Chronic renal failure refers to the irreversible deterioration of renal function over years. It eventually leads to uraemia as the kidneys lose their excretory, metabolic and endocrine functions. The main causes are diabetes, hypertension, and glomerulonephritis. Management involves identifying the underlying disease, controlling blood pressure and other reversible factors to slow progression, managing complications like anaemia, and initiating renal replacement therapy like dialysis for end-stage disease.
Acute Tubular Necrosis | DR RAI M. AMMAR | ALL MEDICAL DATA
by DR RAI M. AMMAR
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Acute Tubular Necrosis | DR RAI M. AMMAR | ALL MEDICAL DATA
by DR RAI M. AMMAR
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www.linkedin.com/in/drraiammar
www.medicall.com.pk/blog/auther/drraiammar/
For Any Book or Notes Visit Our Website:
www.allmedicaldata.wordpress.com
www.drraiammar.blogspot.com
YOUTUBE CHANNEL :
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Acute renal failure (ARF) is a common and serious problem in clinical medicine. It is characterized by an abrupt reduction (usually within a 48-h period) in kidney function.
This results in an accumulation of nitrogenous waste products and other toxins. Many patients become oliguric (low urine output) with subsequent salt and water retention. In
patients with pre-existing renal impairment, a rapid decline
in renal function is termed ‘acute on chronic renal failure’.
The nomenclature of ARF is evolving and the term acute
kidney injury (AKI) is being increasingly used in clinical
practice.
Acute kidney injury (AKI) is a sudden episode of kidney failure or kidney damage that happens within a few hours or a few days.It's most common in those who are critically ill and already hospitalized.
Acute renal failure (ARF) is a common and serious problem in clinical medicine. It is characterized by an abrupt reduction (usually within a 48-h period) in kidney function.
This results in an accumulation of nitrogenous waste products and other toxins. Many patients become oliguric (low urine output) with subsequent salt and water retention. In
patients with pre-existing renal impairment, a rapid decline
in renal function is termed ‘acute on chronic renal failure’.
The nomenclature of ARF is evolving and the term acute
kidney injury (AKI) is being increasingly used in clinical
practice.
Acute kidney injury (AKI) is a sudden episode of kidney failure or kidney damage that happens within a few hours or a few days.It's most common in those who are critically ill and already hospitalized.
Topics Covered:
Basic kidney physiology (just enumeration).
Manifestations of renal impairment.
AKI vs. CRF , definitions, causes and their classifications (in brief) .
Clinical evaluation of a case of renal failure.
indications for renal replacement therapy.
Approach for real-Life patient with renal impairment: group-case discussion.
Chronic renal failure or chronic kidney disease management, pharmacist role, medical management objectives, goals of the therapy .
What are the risk factors of chronic renal failure, clinical manifestations of chronic renal failure, renal failure complications, pathophysiology of chronic renal failure.
Chapter 12 Chronic Kidney Disease and DialysisKalvinSmith4
For DH Theory III, students must give a presentation on a specific module in the class. The purpose of these presentations is to inform students on how treat patients in a dental setting who may be compromised by a certain medical condition. I was tasked with presenting on chronic kidney disease and dialysis, as well as on sexually transmitted diseases. This is the presentation that I modified on CKD and dialysis.
pathophysiology of acute and chronic renal failure - Bestha Chakrapani associate professor Deparrtment of Balaji college of pharmacy , ananthapuramu-515004
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
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
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.
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.
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.
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These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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
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
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.
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
2. CHRONIC RENAL FAILURE Chronic renal failure (CRF) refers to an irreversible deterioration in renal function which classically develops over a period of years .
3. Initially, CRF manifest only as a biochemical abnormality. Eventually, loss of the excretory, metabolic and endocrine functions of the kidney leads to the development of the clinical symptoms and signs of renal failure, which are referred to as uraemia. End stage renal disease (ESRD):renal failure which need renal replacement therapy. When death is likely without renal replacement therapy, it is called end-stage renal failure (ESRF).
