chronic kidney disease, diagnosis, management, prognosis, complications, renal replacement therapy, when to initiate hemodialysis, complication of hemodialysis, mortality and morbility.
chronic kidney disease, diagnosis, management, prognosis, complications, renal replacement therapy, when to initiate hemodialysis, complication of hemodialysis, mortality and morbility.
Chronic kidney disease (CKD) consists of a spectrum of different pathophysiologic processes associated with abnormal kidney function, and a progressive decline in glomerular filtration rate (GFR).
Chronic kidney disease (CKD) means your kidneys are damaged and can't filter blood the way they should. The disease is called “chronic” because the damage to your kidneys happens slowly over a long period of time.
Cardiogenic shock is a condition of diminished cardiac output that severely impairs cardiac perfusion. In this condition in which the heart suddenly can't pump enough blood to meet the body's needs.
LKM1 – Antibodies to Liver Kidney Microsomes test is to diagnose autoimmune hepatitis and distinguish it from other causes of liver injury. When you have hepatitis that your healthcare practitioner suspects may be due to an autoimmune-related process and then can order to to this blood test.
When you have hepatitis that your doctor suspects may be due to an autoimmune-related process, this test is to be done.
Test Include: < or =20.0 Units (negative)20.1-24.9 Units (equivocal)> or =25.0 Units (positive)
Reference values apply to all ages.
- Antibodies To Liver Kidney Microsomes
Visit us @ http://bit.ly/2LZQVoY
Acute kidney injury is common among hospitalized patients. It affects some 3–7% of patients admitted to the hospital and approximately 25–30% of patients in the intensive care unit.
Peritoneal dialysis is a treatment for kidney failure that uses the lining of your abdomen, or belly, to filter your blood inside your body. Health care providers call this lining the peritoneum. A more convenient method of dialysis in home itself.
Chronic kidney disease (CKD) consists of a spectrum of different pathophysiologic processes associated with abnormal kidney function, and a progressive decline in glomerular filtration rate (GFR).
Chronic kidney disease (CKD) means your kidneys are damaged and can't filter blood the way they should. The disease is called “chronic” because the damage to your kidneys happens slowly over a long period of time.
Cardiogenic shock is a condition of diminished cardiac output that severely impairs cardiac perfusion. In this condition in which the heart suddenly can't pump enough blood to meet the body's needs.
LKM1 – Antibodies to Liver Kidney Microsomes test is to diagnose autoimmune hepatitis and distinguish it from other causes of liver injury. When you have hepatitis that your healthcare practitioner suspects may be due to an autoimmune-related process and then can order to to this blood test.
When you have hepatitis that your doctor suspects may be due to an autoimmune-related process, this test is to be done.
Test Include: < or =20.0 Units (negative)20.1-24.9 Units (equivocal)> or =25.0 Units (positive)
Reference values apply to all ages.
- Antibodies To Liver Kidney Microsomes
Visit us @ http://bit.ly/2LZQVoY
Acute kidney injury is common among hospitalized patients. It affects some 3–7% of patients admitted to the hospital and approximately 25–30% of patients in the intensive care unit.
Peritoneal dialysis is a treatment for kidney failure that uses the lining of your abdomen, or belly, to filter your blood inside your body. Health care providers call this lining the peritoneum. A more convenient method of dialysis in home itself.
Seminar presentation on AKI and CKD in pediatricsfasil wagnew
acute kidney injury is Rapid deteriotion of renal function resulting in retention of nitrogenous wastes and inability of kidney to regulate fluid and electrolyte homeostasis
Acute renal failure or acute kidney injury is characterized by determination of renal functions over a period of hours to few days, resulting in failure of the kidney to excrete nitrogenous waste product and to maintain fluid, electrolytes and acid-base homeostasis.
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
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.
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
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
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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
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.
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
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
1. Reynel Dan L. Galicinao
HD Nurse Trainee
Nephrology Center of St.
