This document discusses chronic liver disease and provides details on its epidemiology, risk factors, etiology, pathophysiology, clinical presentation, diagnosis, complications, and treatment. It defines chronic liver disease as the progressive decline of liver function for more than six months. It describes the major causes as alcohol, viral infections like hepatitis B and C, and non-alcoholic fatty liver disease. Complications discussed include portal hypertension, ascites, spontaneous bacterial peritonitis, variceal bleeding, and hepatic encephalopathy.

1. UNIVERSAL MEDICALAND
BUSINESS COLLEGE,
DEPARTMENT OF PHARMACY
EMERGENCY WARD ATTACHMENT SEMINAR
IN Y12HMC
1/29/2024
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2. CHRONIC LIVER DISEASE (CLD)
Prepared by: Eyael surafel
1/29/2024
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3. OUTLINE
 INTRODUCTION
 EPIDMOLOGY
 RISK FACTOR
 Etiology
 Pathophysiology
 Clinical presentation
 Diagnosis
 complication
 Treatment
 Reference
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4. INTRODUCTION
 Definition- Chronic liver disease (CLD) is a
progressive decline of liver functions for more than
six months.
 Progressive destructions of liver parenchyma over 6
month lead to fibrosis and cirrhosis
 CLD includes: cirrhosis , alcoholic liver disease ,Non-
alcholic fatty liver disease(NAFLD), chronic Hepatitis
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5. FUNCTION OF LIVER
 Detoxification
 Albumin production
 Bilirubin conjugation
 Synthesis of cloting factor
 Estrogen metabolism
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6. EPIDEMIOLOGY
 An estimated 1.5 billion person have CLD
 There are 257 million people worldwide who are living
with chronic HBV.
 20% will die early of liver failure or hepatocellular
carcinoma. only 11% of infected persons are aware of
their infection, and 17% of those receive treatment.
 In Ethiopia, liver diseases accounted for 11.4% of all
medical admissions
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7. RISK FACTORS
 Heavy alcohol use.
 Obesity and metabolic syndrome
 Iv drug use and exposure to toxin
 Tattoos or body piercings.
 Injecting drugs using shared needles.
 Exposure to other people's blood and body fluids.
 Unprotected sex
 infection(viral hepitites, cmv)
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8. ETIOLOGY
1. Alcohol: common cause
2. Viral infection: except HAV $ HEV
3. NAFLD: metabolic syndrome (like obesity
,high cholesterol, TG,HTN)
4. Genetic
5. Autoimmune
6. Drug : phenytoin, Isoniazid, methotrexate,
amiodarone
7. idiopathic
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9. PATHOPHYSIOLOGY
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10. CLINICAL PRESENTATION
 Early - compensated asymptomatic and non specfic wt.
loss weakness
 Later-extensive fibrosis
 jaundice
 Abnormal pain and swelling in leg and ankle
 Ascites(fluid in the belly)
 Gallstone
 Itching SKIN
 Kidney failure
 Loss of appetite
 Confusion
 Dark urine
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11. DIAGNOSIS
 Liver function test (ALT,AST, APT. GGT,
Bilirubin)
 CT scan, MRI Ultrasound
 LIVER BIOPSY
normal AST:ALT ratio is<1.
in alcoholic liver patient it is >1
in NAFLD liver patient it is <1
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12. COMPLICATION
 Portal hypertension
 Ascites
 SBP
 Variceal bleeding
 Hepatic encephalopathy
 hepatocellular carcinoma(hepatoma)
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13. 1) PORTAL HYPERTENSION
• is defined as elevation of hepatic venous pressure
>5mmhg.
• Clinically significant portal HTN occur >10mmhg.
• Risk of variceal bleeding increase beyond 12mmhg.
• Extra hepatic portal vein obstruction is usual source in
children and adolescence. while cirrhosis cause at least
90% of cases in adults
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14. TREATMENT
 Management in portal hypertension is aimed at
preventing and treating its complications.
 In the case of varices, this includes endoscopy
to screen for varices,
 nonselective beta blockers and/or endoscopic
variceal ligation to prevent bleeding, and
 treatment of active hemorrhage with endoscopic
therapy or transjugular intrahepatic
portosystemic shunt (TIPS) placement.
