internal medicine logy 2008

8/6/2019 Internal Medicine logy 2008

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INTERNAL MEDICINE DEPARTMENTHEAMATOLOGY UNIT 1

ALEXINTERNAL.TK THE OFFICIAL WEBSITE OF INTERNAL MEDICINE DEPARTMENT

ALEXMEDONLINE.COM ------ THE OFFICIAL WEBSITE OF ALEXANDRIA FACULTY OF MEDICINE

ALEXMEDONLINE.COM/STUDENTS ------ STUDENTS WEBPAGE OF ALEXANDRIA MEDICAL STUDENTS


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HEPATOLOGYDEPARTMENT BOOK

TABLE OF CONTENT

VIRAL HEPATITIS ----------------------------------------------------------- 3

JAUNDICE ------------------------------------------------------------------------- 4

ASCITIS ------------------------------------------------------------------------------ 12

CIRRHOSIS ----------------------------------------------------------------------- 28

HEPATIC TUMOUR ------------------------------------------------------- 33

ACUTE LIVER FAILURE ---------------------------------------------- 37

GALL BLADDER DISEASES----------------------------------------- 43

PANCREATIC DISEASES --------------------------------------------- 46


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Viral HepatitisDr. Fathalla Sedky

Assistant Prof of Hepatology

Faculty of Medicine, Alex UN

Clinical types:Asymptomatic: only elevated transaminases.Anicteric: GI and influenza like symptoms, no jaundice.Classic: 3 stages.

1- Prodromal 3-4 days.Profound malaise, fever, anorexia nausea, vomiting, abdominal Pain.

2- Icteric 1-4 weeks.- Change of urine color followed by jaundice and itching.- Patient feels generally better and appetite returns.

- Tender hepatomegaly.3- Convalescent.

Prolonged cholestasis:- Classic acute hepatitis but the icteric stage is prolonged 8-29 weeks with

manifestations of cholestasis.- More with HAV.

Fulminant hepatitis:- Patient after a typical acute onset becomes deeply jaundiced, ominous

manifestations persistent vomiting, fetor hepaticus, drowsiness, flappy tremors,finally coma.

- Commonly with HAV, HBV, HEV.

Relapse:- 1.8-15 % especially HAV.- Attack is usually milder.- Precipitated by premature activity.

Diagnosis:- SGOT, SGPT:Peak levels 1-2 days before or after onset of jaundice.

- Useful in early diagnosis and detection of anicteric cases.- Bilirubin & ALP usually elevated.- PT prolonged.- CBC --- Leucopenia, lymphopenia in anicteric stage

--- Aplastic anemia may occur weeksmonths after acute attack.

Treatment- Bed rest.- Diet: low fat high carbohydrate diet more palatable to the patient.Symptomatic and supportive.- Corticosteroids only in cholestatic HAV.

Convalescence is not allowed till patient is symptom free, liver no longer tender & sbilirubin


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Basics of Hepatitis A- RNA Picorna virus- Acute disease and asymptomatic infection- No chronic infection- Protective antibodies develop in response to infection - confers lifelong immunity.- Rare complicationsfulminant hepatitis, cholestatic hepatitis, relapsing hepatitis.

Hepatitis B VirusExtra hepatic manifestations- Polyartritis.- Glomerulonephrits.- Essential mixed cryoglobulinemia.- Guillain-Barre syndrome.

TreatmentAcute:- Symptomatic.- Liver support (silymarine).

Chronic:- Interferon.- Lamivudine.

Hepatitis C VirusSexual Transmission of HCV

Occurs, but efficiency is low

Rare between long-term steady partners (1.5-3%)Factors that facilitate transmission between partners unknown (e.g., viral titer)

Perinatal Transmission of HCV

Transmission only from women HCV-RNA positive at deliveryAverage rate of infection 6%Higher (17%) if woman co-infected with HIVRole of viral titer unclear

No association with delivery method Infected infants do wellSevere hepatitis is rare

Household Transmission of HCV Rare but not absent Could occur through percutaneous/mucosal exposures to bloodTheoretically through sharing of contaminated personal articles (razors,

toothbrushes)

Contaminated equipment used for home therapiesIV therapyInjections


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Natural History of HCV InfectionExtra hepatic manifestations- Polyartritis.- Glomerulonephrits.

- Essential mixed cryoglobulinemia.- Lymphocytic sialadenitis.- Thyroiditis.- Lichen plannus.

Treatment

Acute:- Symptomatic.- Liver support.- ?? Interferon.

Chronic:1- Antiviral drugs (interferon, ribavirin).

- Treatment might take as long as a year.- About 80% of patients get rid of the virus.

2- ?? Liver support.

Liver transplant For end-stage cases.

Problem III: needle stick injury from a known HCV patient.

HCV RNA becomes positive 2 weeks after exposure and remains positive throughoutthe acute illness.

Symptoms appear by week 6.

ALT tests do not become abnormal until weeks 4-8. Anti-HCV antibody (ELISA) generally does not become positive until 6-8 weeks.

Therefore, the HCV RNA test is the most valuable tool for detecting an acuteinfection, and we use it routinely at our institution to identify infection after a needlestick. If the HCV RNA is negative at week 2, we repeat the test 4 weeks later, and if itremains negative, the patient is advised that there has been no transmission.

Spontaneous viral clearance occurs in the first 3 months after exposure in mostcases, after that spontaneous clearance is unlikely.

In those who remain viraemic at 12 weeks after initial seroconversion, antiviraltherapy is recommended if there are no absolute contraindications to its use. 95% of interferon treated patients will achieve a sustained virological response with

only 6 months of therapy.


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Chronic hepatitisDefinition:chronic inflammatory reaction in the liver for more than 6 ms.Etiology:

1- Viral: B& D, C2- Autoimmune.

3- Drugs.4- Genetic.

PathologyHAI: histological activity index

A scoring system based on 3 categories for necro-inflammation & one for fibrosis.Inflammation (grade):1- Periportal necrosis bridging necrosis score 0-10.2- Intralobular degeneration & focal necrosis.score 0-4.3- Portal inflammation score 0-4.Minimal G 1-3.Mild G 4-8.

Moderate G 9-12.Severe G 13-18.

PathologyFibrosis (stage):

None stage 0.Mild portal expansion stage 1.Moderate portal-portal septa stage 2.Severe bridging with distortion stage 3.Cirrhosis cirrhosis stage 4.

Clinical pictureFatigue (most common), RT hypochondrial pain, nausea, jaundice, muscle and jointpains.

Tender hepatomegaly, occasionally vascular spiders.

Investigations:CBC, liver function tests, US, liver biospy.Investigations of the cause

Autoimmune hepatitisType 1

In most of cases.Usually in young females.Asymptomatic for long time.Endocrinal manifestations, acne, cuchingoid features, amenorrhea.Associated conditions: prolonged fever, polyarthritis of large joints, purpura, hemolyticanemia, splenomegaly & lymphadenopathy, lupus kidney, diabetes, pleurisy, primaryPH.


