1. Aspirin is used after myocardial infarction to inhibit platelet aggregation and reduce the risk of reinfarction through inhibition of TXA2 synthesis. It is given at doses of 60-100 mg/day.
2. Disulfiram is used as an aversion therapy in motivated alcoholics to help them stop drinking. It inhibits alcohol metabolism causing distressing symptoms when alcohol is consumed after taking disulfiram.
3. Folic acid is used in pregnancy to prevent anemia and support healthy development of the baby's brain and spinal cord by ensuring adequate folic acid levels during this critical time of development.
This PPT covers drugs used as diuretics. Pharmacotherapy of all drugs used as diuretics are covered here. Thiazides, high ceiling, aldosterone antagonist, osmotic diuretics are explained
Diuretic and Urinary alkalizes-Dr.Jibachha Sah,M.V.ScDr. Jibachha Sah
Dr.Jibachha Sah,M.V.Sc (Veterinary pharmacology),Lecture,College of Veterinary science,NPI,Bhojard,Chitwan,Nepal.This is part of lecture note on veterinary pharmacologyAUTONOMIC AND SYSTEMIC PHARMACOLOGY, Sixth Semester, B.V.Sc & A.H 6th semester.
Dr.Jibachha sah,Email: jibachhashah@gmail.com,Mobile:00977-9845024121
This PPT covers drugs used as diuretics. Pharmacotherapy of all drugs used as diuretics are covered here. Thiazides, high ceiling, aldosterone antagonist, osmotic diuretics are explained
Diuretic and Urinary alkalizes-Dr.Jibachha Sah,M.V.ScDr. Jibachha Sah
Dr.Jibachha Sah,M.V.Sc (Veterinary pharmacology),Lecture,College of Veterinary science,NPI,Bhojard,Chitwan,Nepal.This is part of lecture note on veterinary pharmacologyAUTONOMIC AND SYSTEMIC PHARMACOLOGY, Sixth Semester, B.V.Sc & A.H 6th semester.
Dr.Jibachha sah,Email: jibachhashah@gmail.com,Mobile:00977-9845024121
Basics of hypertension and available treatment.
Overview of mechanism of action, risks/benefits of various classes of drugs.
Prevalent prescription trends and future market review.
ACE inhibitors block the angiotensin-converting enzyme found throughout vascular tissue that converts angiotensin I to angiotensin II. Let us know how do ACE Inhibitors work?
in this presentation i have tried to briefly discuss about diuretics (water pills), their classification, mechanism of action, pharmacokinetics and pharmacodynamics of these drugs
In medicine, diuretics are used to treat heart failure, liver cirrhosis, hypertension, influenza, water poisoning, and certain kidney diseases.
different major types of diuretic drug
1. Carbonic Anhydrase Inhibitors2. Loop 3. Osmotic4. Potassium- sparing5. Thiazides
Basics of hypertension and available treatment.
Overview of mechanism of action, risks/benefits of various classes of drugs.
Prevalent prescription trends and future market review.
ACE inhibitors block the angiotensin-converting enzyme found throughout vascular tissue that converts angiotensin I to angiotensin II. Let us know how do ACE Inhibitors work?
in this presentation i have tried to briefly discuss about diuretics (water pills), their classification, mechanism of action, pharmacokinetics and pharmacodynamics of these drugs
In medicine, diuretics are used to treat heart failure, liver cirrhosis, hypertension, influenza, water poisoning, and certain kidney diseases.
different major types of diuretic drug
1. Carbonic Anhydrase Inhibitors2. Loop 3. Osmotic4. Potassium- sparing5. Thiazides
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.
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.
Non-steroidal anti-inflammatory drugs is a class of analgesic medication that reduces pain, fever and inflammation. Since most episodes of back pain involve inflammation, NSAIDs such as ibuprofen and naproxen are often an effective treatment option.
Drugs for Gout ( Acute and Chronic gout)ANUSHA SHAJI
The current presentation include the pharmacotherapy of drugs for acute and chronic gout. Details include definition, classification of drugs, mechanism, pharmacokinetics, adverse effects, uses and contraindications.
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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
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
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New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
- 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
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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.
