Cirrhosis is a chronic liver disease characterized by scarring of the liver and loss of liver function. It has a prevalence of 0.27% in the United States. Common causes include chronic alcohol use, hepatitis B and C, and nonalcoholic fatty liver disease. Cirrhosis results in complications like ascites, portal hypertension, and hepatic encephalopathy due to fibrotic changes and elevated portal pressure. Treatment focuses on managing complications, lowering portal pressure, and potentially liver transplantation for advanced disease.
Hepatorenal Syndrome is one of major complication of Liver Cirhosis.......Early detection & Accurate Treatment....26/6/2016 at Kafrelsheik University ( Resident Lectures).
Hepatorenal Syndrome is one of major complication of Liver Cirhosis.......Early detection & Accurate Treatment....26/6/2016 at Kafrelsheik University ( Resident Lectures).
Anaesthesia to patiens with liver disease or a liver transplantscanFOAM
A presentation by Anna Januszkiewicz at the 2017 meeting of the Scandinavian Society of Anaestesiology and Intensive Care Medicine.
All available content from SSAI2017: https://scanfoam.org/ssai2017/
Delivered in collaboration between scanFOAM, SSAI & SFAI.
A simple description of a less understood topic in Intensive Care Medicine. Aim to make understanding and management easy for the residents and prevention steps for all ICU workers.
Devascularization in portal hypertension.dr quiyumMD Quiyumm
role of surgery in portal hypertension is promising. Devascularization is one of the procedure of choice in unshuntable portal vein. Though LT is treatment of choice
outh Africa has one of the highest incidences of human immunodeficiency virus (HIV) infection in Africa. The rollout of antiretroviral therapy (ART) in South Africa has been tremendously successful in extending the lives of HIV-infected persons. Consequently, more patients who would have died before the availability of ART are now receiving a diagnosis of HIV-associated nephropathy.1
The rates of disease progression and death in the population of HIV-positive patients with chronic kidney disease can be modified by ART, which reduces the risk of advanced chronic kidney disease among patients with HIV-associated nephropathy by approximately 60%.2,3 It has been estimated that the prevalence of chronic kidney disease among HIV-infected patients receiving treatment is between 8% and 22%4-7; among untreated patients, it is estimated to be between 20% and 27%.8,9 Confronted with a high burden of HIV disease and limited resources, South Africa faces considerable challenges in providing renal-replacement therapy for the large numbers of HIV-infected persons in whom chronic kidney disease will develop during their lifetime.
In patients with terminal renal failure, left ventricular hypertrophy (LVH) is extremely common. It is found in approximately 60 to 80% of patients starting renal replacement therapy.
In renal failure, both preload and afterload are increased because of hypervolemia and increased peripheral vascular resistance respectively .
Anaesthesia to patiens with liver disease or a liver transplantscanFOAM
A presentation by Anna Januszkiewicz at the 2017 meeting of the Scandinavian Society of Anaestesiology and Intensive Care Medicine.
All available content from SSAI2017: https://scanfoam.org/ssai2017/
Delivered in collaboration between scanFOAM, SSAI & SFAI.
A simple description of a less understood topic in Intensive Care Medicine. Aim to make understanding and management easy for the residents and prevention steps for all ICU workers.
Devascularization in portal hypertension.dr quiyumMD Quiyumm
role of surgery in portal hypertension is promising. Devascularization is one of the procedure of choice in unshuntable portal vein. Though LT is treatment of choice
outh Africa has one of the highest incidences of human immunodeficiency virus (HIV) infection in Africa. The rollout of antiretroviral therapy (ART) in South Africa has been tremendously successful in extending the lives of HIV-infected persons. Consequently, more patients who would have died before the availability of ART are now receiving a diagnosis of HIV-associated nephropathy.1
The rates of disease progression and death in the population of HIV-positive patients with chronic kidney disease can be modified by ART, which reduces the risk of advanced chronic kidney disease among patients with HIV-associated nephropathy by approximately 60%.2,3 It has been estimated that the prevalence of chronic kidney disease among HIV-infected patients receiving treatment is between 8% and 22%4-7; among untreated patients, it is estimated to be between 20% and 27%.8,9 Confronted with a high burden of HIV disease and limited resources, South Africa faces considerable challenges in providing renal-replacement therapy for the large numbers of HIV-infected persons in whom chronic kidney disease will develop during their lifetime.