4. Aetiology of CRF CRF may be caused by any condition which destroys the normal structure and function of the kidney. Patients often have bilateral small kidneys at presentation, and in such a situation renal biopsy is usually inadvisable because of the difficulty in making a histological diagnosis in severely damaged kidneys and the fact that treatment is unlikely to improve renal function significantly.
7. Pathogenesis of CRF Disturbances in water, electrolyte and acid-base balance contribute to the clinical picture in patients with CRF, but the exact pathogenesis of the clinical syndrome of uraemia is unknown. Many substances present in abnormal concentration in the plasma have been suspected as being 'uraemic toxins', and uraemia is probably caused by the accumulation of various intermediary products of metabolism.
11. Clinical assessment Renal failure may present as a raised blood urea and creatinine found during routine examination, often accompanied by hypertension, proteinuriaoranaemia. When renal function deteriorates slowly, patients may remain asymptomatic until GFR falls below 20 - 30 ml/minute( normal range 80 – 120 mL/ min ). Nocturia, due to the loss of concentrating ability and increased osmotic load per nephron, is often an early symptom. Thereafter, due to the widespread effects of renal failure, symptoms and signs may develop that are related to almost every body system .
12. Patients may present with complaints which are not obviously renal in origin, such as tiredness or breathlessness. In ESRF (stage 5) patients appear ill and anaemic. There may be unusually deep respiration related to metabolic acidosis (Kussmaul's respiration), anorexia and nausea. Later, hiccoughs, pruritus, vomiting, muscular twitching, fits, drowsiness and coma ensue.
14. Specific manifestations of Uremia Gastrointestinal manifestations Are common at low GFRs, including: anorexia followed by nausea, and vomiting is commonly seen. There is a higher incidence of peptic ulcer disease in uraemic patients.
15. Anaemia Anaemia is common in CRF; it usually correlates with the severity of renal failure and contributes to many of the non-specific symptoms of CRF. Several mechanisms are implicated(causes of anaemiainCRF): 1- Relative deficiency of erythropoietin 2- Diminished erythropoiesis due to toxic effects of uraemia on marrow precursor cells 3- Reduced red cell survival 4- Increased blood loss due to capillary fragility and poor platelet function 5- Reduced dietary intake and absorption of iron and other haematinics.
16. Plasma erythropoietin is usually within the normal range and thus inappropriately low for the degree of anaemia. In patients with polycystic kidneys, anaemia is often less severe or absent, while in some interstitial disorders it appears disproportionately severe for the degree of renal failure. This is probably because of the effects of these disorders on the interstitial fibroblasts that secrete erythropoietin
17. Acidosis Declining renal function is associated with metabolic acidosis , which is often asymptomatic. There may be unusually deep respiration related to metabolic acidosis (Kussmaul's respiration). Effects of metabolic acidosis : Sustained acidosis results in protons being buffered in bone in place of calcium, thus aggravating metabolic bone disease. Acidosis may also contribute to reduced renal function and increased tissue catabolism.
18. Cardiovascular disease and lipids CRF is an independent risk factor for occlusive cardiovascular disease. Hypertensiondevelops in approximately 80% of patients with CRF. In part, this is caused by sodium retention. Chronically diseased kidneys also tend to hypersecreterenin, leading to high circulating concentrations of renin, angiotensin II and aldosterone. This is exaggerated if there is renal under-perfusion related to renal vascular disease. Hypertension must be controlled, as it causes further vascular and glomerular damage and worsening of renal failure Atherosclerosisis common and may be accelerated by hypertension.
19. Pericarditisis common in untreated or inadequately treated ESRF. It may lead to pericardial tamponade and, later, constrictive pericarditis. Hypercholesterolaemia is almost universal in patients with significant proteinuria, and increased triglyceride levels are also common in patients with CRF. It has been suggested that as well as influencing the development of vascular disease, this may accelerate the progression of chronic renal disease.
