1. Liver diseases- Yakrut Vikara Dr. Prathamesh V. Karpe
2. Anatomy and physiology A Liver B Hepatic vein C Hepatic
artery D Portal vein E Common bile duct F Stomach G Cystic duct H
Gallbladder
3. Anatomy- 1) 2 anatomical lobe with separate blood supply,
bile-duct & venous drainage. 2) Dual blood supply- 80% PV and
20% H.Artery 3) Liver regenrates fully after partial ressection. 4)
Ressection is based on anatomical lines to preserve Max.
functioning of the liver.
4. Physiology 1) Maintaining core body temperature. 2) pH
balance and correction of lactic acidosis. 3) Synthesis of clotting
factors. 4) Glucose metabolism, Glycolysis, gluconeogenesis. 5)
Urea, Bilirubin formation from protein catabolism. 6) Drug &
Hormone metabolism and excretion. 7) Removal of gut endotoxins
& Foreign antigen.
5. Normal LFTs 1 Blirubin 5 7 mol /L 2 Alkaline phosphatase
(ALP) 35 130 IU/L 3 Alanine transaminase (ALT) 5 40 IU / L 4
Asparate transaminase (AST) 5 40 IU / L 5 Gamma-Glutamyl
transpeptidase 10 48 IU / L 6 Albumin 35-50 g/L 7 Prothrombin time
(PT) 12 16 secs
6. ALT and AST Enzymes, found in Hepatocytes Released when
liver cells damaged ALT is specific for liver injury AST (SGOT) is
also found in skeletal and cardiac muscle
7. Transaminitis: < 5 x normal ALT predominant Chronic Hep B
/ C Acute A-E, EBV, CMV Steatosis / Steatohep Hemochromatosis
Medications / Toxins Autoimmune Hepatitis Alpha-1-antitrypsin
Wilsons Disease Celiac Disease AST predominant Alcohol-related
liver dz Steatosis/ Steatohep Cirrhosis Non-hepatic source
Hemolysis Myopathy Thyroid disease Strenuous exercise
8. Severe AST & ALT Elev: >15x Acute Viral Hepatitis
does not predict outcome Bili > 20 poor prognosis Ischemic
Hepatitis hypotension sepsis hemorrhage MI Autoimmune Hepatitis
Wilsons Disease Acute bile duct obstr Hepatic Artery ligation
Budd-Chiari Syndrome Medications / Toxins acetaminophen CCl4
9. ALKALINE PHOSPHATASE Found in hepatocytes that line the bile
canaliculi Level is raised in Biliary obstruction (causes stretch
of the bile canaliculi) BUT also found in BONE and PLACENTA GGT is
also found in bile canaliculi and therefore can be used in
conjunction with Alk Phos for predicting liver origin BUT GGT can
be raised by many drugs including Alcohol and therefore non
specific
10. BILIRUBIN Water insoluble product of heme metabolism Taken
up by liver and conjugated to become water soluble so it can be
excreted in bile and into bowel. Patient looks Jaundiced if
bilirubin >2.5 If patient is vomiting GREEN, then they have
bowel obstruction below the level of the Ampulla of Vater.
11. WHAT IS THE DEAL WITH DIRECT AND INDIRECT BILIRUBIN?
Prehepatic disease (eg hemolysis) causes high bilirubin which is
non conjugated ie. Indirect fraction higher Hepatic disease causes
increased conjugated and unconjugated bilirubin Post hepatic
disease eg. Gallstones have increased conjugated (direct) bilirubin
and lead to dark urine and pale stool.
12. PROTHROMBIN TIME/INR Measure of the Vitamin K dependent
clotting factors ie. II, VII, IX and X. The liver is involved in
activating Vitamin K. Therefore in liver damage, these clotting
factors cannot be produced. Before you believe that prolonged INR
is due to liver disease just make sure the patient has adequate
Vitamin K by giving 10mg sc. Giving Vitamin K has no effect on INR
if patient has impaired synthetic function.
13. ALBUMIN Albumin has a half life of 21 days, so the drop
that occurs with hepatic dysfunction does not occur acutely That
said, acute illness can cause albumin to drop rapidly a process
thought to be due to cytokines increasing the rate of albumin
metabolism HOWEVER, dont forget that low albumin also occurs in
NEPHROTIC syndrome, so always check the urine for protein.
14. TYPICAL PATTERNS HEPATOCELLULAR Increased transaminases
Viral Hepatitis Drugs/alcohol Autoimmune NASH Hemochromatosis
CHOLESTATIC Increased Alk Phos and Bilirubin Also may cause
increased transaminases Gallstones Primary Biliary Cirrhosis
Sclerosing Cholangitis Pancreatic C/a
16. Clinical features Early stage- no objective sign, severe
liver dysfunction Onset of clinical jaundice + neurological
signs(hepatic encephalopathy)- drowsiness, confusion, coma
17. Treatment 1) Fluid balance and electrolytes 2) Acid base
balance and blood glucose monitoring 3) Nutrition 4) Renal function
(hemofiltration) 5) Respiratory support ( ventillation) 6)
Monitering and treatment of cerebral oedema 7) Treat bacterial and
fungal infection 8) Liver transplant
18. Chronic liver disease Lethargy and weakness Jaundice
(inability to metabolise bilirubin) Hyperdynamic circulation with
High cardiac output, large pulse volume, low BP, flushed warmed
extremities Fever- due to inflammation and cytokinin released from
the diseased liver or bacterial infection. Skin changes spider
naevi, palmar erythema, white nails Endocrinological hypogonadism
and gynaecomastia. Hepatic encaphalopathy- mental derrangement-
memory impairement, confusion, personality changes, altered speech
pattern, slow slurred speech, flapping tremors (Asterixis).
