2. ALCOHOLIC LIVER CIRRHOSIS IS LIVER INJURY ATTRIBUTED TO ALCOHOL ABUSE.
ENCOMPASSES THE HEPATIC MANIFESTATION, INCLUDING FATTY LIVER, ALCOHOLIC
HEPATITIS WITH HEPATIC FIBROSIS.
MAJOR CAUSE OF LIVER DISEASE IN WESTERN COUNTRIES.
TERM WAS 1ST COINED BY LAENNEC IN 1826.
PRIMARY HISTOLOGICAL FEATURES
1. MARKED FIBROSIS
2. DESTRUCTION OF VASCULAR AND BILIARY ELEMENTS
3. REGENERATION
4. NODULE FORMATION
ALCOHOLIC LIVER CIRRHOSIS
4. PREVALENCE OF ALCOHOL RELATED DISORDERS WAS 1.7% WORLDWIDE.
WORLDWIDE MORTALITY IS ESTIMATED TO BE 150 000 PER YEAR.
AMONG HEAVY DRINKERS 90-100% WILL DEVELOP HEPATIC STEATOSIS IN 10 YEARS.
ONLY 10-35% DEVELOP CIRRHOSIS IN THE SAME PERIOD.
LIVER CIRRHOSIS DEVELOPS IN 6-14% OF THOSE WHO CONSUME > 60-80g ALCOHOL DAILY FOR
MEN AND > 20g DAILY IN WOMEN.
WHO DRINK > 120g DAILY ONLY 13.5% WILL SUFFER SERIOUS ALCOHOL RELATED INJURY.
DESPITE CESSATION OF ALCOHOL USE OF ONLY 10% WILL HAVE NORMALIZATION OF HISTOLOGY
AND LFTs.
INCIDENCE
5. ALCOHOL BEVARAGE IS A DRINK THAT CONTAINS ETHANOL.
IN THE BLOODSTREAM, FROM THE STOMACH, ALCOHOL IS ABSORBED BETWEEN 5-10 TIMES.
FACT: FEMALES ABSORB ALCOHOL FASTER THAN MALES BECAUSE THEIR BODIES CONTAIN LESS
WATER.
ABOUT ALCOHOL
6. THERE ARE THREE MAIN STAGES OF ALCOHOLIC LIVER DISEASE, ALTHOUGH THERE IS OFTEN AN
OVERLAP BETWEEN EACH STAGE. THE THREE STAGES ARE EXPLAINED.
STAGES OF ALCOHOLIC LIVER
DISEASE
7. ALCOHOLIC FATTY LIVER DISEASE IS THE FIRST OF ALCOHOLIC LIVER DISEASE.
DRINKING A LARGE AMOUNT OF ALCOHOL, EVEN FOR ONLY A FEW DAYS, CAN LEAD TO A BUILD-
UP OF FATTY ACIDS IN THE LIVER.
FATTY LIVER DISEASE RARELY CAUSES ANY SYMPTOMS BUT IT IS AN IMPORTANT WARNING SIGN
THAT YOU’RE DRINKING AT A LEVEL THAT IS HARMFUL TO YOUR HEALTH.
FATTY LIVER DISEASE IS REVERSIBLE IF YOU STOP DRINKING ALCOHOL FOR TWO WEEKS, YOUR
LIVER SHOULD RETURN TO NORMAL.
1. ALCOHOLIC FATTY LIVER DISEASE
8. ALCOHOLIC HEPATITIS (NOT RELATED TO INFECTIOUS HEPATITIS) IS THE SECOND, MORE
SERIOUS STAGE OF ALCOHOLIC DISEASE.
PROLONGED ALCOHOL MISUSE OVER MANY YEARS CAUSE THE TISSUES OF THE LIVER TO
BECOME INFLAMED. THIS IS KNOWN AS ALCOHOLIC HEPATITIS.
ALCOHOLIC HEPATITIS IS USUALLY REVERSIBLE IF YOU STOP FOR SEVERAL MONTHS.