Alexius
2. Renal Failure
• Kideny Failure, Renal Insufficiency
• Loss of kidney function
• Retention of wastes
• Retention of fluids
• Inability of the kidneys to regulate
electrolytes
6. Prerenal
• Conditions that dec renal blood flow
Intrarenal
• Injury to renal tissue
• usually associated with intrarenal ischemia,
toxins, immunologic processes, systemic &
vascular disorders
Postrenal
• obstruction or disruption to urine flow anywhere
along the urinary tract
9. ARF/AKI
• Sudden loss of kidney fcn
• Caused by renal cell damage from ischemia or toxic
substances
• Occurs abruptly, can be reversible
• Leads to hypoperfusion, cell death, decompensation in
renal fcn
• Near-N or N kidney fcn may resume gradually
10. Causes of ARF
• Infection
• Renal artery occlusion
• Obstruction
• Acute kidney disease
• Dehydration
• Diuretic therapy
• Ischemia
o From hypovolemia,
heart failure, septic
shock, blood loss
• Toxic substances
o Medications,
antibiotics
13. Oliguric
Phase
• Duration: 8-15 days
o Longer duration, less chance of
recovery
• Sudden drop in urine output
o UO > 400mL/day
• Dec. urine specific gravity
14. Oliguric Phase S/sx
• Anorexia, N&V
• HPN
• Dec. skin turgor
• Pruritus
• Tingling of the etremities
• Drowsiness → disorientation
→ coma
• Edema
• Dysrhythmias
• Signs of CHF & pulmonary
edema, pericarditis, acidosis
15. • UO rises slowly, then diuresis occurs
o 4-5L/day
• Excessive UO indicates recovery of
damaged nephrons
• Hypotension
• Tachycardia
• LOC improves
Diuretic
Phase
16. • Recovery is a slow process
• N urine volume
• Inc in strength
• LOC improves
• BUN: stable, N
• Pt can develop CRF
Recovery Phase
(Convalescent)
17. Oliguric
• Dec GFR
• Hyperkalemia
• N or dec Na+
level
• Fluid overload
• Elevated
BUN, crea
Diuretic
• Inc GFR
• Hypokalemia
• Hyponatremia
• Hypovolemia
• Gradual
decline in
BUN, crea
Recovery
• Stable & N
BUN
18. Diagnostic Evaluation
• U/A— proteinuria, hematuria, casts
• Rising serum creatinine & BUN levels
• Urine chemistry examinations to distinguish various forms
of ARF; decreased sodium
• Renal ultrasonography—for estimate of renal size & to
exclude a treatable obstructive uropathy
21. Preventive Measures
• Identify pts with preexisting renal disease.
• Initiate adequate hydration before, during, & after any
procedure requiring NPO status.
• Avoid exposure to nephrotoxins.
• Majority of drugs or their metabolites are excreted by the
kidneys.
• Monitor chronic analgesic use—some drugs may cause
interstitial nephritis & papillary necrosis.
22. • Prevent & treat shock with blood & fluid replacement
• Prevent prolonged periods of hypotension
• Monitor UO & CVP hourly in critically ill pts to detect onset
of renal failure at the earliest moment
• Schedule diagnostic studies requiring dehydration so there
are “rest days,” especially in elderly pts who may not have
adequate renal reserve
23. • Pay special attention to draining wounds, burns, which can
lead to dehydration, sepsis & progressive renal damage.
• Avoid infection; give meticulous care to pts with indwelling
catheters & I.V. lines.
• Take every precaution to make sure that the right person
receives the right blood to avoid severe transfusion
reactions, which can precipitate renal complications.
25. Corrective & Supportive Measures
• Correct reversible cause of ARF (eg, improve renal
perfusion, maximize cardiac output, surgical relief of
obstruction).
• Correct underlying fluid excesses or deficits.
• Correct & control biochemical imbalances—tx of
hyperkalemia.
• Restore & maintain BP.
• Maintain nutrition.
• Initiate HD, PD, or CRRT for pts with progressive renal
failure & other life-threatening complications.
26.
27. Other Therapy
• Sodium polystyrene sulfonate (Kayexelate) can be
administered PO or PR to reduce potassium.
• Sodium bicarbonate may be ordered to correct metabolic
acidosis.
• HD pts need water-soluble vitamins supplements because
they are removed during dialysis
• Antihypertensives to control BP
• Antibiotics to manage secondary infections
• Diphenhydramine (Benadryl) to manage itching
• Recombinant human erythropoietin to inc RBC production.