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Type 22a: affects mainly girls.

Extra-hepatic immunologic disease.2b: patients are usually males and older.

No clear association with otherAutoimmune disease.Respond better to antiviral.

TreatmentCorticosteroids:

- At least 2 Y.- 1st week: 10 mg x3 daily.- 2nd & 3rd weeks: reduce to 10-15 mg/day.- Monthly check.- Full check at 6ms, no remission continues for 6m + azathioprine 50-100 mg /day.- Stop after 2 yrs, normal SGOT, SGPT,

S bilirubin, negative ANA, inactive liver biopsy.

HBV

15 % chronicity.Acute HBV: no treatment.Chronic hepatitis B: antiviral

- Interferon, for 6 ms.- Oral: lamivudine, adefovir, entecaver, continued for 6 m after seroconversion.

HCVPredictors of good response:

- Host: age < 45, non obese, female,Duration of infection


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JaundiceDr. FathAlla Sidkey

Assistant Prof. of Internal Medicine

DEFINITION:Yellow color of skin, mucous membranes and sclera due increased amount of bilirubin.Also caused by carotenemia, and some drugs e.g. quinacrine.

Bilirubin is readily bound to elastic tissue. Skin ocular sclera and blood vessels havehigh elastic tissue content and hence become easily icteric.

PHYSIOLOGY OF BILEBILE ACID: Primary acids CA, CDCA conjugated with glycine or taurine to form bile salts. function--- lipid solubilization (mixed micelles) Canalicular secretion is an active transport process ---osmotic force--- drive bile flow

(bile salt dependent flow). Enterohepatic circulation (95%) mainly in terminal ileum. Bacterial deconjugation in intestine--- 2ry bile salts.

PHYSIOLOGY OF BILE SECRETION Total bile flow---500-600ml /day. Active Na-K-ATPase pump at the canalicular membrane. Part of the secretion is dependent on bile salts. Active secretion in the ductules (secretin) Cholecystokinin-pancerozymin--GB contraction.

CLASSIFICATION Primarily uncojugated:

- CB fraction < 20 % total bilirubin.- dt increased production, defective uptake, defective conjugation.

Mixed:- CB fraction = 20-50 %.- dt hepatitis, cirrhosis.

Primarily conjugated (cholestatic):- CB > 50 %. Prehepatic, hepatic, posthepatic.

NormalConjugated unconjugated


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Diagnosis

OCCUPATION:Employment involving alcohol.Contact with rats in sewage disposal

Wiels disease.

PLACE OF ORIGIN:Mediterranean, African or Far East may suggest carriage of hepatitis B or C.

ONSET OF ILLNESS: Abrupt onset of nausea, anorexia followed by progressive jaundice---acute viral

hepatitis. Gradual onset of jaundice + pruritus---cholestasis. Intermittent rt. upper quadrant abd. Pain followed by jaundice---GS. Gradual onset of painless jaundice + wt. loss---tumor.

In hepato-cellular jaundice, dark urine precedes the onset of jaundice by a few days. In hepatocellular jaundice patient feels ill, while in cholestatic jaundice patient feels

well despite deep jaundice and itching.

SYMPTOMS: Past history:

-contact with jaundiced patient.-injection, blood transfusions,Operations.

Family history:-Jaundice, anemia, splenectomy---hemolytic anemia.

Drugs.

LAB INVESTIGATION: Serum bilirubin (total, direct) ALP > 3 times normal ---- cholestasis. Other cholestatic markers ---- GGT. SGOT, SGPT high in hepatocellular jaundice, lower level in cholestasis. High levels

may be found transiently with acute bile duct obstruction due to a stone. PT may be prolonged --- 10 mg vit K IV /day for 3 days --- return to normal in

cholestasis, but little change in hepatocellular jaundice. CBC for anemia (hemolysis), leucocytosis.


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Gilberts syndrome: Autosomal recessive. Deficiency UDPG enzyme, about 30 % of normal. Mild Inc in serum bilirubin (1-5 mg/dl). Jaundice is mild & intermittent, Inc by fasting and intercurrent infection, fall by

phenobarbitone. Excellent prognosis, reassurance.

Crigler-Najjar syndrome Autosomal recessive.

Type I:- No conjugating enzyme.- Very high s. bilirubin since birth.- Risk of kernictrus.- No response to phenobarbitone.- Phototherapy degrades unconjugated bilirubin to products which are water solubleand can be secreted into the bile.- Liver transplantation is the only definitive line of treatment.

Type II:- UDBG is reduced to > 10 % of normal.- Dramatic response to phenobarbitone, pat. Survive to adult life.

Dubin-johnson syndrome Mainly conjugated hyperbilirubinemia. Autosomal recessive. Defect in cMOAT transporter. Prolonged BSP retention test, serum value at 120 min >at 45 min due to regurgitation

into the circulation of the glutathione conjugate (normally excreted via cMOAT) Liver is black (black liver jaundice).

Rotor syndrome Similar to DJ syndrome. Two differences:

- Liver is not pigmented.- No 2ry rise in BSP retention test. Defect is in hepatic uptake rather than excretion ofBSP.

Cholestasis Failure of normal bile to reach the duodenum.

Intra-hepatic or extra-hepatic.

Intra-hepatic bile ductsIntra-hepatic cholestasis


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Clinical effects: -Pruritus and malapsorption (bile salts). -Bleeding tendency (vit K). -Bone disease (vit D and Ca). -Xanthoma and xanthelasma (cholesterol). -Hyperpigmentation (melanin).

Intermittent jaundice Hemolytic anemia. Gilbert syndrome. Relapsing hepatitis. Drugs. Benign recurrent intrahepatic cholestasis. Cholestasis of pregnancy. Bilary parasites. Periampullay tumors.

CBD stones. Wilsons disease.


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ASCITESDr. Amr Aly Abd El Moety

Assistant professor of Hepatology

Definition

Pathologic fluid accumulation within the peritoneal cavity.

Pathogenesis of ascites

A- Cirrhotic Ascites

The most recent theory of ascites formation, the "peripheral arterial

vasodilation hypothesis," proposes that both older hypotheses, the underfill and

overflow theories,are correct, but that each is operative at a different stage.


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B- Noncirrhotic Ascites

1-Peritoneal carcinomatosis:

Appears to cause ascites through the production of proteinaceous fluid by tumor

cells lining the peritoneum. Extracellular fluid enters the peritoneal cavity to reestablish

oncotic balance.

2-Massive liver metastases:

Portal hypertension due to occlusion of portal veins by tumor nodules.

3-Hepatocellular carcinoma:

Ascites forms because of the underlying cirrhosis-related portal hypertension,

tumor-induced portal vein thrombosis, or both.