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
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.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
1. WRITE DOWN THE RATIONAL OF
FOLLOWINGS:
1. Aspirin in post myocardial infarction.
ANS: By inhibiting the platelet aggregation aspirin lowers the incidence of
reinfarction. TXA2 synthesis in platelet is inhibited in low doses. Aspirin
reduces the transient ischaemic attack and lowers the incidence of stroke in
such patients. But the risk of stroke in postMI patients is not reduced.
Dose: 60-100 mg/day
But it has been argued that high dosecan reverse the beneficial effects
concurrently inhibiting PGI2 synthesis in vessel wall.
2. Disulfuram in alcoholism:
ANS: Disulfuram has been used as an aversion technique in chronic
alcoholics who are motivated and sincerely desire to leave the habbit. It
inhibits the enzyme aldehyde dehydrogenase probably after conversion into
active metabolites. When alcohol is ingested after taking disulfuram, the
concentration of acetaldehyde in tissue and blood rises and a number of
highly distressing symptoms (aldehyde syndrome) are produced promptly.
Due to which the personstops the drinking.
3. Folic acid in pregnancy:
ANS: Folic acid is used in the pregnancy due to the increased demand to
meet the metabolic functions of the bodyand prevents the anaemia in
pregnancy. Folic acid is vital to supportthe healthy development of a baby’s
brain and spinal cord. Before you are even aware that you’re pregnant, your
baby’s brain and spinal cord are already forming. By having enough folic
acid in your blood at this important time you help to ensure that they
develop properly. Many women don't realise that taking folic acid can help
to avoid the possibility of some very serious consequences.
2. 4. Naloxone usedfor morphine poisoning:
ANS: Naloxone is the drug of choice for morphine poisoning. It is N-
alylnor-oxymorphine and a competitive antagonist on all type of opioid
receptors. However, it blocks µ- receptors at much lower dosethan those
needed to block kappa and delta receptors. So, it blocks the effects of
morphine completely.
5. Acetazolamide in mountain sickness:
ANS: Acute altitude sickness usually occurs during the first few days at
altitude, before respiratory acclimatization is complete. Thus at high
altitudes, climbers hyperventilate in responseto lower oxygen levels. This
results in reduced carbon dioxide(an acid) and reduced oxygen level in the
body.
Herein, lies the rational for prophylaxis with acetazolamide inhibits renal
carbonic anhydrase causing bicarbonate dieresis and extracellular acidosis.
Acetazolamide has, however been shown repeatedly to lower blood pH,
improve blood gas, and improve symptoms scores for acute mountain
sickness.
In nephron, CO2 is lipophilic and rapidly diffuse across the luminal
membrane into the epithelial cell, where it reacts with water to form
bicarbonate, a reaction catalyzed by cytoplasmic carbonic anhydrase.
Acetazolamide increases CO2 levels in peripheral tissues and decrease CO2
levels in expired gas.
It is usefull in treating established acute mountain sickness. Doses used have
varied from 250mg to 1 gm, and probably 500mg daily as a sustained release
preparation begun in nthe 24 hours before ascent is adequate.
3. 6. Sublingual nitroglycerine tablets:
ANS: When nitroglycerine is administered orally, most of each doseis
destroyed on its first pass through liver. The sublingual route is used when
terminating an attack or aborting an imminent one is the aim. The tablet may
be crushed under the teeth and spread over the buccal mucosa. It acts
within 1-2 min becauseof direct absorptioninto the systemic circulation
bypassing the liver where 90% is metabolized.
7. Sodium intake is restrictedin hypertension:
ANS: salt is essential to our bodies. Normally the kidneys control the level
of salt. If there is too much salt, the kidneys pass it into urine. But when our
salt intake levels are very high, the kidneys can not keep up and the salt ends
up in our bloodstream. Salt attracts water. When there is too much salt in
the blood, the salt draws more water into the blood. More water increases the
volume of blood which raises blood pressure.
Almost 80% of the average person’s daily salt intake comes from processed
foods. If we ate only natural foods and limited the use of table salt, we
would be able to eliminate excess salt in our body.
A lower sodium diet is good for people who are older, who are of
African American descent, or who have high blood pressure or diabetes.
These folks should limit their sodium intake to no more than 2300-2400mg a
day.people with heart failure or kidney disease are advised to keep their
sodium intake under 2000mg per day.