20. Renal osteodystrophy This metabolic bone disease which accompanies CRF consists of a mixture of osteomalacia,hyperparathyroid bone disease (osteitisfibrosa), osteoporosis and osteosclerosis. Osteomalacia Results from diminished activity of the renal 1α-hydroxylase enzyme, with failure to convert cholecalciferol to its active metabolite, 1,25-dihydroxycholecalciferol. A deficiency of the latter leads to diminished intestinal absorption of calcium, hypocalcaemia and reduction in the calcification of osteoid in bone.
21. Osteitisfibrosaresults from this secondary hyperparathyroidism . The parathyroid glands are stimulated by the low plasma calcium, and also by hyperphosphataemia. In some patients tertiary or autonomous hyperparathyroidism with hypercalcaemia develops. Osteoporosis occurs in many patients , possibly related to malnutrition. Osteosclerosisis seen mainly in the sacral area, at the base of the skull and in the vertebrae; the cause of this unusual reaction is not known.
22. Myopathy Generalisedmyopathyis due to a combination of poor nutrition, hyperparathyroidism, vitamin D deficiency and disorders of electrolyte metabolism. Muscle cramps are common, and quinine sulphate may be helpful. The 'restless leg syndrome', in which the patient's legs are jumpy during the night, may be troublesome and is often improved by clonazepam
23. Neuropathy Neuropathy results from demyelination of medullatedfibres, with the longer fibres being involved at an earlier stage. Sensory neuropathy may cause paraesthesiae. Amitriptyline and gabapentin may provide some symptom relief. Motor neuropathy may present as foot drop. Uraemic autonomic neuropathy may cause delayed gastric empty-ing, diarrhoea and postural hypotension. Clinical manifestations of neuropathy appear late in the course of CRF but may improve or even resolve once dialysis is established.
24. Endocrine Function A number of hormonal abnormalities may be present of which the most important are hyperprolactinaemia & hyperparathyroidism . In both sexes there is loss of libido and sexual function, related at least in part to hyperprolactinaemia . In women amenorrhoea is common. The half-life of insulin is prolongedin CRF due to reduced tubular metabolism of insulin; insulin requirements may therefore decline in diabetic patients in end-stage CRF. However, there is also a post-receptor defect in insulin action, leading to relative insulin resistance. This latter abnormality is improved by dialysis treatment.
25. Bleeding There is an increased bleeding tendency in renal failure which manifests in patients with advanced disease as cutaneousecchymoses and mucosal bleeds. Platelet function is impaired and bleeding time prolonged. Adequate dialysis treatment partially corrects the bleeding tendency.
26. Infection Cellular and humoral immunity are impaired, with increased susceptibility to infection. Infections are the second most common cause of death in dialysis patients, after cardiovascular disease; they must be recognised and treated promptly.
27. Acute or Chronic? History Previous renal function test. Small kidneys on u/s Anaemia. Bone changes.
28. Acute or Chronic Renal failure? History Previous renal function test. Small kidneys on u/s Anaemia. Bone changes.
30. Investigations and management of CRF There are several aspects to the management of CRF: Identify the underlying renal disease. Look for reversible factors which are making renal function worse . Attempt to prevent further renal damage. Attempt to limit the adverse effects of the loss of renal function. Institute renal replacement therapy (dialysis or transplantation)
31. .At presentation the nature of the underlying disease should be determined, if possible, by history, examination, testing of biochemistry, immunology, radiology and biopsy . The degree of renal failure is assessed and complications are documented.
32. Investigations -Blood urea & serum creatinine: increased - Serum electrolytes .serum calcium :decreased .serum potassium : increased ( risky ) .serum uric acid : increased(but rarely cause gout ) .serum phosphate : increased General urine examination: for: protein , RBC , features of UTI ( may need urine culture ) , cast ( waxy broad cast is characteristic for CRF) Complete blood picture: usually there is anaemia. PH of blood : metabolic acidosis. Viral markers : HBsAg , Anti-HCV Ab & HIV test (if dialysis is needed) (vaccination against hepatitis B if no previous infection; isolation of dialysis machine if positive) .
