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Renal Replacement Therapy: modes and evidenceMohd Saif Khan
Renal replacement therapy is a supportive care often required in critically ill patients who develop acute renal failure and its complications. Complexity arises when such patients become hemodynamically unstable and pose special challenge to critical care clinicians in ICU to carefully choose dialytic modality to tackle volume and solute overload. This presentation is about short description of modalities of RRT and current evidence regarding initiation, dose and type of modality.
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Renal Replacement Therapy: modes and evidenceMohd Saif Khan
Renal replacement therapy is a supportive care often required in critically ill patients who develop acute renal failure and its complications. Complexity arises when such patients become hemodynamically unstable and pose special challenge to critical care clinicians in ICU to carefully choose dialytic modality to tackle volume and solute overload. This presentation is about short description of modalities of RRT and current evidence regarding initiation, dose and type of modality.
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https://youtu.be/XRD-QqGFP18
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https://youtu.be/c9PoavAtNKM
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- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
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Thrombotic Microangiopathy (TMA) in Adults and Acute Kidney Injury - Dr. GawadNephroTube - Dr.Gawad
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Infection-related Glomerulonephritis (KDIGO 2021 Guidelines) - Dr. GawadNephroTube - Dr.Gawad
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Insights from the FIGARO-DKD and FIDELIO-DKD trials - Dr. GawadNephroTube - Dr.Gawad
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Diabetes Mellitus Management in CKD (Clinical Tips) - Dr. GawadNephroTube - Dr.Gawad
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Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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
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.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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
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
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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
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
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1. Hypernatremia
Practical Approach
Mohammed Abdel Gawad
Nephrology Consultant - Alexandria - Egypt
MD Nephrology - Mansoura University
European Specialty Examination in Nephrology (ESENeph)
NephroTube Founder/Admin
Member of ISN education SoMe team
Co-chair of AFRAN Web & Media Committee
drgawad@gmail.com
@Gawad_Nephro
NephroTube Webinar, 08-July-2021
2.
3. To download the lecture
contact me
drgawad@gmail.com
For more Nephrology lectures visit
www.NephroTube.com
11. Question 1
Is the patient’s hypernatremia related to water deficit or gain of
Na+?
Question 2
Calculate his water deficit for serum [Na+] of 140 mEq/L?
Question 3
What is your choice of fluid administration?
Question 4
Estimate the reduction in serum [Na+], if 1 L of a fluid is infused
in 1 h?
12. Question 1
Is the patient’s hypernatremia related to water deficit or gain of
Na+?
Question 2
Calculate his water deficit for serum [Na+] of 140 mEq/L?
Question 3
What is your choice of fluid administration?
Question 4
Estimate the reduction in serum [Na+], if 1 L of a fluid is infused
in 1 h?
13. 2 Steps
13
Development of Hypernatremia
In the ICU, patients are often unable to
respond to normal thirst because of
altered mentation, sedation, or intubation
14.
15. UNa < 20
UNa > 20 UNa < or > 20 UNa > 20
Orthostatic changes Edema
16. UNa < 20
UNa > 20 UNa > 20
Orthostatic changes Edema
Blood Glucose level
UNa < or > 20
17. UNa < 20
UNa > 20 UNa > 20
Orthostatic changes Edema
Hypernatremia,
Hypokalemia,
Metabolic Alkalosis,
HTN
Blood Glucose level
UNa < or > 20
18. UNa < 20
UNa > 20 UNa > 20
Orthostatic changes Edema
Hypernatremia,
Hypokalemia,
Metabolic Alkalosis,
HTN
Blood Glucose level
Polyuria
Polyuria
UNa < or > 20
19. Question 1
Is the patient’s hypernatremia related to water
deficit or gain of Na+?
20. Question 1
Is the patient’s hypernatremia related to water
deficit or gain of Na+?
The patient’s hypernatremia is due to water deficit rather
than Na+ gain, as the patient has orthostatic changes
21. UNa < 20
UNa > 20 UNa > 20 UNa > 20
Orthostatic changes Edema
Hypernatremia,
Hypokalemia,
Metabolic Alkalosis,
HTN
Blood Glucose level
Polyuria
Polyuria
33. Question 1
Is the patient’s hypernatremia related to water deficit or gain of
Na+?
Question 2
Calculate his water deficit for serum [Na+] of 140 mEq/L?
Question 3
What is your choice of fluid administration?
Question 4
Estimate the reduction in serum [Na+], if 1 L of a fluid is infused
in 1 h?
34. Question 1
Is the patient’s hypernatremia related to water deficit or gain of
Na+?
Question 2
Calculate his water deficit for serum [Na+] of 140 mEq/L?
