Diuretics work by inhibiting sodium reabsorption in the kidney, which increases water excretion and urine output. They are classified based on their site of action along the nephron. Loop diuretics like furosemide act in the ascending loop of Henle. Thiazides such as hydrochlorothiazide act in the distal convoluted tubule. Potassium-sparing diuretics including spironolactone and amiloride act in the collecting duct. Each class of diuretic has distinct mechanisms of action, pharmacokinetics, indications, and toxicities.
short and simple study on the topic of laxative and purgatives which is very usefull for the student , teachers, as well as health cares peoples. this study is done by the student with the help of teachers
Introduction to diuretics.
Therapeutic approaches.
Normal physiology of urine formation.
Classification of drugs .
Mechanism of action of Acetazolamide.
Mechanism of action of Thiazides.
Mechanism of action of Loop diuretics.
Mechanism of action of potassium sparing diuretics &aldosterone antagonists.
Anti anginal drugs, uses, mechanism of action, adverse effectsKarun Kumar
A presentation outlining the causes of angina, mechanism of action of various anti-anginal drugs, their uses and side effects alongwith contraindications
Seretonin (5HT) and Its Antagonists PharmacologyPranatiChavan
Serotonin is a chemical that has a wide variety of functions in the human body. It is sometimes called the happy chemical, because it contributes to wellbeing and happiness.
The scientific name for serotonin is 5-hydroxytryptamine, or 5-HT. It is mainly found in the brain, bowels, and blood platelets.
Serotonin is used to transmit messages between nerve cells, it is thought to be active in constricting smooth muscles, and it contributes to wellbeing and happiness, among other things. As the precursor for melatonin, it helps regulate the body’s sleep-wake cycles and the internal clock.
It is thought to play a role in appetite, the emotions, and motor, cognitive, and autonomic functions. However, it is not known exactly if serotonin affects these directly, or if it has an overall role in co-ordinating the nervous system.
Pharmacology of drugs acting on Renal System.pdfAFFIFA HUSSAIN
Diuretics also known as water pills increases the excretion of water and electrolytes (Na+) in
urine.
Natriuresis – large amount of sodium excreted in urine due to the action of kidneys.
Promoted by – ventricular and atrial natriuretic as well as calcitonin.
Inhibited by chemicals such as aldosterone. The drugs which increases sodium excretion are
known as natriuretic.
Diuresis – increased or excessive production of urine. The drugs which enhances the excretion
of water without loss of electrolyte is called as aquaretic.
short and simple study on the topic of laxative and purgatives which is very usefull for the student , teachers, as well as health cares peoples. this study is done by the student with the help of teachers
Introduction to diuretics.
Therapeutic approaches.
Normal physiology of urine formation.
Classification of drugs .
Mechanism of action of Acetazolamide.
Mechanism of action of Thiazides.
Mechanism of action of Loop diuretics.
Mechanism of action of potassium sparing diuretics &aldosterone antagonists.
Anti anginal drugs, uses, mechanism of action, adverse effectsKarun Kumar
A presentation outlining the causes of angina, mechanism of action of various anti-anginal drugs, their uses and side effects alongwith contraindications
Seretonin (5HT) and Its Antagonists PharmacologyPranatiChavan
Serotonin is a chemical that has a wide variety of functions in the human body. It is sometimes called the happy chemical, because it contributes to wellbeing and happiness.
The scientific name for serotonin is 5-hydroxytryptamine, or 5-HT. It is mainly found in the brain, bowels, and blood platelets.
Serotonin is used to transmit messages between nerve cells, it is thought to be active in constricting smooth muscles, and it contributes to wellbeing and happiness, among other things. As the precursor for melatonin, it helps regulate the body’s sleep-wake cycles and the internal clock.
It is thought to play a role in appetite, the emotions, and motor, cognitive, and autonomic functions. However, it is not known exactly if serotonin affects these directly, or if it has an overall role in co-ordinating the nervous system.
Pharmacology of drugs acting on Renal System.pdfAFFIFA HUSSAIN
Diuretics also known as water pills increases the excretion of water and electrolytes (Na+) in
urine.
Natriuresis – large amount of sodium excreted in urine due to the action of kidneys.