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15. 2. ASCITES
 Is accumulation of fluid in peritoneal cavity.
 The decrease in LFT combine with portal HTN cause ascites
symptom.
 Symptom
 swelling of ankle
 Back pain
 SOB
 Fatigue
 Abdominal pain
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16. TREATMENT
 In patients with ascites, treatment often starts with dietary
sodium restriction and diuretics.
 Stop drinking alcohol
 Attainment of sodium balance
 dietary sodium restriction(<2gm/d)
 Fluid restriction(1.5L/d)
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17.  Diuretics
 urine Na>30mEQ/L: Spironolactone 400mg/d
 urine Na(10-30) mEq/L: Furosemide 160mg/d in
40:100 ratio of spironolactone.
-urine Na<10 mEq/L: high dose loop + albumin
8-10g/L
-cefotaxime 2gm iv tid
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18. 3. SPONTANEOUS BACTERIAL PERITONITIS (SBP]
 Is defined as bacterial infection of the ascetic fluid. Due to
enterobacteria or pneumococci
 SBP is defined as ascetic fluid polymorph nuclear leukocyte (PMN)
count level ≥ 250 cells/µL without a surgical, intra-abdominal cause
of infection
 Incidence: 10-30% of hospitalized patients with cirrhosis and ascites
 Clinical presentation: Fever, abdominal pain, nausea, vomiting,
diarrhea, rebound tenderness, and exacerbation of encephalopathy
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19. TREATMENT
 surgical drainage,
 repair or removal of the ruptured viscus
 fluid resuscitation
 Antibiotics
 first line-cefotaxime 2gm iv bid for 5 day
alternative ceftriaxone 1gm iv bid or
2gm iv qd for 5 day
 Uncomplicated - ciprofloxacillin 500mg po bid
-levofloxacin 500mg po qd
Duration: 5-10 days
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20.  Nosocomial –extended spectrum
( carbapenems, piperacillin-tozobactam)
depend on local resistance pattern
 Advanced liver & cr>1mg/dl, BUN >30mg/dl or bilirubin >4mg/dl
cefotaxime 2gm iv qid for 5day
+
iv albumin 1.5 g/kg on day 1
 albumin used to reduce renal impairment and mortality
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21. 4. VARICEAL BLEEDING
 Esophageal varices are a common complication of cirrhosis
Approximately 1/3 of all cirrhotic patients will develop a
variceal bleed
 Occur when large vein often esophagus get swollen and
break then open this caused by a condition called portal
HTN .
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22. TREATMENT
 Vasopressin (0.2-0.4 U/min )
-Octreotide is a parenteral synthetic
analog of the naturally occurring hormones
omatostatis.
-sandostatin dose-50mcg iv bolus
* 20-50 mcg/hr infusion(1-
5day)
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23. 5. HEPATIC ENCEPHALOPATHY
 Disturbance in CNS function by toxin
secondary to hepatic insufficiency
 Clinical presentation- confusion excess
sleepiness slurred speech
Altered mental status and progression to
coma if untreated
Asterixis: “Hand flap” – classic PE finding
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24.  abnormal metabolism most likely is a cause
(ammonia is the by product of protein
metabolism , healthy liver converts
ammonia
in to urea then excreted by kidney)
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25. TREATMENT
1.supportive care
2. identify the cause
3.treatment
 removing toxin from intestine(ammonia)
 Antibiotics (rifaximin)
 Lactulose(ammonia reduction)
30ml po qd/bid
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26. Antibiotics
Goal: intraluminal urease-producing
bacteria
*Neomycin 3-6 g/day 1-2 weeks; then
1-2 g/day
*Metronidazole 250 mg BID
*Rifaximin 400 mg tid
As effective as lactulose
Costly but better tolerated
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27. REFERENCE
 Fourth edition, Pharmacotherapy Principles &
Practice, E-book Marie A. Chisholm-Burns, Terry
L. Patrick M. Malone,
 By E, Alldredge BK, Affairs A, Francisco S,
Francisco S, Corelli RL, et al. Applied
Therapeutics The Clinical Use of Drugs TENTH
EDITION Edited
 Dipiro 9th edition
 Who guideline
 Up-to-date
 Medscape
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