4-Chylous ascites:In patients with malignant lymphoma may be caused by lymph node obstruction

by tumor and rupture of chyle-containing lymphatics.

5-High-output or low-output heart failure or nephrotic syndrome:

As in cirrhosis, effective arterial blood volume appears to be decreased, and the

vasopressin, renin-aldosterone, and sympathetic nervous systems are activated. These

changes lead to renal vasoconstriction and sodium and water retention.

6-Tuberculosis, Chlamydia infection, and coccidioidomycosis:

Probably cause ascites through the production of proteinaceous fluid, as in

peritoneal carcinomatosis.

7-Spontaneous bacterial peritonitis (SBP):

Does not appear to cause fluid to accumulate; infection develops only in

preexisting ascites.

8-Pancreatic or biliary ascites fluid:

Forms by leakage of pancreatic juice or bile into the peritoneal cavity or by a

"chemical burn" of the peritoneum.

9-Abdominal surgery:

Especially extensive retroperitoneal dissection, lymphatics may be transected.


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A-History Taking

1- History of alcohol intake, intravenous drug use, blood transfusions, sex with a

member of the same sex, acupuncture, tattoos, ear piercing, and country of origin.2- Long-standing obesity (NASH).

3- Patients with a long history of stable cirrhosis and the sudden development of

ascites should be suspected of harboring a hepatocellular carcinoma.

4- History of cancer malignancy-related ascites. However, cancer in the past does

not guarantee a malignant cause of ascites.

5- History of heart failure may raise the possibility of cardiac ascites. Alcoholics in

whom ascites develops may have alcoholic cardiomyopathy or alcoholic liver

disease, but usually not both.6- Tuberculous peritonitis is usually manifested by fever and abdominal pain.

7- Fitz-Hugh-Curtis syndrome caused by Chlamydia may cause inflammatory

ascites in a sexually active woman.

8- Patients in whom ascites and anasarca develop in the setting of diabetes should be

suspected of having nephrotic ascites.

1. Liver Cirrhosis

2. Non alcoholic

steatohe atitis

3. Alcohol

4. Hepatocellular

Carcinoma

5. Congestive heart

ailure

6. Tuberculous

eritonitis

7. Acute hemorrhagic

ancreatitis.

8. Fitz-Hugh-Curtis

s ndrome

9. Nephrotic syndrome

10. Myxedema

11. Connective tissue

disease

Causes of Ascites


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9-Ascites in a patient with symptoms and signs of myxoedema should prompt

measurement of thyroid function.

10- Serositis in connective tissue disease may be complicated by ascites.

B-Physical examination

Full bulging abdomen should lead to percussion of the flanks. If they are dull then

check for "shifting." Approximately 1500 mL of fluid must be present before dullness is

detected.

A fluid wave is not worth testing for gaseous distention of the bowel, a

thick panniculus, and anovarian masscan mimic ascites.

*Gaseous distentionshould be readily apparent on percussion.

*Ovarian masses usually cause tympanic flanks with central dullness. An

obese abdomen may be diffusely dull to percussion, and abdominal ultrasonography

may be required to determine if fluid is present.

The presence of;

Palmar erythema

Large pulsatile spider angiomata

Large abdominal wall collateral veins

Fetor hepaticus

Large veins on the patient's back suggests inferior vena cava blockage.

An immobile mass in the umbilicus, the Sister Mary Joseph nodule, is

suggestive of peritoneal carcinomatosis.

Congested neck veins Constrictive pericarditis.

Determination of the cause of ascites is based on the results of the

history, physical examination, and ascitic fluid analysis.

Abdominal Paracentesis

Indications: Ascitic fluid should be sampled in all inpatients and outpatients with the new onset of

ascites and in all patients with ascites who are admitted to the hospital to exclude

infection.

Paracentesis should be repeated in patients with suspected infection.

Contraindications: Coagulopathy

Liver cirrhosis


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C-Ascitic Fluid Analysis

Gross Appearance

1- Neutrophil count

If Neutrophil count >1000/mm3 fluid is clear

If Neutrophil count


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B- Exudate/Transudate

Before the 1980s, the ascitic fluid total protein concentration was used to classify

ascites into exudates (>2.5 g/dL [25 g/L]) and transudates (


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G- Lactate Dehydrogenase

LDH enters ascitic fluid by diffusion from blood and by release from disintegrating

ascitic fluid WBCs. In SBP, the ascitic fluid LDH level rises because of the release of

LDH from disintegrated neutrophils.

H- Amylase

In patients with acute pancreatitis or gut perforation the ascitic fluid amylase

concentration is elevated markedly, usually greater than 2000 U/L

I- Gram's Stain

Bacteria are present only when there is an overwhelming infection, as in

advanced SBP or asplenic pneumococcal sepsis.

J- Smear and Culture for Tuberculosis

The direct smear of ascitic fluid to detect mycobacteria is almost never positive

because of the rarity of tuberculous peritonitis and the low concentration of mycobacteria

in ascitic fluid in tuberculous peritonitis.

In contrast to a sensitivity rate of approximately 50% for ascitic fluid

mycobacterial culture with optimal processing, laparoscopy with histology and culture of

peritoneal biopsies has a sensitivity rate of approximately 100% in detecting tuberculous

peritonitis.

K- Cytology

To detect Malignant cells.

L- Triglyceride

Chylous ascites has a triglyceride concentration greater than 200 mg/dL (2.26

mmol/L) and greater than the serum level; usually the level is greater than 1000 mg/dL

(11.30 mmol/L).

Chylous ascites has a triglyceride concentration greater than 200 mg/dL (2.26

mmol/L) and greater than the serum level; usually the level is greater than 1000 mg/dL

(11.30 mmol/L).

M- Bilirubin

Ascitic fluid bilirubin level greater than 6 mg/dL (102 mol/L) and greater than the

serum level of bilirubin suggests biliary or upper gut perforation into ascites.


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Shrunken cirrhotic liver

Surrounded by ascitic fluid

Complication of Ascites

1- Infection

1. SBP

a- Positive ascitic fluid culture.

b- Elevated ascitic fluid absolute PMN count (i.e., at least 250

cells/mm3 [0.25 109/L]).

c- No evidence of an intra-abdominal surgically treatable source of infection.

2. Polymicrobial bacterascites is diagnosed by;

Polymicrobial bacterascites is essentially diagnostic of gut perforation by the

paracentesis needle.


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Pathogenesis of SBP


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Symptoms and Signs of Ascitic Fluid Infection

Fever

Abdominal pain

Tender abdomen

Rebound

Altered mental status

Bacteriology

SBP:Escherichia coli, streptococci (mostly pneumococci), and Klebsiella .

Polymicrobial bacterascites: is by definition polymicrobial

Risk Factors of infection

1- Low ascitic fluid total protein concentrations

2- Paracentesis Needle-induced ascitic fluid infections does not occur unless the

bowel is penetrated by the paracentesis needle.