4. 8. Atropine is given in organophosphorus poisoning:
ANS: Atropine is the specific antidote for anticholinesterase
( organophosphate)so, it is highly effective in counteracting the muscarinic
symptoms, in higher doses it also antagonize the central effects. It does not
reverse the peripheral muscular paralysis which is a nicotinic action. In all
cases of anti-ChE (carbamate or organophosphate) poisoning must be
promptly given atropine 2mg i.v. repeated every 10 min till dryness of
mouth or other signs of atropinization appear. Continued treatment with
maintainance dosemay be required for 1-2 weeks.
9. Salicylates are not given in empty stomach:
ANS: The most important adverse effect of salicylate is gastric mucosal
damage and peptic ulceration especially when given in empty stomach. This
is due to the inhibition of COX-1 mediated synthesis of gastroprotective
prostaglandins i.e. PGE2, PGI2.deficiency of PGEs reduces mucus and
HCO₃⁻ secretion tends to enhance acid secretion and may promotemucosal
ischaemia leading to peptic ulceration and the chance of inhibition of PGs
synthesis is more when given in empty stomach. So, these drugs are not used
in empty stomach.
WRITE DOWN THE RATIONAL OF:
10.Carbidopa and le vodopa combination:
ANS: Levodopa undergoes high first pass metabolism in gastrointestinal
mucosa and liver. About 1% of administered levodopa that enters brain
when used alone.
Carbidopa is an extracerebral dopadecarboxylase inhibitors; they do not
penetrate the blood-brain barrier and do not inhibit conversion of levodopa
to dopamine in the brain. Administered along with levodopa, they increase
its half-life in the periphery and make more of it available to cross blood-
brain barrier to reach its site of action.
5. The benefits of the combination are:
i. The plasma half-life of levodopa is prolonged and its doseis
reduced to approximately 1/4th.
ii. Systemic concentration of dopamine is reduced, nausea and
vomiting are not prominent, therapeutic doseof levodopa can be
attained quickly.
iii. Cardiac complications are minimized.
iv. Pyridoxine reversal of levodopa effects does not occur.
v. “on-off” effect is minimized since cerebral dopamine levels are
more sustained.
vi. Degree of improvement may be higher; some patients, not
responding adequately to levodopa alone, also improve.
Combination of levodopa with carbidopahas been given the name
“co-careldopa”.
11. Furosemide with amiloride:
ANS: furosemide is high efficacy loop diuretics and inhibits the Na⁺-k⁺-
2Cl⁻ cotransport in ascending limb of loop of hanle. Potassium excretion is
increased due to high sodium load reaching distal tubule.
Amiloride is non-seroidal organic bases which cause decrease potassium
excretion, particularly when it is high due to large K⁺ intake or use of
diuretic that enhances K⁺ loss i.e. furosemide. Unlike spironolactone their
action is independent of aldosterone.
They act on luminal membrane of distal tubule cells to inhibit elecrogenic
Na⁺ reabsorption.
Therefore, by giving these two drung in combination the level of K⁺ can be
maintained in the blood and the risk of hypokalemia is minimized.
6. 12.Nifidipine and beta-blockers:
ANS: Nefidipine is a calcium channel blocker which cause reflex
tachycardia, increased contractility and cardiac output.
Beta-blockers cause ventricular dilatation.
By giving combination of these two drugs, following advantages can be
achieved:
I. Reflex tachycardia due to CCBs is blocked by beta-blockers.
II. The tendency of beta-blockers to cause ventricular dilatation is
counteracted by CCBs.
III. The tende3ncy of beta-blockers to reduce total coronary flow is
opposedbyCCBs.
13. Thiazide and spironolactone:
ANS: Thiazidse diuretics cause hypokalemia by increasing the loss of
potassium leading to weakness, fatigue, muscle cramps, cardiac arrhythmias.
Decrease plasma potassium level also inhibits the release of insulin leading
to hyperglycemia.
Spironolactone is a aldosterone antagonist. It blocks the receptor on
which aldosterone acts. This leads to inhibition of reabsorption of sodium
and inhibition of secretion of potassium in the late part of distal tubule
resulting in i9ncreased excretion of sodium and retention of potassium in the
body.
So, by giving these two drugs in combination, the level of potassium can
be maintained in the bodyand the risk of hypokalemiaa is minimized.