In patients with terminal renal failure, left ventricular hypertrophy (LVH) is extremely common. It is found in approximately 60 to 80% of patients starting renal replacement therapy.
In renal failure, both preload and afterload are increased because of hypervolemia and increased peripheral vascular resistance respectively .
Some slides are taken from different textbooks of medicine like Davidson, Kumar and Clark and Oxford, and some from other presentations made by respected tutors. I'm barely responsible for compilation of various resources per my interest. These resources are free for use, and I do not claim any copyright. Hoping knowledge remains free for all, forever.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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.
Follow us on: Pinterest
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
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.
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
263778731218 Abortion Clinic /Pills In Harare ,ABORTION WOMEN’S CLINIC +27730423979 IN women clinic we believe that every woman should be able to make choices in her pregnancy. Our job is to provide compassionate care, safety,affordable and confidential services. That’s why we have won the trust from all generations of women all over the world. we use non surgical method(Abortion pills) to terminate…Dr.LISA +27730423979women Clinic is committed to providing the highest quality of obstetrical and gynecological care to women of all ages. Our dedicated staff aim to treat each patient and her health concerns with compassion and respect.Our dedicated group ABORTION WOMEN’S CLINIC +27730423979 IN women clinic we believe that every woman should be able to make choices in her pregnancy. Our job is to provide compassionate care, safety,affordable and confidential services. That’s why we have won the trust from all generations of women all over the world. we use non surgical method(Abortion pills) to terminate…Dr.LISA +27730423979women Clinic is committed to providing the highest quality of obstetrical and gynecological care to women of all ages. Our dedicated staff aim to treat each patient and her health concerns with compassion and respect.Our dedicated group of receptionists, nurses, and physicians have worked together as a teamof receptionists, nurses, and physicians have worked together as a team wwww.lisywomensclinic.co.za/
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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.
1.
LIVER CIRRHOSIS
Pharmacy Practice
To: Sir Narendar Sharma
By: Mohammad Waqas Mairaj
2K16-PHA-56 (morning)
Epidemiology & Etiology 2
Pathophysiology of cirrhosis 3
Clinical Presentation 5
Diagnosis 6
Treatment 7
Drug monitoring guidelines 11
Liver transplant surgery 12
2.
2
EPIDEMIOLOGY
❖ The Prevalence of cirrhosis in the United States was approximately 0.27%, corresponding to
633,323 adults. 69% reported that they were unaware of having liver disease.
High risk groups:
➔ The prevalence was higher in non-Hispanic blacks and Mexican Americans.
➔ Diabetes, alcohol abuse, hepatitis C and B, male sex, and older age were all independently
associated with cirrhosis, with a population attributable fraction of 53.5% from viral hepatitis
(mostly hepatitis C), diabetes, and alcohol abuse.
❖ Mortality was 26.4% per 2-year interval in cirrhosis compared with 8.4% in propensity-matched
controls.
ETIOLOGY
Causes of Cirrhosis maybe following:
❖ Chronic alcohol consumption.
❖ Chronic viral hepatitis (types B and C).
❖ Metabolic liver disease.
❖ Hemochromatosis, Wilson disease, antitrypsin deficiency, nonalcoholicα − 1
steatohepatitis (NASH), cystic fibrosis.
❖ Immunologic disease
❖ Autoimmune hepatitis, primary biliary cirrhosis.
❖ Vascular disease
❖ Budd-Chiari syndrome, cardiac failure.
❖ Drugs
❖ Isoniazid, methyldopa, amiodarone, dronedarone, methotrexate, tamoxifen, retinol
(vitamin A), propylthiouracil and didanosine.
3.
3
PATHOPHYSIOLOGY of CIRRHOSIS
❖ Cirrhosis results in elevation of portal blood pressure because of fibrotic changes in the hepatic
sinusoids, changes in the levels of vasodilator and vasoconstrictor mediators, and an increase in
blood flow to the splanchnic vasculature.
❖ The pathophysiologic abnormalities that cause it results in the commonly encountered problems
of ascites, portal hypertension and esophageal varices, HF and coagulation disorders.
Portal hypertension and varices
❖ The most common sequelae of the portal hypertension is the development of varices and
alternative routes of blood flow resulting in acute variceal bleeding.
❖ Portal hypertension is defined by the presence of a gradient of greater than 5 mm Hg between the
portal and central venous pressure.
❖ Portal hypertension is characterized by the hypervolemia, Increased cardiac index, hypotension
and decreased systemic vascular resistance.