33. ECG: look for -Features of hyperkalemia (hyperacute T- wave ,then prolongation of PR- interval & QRS ,then loss of P-wave , & if not managed may cause asystole ) -Features of pericardial effusion( low voltage ECG ). -Features of IHD. Echocardiography: look for any evidence of pericardial effusion or cardiomyopathy ( DCMP). CXR: look for features of pulmonary oedema , pleural effusion , chest infection , enlarged cardiac shadow. Abdominal Ultrasoud: look for the size & ecchogenecity of the kidneys & if there is ascitis. In CRF , usually bilateral small kidneys (except polycystic kidney disease , amyloidosis , hydronephrosis , diabetic nephropathy )
34. X- ray of bone : for evidence of renal osteodystrophy. Renal biopsy : only indicated in CRF with normal size kidneys ( not indicated in CRF with small size kidneys ). GFR If diagnosis is not known further investigation needed as : Immunoglobulins and protein electrophoresis Urinary Bence Jones protein Complement ANA: and dsDNA if ANA is positive Rheumatoid factor ANCA: in all possible inflammatory renal disease Anti-GBM: in all possible inflammatory renal disease Cryoglobulins: if cryoglobulinaemia is clinically suspected
35. Hyperkalemia & EKG K > 5.5 -6 Tall, peaked T’s Wide QRS Prolong PR Diminished P Prolonged QT QRS-T merge – sine wave
38. Retarding the progression of CRF Unless dialysis or transplantation is provided , CRF is eventually fatal. Once the plasma creatinine exceeds about 300 μmol/l (3.4 mg/dl), there is usually progressive deterioration in renal function, irrespective of aetiology. The rate of deterioration is very variable between patients but is relatively constant for an individual patient.
39. REVERSIBLE FACTORS IN CHRONIC RENAL FAILURE 1- Hypertension 2- Reduced renal perfusion Renal artery stenosis Hypotension due to drug treatment Sodium and water depletion Poor cardiac function 3- Urinary tract obstruction 4- Urinary tract infection 5- Other infections: increased catabolism and urea production 6- Nephrotoxic medications CRF is usually irreversable , by controlling the reversable factors we may delay the progression of renal impairement to ESRD.
40. Control of blood pressure In many types of renal disease, particularly in diseases affecting glomeruli (particularly those associated with heavy proteinuria), control of blood pressure may retard deterioration of GFR & delay the progression to ESRD. The target blood pressures is 130/85 mmHg for CRF alone, & lowered to 125/75 mmHg for those with proteinuria > 1 g/day. Drugs can be used : ACE inhibitors like captopril Angiotensin II receptor antagonists like valsartan calcium channel blockers like diltizem
41. ACE inhibitors like captoprilhave been shown to be more effective at retarding the progression of renal failure , because they reduce glomerular perfusion pressure by dilating the efferent arteriole & reduce proteinuria ACE inhibitors should be used, where tolerated (check creatinine and potassium), in all patients with diabetic nephropathy or protein-uria> 1 g/day independent of the presence of hypertension. Using ACE inhibitors need monitoring of serum potassium. ACE inhibitors should not be used when there is renal artery stenosis
42. Diet Dietary protein For patients on renal replacement therapy , severe protein restriction is not recommended because carry a risk of inducing malnutrition. Moderate restriction (to 60 g protein per day) should be accompanied by an adequate intake of caloriescalories(30-35kcal/kg/d) to prevent malnutrition. Anorexia and muscle loss may indicate a need to commence dialysis treatment.
43. Treatment of Anaemiaof CRF Recombinant human erythropoietin (Eprex) is effective in correcting the anaemia of CRF . dose : 50 Iu / kg once or twice wk.ly route : subcutaneously (or IV for patients on haemodialysis ). The target haemoglobin is usually between 10 and 12 g/dl. Complications of treatment include increased blood pressure, and adjustment of antihypertensive medication is often necessary. There is also an increase in blood coagulabilityand an increased incidence of thrombosis of the arteriovenous fistulae used for haemodialysis.
