Internal Medicine Logy 2008

INTERNAL MEDICINE DEPARTMENT HEAMATOLOGY UNIT 1
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HEPATOLOGY
DEPARTMENT 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



Viral Hepatitis

Dr. 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 weeks months 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 & s
bilirubin <1.5 mg/dl.
- Follow up for monthly for 3ms.


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 Virus

Extra hepatic manifestations
- Polyartritis.
- Glomerulonephrits.
- Essential mixed cryoglobulinemia.
- Guillain-Barre syndrome.

Treatment
Acute:
- Symptomatic.
- Liver support (silymarine).
Chronic:
- Interferon.
- Lamivudine.
Hepatitis C Virus

Sexual 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 delivery
Average rate of infection 6%
Higher (17%) if woman co-infected with HIV
Role of viral titer unclear
No association with delivery method
Infected infants do well
Severe hepatitis is rare
Household Transmission of HCV
Rare but not absent
Could occur through percutaneous/mucosal exposures to blood
Theoretically through sharing of contaminated personal articles (razors,
toothbrushes)
Contaminated equipment used for home therapies
IV therapy
Injections


Natural History of HCV Infection
Extra 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 throughout
the 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 acute
infection, and we use it routinely at our institution to identify infection after a needle
stick. If the HCV RNA is negative at week 2, we repeat the test 4 weeks later, and if it
remains negative, the patient is advised that there has been no transmission.

Spontaneous viral clearance occurs in the first 3 months after exposure in most
cases, after that spontaneous clearance is unlikely.
In those who remain viraemic at 12 weeks after initial seroconversion, antiviral
therapy 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.


Chronic hepatitis
Definition: chronic inflammatory reaction in the liver for more than 6 ms.
Etiology:
1- Viral: B& D, C
2- Autoimmune.
3- Drugs.
4- Genetic.

Pathology
HAI: 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.

Pathology
Fibrosis (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 picture
Fatigue (most common), RT hypochondrial pain, nausea, jaundice, muscle and joint
pains.
Tender hepatomegaly, occasionally vascular spiders.

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

Autoimmune hepatitis
Type 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, hemolytic
anemia, splenomegaly & lymphadenopathy, lupus kidney, diabetes, pleurisy, primary
PH.


Type 2
2a: affects mainly girls.
Extra-hepatic immunologic disease.
2b: patients are usually males and older.
No clear association with other
Autoimmune disease.
Respond better to antiviral.
Treatment
Corticosteroids:
- 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.
HCV
Predictors of good response:
- Host: age < 45, non obese, female,
Duration of infection <5 yrs,
ALT moderate elevation, normal
GGT, no cirrhosis, low liver iron.
- Virus: low HCV RNA, genotype 2, 3.
Interferon
Side effects:
- Early: flu like, myalgia, nausea, headache
- Late: anorexia, alopecia, wt loss, anxiety & depression, diarrhoea, muscle aches,
bone marrow depression, optic neuropathy, thyroid dysfunction.
Contraindications: psychatric illness, thyroid dysfunction, neutropenia,
thrombocytopenia, CHD, arrhythmia, decomensated cirrhosis, renal transplant.
Ribavirin
Side effects: hemolytic anemia (dose dependent), hyperuricemia
Contraindications: during pregnancy, anemia, renal insufficiency, severs heart disease.
Problems!!
Problem I: needle stick injury from a known HBV patient.
Wounds and skin sites that have been in contact with blood or bloody body fluids
should be washed with soap and water. Exposed mucous membranes should be
flushed with water. Squeezing the wound and treating with topical antiseptics are not
recommend



Jaundice

Dr. 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 have
high elastic tissue content and hence become easily icteric.

PHYSIOLOGY OF BILE
BILE 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.
Normal
Conjugated unconjugated


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.


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
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 soluble
and 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.
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 of
BSP.

Cholestasis
Failure of normal bile to reach the duodenum.
Intra-hepatic or extra-hepatic.
Intra-hepatic bile ducts
Intra-hepatic cholestasis


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.


ASCITES

Dr. 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.


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.