7. 14. Classifyantipsychotic and antiepileptic. Explain pharmacological action
and use of chlorpropamide and carbamazepine:
ANS: Psychoses are the severe psychiatric illness with serious distortion of
thought, behavior, capacity to recognize reality and of perception (delusions
and hallucinations). There is in explicable misperception and misevaluation;
the patient is unable to meet the ordinary demands of life.
Anti-psychotic drugs are the agents having primary effects on psyche
(mental process)and are used for treatment of psychiatric disorders.
CLASSSIFICATIONOF ANTI-PSYCHOTIC DRUGS:
I. Phenothiazines:
Chlorpromazine
Triflupromazine
Trifluperazine
II. Butyurophenones:
Haloperidol
Trifluperidol
Penfluperidol
III. Thioxanthenes:
Flupenthixol
IV. Other heterocyclics:
Pimozide
Loxapine
8. V. Atypical antipsychotics:
Clozapine
Risperidone
Olanzapine
Ziprasidone
Pharmacological actions of chlorpromazine:
a) CNS: effects differ in normal and psychotic individuals:
In normal individuals chlorpromazine produces indifference to
surroundings, paucity of thought, psychomotorslowing, emotional
quietening, reduction in initiative and tendency to go off to sleep from which
the subject is easily arousable. Spontaneous movements are minimized butr
slurring of speech, ataxia or motor incoordination does not occur.
In a psychotic individual, chlorpromazine reduces irrational behavior,
agitation and aggressiveness and controls psychotic symptomology.
Disturbed thought and behavior are gradually normalized, anxiety is
relieved. Hyperactivity, hallucination and delusions are suppressed.
b) ANS: chlorpromazine have varying degree of alpha adrenergic blocking
activity. It also have a weak H₁-antihistamine and anti-5HT actions as well.
c) Local anaesthetics: chlorpromazine is as potent a local anaesthetic as
procaine. However, it is not used for this purposebecause of its irritant
action.
d) CVS: high doseof chlorpromazine directly depress the heart and produce
EEG changes. Chlorpromazine exerts some antiarrhythmic action, probably
due to membrane stabilization. Arrhythmia may occurin overdose.
9. e) Skeletal muscle: neuroleptics have no effect on muscle fibres or
neuromuscular transmission. They reduce certain types of spasticity; the site
of action being in the basal ganglia or medulla oblongata. Spinal reflexes are
not affected.
f) Endocrine: neuroleptics consistently increase prolactin release by blocking
the inhibitory action of dopamine on pituitary lactotropes. This may result in
galactorrhoea and gyaecomastia.
Uses of chlorpromazine:
i. Psychoses:
Schizophrenia
Mania
Organic brain syndromes
ii. Anxiety
iii. As anti-emetics
iv. Other uses:
To potentiate hypnotics, analgesics and anaesthetics.
Tetanus, CPZ is secondarydrug to achieve muscle relaxation.
Alcoholic hallucinations.
CLASSIFICATIONOF ANTI-EPILEPTICS:
i. Barbiturates:
Phenobarbitone
ii. Deoxybarbiturate:
Primidone
iii. Hydantoin:
10. Phenytoin
Fosphenytoin
iv. Iminostilbene:
Carbamazepine
Oxcarbazepine
v. Succinimide:
Ethosuximide
vi. Aliphatic carboxylic acid:
Valproic acid
Divalproex
vii. Benzodiazepines:
Clonazepam
Diazepam
Lorazepam
Clobazam
viii. Phenyltriazine:
Lamotrigine
ix. Cyclic gaba analogue:
Gabapentin
x. Newer drugs:
Vigabatrin
Topiramate
Tiagabine
Zonisamide
Uses of carbamazepine:
a) Complex partial seizures
b) General tonic clonic seizure
c) Simple partial seizure
d) Trigeminal and related neuralgias
e) Manic depressive illness and acute mania.
11. 15.Describe the pharmacotherapy of hypertension and gout:
ANS: the general principles of antihypertensive therapy enunciated in JNC7
and WHO-ISH guidelines is as follows:
a) Except for stage-2 hypertension, starts with a single most appropriate
drug which for majority of patients is thiazide. However, a beta-
blocker, ACE inhibitor or CCB may also be considered.
b) Initiate therapy at low dose;if needed increase dosemoderately.
