1) Blocking the renin-angiotensin-aldosterone system (RAAS) through ACE inhibitors or ARBs reduces oxidative stress, improves endothelial function, and lowers rates of atherosclerosis progression compared to other antihypertensives.
2) RAAS blockade improves glucose metabolism by increasing nitric oxide, reducing angiotensin II levels, and enhancing insulin sensitivity and glucose transport in skeletal muscle. Clinical trials show reduced cardiovascular events and nephropathy in diabetes patients treated with ACE inhibitors.
3) Multiple clinical trials demonstrate that targeting lower diastolic blood pressure goals or using RAAS blockade reduces cardiovascular events and new onset diabetes compared to other antihypertensive classes.
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
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
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
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
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.
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.
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
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
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
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
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.
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.
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.
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
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.
Riesgo Cardiometabolico: Papel de la Hipertension (3)
1. SRAA y Ateroesclerosis SRAA y Ateroesclerosis
drpp 2009 drpp 2009
Mecanismos de Inhibición del Bloqueo del SRAA y Stress Oxidativo
SRAA comparado con otros antihipertensivos
Valsartan Ramipril Doxazosin Metoprolol Amlodipine
80 mg od 5 mg od 4 mg od 100 mg od 10 mg od
(n = 20) (n = 20) (n = 20) (n = 22) (n = 20)
0
–10 –2.7% * –2.4% *
–20 –15.9% *
Aldosterone ! in MDA
blockers
Formation –30
(%) –40 *P <0.001 vs baseline.
–50
–60 –57.6%
–70
–67.2%*
Change from baseline in formation of malondialdehyde (MDA), a marker of lipid peroxidation, after 3
months treatment (N = 102).
drpp 2009 Baykal Y et al. J Hypertens. 2003;21:1207-1211. drpp 2009
Bloqueo de Receptor AT1 Efectos del Ramipril en la
Vasodilatación mediada por flujo Ateroesclerosis Carotídea
N=732 patients with vascular disease or diabetes
122 Hypertensive patients treated for 2 months
0.025 Mean Changes in BP:
2.0 RR -37 (P=0.028) Baseline to Study End
Mean Max. Carotid IMT Slope (mm/year)
1.66*
0.020 Systolic BP (mmHg)
1.5 1.32* Placebo: 0.1 ± 12.2
! 1.14* 0.015 Ramipril 2.5 mg/d: -4.6 ± 13.5*
FMD 1.0 Ramipril 10 mg/d: -4.1 ± 12.4*
(%)
0.010 Diastolic BP (mmHg)
0.5 Placebo: -0.4 ± 7.3
0.15 0.005 Ramipril 2.5 mg/d: -2.9 ± 7.9*
Ramipril 10 mg/d: -2.8 ± 7.6*
0.0
Placebo Losartan Irbesartan Candesartan 0
(n = 44) 100 mg 300 mg 16 mg Values are mean ± SD.
*P<0.001 for mean BP changes compared with
(n = 31) (n = 30) (n = 30) Placebo Ramipril Ramipril placebo. There were no significant differences in
*P < 0.05 vs baseline and vs placebo 2.5 mg 10 mg BP changes between the two active ramipril groups.
Referencia al. Am J Cardiol. 2004;93:1432-5.
Koh KK et drpp 2009 Lonn EM, et al. Circulation 2001; 103:919–25. drpp 2009
2. Val-PREST: Re-estenosis intra-Stent Mortalidad in SAVE,
y Reintervención a 6 meses TRACE, AIRE, y VALIANT
Valsartan 80 mg (n = 99)
Hazard Ratio for Mortality
Placebo (n = 101)
50
SAVE
50% reduction
with valsartan vs placebo
40
58% reduction
TRACE
with valsartan vs placebo
Restenosis (%)
Patients with
30
AIRE
*
20
* Combined
10
VALIANT
(imputed placebo)
0
0.5 1 2
Restenosis Reintervention
*P <0.005 vs placebo.
