Acute renal failure or acute kidney injury is characterized by determination of renal functions over a period of hours to few days, resulting in failure of the kidney to excrete nitrogenous waste product and to maintain fluid, electrolytes and acid-base homeostasis.
Acute renal failure or acute kidney injury is characterized by determination of renal functions over a period of hours to few days, resulting in failure of the kidney to excrete nitrogenous waste product and to maintain fluid, electrolytes and acid-base homeostasis.
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.
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.
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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.
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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.
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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
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
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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.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
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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.
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
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
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
3. OBJECTIVES
• Identify normal functioning of the kidney and laboratory
tests that assess kidney function
• Define renal failure
• Discuss the causes of acute renal failure and compare
those with chronic renal failure
• Compare prerenal, intrarenal and postrenal conditions
• Identify the alterations seen in patients, explaining why
they exist
• Identify nursing measures appropriate to the
alterations
4. NORMAL KIDNEY
FUNCTION
What does the kidney do in terms of?
• wastes and water balance?
• Acid base balance?
• Controlling BP?
• Controlling anemia?
5. RENAL FAILURE DEFINED
• Kidneys no longer function properly
• Kidneys unable to excrete waste
• kidneys cannot concentrate urine
• Kidneys cannot conserve electrolytes
6. HORMONES WHICH
INFLUENCE THE KIDNEY
• ALDOSTERONE
– Produced:
– Action:
• RENIN/ANGIOTENSIN
– Produced:
– Action:
7. HORMONES WHICH
INFLUENCE THE KIDNEY
• ANTIDIURETIC HORMONE
– Produced:
– Action:
• ERYTHROPOIETIN (EPO)
– Produced:
– Action:
8. IDENTIFYING THE THREE
PRIMARY RENAL FUNCTIONS
• GLOMERULAR FILTRATION:glucose, amino acids,
creatinine, urea, phosphates, uric acid
• GLOMERULAR REABSORPTION:bicarbonate,
phosphates, sulfates, 65% of Na and water, glucose,
K, amino acids, H ions, urea
• GLORMERULAR SECRETION: hydrogen and
potassium, remove acids (hydrogen) to maintain
appropriate acid base balance, potassium, urea
9. ASSESSMENTS OF RENAL
FUNCTION
• u/a: negative for glucose, protein, blood,
leukocytes, nitrites, ketones
• Specific gravity: measures concentration of
the urine; normal values: 1.010-1.025
• Urine osmolality: normal 300-900 mOsm/
kg/24
• Serum creatinine: 0.6-1.2mg/dl
• BUN: 7-18mg/dl
• BUN to creatinine ratio: about 10:1
10. DIAGNOSTIC ASSESSMENTS
CONTINUED
• STANDARD FOR RENAL FUNCTION:
assess glomerular filtration rate (GFR)
• Norm for this assessment is the
creatinine clearance test done over 24
hours: normal rate is 80-125ml/min
11. DEFINITIONS
• OLIGURIA: urine output is less than 30
ml/hr
• ANURIA: no urinary output
• NORMAL URINARY OUTPUT: 1500-
1800ml/day
12. CAUSES OF ACUTE RENAL
FAILURE
• PRERENAL or factors external to the kidney
which interferes with renal perfusion (55%
cases of ARF)
• INTRARENAL: conditions that cause direct
damage to renal tissue (35-40% cases of
ARF)
• POSTRENAL: mechanical obstruction in the
urinary tract (5% cases of ARF)
13. CAUSES OF RENAL FAILURE
CONTINUED
• Multiple problems may exist at same
time
• AGING
14. RENAL FAILURE DEFINED
• To define renal failure ask yourself: How
is the kidney functioning with regard to?
• Excreting nitrogenous wastes
• Concentrating urine
• Conserving electrolytes
15. PROBLEMS FOR PATIENT
• Retention of metabolic wastes
• Imbalance of fluid and electrolytes
• Alterations of sensorium
19. DIURETIC PHASE (lasts 1-3
wks)
Gradual increase of urine output as a
result of osmotic diuresis
• Why does this happen?
• What is the state of nephron?
• Can the kidney excrete wastes?
• Can the kidney concentrate urine?
• What would we see in the patient during
this stage?
22. MAINTAINING FLUID AND
ELECTROLYTE BALANCE
• How do we assess fluid excess?
• How can we control fluid intake?
• What physical assessments would be
done?
• What would you expect to see?
• What laboratory tests would be used to
assess client status?