28. Complications
• Infection
• Arrhythmias due to hyperkalemia
• Electrolyte abnormalities
o sodium, potassium, calcium, phosphorus
• GI bleeding due to stress ulcers
• Multiple organ systems failure
30. Nursing Assessment
• Assess hx of cardiac disease, malignancy, sepsis,
intercurrent illness
• Determine if pt has been exposed to potentially nephrotoxic
drugs (antibiotics, NSAIDs, contrast agents, solvents)
• Physical examination for tissue turgor, pallor, alteration in
mucous membranes, BP, HR changes, pulmonary edema,
peripheral edema.
• Monitor I&O.
31. Nursing Diagnoses
• Excess Fluid Volume r/t decreased GFR & sodium
retention
• Risk for Infection r/t alterations in the immune system &
host defenses
• Imbalanced Nutrition: Less Than Body Requirements r/t
catabolic state, anorexia, & malnutrition associated with
ARF
• Risk for Injury r/t GI bleeding
33. Nursing Interventions
• Achieving Fluid and Electrolyte Balance
• Preventing Infection
• Maintaining Adequate Nutrition
• Preventing GI Bleeding
• Preserving Neurologic Function
34. Achieving Fluid & Electrolyte Balance
• Monitor for s/sx of hypo/hypervolemia
• Monitor UO & urine sp. gr.
• Measure & record I&O including urine, gastric suction,
stools, wound drainage, perspiration (estimate).
• Monitor serum & urine electrolyte concentrations.
• Weigh pt daily to provide an index of fluid balance;
expected wt loss is ½ to 1 lb (0.25 to 0.5 kg) daily.
35. • Adjust fluid intake to avoid volume overload & dehydration.
• Fluid restriction is not usually initiated until renal fcnis quite
low.
• During oliguric-anuric phase, give only enough fluids to
replace losses (usually 400 to 500 mL/24 hours plus
measured fluid losses).
• Fluid allowance should be distributed throughout the day.
• Avoid restricting fluids for prolonged periods for laboratory &
radiologic examinations because dehydrating procedures
are hazardous to pts who cannot produce concentrated
urine.
• Restrict salt & water intake if there is evidence of
36. • Regular BP with pt in supine, sitting, standing
• Auscultate lung fields for rales
• Inspect neck veins for engorgement & extremities,
abdomen, sacrum, & eyelids for edema.
• Evaluate for s/sx of hyperkalemia, monitor serum potassium
levels
• Notify health care provider of value above 5.5 mg/L.
• Watch for ECG changes—tall, tented T waves;
depressed ST segment; wide QRS complex.
• .
37. • Administer sodium bicarbonate or glucose & insulin to shift
potassium into the cells.
• Administer cation exchange resin (sodium polystyrene
sulfonate [Kayexalate]) PO/PR to provide more prolonged
correction of elevated potassium.
• Watch for cardiac arrhythmia & heart failure from
hyperkalemia, electrolyte imbalance, or fluid overload.
• Resuscitation equipment on hand in case of cardiac arrest.
• Instruct on importance of following prescribed diet; avoid
foods high in potassium.
38. • Prepare for dialysis when rapid lowering of potassium is
needed.
• Administer BT during dialysis to prevent hyperkalemia from
stored blood.
• Monitor acid-base balance.
• Monitor ABG
• Ventilator therapy for severe acidosis
• Administer sodium bicarbonate for symptomatic acidosis
(bicarbonate deficit).
• Be prepared to implement dialysis for uncontrolled
acidosis
39. Preventing Infection
• Monitor for all signs of infection. Renal failure pts do not
always demonstrate fever & leukocytosis.
• Remove bladder catheter as soon as possible; monitor for
UTI.
• Use intensive pulmonary hygiene—high incidence of lung
edema & infection.
• Carry out meticulous wound care.
• If antibiotics are administered, care must be taken to adjust
the dosage for renal impairment.
40. Maintaining Adequate Nutrition
• Work collaboratively with dietitian to regulate protein intake
according to impaired renal fcn
• High biologic value protein—rich in essential amino
acids (dairy products, eggs, meat)
• Low-protein diet may be supplemented with essential
amino acids & vitamins.
• As renal fcn declines, protein intake may be restricted
proportionately.
• Pt on dialysis: inc. protein to allow for the loss of amino
acids occurring during dialysis
41. • Offer high-carbohydrate feedings because carbohydrates
have a greater protein-sparing power & provide additional
calories.
• Weigh pt daily.
• Monitor BUN, creatinine, electrolytes, serum albumin,
prealbumin, total protein, transferrin.