Favors Favors
Active Drug Placebo
Adapted with permission from Peters S et al. J Invasive Cardiol. 2001;13:93-97. drpp 2009 Pfeffer, McMurray, Velazquez, et al. N Engl J Med 2003;349 drpp 2009
MICRO-HOPE: IECAs Mejoran
Metas CV y Renales en Diabetes
N=3577 patients with diabetes
(SRAA) Sistema Overt
CV nephro-
Renina-Angiotensina-
MI Stroke death pathy Mean albumin:
0 creatinine ratio
3.0 Placebo
–10
2.5
Aldosterona:
Risk 2.0
Reduction –20 P=0.02
(%) 1.5 Ramipril 10 mg
1.0
Efectos Renales
–30 P=0.001
P=0.01
P=0.027 0.5
–40 0 1 2 3 4.5
P=0.007 Years
P=0.0001
drpp 2009 HOPE Study Investigators. Lancet. 2000;355:253–259. drpp 2009
(SRAA) Sistema
Renina-Angiotensina-
Aldosterona:
Diabetes
N Engl J Med.
www.mechanismsincardiology.com
2001;345:851-860. drpp 2009 drpp 2009
3. Bloqueo del SRAA y metabolismo de Bloqueo del SRAA: Mejoría del
glucosa: Insulina y mediadores Metabolismo de glucosa
BK
NO
Angiotensin I Bradykinin
BK2 +
Receptor "NO Glucose ACE/Kininase II
Transport
Akt1 Degradation
+ Angiotensin II
Insulin products
Receptor + +
+ GLUT-4
Insulin IRS-1 PI3-K
+ Trans-
location
SRAA Blockage
- GLUT-4
Biosynthesis $Angiotensin II "Bradykinin
- GLUT-4
AT1
Receptor
!Skeletal muscle "Nitric oxide
blood flow
Ang II !Glucose metabolism
Adapted from Henriksen EJ, Jacob S. J Cell Physiol. 2003;196:171–9. drpp 2009 Henriksen EJ, Jacob S. J Cell Physiol. 2003;196:171–9. drpp 2009
Efecto de los IECA’s en Diabetes Metas de PA diastólica:
Estudio HOPE Estudio HOT
Reducción relativa del riesgo con Ramipril vs
Placebo en pacientes con Diabetes 30
-2.1 mmHg = -2.1 mmHg =
CV Events /1,000 Patient-Years in
Patients with Diabetes at Baseline
- 5.8 events/1000 py - 6.7 events/1000 py
25
22% de Infarto de Miocardio p = 0.01 20
33% de EVC p = 0.0074 15
37% de muerte cardiovascular p = 0.0001
24% de nefropatía p = 0.027 10
17% de revascularización p = 0.031
5
20% de Insuficiencia Cardíaca p = 0.019
0
Target: # 90 mmHg DBP # 85 mmHg DBP #80 mmHg DBP
(Achieved): (mean 85.2 mmHg) (mean 83.2 mmHg) (mean 81.1 mmHg)
p for trend = 0.005
HOPE investigators. Lancet 2000;355:253-259. drpp 2009 Referencia
Adapted from Hansson et al. Lancet 1998;351(9118):1755-1762. drpp 2009
Antihipertensivos: Prevención de Nuevos Casos de
Sensibilidad a la Insulina Diabetes tipo 2
Mejor Nuevo Mejor convencional
Estudio Seguimiento RR (IC 95%)
18 20 CAPPP (IECA vs Diu-BB) 6,1
16 0,86 (0,74-0,99); p= 0,03
12 HOPE (IECA vs Placebo)* 5,0 0,66 (0,51-0,85); p= 0,001
Cambio (%)
10
NORDIL (CA vs Diu-BB) 4,5 0,87 (0,73-1,04); p= 0,14
0 INVEST (CA vs BB) 2,7 0,85 (0,77-0,95); p= 0,01
-4
ALLHAT (IECA vs Diu) 4,6
-10 0,77 (0,66-0,89); p= 0,001
-15 LIFE (ARA II vs BB) 4,8
-22 -18 0,75 (0,63-0,88); p= 0,001
-30 -27 -20 CHARM (ARA II vs Placebo) 3,1
0,78 (0,64-0,96); p= 0,01
PRO
MET
-30
VALUE (ARA II vs CA) 4,2 0,77 (0,69-0,86); p= 0,0001
ATEN
HCTZ
NIF
VER
DOXA -40 0,50 0,75 1 1,25
IECA
ARA II
drpp 2009 drpp 2009
4. ARA II en Nefropatía Diabética
Referencia drpp 2009 Referencia drpp 2009
