This document provides an overview of the management of chronic kidney disease (CKD). It defines CKD and outlines criteria for diagnosis based on markers of kidney damage and glomerular filtration rate (GFR). It describes tools for screening and staging CKD, including estimated GFR (eGFR) calculators and urine albumin-to-creatinine ratio. Common clinical manifestations of CKD like fluid and electrolyte disorders, anemia, bone disease, and cardiovascular complications are summarized. Treatment strategies are covered for managing complications involving hypertension, acid-base abnormalities, mineral and bone disorders, anemia, and diabetes in CKD patients.
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.
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.
Approach to chronic kidney disease abhijithV Abhijith
Contain almost all major topics associated with chronic kidney disease. Useful for medicine post graduates. I hope this presentation will help you all. Best of luck, thankyou
Renal failure and its homeopathy treatment in Chembur, Mumbai, India Shewta shetty
"Treatment & remedies for renal failure and its homeopathy treatment.Personalised online consultancy & treatments provided at our clinic by efficient panel of doctors in our center at mumbai,Bombay,Chembur, India.Contact us."/>
8 July is World Hepatitis Day
World Hepatitis Day, 28 July, is an opportunity to step up national and international efforts on hepatitis, encourage actions and engagement by individuals, partners and the public and highlight the need for a greater global response as outlined in the WHO's Global hepatitis report of 2017.
The date of 28 July was chosen because it is the birthday of Nobel-prize winning scientist Dr Baruch Blumberg, who discovered hepatitis B virus (HBV) and developed a diagnostic test and vaccine for the virus.
Low coverage of testing and treatment is the most important gap to be addressed in order to achieve the global elimination goals by 2030.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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
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
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
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.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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
2. Definition:
• CKD is defined as abnormalities of kidney structure or function,
present for >3 months
Criteria for CKD (either of the following present for >3 months)
Markers of kidney damage (one or more) Albuminuria (AER >30 mg/24 hours; ACR >30 mg/g
[>3 mg/mmol])
Urine sediment abnormalities
Electrolyte and other abnormalities due to tubular
disorders
Abnormalities detected by histology
Structural abnormalities detected by imaging
History of kidney transplantation
Decreased GFR GFR <60 ml/min/1.73 m2 (GFR categories G3a–G5)
3. CKD is classified based on cause, GFR category, and albuminuria
category (CGA).
4. Screening Tools: eGFR
• Considered the best overall index of kidney function.
• Normal GFR varies according to age, sex, and body size, and declines
with age.
• The NKF(National kidney foundation) recommends using the CKD-
EPI Creatinine Equation (2009) to estimate GFR. Other useful
calculators related to kidney disease include MDRD and Cockroft
Gault.
6. Cockcroft-Gault Formula :
• Creatinine clearance =
[{(140-age)* weight}/ (72*serum creatinine)] *0.85 (if female)
• GFR calculators are available online at www.kidney.org/GFR
7. Small changes make a big difference
Lee A Hebert et al. Kidney International (2001) 59, 1211–1226
•A GFR loss of
> 1 mL/min/year
beginning at age
25 can result in
end-stage renal
disease within a
normal lifespan.
8. Screening Tools: ACR
• Urinary albumin-to-creatinine ratio (ACR) is calculated by dividing
albumin concentration in milligrams by creatinine concentration in
grams.
• Spot urine albumin-to-creatinine ratio for quantification of
proteinuria
• First morning void preferable
• 24hr urine test rarely necessary
11. Fluid and Electrolyte disorder
• Patients with CKD, the tubular reabsorption of filtered sodium and
water is adjusted ,so that urinary excretion matches intake.
• Many form of kidney disease disrupt this balance leading to sodium
retention and extracellular fluid volume(ECFV)
• Dietary salt restriction and use of loop diuretics, occasionally in
combination with metalozone maintain euvolemia
• In contrast overzealous salt restriction or diuretic use can lead to
ECFV depletion and precipitate further decline in GFR.
12. Hyperkalemia
• Decline in GFR doesn’t necessarily parallel decline in urinary potassium
excretion
• Hyperkalemia may precipitate due to increased dietary potassium intake,
protein catabolism, hemolysis, blood transfusion and metabolic acidosis
• RAS inhibitor and potassium sparing diuretics also cause hyperkalemia.
• In diabetic nephropathy and renal disease involving distal nephron such as
obstructive uropathy and sickle cell nephropathy are associated with
earlier and more severe disruption of potassium secreting mechanism in
distal nephron out of proportion to decline in GFR.