2. ALCOHOLIC HEPATITIS
9. CIRRHOSIS IS THE FINAL STAGE OF ALCOHOLIC LIVER DISEASE.
CIRRHOSIS HAPPENS WHEN PROLONGED INFLAMMATION CAUSES SCARRING OF THE LIVER AND
LOSS OF FUNCTION.
LOSS OF LIVER FUNCTION CAN BE LIFE THREATNING.
THE DAMAGE CAUSE BY CIRRHOSIS IS NOT RERVISIBLE.
IN MILD TO MODERATE CASES, STOPPING DRINKING ALCOHOL IMMEDIATELY SHOULD PREVENT
FURTHER DAMAGE AND LEAD TO THE GRADUAL RECOVERY OF LIVER FUNCTION.
IN MORE SEVERE CASES, A LIVER TRANSPLANT MAY BE REQUIRED.
3. ALCOHOLIC CIRRHOSIS
10. HEPATITIS C, FATTY LIVER, AND ALCOHOL ABUSE ARE THE MOST COMMON CAUSES OF
CIRRHOSIS OF THE LIVER, BUT ANYTHING THAT DAMAGES THE LIVER CAN CAUSE CIRRHOSIS,
INCLUDING:
FATTY LIVER ASSOCIATED WITH OBESITY AND DIABETES
CHRONIC VIRAL INFECTIONS OF THE LIVER
BLOCKAGE OF THE BILE DUCT
REPEATED BOUTS OF HART FAILURE WITH FLUID BACKING UP TO THE LIVER
CERTAIN INHERITED DISEASES SUCH AS :
I. CYSTIC FIBROSIS
II. GLYCOGEN STORAGE DISEASES
III. ALPHA 1 ANTITRYPSIN DEFICIENCY
ALTHOUGH LESS LIKELY, OTHER CAUSES OF CIRRHOSIS INCLUDE REACTIONS TO PRESCRIPTION
DRUGS, PROLONGED EXPOSURE TO ENVIRONMENT TOXINS OR PARASITIC INFECTIONS.
AETIOLOGY OF LIVER CIRRHOSIS
11. THE RISK FACTORS PRESENTLY KNOWN ARE:
QUANTITY OF ALCOHOL TAKEN: CONSUMPTION OF 75-100ml/DAY FOR 20 YEARS OR MORE IN MEN, OR
25ml/DAY FOR WOMEN SIGNIFICANTLY INCREASES THE RISK OF HEPATITIS AND FIBROSIS BY 7 TO 47%
PATTERN OF DRINKING: DRINKING OUTSIDE OF MEAL TIMES INCREASES UP TO 2.7 TIMES THE RISK OF
ALCOHOLIC LIVER DISEASE.
GENDER: FEMALES ARE TWICE SUSCEPTIBLE TO ALCOHOL RELATED LIVER DISEASE, AND MAY DEVELOP
ALCOHOLIC LIVER DISEASE WITH SHORTER DURATIONS AND DOSES OF CHRONIC CONSUMPTION.
GENETIC FACTORS: MONOZYGOTIC TWINS ARE MORE LIKELY TO BE ALCOHOLIS AND TO DEVELOP LIVER
CIRRHOSIS THAN ZYGOTIC TWINS.
IRON OVERLOAD: (HEMOCHROMATOSIS)
DIET: MALNUTRITION, PARTICULARLY VITAMIN A AND E
RISK FACTORS
13. SYMPTOMS VARY BASED ON HOW BAD THE DISEASE IS. YOU MAY NOT HAVE SYMPTOMS IN EARLY
STAGES. SYMPTOMS TEND TO BE WORSE AFTER A PERIOD OF HEAVY DRINKING.