Thiazide doseshould be 12.5-25mg/day hydrochlorthiazide or
equivalent.
c) Majority of stage-2 hypertension are started on a 2 drug combination;
one of which usually is a thiazide diuretic.
d) If only a partial response, add a drug from another complimentary class
or change to low dosecombination.
e) If no response, change to a drug from another class or low dose
combination from another classes.
f) In case of side effect to the initially choosendrug, either substitute with
drug of another class or reduce doseand add a drug from another class.
Drugs and their doses:
Hydrochlorthiazide- 12.5 mg OD
Furosemide-20-80mg/day
Atenolol-25-50mg OD
Amlodipine-2.5-5mg OD
Lisinipril-2.5-5mg OD
Losarton-25-50mg OD
Pharmacotherapy of gout:
For acute gout:
a. NSAIDs: one of the strong anti-inlammatory drugs, e.g. indomethacin,
naproxen, piroxicam, or etoricoxib is given in relatively high doseand
quickly repeated doses. Theyare quite effective in terminating the attack.
12. b. Colchicines is neither analgesic nor anti-inflammatory, but it especially
suppress gouty inflammation. It does not inhibit the synthesis or promote the
excretion of uric acid. Thus, it has no effect on blood uric acid levels.
c. Corticosteroids: intraarticular injection of a soluble steroid suppress the
symptoms of acute gout. Crystalline preparations should not be used. It is
indicated in refractory cases and those not tolerating NSAIDs/ colchicines.
E.g. prednisolone 40-60mg/day
For chronic gout:
a. Uricosuric drugs:
Probenecid: uric acid is largely reabsorbed by active transport,
while less of it is secreted; only 1/10th of filtered load is
excreted in urine. Probenecid therefore, promotes its excretion
and reduces its blood level.
Dose 0.25-0.5mg BD
Sulfinpyrazone: it is a pyrazolone derivative related to
phenylbutazone having consistent uricosuric action, but is
neither analgesic nor anti-inflammatory. At the usual
therapeutic doses, it inhibits tubular reabsorption of uric acid.
Dose: 100-200mg BD.
b. Uric acid synthesis inhibitors:
Allopurinol: allopurinol is the first choice drug in chronic gout.
It can be used in both over producers and under excretors of
uric acid, particularly more serious case, with tophi or
nephropathy.
Dose start with 100mg OD , gradually increase to maintenance
doseof 300mg/day; maximum 600mg/day
13. 16.Describe vasomotorreversalofdale:
ANS: Rapid i.v. injection of adrenaline produces a marked increase in both
systoloic as well as diastolic blood pressure(at high concentration α-response
predominates and vasoconstriction occurs even in skeletal muscle). The blood
pressure returns to normal within a few minutes and a secondaryfall in mean
BP follows. The mechanism is rapid uptake and dissipation- concentration of
adrenaline decreases, This adrenaline concentration cannot stimulate alpha
receptors but is enough to stimulate Beta receptors. Hence there is a secondary
fall in blood pressure. So when rapid i.v. injection of adrenaline is given in
combination with Alpha blockers, only fall in BP is seen which is called
Vasomotor Reversal Of Dale.
17. Differentiatebetween:
A. Drug potency and drug efficacy:
Drug potency:
1) It is the relationship between the the doseof a drug and the therapeutic effect.
2) It refers to the drug's strength.
3) A drug is considered potent when a small amount of the drug achieves the
intended effect.
4) It depends on bothaffinity and efficacy of drug.
5) It is a factor in choosing the doseof drug.
14. Drug efficacy:
1) It is the ability of a drug to producethe desired therapeutic effect.
2) It refers to the drug's effectiveness.
3) A drug is considered efficacious when a drug achieves the maximal responses
that can be elicited by it.
4) It depends on bothdrug binding and drug bound receptor.
5) It is a decisive factor in choosing the drug.
B. Synergism and antagonism:
Antagonism
1) When one drug decreases or abolishes the action of another, they are said to be
antagonistic and the phenomena is called antagonism.
2) In an antagonistic pair one drug is inactive as such but decreases the effect of
other.
