1. Topic --- CIRRHOSIS

2.  Should be able to define cirrhosis
 Should be able to classify cirrhosis
 Should be able to work up CLD
 be able to mention complications of CLD

3.  Introduction -------------------- 1’
 Definition ------------------------0.5’
 Etiologic classification----------25’
 Pathogenesis ---------------------3’
 Clinical presentation ------------10’
 Diagnosis --------------------------10’
 Staging ----------------------------- 3’
 Management outline--------------3’

4.  liver -- receives a dual blood supply; ~20% of
the blood flow is oxygen-rich blood from the
hepatic artery, and 80% is nutrient-rich blood
from the portal vein arising from the
stomach, intestines,pancreas,andspleen
(almost from entire GI- through Superior /
Inferior mesentry)

9.  hepatocytes, constitute 2/3
 stellat(13% )
 Kupffer cells
 endothelial cells and blood vessels, bile
ductular cells, and supporting structures

10. Liver cells :
1-- hepatocytes, constitute 2/3.has distinct
polarity; Disse space & microvilli with passive
and active uptake of nutrients, proteins, and
other molecules.
Plays vital roles in maintaining homeostasis and
health; synthesis serum proteins
(albumin, carrier proteins, coagulation
factors, many hormonal and growth factors), the
production of bile and its carriers (bile
acids, cholesterol, lecithin, phospholipids), the
regulation of nutrients
(glucose, glycogen, lipids, cholesterol, amino
acids), and metabolism and conjugation of
lipophilic compounds
(bilirubin, anions, cations, drugs) for excretion in
the bile or urine.

11. 2-- Kupffer cells (reticuloendothelial
system), lie within the sinusoidal vascular
space and represent the largest group of
fixed macrophages in the body.
3---stellate (Ito,fat-storing ) 13%-
(retinoid;vitA metabolite storage), not
prominent unless activated, when they
produce collagen and matrix in large.
4-- endothelial cells and blood vessels, bile
ductular cells, and supporting structures.

15.  Def : cirrhosis is irreversible hepatic damage
; histologically characterized by loss of
hepatic architecture with fibrosis & nodular
regeneration.

16. ALCOHOL
HEPATOTROPHIC VIRAL HEPATITIS:
- HCV
-HBV
-HV-Coinfection(HBV+HCV, HBV+HDV)
-HV-Coinfection with HIV
-HV-Alcohol abuse
AUTOIMMUNE HEPATITIS (AIH)
BILLIARY DISEASES:
 PRIMARY(Psc/PBC)
 SECONDARY: obstructive;cholangitis

17.  HERIDETARY METABOLIC DISEASES
-HEMOCHROMATOSIS
-WILSON’S DISEASE
-ALPHA1-ANTITRYPSIN DEFICIENCY(AAT )
-CYSTIC FIBROSIS
-GLYCOGEN DISEASE
VASCULAR DISEASES:
-VENO-OCCLUSIVE DISEASE(VOD)
-BUDD-CHIARI SYNDROME(BCS)
-CHF/ Percarditis( CARDIAC CIRRHOSIS)
Drugs: Metotrixate, amiodarone,
Toxins: Carbon tetrachloride, diethylmitrosamide
Idiopathic Indian childhood cirrhosis
 Cryptogenic

19.  Alcoholic cirrhosis :
Chronic & excessive ingestion
Risk factors:
A, quantity-M-60-80g/d for 10-20yrs
F -20-40g alcohol/d for shorter
NB-1beer =12g alcohol(ethanol)
B, duration –chronic consumption
C, gender
D, concurrent hepatitis
E,genetic –genepolymorphism; ADH
F, malnutrition –obesity – fatty liver

20. ADH ALDH
Alcohol ---------- acetaldehyde --Acetate

highly reactive with
protein(by reactive O2)
& form adduct

Stellate cells ACTIVATION

COLLAGEN PRODUCTION

21. HCV
Predictive factors for diseases progression :
A-host factor ;
age 40+ at acquisition,Cimminity –rapid p
B-viral factors : d/t genotype,viral load
C- alcohol intake
D- HIV –coinfection  HCC

23.  Progression vary with :
1-function of age(viralrepli/immunit-interplay)
NB –perinatal infection  90%cirrhosis
- adult infection  < 5%
2 –alcohol consumption
3 –concomitant HDV ,HIV infection

