This document describes various complications that can arise in patients with end-stage renal disease (ESRD). It discusses difficulties regulating sodium, water, potassium and acid-base balance as kidney function declines. It also covers bone disease manifestations like osteitis fibrosa and adynamic bone disease. Treatment focuses on restricting dietary sodium/potassium and using binders/supplements to manage electrolytes and bone abnormalities. The document also notes anemia is common in later-stage CKD due to insufficient erythropoietin production.
End-stage renal disease is a condition in which the kidneys no longer function normally and required excellent medical and nursing care for the managing this condition.
Diabetic ketoacidosis is a serious complication of diabetes that occurs when your body produces high levels of blood acids called ketones. The condition develops when your body can't produce enough insulin.
When your cells don't get the glucose they need for energy, your body begins to burn fat for energy, which produces ketones. Ketones are chemicals that the body creates when it breaks down fat to use for energy. The body does this when it doesn’t have enough insulin to use glucose, the body’s normal source of energy. When ketones build up in the blood, they make it more acidic.
End-stage renal disease is a condition in which the kidneys no longer function normally and required excellent medical and nursing care for the managing this condition.
Diabetic ketoacidosis is a serious complication of diabetes that occurs when your body produces high levels of blood acids called ketones. The condition develops when your body can't produce enough insulin.
When your cells don't get the glucose they need for energy, your body begins to burn fat for energy, which produces ketones. Ketones are chemicals that the body creates when it breaks down fat to use for energy. The body does this when it doesn’t have enough insulin to use glucose, the body’s normal source of energy. When ketones build up in the blood, they make it more acidic.
This PPT is mainly useful for MBBS as well as other branch of Medicine to have an basic idea about Electrolytes. Also about What to see & What to do in cases of Electrolytes Imbalances.
This PPT is mainly useful for MBBS as well as other branch of Medicine to have an basic idea about Electrolytes. Also about What to see & What to do in cases of Electrolytes Imbalances.
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.
Introduction to Chronic Kidney Disease epidemiology, diagnosis, treatment of complications and system issues (e.g. interface between nephrology and primary care, specialty referrals) for medical students
Renal failure and its homeopathy treatment in Chembur, Mumbai, India Shewta shetty
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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.
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.
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.
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.
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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.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
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NVBDCP.pptx Nation vector borne disease control programSapna Thakur
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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
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
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.
5. 2 weeks PTC
• Complained of cough, whitish phlegm
• Associated with runny nose
• No fever
• No difficulty of breathing
• No chest pain
• No consult was done
6. 1 week PTC
• Persistence of symptoms
• Sought consult to local clinic
• Sent home without any meds
7. 5 days PTC
• Still with cough, whitish phlegm
• Already associated with orthopnea
(sitting position)
• Sought consult to clinic
• Given mucolytic and sent home
8. Day of admission
• Persistent of symptoms, patient sought
consult to local clinic
• Chest Xray was done
• Transferred to our institution
9. Physical Examination
• Awake, dyspnea
• BP unappreciated; HR 112; RR 42; T
36.8
• Neck vein engorgement (+)
• Crackles all over
• Abdomen soft, nontender
• No edema
10. In the ER
• Norepinephrine 0.1 mcg/kg/min
• Ipratropium bromide + Salbutamol
nebulization 2 doses
• 12 lead ECG ▶ sinus tachycardia
• ABG ▶ FiO2 60%
Ph 7.19
PaCO2 20
PaO2 81
HCO3 7
O2 94%
11. • NaHCO3 50 meq SIVP
• Intubated
• NaHCO3 150 meq in 250 cc D5W x 24o
• Piperacillin-Tazobactam 4.5 gr IV
loading then 2.25 gr IV q8
• BP 150/80
– Furosemide 80 mg IV
FiO2 100%
Ph 7.09
PaCO2 44
PaO2 50
HCO3 13
O2 71%
17. Chronic Kidney Disease
• Kidney damage or eGFR below 60
ml/min/1.73 m2 persisting for 3 months
• Abnormalities of kidney structure
• Irrespective of the cause
18.
19.
