The document discusses liver failure and its types, causes, clinical features, and management. It covers topics like acute liver failure, acute-on-chronic liver failure, hepatic encephalopathy, complications of cirrhosis including ascites and variceal bleeding, and criteria for liver transplantation. Key points are acute liver failure can result from infections, drugs, ischemia, while cirrhosis leads to complications managed through treatments like TIPS procedure, antibiotics for SBP, and vasopressors for HRS. Liver assist devices help improve organ function and cerebral/renal parameters in acute liver failure.
neonatal sepsis is commonest cause of death in neonatal period,but it is preventable by prevention,timely recognition appropriate antibiotics and supportive care.
neonatal sepsis is commonest cause of death in neonatal period,but it is preventable by prevention,timely recognition appropriate antibiotics and supportive care.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
2. LIVER STRUCTURE AND BLOOD SUPPLY
• LARGEST ORGAN OF BODY.
• WEIGHT 1-1.5 KG. RECIEVES 25% OF CARDIAC OUTPUT.
• CONTAINS SINUSOIDS WHICH ARE COMPOSED OF FENESTRATED
ENDOTHELIAL CELLS ,KUPFFER CELL,STELLATE CELL AND NATURAL KILLER
CELL.
• ENDOTHELIAL CELLS : 50% OF SINUSOIDAL CELLS.FUNCTIONS INCLUDES
ENDOCYTOSIS,SECRETION(INTERLEUKIN,INTERFERON,ENDOTHELIN,AND
NITRIC OXIDE)
• KUPFFER CELLS :PHAGOCYTIC.
• STELLATE CELLS: LIPOCYTE ,FAT STORING CELL OR ITO CELLS.
• NATURAL KILLER CELLS: LIVER ASSOCIATED LYMPHOCYTES.
7. TYPES OF LIVER FAILURE
1. ACUTE LIVER FAILURE
2. ACUTE ON CHRONIC LIVER FAILURE
8. ACUTE LIVER FAILURE
• ABRUPT AND RAPID DETERIORATION IN LIVER FUNCTION WITHOUT
PRIOR LIVER DISEASE.
• INCLUDES 3 PARAMETER:
1.DEVELOPMENT OF JAUNDICE.
2.COAGULOPATHY,INR>1.5.
3.ALTERED MENTATION OF ANY GRADE.
9. CLASSIFICATION OF ACUTE LIVER FAILURE
• O GRADY CLASSIFIED INTO 3 CATEGORIES.
• DEPENDS UPON DURATION BETWEEN THE ONSET OF JAUNDICE AND
ENCEPHALOPATHY WITHOUT PREEXISTING CIRRHOSIS AND WITH AN
ILLNESS OF <26 WEEKS.
1.HYPERACUTE LIVER FAILURE: <7 DAYS (G00D SURVIVAL RATE)
2.ACUTE LIVER FAILURE : 7-28 DAYS.
3.SUB ACUTE LIVER FAILURE : 5-12 WEEKS (WORST PROGNOSIS).
11. 1.INFECTIONS
SYSTEMIC INFECTION AFFECTING THE LIVER BY HEP A,C,D,E (RNA VIRUS)ONLY
HEP B (DNA VIRUS)
IN THIS FEVER WITH JAUNDICE.
FROM ASYPTOMATIC TO INAPPARENT TO FULMINANT FATAL INFECTIONS.
2.ISCHAEMIC CONGESTIVE HEPATOPATHY
COMMONEST CAUSES OF DERRANGED LFT IN ICU.
PREDISPOSING FACTOR ARE SHOCK,HAEMORRHAGE,DEHYDRATION,HEAT
STROKE,AORTIC DISSECTION,PULMONARY EMBOLUS,CARDIOGENIC SHOCK.
PREDISPOSING FACTOR FOR CONGESTIVE HEPATOPATHY
ISCHAEMIC CARDIOMYOPATHY,HEART FAILURE,MITRAL VALVE
STENOSIS,TRICUSPID REGURGITATION.
PEAK ELEVATION IN FIRST 72 HR.
FACTOR RESOLVES NORMALISES LFT IN 7-10 DAYS.
TREATMENT BY IMPROVE CARDIAC STATUS AND ORGAN PERFUSION.
12. 3.SEPSIS INDUCED LIVER DYSFUNCTION
• BY RELEASE OF BACTERIAL AND INFLAMMATORY MEDIATOR.
• IN SEPSIS
1.BACTERIAL AND LIPOPOLYSACCHARIDES INHIBIT TRANSPORTER WHICH
TRANSPORT BILE SALT AND BILIBURIN IN BILE CANALICULI CAUSES
CHOLESTASIS.
2.ENDOTHELIAL CELL PRODUCE CYTOKINES (TNF,IL-1,IL-6 )AND NITRIC
OXIDE PRODUCTION.
3.RELEASE OF OXYGEN FREE RADICAL PROTEASE AND ELASTASE.
