1. Autosomal dominant polycystic kidney disease (ADPKD) is a genetic disorder characterized by multiple bilateral renal cysts and cysts in other organs caused by mutations in PKD1 and PKD2 genes.
2. The renal cysts enlarge over time, ultimately leading to renal failure in half of patients by age 60.
3. Treatment focuses on controlling blood pressure, treating infections, reducing pain, and delaying renal failure through medications such as ACE inhibitors or ARBs.
Polycystic disease of the kidney (PKD) is a disorder in which major portion of the renal parenchyma is converted into cysts of varying size .
Fluid-filled cysts distributed over the kidney results in massive enlargement of the kidneys.
In this presentation I have tried to cover renal disorder associated with vascular pathology of kidney. Classification, various disorder in detail with histopathology images H&E and special stains and clinical presentations. Hope it helps understanding the entity better.
Polycystic disease of the kidney (PKD) is a disorder in which major portion of the renal parenchyma is converted into cysts of varying size .
Fluid-filled cysts distributed over the kidney results in massive enlargement of the kidneys.
In this presentation I have tried to cover renal disorder associated with vascular pathology of kidney. Classification, various disorder in detail with histopathology images H&E and special stains and clinical presentations. Hope it helps understanding the entity better.
Antenatal diagnosis of Congenital Anomalies of Kidneys and Urinary Tract (CAKUT)Durre Sabih
Antenatal Diagnosis of Kidney Disease. This presentation gives an overview of the role of ultrasound in the diagnosis of fetal renal disease and congenital renal anomalies
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
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.
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.
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
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.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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
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.
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.
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
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3. Definition
ADPKD is a multisystem disorder characterized by multiple,
bilateral renal cysts associated with cysts in other organs,
such as liver, pancreas, and arachnoid membranes.
It is a genetic disorder mediated primarily by mutations in two
different genes and is expressed in an autosomal dominant
pattern, with variable expression.
4. Typically leads to renal failure mainly due to continued
enlargement of cysts.
ADPKD is the most common life-threatening monogenic
disease, affecting 12 million people worldwide.
Approximately 5% of patients who initiate dialysis annually in
the United States.
5. Etiology and Pathogenesis
The polycystic kidney disease (PKD) proteins now known as
polycystin 1 (PC1) and polycystin 2 (PC2) play a critical role in the
normal function of the primary cilium that is essential to
maintaining the differentiated phenotype of tubular epithelium.
Disordered function of polycystins is the basis for cyst formation
in PKD by permitting a less differentiated tubular epithelial
phenotype.
7. PKD1 PKD2
Located on Chromosome 16
[16p13]
Located on Chromosome 4
[4q21-q23]
Codes for Polycystin 1 protein
(PC1)
Codes for Polycystin 2 protein
(PC2)
Associated with more severe
phenotype
Less severe phenotype
Incidence: 85% Incidence: 15%
Median age of ESRD 53 years Median age of ESRD 73 years
Code PC1: Cilia, Basolateral
membranes, inter-membrane
junctions.
Helps in cell-cell adhesions.
Code PC2: non-selective cation
channel, permeable to Calcium.
Located mainly in SER.
8. Mutations in PKD1 and PKD2
Loss of ciliary function of PC1 and PC2
Reduced calcium signaling
Increase of adenylyl cyclase activity + decrease
of phosphodiesterase activity
Increased cellular cyclic AMP (camp)
Promotes protein kinase A activity
Proliferation and fluid secretion of cyst-lining cells through
chloride and aquaporin channels
Cyst growth
Increased cell proliferation and fluid secretion, decreased cell differentiation,
and abnormal extracellular matrix.
9. Cysts only occur in 5% of the tubules
in the kidney
Enormous growth of these cysts
ultimately leads to the loss of normal
surrounding tissues
Loss of renal function
11. Clinical Manifestations
Asymptomatic [until the fourth to fifth decade of life and are
diagnosed by incidental discoveries]
Pain—in the abdomen, flank, or back—is the most common initial
complaint. [may result from renal cyst infection, hemorrhage or
nephrolithiasis]
Gross hematuria [resulting from cyst rupture occurs in ~40% of
patients and many of them will have recurrent episodes.]