24.  HBsAg Anti-HBs IgM anti-HBc IgG anti-HBc HBeAg Anti-HBe viral
copies/mL Interpretation
 + − + − + − + Acute infection; occasionally
 ―reactivation‖ of chronic
 hepatitis B
 − + − + − −/+ − Prior infection with immunity
 − + − − − − − Vaccination with immunity
 + − − + − + <105 Chronic hepatitis B without
 replication
 + − − + + − >105 Chronic hepatitis B with
 replication
 + − − + − + >105 Chronic hepatitis B with
 precore mutant
 Anti-HBc, hepatitis B core antibody; anti-HBe, hepatitis B
e antibody; anti-HBs, hepatitis B surface antibody;
HBeAg, hepatitis B e antig

25. Risk : obesity, hyperlipidemia,DM,
Histology: fatty change & inflammation

26.  Primary biliary cirrhosis(PBS) :
progressive granulomatous inflamm
interlobular bile ducts damage cirrhosis
Cause : unknown ? Autoimmune ,
Affect : 90% middle age women

27.  Primary sclerosing cholangitis(PSC)
Progressive obliterative inflamm of intra &
extra hepatic bile ducts fibrosis cirrhosis
Cause : unknown ? Autoimmune
>70% asssociate with Ulcerative colitis

28.  Hemochromatosis:
Autosom disorder of Fe metabol X-ed by high
Fe absorption deposition in multiple organs
(LIVER, PANCREASE, HEART
,PITIUTARY, JOINT)
Affect : middle age men, loss through mensus
protect women.

29.  Wilson’s Disease :
Inherited disorder X-ed by failure to
excrete copper(failure to prepare
Cu,transportingATPase , for biliary excretion)
 accummulation of toxicCu in LIVER&BRAIN
Kayser-Fleischer ring : pathognomonic(usually)
brownish pigment ring at the periphery of
cornea

30.  Alpha 1-antitrypsin deficiency
Inherited disorder causes abnormal folding of AAT
protien  failure of Liver secretion  accumulation
in hepatocytes  Liver damage
NEONATE :cholestasisearlychildhood cirrhosis
ADULT :- cirrhosis HCC

31. NB:-lung is affected due to destrucion
ELASTASE
AAT -
Elastin (protien)  destruction of protien

32. LIVER INJURY( CHRONIC) OF ANY CAUSE

ACTIVATION
STELLATE,Endothelial,Kupffer,..Cells

Collagen production

Fibrogenesis(wound healing)


33. Hepatocytes microvilli & Endothelial
fenestration lost

Micro/Macronodular Regeneration

Metabolic &synthetic dysfunction of
hepatocytes

DECOMPANSETED LIVER

END STAGE

39.  1/3 asymptomatic
 History:
 Hx of alcohol, drug abuse, blood Tx, familly
ds,
 Weakness, fatigue, wt
loss, anorexia, flatulent dyspepsia,abdominal
pain, impotence/↓libido, jaundice, leg/abdo
m swelling, GI/skin hemorrhage

40.  may present with life-threatening
complications:
 ~variceal hemorrhage,
 ~ascites,
 ~spontaneous bacterial peritonitis (SBP)
 ~hepatic encephalopathy.

41.  Physical signs:
 Fever
 Atrophic legs and arms
 Parotid enlargement
 Testicular atrophy
 Ascites & edema, hydrothorax/effusion
 Portal HTN/splenomegally
 Asterixis, confusion,fetor hepaticus

42.  Spider angiomas/nevi,
 Abdominal collaterals
(found in 50% pregnant)
 Axillary & pubic hair
 Telangectasias
loss
 Palmar erythema
 Kayser-Fleischer ring(
 Pigmentation
cornea)
 Purpura, white nails
 Asterixic(flapping)
 Finger clubbing,
 Testicular atrophy
 Dupytrens contructure

43.  Spiderangiomata/ spider
telangiectasias-- are vascular lesions consisting of
a central arteriole surrounded by many smaller vessels on
trunk, face, and upper limbs.
pathogenesis is incompletely understood, believed to
result from alterations in sex hormone metabolism; in men
increase in the estradiol/free testosterone ratio
not specific for cirrhosis can be seen during pregnancy
, severe malnutrition.
As a general rule, the number and size of spider angiomata
correlate with the severity of liver disease . Patients with
numerous and large spider angiomata may be at increased
risk for variceal hemorrhage.

45.  Palmar erythema — exaggeration of the normal
speckled mottling of the palm, believed to be
caused by altered sex hormone metabolism . on
the thenar and hypothenar eminences while
sparing the central portions of the palm. not
specific for liver disease ,can be seen in
pregnancy rheumatoid
arthritis, hyperthyroidism, and hematological
malignancies.

