Download - Gall Bladder & Pancreas 2010
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Diseases ofGallbladder &
Pancreas
Presented by:Dr. Tarek ElSharkawy
Pathology Department
University of Dammam
2010
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EXTRAHEPATIC BILIARY SYSTEM
Congenital anomalies:
Gall bladder: may be absent, duplicated or in aberrant location.
Choledochal cyst:
Congenital dilation of the C.B.D., Children. Recurrent abdominal pain and jaundice.
Complications: Gall stones, pancreatitis and CBD ca. in adults
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Cholecystitis
Acute -Calculous- Non-calculous
Chronic
Acute on top of chronic
Normal Gall Bladder
Velvety dark
green mucosa
Thin wall3Dr.Tarek ElSharkawy
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Acute Cholecystitis
Calculous Obstructive 90% Non-Calculous 10%Obstruction in the neck of gall
bladder or cystic duct by a gall stone
Severe septicemia
Non-biliary surgery
Severe trauma
Torsion of gall bladder
Diabetes Mellitus
BurnsRecent childbirth
Dehydration
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Acute Cholecystitis Gross
Gall bladder distended and tense
Serosa: Congestion, fibrinous exudate & hemorrhage
Mucosa: Congested and bright red
Lumen: Pus, green bile, stones
Wall remarkably thick (edema)
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Acute Cholecystitis
Neutrophilic infiltration Focal or extensive mucosal ulceration
Striking edema and hemorrhage
Acute Gangrenous Cholecystitis
Widespread gangrenous necrosis
Frank abscess in wall
Rupture into peritoneal cavity
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Gall Bladder Empyema
Rare
Bacteria invade gall bladder wall
Complete obstruction of cystic duct
Cavity distended by
cloudy purulent fluid
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Size: Normal or contracted
Mucosa: Intact or focally ulcerated, atrophic
Stones usually seen in lumen
Chronicity
Repeated AcuteCholecystitis
Long StandingStones
Thick fibrous wall
Shaggy exudative serosa adhesionsVague symptoms
Female, Fertile, Fatty, Forty or fifty
Abdominal distension
Epigastric discomfort (fatty meals)
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Chronic CholecystitisMononuclear cell infiltration
Mucosa: Normal/atrophic/hyperplastic/metaplastic
Fibrosis
Muscle hypertrophy
Rokitansky Aschoff sinuses:Irregular tubular mucosal structures dipping
deep into the wall up to muscularis
Muscle hypertrophy
Atrophic mucosa
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Cholelithiasis Gall Stones
Formed from bile constituents (cholesterol, bile pigments, calciumsalts & other organic components)
Site:Gallbladder
Extrahepatic biliary passages
Larger Intrahepatic bile ducts
Imaging:
Cholesterol stones (radiolucent filling defects)
Ca salts renders gallstones radio-opaque)
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Gall Stones Types
Pure (10%) - Pure cholesterol- Pure bile pigment (bilirubin)
- Calcium carbonate
Mixed (80%) - Cholesterol
- Bile pigment
- Calcium
- Proteins
Combined (10%)Pure stone nucleus
Mixed stone shell
or vice versa
Cholecystitis
invariably present
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Gall Stones Predisposing Factors
4F Geographic: Entire western world
Genetic: Family members of gall stone patients
Age: Incidence increases above 40, presentation 50s or 60s
Sex: Twice more frequent in females ( Fertile )
Drugs: Estrogen therapy or oral contraceptives
Obesity: Increased cholesterol synthesis and excretion(Fatty)
Diet: Deficiency of dietary fibers
Hemolytic anemia (pigment stones) GIT diseases that interrupt enterohepatic circulation
(Crohns disease, ileal resection, ileal bypass surgery)
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Pure Gall Stones
Cholesterol Pigment Calcium
Number Single (nearly always) Multiple Multiple
Color Yellow Shiny Jet Black Gray-white
Size Few mm- 5 cms Few mms (rice grain) Few mms
Shape Round/oval Irregular Irregular
Surface Smooth Irregular Multifaceted
Consistency Firm Friable Hard
Location Gall bladder (exclusive) Hartmanns Pouch Commonly bile ducts Gall bladder
Cut surface Radial crystals Glassy, soft
Association Cholesterolosis (Fatty fertile females forty) Sterile bile (hemolysis)