Promoted by – ventricular and atrial natriuretic as well as calcitonin.
Inhibited by chemicals such as aldosterone. The drugs which increases sodium excretion are
known as natriuretic.
Diuresis – increased or excessive production of urine. The drugs which enhances the excretion
of water without loss of electrolyte is called as aquaretic.
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
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.
- 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
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.
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.
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.
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
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.
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.
This document describes the acute management of AV block.
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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
2. • Diuresis: increased urine flow
• Diuretics: substances which elicit diuresis
• In the kidney, water reabsorption dependent
primarily on Na+ reabsorption
• Thus a diuretic is an agent which inhibits tubular Na+
reabsorption (along with Cl-, HCO3-) resulting in
increased excretion of these ions
3.
4.
5. Classification of diuretics
A)
According to the site of Action:
1) Site –I ( Proximal convoluted tubule) acting drugs :
–
Osmotic diuretics: mannitol, isosorbide , urea
–
Carbonic anhydrase inhibitors : acetazolamide , methazolamide ,
dichlorphenamide
–
Xanthene drugs : aminophylline , theophylline , theobromide , caffeine
2) Site-II (Ascending limb of loop of Henle) acting drugs:
–
Furosemide , bumetanide, ethacrynic acid , mefruside, piretanide
3) Site –III ( Distal convoluted tubule )acting drugs :
–
Thiazides: chlorothiazide, hydrochlorthiazide, benzthiazide ,
hydroflumethiazide , clopamide
–
Thiazide like( related heterocyclics ) : cholrthalidone , metolazone ,
Xipamide , Indapamide
–
Mercurials: mercaptomerin, mersibid, mercurophyll, mersalyl
4) Site –IV ( Collecting Duct) :
–
K+ sparing diuretics : spironolactone , triamterene , amiloride
6. B) According to potency:
1) High ceiling(efficacy)
diuretics (loop
diuretics)
–
–
–
–
–
Furosemide
Bumetanide
Piretanide
Ethacrynic acid
Mefruside
2) Moderate efficacy
diuretics ( thiazides )
– Hydrochlorthiazide
– Bendroflumethiazide
3) Low efficacy diuretics
a) Osmotic diuretics :
b) Potassium sparing
c) Carbonic anhydrase
inhibitors
d) Xanthene groups
7. Proximal Convoluted tubule
• 66% of total sodium ions
(Na+, but 85% of the
filtered NaHCO3), 65% of
the K+, 60% of the water,
and virtually all of the
filtered glucose and
amino acids are
reabsorbed.
• Specific transport
• Passive transport
• Paracellular pathways
8. Carbonic anhydrase inhibitor:
Acetazolamide
• Pharmacokinetics
– The carbonic anhydrase inhibitors are well
absorbed after oral administration. An increase in
urine pH from the HCO3– diuresis is apparent
within 30 minutes, maximal at 2 hours, and
persists for 12 hours after a single dose. Excretion
of the drug is by secretion in the proximal tubule
S2 segment. Therefore, dosing must be reduced in
renal insufficiency
9. • Mechanism
– By inhibiting the action of carbonic anhydrase ,
inhibits reabsorption of sodium
– Blocks NaHCO3 reabsorption causing bicarbonate
diuresis
– Metabolic acidosis
10. Clinical Indications
•
•
•
•
•
•
Glaucoma
Urinary alkalinization.
Metabolic alkalosis
Acute mountain sickness
Premenstrual oedema
Other uses:
– adjuvants in the treatment of epilepsy, in some forms of
hypokalemic periodic paralysis, and to increase urinary
phosphate excretion during severe hyperphosphatemia.
11. Toxicity
• HYPERCHLOREMIC METABOLIC ACIDOSIS
• RENAL STONES
– Phosphaturia and hypercalciuria occur during the bicarbonaturic response to
inhibitors of carbonic anhydrase.
• RENAL POTASSIUM WASTING
– Potassium wasting can occur because Na+ presented to the collecting tubule is
partially reabsorbed, increasing the lumen-negative electrical potential in that
segment and enhancing K+ secretion. This effect can be counteracted by
simultaneous administration of potassium chloride.
