Cirrhosis: etiology: virus B , alcohol, alpha 1

anti-trypsin deficiency, toxins, chemical, essential

variant when no etiologic factor (cryptogenic).
Pathogenesis: 1- influences of factors that cause
necrosis directly. Necrosis result in some way of
pathogen activate mesenchymal tissue which
leads to further degradation of hepatocytes. 2appearance of necrosis since onset stimulate
generation of the liver but unable to provide
normal function nodules or false liver
lobules.3- inflammation in portal fields that block
normal tissue blood stream to parenchyma,
activate fibroblast new collagen fibers which
cause shrinkage in parenchyma + decrease flow
of blood. 4- cirrhosis include portal H ascites+
splenomegaly: a- increase hydrostatic pressure in
portal vein + decrease oncotic pressure, bsplenomegaly + hyper function of spleen, cexudative enteropathy stagnation of blood, when
drainage of mucous layer in bowel is broke
decrease absorption of nutrient from lumen,
increase hydrophilia, inc transudation of H2O
from lumenor loss of H2O + decrease digestion
+absorption, d- shunting of blood through
commissure result endotoxicosis then
bacteremia. Decrease high risk for secondary
infection, shunting of blood increase risk of
encephalopathy that result coma due to toxins.
Syndrome:
asthenic,
dyspepsia,
pain,
inflammation (fever), cytolytic syndrome,
cholestasis,
hepatosplenomegaly
synd,
hyperspleni in prolonged state of disease, acites +
edema syn, hemorrhagic syn, liver insuf syn,
portal hypertension synd.Classification: 1Micronodular
in
alcoholic
variant.2macronodule. 3- mixed variant. 4- biliary
cirrhosis
Acc to clinic: compensated &
decompensated. Biliary disease: etiology: drugs
as sulphonamide, antibiotis as tetracycline,
contraceptive, diuretics as thyazide, infl in
liver because they are heptans. Endocrinology as
thyrotoxicosis, pregnancy, signs: 1- changes of
skin typical jaundice that last for a long time,
itching, stria, lipoma of skin, pigmentation of
skin.& hepatomegaly is the most imp synd,
abnormal digestion of bowel, bones problems as
osteoperosis+ typical dypeptic syndrome with
diarrhea. Investigation: inflam is syn of liver
affection, increase ALT, AST, phospholipid, bile
acid, cholesterol, direct bilirubin. Ultra sound:
enlargement of liver, widening of bile
channel.Micronodular
(alcohlic
cirrhosis):
Anemnesis if age > or = 40 yrs, false cushingoid
synd: moon face, red cheek, alcoholic
polyneuritis, peripheral myopathy, cardiac
myopathy, cardialgia, increase IgA globulin, if
biopsy is possible centrilobular of collecting
Mallory bodies. Mechanism: over 20 yrs often
alcohol stoppage the function of liver will be
reversed. 80% slow development, 20 % quick
dev.- ascites + quick commissures formation