. ABNORMAL JAUNDICE ,LFT AFTER 2,3 DAYS.LIVER ENZYMES>3
TIMES,BILURUBIN >5 TIMES.
TREATMENT WITH SUPPORTIVE AND ANTI BIOTICS THEARAPY
15. ACETAMINOPHEN
• MOST COMMON CAUSE OF DRUG INDUCED HEPATIC DYSFUNCTION.
• UPTO 4GM/DAY IS SAFE IN HEALTHY INDIVIDUAL.
• 95 PERCENT ELIMINATED BY HEPATIC CONJUGATION.
• 5 PERCENT IS CONVERTED TO N- ACETYL- P- BENZOQUINONE-
IMINE(NAPQI).IT INACTIVATES WITH GLUTAHIONE AND EXCRETES.
• GLUTATHIONE STORES DEPLETED AND NAPQI IS HIGHLY TOXIC AND
CAUSES LIVER NECROSIS.
16. TOXICITY PRESENT IN THREE PHASES:
FIRST PHASES :GI SYMPTOMS OF NAUSEA,VOMITING AND
ABDOMINAL PAIN IN FIRST FEW HOUR AFTER INGESTION.
SECOND PHASE(24-72 HR):MARKED ELEVATION OF LIVER
ENZYMES.
THIRD PHASES(72-96 HR):JAUNDICE AND ENCEPHALOPATHY.
ANTIDOTE:
NAC 150 MG/KG OVER 1 HOUR FOLLOWED BY 12.5 MG/KG/HR
FOR 4 HR THEN 6.25 MG/KG/HR FOR 67 HRS
17. ACUTE FATTY LIVER OF PREGNANCY
• PRESENT BETWEEN 30-38 WEEKS OF GESTATION.
• SYMPTOMS INCLUDE MALAISE HEADACHE,NAUSEA,VOMITTING.
• HELLP SYNDROME
• HAEMOLYSIS ,ELEVATED LIVER ENZYMES LOW PLATELET COUNT.
18. TOTAL PARENTERAL NUTRITION
• ON PROLONGED PARENTERAL NUTRITION (BEYOND 2 WEEKS).
• MORE COMMON IN INFANT THAN ADULT.
• LIPID EMULSIONS > 1GM/KG/DAY DEVELOP ACUTE LIVER DISEASE.
• SOYABEAN OIL DERIVATIVE LIPIDS EMULSION CONTAINS OMEGA 6
POLYUNSATURATED FATTY ACIDS STIMULATE PROINFLAMMATORY
RESPONSE AND INHIBIT BILIARY SECRETION.
20. HEPATIC ENCEPHALOPATHY
• SPECTRUM OF NEUROLOGIC OR PSYCHIATRIC ABNORMALITY
RESULTING FROM LIVER INSUFFICIENCY OR PORTOSYSTEMIC
SHUNTING.
• SUBTYPES DUE TO UNDERLYING DISEASES:
1.ACUTE LIVER FAILURE.
2.PORTOSYSTEMIC SHUNTING.
3.CIRRHOSIS.
IN ACUTE LIVER FAILURE RISK OF CEREBRAL OEDEMA WITH INCREASE
ICP AND CEREBRAL HERNIATION.
22. IN HIGH GRADE HEPATIC ENCEPHALOPATHY ARTERIAL
AMMONIA LEVEL USEFUL.
1.LEVEL>100 MICROMOL/L PREDICT SEVERE
ENCEPHALOPATHY.
2.LEVEL >200 MICROMOL/L IS ASSOCIATED WITH
INTRACRANIAL HYPERTENSION IN HALF CASES.
3.LEVEL> 122 MICROMOL/LITRE FOR 3 DAYS (POOR
PROGNOSIS)
24. DUE TO INCREASED AMMONIA CAUSES
PRODUCTION OF GLUTAMINE IN ASTROCYTES
WHICH CAUSES INCREASE OSMOTIC ACTION AND
CAUSES BRAIN OEDEMA CAUSES LOSS OF
CEREBRAL AUTOREGULATION AND ITS
COMPLICATIONS
INTRACRANIAL HYPERTENSION AND BRAIN
HERNIATION.
25. MEDICAL THERAPY TO CONTROL
ENCEPHALOPATHY AND CEREBRAL OEDEMA
• NEUROLOGICAL SUPPORT.
• INTRACRANIAL PRESSURE MONITORING.
• JUGULAR BULB VENOUS SATURATION MONITORING.
• OSMOTHERAPY.
• THIOPENTONE.
• HYPOTHERMIA.
• PROPHYLACTIC PHENYTION.
• HYPERVENTILATION.
• AMMONIA LOWERING STRATEGIES.
• LOLA (L ORNITHINE L ASPARTATE).
• L ORNITHINE PHENYLACETATE.
• SODIUM BENZOATE.
• RIFAXIMIN.
26. 1.INTRACRANIAL PRESSURE MONITOR:
BY EPIDURAL TRANSDUCER.
GOAL IS TO MAINTAIN AN ICP <20 MM HG.
