in this presentation i have tried to briefly discuss about diuretics (water pills), their classification, mechanism of action, pharmacokinetics and pharmacodynamics of these drugs
A power point presentation on "Drugs affecting coagulation and anticoagulants" suitable for undergraduate medical students. Also suitable for Post Graduate students of Pharmacology and Pharmaceutical Sciences.
Diuretics
Pharmacology
Katzung
Abnormalities in fluid volume and electrolyte composition are common and important clinical disorders. Drugs that block specific transport functions of the renal tubules are valuable clinical tools in the treatment of these disorders. Although various agents that increase urine volume (diuretics) have been described since antiquity, it was not until 1937 that carbonic anhydrase inhibitors were first described and not until 1957 that a much more useful and powerful diuretic agent (chlorothiazide) became available. Technically, a “diuretic” is an agent that increases urine volume, whereas a “natriuretic” causes an increase in renal sodium excretion and an “aquaretic” increases excretion of solute-free water. Because natriuretics almost always also increase water excretion, they are usually called diuretics. Osmotic diuretics and antidiuretic hormone antagonists (see Agents That Alter Water Excretion) are aquaretics that are not directly natriuretic.
Hypolipidemic agents, also known as cholesterol-lowering drugs or antihyperlipidemic agents, are a diverse group of pharmaceuticals that are used in the treatment of high levels of fats (lipids), such as cholesterol, in the blood (hyperlipidemia). They are also called lipid-lowering drugs.
Lecture covers the pharmacology of anticholinergic drugs. Includes classification, therapeutic uses, adverse effects of anticholinergics. Atropine has been described as prototype drug.
Diuretics | Definition | Mechanism of Action | Classes of DrugsChetan Prakash
This presentation provides knowledge about Diuretics,Role of sodium, types of urine output, General mechanism of action, Normal Physiolofy of urine formation, GFR Formation, Classes of Diuretics, diuretics abuse and recent discovery. An assignment for the subject, Advanced Pharmacology-I, 1st year M.Pharm, 1st semester.
Mechanism of urine formation
Definition and classification of diuretics
MOA and SAR of each class
Their dose and adverse effects
Pharmacologicaol uses
all about diuretics
A power point presentation on "Drugs affecting coagulation and anticoagulants" suitable for undergraduate medical students. Also suitable for Post Graduate students of Pharmacology and Pharmaceutical Sciences.
Diuretics
Pharmacology
Katzung
Abnormalities in fluid volume and electrolyte composition are common and important clinical disorders. Drugs that block specific transport functions of the renal tubules are valuable clinical tools in the treatment of these disorders. Although various agents that increase urine volume (diuretics) have been described since antiquity, it was not until 1937 that carbonic anhydrase inhibitors were first described and not until 1957 that a much more useful and powerful diuretic agent (chlorothiazide) became available. Technically, a “diuretic” is an agent that increases urine volume, whereas a “natriuretic” causes an increase in renal sodium excretion and an “aquaretic” increases excretion of solute-free water. Because natriuretics almost always also increase water excretion, they are usually called diuretics. Osmotic diuretics and antidiuretic hormone antagonists (see Agents That Alter Water Excretion) are aquaretics that are not directly natriuretic.
Hypolipidemic agents, also known as cholesterol-lowering drugs or antihyperlipidemic agents, are a diverse group of pharmaceuticals that are used in the treatment of high levels of fats (lipids), such as cholesterol, in the blood (hyperlipidemia). They are also called lipid-lowering drugs.
Lecture covers the pharmacology of anticholinergic drugs. Includes classification, therapeutic uses, adverse effects of anticholinergics. Atropine has been described as prototype drug.
Diuretics | Definition | Mechanism of Action | Classes of DrugsChetan Prakash
This presentation provides knowledge about Diuretics,Role of sodium, types of urine output, General mechanism of action, Normal Physiolofy of urine formation, GFR Formation, Classes of Diuretics, diuretics abuse and recent discovery. An assignment for the subject, Advanced Pharmacology-I, 1st year M.Pharm, 1st semester.