3- Gastrointestinal hemorrhage.

4- Urinary tract infections are also an under-recognized risk factor for SBP.

Diagnosis

Patient with ascites who develop;

Clinical deterioration

Fever ,abdominal pain, elevated PMN count .Treatment

Indications for Empirical Antibiotic. Therapy of Suspected Spontaneous Ascitic.

Fluid Infection

Ascitic fluid neutrophil count 250/mm3 (0.25 109/L)

Convincing symptoms or signs of infection

Intravenous Albumin Plus Antibiotic

Intravenous albumin (1.5 g/kg body weight at the time the infection is detected

and 1.0 g/kg on day 3) in combination with cefotaxime reduce the risk of renal failure and

improve survival.


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Treatment of Subtypes of Ascitic Fluid Infection

Diagnosis Treatment

Spontaneous bacterial

peritonitis

Five days of intravenous antibiotic to which the organism ishighly susceptible (e.g., cefotaxime 2 g every 8 hours

empirically followed by more narrow spectrum therapy after

susceptibility results are available)

Polymicrobial

bacterascites

Intravenous third-generation cephalosporin (e.g., cefotaxime

2 g q 8h) plus an antianaerobic drug such as metronidazole.

Duration is determined by clinical response and serial ascitic

fluid PMN counts and cultures

Narrowing the Spectrum of Coverage

After the results of susceptibility testing are available.

Duration of Treatment

10 - 14 days of antibiotic therapy for life-threatening infections.

Follow-Up Paracentesis in Spontaneous Bacterial Peritonitis

Not needed except after 48 hours if the course is a typical.

Prognosis

In the past, 48% - 95% of patients with a spontaneous ascitic fluid infection died.

Now less than 5% of patients die.

Paracentesis should be performed at the time of hospital admission so that

infection can be detected and treated promptly.

Paracentesis should be repeated during the hospitalization if any clinical

deterioration occurs.

Prevention

Norfloxacin 400 mg/day twice daily for 7 days. During hospital stay with

discontinuation of the drug at the time the patient is discharged from the hospital.


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2-Tense Ascites

Tense ascites requires urgent therapeutic paracentesis. "Total paracentesis,"

even more than 20 L, has recently been safe.

3-Pleural Effusions

Unilateral and right-sided but occasionally may be bilateral .

A unilateral left-sided effusion suggests tuberculosis.

A large effusion in a patient with cirrhotic ascites is referred to as hepatic

hydrothorax.

It is due to small defects small defect in the right hemidiaphragm.

Symptoms

Shortness of breath.

Infection may complicate in case of SBP.

Treatment

1- Sodium restriction + Diuretics

2- TIPS.

4-Abdominal Wall Hernias

Umbilical, incisional or inguinal.

Complications; Incarceration or perforation.

Elective surgical treatment should be considered in all patients with hernias and

ascites.

Therapy of Low Albumin-Gradient Ascites

1- Nonovarian peritoneal carcinomatosis is treated by outpatient therapeutic

paracentesis.

2- Ovarian malignancy have a good response to surgical debulking and chemotherapy.

3- Tuberculous peritonitis (without cirrhosis) is cured by antituberculous therapy.

Diuretics do not speed weight loss unless the patient has underlying portal

hypertension from cirrhosis.

4- A postoperative lymphatic leak from a distal splenorenal shunt or radical

lymphadenectomy also may resolve spontaneously but on occasion may require

surgical intervention or peritoneovenous shunting.


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5- Chlamydia peritonitis is cured by tetracycline.

6- Ascites caused by lupus serositis may respond to glucocorticoids.

7- Dialysis-related ascites may respond to aggressive dialysis.

Therapy of High Albumin-Gradient Ascites

Treat the underlying liver disease eg stop drinking alcohol.

Patients with other forms of treatable liver disease (e.g., autoimmune hepatitis,

hemochromatosis, or Wilson disease) should receive specific therapy for these

diseases.

Hospitalization

For Patients with large-volume ascites and those who are resistant to outpatient

treatment usually require hospitalization for definitive diagnosis and management of the

fluid overload.Diet Education

Sodium restriction for inpatients and outpatients is 2 grams (88 mmol) per day.

Fluid Restriction

Not required

No Bed Rest

Urine Sodium/Potassium Ratio

A random urine sodium/ potassium concentration ratio greater than 1 predicts

that the patient should lose weight if the sodium-restricted diet is followed.

Diuretics

Spironolactone 100 mg + furosemide 40mg.

If the combination of spironolactone is ineffective in increasing urinary sodium or

decreasing body weight, the doses of both drugs should be increased

simultaneously as needed (e.g., spironolactone 200 mg plus furosemide 80 mg, then

300 mg plus 120 mg, and finally 400 mg plus 160 mg).

Intravenous diuretics cause acute decreases in the glomerular

filtration rate in cirrhotic patients with ascites and should be avoided.

Once the edema has resolved, a reasonable maximum weight loss is probably 0.5

kg/day.


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Stop diuretics and reasse the situation if:

Encephalopathy develops.

Serum sodium concentration less than 120 mmol/L.

Serum creatinine level greater than 2.0 mg/dL.(180 mol/L).

Reducing the quantity of fluid in the abdomen

A- Improve the patient's comfort and prevent hepatic hydrothorax and hernias.

B- Concentrating the ascitic fluid, diuresis increases the opsonic activity of fluid 10-

fold, and theoretically, may be of value in preventing spontaneous ascitic fluid

infection.

Refractory Ascites

Definition

Ascites unresponsive to a sodium-restriction diet and high-dose diuretic

treatment.

Refractoriness is manifested by

No weight loss or the development of complications of diuretics.

Treatment; liver transplantation, serial therapeutic paracenteses, TIPS, and

peritoneovenous shunts.

Abandoned procedures:

Portacaval shunts: (for encephalopathy).

Paris pump: ultrafilterates ascitic fluid and reinfuse it intravenously. Unfortunately

leads disseminated intravascular coagulation.


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Liver Transplantation

Orthotopic liver transplantation should be considered among the treatment

options of patients with cirrhosis and ascites

Serial Paracenteses

Therapeutic paracentesis now appears to befirst-line therapy for patients

with tense ascitesandsecond-line therapy for cirrhotic patients who

are refractory to diuretics.

Colloid Replacement

Recent consensus statements and systematic reviews have pointed out some of

the hazards of albumin infusion.

1- Avoid serial large-volume paracenteses in patients with diuretic-sensitiveascites.

2- Withhold albumin after taps of 5 L or less.

3- Consider albumin infusion optional after taps of larger volume in patients

with diuretic-resistant ascites.

Transjugular Intrahepatic Portosystemic Stent Shunt (TIPS)

For diuretic-resistant ascites.

