1. Hepatic Encephalopathy
By Charis Conradi

2. Overview
Name
Epidemiology
Classification
Treatment
Future
Sources

3. What is HE Heaptic= Liver Encephalo = brain -pathy = disorder
 „spectrum of neuropsychiatric abnormalities in patients with liver dysfunction”
Blood test – ammonia concentration
characterized by personality changes, intellectual impairment, and a depressed level of consciousness
Normal ammonia level : The lower limit of the reference range is μmol/L.
The upper limit of the reference range is μmol/L

4. Epiology accumulation in the bloodstream of toxic substances
Excessive nitrogen load
Drugs and medications
Excessive alcohol consumption
Infections
portosystemic shunt surgery
Unknown 20-30%

5. Liver functions Protein metabolsim Carbohydrate metabolism
Fat metabolsim
Bile production
Vitamin storage
Fibrinogen, prothrombin, factor VII (vitamin K dependent)
Excrition of Hormones and Drugs
Protein metabolism : Deamination of amino acids, UREA formation
Plasma protein formation ( 90%)
Carobohydrate metabolism: Glycogen storage
Conversion of galactose and fructose to glucose
Gluconeogenesis
Fat metabolism : Synthesis of cholesterol, lipoproteins
Vitamin Storage : A retina : combines with protein opsin to form rhodopsin = rod photoreceptors thus function in case of less light situations ; D : needed for calcium and phosphate regulation, enhances mineralization of bone; B12
Hormons: steroid hormons – estrogen, cortisol, aldosterone

6. Epidemology
total deaths worldwide from cirrhosis and liver cancer rose by 50 million per year over 2 decades, according to the first-ever World Health Organization (WHO) study of liver disease mortality.4
Alcohol-attributable liver cirrhosis deaths per 100,000 people in 2010 by global-burden-of-disease region

7. Causes Liver failure observed in nearly 70% of patients with cirrhosis
acute  onset between 7 and 28 days
chronic
observed in nearly 70% of patients with cirrhosis
24-53% of patients who undergo portosystemic shunt surgery
Liver failure : liver become damaged beyond repair and the liver is no longer able to function, occurs gradually and over many years Hepatitis B Hepatitis C Long-term alcohol consumption
Acute :rapid development of hepatocellular dysfunction

8. from liver failure to brain damage
Nitrogen compounds  portal vein urea cycle  excreted by kidney
impaired due to damaged hepatocytes or due to portosystemic shunts (venous blood bypasses the liver)  Nitrogenous waste products accumulate in the systemic circulation
ammonia (NH3)  blood brain barrier
organic compounds containing amine (-NH2) and carboxylic acid (-COOH) functional groups, usually along with a side-chain specific to each amino acid.[1][2][3] The key elements of an amino acid are carbon, hydrogen, oxygen, and nitrogen
small molecule crosses the blood–brain barrier and is absorbed and metabolised by the astrocytes, a population of cells in the brain that constitutes 30% of the cerebral cortex. Astrocytes use ammonia when synthesising glutamine from glutamate.

9. NH3 Astrocytes : glutamine glutamate
Increased amount of glutamine Increased osmotic pressure  brain edema
small molecule crosses the blood–brain barrier and is absorbed and metabolised by the astrocytes, a population of cells in the brain that constitutes 30% of the cerebral cortex. Astrocytes use ammonia when synthesising glutamine from glutamate. The increased levels of glutamine lead to an increase in osmotic pressure in the astrocytes, which become swollen. There is increased activity of the inhibitory γ-aminobutyric acid (GABA) system, and the energy supply to other brain cells is decreased. This can be thought of as an example of brain oedema of the "cytotoxic" type.[10]

10. Stages - West Haven Criteria
Grades
State of consciousnes
Intellectual function
Personality behavior
Neuromuscular disorders 1
Trivial lack of awareness
Sleep disorder
Shortened attention span
 Euphoria or depression
Asterixis
tremor 2
Lethargy
„forgefulness“
Disorientation to time Amnesia of recent events
Inappropriate behavior  Anxiety
-Slurred speech  -Hyperactive reflexes 3
Somnolence ( sleepiness) to stupor
Confusion  Gross disorientation
Bizarre behavior
Babinski relfex, rigidity 4
Coma (unresponsive to verbal/noxious stimuli)
Unable to test
Asterixis : flapping tremor (patient in front of you, wrist extended! Physician further extends patiends hands which leads to a uncontrolled flapping tremor!!! Either symmetric or asymmetric
Stupor is the lack of critical cognitive function and a level of consciousness wherein a sufferer is almost entirely unresponsive and only responds to base stimuli such as pain.
Babinski reflex is one of the normal reflexes in infants. Reflexes are responses that occur when the body receives a certain stimulus.
The Babinski reflex occurs after the sole of the foot has been firmly stroked. The big toe then moves upward or toward the top surface of the foot. The other toes fan out.

12. Treatment Type 1 due to acute liver failure Type 2 (bypass)
Intubation
Transplantation
Type 2 (bypass)
Occlusion of bypass
Type 3 (infections)
Antibiotics

13. Perspective
Multiple causes
Vaccination
Less alcohole consumption

14. Sources
criteria
normal Nh3 levels
Gython and Hall Textbook of physiology
Medscape : Hepatic Encephalopathy 
Medscape : Global Burden of Liver Disease Substantial

15. https://www. google. com/search
( babinski relfex)