SYMPTOMS
14. PAIN AND SWELLING IN THE ABDOMEN
DECREASED APPETITE AND WEIGHT LOSS(RARE)
NAUSEA AND VOMITTING
FATIGUE
DRY MOUTH AND INCREASED THIRST
1.DIGESTIVE SYMPTOMS INCLUDE
15. YELLOW COLOR IN THE SKIN, MUCUS MEMBRANES, OR EYES (JAUNDICE)
SMALL, RED SPIDER-LIKE VEINS ON THE SKIN
VERY DARK OR PALE SKIN
REDNESS ON THE FEET AND HANDS
ITCHING
2.SKIN PROBLEMS SUCH AS:
16. PROBLEMS WITH THINKING, MEMORY AND MOOD
FAINTING AND LIGHTHEADNESS
NUMBNESS IN LEGS AND FEET
3.BRAIN AND NERVOUS SYSTEM
SYMPTOMS INCLUDE:
17. DIAGNOSTIC TESTS
COMPLELETELY BLOOD COUNT (CBC)
LIVER BIOPSY
LIVER FUNCTION TESTS
ABDOMINAL CT SCAN
BLOOD TESTS FOR OTHER CAUSES OF LIVER DISEASE
ULTRASOUND OF THE ABDOMEN
PATIENT SOCIAL HISTORY
18. ABNORMALITY DIAGNOSTIC CHARACTERISTICS
SERUM AST > ALT (RATIO >2,0.
BOTH <300 IU/L
SENSITIVITY & SPECIFICITY
HAVEN’T BEEN WELL STUDIED
ELEVATED SERUM AST SENSITIVITY 50%
SPECIFICITY 82%
ELEVATED SERUM ALT SENSITIVITY 35%
SPECIFICITY 86%
ELEVATED SERUM GGT SENSITIVITY APPROX. 70%
SPECIFICITY APPROX 60-80%
HIGH MCV SENSITIVITY APPROX. 30-50%
SPECIFICITY APPROX.85-90%
ELEVATED CARBOHYDRATE
DEFICIENT TRANSFERRIN
SENSITIVITY APPROX. 60-70%
SPECIFICITY APPROX.80%
INDICATORS-OF-ALCOHOL-ABUSE
19. ABSTINENCE
NUTRITION
MEDICAL THERAPY
CESSATION OF ALCOHOL CONSUMPTION
LIVER TRANSPLANTATION
TREATMENT
20. WONDERBOY KHAWULA AGE(70) WAS ADMITTED IN ADDINGTON HOSPITAL ON 10/07/2017
CHIEF COMPLAINTS
C/O: ABDOMINAL DISTENTION SINCE 4 DAYS.
WEAKNESS SINCE 15 DAYS
DECREASED APPETITE SINCE 15 DAYS
WEIGHT LOSS SINCE 15 DAYS
ON EXAMINATION
PATIENT IS CONSCIOUS AND ORIENTED
NO CYANOSIS/ICTERUS/CLUBBING
B.P-120/80mm Hg
PR-80b/m
PATIENT MEDICAL HISTORY
NOT A K/C/O: HTN/BA/DM
PAST MEDICATION HISTORY
NOT AVAILABLE
SOCIAL HISTORY
ALCOHOLIC
SMOKER
BELONGS TO LOW ECONOMIC STATUS
MARRIED
NON-ALLERGIC
CASE STUDY
21. CBC
Hb----12g/Dl (DECREASED)
RBC---3.2M/MICRO L (DECREASED)
WBC---6700/mm3
ESR---20mm/hr (INCREASED)
LFT
SGOT---169 MICRO L (INCREASED)
SGPT---162 MICRO L (INCREASED)
ALP---58 MICRO L (INCREASED)
ALBUMIN---3.1 gm/dl (DECREASED)
GLOBULIN---21gm
RFT
BUN----12mg/dl
Sr. Cr----0.7 mg/dl
SPECIAL INVESTIGATIONS
HbS ag : NEGATIVE (IMPRESSION)
US ABDOMEN : COARSE TEXTURE
GALL BLADDER : WALL THICKNING
SPLEEN: ENLARGED MASS
DIAGNOSIS: ALCOHOLIC LIVER CIRRHOSIS!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!
LAB INVESTIGATIONS
As the name implies, alcoholic liver disease is liver injury attributed to alcohol abuse
That’s 191 years from today
The liver breaks down alcohol so it can be removed from your body
This process involves breaking down ethanol, the alcohol in wine, beer and liquor. You can name it, I don’t drink by the way.
Some of the by-products of this process are toxic chemicals that, in high concentration, trigger inflammation and injure liver ells
For those who haven’t started yet. Just like me.
And for those who have started, the first treatment of alcohol-induced liver disease is cessation of alcohol consumption.