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.
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.
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.
The all the content in this profile is completed by the teachers, students as well as other health care peoples.
thank you, all the respected peoples, for giving the information to complete this presentation.
this information is free to use by anyone.
Peptic ulcers are open sores that develop on the inside lining of esophagus, stomach and/or the upper portion of small intestine. Peptic ulcer occur mainly due to imbalance between aggressive and defensive factors in the stomach.
Respiratory stimulants: types, complete discussion on indications, contraindications, assessment, patient notes and examples of stimulants both central and respiratory
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.
The all the content in this profile is completed by the teachers, students as well as other health care peoples.
thank you, all the respected peoples, for giving the information to complete this presentation.
this information is free to use by anyone.
Peptic ulcers are open sores that develop on the inside lining of esophagus, stomach and/or the upper portion of small intestine. Peptic ulcer occur mainly due to imbalance between aggressive and defensive factors in the stomach.
Respiratory stimulants: types, complete discussion on indications, contraindications, assessment, patient notes and examples of stimulants both central and respiratory
Expectorants and Antitussives: types, complete discussion on indications, contraindications, assessment, patient notes and examples of expectorants and antitussives
Complete pharmacology of Non steroidal Anti inflammatory Drugs, classification, Mechanism of action, Pharmacological actions, Indications, Contraindications, Adverse effects
Pharmacology laboratory experiment, both invivo and invitro includes interpolation, matching , bracketing, three point, four point bioassays with a note on hypoglycemic activity, acute skin irritation, acute eye irritaiton, pyrogen test, gastrointestinal motility test, physiological salt solutions
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.
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
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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
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
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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.
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.
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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
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...
Anti gout drugs.pdf
1. Gout
Gout: It is a metabolic disorder characterized by hyperuricaemia (normal plasma urate 2–6
mg/ dl). Uric acid, a product of purine metabolism, has low water solubility, especially at low
pH. When blood levels are high, it precipitates and deposits in joints, kidney and
subcutaneous tissue (tophy).
Secondary hyperuricaemia occurs in:
A. Leukaemias, lymphomas, polycythaemia— especially when treated with
chemotherapy or radiation: due to enhanced nucleic acid metabolism and uric acid
production.
B. Drug induced—thiazides, furosemide, pyrazinamide, ethambutol, levodopa reduce
uric acid excretion by kidney.
Acute Gout
Acute gout manifests as sudden onset of severe inflammation in a small joint
(commonest is metatarso-phalangeal joint of great toe) due to precipitation of urate
crystals in the joint space.
The joint becomes red, swollen and extremely painful: requires immediate treatment.
Chronic Gout
When pain and stiffness persist in a joint between attacks, gout has become chronic.
Other cardinal features are hyperuricaemia, tophi (chalk-like stones under the skin in
pinna, eyelids, nose, around joints and other places) and urate stones in the kidney.
In majority of patients, hyperuricaemia is due to undersecretion of uric acid, while in
few it is due to over production.
Chronic gouty arthritis may cause progressive disability and permanent deformities.
Acute gout
Uricosurics
Probenecid
Sufinpyrazone
Synthesis inhibitors
Allopurinol
Febuxostat
For chronic gout/
hyperuricaemia
NSAIDs
Colchicine
Corticosteroids
ANTI-GOUT DRUGS
2.
3. CATEGORY FEATURES ADME USES ADVERSE EFFECTS
NSAIDs
Naproxen
Piroxicam
Diclofenac
Indomethacin
Etoricoxib
Given in relatively high and
quickly repeated doses.
They are quite effective in
terminating the attack
Naproxen and Piroxicam
specifically inhibit
chemotactic migration of
leucocytes into the inflamed
joint.
May take 12–24 hours,
Better tolerated
Prefer them over
colchicine
They may be continued
At lower doses for 3–4
weeks
Not recommended for
long term management
due to risk of toxicity.
The NSAIDs in initiation of
therapy (6–8 weeks) with
allopurinol or uricosurics in
chronic gout.
Colchicine
(Colchicum
autumnale which
was used in gout
since 1763. The
pure alkaloid was
isolated in 1820.)
Neither analgesic nor anti-
inflammatory,
Suppresses gouty
inflammation
Does not inhibit the synthesis
or promote the excretion of
uric acid
Colchicine does not affect
phagocytosis of urate crystals
Inhibits release of
chemotactic factors
Binding to tubulin, It inhibits
granulocyte migration
Antimitotic: causes
metaphase arrest by binding
to microtubules of mitotic
spindle.
Increases gut motility
through neural mechanisms.
Colchicine is rapidly
absorbed
Orally,
Partly metabolized
Excreted in bile
Undergoes
enterohepatic
circulation;
Ultimate disposal urine
and faeces
Binding to tubulin
contributes to its large
volume of distribution
and slow elimination.
Inhibitors of CYP3A4
retard colchicine
metabolism and
enhance its toxicity.
Treatment of acute gout
Colchicine is the fastest acting
drug to control an acute attack of
gout;
0.5 mg 1–3 hourly/ 3 doses in
a day;
A second course should not be
started before 3–7 days.
Prophylaxis
Colchicine 0.5–1 mg/day can
prevent further attacks of acute
gout.
Nausea, vomiting,
Watery or bloody
diarrhoea
Abdominal cramps
Kidney damage,
CNS depression,
Intestinal bleeding
Death is due to
muscular paralysis and
respiratory failure.