Mechanism of urine formation
Definition and classification of diuretics
MOA and SAR of each class
Their dose and adverse effects
Pharmacologicaol uses
all about diuretics
Diuretics and antidiuretics detail STUDYNittalVekaria
diuretics and antidiuretics detail study
-diuretic are the drug which increase the urine formation and excretion.
- antidiuretic work by decrease the urine formation.
classification, mechanism of action, use ,pharmacokinetic, pharmacodynamic,adverse effect
-newer drug
-banned diuretic and antidiuretic drug
Diuretics are medicines that help reduce fluid buildup in the body. They are sometimes called water pills. Most diuretics help the kidneys remove salt and water through the urine. This lowers the amount of fluid flowing through the veins and arteries. As a result, blood pressure goes down.
Diuretics are drugs that increase the flow of urine. They are commonly used to treat edema, hypertension, and heart failure. Typically, the pharmacological group consists of five classes: thiazide diuretics, loop diuretics, potassium-sparing diuretics, osmotic diuretics, and carbonic anhydrase inhibitors.
There are three main types of diuretic: loop diuretics, thiazide diuretics and potassium-sparing diuretics.
the detail study of diuretics which include their drugs, use,classification of diuretics, side effect, mechanism of action, metabolism, synthesis etc. this all things are cover in this presentation.
The Emerging Role of Pharmacists in Public Health.pptxDr. Ankit Gaur
The Emerging Role of Pharmacists in Public Health: Opportunities and Challenges
General system theory, steven's system model, Pharmacists in india, Disaster management and emergency care, rational use of medicine, RNTCP programme. National Aids Control Programme.
This presentation is about Stress and its impact on health. I have tried to cover everything related to it, stressors, coping mechanisms, tools, types etc.
Gastro esophageal Reflux Disease (GERD) and its managementDr. Ankit Gaur
In this presentation I have tried to explain in brief about gastro esophageal Reflux Disease (GERD), its etiology, risk factors, diagnosis, and its management via pharmacotherapy.
In this presentation I have tried to discuss in brief about obsessive compulsive disorder and its treatment both pharmacological and non pharmacological.
In this presentation I have tried to explain in brief about pain management, different types of pain, its diagnostic criteria, its physiology, and its treatment approaches both pharmacological and non pharmacological
Respiratory Tract Infections- A Pharmacotherapeutic ApproachDr. Ankit Gaur
In this presentation I have tried to explain the types, etiology, pathophysiology of respiratory tract infections such as bronchitis, pnemonia, otitis media, sinusitis, pharyngitis, and their treatment
In this presentation I have tried to explain in brief about the dosage adjustment in renal disorders, how to carry out this process and the important formulae which are used in it.
In this presentation i have tried to explain in brief about nomograms and their applications, the general approach to individualise doage regimen by using pharmacokinetic data
In this presentation I have tried to explain in detail about tablets, their different types, ingredients which are used to prepare them, and the procedure to prepare them as well. This presentation is very useful for pharmacy students.
In this presentation i have tried to explain in details about the Total Parenteral Nutrition (TPN) , what is it, who needs it, and how to prepare it and the necessary procedure with instructions. It is very useful for the individuals from Nutrition, Nursing, Pharmacists, and Medical background.
In this presentation i have tried to explain in brief about CPR, how and when it has to be done and the important things to be kept in mind while doing it. This ppt is very helpful for every individual who is looking for the info regarding CPR.
In this presentation i have tried to explain in detail about the nux vomica and khurchi bark. This presentation is useful for the individuals who are looking for information on this topic especially for those students who are studying Pharmacognosy.
In this presentation i have tried to explain in detail about the measurements of the outcomes which are used in epidemiology such as prevalence, incidence, fatality rate, crude death rate etc.
In this presentation i tried to explain in detail about cohort studies, their types, how to conduct them, their outcomes, and how to calculate sample size of these studies.
In this presentation i have tried to thoroughly discuss about the concept of Drug induced kidney disease or injury, the mechanism behind it, its classification and how to access it.
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
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
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.