46.  Muehrcke's nails --paired horizontal white
bands separated by normal color. caused by
hypoalbuminemia .not specific for
cirrhosis, also be seen in other conditions
with hypoalbuminemia.
 Clubbing — angle b/n nail plate and proximal
nail fold >180degree. severe form[grade4] is
drum stick. more common in biliary causes of
cirrhosis (particularly primary biliary
cirrhosis) ,but not specific for liver disease.

48.  Dupuytren'scontracture — thickening and
shortening of the palmar fascia with flexion
deformity ,fibroblastic proliferation and
disorderly collagen deposition with fascial
thickening. The pathogenesis is unknown but
may be related to free radical formation
generated by the oxidative metabolism of
hypoxanthine

50.  Gynecomastia — benign proliferation of the glandular
tissue of the male breast and clinically by the presence of
a rubbery or firm mass extending concentrically from the
nipple(s). Fat deposition without glandular proliferation is
termed pseudogynecomastia ( obese men). These two
entities can be distinguished by having the patient lie on
his back with his hands behind his head. The examiner
then places his or her thumb and forefinger on each side of
the breast, and slowly brings them together.
caused by increased production of androstenedione from
the adrenals, enhanced aromatization of androstenedione
to estrone, and increased conversion of estrone to
estradiol. Men may also develop other features reflecting
feminization such as loss of chest or axillary hair and
inversion of the normal male pubic hair pattern.
Gynecomastia can be seen in a variety of conditions other
than cirrhosis.

52.  Testicular atrophy — Hypogonadism is manifested
by impotence, infertility, loss of sexual
drive, and testicular atrophy. It is a feature seen
predominantly in patients with alcoholic
cirrhosis and hemochromatosis. More than one
mechanism appears to be involved. In some
cases, primary gonadal injury appears to be
more prominent, as suggested by increased
serum FSH and LH concentrations, while in
others suppression of hypothalamic or pituitary
function appears to have a primary role, as
suggested by serum LH concentrations that are
not elevated. The toxic effects of alcohol or iron
may also contribute to its development.

53.  Hepatomegaly — cirrhotic liver may be enlarged, normal sized, or
small. While the presence of a palpable liver may indicate liver
disease, a non-palpable liver does not exclude it. When
palpable, the cirrhotic liver has a firm and nodular consistency.
 Splenomegaly — caused by congestion as the result of portal
HTN .
other several ddx are possible.
. Ascites — accumulation of fluid in the peritoneal cavity. The
accuracy of physical findings is variable depending in part upon
the amount of fluid present, the technique used to examine the
patient, and the clinical setting (eg, detection may be more
difficult in patients who are obese). In one study, the absence of
flank dullness was the most accurate predictor against the
presence of ascites; the probability of ascites being present was
less than 10 percent in such patients . However, approximately
1500 mL of fluid had to be present for flank dullness to be
detected. Shifting dullness is more specific.

54.  Caput medusae — The veins of the lower
abdominal wall normally drain inferiorly into the
iliofemoral system while the veins of the upper
abdominal wall drain superiorly into the veins of
the thoracic wall and axilla. When portal
hypertension occurs as the result of
cirrhosis, the umbilical vein, normally
obliterated in early life, may open. Blood from
the portal venous system may be shunted
through the periumbilical veins into the
umbilical vein and ultimately to the abdominal
wall veins, causing them to become prominent.
This appearance has been said to resemble the
head (caput) of the mythical Gorgon Medusa.

55.  Dilated abdominal veins can also be seen in the IVCS
and SVCS (if obstruction includes the azygous system)
. In these conditions, collateral veins tend to be more
prominent in the lateral aspect of the abdominal
wall. One maneuver that has been proposed to
distinguish vena caval obstruction from portal
hypertension is to pass the finger along dilated veins
located below the umbilicus to strip them of blood
and determine the direction of blood flow during
refilling. In portal-systemic collateral veins, the
blood flow should be directed inferiorly away from
the umbilicus in contrast to vena caval collateral vein
flow in which the flow should be cephalad.
However, the actual ability of this maneuver to
discriminate between the two is poor since in both
conditions the dilated veins may lack valves and thus
have bidirectional blood flow .