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
steatohepatitis
3. Alcohol
4. Hepatocellular
Carcinoma
5. Congestive heart
failure
6. Tuberculous
peritonitis
7. Acute hemorrhagic
pancreatitis.
8. Fitz-Hugh-Curtis
syndrome
9. Nephrotic syndrome
10. Myxedema
11. Connective tissue
disease
Causes of Ascites

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 an ovarian mass can mimic ascites.
*Gaseous distention should 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

C-Ascitic Fluid Analysis
Gross Appearance
1- Neutrophil count
If Neutrophil count >1000/mm3 fluid is clear
If Neutrophil count <5000/mm3 fluid is cloudy
If Neutrophil count < 50,000/mm3 Fluid resembles mayonnaise
2- RBC, count < 10,000 /mm3, the ascitic fluid looks pink. But more than
20,000/mm3 it will be distinctly red.
Red Ascitic fluid is due to:
a- Traumatic: Ascitic fluid will clot.
b- Rupture lymphatics in liver cirrhosis.
c- HCC
d- Peritoneal carcinomatosis
e- Tuberculous Ascites
3- Chylous Ascites: Due to increase in Triglyceride level above 200 mg/dL .
4- Dark brown colored Ascites indicates biliary perforation.
5- Black Ascites
Hemorrhagic pancreatitis
Malignant Melanoma
Ascitic Fluid Tests
A- Cell count
The WBC count in uncomplicated cirrhosis is less than 500 cells/mm3.
The absolute polymorphonuclear leukocyte count in uncomplicated cirrhosis is
less than 250/mm3.
Elevated ascitic fluid WBC count is seen in
/ Spontaneous bacterial peritonitis.
/ Tuberculous peritonitis.
/ Peritoneal carcinomatosis
lymphocytes are mainly elevated)

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 (<2.5 g/dL [25 g/L]).
Unfortunately, this classification does not work well in ascitic fluid.
C- Serum-Ascites Albumin Gradient
Serum albumin Ascitic fluid albumin.
(SAAG) categorize ascites better than either the total protein concentration or
other parameters do.

D- Culture
Blood culture is sensitive in detecting monomicrobial infection which is a feature
of Spontaneous Bacterial Peritonitis.
E- Total protein
SAAG ratio is more sensitive in differentiating type of ascites than evaluating total
protein.
F- Glucose
In SBP and in the setting of gut perforation into ascitic fluid, the ascitic glucose
concentration usually drops to 0 mg/dL (0 mmol/L) because of large numbers of
stimulated neutrophils and bacteria.


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.



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.


Pathogenesis of SBP


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.


Treatment of Subtypes of Ascitic Fluid Infection
Diagnosis Treatment
Spontaneous bacterial
peritonitis
Five days of intravenous antibiotic to which the organism is
highly 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.


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.

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.

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.




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 be first-line therapy for patients
with tense ascites and second-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-sensitive
ascites.
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.



CIRRHOSIS

DR. NAGLAA M. MASHAAL
PROFESSOR OF HEPATOLOGY
HEPATOBILIARY UNIT

LEARNING OBJECTIVES:
Define Cirrhosis
List Causes of Cirrhosis
Outline Different Classifications
Recognize the Clinical Picture
Assess the Severity of Liver Disease
Recognize the Complications
Outline the Evolution and Prognosis
Mention Different Lines of Managements

What is Cirrhosis?
Cirrhosis represents the final common histologic pathway for a wide variety of chronic
liver diseases. The term cirrhosis was first introduced by Laennec in 1826. It is derived
from the Greek term scirrhus and is used to describe the orange or tawny surface of the
liver 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 abnormal
nodules.
Cirrhogenic stimulus (Injury)
Necrosis (degeneration) & Parenchyma regeneration
+
Fibrogenesis
Stellate cells, located in the perisinusoidal space, are essential for the production of
extracellular matrix; they are activated into collagen-forming cells by a variety of
paracrine factors.This lead into an alteration in the normally balanced processes of
extracellular 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, and
stimulating matrix degradation.


