Chronic renal failure refers to the irreversible deterioration of renal function over years. It initially presents as biochemical abnormalities and eventually leads to uraemic symptoms as the excretory, metabolic and endocrine functions of the kidneys fail. Common causes include diabetes, hypertension, and glomerulonephritis. Management involves identifying and treating the underlying disease, slowing progression, managing complications, and renal replacement therapy for end-stage disease.
A decrease in red blood cells when the body can't absorb enough red blood cells.It is an organ specific autoimmune diseases in which the body’s immune system attacks the lining of the stomach.
It was considered as a deadly disease due to the lack of available treatment.
Pernicious anemia is most common in caucasian persons of north European ancestry than in other racial groups.
Carbidopa is given in combination L-dopa in Parkinsonian A M O L D E O R E
Carbidopa/levodopa remains the most effective drug to treat PD. In addition to helping prevent nausea, carbidopa prevents levodopa from being converted into dopamine prematurely in the bloodstream, allowing more of it to get to the brain.
A decrease in red blood cells when the body can't absorb enough red blood cells.It is an organ specific autoimmune diseases in which the body’s immune system attacks the lining of the stomach.
It was considered as a deadly disease due to the lack of available treatment.
Pernicious anemia is most common in caucasian persons of north European ancestry than in other racial groups.
Carbidopa is given in combination L-dopa in Parkinsonian A M O L D E O R E
Carbidopa/levodopa remains the most effective drug to treat PD. In addition to helping prevent nausea, carbidopa prevents levodopa from being converted into dopamine prematurely in the bloodstream, allowing more of it to get to the brain.
Acyclovir is in a class of antiviral medications called synthetic nucleoside analogues. It works by stopping the spread of the herpes virus in the body.
is used to decrease pain and speed the healing of sores or blisters in people who have varicella (chickenpox)), herpes zoster
Migraine pathophysiology, diagnosis and treatmentsYung-Tsai Chu
Introduction of migraine, including symptoms, epidemiology, pathophysiology(neurotransmitter, neural network, channel, CGRP), diagnostic criteria and treatment (oral, intravenous therapy at ED and long-term prevention)
To enjoy the presentation kindly download it.
For Original view, download "Poetsen One" font style from dafont website.
Here I have discussed pharmacology of penicillin G.
Acyclovir is in a class of antiviral medications called synthetic nucleoside analogues. It works by stopping the spread of the herpes virus in the body.
is used to decrease pain and speed the healing of sores or blisters in people who have varicella (chickenpox)), herpes zoster
Migraine pathophysiology, diagnosis and treatmentsYung-Tsai Chu
Introduction of migraine, including symptoms, epidemiology, pathophysiology(neurotransmitter, neural network, channel, CGRP), diagnostic criteria and treatment (oral, intravenous therapy at ED and long-term prevention)
To enjoy the presentation kindly download it.
For Original view, download "Poetsen One" font style from dafont website.
Here I have discussed pharmacology of penicillin G.
Musculoskeletal Masqeuraders - Rolling the 'Clinical Dice'Steve Nawoor
I recently delivered this presentation on 'MSK Masqueraders' at the National Exhibition Center (NEC) in Birmingham for the 2015 Therapy Expo conference.
Basically this was a brief insight and overview of MSK Masqueraders and the impact on clinical practice. The context of each slide was expanded during the conference session and hopefully the presentation below gives you a flavour of the topics I covered. Be mindful that this presentation is a snippet of what I would usually cover so, is not a complete overview of the topic of Masqueraders, which is a challenging area of clinical practice.
Having knowledge of conditions that can masquerade as MSK pathology is a key aspect of the physiotherapist’s clinical development. More and more roles and opportunities are arising where we are responsible for first line assessment and care, which means we must have an ability to screen effectively, systematically and understand when the patient is presenting with symptoms that don't quite fit with an MSK presentation.
Index of suspicion, pattern recognition and understanding when and how to streamline you assessment to ascertain clarity on the next steps for a patient that you are concerned about can be challenging but is vital.
Twitter Handle: @stevenawoor
The Musculoskeletal System under the Unit HUMAN BODY
~now active with hyperlinks.
Please note that this presentation will be more appreciated if your computer is under Microsoft 2013. Kindly consider the compatibility for more convenient and pleasing slides.
Chronic kidney disease, also called chronic kidney failure, describes the gradual loss of kidney function. Your kidneys filter wastes and excess fluids from your blood, which are then excreted in your urine.
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.
Brief Information regarding the disorders of the genitourinary system. This presentation involves the disorders of the urinary system including Chronic Kidney Disease, Congenital problems related to the urinary system, and renal cancers.
Acute kidney injury (AKI), also known as acute renal failure (ARF), is a sudden episode of kidney failure or kidney damage that happens within a few hours
CKD is a condition in which the kidneys are damaged and cannot filter blood as well as they should. Because of this, excess fluid and waste from blood remain in the body and may cause other health problems, such as heart disease and stroke.
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.
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 Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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.
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Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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
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
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.
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.
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.
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, proteinuria or anaemia.
• 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 anaemia inCRF):
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.
• Hypertension develops in approximately 80% of patients
with CRF.
In part, this is caused by sodium retention.
Chronically diseased kidneys also tend to hypersecrete
renin, 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
• Atherosclerosis is common and may be accelerated by
hypertension.
19. • Pericarditis is 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 (osteitis fibrosa), 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. • Osteitis fibrosa results 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.
• Osteosclerosis is 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
• Generalised myopathy is 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 medullated
fibres, 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 prolonged in 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 cutaneous
ecchymoses 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 Renal failure?
• History
• Previous renal function test.
• Small kidneys on u/s
• Anaemia.
• Bone changes.
29. 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)
30. .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.
31. 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 the patient need
dialysis ) (vaccination against hepatitis B if no previous infection;
isolation of dialysis machine if positive) .
32. 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 )
33. X- ray of bone : for evidence of renal osteodystrophy.
GFR
Renal biopsy : only indicated in CRF with normal size kidneys
( not indicated in CRF with small size kidneys ).
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.
34. • 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
37. Chronic Kidney Disease Staging
Stage Description GFR
(ml/min/1.73 m2)
1 Kidney damage with normal or 90
GFR
Kidney damage with mild GFR 60-89
2
Moderate GFR 30-59
3
Severe GFR 15-29
4
Kidney failure < 15
5
(or dialysis)
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.
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 , amlodipine …
41. • ACE inhibitors like captopril have 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 calories
calories(30-35kcal/kg/d) to prevent malnutrition.
Anorexia and muscle loss may indicate a need to
commence dialysis treatment.
43. Treatment of Anaemia of 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 coagulability and 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
phosphate should 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, parathyroidectomy may become necessary
53. Treatment of renal osteodystropy
Vitamin D (0.25ug/d for prophylactic, 0.5ug/d
for symptomatic)
Low phosphate diet
Calcium carbonate (1-6g/d)
parathyroidectomy
54. Treatment of Myopathy
• 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
55. 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. Amitriptyline
and gabapentin may provide some symptom relief.
56. Treatment of Endocrine disorders
• Treatment with dopamine agonists is sometimes
useful for amenorrhoea or galactorrhoea in women
• Insulin requirements usually decline in diabetic
patients in end-stage CRF ( CRF patients are liable for
hypoglycemia ).
• insulin resistance is improved by dialysis treatment.
57. 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.
58. Depression
• Depression is common in patients on or
approaching renal replacement therapy and
support should be provided for both them and
their relatives