• Be aware that food & fluids containing large amounts of Na,
K, and Ph may need to be restricted.
42. Preventing GI Bleeding
• Examine all stools & emesis for gross & occult blood.
• Administer H2-receptor antagonist (or PPI) or nonaluminum
or magnesium antacids as prophylaxis for gastric stress
ulcers. If H2-receptor antagonist is used, care must be taken
to adjust the dose for the degree of renal impairment.
• Prepare for endoscopy when GI bleeding occurs.
43. Preserving Neurologic Function
• Speak to the pt in simple orienting statements, use
repetition when necessary
• Maintain predictable routine, keep change to a minimum.
• Watch for & report mental status changes
• Somnolence, lassitude, lethargy, fatigue progressing to
irritability, disorientation, twitching, seizures.
• Correct cognitive distortions.
44. • Use seizure precautions—padded side rails, airway, suction
equipment at bedside.
• Encourage & assist pt to turn & move because drowsiness
& lethargy may prevent activity.
• Use music tapes to promote relaxation.
• Prepare for dialysis, which may help prevent neurologic
complications.
45. Patient Education & Health
Maintenance
• Explain that the pt may experience residual defects in
kidney fcnfor long period after acute illness.
• Routine U/A; follow-up examinations.
• Avoid any medications unless specifically prescribed.
• Resume activity gradually because muscle weakness will
be present from excessive catabolism.
46. Evaluation: Expected Outcomes
• BP stable, no edema or SOB
• No signs of infection
• Food intake adequate, maintaining wt
• Stools heme negative
• Appears more alert, sleeps less during the day
47.
48. CRF/CKD
• Progressive loss & ongoing deterioration in kidney
function
• Occurs slowly over a period of time
• Irreversible
• Results in uremia or ESRD
• Affects all major body systems
53. Dec Renal
Fcn
Retention of
Na & H20
Edema
HF
HPN
Ascites
Dec GFR
RAAS
stimulation
Inc BP
Inc serum Ph
Dec serum
Ca
Bone
resorption of
Ca
Inability to
Metabolic
Acidosis
Excrete
hydrogen
ions
Produce
ammonia
Coserve
bicarbonate
Dec EPO
production
Profound
anemia
Uremia
CNS
Altered
mental fcn
Personality
change
Seizure
Coma
56. Stage
1
2
3
4
5
Description
Kidney damage with N /supraN GFR
Mild dec in GFR
Moderate dec in GFR
Severe dec in GFR
Kidney failure
GFR
(ml/min)
>90
60-89
30-59
15-29
<15
KDOQI Suggested Stages of CKD
57.
58. • Diagnosis & tx; treat comorbid dses
• Slow progression of dse (diet, meds)
• Evalauate and tx
• Monitor progression of dse
• Evaluate & treat complications
• Monitor progress of dse
• Prepare for RRT
• RRT: HD, PD, KT
67. • Detection & tx of reversible causes of renal failure
(eg, bring diabetes under control; treat HPN)
• Dietary regulation—low-protein diet supplemented with
essential amino acids
• Minimize uremic toxicity; prevent wasting & malnutrition
Goal:
Conservation of renal function as long as possible
68. • Treatment of associated conditions to improve renal
dynamics
• Anemia—ESAs: epoetin alfa, darbepoetin
• Acidosis—infusion or oral administration of sodium
bicarbonate
• Hyperkalemia—restriction of dietary potassium;
administration of cation exchange resin
• Phosphate retention—dec in dietary phosphorus
(chicken, milk, legumes, carbonated beverages);
phosphate-binding agents because they bind
phosphorus in the intestinal tract
• Maintenance dialysis or KT when symptoms can no longer
be controlled with conservative management
69.
70. Other Drugs
• Hypocalcemia & hyperphosphatemia may be treated with
aluminumantacids that bind dietary phosphorus. If long-
term effects of aluminum hydroxide are a concern, an oral
calcium (with vitamin D) preparation may be given.
• Recombinant erythropoietin (Epogen) may be given for the
tx of anemia.
• If the pt undergoes renal
transplantations, immunosuppressives
• azathioprine (Imuran) or cyclosporine (Sandimmune)
• Corticosteroids to dec antibody formation
73. Nursing Assessment
• Obtain hx of chronic disorders & underlying health status
• Assess degree of renal impairment & involvement of other
body systems; obtain a ROS, review lab results
• Perform thorough PE, including
VS, cardiovascular, pulmonary, GI, neurologic, dermatolog
ic, musculoskeletal systems.