❖ Progression to bleeding can be predicted by Child-Pugh score, size of the varices, and the
presence of red wale markings on the varices. First variceal hemorrhage occurs at an annual rate
of about 15% and carries a mortality of 7% to 15%.
4.
4
Hepatic Encephalopathy
❖ Hepatic encephalopathy is a metabolically induced functional disturbance of the brain that is
potentially reversible.
❖ The symptoms of HE are thought to result from an accumulation of gut-derived nitrogenous
substances in the systemic circulation as a consequence of shunting through portosystemic
collaterals bypassing the liver.
❖ These substances then enter the central nervous system (CNS) and result in alterations of
neurotransmission that affect consciousness and behavior.
❖ Type A HE is induced by acute liver failure, type B results from portal-systemic bypass without
intrinsic liver disease, and type C occurs with cirrhosis. HE may be classified as episodic,
persistent, or minimal.
5.
5
Coagulation Defects
❖ Complex coagulation derangements can occur in cirrhosis. These derangements include the
reduction in the synthesis of coagulation factors, excessive fibrinolysis, disseminated
intravascular coagulation, thrombocytopenia, and platelet dysfunction.
❖ Vitamin K–dependent clotting factor levels are decreased, with factor VII affected first because it
has a short half-life. The net effect of these events is the development of bleeding diathesis.
CLINICAL PRESENTATION
Signs and Symptoms
❖ The range of presentation of patients with cirrhosis maybe from asymptomatic.
❖ Some presenting characteristics with cirrhosis are
1. Anorexia
2. Weight loss
3. Weakness
4. Fatigue
5. Jaundice
6. Pruritus
7. Gastrointestinal bleeding
8. Coagulopathy
9. Increased abdominal girth with shifting flank dullness
6.
6
10. Mental status changes
11. Vascular spiders
12. Gynecomastia and reduced libido
13. Ascites, edema, pleural effusion and respiratory difficulties
14. Malaise
15. Encephalopathy
DIAGNOSIS
Laboratory tests
❖ Hypoalbuminemia
➔ Albumin and coagulation factors are markers of hepatic synthetic activity and are used to
estimate hepatocyte functioning in cirrhosis.
❖ Elevated prothrombin time (PTT)
❖ Elevated serum conjugated bilirubin indicate that the liver has lost at least half its excretory
capacity. When alkaline phosphatase is elevated and aminotransferases levels are normal,
elevated conjugated bilirubin is a sign of cholestatic disease.
❖ Thrombocytopenia
➔ It is found in 15% to 70% of cirrhotic patients.
❖ Elevated aspartate transaminase, alanine transaminase (ALT)
➔ These enzymes has increased concentration in plasma after hepatocellular injury
❖ Alkaline phosphatase (AST) and -glutamyl transpeptidase (GGT) are elevated in plasmaγ
with obstructive disorders that disrupt the flow of bile from hepatocytes to bile ducts.
Non-invasive techniques
❖ Imaging tests. Magnetic resonance elastography (MRE) may be recommended. This
noninvasive advanced imaging test detects hardening or stiffening of the liver. Other imaging
tests, such as MRI, CT and ultrasound, may also be done.
❖ Liver biopsy. A liver biopsy can diagnose cirrhosis when the results of other tests are uncertain.
The biopsy may show the cause of cirrhosis.
7.
7
TREATMENT
❖ Treatment goals are clinical improvement or resolution of acute complications, such as
variceal bleeding, and resolution of hemodynamic instability for an episode of acute
variceal hemorrhage.
❖ Other goals are prevention of complications, adequate lowering of portal pressure with medical
therapy using β-adrenergic blocker therapy, and support of abstinence from alcohol.
❖ General approach to Treatment
● Approaches to treatment include the following:
➔ Identify and eliminate the causes of cirrhosis (eg, alcohol abuse).
➔ Assess the risk for variceal bleeding and begin pharmacologic prophylaxis where
➔ indicated, reserving endoscopic therapy for high-risk patients or acute bleeding
➔ episodes.
➔ The patient should be evaluated for clinical signs of ascites and managed with
➔ pharmacologic treatment (eg, diuretics) and paracentesis. Spontaneous bacterial
➔ peritonitis (SBP) should be carefully monitored in patients with ascites who
➔ undergo acute deterioration.
➔ HE is a common complication of cirrhosis and requires clinical vigilance and
➔ treatment with dietary restriction, elimination of CNS depressants, and therapy to
➔ lower ammonia levels.