CAUSES:
Schistosomal Hepatic Fibrosis & Viral Hepatitis
Alcoholic
Biliary obstruction: (Primary & secondary)
Outflow obstruction: Heart failure , Bud- Chiari syndrome
Syphilis
Autoimmune
Drugs
Metabolic: Haemochromatosis, Wilson's disease, Alfa 1 antirypsin
deficiancy
CLASSIFICATION:
Morphologic
Micronodular
Macronodular
Mixed
Histopathologic
Portal
Biliary obstruction
Post-necrotic and post-hepatitis
Congestive
Bilharzial Hepatic Fibrosis
Functional
Compensated: -No hepatic dysfunction
-No portal hypertension
Decompensated:(active)
-Hepatic dysfunction
-Portal hypertension

CLINICAL PICTURE:

- MANIFESTATIONS OF THE UNDERLYING ETIOLOGY
Examples:
Primary Biliary Cirrhosis
Congestive Heart failure
Systemic Lupus Erythematosis
Hemochromatosis
- ABNORMAL HEPATIC FEATURES
Change in liver size: normal, enlarged or shrunken.
Change in consistency: firm
Abnormal edge: sharp or irregular
- MANIFESTATIONS OF CHRONIC LIVER DISEASE
General Manifestations:
Fatigue
Anorexia, weight loss & muscle wasting
Anemia
Osteoporosis


Cutaneous manifestations:
Spider angiomata, skin telangiectasias paper money skin, palmar erythema, white
nails, 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 angiomata
Palmar erythema
-Hepatic encephalopathy

- MANIFESTATIONS OF PORTAL HYPERTENSION
Congestive gastropathy
Porta-systemic collaterals
Ascites
Splenomegaly

- Other Manifestations:
Hyperkinetic circulation
Low grade fever
Hypersplenism
Insulin resistance and type 2 diabetes


ASSESSMENT OF THE SEVERITY OF LIVER DISEASE:

3points

2points

1 point

Clinical variable

Stage 3-4 Stage 1-2 None Encephalopathy
Moderate Slight Absent Ascites
>3 2-3 <2 Bilirubin (mg/dL)
<2. 8 2.8-3.5 >3.5 Albumin (g/dL)
>6 s or
INR >2.3
4-6 s or
INR 1.7-2.3
<4 s or
INR <1.7
Prothrombin time
(seconds prolonged
or INR)

Child-Pugh Classification
Child Class A = 5-6 points
Child Class B = 7-9 points
Child Class C = 10-15 points

COMPLICATIONS:
Esophageal varices
Spontaneous bacterial peritonitis (SBP)
Portosystemic encephalopathy
Hepatorenal syndrome
Hepatocellular carcinoma

EVOLUTION:
Progressive
Regressive
Stationary
Depending on:
Clinical assessment
Biochemical assessment
Histological assessment


PROGNOSIS:
Child's Classification
A Good
B Moderate
C Poor

DIAGNOSIS:
Diagnosis should include:
Etiology
Pathology & Pathophysiology
Severity of liver disease
Complications
Diagnosis depends on:
Medical History
Clinical Picture
Investigations
Imaging Techniques
Liver Biopsy

MANAGEMENT:
Depends on the Type and Stage of the Cirrhosis
Removal and/ or treatment of the cause
Support liver functions
Reduce portal hypertension
Treat complications e.g. ascites, haematemesis
Treatment of contributing factors e.g. anaemia
Consider transplantation in end stage cirrhosis



HEPATIC TUMOURS

Prof. Dr/ EL-SAID IBRAHIM
Hepatobiliary Unit

I. Benign
(A) Epithelial:
1- Liver cell adenoma
2- Bile duct adenoma
3- Focal nodular hyperplesia
4- Nodular regenerative hyperplesia
(B) Mesenchymal:
1- Haemangiomas
2- Mesenchymal hamartoma
II. Malignant
1-Primary
A- Epithelial:
I Hepatocellular carcinoma
II Hepatoblastoma
III Cholangiocarcinoma
B- Mesenchymal
I Angiosarcoma
II Infantile hemangioendothelioma
III Other Sarcomas
2- Metastatic:
The liver is the second most common site of metastasis next to lymph nodes

FOCAL NODULAR HYPERPLASIA
FNH is defined as a nodule composed of benign appearing hepatocytes in a liver
which is other wise normal
It varies in size between 1-15 cm
Diagnosis: US, CT, MRI
Treatment: Conservative without surgery

HEPATIC ADENOMA
There is an association with oral contraceptive use particularly over many years and in
older women
May present with right upper quadrant pain or mass, hemorrhage within the tumor,
hemoperitoneium or hypovolemic shock may occur
Treatment: Surgical resection may be indicated in young women, especially when
pregnancies are desired


HEMANGIOMAS
This 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.
Treatment: Surgery is usually unnecessary

NODYLAR REGENERATION HYPERPLASIA
Monoacinar 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 drugs
and anabolic steroids.
Diagnosis: US< CT.
Portal hypertension is marked and sometimes there is hemorrhage into the nodule.