X-ray Radiolucent 50 % Radiopaque Radiopaque
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Cholesterolosis
Bile supersaturated with cholesterol (no hypercholesterolemia)
Small yellow mucosal flacks
Strawberry Gall Bladder
cholesterol-laden macrophages in mucosa or epithelium 14Dr.Tarek ElSharkawy
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Mixed Stones
Number Multiple (formed in crops)Color Tan to gray-black
Size 1-2 cm
Shape Multifaceted
Outer surface Smooth
Consistency Firm
Location Gall bladder
Cut surface Laminated
Associated with Cholecystitis
X-Ray Hollow Ring
Hollow Ring
Concentric rings of dark pigment
layer and pale white calcium layer
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Gall Stones Clinical
50% asymptomatic accidentally discovered (silent)
Symptomatic (only when complicated)
Cholecystitis
Mucocele / Empyema
Choledocholithiasis (stone in CBD)
Biliary fistula
Gall stone ileus
Gall bladder cancer
Chronic
Obstruction
Suppurative
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Gall Stones Complications Perforation
Acute Suppurative Peritonitis
With or without stones
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Gall Stones Complications Obstruction
Common hepatic duct
Abscess
Perforation
Fistula
(duodenum or intestine)
Obstructive
Jaundice
Hydrops
Empyema
Cholecystoenteric fistula
Intestinal obstruction (gall stone ileus)
Pancreatitis
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Tumors of Biliary System
Benign: Papilloma, adenoma, adenomyoma,
fibroma, lipoma, myxoma, hemangioma
Malignant
Carcinoma of gall bladder
Carcinoma of bile ducts & ampulla of Vater
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Gall Bladder Carcinoma Etiology
Cholecystitis (particularly porcelain gall bladder)
Cholelithiasis
Genetic (higher incidence in certain populations
living in then same geographical area)
Chemical carcinogens: Methyl cholantherene
Nitrosamines
PesticidesRubber industries
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Gall Bladder Carcinoma
Site: Commonest is fundus, followed by neck 2 gross types: Infiltrating
Fungating
Microscopy
Adenocarcinoma (90%)
Papillary or infiltrative
Most non-mucin producing (some colloid)
Well or poorly differentiatedSquamous cell carcinoma (5%)
Epithelial metaplasia
Adenosquamous carcinoma
Infiltrative (thick leathery wall)
Adenocarcinoma
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Carcinoma of bile ducts & ampulla of Vater
More in males (unlike other biliary diseases)6th decade
No association with gall stones
Associated withUlcerative colitis
Sclerosing cholangitis
Bile duct parasites: Fasciola hepatica liver fluke
Ascaris lumbricoides
Clonorchis sinensis
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Lies obliquely in concavity of duodenum
Elongated structure 15 cm long, 100 gm
Exocrine Part
Endocrine PartPANCREAS
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Proteases (trypsin and chymotrypsin): Protein digestion
Amylase: Carbohydrate digestion Lipase: Fat digestion
Causes stomach to produce acid
(Growth hormone inhibiting hormone)Produced in pancreatic islets and CNS
Inhibits release of growth
hormone from anterior pituitary
Acinar cells
digestive enzymes
Endocrine portionIslets of LangerhansDuctal
cells
Exocrine portion
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Glucagon Insulin
Glycogen
Glucose
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Diseases of Exocrine Pancreas
Cystic Fibrosis (fibrocystic disease)- MUCOVISCIDOSIS
Pancreatitis (acute and chronic)
Tumors and tumor-like lesions
Exocrine part is divided into rhomboid lobules composed of acini
Separated by thin fibrous septa containing blood vessels, nerves, and ducts
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Mucoviscidosis( Viscid mucus secretionObstruct pancreatic ducts,sweat gland&salivary gland ducts )
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Acute Pancreatitis
Present clinically with acute abdomen serum amylase in first 24 hours
serum lipase after 3-4 days (more specific)
Gall stone or
metaplasia
Release of pancreatic enzymes
Duct rupture
Autodigestion of pancreas
Enzymatic fat necrosis (peripancreatic and omental)
Released fatty acids combine with calcium