treated successfully. But if they still drink till 2

mo.can be compensated but then after that
decrease
function,
bleeding,
death.
Macronudalr: no enough parenchyma to func
normally hepatodepression. First appears then
later or portal H. s Ag is seen, liverinsufficiency
looks like hepatitis, episodes of the jaundice,
duration is less 30 %. 10 yrs of disease even less
before last stage. May have compensative stage
but shorter in time, compared to alcoholic
cirrhosis. Decompensation all clinical picture.
Portal H. Real encephalopathy. Fever is more
typical. If upon palpation nodules macro.
Investigation: blood; different finding: anemia:
hemolytic, hyperregenerative, abnormal RBC in
bone marrow, Fe deficiency if hemorrhage,
pernicious anemia. Leukocytosis or leukopenia,
thrombocytopenic. Urine: hepatorenal synd,
increase SG hemotouria + casts. Biochemical
detoxification bromosulfin test. Ultra sound of
liver: portal increase, increase size of liver or
decrease enlargement of veins inside the liver.
Gastroscopy,
duodenoscopy,
angiography:
control of portal vein, laporoscopy: nodules,
enlargement vessels, biopsy. Treatment: Ihepatitis: active: 1- avoid dysbacteriosis that get
to permanent level of toxicity. 2-diet number 5 do
not irritate liver. 3- drug to stimulate digestion: aantibacterial drugs, bactoseptal, lactobacterin. Bpancreas enzymes for digestion solve asthenia &
dyspepsia. Immunosupression indication: 1clinical active hepatitis (enlargement of liver,
jaundice, increase ALT more or = 5 times, bridge
necrosis or biopsy) 2- Transaminase not more or
= 5times but associated. Other lupoid must be
treated with glucocorticoid 20 30 mg , 5 tablets
daily for 2 weeks then 50 mg per day if still signs
of aggrevation we can give 10 15 mg for 2 or
3 monthstill remission, if remission is stable then
decrease tablet during 1 week. Associate
glucocort with azathioprin 25-30 mg/day 3 to 5
months. If unstable remission use smooth
cytostatic for 1 year. If virus hepatitis:
immunosupressors are debated we must know the
phase of hepatitis, if persistent there is conversion
of eAg to eAb & if only Ab against s,c,e treat
of immusupressnat may be useful. If in
replication phase s Ag + eAg are found
prohibited
immunosupresant.
Cirrhosis:1compensated: liver can detoxicate.(complex of
vit, gluc, hemodiesis, avoid dysbacteriosis,
increase digestion).
2- subcompensative:
phospholipid, vit E, anabolic hormone,
detoxification. 3- decompensative: if portal
hypertension
+
ascites

diuretics+
sprinolactone. If huge ascites puncture slow
evacuation to avoid toxicity. Antibiotics:
cephalosporine for cleaning of bowels + prevent
infection. Coma: catheterization of CV, gluc
3l/day+ vit B +lipoid acids. Prednizalone,
solution of alpha-arginine, cleaning of the bowel,

transfusion of blood each day or intranasal

catheter, bicarbonate 400 mg for acidosis.
Syndromes: that shows the coma will appear are
fetor smell, aggrevation of encephalopathy
stupor, flatter of hands. Jaundice: Class: 1extrahepatic
jaundice:
hemoglobulinemia,
changes in RBC structures, direct hemolytic
agents like drugs( methyldopa), chemical
hemotransfusion, infection as mycoplasma,
autoimmunological changes, sepsis, some tumors
as leukemia. 2- interhepatic jaundice when some
process in liver block capyure of bilirubin:
toxical influences of some drugs, thyrotoxicosis,
some sepsis decrease ability of liver to detoxify
non conjugated bilirubin. Congenital syndrome as
gilbert and najjar Gilbert: special biological
signs, seen in family autosomal dominant, yellow
skin, bradycardia, severe headache as migrane,
decrease temp, diarrhea, albuminuria. Najjar:
post-natal period, recessive, enlargement of
liver+ spleen, encephalopathy. Parenchymal
jaundice: cirrhosis, hepatitis, signs of affected
liver as ncrease AST, ALT, abnormal structure of
membrane--. Bilirubin directly to blood +
inability to conjugate. Rotor + dubin jonson:
when no inflam of liver but congenital properties,
abnormal to secrete conjugate of bilirubin to
outside cells, Rotor: dominant, increase bilirubin
in blood, liver not enlarged, Dubin jonson:
recessive, no inflammation. 3- extrahepatic
jaundice: a- intrahepatic cholestasis: blocking of
flow of bile at level of channels, abnormal
content of bile. B- extrahepatic cholestasis:
mechanical blocking of bile due to stones,
scaring, pancreatitis. Investigat: all functional
examination, blood deny hemolysis, RECP,
Cholecystography, US, gastroscopy with
duodenoscopy, Treatm: anti- inflammatory drugs
that support bowel spasmolytic.