Aplastic anaemia,
Agranulocytosis,
Myopathy
Loss of hair.
4. Corticosteroids
Intraarticular injection of a
soluble steroid suppresses
symptoms of acute gout.
Systemic steroids are rarely
needed. They are highly
effective and produce nearly
as rapid a response as
colchicine
Prednisolone 40–60
mg may be given in
one day, followed by
tapering doses over
few weeks.
It is indicated in refractory
cases and those not tolerating
NSAIDs/colchicine.
Systemic steroids are reserved
for patients with renal
failure/history of peptic ulcer
bleed in whom NSAIDs are
contraindicated.
Crystalline preparations
should not be used
Probenecid
It is a highly lipid-soluble
organic acid developed in
1951 to inhibit renal tubular
secretion of penicillin so that
its duration of action could
be prolonged.
It competitively blocks
active transport of organic
acids by OATP at all sites;
that in renal tubules being
the most prominent
It is neither Analgesic nor
anti-inflammatory.
Probenecid is completely
absorbed orally; 90%
plasma protein bound:
partly conjugated in liver
and excreted by the
kidney; Plasma t½ is 6–8
hours.
Chronic gout and
hyperuricaemia:
Probenecid is also used to
prolong penicillin or
ampicillin action in
gonorrhoea, SABE.
Probenecid is given along
with cidofovir, a drug for
CMV retinitis in AIDS
patients, to prevent its
nephrotoxicity.
Dyspepsia
Rashes
convulsions
Respiratory failure.
Interactions
Probenecid inhibits
the urinary excretion
of cephalosporin’s,
sulphonamides,
Mtx and indomethacin.
It inhibits biliary
excretion of
rifampicin.
Pyrazinamide
Probenecid inhibits
tubular secretion of
nitrofurantoin
Salicylates block
uricosuric action of
probenecid.
Sulfinpyrazone It is a pyrazolone derivative,
related to phenylbutazone,
It inhibits tubular
reabsorption of uric
Sulfinpyrazone has gone into
disuse because of more gastric
Sulfinpyrazone
inhibits platelet
5. having uricosuric action, but
is neither analgesic nor anti-
inflammatory.
acid, but smaller
doses can decrease
urate excretion as do
small doses of
probenecid. Though
equally efficacious as
probenecid
irritation and other side
effects. It has been withdrawn
in USA.
aggregation as well.
Uricacid synthesis
inhibitors
Allopurinol
This hypoxanthine analogue
was synthesized as a purine
antimetabolite for cancer
chemotherapy.
a substrate as well as
inhibitor of xanthine oxidase
Short-acting (t½ 2 hrs)
competitive inhibitor
of xanthine oxidase,
But its major
metabolitealloxanthine
(oxypurine) is a long-
acting (t½ 24 hrs) and
non-competitive
inhibitor
At high
concentrations,
Allopurinol also
becomes non-
competitive inhibitor.
During allopurinol
administration, plasma
concentration of uric
acid is reduced and
that of hypoxanthine
and xanthine is
somewhat increased.
About 80% of orally
administered
allopurinol is
absorbed.
Chronic gout.
It can be used in both over
producers and under
excretors of uric acid less
effective when G.F.R. is low
and are Inappropriate in stone
formers.
The two classes of drugs can
also be used together when
the body Load of urate is
large.
With long-term allopurinol
therapy, tophi gradually
disappear and nephropathy is
halted, even reversed.
Secondary hyperuricaemia
Due to cancer chemotherapy
radiation/thiazides or other
drugs: can be controlled by
allopurinol.
It can even be used
prophylactically in these
situations.
Hypersensitivity
reaction consisting of
Rashes,
Fever,
Malaise
Muscle pain
Renal impairment
increases
Stevens-Johnson
syndrome
Gastric irritation,
Headache,
Nausea
Dizziness
Liver damage is rare.
6. It is not bound to
plasma proteins
Metabolized largely to
alloxanthine.
During chronic
medication, it inhibits
its own metabolism
and about 1/3rd is
excreted unchanged,
the rest as
alloxanthine.
To potentiate 6-mercaptopurine
or azathioprine
In cancer
Kala-azar
Allopurinol inhibits
Leishmanial by altering its
purine metabolism. It was
tried as adjuvant to sodium
Stibogluconate, but
abandoned due to poor
efficacy.
Febuxostat
It is a recently introduced
nonpurine xanthine oxidase
inhibitor, equally or more
effective than allopurinol in
lowering blood uric acid level in
patients with hyperuricemia and
gout.
It is rapidly
absorbed orally,
highly plasma protein
bound,
oxidized as well as
glucuronide
conjugated in
the liver and
excreted by kidney
The plasma t½ is ~ 6
hours.
Febuxostat is an alternative
drug for treating
symptomatic gout only in
patients intolerant to
allopurinol,
It is not indicated in
malignancy associated
Hyperuricemia.
NSAID/colchicine cover
should be provided for 1–2
months while initiating
Febuxostat therapy.
Liver
Damage (liver
function needs to be
monitored
During febuxostat
therapy)
Diarrhoea,
Nausea
Headache
By inhibiting xanthine
oxidase, it has the
potential to interact
with mercaptopurine,
azathioprine and
theophylline; should
not be given to
patients receiving
these drugs.