44. Erythropoietin is less effective in the presence of : iron deficiency, active inflammation or malignancy, or in patients with aluminium overload which may occur in dialysis. Causes of Erythropoietin resistant Iron deficiency Active inflamation Malignancy Secondary hyperparathyroid Aluminum overload Pure red cell aplasia These factors should be sought and, if possible, corrected before treatment. Iron supplementation should be used to keep ferritin > 100 μg/l and transferrin saturation > 20%.
45. Fluid and electrolyte balance Due to the reduced ability of the failing kidney to concentrate the urine, a relatively high urine volume is needed to excrete products of metabolism and a fluid intake of around 3 litres/day is desirable ( when there is no fluid overload “ no oedema “ ) fluid retention sometimes lead to episodic pulmonary oedema . Fluid intake:urine volume +500ml .Limitation of potassium intake (e.g. 70 mmol/day) and sodium intake (e.g. 100 mmol/day) may be required in late CRF if there is evidence of accumulation .Low phosphate diet(600-1000mg/d)
47. Some patients with so-called salt-wasting' disease may require a high sodium and water intake, including supplements of sodium salts, to prevent fluid depletion and worsening of renal function. This is most often seen in patients with renal cystic disease, obstructive uropathy, reflux nephropathy or other tubulo-interstitial diseases, and is not seen in patients with glomerular disease.
48. Treatment of Acidosis The plasma bicarbonate should be maintained above 22 mmol/l by giving sodium bicarbonate supplements (starting dose of 1 g 8-hourly, increasing as required). The increased sodium intake may induce hypertension or oedema. calcium carbonate (up to 3 g daily) is an alternative that is also used to bind dietary phosphate.
49. Treatment of Hypercholesterolaemia Statin ( as simvastatin ) achieve substantial reductions in lipids in chronic renal disease. Hyperlipidemia is more if the CRF is due to glomerular diseases due to the increased hepatic lipoprotein synthesis that is triggered by reduced oncotic pressure
50. Treatment of Bleeding Adequate dialysis treatment partially corrects the bleeding tendency.
51. Renal osteodystrophy To minimise the effects of CRF on bone, plasma calcium and phosphateshould be kept as near to normal as possible. Treatment of Hypocalcaemia is corrected by giving 1α-hydroxylated synthetic analogues of vitamin D. The dose is adjusted to avoid hypercalcaemia. This will usually prevent or control osteomalacia. .
52. Treatment of Hyperphosphataemia Is controlled by dietary restriction of foods with high phosphate content (milk, cheese, eggs) The use of phosphate-binding drugs administered with food. These agents form insoluble complexes with dietary phosphate and prevent its absorption (e.g. calcium carbonate 500 mg with each meal and aluminium hydroxide 300 – 600 mg before each meal).we should avoid aluminium toxicity. Secondary hyperparathyroidism is usually prevented or controlled by these measures but, in severe bone disease with autonomous parathyroid function, parathyroidectomymay become necessary
57. Treatment of Neuropathy Clinical manifestations of neuropathy appear late in the course of CRF but may improve or even resolve once dialysis is established. Sensory neuropathy may cause paraesthesiae. Amitriptylineandgabapentinmay provide some symptom relief.
58. Treatment of Endocrine disorders Treatment with dopamine agonists is sometimes useful for amenorrhoea or galactorrhoea in women Insulin requirementsusually decline in diabetic patients in end-stage CRF ( CRF patients are liable for hypoglycemia ). insulin resistance is improved by dialysis treatment.
59. Gastrointestinal manifestations Are common at low GFRs, including anorexia followed by nausea, and vomiting is commonly seen & improve by dialysis. There is a higher incidence of peptic ulcer disease in uraemic patients and H2-receptor antagonists or proton pump inhibitors are commonly used.
60. Depression Depression is common in patients on or approaching renal replacement therapy and support should be provided for both them and their relatives
63. RENAL REPLACEMENT THERAPY The facility to replace some functions of the kidney artificially by dialysis has been available since the 1960s. Such treatment is now routine in patients with acute or chronic renal failure. It does not replace the endocrine and metabolic functions of the kidney, but aims to maintain the plasma biochemistry (uraemic toxins, electrolytes and acid-base status) at acceptable levels. Dialysis can also remove fluid from the circulation (ultrafiltration) to maintain euvolaemia.
