This document discusses cirrhosis of the liver and its dietary management. It begins with defining cirrhosis as a diffuse process characterized by liver necrosis, fibrosis and conversion of normal liver architecture into abnormal nodules. It then outlines the common causes of cirrhosis including chronic alcoholism, hepatitis B/C, autoimmune diseases and others. The document discusses the pathophysiology of cirrhosis and its clinical manifestations. It also covers nutritional assessment of patients with cirrhosis and recommendations for their dietary management including adequate caloric, protein and fiber intake as well as supplementation of vitamins, minerals and branched-chain amino acids.
Hepatitis affects liver cells. it needs proper nutritional support. If proper diet and medicinal treatment given, easy recovery from this disease is possible. As this disease affects your nutritional status, taking care of your nutritional health is equally important.
Nutritional assessment using anthropometric, biochemical, clinical, and dietary methods with a larger understanding of anthropometric methods used in Ethiopia
Diet does not substitute drugs but it is considered a complementary therapy.
The goals of dietary advice are:
To prevent or manage some medical conditions
To maintain or improve health through the use of appropriate and healthy food choices
To achieve and maintain optimal metabolic and physiological outcome
Hepatitis affects liver cells. it needs proper nutritional support. If proper diet and medicinal treatment given, easy recovery from this disease is possible. As this disease affects your nutritional status, taking care of your nutritional health is equally important.
Nutritional assessment using anthropometric, biochemical, clinical, and dietary methods with a larger understanding of anthropometric methods used in Ethiopia
Diet does not substitute drugs but it is considered a complementary therapy.
The goals of dietary advice are:
To prevent or manage some medical conditions
To maintain or improve health through the use of appropriate and healthy food choices
To achieve and maintain optimal metabolic and physiological outcome
NAFLD is a vast topic and recently gaining a lot of importance. Fatty liver, NASH, are other topics discussed here. sleissenger, sheila sherlock and Harrisons are used for reference
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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
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
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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.
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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.
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
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Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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.
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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
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ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
2. OBJECTIVE
At the end of presentation, participants will be able to:
1. Define liver Cirrhosis
2. Enumerate the different types of liver cirrhosis
3. Enumerate the predisposing/ contributing factors
of liver cirrhosis
4. Discuss the pathophysiological changes and
clinical manifestations of patients with liver
cirrhosis.
5. Nutritional assessment in CLD patient
6. Dietary management
2
3. OUTLINE
Definition
Causes and predisposing factor in cirrhosis
of liver
Pathophysiology
Type of cirrhosis and clinical manifestation
Complication
Nutritional assessment
Dietary management
Conclusion
3
4. DEFINITION OF CIRRHOSIS
Cirrhosis is derived from Greek word
kirros=orange or tawny and osis=condition
-WHO definition: a diffuse process characterized
by liver necrosis and fibrosis and conversion of
normal liver architechture into structurally
abnormal nodules that lack normal lobular
organisation.
4
6. PREDISPOSING/ PRECIPITATING FACTORS:
malnutrition
effects of alcohol abuse
chronic impairment of bile excretion
– biliary obstruction in the liver and
common bile duct (gallbladder
stones)
necrosis from hepatotoxins or viral
hepatitis
Congestive heart failure 6
21. COMPLICATIONS
The ultimate mechanism of deaths in most cirrhotic
patients is
(1) progressive liver failure,
(2) a complication related to portal
hypertension, or
(3) the development of hepatocellular
carcinoma.
21
Ascites
Esophageal variceal bleeding
Hepatic encephalopathy
Hepatorenal syndrome
Spontaneous bacterial peritonitis
Portal hypertensive gastropathy
Infection
Liver failure
Hepatocellular carcinoma
25. The measures in dietetic treatment are:
• Assuring the adequate intake of protein and
of the correct types of proteins
• Assuring an adequate supply of energy
• Increased dietary intake of fiber
• Administration of branched-chain amino
acids
• Reduced intake of sodium
• Restriction of fluid
• Increased intake of potassium
26. A. ENERGY REQUIREMENTS
26
Patients usually need 35-45 kcal/kg/day.
They should supply 60-70% of non nitrogen
calories.
Cirrhosis is a disease of accelerated starvation ,so
patients should avoid long time without feeding.
Patients often do better on multiple small meals
with alate bed-time meal.
27. B. LIPIDS
27
Around 20- 30% of total calorie intake should
be supplied as fat.
MCT oil are preferred as they are easily
digestible and assimilable
A mixed fuel system improves nitrogen
balance compared to glucose alone.
Even in decompensated cirrhosis, high lipid
containing parenteral mixtures were found to
be well tolerated and improve
encephalopathy.
28. B. LIPIDS CONT..
28
Thus lipid restriction has no scientific basisin
patients withcirrhosis.
Fat should be provided aspolyunsaturated
fatty acids, with less than 50% long chain
triglycerides.
Fat helps make food tastier. This is important
for people who suffer from a suppressed
appetite due to chronic liverdisease.
29. B. LIPIDS CONT..
29
fat need in order to properly absorb the
four fat-soluble vitamins—A, D,E, and
K.
Without some fat, these vitamins may
become deficient in the body, even if
they are taken in supplemental form.
30. C. PROTEINS.
30
Proteins should not be restricted in patients
with liver disease unless they become protein
intolerant due to encephalopathy.
Protein intakeshould be in the rangeof 1-1.5
g/kg/day.
Several studies have shown that a daily protein
supply of 1.0-1.2g/kg/day may be sufficient to
prevent negative N2 balance in cirrhosis
With mild stress, this has to increase to 1.5
g/kg/day, and with acute exacerbations of
hepatitis or decompensation to 2.0g/kg/day
31. C. PROTEINS. CONT.
31
Special attention should be paid topatients
on beta-blockers for prevention of variceal
bleeding.