56.  Fetor hepaticus — A sweet, pungent smell to the
breath of a cirrhotic patient may occasionally be
encountered. It is caused by increased concentrations
of dimethylsulphide, the presence of which suggests
underlying severe portal-systemic shunting .
 Jaundice — yellow coloring of the skin and mucus
membranes that results from increased serum
bilirubin. It is usually not detectable until Tbil > 3
mg/dL. The hyperbilirubinemia may also cause the
urine to appear dark or "coca-cola" colored.
Yellow discoloration to the skin can also be caused
by excessive consumption of carotene ( carrots). But
can be distinguished from jaundice by the absence of
yellow discoloration in the sclera in the former.

57.  Asterixis— bilateral but asynchronous
flapping motions of outstretched, dorsiflexed
hands ,is seen in patients with hepatic
encephalopathy, ?may also be seen in
patients with uremia and severe heart
failure.

58.  In most instances can be made accurately by
a careful history, physical examination, and
application of a few laboratory tests.
 In some circumstances, radiologic
examinations are helpful
or, indeed, diagnostic.
 Liver biopsy is considered the "gold standard"
in evaluation of liver disease but is now
needed less for diagnosis than for grading
and staging disease.

59. Lab
LFT can be normal, >3-5x UNL or 
1, AST(SGOT)
ALT(SGPT) <40Iu/ml
AST/ALT <0.8 , >2 in alcoholic LD
2,Alk ph - usually elevated but <3X the
upper normal limit. Higher levels in psc &
pbc

60. 3,Bilirubin (N T <1mg/dl;17microg/dl ,D<0.3
N in compensated,  in advanced cirrhosis
4,Albumin-  as the synthetic function of the liver
declines with worsening cirrhosis;helps to grade the severit
of cirrhosis.But not specific for liver disease,can be seen
CHF, NS, protein losing enteropathy, or malnutrition.

61. 5, Prothrombin time
liver synthesize 11 blood coagulation proteins; Factor I
(fibrinogen), II (prothrombin), V , VII , IX , X , XII and XIII
can be measured individually or indirectly by more general
measures of clotting ability such as the PT.
CoagFactors ( liver capacity to synthesize) = PT prolong
Globulins- in cirrhosis(infection), IgG in AIH ,IgM in
PBC

62. Serum Na+ — Hyponatremia is common
in cirrhosis with ascites &severe in ESLD ;
inability to excrete free water; high levels of
ADHsecretion.
Hematologic abnormalities
Anemia — multifactorial ; acute and
chronic GI blood loss, folate
deficiency, direct toxicity due to
alcohol, hypersplenism,BMsuppression,ACD
(inflammation), & hemolysis may all
contribute.

63. Thrombocytopenia
- portal HTN congestive splenomegaly
sequestration of up to 90 % of circulating
platelet mass.
-  thrombopoietin
Leukopenia and neutropenia —
due to hypersplenism

64. Imaging studies
: U/S, Ctscan,MRI
Angiography , ERCP/MRCP, UGIE,Echo
 LIVER BIOPSY

65.  Alcoholic liver disease- History of alcohol abuse , AST/ALT >2
 Chronic hepatitis C- ELISA assay for anti-HCV ,PCR for HCV-RNA
 PBC- Antimitochondrial antibodies
 PSC holangitis - Strong association with IBD, cholangi
 AIH -Hypergammaglobulinemia ,AntinuclearASMA,ALKA
 Chronic hepatitis B - HBsAg and HBeAg and, HBV DNA
 Hereditary hemochromatosis- Family history of cirrhosis
,Serum ferritin & iron,transferritin satur>80% , TIBC ,biopsy-
hepatic Fe index,genetic tes
 Wilson's disease - Family or personal history of cirrhosis at a
young age ,serum ceruloplasmim,biopsy -Co
 AATdeficiency- Family or personal history of cirrhosis at a young
age,serumAAT,phenotyping
 NASH - History of diabetes mellitus or metabolic
syndrome, hepatic imaging , biopsy

66. parameter score
1 2 3
1.ASCITES Abscent Slight Moderat
2.BILIRUBIN <2mg/dl 2-3 >3
3.ALBUMIN >3.5g/dl 2.8-3.5 <2.8
4.PT <4sec 4-6 >6
INR <1.7 1.7-2.3 >2.3
5.HENCEPH None Grade1-2 G3-4

67.  grade A- total score of 5-6 ;well-compensated
disease ;100-85% of 1-2yr survival
 grade
B- total score7-9 ;significant functional
compromise ;80-60%of 1-2yr survival
 gradeC- total score 10-15 decompensated disease
;45-35% 0f 1-2yr survival.