12. Physical Examination
Hypertension
Palpable, bilateral flank masses
Nodular hepatomegaly occurs in those with severe polycystic
liver disease
Symptoms related to renal failure (eg, pallor, uremic fetor, dry
skin, edema) are rare upon presentation.
13. Complications
Hypertension 60-100% [Cardiovascular complications are the major
cause of mortality in patients with ADPKD]
Infection [second most common cause of death for patients with
ADPKD]
Gross hematuria 50%
Nephrolithiasis 20-25%
Renal failure 50% by age 60 (PKD1) and 85% in lifetime
Polycystic liver disease
Cerebral aneurysms [occur in 4-10% of patients]
14. Hypertension
Increased activation of the renin-angiotensin-aldosterone
system,
Increased sympathetic nerve activity,
And impaired endothelial cilium function-dependent
relaxation of small resistant blood vessels.
15.
16. Nephrolithiasis
More than half of the stones in patients with ADPKD are composed of uric
acid, with the remainder due to calcium oxalate.
Distal acidification defects,
Abnormal ammonium transport,
Low urine pH and
Hypocitraturia
17. Intracranial aneurysm (ICA)
The disease gene products PC1 and PC2
may be directly responsible for defects in
arterial smooth muscle cells and
myofibroblasts.
Other vascular abnormalities in ADPKD
patients include diffuse arterial
dolichoectasias of the anterior and
posterior cerebral circulation, which can
predispose to arterial dissection and
stroke. Mitral valve prolapse occurs in up
to 30% of patients with ADPKD.
22. Investigations
Serum electrolytes, including calcium and phosphate
Complete blood cell count [An increased hematocrit may result
from increased erythropoietin secretion from cysts]
Urinalysis
Urine culture
Uric acid determination
parathyroid hormone assay
23. Complete blood cell count :
An increased hematocrit may result from increased
erythropoietin secretion from cysts.
Urinalysis:
Decrease in urine-concentrating ability,
Microalbuminuria occurs in 35% of patients,
Nephrotic-range proteinuria is uncommon]
24. Imaging
Ultrasonography [is the procedure of choice]
Computed tomography (CT) scan
Magnetic resonance imaging (MRI)
Genetic testing
Genetic testing by linkage analyses and mutational analyses
25. Ultrasonography
Ultrasonography is the most widely used imaging technique to help diagnose ADPKD. It can
detect cysts from 1-1.5 cm. This study avoids the use of radiation or contrast material, is
widely available, and is inexpensive.
26. At-risk subjects between 15
and 29 years of age
At least two renal cysts
(unilateral or bilateral)
Sensitivity of 96%
And specificity of 100%
Age 30 to 59 years At least two cysts in each
kidney
Sensitivity of 100% and
specificity of 100%
Age 60 years or
Older
At least four cysts in each
kidney
Sensitivity of 100% and
specificity of 100%
27. Computed tomography (CT) scan
CT is more sensitive than ultrasonography and can detect
cysts as small as 0.5 cm.
Useful in doubtful cases in children or in complicated cases
(eg, kidney stone, suspected tumor).
It exposes the patient to radiation and is more expensive.
28. Unenhanced axial computed tomography scan of the abdomen in a 45-year-old woman with autosomal
dominant polycystic kidney disease. The scan shows numerous cysts of different sizes involving the kidneys,
liver, and pancreas
29. Magnetic resonance imaging (MRI)
MRI is the best imaging tool to monitor kidney size after treatment to
assess progress.
Mri is more sensitive than either ultrasonography or ct scanning.
It may be more helpful in distinguishing renal cell carcinoma from
simple cysts.
Renal cysts show a homogeneous, low to intermediate signal intensity
on t1-weighted images and a homogeneous, high signal intensity on
t2-weighted images.
30. Treatment
Approach considerations
Control blood pressure
Control abnormalities related to renal failure
Treat urinary tract infections
Treat hematuria
Reduce abdominal pain produced by enlarged kidneys
31. Control blood pressure
Blood pressure control to a target of 140/90 mmhg is recommended
according to the guidelines from JNC VIII report
If more than 1 g/day of urinary protein is present, the target blood
pressure is less than 125/75 mm hg.