64. Haemodialysis Haemodialysis is started when the patient has symptomatic advanced renal failure but before the development of serious complications, often with a plasma creatinine of 600-800 μmol/l (6.8-9.0 mg/dl). Vascular access is required; an arteriovenous fistula should be formed, usually in the forearm, when the patient reaches stage 4 kidney disease, so that the fistula has time to develop. After 4-6 weeks, increased pressure in the vein leading from the fistula causes distension and thickening of the vessel wall (arterialisation). Large-bore needles can then be inserted into the vein to provide access for each haemodialysis treatment If this access is not possible, plastic cannulaein central veins can be used for short-term access
65. Haemodialysis is usually carried out for 3-5 hours, three times weekly. Most patients notice an improvement in symptoms during the first 6 weeks of treatment. Plasma urea and creatinine are lowered by each treatment but do not return to normal. Many patients lead normal and active lives, and patient survival for more than 20 years is commonplace in young patients without extrarenal disease.
66. Hemodialysis 3-4 times a week Takes 3-5 hours Machine filters blood and returns it to body
72. PROBLEMS WITH HAEMODIALYSIS Hypotension during dialysis Cardiac arrhythmias Haemorrhage Blood loss (overt or occult), ↓BP Air embolism Circulatory collapse, cardiac arrest Dialyser hypersensitivity Acute circulatory collapse , may be due to Allergic reaction to dialysis membrane or sterilisant Other Emergencies conditions Pulmonary oedema ,Systemic sepsis, Breathlessness ,Rigors, fever.
73. Hemo Advantages & Disadvantages Advantages Disadvantages Rapid fluid removal Rapid removal of urea & creatinine Effective K+ removal Less protein loss Home dialysis possible Temporary access at the bedside Vascular access problems Dietary & fluid restrictions Heparinization Extensive equipment Hypotension Added blood lost Trained specialist
74. Contraindications of HD Shoke Severe caidiaccomplications Severe bleeding malignency , sepsis poor condition in vascular system
75. Peritoneal dialysis Peritoneal dialysis uses peritoneum as a semi-permeable dialysis membrane. Solutes move down a concentration gradient, and water down an osmotic gradient achieved by using an osmolar compound (typically glucose) in the dialysis fluid.
76. PD Advantages and Disadvantages Advantages Disadvantages Bacterial/chemical periotonitis Protein loss Exit site of catheter Hyperglycemia Surgical placement of catheter Multiple abdominal surgery Immediate initiation Less complicated Portable (CAPD) Fewer dietary restrictions Short training time Less cardio stress Choice for diabetics
77. Continuous ambulatory peritoneal dialysis (CAPD) CAPD is a form of long-term dialysis involving insertion of a permanentSilastic catheter into the peritoneal cavity. Two litresof sterile, isotonic dialysis fluid are introduced and left in place for approximately 6 hours. During this time, metabolic waste products diffuse from peritoneal capillaries into the dialysis fluid down a concentration gradient. The fluid is then drained and fresh dialysis fluid introduced. This cycle is repeated four times daily, during which time the patient is mobile and able to undertake normal daily activities. CAPD is particularly useful in young children, and in elderly patients with cardiovascular instability. Its long-term use may be limited by episodes of bacterial peritonitis and damage to the peritoneal membrane, but patients have been treated successfully for more than 10 years.
78. Automated peritoneal dialysis (APD) The use of automated peritoneal dialysis (APD) is now widespread. This system is similar to CAPD but uses a mechanical device to perform the fluid exchanges during the night, leaving the patient free, or with only a single exchange to perform, during the day.