68. goals :
- Slowing or reversing the progression of liver
disease
- Preventing superimposed insults to the liver
-Preventing and treating the complications
-Determining the appropriateness and optimal
timing for liver transplantation

69.  Abstinence from alcohol .
 Interferon therapy to HCVslows the
progression,fibrosis &risk of HCC.
 Rx of chronic HB with lamivudinsignificant
improvement in liver function and histology
& risk of HCC
 Rx autoimmune hepatitis with
immunosuppressive agents10yr survi 90 %

70.  Phlebotomy , Chelation ,Dietary restriction
of iron – for HH
 Chelating –for wilson D

71. AVOID
 substance abuse; alcohol,
 acetaminophen ,NSAIDs
 hepatotoxic drugs & herbal remedies.
 Give Vaccination — against HAV & HBV can
prevent a superimposed insult to a liver
Pneumococcal vaccine
yearly influenza vaccination

72. xumura
ULFAADHA !

73. COMPLICATION OF END-STAGE CLD

74. AT THE END :
 Mention the complication.
 Rescribe the mechanism
 Work up principile
 Outline the managment

75.  Portal hypertension -------------------------5’
 Variceal hemorrhage -----------------------10’
 Ascites -----------------------------------10’
 Spontaneous bacterial peritonitis ------10’
 Hepatic encephalopathy ------------------10’

76.  Portalhypertension
 Variceal hemorrhage
 Ascites
 Spontaneous bacterial peritonitis
 Hepatorenal syndrome
 Hepatic encephalopathy
 Hepatopulmonary syndrome
 Hepatocellular carcinoma
 Coagulopathy
 malnutrition

77.  Def
 Causes
 Types
 consequence

78.  Def: hepatic venous pressure gradient (HVPG)
> 5 mmHg.
Portal pressure = Portal venous flow x portal venous
outflow resistance
-R blood flow
- vasodilatation within the splanchnic vascular
bed  splanchnic blood flow.
 Cause : cirrhosis-commonst >60%
: noncirrhotic
: ?idiopathic

79. 1 Prehepatic :Portal &/ or splenic vein thrombosis ,
: Massive splenomegaly (Banti's syndrome)
2 Hepatic :commonst type 95%
2a PresinusoidalSchistosomiasis –fibrosis,Congenital hepaticfibrosis
2b Sinusoidal  Cirrhosis
2c Postsinusoidalsinusoidal obstruction syndrome(VOD),BCS
3 Posthepatic : IVC obstruction ,
: Budd-Chiari syndrome
: Cardiac causes ;RCM
Constrictive pericarditis

80.  1-- UGIB
 2-- ascites
 3—splenomegaly with hypersplenism.

81.  Def
 Location
 Risk
 Dx
 Rx

82. VARICES - are collateral vessels that develop
because of PHT; 1/3of pts with cirrhosis & 1/3 of
them will develop bleeding.
LOCATION—
-distal esophagus (commonst) ; thinnest coat
and at risk to bleed, - stomach, -Rectum, -
Umbilicus,…
FACTORS  risk of bleeding : --PHTN >12mmhg ,--
severity of cirrhosis (Child's class),--size of the
varix ,--location of the varix,-- endoscopic
stigmata(red wale signs& …)

83. Endoscopy.
Abdominal imaging, CT or MRI demonstre
nodular lesion
Thrombocytopenia

84. a--Pharmacologic =nonselective beta blockade
(propranolol ,nadolol )
b--Endoscopic variceal band ligation(EVL) &/or
variceal injection therapy (sclerotherapy)

85. a --- fluid and blood product replacement
b ---medical ;
1-somatostatin or Octreotide , Vasopressin= direct
splanchnic vasoconstrictor, is given at dosages of 50–100
g/h by continuous infusion.
c---surgical ;
1-Balloon tamponade (Sengstaken-Blakemore tube or
Minnesota tube)
2- endoscopic therapy ( first-line to control active-vigorous
bleeding by EVL & /or variceal injection therapy
(sclerotherapy)
3- transjugular intrahepatic portosystemic shunt (TIPS)under
angiographic guidance

86. a---repeated variceal band ligation until
varices are obliterated.
b---adjunctive Beta blockade (for recurrent
variceal band ligation ,But no need once
obliteration achieved)
c---TIPS

87.  Highrisk group to develop reccurrent
variceal bleeding ?
 Prognosis of variceal bleeding ?
 Other causes for UGIB ?

88. Risk factors for recurrent variceal hemorrhage
 Age >60 years
 Severity of initial bleed
 Renal failure
 Severity of liver failure
 Ascites
 Hepatoma
 Active alcoholism
 Active bleeding on endoscopy
 Increasing varix size
 Red signs yes
 coagulopathy
 Portal pressures