Peritoneovenous Shunt

Patients who are not candidates for liver transplantation and who have a

scarred abdomen that is not amenable to repeated paracenteses or who

have failed an attempt at TIPS make up this small subset of patients.


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CIRRHOSISDR. NAGLAA M. MASHAAL

PROFESSOR OF HEPATOLOGY

HEPATOBILIARY UNIT

LEARNING OBJECTIVES:Define CirrhosisList Causes of CirrhosisOutline Different ClassificationsRecognize the Clinical PictureAssess the Severity of Liver DiseaseRecognize the ComplicationsOutline the Evolution and PrognosisMention Different Lines of Managements

What is Cirrhosis?Cirrhosis represents the final common histologic pathway for a wide variety of chronicliver diseases. The term cirrhosis was first introduced by Laennec in 1826. It is derivedfrom the Greek term scirrhus and is used to describe the orange or tawny surface of theliver seen at autopsy.

DEFINITION:Cirrhosis is defined histologically as a diffuse hepatic process characterized by

fibrosis and the conversion of normal liver architecture into structurally abnormalnodules.

Cirrhogenic stimulus (Injury)Necrosis (degeneration) & Parenchyma regeneration

+FibrogenesisStellate cells, located in the perisinusoidal space, are essential for the production ofextracellular matrix; they are activated into collagen-forming cells by a variety ofparacrine factors.This lead into an alteration in the normally balanced processes ofextracellular matrix production and degradation.

Future drug strategies to prevent fibrosis may focus on reducing hepatic inflammation,inhibiting stellate cell activation, inhibiting the fibrogenic activities of stellate cells, andstimulating matrix degradation.


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CAUSES:Schistosomal Hepatic Fibrosis & Viral Hepatitis

AlcoholicBiliary obstruction: (Primary & secondary)Outflow obstruction: Heart failure , Bud- Chiari syndrome

SyphilisAutoimmuneDrugsMetabolic: Haemochromatosis, Wilson's disease, Alfa 1 antirypsindeficiancy

CLASSIFICATION:Morphologic

MicronodularMacronodularMixed

HistopathologicPortalBiliary obstructionPost-necrotic and post-hepatitisCongestiveBilharzial Hepatic Fibrosis

FunctionalCompensated: -No hepatic dysfunction

-No portal hypertensionDecompensated:(active)

-Hepatic dysfunction-Portal hypertension

CLINICAL PICTURE:

- MANIFESTATIONS OF THE UNDERLYING ETIOLOGYExamples:

Primary Biliary CirrhosisCongestive Heart failureSystemic Lupus ErythematosisHemochromatosis

- ABNORMAL HEPATIC FEATURESChange in liver size: normal, enlarged or shrunken.Change in consistency: firm

Abnormal edge: sharp or irregular- MANIFESTATIONS OF CHRONIC LIVER DISEASEGeneral Manifestations:FatigueAnorexia, weight loss & muscle wastingAnemiaOsteoporosis


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Cutaneous manifestations:Spider angiomata, skin telangiectasias paper money skin, palmar erythema, whitenails, and finger clubbing.

Impaired metabolic functions:

-Dysproteinaemia(Edema and ascites)-Diminished clotting factors-Skin pigmentation

Impaired secretary functions:- Jaundice- Itching & gallstones

Impaired detoxification functions:-Hyperestrogenemia

Gynecomastia & impotence ( in males)

Loss of axillary and pubic hair is noted( in both men and women)Spider angiomataPalmar erythema

-Hepatic encephalopathy

- MANIFESTATIONS OF PORTAL HYPERTENSIONCongestive gastropathyPorta-systemic collateralsAscitesSplenomegaly

- Other Manifestations:Hyperkinetic circulationLow grade feverHypersplenismInsulin resistance and type 2 diabetes


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ASSESSMENT OF THE SEVERITY OF LIVER DISEASE:

3points2points1 pointClinical variable

Stage 3-4Stage 1-2NoneEncephalopathy

ModerateSlightAbsentAscites

>32-36 s orINR >2.3

4-6 s orINR 1.7-2.3


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PROGNOSIS:Child's Classification

A GoodB ModerateC Poor

DIAGNOSIS:Diagnosis should include:

EtiologyPathology & PathophysiologySeverity of liver diseaseComplications

Diagnosis depends on:Medical HistoryClinical PictureInvestigations

Imaging TechniquesLiver Biopsy

MANAGEMENT:Depends on the Type and Stage of the Cirrhosis

Removal and/ or treatment of the causeSupport liver functionsReduce portal hypertensionTreat complications e.g. ascites, haematemesisTreatment of contributing factors e.g. anaemiaConsider transplantation in end stage cirrhosis


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HEPATIC TUMOURS Prof. Dr/ EL-SAID IBRAHIMHepatobiliary Unit

I. Benign(A) Epithelial:

1- Liver cell adenoma2- Bile duct adenoma3- Focal nodular hyperplesia4- Nodular regenerative hyperplesia

(B) Mesenchymal:1- Haemangiomas2- Mesenchymal hamartoma

II. Malignant1-Primary

A- Epithelial:I Hepatocellular carcinomaII HepatoblastomaIII Cholangiocarcinoma

B- MesenchymalI AngiosarcomaII Infantile hemangioendotheliomaIII Other Sarcomas

2- Metastatic:The liver is the second most common site of metastasis next to lymph nodes

FOCAL NODULAR HYPERPLASIAFNH is defined as a nodule composed of benign appearing hepatocytes in a liverwhich is other wise normalIt varies in size between 1-15 cm

Diagnosis:US, CT, MRITreatment:Conservative without surgery

HEPATIC ADENOMAThere is an association with oral contraceptive use particularly over many years and inolder womenMay present with right upper quadrant pain or mass, hemorrhage within the tumor,hemoperitoneium or hypovolemic shock may occur

Diagnosis:US, CT, MRITreatment: Surgical resection may be indicated in young women, especially whenpregnancies are desired


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HEMANGIOMASThis is the commonest benign tumor of the liver being found in 5% of autopsies.Usually single or small but may be multiple or very large.The majority are asymptomatic and discovered accidentally.

Diagnosis:US, CT, MRI

Treatment:Surgery is usually unnecessary

NODYLAR REGENERATION HYPERPLASIAMonoacinar nodules of cells resembling normal hepatocytes involve liver diffusely.They are related to the obliteration of small portal veins at the level of the acinus.The commonest association is with Rheumatoid arthritis and Felty`s syndrome,myeloproliferative disorders, hyper viscosity syndrome or drug reactions cytotoxic drugsand anabolic steroids.

Diagnosis:US< CT.Portal hypertension is marked and sometimes there is hemorrhage into the nodule.