The drugs of choice for this condition are angiotensin-converting enzyme
(ace) inhibitors (ie, captopril, enalapril, lisinopril) or angiotensin ii receptor
blockers (arbs) such as telmisartan, losartan, irbesartan, and candesartan.
Calcium channel blockers are not recommended.
32. Urinary tract infections
Gram-negative bacteria are the most common pathogens.
Treating infected cysts requires antibiotics that penetrate into
the cyst. Useful agents are ciprofloxacin, trimethoprim-
sulfamethoxazole, clindamycin, and chloramphenicol.
33. Hematuria
It usually results from cyst rupture or stone passage.
Drink large amounts of water, rest and pain killer if necessary.
Hematuria is usually self-limited.
34. Abdominal pain from enlarged kidneys
Avoid Non-steroidal anti-inflammatory drugs (NSAIDs), because they can
worsen renal function and potentiate hyperkalemia.
Treatment involves surgical cyst decompression which is effective for pain
relief in 60-80% of patients.
Infected renal or hepatic cysts do not respond to conventional antibiotic
therapy
Very large cyst
Acute pain is from cyst hemorrhage or an obstruction by a clot, stone, or
infection
Nephrectomy is used as a last resort to control the pain and to make room
for a kidney graft.
35. Renal Failure
More than half of ADPKD patients eventually require
peritoneal dialysis, hemodialysis, or kidney transplantation.
Peritoneal dialysis may not be suitable for some patients with
massively enlarged polycystic kidneys due to the small intra-
abdominal space for efficient peritoneal exchange of fluid and
solutes and increased chance of abdominal hernia and back
pain.
36. Specific treatment strategies
No specific medication is available for autosomal dominant polycystic
kidney disease (ADPKD)
Specific treatment strategies for ADPKD have focused on slowing renal
disease progression and lowering cardiovascular risk.
Most approaches target the slowing of renal disease progression by
inhibiting cell proliferation and fluid secretion.
Targeting cell proliferation: sirolimus and everolimus
Inhibitors of the mTOR pathway; OPC31260 and tolvaptan
Reduce camp levels: somatostatin analogues.
A combination of different growth inhibitors may enhance efficacy and
reduce side effects.
37. Vasopressin Receptor Antagonists:
OPC 31260, Tolvaptan
Multicenter, placebo-controlled, double-blinded trial (TEMPO 3:4)
Inclusion: 18 to 50 years, GFR >60ml/min, TKV >750ml.
Dose: 60 to 120mg daily, 2:1 Drug: Placebo
Results after 3 years:
Tolvaptan Placebo
Increase in TKV 2.8% 5.5%
Decline in kidney
function
-2.61 mg/ml -3.81mg/ml
Adverse effects noted with Tolvaptan:
1. Increased liver enzymes (4.9%)
2. Chest pain (0.8%)
3. Headache (0.5%)
Torres VE, Chapman AB, Devuyst O et al. Tolvaptan in patients with autosomal dominant polycystic kidney disease. NEJM 2012;
367:407
38. Somatostatin:
RCT on 34 patients with ADPKD with Somatostatin or placebo.
Large multicentric trials required.
Results after one year:
Somatostatin Placebo
Mean kidney
volume
Stable, 0.25%
increase
8.60% increase
GFR Reduced to same
degree
Reduced to same
degree
Hogan et al. Randomized ClinicalTrial of long-acting Somatostatin for ADPKD and liver disese. J Am Soc Nephro 2010; 21: 1052
39. mTOR inhibitors:
*Double blind, two year. 431 patients with PKD (mean GFR 55 ml/min/1.73m2) with
placebo or everolimus.
Increase in protein: creatinine in Everolimus group.
S/e: Leukopenia, thrombocytopenia, hyperlipidemia.
**Trial 2:
Open-label RCT, 18 months. 100 patients with PKD (mean GFR 70 ml/min) with placebo or
sirolimus.
NO CHANGE IN TKV OR GFR after 18 months.
Albumin: creatinine 38% increased in Sirolimus group.
***Novel strategy:
Kidney-targeted folate-conjugated form of rapamycin inhibited mTOR activity in the kidney but not
other organs in a mouse model.
Everolimus Placebo
Increase in TKV 230ml 310ml
Decrease in GFR 8.9ml/min 7.7 ml/min