89.  Def
 Mechanism
 Dx
 Rx

90.  def: pathologic accumulation of fluid in the peritoneal
cavity
 mechanism: multifactors
1] PORTAL HYPERTENSION
is the first step toward fluid retention in cirrhosis.
>12 mmHg required.
cirrhosis without PHT do not develop ascites
 ascites disappear if <12 mmHg
■Portal hypertension exerts a local hydrostatic pressure
hepatic and splanchnic production of lymph
&transudation of fluid into the peritoneal cavity.

91. 2] Na RETENTION :
splanchnic vasodilatation-Arterial underfilling
- Activation Renin-Ang-Aldos -- Na retent-
3] HYPOALBUMINEMIA :
 synthetic function of cirrhotic liver 
Hypoalbuminemia   plasma oncotic
pressure  loss of fluid from the vascular
compartment into the peritoneal cavity.

92.  incidious abdominal distension ;
( high Na diet,HCC ,splanchnic vein thrombosis
Precipitate)
 Abdominal pain ; SBP
 Respiratory distress ( Rt pleural effussion )
 Malnourish; muscle wasting and excessive
fatigue and weakness.
 bulging flanks, fluid Waves ,shifting dullness
+v ,sign of pleural effussion.

93.  abdominal imaging ; U/s , CT scan
 Paracentesis : Analysis
Color (clear,straw,cloudy,bloody,milky,brown)
cirrhosis –straw/clear(if n-Bilir, protien)
SBP –cloudy
HCC –bloody

94. test
1-Cell cout & diff - N >250  SBP
2-Gram stain,AFB and culture -
3-Protein -3.1 SAAG
-3.2 [total protein]
4-Cytology - for malignant cells.
5-Amylase - to exclude pancreatic ascites

95. test
1-Cell cout & diff - N >250 SBP
2-Gram stain,AFB and culture -
3-Protein- serum ascites-to-albumin gradient (SAAG) ;
[total protein] in ascites is quite low in cirrhosis; <1 g/dL
SAAG=serum alb minus ascitic albumin ( not ratio )
>1.1 g/dL indicates PHT-cirrhosis with 97%accuracy &
High-gradient (transudative
remains stable unless PHT
<1.1 g/dl indicates abscence of PHT,
Low-gradient (exudative)
but infectious(opsonization) or malignant (peritoneal carcinomatosis, tuberculous
peritonitis, pancreatitis, serositis, pyogenic peritonitis, and nephrotic syndrome)
4-Cytology - for malignant cells.
5-Amylase - to exclude pancreatic ascites

96.  Bilirubin — in brown ascites. As mentioned
above, an ascitic bilirubin > of serum
suggests bowel or biliary perforation into
ascites
 Glucose —
 Lactate dehydrogenase
 Triglycerides — milky/ Chylous ascites has TG
> 200 mg/dL

97.  dietary sodium restriction
 spironolactone at 100–200 mg/d- 400–600mg
 furosemide 40–80 mg/d- 120–160 mg/d
 repeated large-volume paracentesis(refractory
ascites)
 TIPS (refractory ascites)
liver transplantation
 prognosis of cirrhosis with ascites is
poor, survive 2 years <50%

98.  LIST Other causes of ASCITES

99.  Def
 Etiology
 Precipitant
 Distinction from secondary BP
 Dx
 Rx

100.  Def:ascitic fluid infection without an
evident intraabdominal surgically-treatable
source.
 ETIOLOGIES ?

101.  Escherichia coli 43%
 Klebsiella pneumoniae 11%
 Streptococcus pneumoniae 9%
 Other streptococcal species 19%
 Enterobacteriaceae 4%
 Staphylococcus 3%
 Pseudomonas 1%
 Miscellaneous* 10%

102.  cirrhosis,& associated conditions
 Ascitic [total protein] <1 g/dL (<10 g/L)
 Prior episode of SBP
 Serum [total bilirubin] > 2.5 mg/dL
 Variceal hemorrhage
 malnutrition
 Proton pump inhibitors
 Nephrotic ascites

104.  Subtel- due to separation of visceral & parietal
peritoneum
 Fever 69
 Abdominal pain 59
 Altered mental status 54
 Abdominal tenderness 49
 Diarrhea 32
 Paralytic ileus 30
 Hypotension 21
 Hypothermia 17

105. Def : ascitic fluid infection in which there is a positive ascitic
fluid bacterial culture and an ascitic fluid PMN count ≥ 250
cells/mm3 with an evident intraabdominal surgically-
treatable source of infection .
Two varieties :
1--perforation peritonitis (eg, perforated peptic ulcer into
ascites)
2--nonperforation peritonitis (eg, perinephric absces
NB-mortality 100% if treatment consists only of antibiotics
with no surgical intervention . And 80% if a patient with
SBP receives an unnecessary exploratory laparotomy .