3) It can be represented as:
•Effects of drugs (A+B) <Effects of drug A+ Effects of drug B
4) Eg:
•Atropine - ACh
•Morphine - Naloxone
•Glucagon and insulin on blood sugar level.
Synergism:
1) When the action of one drug is facilitated or increased by the other, they are
said to be synergistic and the phenomena is called synergism.
15. 2) In a synergistic pair, both the drugs can have action in same direction or given
alone one may be inactive but still enhance the action of the other when given
together.
3) It can be represented as :
•Effects of drugs (A+B) =Effects of drug A+ Effects of drug B
•Effects of drugs (A+B) >Effects of drug A+ Effects of drug B
4) Eg :
•Aspirin + Paracetamol= as analgesic / anripyreti
•Ephedrine + Theophylline= as bronchodilator
•Amlodipine+ Atenolol = as antihypertensive
•Levodopa+ Carbidopa = Inhibition of peripheral metabolism
C. Tubocurarine and succinylcholine
Tubocurarine:
1) It belongs to non- depolarizing or competitive blockers.
2) It work by competitively blocking the binding of acetylcholine to its receptors.
3) They bind to acetlycholine receptors as antagonist and leaves fewer receptors
available for acetylcholine to bind.
Succinylcholine:
1) It belongs to depolarizing blockers.
2) It work by depolarizing the plasma membrane of muscle fibre.
3) They bind to acetylcholine receptorand cause depolarization by opening sodium
ion channels just like acetylcholine does.
16. D. Respiratoryalkalosis andrespiratory acidosis:
Respiratory alkalosis:
1) When the pH value of bodyfluids becomehigher than 7.45 due to
abnormalities in respiratory system then it is called respiratory alkalosis.
2) It is caused by hyperventilation of lungs.
3) In this, rate at which CO2 is eliminated from body fluids through the lungs
increases.
4) It may be produced accidentally during excessive mechanical ventilation. Other
causes include: psychiatric causes like anxiety , hysteria, stress ; CNS causes like
stroke, subarachnoid haemorrhage, meningitis ; drugs like doxapram , aspirin ,
caffeine; high altitude; lung disease such as pneumonia; pregnancy.
5) Kidneys help to compensate for respiratory alkalosis by decreasing the rate of
secretion of hydrogen ions into filtrate and reabsorption of bicarbonate ions.
Respiratory acidosis:
1) When the pH value of bodyfluids becomelower than 7.35 due to abnormalities
in respiratory system then it is called respiratory acidosis.
2) It is caused by hypoventilation of lungs.
3) In this, rate at which CO2 is eliminated from body fluids through the lungs
decreases.
4) Its causes include : CNS problems such as myasthenia gravis, muscular
dystropy; traumas ;airway obstruction related to asthma or chronic obstructive
pulmonary disease (COPD) exacerbation; hypoxia.
5) Kidneys help to compensate for respiratory acidosis by increasing the rate of
secretion of hydrogen ions into filtrate and reabsorption of bicarbonate ions.
18. Write down the adverse drug reactions of the following:
a) Amphetamine:
17. More common
Bladder pain
bloody or cloudy urine
difficult, burning, or painful urination
fast, pounding, or irregular heartbeat or pulse
frequent urge to urinate
lower back or side pain
Anxiety
dry mouth
lack or loss of strength
stomach pain
weight loss
Less common
Cold or flu-like symptoms
cough or hoarseness
fever or chills
b) Lignocaine:
More common
Flushing, redness of the skin
small red or purple spots on the skin
swelling at the site of application
unusually warm skin
Less common
Bruising, burning, pain, or bleeding at the site of application
itching skin
18. c) Warfarin:
Abdominal or stomach pain with cramping
bleeding gums
blood in the urine
bloody stools
blurred vision
burning, crawling, itching, numbness, prickling, "pins and needles", or tingling
feelings
chest pain or discomfort
confusion
coughing up blood
difficulty with breathing or swallowing
dizziness, faintness, or lightheadedness when getting up suddenly from a lying
or sitting position
excessive bruising
headache
increased menstrual flow or vaginal bleeding
nosebleeds
paralysis
peeling of the skin
prolonged bleeding from cuts
red or black, tarry stools
red or dark brown urine
shortness of breath
sweating
unexplained swelling
unusual tiredness or weakness
19. red, sore, or itching skin
sores, welting, or blisters
unusual drowsiness, dullness, or feeling of sluggishness
d) Furosemide:
Chest pain
chills
cough or hoarseness
fever
general feeling of tiredness or weakness
headache
lower back or side pain
painful or difficult urination
shortness of breath
sore throat
sores, ulcers, or white spots onthe lips or in the mouth
swollen or painful glands
tightness in the chest
unusual bleeding or bruising
unusual tiredness or weakness
wheezing
e) Acetylcholine:
Hypotension
Bradycardia
Flushing, and sweating
20. Ocular side effects have rarely included corneal clouding, corneal decompensation,
and corneal edema
Bronchospasmin a patient on concomitantmetoprolol therapy.