13. Hyperkalemia Treatment:
• Respond to reduce dietary potassium
• Stop potassium sparing diuretics (spironolactone)
• Stop or reduce beta blockers, ACE inhibitor/ARBs
• Hypokalemia is not common in CKD.
14. Hyperkalemia Treatment continue…
Large amounts of potassium are found in:
•certain fruits and vegetables (like bananas, melons, oranges, potatoes,
tomatoes, dried fruits, nuts, deep-colored and leafy green vegetables,
and some juices)
•milk and yogurt
•dried beans and peas
•most salt substitutes
•protein-rich foods, such as meat, poultry, pork, and fish
15. Metabolic acidosis
• Mild degree of non-anion gap metabolic acidosis (PH < 7.35)often
present in CKD stage 1-3
• With the worsening renal function non-anion gap metabolic
acidosis complicated by anion gap metabolic acidosis
• Respond to alkali supplementation, typically with sodium
bicarbonate if serum bicarbonate concentration falls below 20-23
mmol/L
• Correction of metabolic acidosis may slow CKD progression and
improve patients functional status by attenuating catabolic state.
16. Hypertension
• Effective reduction in BP with antihypertensive medication can decrease the
urinary excretion of albumin and slow the rate of progression of CKD
• Dual blockade of the renin-angiotensin system with an ACE inhibitor and
angiotensin receptor blocker has been shown to have an additive effect in
reducing albumin excretion.
• Avoid ACE inhibitor and ARB in combination because Risk of impaired kidney
function and hyperkalemia
17. Blood pressure control
• Single most important measure to slow the progress of CKD
• Individualize targets and agents according to age, coexistent CVD, and other
comorbidities
• ACE or ARB
• Diuretics enhance the antihypertensive and antiproteinuric effects of other
agents.
18. ACEi and ARB: Slowing CKD Progression
• ACE inhibitor and ARBs appear to slow the decline of renal function in
a manner beyond reduction in systemic blood pressure
• Check labs after initiation
• If less than 25% SCr increase, continue and monitor
• If more than 25% SCr increase, stop ACEi
• Better proteinuria suppression with low Na diet and diuretics
19. Clinical Practice Guidelines for Management of Hypertension in
CKD
Type of Kidney Disease Blood Pressure
Target
(mm Hg)
Preferred Agents for
CKD, with or without
Hypertension
Other Agents
to Reduce CVD Risk and
Reach Blood Pressure
Target
Diabetic Kidney Disease
<140/90
ACE inhibitor
or ARB
Diuretic preferred, then BB
or CCB
Nondiabetic Kidney
Disease with Urinary
albumin-to-creatinine ratio
(ACR) 30 mg/g
<130/80
Nondiabetic Kidney
Disease with Urinary
albumin-to-creatinine ratio
(ACR) <30 mg/g None preferred
Diuretic preferred, then ACE
inhibitor, ARB, BB or CCB
Kidney Disease in Kidney
Transplant Recipient
CCB, diuretic, BB, ACE
inhibitor, ARB
20. Diabetes and Glycemic Control in CKD
• Target HbA1c ~7.0%
• Improved glycemic control reduces the rate at which
microalbuminuria appears and progresses
• Risk of hypoglycemia increases as kidney function becomes
impaired
• Declining kidney function may necessitate changes to
diabetes medications and renally-cleared drugs
21.
22. Modification of Other CVD Risk Factors in CKD
• Smoking cessation
• Alcohol restriction
• For those who drink alcohol, consume </=2 drink/day in men and </= 1 drink
in women
• Exercise
• 30 -60 minutes of moderate intensity dynamic exercise 4-7 days/ week.
• Weight reduction
• target BMI 18.5 – 24.9 kg/m2 and waist circumference in men <102 cm and
female < 88 cm.
23. Modification of Other CVD Risk Factors in CKD
• Lipid lowering therapy
• In adults >50 yrs : statin when eGFR ≥ 60 ml/min/1.73m2;
:statin or statin/ezetimibe combination when eGFR < 60
ml/min/1.73m2
• In adults < 50 yrs, statin if history of known CAD, MI, DM, stroke
• Aspirin is indicated for secondary but not primary prevention
• Dietary salt restriction less than 5-6 gm daily
24. Anemia in CKD
• Normocytic normochromic anemia is observed as early as stage 3
CKD and is almost universal by stage 4.
