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Shodhana Chikitsa in Liver Disease & Diseases of the Hepatobiliary tract
1. DR.PRASHANTH.A.S
Professor and Head
Department of Post Graduate
Studies in Kayachikitsa
Ayurveda Maha Vidyalaya
Hubli, Karnataka – 580024
Mob: +91-94481-35575
Mail: drprashanthas@gmail.com
2. • Liver is a large solid gland
• Occupies rt. Hypochondria, epigastrium, lt.
hypochondria
• 2 lobes- right and left
• Functional unit are the lobules, each lobule consists
of hepatocytes
• Portal Triad- Hepatic artery, Portal vein and Bile duct
LIVER AN OVERVIEW
4. Importance of Digestive System
Ayurveda says seven tissues are harboring in
the body as primitive anatomical structure. These are Rasa,
Rakta, Mamsa, Meda, Asthi, Majja, Sukra. Out of them Rasa
is the first one. It is the precursor. It moves throughout the
body to facilitate required nutrition to other anatomical
integrity like Rakta, Mamsa etc. and work like a feed back.
5. CONCEPT OF AGNI
Food Substances
Jataragni
Ahara Rasa Ahara Mala
Bhutagni
Poshaka Rasa
Dhatu Poshya
Dhatwagni
Dhatu
Poshaka UpaDhatu
6. HEPATO – BILLIARY SYSTEM
MAJOR MANIFESTATION OF LIVER DISEASE
• Viral hepatitis
• Ascities
• Alcoholic liver disease
• Cirrhosis of the liver
• Fatty Liver changes
• Diminished Liver Function
GALLBLADDER & OTHER BILLIARY DISEASES
• Gallstone
• Cholecystitis
• Tumors of gallbladder and bile duct
7. DIMINISHED LIVER FUNCTION
• Liver failure is the inability of the liver to perform its
normal synthetic and metabolic function as part of normal
physiology.
• Chronic liver failure usually occurs in the context of cirrhosis,
itself potentially the result of many possible causes, such as
excessive alcohol intake, hepatitis B or C, autoimmune, hereditary
and metabolic causes
Common Symptoms
•Yellowish discoloration of skin which is obvious
•Yellowish discoloration of eyes (icterus)
•Pale stools
•Dark or black urine
•Nausea and vomiting
•Abdominal distension primarily due to fluid (Ascites)
•Excessive Fatigue
•Itchy skin, Dry skin
8. VIRAL HEPATITIS
• Hepatitis implies inflammation of
the liver characterized by the presence
of inflammatory cells in the tissue of the organ.
• Symptoms may include malaise, muscle and join
aches, fever, nausea or vomiting, diarrhea,
headache, profound loss of
appetite, aversion to smoking among smokers, da
rk urine, yellowing of
the eyes and skin (i.e., jaundice) and abdominal
discomfort. Physical findings are usually
minimal, apart from jaundice (33%) and
tender hepatomegaly (10%). There can be
occasional lymphadenopathy (5%)
or splenomegaly (5%).
9. ALCOHOLIC LIVER DISEASE
• Alcoholic hepatitis is inflammation of the
liver due to excessive intake of alcohol, it is
regarded as the earliest stage of alcoholic
liver disease.
• Alcoholic hepatitis is characterized by a
variable constellation of symptoms, which
may include feeling unwell, enlargement of
the liver, development of fluid in the
abdomen (ascites), and modest elevation of
liver enzyme levels (as determined by liver
function tests).
10. FATTY LIVER
• Fatty liver, also known as fatty liver
disease, is a reversible condition where
huge large vacuoles of triglyceride fat
accumulate in liver cells via the process
of steatosis.
• Despite having multiple causes, fatty
liver can be considered a
single disease that occurs worldwide in
those with excessive alcohol intake and
those who are obese.
11. LIVER CIRRHOSIS
• Cirrhosis is a consequence of
chronic liver disease characterized
by replacement of
liver tissue by fibrosis,scar tissue
and regenerative nodules leading to
progressive loss of liver function.
• Causes include Alcoholic Liver
Disease, Chronic Hepatitis etc
12. CHOLECYSTITIS
• Cholecystitis is inflammation of the gall
bladder.