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.
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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.
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
2. Background
Primary effect of diuretics is to increase solute excretion,
mainly as NaCl
Causes increase in urine volume due to increased osmotic
pressure in lumen of renal tubule.
Causes concomitant decrease in extra-cellular volume (blood
volume)
Certain disease states may cause blood volume to increase
outside of narrowly defined limits
Hypertension
Congestive heart failure
Liver cirrhosis
Nephrotic syndrome
Renal failure
Dietary Na restriction often not enough to maintain ECF and
prevent edema diuretics needed
9. Types of diuretics and therapeutic uses
Carbonic anhydrase inhibitors (work in proximal
tubule)
Cystinuria (increase alkalinity of tubular urine)
Glaucoma (decrease occular pressure)
Acute mountain sickness
Metabolic alkalosis
Osmotic diuretics (proximal tubule, loop of Henle)
Acute or incipient renal failure
Reduce preoperative intraocular or intracranial pressure
10. Types of diuretics and therapeutic uses
Loop diuretics (ascending limb of loop)
Hypertension, in patients with impaired renal
function
Congestive heart failure (moderate to severe)
Acute pulmonary edema
Chronic or acute renal failure
Nephrotic syndrome
Hyperkalemia
Chemical intoxication (to increase urine flow)
11. Types of diuretics and therapeutic uses
Thiazide diuretics (distal convoluted tubule)
Hypertension
Congestive heart failure (mild)
Renal calculi
Nephrogenic diabetes insipidus
Chronic renal failure (as an adjunct to loop
diuretic)
Osteoporosis
12. Types of diuretics and
therapeutic uses
Potassium-sparing diuretics (collecting tubule)
Chronic liver failure
Congestive heart failure, when hypokalemia is a problem
Osmotic agents (proximal tubule, descending loop
of Henle, collecting duct)
Reduce pre-surgical or post-trauma intracranial pressure
Prompt removal of renal toxins
One of the few diuretics that do not remove large amounts
of Na+
Can cause hypernatremia
13. Background to Mechanisms of Action of Diuretics
Previously told that reabsorption, secretion occurred along
renal tubule but not how this was accomplished
Movement from tubular fluid through renal epithelial cells and
into peritubular capillaries accomplished by three transport
mechanisms after cell interior is polarized by Na+/K+ pump
1. Channels
formed by membrane proteins
Allows only sodium to pass through
1. Cotransport
Carrier mediated
Simultaneously transports both Na+ and other solute (Cl-, glucose,
etc) from tubular lumen into renal epithelial cell
1. Countertransport
Carrier mediated
Transports Na in, another solute (H+) out of renal epithelial cell
Water moves transcellularly in permeable segments or via tight
junctions between renal epithelial cells
15. Mechanisms of Action:
Carbonic anydrase inhibitors
CAIs work on cotransport of Na+
, HCO3
-
and Cl-
that is coupled to
H+
countertransport
Acts to block carbonic anhydrase (CA),
1. CA converts HCO3
-
+ H+
to H2O + CO2 in tubular lumen
2. CO2 diffuses into cell (water follows Na+
), CA converts CO2 + H2O
into HCO3
-
+ H+
3. H+
now available again for countertransport with Na+, etc)
4. Na+
and HCO3
-
now transported into peritubular capillary
CA can catalyze reaction in either direction depending on
relative concentration of substrates
17. 3. Carbonic anhydrase inhibitors
Acetazolamide inhibits carbonic
anhydrase (CA) manly in proximal tubules.
H2O + CO2
CA
H2CO3 H2CO3
–
+ H+
18. •Acetazolamide: has weak diuretic action.
•It significantly enhances urine K+
excretion.
•The loss of HCO3
–
anions decreases blood alkaline
reserve (for 48–72 h) and causes metabolic acidosis.
•In this state the drug becomes ineffective.
•Acetazolamide blocks not only renal CA, but also CA
in the ciliary body in the eye (reducing production of
eye liquid) and in the brain (facilitates GABA
synthesis).