• Diagnose anemia in adults and children >15 years with CKD when the
Hb concentration is
<13.0 g/l in males and
<12.0 g/dl in females.
• Anaemia in CKD should include assessment of secondary causes
including iron deficiency.
25.
26. Anaemia continue….
• Iron replacement is often effective in anaemia of CKD as initial
therapy.
• ESA (erythropoiesis stimulating agents): Start ESA if Hb <10 g/dl, and
maintain Hb <11.5 g/dl. Ensure adequate Fe stores.
• Before initiation of ESA therapy iron saturation should be maintained
at 30 -50 % and serum ferritin at 200-500 ng/ml.
• In addition to iron adeqaute supply of vitamin B12 and folic acid
should be assured.
27. CKD-MBD (Mineral and Bone Disorder)
• Serum calcium , phosphate and PTH should be measured for adults
with stage 4-5 CKD and for with stage 3 CKD with progressive decline
in renal functions.
• Serum phosphate and serum calcium level should be maintained
within the normal range.
• Target PTH levels in CKD is 150-300 pg/ml.
28. Pathophysiology of Secondary Hyperparathyroidism
Decline GFR
Phosphate retention : hyperphosphatemia
Increase PTH
hyperparathyroidism
Increase synthesis of
FGF-23 by osteocytes
Suppression of calcitriol
production by kidney
Decrease level of
ionised Calcium
29. FGF-23 maintain normal serum phosphate level by
• Increase serum phosphate excretion
• Stimulation of PTH , which increase phosphate excretion
• Suppression of calcitriol leading to diminished phosphorus absorption
from GI tract.
FGF-23 is also an independent risk factor for LVH and mortality in CKD,
dialysis and renal transplant patients.
30. Bone Manifestations
• Osteitis fibrosa cystica- due to secondary
hyperparathyroidism
• Adynamic bone disease and osteomalcia-
low or normal PTH
• Occasionally calcium will precipitate
in soft tissue in large concentration
termed “TUMORAL CALCINOSIS”
31. Calciphylaxis
• Calcific uremic arteriolopathy is a
devasting condition seen almost in
patients with advanced CKD and heralded
by livedo reticularis and ischemic necrosis
patches, especially in legs, thigh,
abdomen and breast.
• Pathologically, vascular and extensive soft
tissue calcification.
32. CKD-MBD :Prevention
• Restriction of dietary phosphate:
Large amounts of phosphorus are found in:
•dairy products such as milk, cheese, yogurt, ice cream, and pudding
•nuts and peanut butter
•dried beans and peas, such as kidney beans, split peas, and lentils
•beverages such as cocoa, beer, and dark cola drinks
•bran breads and bran cereals
•processed, convenience, and fast foods, including some meats
33. CKD-MBD : Prevention continue…
• Use of calcium based phosphate binders- calcium carbonate and
calcium acetate and non-calcium based phosphate binders sevalamer
and lanthanum.
• Calcium based phosphate binder have risk of developing
hypercalcemia.
• Prescribe vitamin D analogue if serum level of intact PTH > 53 pg /ml
34. Renal replacement therapy
• Indication:
• Uremic symptoms: anorexia and nausea, impaired nutritional status,
increased sleepiness, and decreased energy level, attentiveness, and
cognitive tasking
• Presence of Hyperkalaemia unresponsive to conservative measure
• Severe metabolic acidosis refractory to medical therapy
• Uremic pericarditis
• Encephalopathy
• Persistent extracellular volume expansion despite of diuretic therapy
• Asymptomatic patients with eGFR 5-9 ml/min/1.73 m2
35. Treatment Options for Renal Replacement
Therapy
There are essentially two options to a patient facing ESRD:
1- Dialysis
2- Transplantation, which has been clearly shown to be the best
treatment option
36. Dialysis Options
• They have to choose between
• hemodialysis and
• peritoneal dialysis
- Hemodialysis can be done at home with a machine that is smaller than
the traditional in-hospital/outpatient clinic machine.
- Peritoneal dialysis can either be done with a cycler or manually
37. Immunizations
CDC recommend following immunization in patients with CKD on
dialysis
• Influenza vaccine annually for all CKD patients
• Pneumococcal vaccine for patients with ESRD
• O, 2 months
• Booster at 5 year
• Hepatitis B vaccine
• O, 1,2, 6 month (2 ml)