Abdominal distention due to ascitis Protein catabolism- coagulation
defect, skin bruising
19. Portal hypertension Causes 1)Prehepatic- PV abnormality
before entering into liver, ex- portal vein thrombosis, splenic
vein thrombosis, congenital atresia. 2) Intrahepatic- liver
cirrhosis, malignancy of liver, polycystic liver (in the liver
causes) 3) Post hepatic- above liver causes- Right sided heart
failure, Budd chiari syndrome
20. Liver cirrhosis Alcohol is commonest cause Viral hepatitis
(B and C commonly) Injury- alcohol, virus (B&C), prolonged
cholestasis Autoimmune (lupoid hepatitis) Metabolic disorders-
hemochromatosis, wilsons disease, - antitrypsin deficiency.
21. 4 Stages Liver cell necrosis Inflammatory cell infiltate
Fibrosis Nodular regeneration which may be macronodular (alcohol),
micronodular (viral) or mixed
22. What is portal HTN? Portal pressure above 5 mm Hg 8-10mm Hg
pressure is required to stimulate porto-systemic collaterisation
Collateral network through coronary vein & short azygous vein
leads to Oesophageal and gastric varices. Recanalised umbilical
vein from the left portal vein to the epigastric venous system-
Caput medusae Retroperitoneal collateral network- hemorrhoidal
veins- hemerrhoids.
23. volume of Portal vein flow is regulated indirectly by
vasoconstriction and vasodilatation of the splanchic Arterial bed.
Hepatic arterioles responds to catecholamines & sympathetic N.
stimulation thus Hep. Art flow is directly regulated. In decreased
Portal flow, hepatic blood flow is kept near to normal as possible
by hepatic Arterial autoregulatory or buffer response.
24. cf Non-specific complaints Weight loss Malaise, weakness
Past H/o alcoholism- chronic Complicated biliary disease Exposure
to hepato-toxins
26. Investigations 1. Anaemia- hemmorhage, nutritional
deficiency, hemolysis, bone marrow depression, alcholism. 2.
Platlet count 3mg/100ml 9. Hepatitis serology B&C 10. Hep A
causes acute liver disease 11. HCC secondary to Hep B and C 12. HCC
elevated Alpha feto protein level 13. CT abdomen 14. Sr.
Electrolytes hypo NA,K, Metabolic Alkalosis
27. Metabolic disorders secondary to hypoaldosteronism,
Diarrhoea and recurrent emesis. Conversion of NH3cl to NH3+
cerebraltoxincrosses blood brain barrier encaphalopathy- coma Liver
biopsy Hepatic veinous wedge pressure assessment USG Doppler
USG
28. Pharmacotherapy Betablockers- propanolol Betablockers+long
acting nitrates(isosorbide 5-mononitrate) more effective than
variceal ligation and alone betablockers.
29. Acute bleeding BT minimum 6 units Ballon tamponade
Endoscopic band ligation Scleronizing agent injection Drugs-
sphlenchic vasoconstrictor- somatostatin 250g iv bolus followed by
continuous infusion 250g/hr 2-4 days Octreotide- 50g iv bolus,
25-50g/hr continuos infusion 2-4 days Combination of endoscopic
procedure and octreotide injection is more effective
30. Vasopressin- 20 IU for 20 mins followed by 0.2-0.4 IU/min,
used with Nitroglycerin- 40g/min and then titrted to achieve BP
control. Adverse effect of vasopressin 1)MI 2) limb/mesenteric
ischemia 3)Arrythemia
31. Terlipressin, Somatostatin,Octreotide are safer option and
more effective. Vit.K injection 10mg IV IV olloid solution till BT
is done TIPS Shunting
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38. General features / / // ../
39. chikitsa repeatedly virechana madhura gana dravya siddha
ghrita snehan and virechan with shyama,triphala,trivrutta siddha
ghrita. Aasthapan basti and anuvasan basti- nyagrodhadi gana
kashaya after mixing with adequate quantity of honey, sugar and
ghrita. Upanaha prepared from payasa should be applied on abdomen
Diet- Vidarigandhadi siddha payasa
40. Plihodara & yakrutodara Rx After performing
snehan-swedan, patient is made to eat curd-rice and after consuming
food siravedh is performed from left kurpar sandhi (elbow), medial
side vein should be punctured. Massage gently on phliha to let more
blood out. Yakrutodar- right kurpar sandhi Agnikarma- daha with
shara after flexing left wrist joint, the vein which is heading
towards the thumb.
41. After samyak shodhan- samudrashukti kshar with milk is
given. Hingu + sarjikshar with milk internally Palash kshar and
yavakshar together with milk Palashapushpa ksharodak with
yavakshar. Parijatak+kekshuraka(talamkhana)+apamarga kshar
Shobhanjana kwatha with taila, pipplai, saindhav and chitrak
Putikaranja kshar mixed with kanji and vid-lavana and pipplai in
large quantity. Shatpala ghrita Varangak kshara Yakrutphlihari
loha