Hepatocellular carcinomaHCC ranks as the 5th most common cancer in the world with an estimated 437000

new cases annually in 19907.4% of all cancers in 3.2% in all cancers in

Aetiological factors:Relation to cirrhosis

Cirrhosis may be premalignant irrespective of etiology.Fine nodular hyperplesia progresses to carcinoma.Liver cell dysplesia may be an intermediate step.

Relation to HBVChronic hepatitis, progressing to cirrhosis, remain the most important precancerous

factor.HBV induces cancer through integration, transactivation, mutations in tumor-suppressorgenes and increases in TGF-

Relation to HCVThere is a four times higher incidence of liver cancer among anti HCV positive

patients than among HBsAg carriers.

Relation to alcoholIn USA, there is a four fold risk of primary HCC in alcoholics particularly in older

patients.

cirrhosis is always present.Mycotoxins

Aflatoxin is produced by a contaminating mould aspergillus flavus.It is highly carcinogenic to rats, guinea big.Aflatoxin can contaminate food such as ground nuts as grains specially when stored intropical condition.


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Miscellaneous factorsA- Autoimmune hepatitis and cirrhosis (rare)B- Wilson`s disease (rare)C- Primary biliary cirrhosis (rare)D- HemochromatosisE- 1- antitrypsin deficiencyF- TyrosinosisG- Type 1 glycogen storage disease

Age and sexThree times more common in male than females.

Increased incidence with advanced age.

Clinical features:It is variable

-Associated cirrhosis

-Pain-GI symptoms-Jaundice-Ascites-Portal vein thrombosis

Systemic effects:Painful gynecomastiaHypercalcemiaHypoglycemiaHyperlipedemia

HyperthyroidismPseudoporphyria

Serological markersAFPSerum ferritinDes gamma carboxy-prothrombin: The protein induced by vitamin K absence orantagonist II (PIVKA-II).Superior to AFP

Tumour localization:

USDoplex and color Doppler sonographyCTTriphasic (spiral)CTMRIHepatic angiographyLipiodol angiographyNeedle liver biopsy: US or CT guided.


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Screening for HCC among high risk patients:AFP- US every 4-6 months

Prognosis and risk factors:Tumor size >50%Serum bilirubin >3 mg/dlSerum albumin


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ACUTE LIVER FAILURE

Prof. Mohamed Elhasafi.Hepatobiliary Unit. Alexandria Faculty

of Medicine.

Acute liver failure is a complex medical emergency that evolves after acatastrophic insult to the liver. The liver damage is sufficiently severe tocause encephalopathy, and this develops within a matter of days orweeks of the insult to the liver.

Definitions:Fulminant hepatic failure:

The development of encephalopathy within 8 weeks of the onset of symptoms inpatients who had no previous history of liver disease. Hyper- acute liver failure:

The development of encephalopathy within 7 days of the onset of jaundice. Acute liver failure:

The development of encephalopathy within 8 28 days after the onset of jaundice. Sub-acute liver failure:

The interval between the onset of jaundice and the development of encephalopathyranges from 8 to 12 weeks.

Etiology:Viral hepatitis:

Hepatitis A virusHepatitis B virusHepatitis C virusHepatitis D virusHepatitis E virusHepatitis due to other viruses:

Herpes virusesEpstein-Barr virusCytomegalovirusDrug-induced liver injury: Acetaminophen

Halothane, Sulfonamides, phenytoins, Statins. Isoniazid/ RifampicineNSAIDs, Ketoconazole, methyldopa.


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Toxins:

Amanita phalloides (mushrooms)Organic solventsPhosphorus

Herbals.Metabolic: Acute fatty liver of pregnancy. Reye syndromeVascular: Acute circulatory failure (cardiogenic shock).

Budd-Chiari syndrome Veno-occlusive diseaseMiscellaneous: Wilson disease

Autoimmune hepatitis Massive infiltration with tumor Liver transplantation with graft failure

Clinical presentations:Acute liver failure causes a syndrome of multi-system failure potentially involving all

the major body systems .

Jaundice is present in most patients, but some cases of hyper-acute liver failuredevelop encephalopathy before jaundice becomes clinically apparent.

Most of the other signs of liver cell failure are notable by their absence.Fetor and flapping tremors are not prominent features associated with the

encephalopathy of acute liver failure, but are more likely to be seen with sub-acuteliver failure.

Ascites is also unusual .Encephalopathy is the most important sign and present in all cases. Intracranial hypertension:

This complicates grade 4 encephalopathy and develops in up to 70% of patientswho have hyper-acute liver failure and in less than 15% of patients who have sub-acute liver failure.

The clinical features of cerebral edema include systemic hypertension, decerebrateposturing, hyperventilation, abnormal pupillary reflexes, and impairment of brain-stemfunction.

Renal failure:

Renal failure occurs in 75% of patients who develop grade 4 encephalopathyfollowing acetaminophen overdose and in 30% of other etiologies of acute liverfailure.


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Metabolic disorders: Hypoglycemia is common and can lead to impairment of consciousness before

the onset of encephalopathy. The classic symptoms of hypoglycemia are oftenmasked and regular monitoring of blood glucose is required.

Metabolic acidosis is present in 30% of patients and is associated with highmortality.

Hyponatremia reflect sodium depletion in patients who are vomiting or it may bedilutional due to excessive anti-diuretic hormone secretion or intracellular sodiumshifts.

Hemodynamics:

The early hemodynamic profile reflects a hyperdynamic circulation with increasedcardiac output and reduced systemic vascular resistance. Profound vasodilatationmay cause relative hypovolemia .

Progressive disease leads to circulatory failure as a result of falling cardiac output oran inability to maintain an adequate mean arterial pressure.

Pulmonary complications :

Hyperventilation may be due to intracranial hypertension or may be due tocoexisting metabolic acidosis.

Intracranial hypertension may also suppress respiratory function by compromising thebrainstem, but most patients are mechanically ventilated before this occurs.

Aspiration of gastric contents may an early risk to pulmonary status in patients whohave encephalopathy who also vomiting.

Coagulopathy:The liver is responsible for the synthesis of most of the coagulation factors (except

factor VIII, which is produced by endothelial cells) and some of the inhibitors ofcoagulation and fibrinolysis.

In acute liver failure circulating levels of fibrinogen, and factors V, VII, IX and X arereduced, and the prothrombin time is widely used as an indicator of the severity ofliver damage.

Hemorrhage is present in 75% of patients who had acute liver failure.Gastrointestinal hemorrhage is common and was attributed to gastric erosions.

Infection :Bacterial and fungal infections are common in acute in acute liver failure and are

important factor for mortality.

Infection may be difficult to detect as there is a poor correlation between the presenceof infection and body temperature or with white cell counts.


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DIAGNOSISThe diagnosis of acute liver failure is a clinical one based on the detection of

encephalopathy in patients who have acute liver disease.

The etiology of acute liver failure must be accurately identified by the appropriateinvestigations.