Hepatocellular carcinoma
HCC ranks as the 5th most common cancer in the world with an estimated 437000
new cases annually in 1990
7.4% 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 HBV
Chronic hepatitis, progressing to cirrhosis, remain the most important precancerous
factor.
HBV induces cancer through integration, transactivation, mutations in tumor-suppressor
genes and increases in TGF-
Relation to HCV
There is a four times higher incidence of liver cancer among anti HCV positive
patients than among HBsAg carriers.
Relation to alcohol
In 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 in
tropical condition.


Miscellaneous factors
A- Autoimmune hepatitis and cirrhosis (rare)
B- Wilson`s disease (rare)
C- Primary biliary cirrhosis (rare)
D- Hemochromatosis
E- 1- antitrypsin deficiency
F- Tyrosinosis
G- Type 1 glycogen storage disease

Age and sex
Three 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 gynecomastia
Hypercalcemia
Hypoglycemia
Hyperlipedemia
Hyperthyroidism
Pseudoporphyria

Serological markers
AFP
Serum ferritin
Des gamma carboxy-prothrombin: The protein induced by vitamin K absence or
antagonist II (PIVKA-II).Superior to AFP

Tumour localization:
US
Doplex and color Doppler sonography
CT
Triphasic (spiral)CT
MRI
Hepatic angiography
Lipiodol angiography
Needle liver biopsy: US or CT guided.


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

Prognosis and risk factors:
Tumor size >50%
Serum bilirubin >3 mg/dl
Serum albumin <3 G/dl
Ascites

Treatment:
Surgical
1- Resection
2- Transplantation
Non Surgical
1- Systemic chemotherapy:
Mitozantrone IV/21 day , tamoxifen
2- Transcatheter arterial chemoembolization
3- Percutaneous ethanol injection
4- Radiofrequency ablation
5- Target gene transfer(Gene therapy)
6- Combined modalities.

Fibrolamellar carcinoma:
Young patients (5-35 years) of both sexes.
It presents with abdominal mass.
The liver is not cirrhotic.
Serum AFP is normal.
Prognosis is better (survival 32-622 months)
Treatment is surgical resection

Hepatoblastoma:
Rare tumor affects children less than 4 years of age.
Progressive enlargement of the abdomen with anorexia, failure to thrive, fever.
Surgery is indicated with preoperative Cisplatin and Adriamycin to reduce tumor size



ACUTE LIVER FAILURE

Prof. Mohamed Elhasafi.
Hepatobiliary Unit. Alexandria Faculty
of Medicine.

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

Definitions:
Fulminant hepatic failure:
The development of encephalopathy within 8 weeks of the onset of symptoms in
patients 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 encephalopathy
ranges from 8 to 12 weeks.

Etiology:
Viral hepatitis:
Hepatitis A virus
Hepatitis B virus
Hepatitis C virus
Hepatitis D virus
Hepatitis E virus
Hepatitis due to other viruses:
Herpes viruses
Epstein-Barr virus
Cytomegalovirus
Drug-induced liver injury: Acetaminophen
Halothane, Sulfonamides, phenytoins, Statins.
Isoniazid/ Rifampicine
NSAIDs, Ketoconazole, methyldopa.

Toxins:
Amanita phalloides (mushrooms)
Organic solvents
Phosphorus
Herbals.
Metabolic: Acute fatty liver of pregnancy.
Reye syndrome
Vascular: Acute circulatory failure (cardiogenic shock).
Budd-Chiari syndrome
Veno-occlusive disease
Miscellaneous: 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 failure
develop 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-acute
liver 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 patients
who 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, decerebrate
posturing, hyperventilation, abnormal pupillary reflexes, and impairment of brain-stem
function.
Renal failure:
Renal failure occurs in 75% of patients who develop grade 4 encephalopathy
following acetaminophen overdose and in 30% of other etiologies of acute liver
failure.