106. Clinical — both can be ( even frank perforation)
subtle b/c peritoneum separation by Ascites
Analysis — PMN count ≥ 250 with two or more of
[Total protein ] >1 g/dL (10 g/L)
[ Glucose ]<50 mg/dL
[ LDH >UNL for serum
Imaging studies —
plain and upright abdo minal films
water-soluble gut contrast studies( extravasation
of contrast
SBP-Rx response follow up ---
with repeat analysis after 48hrs ; PMN is lower

107.  Ascitic fluid analysis :
1] Cell count --- absolute PMNcount≥ 250
2] Culture ---- positive
3] SAAG ----- Low-gradient
4] [Total protien] -----lowest[ ] ; < 1g/dl
5] [glucose] > 50mg/dl
6] LDH (released from lysed PMNs) --[43 +/-
20mU/mL ]
7] [Amylase ]--- in pancreatitis and gut
perforation
8] [ bilirubin] if dark/brown ascites----if > serum
value  choleperitoneum ;GBperforation

108.  1- third-generation cephalosporin
?2-combination of ampicillin
and gentamicin .
Third-gener + metronidazol
For secondary BP

109. third-generation cephalosporin benefits
over ampic/genta-combination:
A-- A higher rate of resolution of the infection — 85 versus 56
%
B--No /less nephrotoxicity versus 5 % with ampicillin-
gentamicin
C-- No superinfection versus 14 percent with ampicillin-
gentamicin
.

110.  Def
 Mechanism
 Precipitant
 Stages
 Rx

111.  Def : ?potentially reversible neuropsychiatric
syndrome seconday to liver diseases
CLD,END-STAGE Or acute fulminant hepatic
failure.

112. Ammonia — cause in >90% + other neurotoxins
Produced--- colonic bacterial catabolism of nitrogenous
source; ingested protein and secreted urea.

Enters the circulation via the portal vein

Liver clears almost all by converting into glutamine &
prevent entry into the systemic circulation

In cirrhosis ,portal blood bypasses the liver via the collaterals
and the 'toxic'metabolites pass directly to the brain
( impaired liver  blood ammonia )

Induced alteration of brain neurotransmitter balance -
especially at the astrocyte-neurone interface

113.  PRECIPITANTS ?

114.  High dietary protein
 GI- haemorrhage
 Constipation
 Vomiting /Diarrhea
 Infection; SBP , sepsis
 Fluid and electrolyte ( k+ )disturbance due to:diuretic therapy,paracentesis
 Drugs (e.g. anyCNSdepressant) Benzodiazepines,Narcotics ,Alcohol
 Portosystemic shunt operations, TIPS Any
 surgical procedure Progressive liver damage
 Development of hepatocellular carcinoma

115. change in personality
confused
Can be quite violent and difficult to manage
Or very sleepy and difficult to arouse
Asterixis "liver flap‖
hepatic coma due Brain edema -herniation

117.  mainstay lactulose--, a nonabsorbable disaccharide
eliminat nitrogenous source
 R x of precipitats
 ?Restriction of dietary protein
 neomycin + metronidazole =Poorly absorbed antibiotics as
adjunctive therapies or alternative to lactulose
 rifaximin.
 ?Zinc supplementation
 Prognostic worse as stage progress

118.  refers === development of acute renal failure in
advanced liver disease, severe alcoholic
hepatitis, (less often) metastatic tumor, and
acute fulminant hepatic failure from any cause.
 MECHANISM :
 portal hypertension -splanchnic
vasodilatation - hypotension-induced
activation of the renin-angiotensin and
sympathetic nervous system- renal perfusion
( GFR )

119.  Type I HRS--- more serious type; progressive
impairment in renal function and a
significant reduction in creatinine clearance
( 50% )within in <2wks,serum Cr.2.5mg/dl
, oliguria
 Type II HRS ; less severe. GFR and Cr

