gall bladder & pancreas 2010

7/31/2019 Gall Bladder & Pancreas 2010

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Diseases ofGallbladder &

Pancreas

Presented by:Dr. Tarek ElSharkawy

Pathology Department

University of Dammam

2010

1Dr.Tarek ElSharkawy


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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


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

Behavior is not predicted by morphology, tumors < 2 cm tend to behave in a benign fashion40Dr.Tarek ElSharkawy


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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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Dr.Tarek ElSharkawy 44


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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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gall bladder & pancreas 2010

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