Metabolic disorders:
Hypoglycemia is common and can lead to impairment of consciousness before
the onset of encephalopathy. The classic symptoms of hypoglycemia are often
masked and regular monitoring of blood glucose is required.
Metabolic acidosis is present in 30% of patients and is associated with high
mortality.
Hyponatremia reflect sodium depletion in patients who are vomiting or it may be
dilutional due to excessive anti-diuretic hormone secretion or intracellular sodium
shifts.

Hemodynamics:
The early hemodynamic profile reflects a hyperdynamic circulation with increased
cardiac output and reduced systemic vascular resistance. Profound vasodilatation
may cause relative hypovolemia .
Progressive disease leads to circulatory failure as a result of falling cardiac output or
an inability to maintain an adequate mean arterial pressure.

Pulmonary complications :
Hyperventilation may be due to intracranial hypertension or may be due to
coexisting metabolic acidosis.
Intracranial hypertension may also suppress respiratory function by compromising the
brainstem, but most patients are mechanically ventilated before this occurs.
Aspiration of gastric contents may an early risk to pulmonary status in patients who
have 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 of
coagulation and fibrinolysis.
In acute liver failure circulating levels of fibrinogen, and factors V, VII, IX and X are
reduced, and the prothrombin time is widely used as an indicator of the severity of
liver 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 presence
of infection and body temperature or with white cell counts.


DIAGNOSIS
The 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 appropriate
investigations.
Hepatitis A
Hepatitis B
Hepatitis C
Acetaminophen
Halothane
Autoimmune
Ischemic hepatitis
IgM anti-HAV
IgM anti-HBc
HCV- RNA
Drug level in blood
Antibody test
Autoantibodies
Very high transaminases.

Histologic assessment of liver tissue aid in the diagnosis of the cause of acute
liver failure, but this is often only available after death or transplantation. Confluent
necrosis 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. Hyponatremia
is 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.


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 continuous
infusion 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- receptor
antagonist).
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 soluble
toxins including ammonia.
The bio-artificial liver support use bio- reactor containing viable hepatocytes in
culture.


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 donor
liver 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 size
graft ( 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.



Gallbladder Disease

Prof Yousri Taher
Head of HPB Unit
Alexandria University

Congenital GB disease

Gallstones and inflammatory GB disease
Three 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 Formation
Impaired GB function

Supersaturated bile

Cholesterol nucleating factors

Absorption /enter hepatic circulation of bile acids

Prevalence Of G Stones
In western countries 10 %(In Egypt 20%)
Prevalence in women is twice that in men
Among 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 Cholecystitis
In 96% cystic duct is obstructed
Clinical features : sufferers are often obese , Fertile female over 40 yr
Pain occur late at night ,in right hypochondrium epigatric referred to right shoulder
Digestive symptoms :flatulence ,nausea vomiting
Fever on occurrence of bacterial infection


ACalculus Cholecystitis
5-10 % of acute cholecystitis in adults
30% in children
Factors associated with critical conditions ,after major surgery ,multiple injuries, major
burns ,severe sepsis mechanical ventilation
Bacterial infection with typhoid bacilli
Actinomycosis
Parasitic cholecystitis

Clinical Findings:
Shallow respiration , fever

Jaundice , Murphys sign is positive

Tender mass at GB region

WBC is high

Clinical Presentation:
Diagnostic tools
Clinical
US
Cholecystography
CT Scan
MRCP
ERCP
PTC

Ultrasound Examination
Accurate In More Than 95%
Biliary Mud
MRCP Perforated GB
CBD Stricture
CT scan After ERCP
Gall Stones
Large GB Stone with Choledochal cyst (ERCP)
Shotty GB Stones With Impacted Stones At The papilla OF Vater
ERCP GB stones
CBD Stricture GB Perforation

Differential Diagnosis
Appendicitis perforated peptic ulcer
Intestinal obstruction, pleurisy myocardial infarction
First aid Treatment antibiotics , analgesia antispasmodic
Surgery


Post Cholecystectomy Problems
Wrong diagnosis
Papillary dysfunction ,stenosis
Psychosomatic disorders
IBS, Biliary stricture
Biliary stones, amputation neuroma Pancreatitis
CBD Injury After Cholecystectomy with Bile Leakage
Endoscopic Sphincterotomy With Stone Extraction
Extraction 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



Acute Pancreatitis

Prof. Yousri Taher
Head of HPB Unit
Alexandria University

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

Spectrum of the disease
Acute edematous or interstitial Pancreatitis : mild , self limited in most patients
Inflammation results in edema of the pancreas
Parenchymal damage is minimal
Pancreas recovers its function after resolution.