➔ Frequent monitoring for signs of hepatorenal syndrome, pulmonary insufficiency,
and endocrine dysfunction is necessary.
❖ Management of PORTAL HYPERTENSION and VARICEAL BLEEDING
➔ The management of varices involves three strategies: (1) primary prophylaxis to prevent rebleeding,
(2) treatment of variceal hemorrhage, and (3) secondary prophylaxis to prevent rebleeding in patients
who have already bled.
Primary Prophylaxis
➔ All patients with cirrhosis and portal hypertension should be screened for varices on diagnosis.
➔ The mainstay of primary prophylaxis is the use of a nonselective β-adrenergic blocking agent such as
propranolol or nadolol. These agents reduce portal pressure by reducing portal venous inflow via
two mechanisms: decrease in cardiac output and decrease in splanchnic blood flow.
8.
8
➔ Therapy should be initiated with propranolol, 20 mg twice daily, or nadolol, 20 to 40 mg once daily,
and titrated every 2 to 3 days to maximal tolerated dose to heart rate of 55 to 60 beats/min.
➔ Patients with contraindications to therapy with nonselective β-adrenergic blockers (i.e, those with
asthma, insulin-dependent diabetes with episodes of hypoglycemia, and peripheral vascular disease)
or intolerance to β-adrenergic blockers should be considered for alternative prophylactic therapy with
EVL. [Endoscopic variceal ligation (EVL) is widely used to prevent esophageal variceal bleeding in
patients with advanced cirrhosis].
Management of ACUTE VARICEAL HEMORRHAGE
❖ Initial treatment goals include
(1) Adequate blood volume resuscitation, prompt stabilization of blood volume to maintain
hemoglobin of 8 g/dL with volume expansion to maintain systolic blood pressure of 90 to 100 mm
Hg and heart rate of less than 100 beats/min is recommended.
➔ Fluid resuscitation involves colloids initially and subsequent blood products. Vigorous
resuscitation with saline solution should generally be avoided.
(2) protection of the airway from aspiration of blood, Airway management is critical.
(3) correction of significant coagulopathy and / or thrombocytopenia with fresh frozen plasma and
platelets,
(4) prophylaxis against SBP and other infections, (5) control of bleeding, (4) prevention of
rebleeding,
(5) preservation of liver function.
❖ Combination pharmacologic therapy plus EVL or sclerotherapy (when EVL is not technically
feasible) is the most rational approach to treatment of acute variceal bleeding.
❖ Octreotide is administered as an IV bolus of 50 mcg followed by a continuous infusion of 50
mcg/h. It should be continued for 5 days after acute variceal bleeding. (Patients should be
monitored for hypo- or hyperglycemia).
❖ Vasopressin, alone or in combination with nitroglycerin, is not recommended as a first line
therapy for the management of variceal hemorrhage.
❖ Antibiotic therapy should be used early to prevent sepsis in patients with signs of infection or
ascites. A short course (up to 7 days) of oral norfloxacin 400 mg twice daily or IV ciprofloxacin is
recommended.
9.
9
❖ If standard therapy fails to control bleeding, a salvage procedure such as balloon tamponade
(with a Sengstaken-Blakemore tube) or transjugular intrahepatic portosystemic shunt
(TIPS) is necessary.
Prevention of BLEEDING
A nonselective β-adrenergic blocker along with EVL is the best treatment option for prevention of
rebleeding.
❖ Propranolol may be given at 20 mg twice daily (or nadolol, 20–40 mg once daily) and titrated
weekly to achieve a goal of heart rate 55 to 60 beats/min.
Ascites
❖ The therapeutic goals for patients with ascites are to control the ascites, prevent or relieve
ascites-related symptoms (dyspnea and abdominal pain and distention).
❖ If the serum–ascites albumin gradient is greater than 1.1 g/dL (>11 g/L), the patient almost
certainly has portal hypertension.
➔ The treatment of ascites secondary to portal hypertension includes abstinence from
alcohol, sodium restriction (to 2 g/day), and diuretics. A goal of therapy is to increase
urinary excretion of sodium to greater than 78 mmol/day.
❖ Diuretic therapy should be initiated with single morning doses of spironolactone, 100 mg, and
furosemide, 40 mg, titrated every 3 to 5 days, with a goal of 0.5 kg maximum daily weight loss.
The dose of each can be increased together, maintaining the 100:40 mg ratio, to a maximum
daily dose of 400 mg spironolactone and 160 mg furosemide.
