Acute kidney injury (AKI) is a potentially life-threatening
syndrome that occurs primarily in hospitalized patients
and frequently complicates the course of critically ill
patient.
Acute Kidney Injury is is (abrupt) reduction in kidney functions as evidence by changed in laboratory values; serum creatinine, blood urea nitrogen(BUN)and urine output
Seminar present the Upper Gastrointestinal Bleeding problems
Edited by : Dr. Inzar Yassen & Dr. Ammar L. Aldwaf
in Hawler Medical Uni. collage of medicine in 14/01/2014
Iraq - Kurdistan - Erbil
Seminar present the Upper Gastrointestinal Bleeding problems
Edited by : Dr. Inzar Yassen & Dr. Ammar L. Aldwaf
in Hawler Medical Uni. collage of medicine in 14/01/2014
Iraq - Kurdistan - Erbil
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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
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.
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.
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
- 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
CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
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.
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.
2. ACUTE KIDNEY INJURY
Acute kidney injury (AKI) is abrupt reduction in kidney
functions as evidence by changed in laboratory values; serum
creatinine, blood urea nitrogen(BUN)and urine output.
Acute kidney injury (AKI) is diagnosed if one of the
following criteria is met :
increase in serum creatinine (SCr) of at least 0.3 mg/dL
within 48 hours,
a 50% increase in baseline SCr within 7 days, or
a urine output of less than 0.5 mL/kg/hour for at least 6
hours.
3. EPIDEMIOLOGY AND ETIOLOGY
Between 5% and 7% of all hospitalized patients develop
AKI.
A greater prevalence of AKI is found in critically ill
patients ( ICU-Acquired AKI).
Despite improvements in the medical care of individuals
with AKI, mortality generally exceeds 50%.
5. CLASSIFICATION OF AKI
Criteria used for AKI classification
RIFLE: Risk, Injury, Failure, Loss of Kidney
Function and End Stage Renal Disease).
AKIN: Acute Kidney Injury Network
KDIGO: Kidney Disease Improving Global
Outcome
9. PRERENAL AKI
Prerenal AKI: is characterized by reduced blood
delivery to the kidney.
A common causes are:
Volume depletion
hemorrhage
dehydration
GI fluid losses.
Decrease effective circulatory blood volume
Decrease cardiac output (CHF, MI, hypotension
Pulmonary hypertension
Liver failure
Sepsis
Functional
ACEIs, NSAIDs, ARBs, Cyclosporine and tacrolimus
Prompt correction of volume depletion can restore kidney
function to normal because no structural damage to the
kidney has occurred.
10. INTRINSIC AKI
Damage is within the kidney (structure of the nephron,);
Vascular damage (renal thrombosis)
Glomerular damage (nephrotic/nephritic
glomerulonephritis
Acute tubular necrosis(ATN)(it accounts for 50% of all cases of AKI)
Ischemia (hypotension, sepsis
Endogenous toxins(uric acid ,hemoglobin
Exogenous toxin
Aminoglycosides
contrast induced nephropathy (CIN)
amphotericin B
Acute interstitial nephritis
NSAIDs
infections
Prerenal AKI can progress to intrinsic AKI if the underlying
condition is not promptly corrected
11. POSTRENAL AKI
Postrenal AKI is due to obstruction of urinary
outflow
Bladder outlet obstruction
Benign prostatic hypertrophy
Prostate cancer
Anticholinergic drug
Ureteral obstruction
Malignancy
Pelvic / renal obstruction
Postrenal AKI accounts for less than 10% of cases of
AKI
Rapid resolution of Postrenal AKI without structural
damage restore kidney function
12.
13. By monitoring Scr on a routine basis, it can be
estimated whether kidney function is improving or
worsening.
Kidney function can also be evaluated based on urine
output. Oliguria and anuria
Oliguria is defined as urine outputs of less than 400 ml
over 24 hours
anuria is defined as urine output of less than 50 mL over
24 hours.