• OTHER TOXICITIES
– Drowsiness and paresthesias are common following large doses of
acetazolamide. Carbonic anhydrase inhibitors may accumulate in patients with
renal failure, leading to nervous system toxicity. Hypersensitivity reactions
(fever, rashes, bone marrow suppression, and interstitial nephritis) may also
occur.
12. Mannitol
• Sugar alcohol
• Characters :
–
–
–
–
–
Freely filtered
No absorption
Pharmacologically inert
IV administration
Entire tubule
• Indications :
– Glaucoma
– Cerebral oedema
– Prevention of acute
renal failure
– Before neurosurgery to
reduce CSF and
intraocular pressure
– Oliguric states (
rhabdomyolysis)
14. Loop of henle
• action of the transporter
contributes to excess K+
accumulation within the
cell. Back diffusion of this
K+ into the tubular lumen
causes a lumen-positive
electrical potential that
provides the driving force
for reabsorption of
cations—including
magnesium and
calcium—via the
paracellular pathway
15. Loop diuretics
• Pharmacokinetics
– rapidly absorbed.
– eliminated by the kidney by glomerular filtration and tubular
secretion.
– Absorption of oral torsemide is more rapid (1 hour) than that of
furosemide (2–3 hours) and is nearly as complete as with
intravenous administration.
– The duration of effect for furosemide is usually 2–3 hours and
that of torsemide is 4–6 hours.
– Half-life depends on renal function.
– Reduction in the secretion of loop diuretics may result from
simultaneous administration of agents such as NSAIDs or
probenecid, which compete for weak acid secretion in the
proximal tubule.
16. Characters :
– Very potent
– Can act in severe renal and heart failure where
other diuretics fail
– Rapid onset
17. Mechanism:
– inhibit NKCC2, the luminal Na+/K+/2Cl– transporter
in the thick ascending limb of Henle's loop
– Decrease intracellular K, back diffusion, positive
potential, increase diuresis
– induce synthesis of renal prostaglandins
– increase renal blood flow
– Massive dose inhibits carbonic anhydrase
18. Indications
•
•
•
•
•
•
•
•
•
Acute pulmonary oedema
Moderate hypertension
Left ventricular failure
Congestive heart failure
Oedema due to liver cirrhosis
Oliguric phase of acute renal failure
Hypercalcemia
Hyperkalemia
anion overdose (treating toxic ingestions of bromide,
fluoride, and iodide, which are reabsorbed in the thick
ascending limb)
19. Toxicity
•
•
•
•
•
•
•
•
•
•
Hypokalemic metabolic alkalosis
Ototoxicity
Nephrotoxicity
Myalgia
Hyperuricemia
Hypomagnesemia
Hypovolemia
severe dehydration. Hyponatremia
Hypovolemic hypotension
Allergic & other reactions
– Except for ethacrynic acid, the loop diuretics are sulfonamides.
Therefore skin rash, eosinophilia and, less often, interstitial nephritis
are occasional side effects of these drugs. This toxicity usually resolves
rapidly after drug withdrawal. Allergic reactions are much less
common with ethacrynic acid.
– Cross allergenicity with thiazides, sulfonamides
22. Distal convoluted tubule
• K+ does not recycle across the
apical membrane of the DCT
as it does in the TAL, there is
no lumen-positive potential in
this segment, and Ca2+ and
Mg2+ are not driven out of the
tubular lumen by electrical
forces. Instead, Ca2+ is actively
reabsorbed by the DCT
epithelial cell via an apical Ca2+
channel and basolateral
Na+/Ca2+ exchanger (Figure
15–4). This process is
regulated by parathyroid
hormone.
23. Thiazides
• Pharmacokinetics
– All of the thiazides can be administered orally
– Chlorothiazide, the parent of the group, is not very
lipid-soluble and must be given in relatively large
doses. It is the only thiazide available for parenteral
administration.
– Chlorthalidone is slowly absorbed and has a longer
duration of action.
– Although indapamide is excreted primarily by the
biliary system, enough of the active form is cleared by
the kidney to exert its diuretic effect in the DCT
24. Pharmacodynamics
• Thiazides inhibit NaCl reabsorption from the
luminal side of epithelial cells in the DCT by
blocking the Na+/Cl– transporter (NCC).