❖ Liver transplant should be considered in patients with refractory ascites.
10.
10
Spontaneous bacterial peritonitis
❖ Antibiotic therapy for the prevention of spontaneous bacterial peritonitis (SBP) should be
considered in all patients who experience variceal hemorrhage and those with low-protein ascites.
❖ Patients with documented or suspected SBP should receive broad-spectrum antibiotic therapy to
cover Escherichia coli, Klebsiella pneumoniae, and Streptococcus pneumoniae.
❖ Cefotaxime 2 g every 8 hours, or a similar third-generation cephalosporin for 5 days is
considered the drug of choice. Oral ofloxacin, 400 mg every 12 hours for 8 days, is equivalent to
IV cefotaxime.
Hepatic Encephalopathy
Treatment Goals: Episodic and Persistent Hepatic Encephalopathy
Episodic HE Persistent HE
Control precipitating factor Reverse encephalopathy
Reverse encephalopathy Avoid recurrence
Hospital/inpatient therapy Home/outpatient therapy
Maintain fluid and hemodynamic
support
Manage persistent neuropsychiatric abnormalities
Manage chronic liver disease
Expect normal mentation after recovery High prevalence of abnormal mentation after
recovery.
❖ To reduce blood ammonia concentrations in episodic HE, lactulose is initiated at 45 mL orally every
hour (or 300 mL lactulose syrup with 700 mL water given as a retention enema held for 60 minutes) until
catharsis begins. The dose is then decreased to 15 to 30 mL orally every 8 to 12 hours and titrated to
produce two or three soft stools per day.
❖ Antibiotic therapy with metronidazole or neomycin is reserved for patients who have not responded to
diet and lactulose. Rifaximin 550 mg twice daily plus lactulose can be used for patients with inadequate
response to lactulose alone.
❖ Zinc acetate supplementation (220 mg twice daily) is recommended for long-term management in
patients with cirrhosis who are zinc deficient.
11.
11
DRUG MONITORING GUIDELINES
Drug Adverse Drug
Reaction
Monitoring
Parameter
Comments
Nonselective
β-adrenergic
blocker
Heart failure,
bronchospasm,
glucose intolerance
BP, HR
Goal HR: 55–60
beats/
min or maximal
tolerated
dose
Nadolol or propranolol
Octreotide Bradycardia,
hypertension,
arrhythmia,
abdominal
pain
BP, HR, EKG,
abdominal
pain
Vasopressin Myocardial ischemia/
infarction,
arrhythmia,
mesenteric ischemia,
ischemia of the limbs,
cerebrovascular
accident
EKG, distal pulses,
symptoms of
myocardial,
mesenteric,
or cerebrovascular
ischemia/infarction
Spironolactone/
furosemide
Electrolyte
disturbances,
dehydration, renal
insufficiency,
hypotension
Serum electrolytes
(especially
potassium),
SCr, blood urea
nitrogen, BP Goal
sodium excretion:
>78 mmol/day
Spot urine sodium
concentration
greater than potassium
concentration
correlates well with
daily sodium excretion
>78 mmol/day
Lactulose Electrolyte
disturbances
Serum electrolytes
Goal number of soft
stools per day: 2–3
Neomycin Ototoxicity,
nephrotoxicity
SCr, annual auditory
monitoring
Metronidazole
Neurotoxicity Sensory and motor
neuropathy
12.
12
LIVER TRANSPLANT SURGERY
❖ In advanced cases of cirrhosis, when the liver ceases to function, a liver transplant may be the
only treatment option.
❖ A liver transplant is a procedure to replace your liver with a healthy liver from a deceased donor
or with part of a liver from a living donor.
❖ Candidates for a liver transplant have extensive testing to determine whether they are healthy
enough to have a good outcome following surgery.
❖ Historically, those with alcoholic cirrhosis have not been liver transplant candidates because of
the risk that they will return to harmful drinking after transplant.
❖ For transplant to be an option if you have alcoholic cirrhosis, you would need:
➔ To find a program that works with people who have alcoholic cirrhosis
➔ To meet the requirements of the program, which would include lifelong commitment to
alcohol abstinence as well as other requirements of the specific transplant center.
REFERENCES
➢ Pharmacotherapy handbook 9th edition
➢ Cirrhosis - Diagnosis and treatment - Mayo clinic
➢ Pubmed.gov (The Epidemiology of Cirrhosis in the United States: A Population-based Study)