f) Aspirin:
epigastric pain
Heartburn
Nausea and vomiting
Ulcers
Gastric mucosal lesions
Hemorrhage and peptic ulcers
Renal side effects include reduction in glomerular filtration rate (particularly in
patients who are sodium restricted or who exhibit diminished effective arterial
blood volume, suchas patients with advanced heart failure or cirrhosis), interstitial
nephritis, papillary necrosis, elevations in serum creatinine, elevations in blood
urea nitrogen, proteinuria, hematuria, and renal failure.
Hypersensitivity side include bronchospasm, rhinitis, conjunctivitis, urticaria,
angioedema, and anaphylaxis
Hepatotoxicity and cholestatic hepatitis
Central nervous system side effects include agitation, cerebral edema, coma,
confusion, dizziness, headache, cranial hemorrhage, lethargy and seizures
g) Morphine in CNS:
Respiratory depression
22. 19. Write down the use of acetazolamide in glaucoma:
An increase in pressurewithin the eye can lead to damage to the optic nerve at the
back of the eye. When this occurs it is called glaucoma. Glaucoma can lead to a
loss of vision if it is not treated. Treatment with acetazolamide helps to reduce eye
pressure, and this helps to prevent further eye damage.
Acetazolamide works by blocking the action of an enzyme called carbonic
anhydrase. Blocking this enzyme reduces the amount of fluid in eye i.e. aqueous
humor and this helps to lower the pressure within the eye.
20. Write the drugs commonly used in the managemaent of myasthenia
gravis and describe their mechanism of action ?
Ans. -Mysthenia gravis is an autoimmune disorder affects 1 in 10000 populations
-characterized by the development of antibodies directed to the nicotinic receptors
at the muscle end plate and
-this results in the reduction of NM cholinoreceptors to 1/3rd of normal or less.
- structural damage to the neutomuscular junction results feel weakness and fatigue
on repeated activity with recovery after rest.
Commonly used drugs to treat this disorder can be listed as-
1) Anticholineesterase : Neostigmine(preferred 15 mg QID), Physostigmine etc
2) Corticosteroids: Prednisolone( 30-60mg od)
3) Other immunosuppresants( eg. Azathioprine, Cyclosporine,etc.)
Other mechanisms
4) Plasmapharesis( plasma exchange)
5) Thymectomy( removal of thymus gland)
Short mechanism of action of drugs
1) Anticholineesterase : Neostigmine(preferred), Physostigmine etc
Reversibly binds at the esteric site of cholinesterase enzyme
23. Prevents the hydrolysis of Ach
Increase the interaction between Ach-nicotinic receptor
2) Corticosteroids: Prednisolone
Inhibit the production of nicotinic receptor antibodies
Immunosuppresant action
May increase the synthesis of nicotinic receptors
3) Other immunosuppresants
Immunosuppresants inhibit the nicotinic receptor antibody by selectively
suppressing the cell mediated immunity.
21. Why acetazolamide is used in Glaucoma?
Ans: Acetazolamide is a carbonic acid anhydrase enzyme inhibitors.
Acetazolamide
( ─)
H2O + CO2 H2CO3 H+ + HCO3-
When acetazolamide (0.25 gm tablet 6-12 hourly) is administered orally, it reduces the
formation of aqueous humor by limiting the generation of bicarbonate in, because
carbonic acid is the main component of aqueous humor. Hence, along with other ocular
hypertensive drug, it reduces the intraocular pressure and thus used in the treatment of
open angle glaucoma.