• Assess psychosocial response to disease
process, availability of resources, support network.
74. Nursing Diagnoses
• Excess Fluid Volume r/t disease process
• Imbalanced Nutrition: Less Than Body Requirements r/t
anorexia, nausea, vomiting, restricted diet
• Impaired Skin Integrity r/t uremic frost & changes in oil &
sweat glands
• Constipation r/t fluid restriction & ingestion of phosphate-
binding agents
• Risk for Injury while ambulating r/t potential fractures &
muscle cramps due to calcium deficiency
• Ineffective Therapeutic Regimen Management r/t
restrictions imposed by CRF & its treatment
76. Nursing Interventions
• Maintain Fluid & Electrolyte Balance
• Maintain Adequate Nutritional Status
• Maintain Skin Integrity
• Prevent Constipation
• Ensure a Safe Level of Activity
• Increase Understanding & Compliance with Treatment
Regimen
77. Maintaining Skin Integrity
• Keep skin clean while relieving itching & dryness.
• Soap for sensitive skin, such as basis soap
• Sodium bicarbonate added to bath water
• Oatmeal baths
• Bath oil added to bath water
• Ointments or creams to relieve itching.
• Keep nails short & trimmed to prevent excoriation.
• Keep hair clean & moisturized.
• Antihistamines for relief of itching; discourage pt from taking
OTC drugs without discussing with health care provider
78. Preventing Constipation
• Phosphate binders cause constipation that cannot be
managed with usual interventions.
• High-fiber diet; bear in mind the potassium content of some
fruits & vegetables.
• Commercial fiber supplements (Fiberall, Fiber-Med)
• Stool softeners as prescribed.
• Avoid laxatives & cathartics that cause electrolyte
toxicities (compounds containing magnesium or
phosphorus).
79. Ensuring a Safe Level of Activity
• Monitor serum Ca & phosphate levels; watch for signs of
hypo/hypercalcemia
• Inspect pt's gait, ROM, muscle strength.
• Administer analgesics, as ordered
• Provide massage for severe muscle cramps.
• Monitor X-rays & bone scan results for fractures, bone
demineralization, joint deposits.
80. • Inc activity as tolerated—avoid immobilization because it
increases bone demineralization.
• Administer medications as ordered:
• Phosphate-binding medications, such as sevelamer
(Renagel) or calcium carbonate (Os-Cal), with meals &
snacks to lower serum phosphorus
• Calcium supplements between meals to inc serum
calcium
• Vitamin D to inc absorption & utilization of calcium
81. Increasing Understanding of &
Compliance with Treatment Regimen
• Prepare pt for dialysis or KT
• Offer hope tempered by reality.
• Assess understanding of tx regimen, concerns, fears
• Explore alternatives that may reduce or eliminate adverse
effects of tx.
• Adjust schedule so rest can be achieved after dialysis.
• Offer smaller, more frequent meals to reduce nausea &
facilitate taking medication.
82. • Encourage strengthening of social support system & coping
mechanisms to lessen the impact of the stress of CKD
• Social work referral
• Contract with pt for behavioral changes if noncompliant with
therapy or control of underlying condition
• Supportive psychotherapy for depression
• Promote decision making by pt
• Refer pts & family members to renal support agencies
83. Patient Education & Health
Maintenance
• Weigh self every morning to avoid fluid overload
• Drink limited amounts of fluids only when thirsty
• Measure allotted fluids, save some for ice cubes; sucking
on ice is thirst quenching
• Eat food before drinking fluids to alleviate dry mouth
• Use hard candy or chewing gum to moisten mouth
84. • Encourage all people with the following risk factors to obtain
screening for CKD:
• elderly people
• native Americans
• Blacks
• Latinos
• Diabetics
• people with HPN, autoimmune disease, with family hx of
kidney disease
85.
86. Evaluation: Expected Outcomes
• BP stable, no excessive wt gain
• Tolerates small feedings of low-protein, high-carbohydrate
diet
• No skin excoriation; reports some relief of itching
• Passes small, firm stool daily
• Ambulates without falls
• Asks questions & reads education materials about dialysis