• ATP dependent K channel openers
• Enhance Calcium reabsorption by two ways :
– In the proximal tubule, thiazide-induced volume
depletion leads to enhanced Na+ and passive Ca2+
reabsorption.
– In the DCT, lowering of intracellular Na+ by thiazideinduced blockade of Na+ entry enhances Na+/Ca2+
exchange in the basolateral membrane and increases
overall reabsorption of Ca2+
26. Toxicity
•
•
HYPOKALEMIC METABOLIC ALKALOSIS AND HYPERURICEMIA
IMPAIRED CARBOHYDRATE TOLERANCE
– Hyperglycemia may occur in patients who are overtly diabetic or who have even mildly
abnormal glucose tolerance tests. The effect is due to both impaired pancreatic release of
insulin and diminished tissue utilization of glucose. Hyperglycemia may be partially reversible
with correction of hypokalemia.
•
HYPERLIPIDEMIA
– Thiazides cause a 5–15% increase in total serum cholesterol and low-density lipoproteins
(LDL). These levels may return toward baseline after prolonged use.
•
HYPONATREMIA
– It is due to a combination of hypovolemia-induced elevation of ADH, reduction in the diluting
capacity of the kidney, and increased thirst. It can be prevented by reducing the dose of the
drug or limiting water intake.
•
ALLERGIC REACTIONS
– The thiazides are sulfonamides and share cross-reactivity with other members of this chemical
group. Photosensitivity or generalized dermatitis occurs rarely. hemolytic anemia,
thrombocytopenia, and acute necrotizing pancreatitis.
•
OTHER TOXICITIES
– Weakness, fatigability, and paresthesias similar to those of carbonic anhydrase inhibitors may
occur. Impotence has been reported but is probably related to volume depletion
27. Collecting tubule
• The principal cells are the
major sites of Na+, K+, and
water transport and the
intercalated cells are the
primary sites of H+
secretion
• principal cells do not
contain cotransport
systems for Na+ and other
ions in their apical
membranes
28. Potassium sparing diuretics :
spironolactone
• Aldosterone antagonist
• Steroid chemically related to mineralocorticoid aldosterone
Mechanism of ALDOSTERONE ACTION
• By combining with aldosterone receptor , promotes gene
mediated mRNA synthesis, induces the formation of
aldosterone induced proteins which promote Na+
reabsorption by :
– Activating sodium channel
– Translocating sodium channels from cytosolic site to luminal
membrane and Na/K ATPase to basolateral membrane
– Increase ATP production by mitochondria
Spironolactone competitively inhibits the formation of aldosterone
induced proteins (AIPs) and blocks all the action of aldosterone
in the principal cell of the collecting duct.
29. • Pharmacokinetics :
– High oral bioavailability
– Highly bound to plasma proteins
– Completely metabolised in liver , converted to
active metabolites –canrenone .
– Undergoes some enterohepatic circulation
30. • Indications
– Edema
– Hyperaldosteronic states
– Adjunct to other
diuretics
– Antiandrogenic to treat
women with hirsuitism
or significant acne
– Congestive heart failure
– Hypertension
• Adverse effects
– Hyperkalemia
– Acidosis
– Antiandrogen ( male
gynecomastia)
– Drowsiness
– Confusion
– Abdominal upset
– Impotence
– Menstrual irregularities
– Peptic ulcer
31. Renal epithelial sodium channel
blockers
• Amiloride , triamterene
Bind to the sodium channel from the luminal side and
block it, reducing the lumen negative transepithelial
potential difference responsible for K+ And H+
secretion and indirectly inhibit K excretion.
Triamterene is metabolized in the liver, but renal
excretion is a major route of elimination for the active
form and the metabolites.
triamterene has a shorter half-life and must be given
more frequently than amiloride (which is not
metabolized).
32. Triamterene:
• Bioavailability :30-70%
• Protein binding: 67%
• Metabolism: conjugated to hydroxytriamterene
• Half-life: 1-2 hours, active metabolite 3 hours
• Excretion: renal <50%, 21% unchanged
Amiloride:
Bioavailability: Readily absorbed
Metabolism: none
Half-life :6 to 9 hours
Excretion :unchanged in urine