

Gall bladder: acute cholecystitis Chronic cholecystitis Empyema of gall bladder Mucocele gall bladder Perforation --> biliary peritonitis Gangrene of gall bladder Carcinoma BILE DUCT: Obstructive jaundice Cholangitis Acute pancreatitis INTESTINE : Acute intestinal obstruction

describe acute cholecystitis ?

Cholecystitis = inflammation of gall bladder Fever, leukocytosis , Right upper quadrat pain RUQ- -> radiate to scapula Pressure builds up in gallbladder and squeezes blood vessels leading to ISCHEMIA, bacterial growth, inflammation --> CONGESTION AND INFLAMMATION Presentation : Fever Increase in WCC- > leukocytosis Nausea and vomitting Increased AP--> contained in epithelium of gall bladder , biliary tree might rupture if untreated

describe chronic cholecystitis ?

Subclinical or pain

investigations of cholecystitis ?

Ultra sound can detect stones well HIDA nuclear study ( biliary ) --> imaging procedure used to diagnose problems of liver, gallbladder, bile ducts we invistigate stones cuz they go hand in hand with cholecystitis If surgery is required = laparoscopic