• Cholecystitis is often caused by the
presence of gallstones in the gallbladder,
with choleliths most commonly blocking
the cystic duct directly. This leads to
inspissation (thickening) of bile, bile stasis,
and secondary infection by gut organisms,
predominantly E.coli and Bacteroides species.
• Symptoms include pain in the right upper
quadrant and some time high fever, shock
and jaundice
13. Gall stones
• Gallstones can occur anywhere within
the biliary tree, including the gallbladder and
the common bile duct.
• Researchers believe that gallstones may be
caused by a combination of factors, including
inherited body chemistry, body
weight, gallbladder motility (movement), and
perhaps diet.
• Gallstones usually remain asymptomatic
initially. A main symptom is biliary colic, in
which a person will experience intense pain in
the upper abdominal region that steadily
increases for approximately thirty minutes to
several hours. Nausea and vomiting may
occur.
14. • Normal level of Bilirubin is .5 – 1 mg/dl
• Jaundice clinically manifest if S. Bilirubin > 3mg/dl
• Skin becomes yellowish, in long standing cases even
greenish- bilirubin oxidized to Biliverdin
• Differentiate from Carotenoderma
• Bilirubin formed by breakdown of haeme
• It is formed in the RE cells of Liver & Spleen
JAUNDICE
15. CLASSIFICATION OF JAUNDICE
• Unconjugated hyperbilirubinamia
• A) increased production of bilurubin without
haemolysis(shunt hyperbiliruninamia)
• B)increased production of bilirubin due to haemolysis
• Intrinsic defects of RBCs
• Extrinsic factors leading to increased haemolysis
• C) impaired uptake of bilurubin into liver
- Gilbert disease, sickle cell anemia
• D) impaired conjugation
-Cligler-naffar syndrome
17. B) intra hepatic cholestasis
C) extra hepatic biliary obstruction
• Gall stones, parasites
• Pancreatitis , strictures
• Tumors, hydait cysts
18. COMPLICATION OF JAUNDICE
1.Obstructive Jaundice
• Skin pigmentation, pruritis, skin thickening, xanthoma
• Defective absorption of fat & fat soluble vitamins
• Copper accumulates in the Liver
• Hepatocellular necrosis, hepatic failure
• Renal failure
2.Hemolytic Jaundice
• Damage to NS in case of newborn
• Excess bilirubin in bile causes formation of pigment gall
stones
19. Bilirubin metabolism
• Bilirubin is the end product of hemedegradation. The majority
of daily production (0.2-0.3mg/dl) is derived from break down of
senescent erythrocytes by the mononuclear phagocytic system,
especially in liver, spleen and bone marrow. Most of the
remaining bilirubin is derived from the turnover of hepatic heme
or hemeprotein (P450 cytochromes) and from premature
destruction of newly formed erythrocytes in the bone marrow.
Bilirubin metabolism and excretion can be explained through
following steps.
• Step 1 In Extrahepatic circulating heme oxygenase oxidizes
heme to biliverdin, which is then reduced to bilirubin by
biliverdin reductase.
20. Step 2 Bilirubin thus formed outside the liver is
released and bound to serum albumi. Albumin binding
is necessary, since bilirubin is virtually in soluble in
aqueous solution. The very small fraction of unbound
bilirubin in plasma may increase in hemolytic disease or
when protein bound binding drugs displace bilirubin
from albumin.
Step 3 Hepatic processing of bilirubin involves carrier
mediated uptake at the sinusoidal membrane
Step 4 Conjugation occurs with one or two molecules
of glucuronic acid which is catalysed by bilirubin UDP
glucuronyl transferase (UGT1A1) in the endoplasmic
reticulum followed by excretion of the water soluble,
non toxic billirubin glucuronide into the bile.
21. • Step 5 Most bilirubin glucuronides are deconjugated
by bacterial b glucuronidases and degraded to colourless
urobilinogens. The urobilinogen and the residue of intact
pigment are largely excreted in faeces. Approximately
20% of urobilinogen formed are reabsorbed in the ileum
and colon, returned to liver and promptly reexcreted into
bile (enterohepatic circulation). Small amount of
urobilinogen escapes this circulation and is excreted in
urine.