20. Mechanism
• Chronic and sustained insults to the
kidney evolve to progressive kidney
fibrosis with destruction of the normal
microarchitecture of the kidney ▶
replaced by fibrous tissue made of
collagenous extracellular matrix ▶ loss
of function
22. • In normal renal function, tubular
reabsorption of filtered sodium and
water is adjusted; urinary excretion =
intake
• In kidney disease, dietary intake of
sodium > urinary excretion ▶ sodium
retention and ↗ extracellular fluid
volume
26. Expansion of ECFV
• Presents as peripheral edema or
unresponsive hypertension
• Salt restriction
• Combination of diuretics and metolazone
can promote salt excretion
• Diuretic resistance with intractable
edema and hypertension: indication to
initiate dialysis
27. In face of extrarenal fluid loss..
• Prone to ECFV depletion because
inability to reclaim filtered sodium
• Compromise kidney function through
underperfusion ▶ acute-on-chronic
kidney failure
29. • Defense for decline in urinary potassium
excretion:
– Aldosterone-dependent secretion in the
distal nephron
– Augmented potassium excretion in the GI
tract
30. • Hyperkalemia may be precipitated:
– Increased dietary potassium intake
– Protein catabolism
– Hemolysis
– Hemorrhage
– Blood transfusion
– Metabolic acidosis
– RAS inhibitors and potassium sparing
diuretics
31. Hypokalemia
• Not common in CKD
• Reflects markedly reduced dietary
potassium intake, excessive diuretic,
concurrent GI losses
33. Metabolic Acidosis in Advanced
CKD
• Caused by failure of the tubular
acidification to excrete normal daily acid
load
• As functional renal mass is reduced;
increase in adaptive ammonia
production and H+ secretion
• Overall production may be decreased
secondary to the decrease in total renal
mass
34. • Majority of patients can still acidify the
urine
• Less ammonia = less proton excretion
• Hyperkalemia will further depresses
ammonia production
35. • eGFR < 30 ml/min, patient may develop
hyperchloremic normal anion gap
metabolic acidosis associated with
normo- or mild hyperkalemia
• eGFR < 15 ml/min, acidosis change to
anion gap metabolic acidosis; inability to
excrete phosphate, sulfate
36. Si & Sy
• Dyspnea as a result of respiratory
compensation
• Aggravates hyperkalemia
• Inhibits protein anabolism
• Accelerates calcium loss from bone (for
buffer of hydrogen ions)
37. Treatment
• NaHCO3 0.5 to 1.5 mmol/kg/day
• Beginning when HCO3
- level is < 22
mmol/L
• If acidosis is refractory to medical
therapy, dialysis needs to be initiated
39. Classification
• High bone turnover with increased PTH
levels (osteitis fibrosa)
• Low bone turnover with low or normal
PTH levels (adynamic bone disease and
osteomalacia)
40. Classification
• High bone turnover with increased PTH
levels (osteitis fibrosa)
• Low bone turnover with low or normal
PTH levels (adynamic bone disease and
osteomalacia)
41. Calcium Metabolism
• Calcium metabolism depends on close
interaction of PTH and vitamin D
• Total serum Ca++ tends to decrease as
result of phosphate retention and
decreased production of calcitriol,
intestinal calcium absorption, and
skeletal resistance to PTH
Levels of free calcium within
normal range
Compensatory
hyperparathyroidism
42. Phosphate Metabolism
• Hyperphosphatemia does not evident
before CKD stage 4
• Compensatory hyperparathyroidism and
increases in FGF-23 result in increased
phosphaturia
43.
44.
45.
46. Clinical Manifestations
• Aches and pains, nonspecific; lower
back, hips, legs; aggravated by weight
bearing
• May be confused with gout or
pseudogout and often respond to
NSAIDs
47. • Bone deformities as a consequences of
fractures; sometimes induced by brown
tumors
48. Treatment
• Prevention of hypocalcemia
– Calcium supplements (CaCO3) with
vitamin D
• Control of Phosphate
– Dietary phosphate restriction (0.8 g/kg/day)
– Phosphate binders (calcium-containing
antacids, magnesium salts, aluminium
hydroxide, etc.)
49.
50. Classification
• High bone turnover with increased PTH
levels (osteitis fibrosa)
• Low bone turnover with low or normal
PTH levels (adynamic bone disease and
osteomalacia)
51. • Consequences of inadequately low PTH
levels
• Iatrogenic oversuppression of PTH
results from high dose active vitamin D,
calcium loading, or after
parathyroidectomy
52.
53.
54. Treatment
• Avoid PTH overexpression and restore
adequate PTH levels without
development of secondary
hyperparathyroidism
– Reduction or withdrawal of active
vitamin D
– Reduction of dialysate calcium
concentration
56. • Isolated normochromic, normocytic
anemia
• Observed as early as stage 3 CKD and is
almost universal by stage 4
• Primary cause: insufficient production of
erythropoietin
57. Treatment
• Erythropoietic-stimulating agents
• Adequate bone marrow iron stores
• Adequate supply of other major
substrates and cofactors (e.g., vitamin
B12 and folate)
• Target hemoglobin: 100-115 g/L
Editor's Notes
Hyponatremia usually responds to water restriction
Aluminium containing antacids are effective but is not recommended because of the risk for aluminium toxicity
Calcium containing phosphate binders cant be used in hypercalcemia, extensive vascular calcification, and calciphylaxis
Anemia resistant to ESA in the face of adequate iron stores may be due to: acute or chronic inflammation, inadequate dialysis, severe hyperparathyroidism, chronic blood loss or hemolysis, chronic infection, or malignancy