Question 3
What is your choice of fluid administration?
Question 4
Estimate the reduction in serum [Na+], if 1 L of a fluid is infused
in 1 h?
39. Calculation of Water Deficit
Add obligatory water output to the calculated infustae volume
• Obligatory water output from sweat and stool, which is approximately 30 to 40 mL/h
• Ongoing urinary and/or gastrointestinal losses is roughly equivalent to losing 50 mL/h
42. Question 1
Is the patient’s hypernatremia related to water deficit or gain of
Na+?
Question 2
Calculate his water deficit for serum [Na+] of 140 mEq/L?
Question 3
What is your choice of fluid administration?
Question 4
Estimate the reduction in serum [Na+], if 1 L of a fluid is infused
in 1 h?
43. Question 1
Is the patient’s hypernatremia related to water deficit or gain of
Na+?
Question 2
Calculate his water deficit for serum [Na+] of 140 mEq/L?
Question 3
What is your choice of fluid administration?
Question 4
Estimate the reduction in serum [Na+], if 1 L of a fluid is infused
in 1 h?
45. Assess volume status
Hypovolemia
Step 1: Correction of volume deficit:
Administer isotonic saline
(only in cases of frank circulatory
compromise until hypovolemia
improves)
Step 2: Correction of water deficit:
Calculate water deficit then replace
Euvolemia
Correction of water deficit:
Calculate water deficit then
replace
Hypervolemia
Step 1: Correction of water deficit:
Calculate water deficit then replace
Step 2: Removal of Na:
Furosemide (20-40mg/6hrs)
The ideal fluid is enteral water.
Often patients in the ICU have various contraindications
to enteral intake and in that case D5W can be used.
46. Assess volume status
Hypovolemia
Step 1: Correction of volume deficit:
Administer isotonic saline
(only in cases of frank circulatory
compromise until hypovolemia
improves)
Step 2: Correction of water deficit:
1- Calculate water deficit
2- Administer 0.45% saline, 5%
dextrose, or oral water
Euvolemia
Correction of water deficit:
1- Calculate water deficit
2- Administer 0.45% saline,
5% dextrose, or oral water
Hypervolemia
Step 1: Correction of water deficit:
1- Calculate water deficit
2- Administer 5% dextrose
Step 2: Removal of Na:
Furosemide (20-40mg/6hrs)
Question 3
What is your choice of fluid administration?
47. Question 1
Is the patient’s hypernatremia related to water deficit or gain of
Na+?
Question 2
Calculate his water deficit for serum [Na+] of 140 mEq/L?
Question 3
What is your choice of fluid administration?
Question 4
Estimate the reduction in serum [Na+], if 1 L of a fluid is infused
in 1 h?
48. Question 1
Is the patient’s hypernatremia related to water deficit or gain of
Na+?
Question 2
Calculate his water deficit for serum [Na+] of 140 mEq/L?
Question 3
What is your choice of fluid administration?
Question 4
Estimate the reduction in serum [Na+], if 1 L of a fluid is infused
in 1 h?
50. Treatment of Acute Hypernatremia
• Correct the serum sodium at an initial rate of 2-3 mEq/L/h (for 2-3 h)
(maximum total, 12 mEq/L/d).
Treatment of Chronic Hypernatremia
• Corrected at a rate not to exceed 0.5 mEq/L/h and a total of 8-10
mEq/d
Measure serum and urine electrolytes every 1-2 hours
Measure serum and urine electrolytes every 1-2 hours
51. >0.5 mmol/L per hour overall and >8, >10, and >12 mmol/L per 24 hours
chronic hypernatremia
128 with chronic
hypernatremia
52. Cerebral adaptation to hypernatremia
(Increase intracellular osmolality)
52
Immediate response:
increase in intracellular electrolytes.
But it is a limited because a there
is a maximum concentration that is
tolerable for cell function
53. Cerebral adaptation to hypernatremia
(Increase intracellular osmolality)
53
Later response:
Organic solutes (osmolytes) as Inositol,
glutamine, glutamate and taurine begin to
accumulate 24 to 48 hours after the onset
of hypernatremia
56. IMPORTANT !!!!
• It must be emphasized that the calculation of fluid deficit is only an
estimate based on several assumptions.
• When treating a patient with hypernatremia, it is important to
frequently assess plasma sodium to assure that the rate of correction
is proceeding as planned.
56
57. Evaluation & Follow up !!!!
• To assure an appropriate rate of correction, plasma sodium should be
measured frequently.
• Initially, plasma sodium checks should be about every two hours; less
frequent checks may occur when the plasma sodium is falling at a
predictable rate.
57