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

Complications
Wide spread of inflammatory process
Any of the following organs might be affected : CBD ,duodenum, T colon splenic
artery , 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 and
retroperitoneal spaces lead to hypovolemia and shock.
Systemic effects of these material include: cardiovascular instability respiratory
failure and renal failure.
Hemorrhage : Cullens sign ,Turners sign, and DIC.
Pseudo cyst
Pancreatic abscess
Fat necrosis polyserositis and adult respiratory distress syndrome.
Pulmonary alveolar capillary membrane may be disrupted forming hyaline lining of
alveoli.


Etiology
Alcoholism
Biliary tract disease
Surgery
Trauma
ERCP
Infections (viral, mycoplasma,
Salmonella mycobacterium cryptosporidium.
*Metabolic disorders
(Hypertriglyceridemia,pregancy,hypercacemia, hyperparathyroidism)
*Drugs , vasculitis
Anatomic abnormality annular pancreas ,choledochal cyst ,penetrating peptic ulcer
,parasites ,renal failure ,renal transplantation .

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

Clinical Criteria for Severe Pancreatitis
Cardiac : BP < 90,tachycardia,ECG changes
Pulmonary : dyspnea , ARDS PO2< 60mmHg
Renal output less than 50 ml/h
Metabolic calcium < 8mg/dl, albumin
< 3.2 mg /dl
Hematological: falling hematocrite and DIC
Abdominal distension, fluid wave ,and ileus

Physical examination
Fever tachycardia ,hypotension
Shock
Jaundice
Abdominal tenderness and rigidity
Ileus
Cullen's sign
Pleural effusion ,pneumonitis subcutaneous fat necrosis ,tetany.

Laboratory Tests
Elevated Serum amylase noted within
24 h persist for 3-5 days
Elevated Serum lipase
Urine amylase remains elevated for 7-10 days from onset.
Leucocytosis
Hyperglycemia
Jaundice
Arterial hypoxemia


Radiology
Plain film ileus, air under diaphragm sentinel loop
USG
CT scan
ERCP

Differential DIAGNOSIS
ACUTE CHOLECYSTITIS
BILIARY COLIC
CHOLANGITIS
PERFORATED VISCUS
ACUTE HEPATITIS ,ACUTE INTESTINAL OBSTRUCTION
MESNTERIC VENOUS OCCLUSION

Treatment
85=90 % self limited
Supportive care
Analgesia
Maintain intravascular volume
Monitor vital signs
Treat complications

Drug Treatment and Nutritional Support
PPI , somatostatin or octreotide (sandostatin )
Prophylactic antibiotics
Intralipid
Enteral feeding is much better
Initial high carbohydrate diet low protein and fat.

For severe case
ICU is highly indicated
Necresectomy
Pancreatectomy
Decompress Biliary tract
CT 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


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 Pancreatitis
Alcohol, cigarette smoking
Hyperparathyroidism
Hypocalcaemia
Hereditary autosomal dominant CCP
Cystic fibrosis

Clinical Presentation
Abdominal pain
Malabsorption
Vitamin B12 deficiency
DM
Obstructive jaundice

Physical Examination
Epigatric tenderness
Mass, pseudocyst
Weight 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


Pancreatic cancer
Exocrine pancreatic cancer account for 95% of pancreatic cancer
75 -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 Cancer
CA19.9
CEA
USG focal pancreatic lesion
CT scan
ERCP
Angiography
Fine needle Aspiration
EUS
Laparoscopy
MRI

Treatment Options
Surgery is the best if early ; 5% are respectable
Chemo radiation
Palliative drainage
Endoscopic
Percutaneous
Surgical


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

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INTERNAL MEDICINE DEPARTMENT HEAMATOLOGY UNIT 1

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