22. LIVER FUNCTION TESTS
• Detect the presence of liver disorders
• Distinguish among different types of liver disorder
• Gauge the extent of known liver damage
• Follow the response to treatment
• Serum bilurubin (0.2 to 1.2 mg/dl)
• Test of excretion by liver
• Increased conjugated bilirubin – hepatic/post
hepatic
• Increased unconjugated bilirubin - prehepatic
23. SGOT/AST (aspartate aminotransferase)
SGPT/ALT (alanine aminotransferase)
evaluation of enzyme activity
• In non hepatic causes SGOT levels tend to be
appreciably higher than SGPT level
• In liver disorders both tend to show similar raises
• In alcoholic hepatitis it is not uncommon to find
SGOT several times the upper limits of normal with
SGPT level in normal range
24. ALP (25 – 85 IU/dl)
• Enzyme that reflect cholestasis
• GGT (gamma glutamyl transpeptidase)
• 5’ nuclotidase
• Prothrobin time
• Serum albumin – (3.5 to 5.5 g/dl)
• Serum globulin (2 – 3.5 g/dl)
• A/G ratio (1.5 to 3.1)
25. Liver biopsy
• Not inacute hepatitis
• Helps in grading and staging of liver diseases
• Unexplained hepatomegely
• Malignancies and tumors
• PUO
• USG
• CT, MRI
• ERCP – Endoscoping retrograde cholengio
pancreatography
26. Ayurvedic Points…
• In Ayurveda there is no proper explanation
of Liver diseases.
• There is explanation of Kamala ,
Yakrutodara,. But no proper explanations
regarding the liver as the pathological
condition.
27. KAMALA
• Panduroga bedha
• One of chaturvimshathi pitta vikaras
• One of rakta doshaja rogas
• “Kamam asham lathi ithi kamala”
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29. samprapti
• Yakrit according to ayurveda is mentioned as the
moola of Raktha vah srothas and kamala as a
disease of raktha vaha srothas more over kamala
belongs to the category of pittja vyadhi and
Ranjaka pitta is a type of pitta that is involved in
its pathogenesis.The seat of ranjaka pitta is liver.
• The outcome of sanga in ranjaka pitta marga ,is
vimarga gamana of pitta to shakha producing the
characteristic symptoms of kamala.
30. samprapti
• Koshtasritha kamala is Bahu pitta because in this type of
kamala, there is Swabhavata vrudhi of pitta due to its own
prakopa hethus. This is a point of defference between
Bahupitta kamala shakhashritha kamala.
• As per sushrutha , those persons who immediately after
getting cured of pandu take amla ahara or other pitta
prakopa apathya, prakupitha pitha leads to mukha
pandutha,tandra,and bala kshaya. In koshtasritha kamala
samprapthi, prakupitha pitta does dusti of rakta and
mamsa . By definition it means dahana modern authors
remind us heamolysis in this type of kamala .
34. VIRECHANA
• YAKRIT IS THE MOOLA OF
RAKTAVAHA SROTAS.
• KAMALA IS A RAKTAPRDOSHAJA
VIKARA.
• VIRECHANA IS THE PREFFERED
SHODHANA THERAPY.
35. VIRECHANA
• MRIDHU VIRECHANA
• VIRECHANA DRAVYA – TIKTA RASA
PRADHANA
• KATUKI- AS A BHEDAKA DRAVYA
• SUSHRUTA-TRIBHANDI, SARKARA,
SHUNTI
36. VIRECHANA IN SAKHASRITA
KAMALA
• INITIAL TREATMENT – KAPHAHARA.
• VIRECHANA WHEN THE MALA TURNS
TO THE NORMAL COLOUR.
• VIRECHANA – A PREFFERED
SHODHANA IN YAKRITODARA.
41. VAMANA
• PREFERRED WHEN THE LIVER
DISORDER ASSOCIATED WITH PANDU
OF SANTARPANA ORIGINE.
• IN OTHER CONDITIONS TO BE
ADAPTED DEPENDING ON THE
CONDITION
48. Dr. PRASHANTH. A. S. M.D. (Ay), (Ph.D.),
PROFESSOR
DEPARTMENT OF POST GRADUATE STUDIES IN KAYACHIKITSA
AYURVEDA MAHAVIDYALAYA, HUBLI (KARNATAKA)
Cell: 09448135575 drprashanthas@gmail.com
For further details:
Ayurveda Mahavidyalaya, Hubli