79. PROBLEMS WITH CONTINUOUS AMBULATORY PERITONEAL DIALYSIS (CAPD) peritonitis Cloudy drainage fluid; abdominal pain and systemic sepsis are variable Usually entry of skin contaminants via catheter; bowel organisms less common Catheter exit site infection Erythema and pus around exit site Ultrafiltration failure Fluid overload ,Damage to peritoneal membrane, leading to rapid transport of glucose and loss of osmotic gradient Peritoneal membrane failure Inadequate clearance of urea etc. Scarring/damage to peritoneal membrane.
80. PD HD eldly young Age yes no Cardiovascular disease Bleeding No bleeding Blood poor good Vascular condition poor better Ecnomic situation Choice of HD or CAPD
81. Renal transplantation Renal transplantation offers the best chance of long-term survival in patients with end-stage renal disease. It can restore normal kidney function and correct all the metabolic abnormalities of CRF. All patients should be considered for transplantation unless there are active contraindications
82. Kidney grafts may be taken from a cadaver or from a living donor. matching of a donor to a specific recipient is strongly influenced by immunological factors, since graft rejection is the major cause of failure of the transplant. ABO (blood group) compatibility between donor and recipient is essential, and the degree of matching for major histocompatability (MHC) antigens-particularly HLA-DR-influences the incidence of rejection. In the transplant operation, the donor vessels are anastomosed to the recipient iliac artery and vein, and the donor ureter to the bladder Peri-operative problems include: Fluid balance. Careful matching of input to output is required. Primary graft non-function. Causes include hypovolaemia, acute tubular necrosis or other pre-existing renal damage, hyperacute rejection, vascular occlusion and urinary tract obstruction. Sepsis (related to immunosuppression).
83. CONTRAINDICATIONS TO RENAL TRANSPLANTATION Absolute Active malignancy-a period of at least 2 years of complete remission is recommended for most tumours prior to transplantation Active vasculitisor anti-GBM disease, with positive serology-at least 1 year of remission is recommended prior to transplantation Severe ischaemic heart disease Severe occlusive aorto-iliac vascular disease Relative Age-while practice varies, transplants are not routinely offered to very young children (< 1 year) or older people (> 75 years) High risk of disease recurrence in the transplant kidney Disease of the lower urinary tract-in patients with impaired bladder function, an ileal conduit may be considered Significant comorbidity
84. Once the graft begins to function, normal or near-normal biochemistry is usually achieved within a few days. All transplant patients require regular life-long clinic follow-up to monitor renal function and immunosuppression. Management after transplantation Immunosuppressive therapy is required to prevent rejection. Different therapeutic regimens are used; a commonly used one is triple therapy consisting of prednisolone, plus ciclosporin or tacrolimus and azathioprine. Newer immunosuppressive drugs such as mycophenolatemofetiland rapamycin are increasing in use ..
85. Immunosuppression, which must usually be taken throughout the life of the transplant, is associated with an increased incidence of infection, particularly opportunistic infections such as cytomegalovirus and Pneumocystiscarinii . There is also an increased risk of malignancy, especially of the skin. Approximately 50% of white patients develop skin malignancy by 15 years post-transplant. Lymphomas are rare but may occur early and are often related to infection with herpes viruses, especially Epstein. Quality of life studies indicate that transplantation offers the best hope of complete rehabilitation and is the most cost-effective treatment for end-stage CRF.
87. Complications Post Transplant Rejection is a major problem Hyperacute rejection: occurs within minutes to hours after transplantation Renal vessels thrombosis occurs and the kidney dies There is no treatment and the transplanted kidney is removed
88. Complications Post Transplant Acute Rejection: occurs 4 days to 4 months after transplantation It is not uncommon to have at least one rejection episode Episodes are usually reversible with additional immunosuppressive therapy (Corticosteroids, ALG, or ATG) Signs: increasing serum creatinine, elevated BUN, fever , decrease output, increasing BP, tenderness over the transplanted kidneys
89. Complications Post Transplant Chronic Rejection: occurs over months or years and is irreversible. The kidney is infiltrated with large numbers of T and B cells characteristic of an ongoing , low grade immunological mediated injury Gradual occlusion renal blood vessels Signs: proteinuria, HTN, increase serum creatinine levels Supportive treatment, difficult to manage Replace on transplant list