14. CLINICAL PRESENTATION AND DIAGNOSIS OF AKI
Peripheral edema
Weight gain
Nausea/vomiting/diarrhea/anorexia
Mental status changes
Fatigue
Shortness of breath
Pruritus
15. LABORATORY TESTS
Elevated Scr (normal range approximately 0.6-1.2
mg/dL [53 to 106 μmol/L])
Elevated BUN concentration (normal range
approximately 8 to 25 mg/dL [2.9-8.9 mmol/L])
Decreased CrCl (normal 90–120 mL/min)
BUN: creatinine ratio
greater than 20:1 in Prerenal AKI
Less than 20:1 in intrinsic or Postrenal AKI
Hyperkalemia
Metabolic acidosis
16. PREVENTION APPROACHES
Non-pharmacology for prevention
Hydration to prevent contrast induced nephrotoxicity
KDIGO guideline recommend using normal saline or
sodium bicarbonate infusion
Normal saline regimen: 1ml/kg/h for 12hours before
and after procedure.
Sodium bicarbonate regimen: 3ml/kg/hours for one
hour before procedure and 1ml/kg/hours for 6 hours
postcontrast.
17. PHARMACOLOGICAL THERAPY
For prevention of CIN
Ascorbic acid:3g orally pre and 2mg orally for two
doses postprocedure and N-acetylcysteine(600-1200mg
orally every 12 hours for 2-3 days, the first two doses
precontrast
Current KDIGO guideline suggest moderate control of
blood glucose to level of 110-149 mg/dl with insulin
prevent ICU-Acquired AKI
19. Goal of treatment:
Minimize the degree of kidney insult
Reduce extrarenal complication
Restoration of renal function to pre AKI is the
ultimate goal
20. TREATMENT APPROACHES
Currently, there is no definitive therapy for
AKI, supportive care is the mainstay of
management regardless of etiology.
21. SUPPORTIVE CARE IN AKI
Supportive care includes :
Adequate nutrition,
correction of electrolyte and acid-base abnormalities
(particularly hyperkalemia and metabolic acidosis)
Fluid management,
Correction of any hematologic abnormalities
Medical management of infections, cardiovascular and
GI conditions, and respiratory failure
all drugs should be reviewed, and dosage adjustments
made based on an estimate of the patient’s GFR.
22. NON-PHARMACOLOGICAL THERAPY
Maintenance of adequate cardiac output and blood
pressure to optimize tissue perfusion
Discontinue medication associated with diminished renal
blood flow
Initiate appropriate fluid and electrolyte
Renal replacement therapy RRT in sever AKI
Hemodialysis
Peritoneal dialysis
Absolute indications for dialysis usually include:
BUN greater than 100 mg/dL (35.7 mmol/L)
Potassium greater than 6 mEq/L (6 mmol/L)
Magnesium greater than 9.7 mg/dL (4.0 mmol/L)
Metabolic acidosis with a pH less than 7.15
Diuretic-resistant fluid overload.
24. PHARMACOLOGIC THERAPY
Loop diuretics : are effective to reduce fluid
overload.
it can worsen AKI.
Thiazide diuretics, when used as single agents, are
generally not effective for fluid removal.
Mannitol is also not recommended for treating volume
overload associated with AK.
Potassium sparing diuretics are not recommended.
low dose dopamine LDD is not indicated in treating the
AKI.
25. Equipotent dose of loop diuretics (Furosemide,
bumetanide, torsemide and ethacrinic acid ) all have
similar efficacy
Ethacrynic acid is reserved for sulfa-allergic patient
Continues infusion of loop diuretic overcome
diuretic resistance
associated with less adverse effect than intermittent bolus
Dose:
Initial iv loading dose equivalent to (40-60mg
furosemide )
Continuous infusion equivalent to 10-20mg/h
26. STRATEGY TO OVERCOME DIURETIC
RESISTANCE
Administration of agents from different
pharmacological classes, they act synergistically
Thiazide (works on: distal convoluted tubule)
loop diuretics (works on: ascending loop of Henle)
27.
28. ELECTROLYTE MANAGEMENT
Serum electrolyte should be monitored
daily.
Hyperkalemia is the most common and serious
electrolyte abnormality in AKI
Hypernatremia and fluid retention commonly
occur …require daily calculation of sodium intake
Phosphorus and magnesium should be
monitored
29. PREVENTION OF ACUTE RENAL
FAILURE
Avoidance
The best preventive measure for AKI, especially in individuals at
high risk, is to avoid medications that are known to precipitate AKI.
Nephrotoxicity is a significant side effect of
aminoglycosides,
ACE inhibitors, angiotensin receptor
antagonists(ARBs),(what are the risk factors?)
Amphotericin B
NSAIDs
Cyclosporine, tacrolimus,
Radiographic contrast agents GFR less than 60 mL/min
, diabetes, dehydration, age more than 65 years,
How to reduce CI-AK?