ICP>40 MM HG FOR 2 HR (CONTRAINDICATION FOR LIVER
TRANSPLANT)
2.JUGULAR BULB VENOUS STAURATION MONITORING:
CATHETER IN JUGULAR BULB.
SJVO2<55 % ISCHAEMIC BRAIN.
SJVO2>85 % HYPEREMIC BRAIN
3.OSMOTHERAPY:
INTRAVENOUS BOLUS OF MANNITOL (0.5-1 MG/KG 20%SOLUTION
OVER 5 MINS.
HIGH DOSES CAUSES ACUTE RENAL FAILURE AND DAMAGE BBB.
27. 4.THIOPENTONE:
LOADING DOSE 3-5 MG/KG OVER 15 MINS
CONTINUOUS INFUSION AT 0.5-2.0 MG/HR.
5.HYPOTHERMIA:
REDUCES CBF CEREBRAL METABOLISM
AMMONIA UPTAKE BY BRAIN GLUTAMINE
SYNTHESIS REDUCES ICP.
28. 6.LACTULOSE(NON ABSORBABLE DISACCHARIDES)
1.THEY DECREASE COLONIC TRANSIST TIME
REDUCES OPPORTUNITY FOR ABSORPTION OF
GUT DERIVED AMMONIA
2.NON ABSORBABLE DISACCHARIDES LOWERS
COLONIC PH CONVERT AMMONIA TO NON
ABSORBABLE AMMONIUM IONS.
29. 7.L ORNITHINE L ASPARTATE:
CONVERT TO GLUTAMATE.
AMMONIA+GLUTAMATE=GLUTAMINE
IN MUSCLE CELL DETOXIFICATION OF
AMMONIA TO GLUTAMINE.
8.L ORNITHINE PHENYLACETATE:
PHENYL ACETATE COMBINE WITH GLUTAMINE
FORM PHEMYL ACETYL GLUTAMINE WHICH IS
WATER SOLUBLE AND EXCRETES IN URINE
30. 9.RIFAXIMIN:
ANTIBIOTICS WITH BROAD SPECTRUM ACTIVITY
AGAINST ENTERIC BACTERIA
REGIMEN:1200MG DAILY (400MG EVERY 8 HRS
FOR 10-21 DAYS.
10.SODIUM BENZOATE:
FOOD PRESERVATIVE COMBINE WITH
AMMONIA AND GLYCINE TO FORM HIPPURATE
WHICH IS WATER SOLUBLE.
31. THERAPIES DIRECTED TOWARD
MANAGEMENT OF COMPLICATIONS
• PREVENTION AND TREATMENT OF INFECTIONS .
• HAEMODYNAMIC SUPPORT.
• COAGULOPATHY.
• MECHANICAL VENTILATION.
• RENAL SUPPORT.
• NUTRITIONAL AND METABOLIC SUPPORT
32. ACUTE ON CHRONIC LIVER FAILURE
• INVOLVES PATIENT WITH CHRONIC LIVER DISEASE DEVELOP DUE TO
DETERIORATION IN LIVER FUNCTION DUE TO ANY PRECIPITATING
EVENTS ASSOCIATED WITH INCREASE 3 MONTH MORTALITY CAUSED
BY MULTI SYSTEM ORGAN FAILURE.
• PRECIPITATING FACTOR:VIRAL HEPATITIS,DRUG,ALCOHAL
ASSOCIATED.
• CHIEF SYMPTOMS :
HYPERBILIRIBINAEMIA.
COAGULOPATHY.
33. CHRONIC LIVER DISEASE
• PERSISTENT LIVER INFLAMMATION ,LIVER CHEMISTRY ABNORMALITY
AND POSITIVE SEROLOGICAL AND MOLECULAR MARKER FOR 6
MONTHS.
• CHRONIC HEPATITIS C,ALCOHALIC LIVER DISEASE,NON ALCOHALIC
STEATOHEPATITIS.
60. LIVER TRANSPLANTATION
• SCORING SYSTEM:
1.MODEL FOR END STAGE LIVER DISEASE(MELD)SCORE.
2.KING COLLEGE HOSPITAL CRITERIA.
3.CLINCY CRITERIA.
• MELD IS USE MORE OFTEN.
• KCH HAS HIGHER ACCURACY IN PRDICTING OUTCOMES COMPARED
WITH CLINCHY CRITERIA.
64. EFFECT OF LIVER ASSIST DEVICES
• ON HAEMODYNAMICS :INCREASES SVR,REMOVAL OF NO.
• ON METABOLISM: REMOVE LACTATE,BILE ACID
,BILIRUBIN,AMMONIA.
• ON HEPATIC FUNCTION: INCREASE FACTOR 7 ANTITHROMBIN 3
ALBUMIN ,PT
• ON CEREBRAL: IMPROVE ENCEPHALOPATHY,DECREASES ICP.
• ON RENAL FUNCTION: DECREASES BUN AND CREATININE.