Hepatitis AHepatitis BHepatitis CAcetaminophenHalothaneAutoimmune Ischemic hepatitis IgM anti-HAV IgM anti-HBcHCV- RNADrug level in bloodAntibody testAutoantibodiesVery high transaminases.

Histologic assessment of liver tissue aid in the diagnosis of the cause of acuteliver failure, but this is often only available after death or transplantation. Confluentnecrosis is the commonest histologic finding and this may be zonal or involve all of

the parenchyma.

Laboratory investigations :Anemia due to hemorrhage, hemolysis.Thrombocytopenia.Leucocytosis due to sepsis.Transaminases are very variable and of no prognostic value.Serum albumin is normal early, but falls with disease progression.Prothrombin time is of strong prognostic value.

Serum sodium often low and may reflect sodium deficiency or dilution. Hyponatremiais a bad prognostic sign .

Blood glucose : Hypoglycemia is frequent.Acid-base status: Alkalosis common but acidosis is associated with a poor prognosis.Serum creatinine is the best indicator of renal dysfunction.


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Management General measures : 1) Temperature, pulse, and blood pressure should be recorded at least hourly

and preferably continuously.

2) A naso-gastric tube is passed. 3) An H2 antagonist or proton pump inhibitor is given to reduce the risk of

gastro-duodenal erosions and bleeding.

4) Enteral nutrition should be given containing appropriate calories.

5) Hypoglycemia is corrected by giving 100 ml of 50% glucose, then continuousinfusion of glucose 5% or 10 %.

6) Respiratory status is monitored using pulse oximetry. Oxygen by mask is given. Mechanical ventilation is necessary if respiratory failure is shown due to adult

respiratory distress syndrome requiring artificial ventilatory support

7) Intravenous antibiotic is given if there is systemic infection, and anti-fugal treatment

is given with fungal infection.8) Hypotension is corrected by crystalloid or albumin infusions. If not corrected, a

vaso-constrictor agent such as norepinephrine may be given.

Renal failure is treated by continuous arteriovenous hemofilteration.Coagulopathy is managed by routine intravenous vitamin K. Fresh frozen plasma and

platelets are given if there is bleeding.

Hepatic encephalopathy is treated by the usual routine with no protein by mouth,lactulose enema and by the naso-gastric tube, flumazenil (a benzodiazepine- receptorantagonist).

Cerebral edema is treated with mannitol 20% intravenously. N- acetylcystein is given intravenously in cases of acute liver failure complicating

acetaminaphen toxicty.

Artificial and bio-artificial liver support : The aim is to provide support until the native liver recovers its function

spontaneously, or until a donor liver is available. The artificial liver support system MARS ( Molecular Absorbent Recirculating

System ) uses albumin , charcoal, and resin adsorbents to remove water solubletoxins including ammonia.

The bio-artificial liver support use bio- reactor containing viable hepatocytes inculture.


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Liver transplantation: Hepatic transplantation gas to be considered for patients reaching grade 3 and 4

coma due to fulminant hepatic failure.

A) Auxiliary liver transplantation : The native liver is left in place, and the donorliver graft either placed in the right upper quadrant alongside the native liver (

heterotopic ) or part of the native liver is resected and replaced with a reduced sizegraft ( orthotopic ) B ) Living related liver transplantation : Either the left or the right lobe of the

living donor is transplanted to the patient. C ) Hepatocyte transplantation : Small number of cells; 0.5 to 3 % of the normal

hepatocyte mass is injected into the portal vein of the patient ( still experimental ).

Questions 1) Definition, causes, clinical presentation and management of acute liver failure. 2) What are the most important two clinical signs in the diagnosis of acute liver failure. 3) what is the most important laboratory test for the prognosis in following patients

with acute liver failure. 4) Treatment of acute liver failure. 5) What are the definitions, value and uses of the artificial and bio-artificial liver

support systems. 6) What are the types of liver transplantation used in the management of acute liver

failure.


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Gallbladder Disease Prof Yousri TaherHead of HPB Unit

Alexandria University

Congenital GB disease

Gallstones and inflammatory GB diseaseThree types of G stones: cholesterol, black pigment and brown Stones. Pigment stones Contain besides Cholesterol;

Bile pigment, calcium carbonate phosphate palmitate phospholipids glycoprotein,mucopolysaccharides

Cholesterol stone: 15 % are radiopaque Black 60%; brown o %.

Factors For GB Stone FormationImpaired GB function

Supersaturated bile

Cholesterol nucleating factors

Absorption /enter hepatic circulation of bile acids

Prevalence Of G StonesIn western countries 10 %(In Egypt 20%)Prevalence in women is twice that in menAmong cirrhotics 30%Prevalence is higher among diabetics after gastrectomy , ileal resection with

hyoplipaedemic drugs ,long term octreotide , and c pills

Natural History of Gall Stones

Acute and Chronic CholecystitisIn 96% cystic duct is obstructed

Clinical features : sufferers are often obese , Fertile female over 40 yrPain occur late at night ,in right hypochondrium epigatric referred to right shoulderDigestive symptoms :flatulence ,nausea vomitingFever on occurrence of bacterial infection


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ACalculus Cholecystitis5-10 % of acute cholecystitis in adults30% in childrenFactors associated with critical conditions ,after major surgery ,multiple injuries, major

burns ,severe sepsis mechanical ventilation

Bacterial infection with typhoid bacilliActinomycosisParasitic cholecystitis

Clinical Findings:Shallow respiration , fever

Jaundice , Murphys sign is positive

Tender mass at GB region

WBC is high

Clinical Presentation:Diagnostic toolsClinicalUSCholecystographyCT ScanMRCPERCPPTC

Ultrasound ExaminationAccurate In More Than 95%Biliary MudMRCP Perforated GBCBD StrictureCT scan After ERCPGall StonesLarge GB Stone with Choledochal cyst (ERCP)Shotty GB Stones With Impacted Stones At The papilla OF VaterERCP GB stonesCBD Stricture GB Perforation

Differential DiagnosisAppendicitis perforated peptic ulcerIntestinal obstruction, pleurisy myocardial infarctionFirst aid Treatment antibiotics , analgesia antispasmodicSurgery


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Post Cholecystectomy ProblemsWrong diagnosisPapillary dysfunction ,stenosisPsychosomatic disordersIBS, Biliary stricture

Biliary stones, amputation neuroma PancreatitisCBD Injury After Cholecystectomy with Bile LeakageEndoscopic Sphincterotomy With Stone ExtractionExtraction of Fasciola Fluke from CBD after EST

Questions Enumerate congenital GB anomalies Mention clinical manifestations of GB disease Enumerate types gall stones Mention diagnostic tools for GB stones Enumerated complications of GB disease

Enumerate GB and biliary parasites Enumerate postcholecystectomy problems Mention Role of endoscopy in the management of GB stones Discuss differential diagnosis of GB disease


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Acute PancreatitisProf. Yousri TaherHead of HPB Unit

Alexandria University

Acute PancreatitisIs discrete episodes of inflammation resulting from intrapancreatic activation ofdigestive enzymes.It is a disease of wide spectrum of severity complications and outcome.