= Insoluble calcium soaps (whitish-yellow calcification)
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Acute Pancreatitis Causes
Alcoholism Cholelithiasis
Trauma
Ischemia
Shock
Extension of inflammation from adjacent tissues
Blood-borne bacterial infections and viral infections
Drugs (thiazides, sulfonamides, oral contraceptives)
Hypothermia
Hyperlipoproteinemia
Hypercalcemia due to hyperparathyroidism
In >80% of cases
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Acute Pancreatitis Gross
Chalky whitish-yellow nodules of fat necrosisEarly: Swollen and edematous
Black-red hemorrhagic necrosis
Peritoneal cavity typically contains blood-stained ascitic fluid
White flecks of fat necrosis can involve omentum. mesentry & peripancreatic tissue
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Acute Pancreatitis Microscopy
Neutrophilic infiltration
(acute inflammation)
Fat necrosis
Dystrophic calcification on fat necrosis
Necrosis of pancreatic lobules and ducts
Necrosis of arteries with areas of hemorrhage
Fat necrosis
Inflammatory infiltrate, mostly polymorphs, around necrosis and hemorrhage
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Acute Hemorrhagic Pancreatitis
Acute Pancreatic Necrosis
Severe form of acute pancreatitis
Acute inflammation with fat necrosis and hemorrhage
In and around the pancreas
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Chronic Relapsing Pancreatitis
Repeated mild and subclinical pancreatitis
progressive destruction of pancreas
Weight loss and Jaundice
Etiology: alcohol consumption
Common bile duct stones or stenosis
Familial hereditary pancreatitis (uncommon)
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Chronic Relapsing Pancreatitis Gross
Pancreas enlarged, firm and nodular
Cut surface smooth gray (loss of lobulations)
Foci of calcification
Tiny concretions or larger stones (frequent)
Pseudocysts may be seen
Fibrotic and hardMain duct is dilated and filled with calcified secretions
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Chronic Relapsing Pancreatitis Microscopy
Ducts: Fibrosis of wall
Luminal protein plugs or stones Obstruction
Squamous metaplasia
Mild dilatation of some inter and intra-lobular ducts
Acini: Atrophy with increase in interlobular fibrous tissue
Chronic inflammatory infiltrate around lobules and ducts
Islet tissue (involved in late stages only)
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Chronic Pancreatitis
Chronic inflammatory cells
Duct dilatation
Loss of islets = Diabetes
Loss of acini = Steatorrhea
(fat in stools)
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Pancreatic Carcinoma
Head 7o%
Body
Tail
Predisposing Factors: Smoking
Diet ( calories & protein)
Chemicals ( naphthylamine, benzidine, nitrosamines)
Diabetes Mellitus
Hereditary Chronic Pancreatitis
Gallbladder diseases
Frequency: Head
Body
Tail
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Ductal AdenocarcinomaSerous & Mucinous
Extension to ampulla and common bile ductHead Bodyand TailLiver
Spleen
Hard fixed mass with poorly defined infiltrative margin
Progressive obstructive jaundice (early detection)
Silent growth and early metastases
Multiple thrombosis in
superficial and deep veins
Migratory ThrombophlebitisTrausseau sign
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Ductal Adenocarcinoma
Invasive disordered malignant glands
Usually poorly differentiated
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Islet Cell Neoplasms Adenoma/Carcinoma
Insulinoma ( cells) Insulin 5-10% malignant
Glucagonoma ( cells) Glucagon
Gastrinoma (G cells) Gastrin
Somatostatinoma ( delta cells) Somatostatin
Smooth homogeneous appearance Sharply circumscribed margins
60-90% malignant
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Islet Cell Adenoma
Encapsulated
Similarity of cells to normal
Nests of homogenous endocrine cells
Round uniform nuclei and granular eosinophilic cytoplasm
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Insulinoma Glucagonoma Somatostatinomacompress neighboring cells
Gastrinoma
Hypoglycemia Mild diabetes mellitus Diabetes mellitus Gastric hyperacidity
Mental confusion Anemia Steatorrhea Peptic ulceration
Loss of consciousness Necrotizing skin erythema Hypochlohydria
Gastrinoma