25. DIET FOR ACUTE RENAL
FAILURE
• dietary protein
• calories
• K and phosphorus
• Na
• Fe
26. CHRONIC RENAL FAILURE
DEFINED
• Progressive deterioration in renal
function resulting in fatal uremia (excess
of urea and other nitrogenous wastes in
the blood)
• Irreversible destruction of nephrons
• Called ESRD (end stage renal disease)
• Dialysis or transplant
27. TERMS ASSOCIATED WITH
CHRONIC RENAL FAILURE
• Azotemia: collection of nitrogenous
wastes in blood
• Uremia: azotemia
• Uremic syndrome: systemic clinical and
laboratory manifestations of ESRD
29. ALTERATIONS OF CHRONIC
RENAL FAILURE CONTINUED
• Gastrointestinal Disturbances: Anorexia, N&V,
metallic taste in mouth, breath smells like
ammonia, stomatitis, ulcers/GI bleeding,
constipation
• Neurological Distrubances: uremic
encephalopathy progresses to seizures &
coma
• CHF: from increased workload on heart from
anemia, hypertension and fluid overload
• Uremic pericarditis: pericardium becomes
inflammed from toxins
30. ALTERATIONS OF CHRONIC
RENAL FAILURE CONTINUED
• Respiratory:
– breath smells like urine: uremic fetor or
uremic halitosis
– Metabolic acidosis: see tachypnea
(increased rate) and hyperpnea (increased
depth) indicates worsening metabolic
acidosis
• See Kussmaul respirations extreme
hyperventilation
31. NURSING CARE FOR PT WITH
CHRONIC RENAL FAILURE
FOR ANEMIA:
FOR HYPOCALCEMIA
FOR FLUID RETENTION AND HYPERTENSION
FOR SKIN ITCHING
36. PERITONEAL DIALYSIS
• Diffusion of solute molecules through a semi-
permeable membrane passing from the side of higher
concentration to that of lower concentration
• Fluids passing through the semi-permeable
membrane via osmosis
• Renal Failure pt has dialysis to remove waste
products and to maintain life until kidney function can
be restored
• Dialysis indicated for high levels of K and fluid
overload
37. PERITONEAL DIALYSIS
• Sterile dialyzing fluid is introduced into
the peritoneal cavity
• Peritoneum is an inert semipermeable
membrane
• The dialyzing solution promotes
osmosis leading to diuresis
• Urea and creatinine are removed
38. NURSING CARE OF PT ON
PERITONEAL DIALYSIS
• Baseline VS and wgt
• Assess for fluid overload
• Maintain highly accurate inflow and outflow
records
• When PD starts the outflow may be bloody
or blood tinged
• This clears within a week/two
• Effluent should be clear and light yellow
39. Nursing care during PD
• Drainage bag is lower than the client’s
abdomen to enhance gravity drainage
• Avoid kinking or twisting, ensure
clamps are open
• Reposition client to stimulate inflow or
outflow
• Sitting/standing/coughing: increases
intraabdominal pressure
40. COMPLICATIONS OF
PERITONEAL DIALYSIS
• Respiratory difficulties
• Hypotension
• Infection:
– peritonitis: see cloudy or opaque dialysate outflow
(effluent), fever, abdominal tenderness, pain, malaise, N&V
• Hypo-albuminemia
• Bowel perforation:
• Bladder perforation:
• Catheter may get clogged
41. COMPLICATION OF PD: Fibrin
Clot formation
• Fibrin Clot formation
• Milking the tubing
• Xray
42. COMPLICATION OF PD:
LEAKAGE
• Dialysate leakage
• See with obese, diabetic, older clients,
those on long term steroids
43. HEMODIALYSIS
• Process by which the uremic toxins and
accumulated waste products are
removed from the blood
44. HEMODIALYSIS
CONTINUED
• A synthetic semi-permeable membrane
replaces the renal glomeruli and tubules
and acts as a filter for the impaired
kidneys
• Must have 3 times/week for 4 hours per
treatment for rest of life
45. Access to pt’s circulation via:
• AV shunt (less common): external silastic
tubing placed in an adjacent artery and vein
• AV Fistula: internal access using pts own
vessels (artery and vein)
• AV Graft: internal access using a foreign
material
47. Assessment during Hemodialysis
– Assess for disequilibrium reaction
– CAUSE:
• due to rapid decrease in fluid volume and BUN levels
• Change in urea levels can cause cerebral edema and
increased intracranial pressure
• Neurologic complications: HA, N&V, restlessness,
decreased LOC, seizures, coma, death
• PREVENTION: starting HD for short periods
with low blood flows
48. Nursing care pre dialysis
• Vasoactive drugs which cause
hypotension are held until after
treatment
• CHECK WITH MD ABOUT WHICH
DRUGS TO BE HELD
• Know pt’s BP predialysis
49. Post dialysis nursing care
• BP and wgt
• Hypotension
• Temperature may also be elevated:
• If client has a fever
• Bleeding risk:
50. KIDNEY TRANSPLANT
• Involves transplanting a kidney from a
living donor or human cadaver to a
recipient who has end-stage renal
disease and requires dialysis to live
51. POSTOPERATIVE CONCERNS
AFTER TRANSPLANT
major concern is rejection
• Drugs given to suppress immunologic
reactions: Imuran, prednisone,
cyclosporin (Cyclosporin A)
Next concern is infection
52. NRSG CARE POST KIDNEY
TRANSPLANT
TO DETECT REJECTION:
• Assess for increased temp, pain or
tenderness over grafted kidney
• Assess for decrease in urine output,
edema, sudden wgt gain
• Assess for rise in serum creatinine and
BUN values