Spectrum of the diseaseAcute edematous or interstitial Pancreatitis : mild , self limited in most patientsInflammation results in edema of the pancreasParenchymal damage is minimal

Pancreas recovers its function after resolution.

Hemorrhagic Pancreatitis (Necrotizing Pancreatitis).May be extensive with progressive coagulative necrosis of the pancreas andsurrounding tissuesAuto digestion of the organ leads to hemorrhage .The mass of inflamed pancreasand surrounding tissues is termed phlegmon.

ComplicationsWide spread of inflammatory processAny of the following organs might be affected : CBD ,duodenum, T colon splenicartery , and vein, spleen, Para renal spaces , lesser sac posterior mediastinum,

abdominal wall and diaphragm .Peritoneal surfaces leading to pancreatic ascites.Leakage of protein rich fluid from systemic circulation into peritoneal andretroperitoneal spaces lead to hypovolemia and shock.Systemic effects of these material include: cardiovascular instability respiratoryfailure and renal failure.Hemorrhage : Cullens sign ,Turners sign, and DIC.Pseudo cystPancreatic abscessFat necrosis polyserositis and adult respiratory distress syndrome.Pulmonary alveolar capillary membrane may be disrupted forming hyaline lining ofalveoli.


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EtiologyAlcoholismBiliary tract diseaseSurgeryTraumaERCPInfections (viral, mycoplasma, Salmonella mycobacterium cryptosporidium.*Metabolic disorders(Hypertriglyceridemia,pregancy,hypercacemia, hyperparathyroidism)*Drugs , vasculitisAnatomic abnormality annular pancreas ,choledochal cyst ,penetrating peptic ulcer,parasites ,renal failure ,renal transplantation .

Drug induced Acute PancreatitisSulfonamides ,estrogen , teracycline, pills, azathioprine , furosemide, ethanol,methanol ,ACE inhibitor ,NSAID, isoniasid,rifampin,metronidazole, eryhthromycin .

Clinical Criteria for Severe PancreatitisCardiac : BP < 90,tachycardia,ECG changesPulmonary : dyspnea , ARDS PO2< 60mmHgRenal output less than 50 ml/hMetabolic calcium < 8mg/dl, albumin < 3.2 mg /dlHematological: falling hematocrite and DICAbdominal distension, fluid wave ,and ileus

Physical examinationFever tachycardia ,hypotension

ShockJaundiceAbdominal tenderness and rigidityIleusCullen's signPleural effusion ,pneumonitis subcutaneous fat necrosis ,tetany.

Laboratory TestsElevated Serum amylase noted within 24 h persist for 3-5 daysElevated Serum lipase

Urine amylase remains elevated for 7-10 days from onset.LeucocytosisHyperglycemiaJaundiceArterial hypoxemia


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RadiologyPlain film ileus, air under diaphragm sentinel loopUSGCT scanERCP

Differential DIAGNOSISACUTE CHOLECYSTITISBILIARY COLICCHOLANGITISPERFORATED VISCUSACUTE HEPATITIS ,ACUTE INTESTINAL OBSTRUCTIONMESNTERIC VENOUS OCCLUSION

Treatment85=90 % self limitedSupportive care

AnalgesiaMaintain intravascular volumeMonitor vital signsTreat complications

Drug Treatment and Nutritional SupportPPI , somatostatin or octreotide (sandostatin )Prophylactic antibioticsIntralipidEnteral feeding is much betterInitial high carbohydrate diet low protein and fat.

For severe caseICU is highly indicatedNecresectomyPancreatectomyDecompress Biliary tractCT guided percutaneous drainage of necrotic pancreas , Endoscopic drainage

For Acute Biliary Pancreatitis Urgent Endoscopic Sphincterotomy is a must as soon as possible within 72 hours of

onset of symptoms


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Chronic Pancreatitis Result from progressive destruction of the pancreas by inflammation and fibrosis Exocrine pancreatic tissue and function are lost earlier followed by Endocrine parenchyma

And function

Classification Obstructive :Tumors, scar of Parenchymal inflammation , congenital anomalies Infiltrative and autoimmune diseases such as hemochromatosis, Sjogren syndrome. Chronic calcifying PancreatitisAlcohol, cigarette smokingHyperparathyroidismHypocalcaemiaHereditary autosomal dominant CCP Cystic fibrosis

Clinical Presentation Abdominal painMalabsorption Vitamin B12 deficiency DM Obstructive jaundice

Physical Examination Epigatric tendernessMass, pseudocystWeight loss bleeding tendency

Jaundice

Diagnosis Serum amylase ,lipase Increased stool fat> 30 -40 g /day USG and CT scan ERCP EUS

Treatment Stop alcohol or tobacco Feedback control Percutaneous injection of alcohol Surgery Drainage procedures Acid suppressant therapy Nutritional support


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Pancreatic cancerExocrine pancreatic cancer account for 95% of pancreatic cancer75 -85% arise from pancreatic duct epithelium Islet cell tumor represent 5 %Manifest themselves by hormone they secrete

Tumors may secrete gastrin, insulin ,glucagon ,VIP, pancreatic peptide somatostatin

Warnings Signs of Pancreatic Cancer Unexplained Recent upper abdominal pain Recent upper abdominal pain with retroperitoneal lesion Jaundice with weight loss Weight loss greater than 5 % Unexplained acute Pancreatitis Unexplained onset of DM

Diagnostic Tools of Pancreatic CancerCA19.9

CEAUSG focal pancreatic lesion CT scanERCPAngiographyFine needle AspirationEUSLaparoscopyMRI

Treatment Options

Surgery is the best if early ; 5% are respectable Chemo radiation Palliative drainage

EndoscopicPercutaneousSurgical


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Questions Enumerate causes of acute Pancreatitis Mention important diagnostic clinical symptoms and signs of acute Pancreatitis Discuss causes of biliary Pancreatitis Discuss complications of acute Pancreatitis Role of endoscopy in emergency management and prophylaxis of acute Pancreatitis Discuss differential diagnosis of acute Pancreatitis Mention role of imaging techniques in acute Pancreatitis Discuss role of surgery in acute Pancreatitis

Questions : Chronic Pancreatitis Describe clinical picture of chronic Pancreatitis Describe complications of Pancreatitis Discuss management of pancreatic pseudo cyst Discuss management of chronic Pancreatitis presented with obstructive

jaundice Mention diagnostics criteria of pancreatic cancer Mention endoscopic management of chronic Pancreatitis and pancreatic

cancer Discuss role of surgery in chronic Pancreatitis Mention differential diagnosis of chronic Pancreatitis

internal medicine logy 2008

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