Duodenum with
scattered ulcers
(also stomach and jejunum)
Gastric
Hyperacidity
Usually have Zollinger-Ellison Syndrome
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Diabetes Mellitus (DM)
Metabolic disorders of glucose utilization
Characterized by:
HyperglycemiaGlycosuria
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Primary DM Secondary DM
Type I(Juvenile, insulin dependent) 10-20%
Type II(Adult, non-insulin dependent) 80-90%
Chronic pancreatitis
Pancreatectomy
Hormone-producing tumors
Drugs (corticosteroids)
Hemochromatosis
Pituitary Adenoma
Acromegaly growth hormone
Hyperthyroidism
Glucagonoma
Cushing Syndrome cortisol
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Hemochromatosis
iron absorption
Iron deposited in Kupffer cells and hepatocytes
iron is stored in tissues,
specifically liver, heart, pancreas
Arthritis Liver (enlargement, cirrhosis, cancer, liver failure)
Pancreas(possibly causing diabetes)
Heart (arrhythmia or congestive heart failure)
Abnormal skin pigmentation (gray or bronze)
Thyroid deficiency/adrenal glands damage
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Primary Diabetes Mellitus
Type I Type II
cell mass Autoimmunity (anti-insulin antibodies)Genetic susceptibility
Environmental (viruses, chemicals)
Patient depends on insulin for survival
Relative insufficiency of insulin relative to glucose load
And / or
Inability of peripheral tissues to respond to insulin
(insulin resistance)
Severe & absolute
lack of insulin
30
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Insulin Resistance
? in number of insulin receptors
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Islets Changes in Diabetes
in number and size of islets (Type I) cell degranulation and depletion of insulin secretory stores (Type I)
Insulitis: Lymphocytic infiltration & edema of islets (Type I)
Amyloid deposition (Type II)
Fibrosis
Normal
Amyloid Deposits
Insulitis
Pink material between cells
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Type II Diabetes
PolyuriaThirst
Blurring of vision Malaise
Nocturia
Weight loss
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Complications of Diabetes CVS
Atherosclerosis
Hypertension
Myocardial infarction
Gangrene of limbs (ischemia)
Diabetic Foot51Dr.Tarek ElSharkawy
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Complications of Diabetes CNS
Cerebral Hemorrhage
Infarction
Coma (Ketosis)
Peripheral Neuritis
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Ketoacids
fatty acids
Acidic pH of blood (toxic)
Glycogenolysis
Ketogenesis
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Complications of Diabetes Ocular
Diabetic Retinopathy
Glaucoma
Cataract
Cataract Opacification of lens
Progressive in insoluble proteins
Macula Optic Disc Hemorrhage Microaneurysms
Rupture
Multiple retinal detachments
Blindness
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Complications of Diabetes Respiratory
Bronchitis and Bronchopneumonia
Lung Abscess and Gangrene
Pulmonary TB
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Complications of Diabetes Diabetic Nephropathy
Glomerulosclerosis Nephrotic SyndromeProteinuria
Hypoalbuminemia
Edema
Pyelonephritis
Necrosis of Renal Papillae
Renal arteriolosclerosis
Chronic Renal Failure
Apex of pyramid
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Diabetic Glomerulosclerosis Nodular
Kimmelsteil-Wilson Lesion
The only lesionspecificfor diabetes mellitus, yet only seen in 10-35% of cases
Obliterating
capillary lumen
Nodular deposits of matrix within mesangial core
In periphery of
glomerulus
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Diabetic Glomerulosclerosis Diffuse
Linear hyalinized thickening of basement membrane
Diffuse mesangial matrix + mesangial cell proliferation
Normal
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Diabetic Glomerulosclerosis Exudative
Hyaline deposits with eosinophilic material
in capillary lumen and glomerular capsule
(hyaline cap) or Bowmans capsule
(capsular drop)
Capsular drop
Hyaline cap
Massons trichrome
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Complications of Diabetes Skin
liability to Infection (Carbuncle/Cellulitis)Stress of infection insulin requirements
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