120.  midodrine --is a systemic vasoconstrictor
 alpha1–agonist--
 octreotide -- inhibitor of endogenous vasodilator
, in combination
 intravenous albumin
 liver transplantation
 prognosis is poor unless transplant can be
achieved within a short period of time

121.  90% of primary hepatic malignancy
 One of the most common malignancies ,4th
leading death , affecr men commonly
 1 million/yr with MR=250,000/yr
 Liver cirrhosis, HBV, HCV are most important
risk factors
 Most Asymtomatic or present with abdomen
pain or liver failure s/s
 Px=survive 2-6 months if unRxed

122.  Causes of HCC:
 Viral infection: B,C,D; cirrhosis from
HBV,HCV, HH --at highest risk, while AIH,NASH
&Wilson's d lower risk.HBV even at carrier state
is high risk.
 Toxins:Alcohol, aphlatoxin B1, tobaco,Thorium
oxide, Vinyl chloride monomers

 Metabolic liver ds:
hemochrom,alpha1,PCT,glycogen storageI, II
 Others: BCS, Liver flukes, androgeic anabolic
hormones, etc

123.  S/S:nonspecific similar
 Hard irregular hepatomegally with bruit and
cachexia and splenomegally
 Portal vein thrombosis
 Coagulopathy
 Multiorgan failure
 Portal HTN

124. Extrahepatic -- most common sites are
lung, intraabdominal lymph nodes, bone, and
adrenal gland; brain metastases are
extremely rare . Extrahepatic metastases are
more common in patients with intrahepatic
tumors >5 cm in diameter

125.  DDX of primary hepatic malignancy:
 1.Epithelial :
 HCC;cholangioca;bilary cystadenoca;Sq cell
ca; mucoepidermoid ca
 2. Mesenchymal:
 Angiosercoma, hemangioendothelioma,
 Leimyosarcoma, fibrosercoma, embryonal ,
 sercoma, rhabdomyosercoma,
 Malignant schewanoma/
histosercoma, lymphoma

126.  3.Mixed tumors:
 Hepatoblastoma
 Mixed HCC &cholangiocellular Ca
 carcinsarcoma

127.  Treatment & prevention
 Quarterly U/s & AFP for CLD for early HCC DX
 RX: Ethanol, chemoembolz, resection, LTx,
palliative care; RT, HormonalRx
 Mass HBV vaccination and CLD Rx for
prevention

128. can be asymptomatic OR can present with
complication of cirrhosis
RUQ pain ,weight loss , early satiety, or a
palpable mass in the upper abdomen.
Obstructive jaundice r ,dyspnea (
metastases), Intraperitoneal bleeding ( tumor
rupture)
Hepato/splenomegaly with bruit
Paraneoplastic syndromes —
hypoglycemia, erythrocytosis, hypercalcemia, se
vere watery diarrhea,and cutaneous
manifestation

129.  Patterns of metastatic spread —
Extrahepatic -- most common sites are
lung, intraabdominal lymph nodes, bone, and
adrenal gland; brain metastases are
extremely rare . Extrahepatic metastases are
more common in patients with intrahepatic
tumors >5 cm in diameter .

130.  Alpha-fetoprotein --- glycoprotein that is
normally produced during gestation by the
fetal liver and yolk sacr can
pregnancy, with tumors of gonadal
origin, and chronic liver disease ;acute or
chronic viral hepatitis
NORMAL=10 and 20 mcg/L
>500 mcg/L in high risk group is suggest to
HCC
IMAGING
BIOPSY

131.  Surgical
 Livertransplant
 Radiotherapy/chemotherapy

132.  regulationof protein and energy metabolism
catabolic, and muscle protein is
metabolized,
poor dietary intake, alterations in gut
nutrient absorption, and alterations in
protein metabolism.
Dietary supplementation is helpful

133.  Coagulopathy is almost universal in cirrhosis.
  synthesis of clotting factors and impaired
clearance of anticoagulants.
 thrombocytopenia from hypersplenism
  Vitamin K absorption – AFFECTdependent
CF ( II, VII, IX, & X )

134.  anemia from --persplenism, hemolysis, iron
deficiency, and perhaps folate deficiency
from malnutrition.
 Macrocytosis
 Neutropenia from -hypersplenism.

135.  Osteoporosis-
malabsorption of vitamin D &
calcium ingestion

136.  HARRISON’S PRINCIPLES OF INT.MEDICINE 17th
EDITION
 UpTODate 17.2
 KUMAR CLINICAL MEDICINE 6th EDITION