Beta-blockers increase protein oxidation
(an alternative method of protein
metabolism withoutenergy production),
and may increase protein requirement.
patients on propranolol should be placed
on the higherend of the protein intake.
33. Oral BCAAs in cirrhosis with or without chronic
encephalopathy
BCCAs supplement can only be recommended in
pat. At high risk of encephalopathy.
branched-chain amino acids, at doses of 12 to
14 grams per day
BCAA-enriched formulations can be useful in p’twhoare
intolerant to protein and malnourished, which can improve
protein synthesis and reduce post injurycatabolism.
Leucine is the most active in promoting protein
synthesis and inhibitingprotein breakdown.
Isoleucine and valine increase nitrogen balance and increase
tissue concentrationof leucine.
33
34. DIETARY RECOMMENDATION :
Energy and protein :
34
Clinical condition Energy
( kcal/kg/day)
Protein
(gm/kg/day)
Compensated cirrhosis 25 – 35 1.0 – 1.2
Decompensated
cirrhosis
35 - 40 1.2 – 1.5
Hepatic encephalopathy
Grade 1 -2
25 - 35 1.0 – 1.5
Hepatic encephalopathy
Grade 3 -4
25 - 35 1.0 – 1.5
BCAA enriched formula
35.
36. 25% of cirrhotics have small intestinal bacterial overgrowth
Probiotics decrease intestinal pH, inhibiting growth of
pathogenic bacteria
Probiotics with fructo-oligosaccharides equal to lactulose for
hepatic encephalopathy
Generally safe and well
36
37. Fluid intake 30-40mL/kg/day maintains fluid
balance
Dilutional hyponatremia develops due to decreased
renal blood flow and greater free water
accumulation
Fluid restriction of 1.5L/day only if with ascites and
hyponatremia <120mEq/L
37
38. Vitamins A, D, E, and K, zinc and selenium
supplementation for all cirrhotics
If with chronic cholestasis, check serum levels of
vitamin A and 25(OH)-D annually
B12 levels falsely elevated due to inactive
cobalamin analogues
Alcoholics need folate and thiamine supplements
38
39. 39
• Strict low sodium diet (1 g of
table salt per day)
• Low sodium diet (3 g of table
salt per day)
• Sodium-reduced diet (6 g of
table salt per day)
44. Diagnosis:- ALD/CLD with HTN with ascites
Total energy requirement= 2100kcal
Serving size:- 26
Nutrient distribution
Protein- 91.5gm(18%)- 1.5gm/kg/BW
Carbohydrate- 320gm(60%)
Fat- 52gm(22%)
45. Food
group
List Unit Protein Fat CHO
CHO 1 11 22 198
2 2 36
Protein 3 3 27 15
4 3.5 14 17.5 21
5 3.5 21 3.5 45.5
Fat 6 1.5 13.5
Vitamin/mi
nerals
7 1.5 7.5 1.5 19.5
46. SAMPLE MENU
बिहानको नास्ता(७:००-८:००)
दूध/चिया:-१ चिलास
अन्डा:- १ वटा पुरै + ३ वटा सेतो मात्रै
पाउरोटी:- २ slice वा ४ पपस बिस्कु ट
फलफु ल:१ वटा
बिहानको खाना(१०:००-११:००)
भात:- ३+१/२ चिलास
दाल:- १ चिलास
सब्जी:- १ चिलास
दही/दूध/मासु/:- १/१ चिलास वा ३-४ पपस
हररयो सलाद:- थोरै
मध्यान्ह(१:००)
फलफु ल:१ वटा
अन्डाको सेतो भाि:- २ वटा
47. दिउँसोको खाजा(३:००-४:००)
िेडािुडी:- १ चिलास
दही:- १ चिलास
पाउरोटी/बिस्कु ट:- १ slice वा ३-४ पपस
िेलुकाको खाना(७:००-८:००)
रोटी:- ३-४ वटा
दाल:- १ चिलास
सािसब्जी:- १ चिलास
दूध/दही/माछा,मासु:- १/१ चिलास/ ३-४ पपस
ग्रीन सलाद:- इच्छाअनुसार
48. CONCLUSION
Adequate caloric intake (35 kcal per kg
body weight daily)
Adequate intake of protein (1.2–1.5 g per kg
body weight daily)
Adequate intake of vegetable fiber or
roughage
Regular exercise to maintain muscle mass
Timely addition of enteral dietary
supplementation
Timely addition of branched-chain amino
acids
49. RFERENCE
https://www.slideshare.net/SNBhattacharya/cirrhosis-of-liver
https://www.slideshare.net/tozki/liver-cirrhosis
Prof. Dr.Plauth M.; Klinik für Innere Medizin and Städtisches Klinikum Dessau
“A Guide for Patientswith Liver Diseases including Guidelines for
Nutrition”2006
www.slideshare.net/dinujustin/liver-cirrhosis-ppt
Gluud LL, Dam G, Borre M, Les I, Cordoba J et al. Oral BCAAs have a
beneficial effect on manifestations of hepatic encephalopathy in a
systematic review with meta-analyses of RCTs. J Nutr 2013;143:1263-
1268.
Johnson TM, Overgard EB, Cohen AD, DiBaise JK. Nutrition assessment and
management in advanced liver disease. Nutr in Clin Practice 2013; 28: 15-
29.
Koretz RL, Avenell A, Lipman TO. Nutritional support for liver disease.
Cochrane Review 2012; issue 5.
Plauth M, Cabre E, Riggio O, Assis-Camilo M, Pirlich M et al.
ESPEN guidelines on enteral nutrition: liver disease. Clin. Nutr.
2006; 25: 285-294.
49