19. Mechanisms of Action: Loop diuretics
No transport systems in descending loop of Henle
Ascending loop contains Na+
- K+
- 2Cl-
cotransporter from lumen to ascending
limb cells
Loop diuretic blocks cotransporter Na+
, K+
, and Cl-
remain in lumen,
excreted along with water
20.
21. Mechanisms of Action: Thiazide Diuretics
in the Distal Convoluted Tubule
Less reabsorption of water and electrolytes in the distal
convoluted tubule than proximal tubule or loop
A Na+
- Cl-
cotransporter there is blocked by thiazides
22. Mechanisms of Action: Collecting tubule
and potassium-sparing diuretics
Two cell types in collecting tubule
1. Principal cells – transport Na, K, water
2. Intercalated cells – secretion of H+
and HCO3
3. Blocking Na+ movement in also prevents K+
movement out
25. Spironolactone is steroid compound,
which is competitive aldosterone antagonis
t increases Na+
excretion and decreases K+
nd urea excretion. Its diuretic action is
week and is achieved slowly.
Spironolactone is effective in oedemas,
aused by increased production of
ldosterone ascites in liver cirrhosis and
oedemas in congestive heart failure.
26. Spironolactone in low doses (25 mg/24 h)
potentiates the effect of ACE inhibitors. It
saves K+
and Mg2+
ions and has antiarrhyth-
mic effect. It also prevents development of
myocardial fibrosis, caused by aldosterone
and in this way contributes to enhancing
myocardial contractility.
27. Diuretidin®
(triamterene/hydrochlorothiazide)
is indicated in oedemas cardiac, renal,
liver or other origin and for the
treatment of hypertension with
other antihypertensive drugs.
Moduretic®
(amiloride/hydrochlorothiazide)
has the same indications too.
29. After oral administration Mannitol is not
bsorbed and has laxative effect. After i.v.
dministration it is not metabolized, it
trates in the glomerulus and not reabsorbed
renal tubules, causing increased osmotic
ressure and excretion of isoosmotic equivalen
water. It increases blood flow in 30%.
30. Мannitol does not influence renin synthesis.
t does not cross tissue barriers (BBB too),
does not penetrate to the eye and brain and
n osmotic way reduces intraocular and intra-
cranial pressure.
t is included in the treatment of brain oedema
nitial stages of acute renal failure, chronic
enal failure, glaucoma, intoxications with
drugs, excreted in the urine.
39. General Background of Diuretics
Pattern of excretion of electrolytes (how
much of which type) depends on class of
diuretic agent
Maximal response is limited by site of action
Effect of two or more diuretics from different
classes is additive or synergistic if there sites
or mechanisms of action are different
40. Osmotic diuretics
No interaction with transport systems
All activity depends on osmotic pressure
exerted in lumen
Blocks water reabsorption in proximal tubule,
descending loop, collecting duct
Results in large water loss, smaller
electrolyte loss can result in hypernatremia
41. Carbonic anydrase inhibitors
Block carbonic-anhydrase catalyzation of
CO2/ carbonic acid/carbonate equilibrium
Useful for treating glaucoma and metabolic
alkalosis but can cause hyperchloremic
metabolic acidosis from HCO3
-
depletion
42. Loop diuretics
Generally cause greater diuresis than
thiazides; used when they are insuffficient
Can enhance Ca2+
and Mg2+
excretion
Enter tubular lumen via proximal tubular
secretion (unusual secretion segment)
because body treats them as a toxic drug
Drugs that block this secretion (e.g.
probenecid) reduces efficacy
43. Thiazide diuretics
Developed to preferentially increase Cl-
excretion over HCO3
-
excretion (as from CAIs)
Magnitude of effect is lower because work on
distal convoluted tubule (only recieves 15%
of filtrate)
Cause decreased Ca excretion
hypercalcemia reduce osteoporosis
45. Potassium-sparing diuretics
Have most downstream site of action
(collecting tubule)
Reduce K loss by inhibiting Na/K exchange
Not a strong diuretic because action is
furthest downstream
Often used in combination with thiazide
diuretics to restrict K loss