1. NSAIDs are a class of drugs that relieve pain and reduce fever and inflammation. They work by inhibiting cyclooxygenase (COX) enzymes and subsequent prostaglandin production.
2. NSAIDs are classified based on selectivity and potency of COX-1 and COX-2 inhibition. Common nonselective NSAIDs include aspirin, ibuprofen, and naproxen. Selective COX-2 inhibitors have fewer gastrointestinal side effects.
3. In addition to analgesic, antipyretic and anti-inflammatory effects, NSAIDs can have antiplatelet, cardiovascular, renal and gastrointestinal adverse effects that require consideration of risks and benefits of treatment options.
This is an interesting and novel PPT on the Pharmacology of NSAIDs, on drugs other than aspirin ( for Aspirin check NSAIDs PART I ) illustrated with beautiful pictures and flowcharts....!!
local anaesthesia is defined as a loss of sensation in a circumscribed area of the body caused by a depression of excitation in nerve endings
Or an inhibition of the conduction process in peripheral nerves; no loss of consciousness occurs
Local anesthetics interfere with the excitation process in the nerve membrane in one or more of the following ways:
1) Altering the basic resting potential of the nerve membrane
2) Altering the threshold potential (firing level)
3) Decreasing the rate of depolarization*
4) Prolonging the rate of repolarization
Classification
Mechanism of action
Duration of action
Absorption and distribution
Mode of action
Theories of action of L.A
Pharmacokinetics of local anaesthetics
Routes of administration
Metabolism or biotransformation
Individual agents
Vasoconstrictors
Systemic effects
Toxicity
Advantages
Disadvantages
Maximum allowable dose
Local anaesthetics in community trust services
This is an interesting and novel PPT on the Pharmacology of NSAIDs, on drugs other than aspirin ( for Aspirin check NSAIDs PART I ) illustrated with beautiful pictures and flowcharts....!!
local anaesthesia is defined as a loss of sensation in a circumscribed area of the body caused by a depression of excitation in nerve endings
Or an inhibition of the conduction process in peripheral nerves; no loss of consciousness occurs
Local anesthetics interfere with the excitation process in the nerve membrane in one or more of the following ways:
1) Altering the basic resting potential of the nerve membrane
2) Altering the threshold potential (firing level)
3) Decreasing the rate of depolarization*
4) Prolonging the rate of repolarization
Classification
Mechanism of action
Duration of action
Absorption and distribution
Mode of action
Theories of action of L.A
Pharmacokinetics of local anaesthetics
Routes of administration
Metabolism or biotransformation
Individual agents
Vasoconstrictors
Systemic effects
Toxicity
Advantages
Disadvantages
Maximum allowable dose
Local anaesthetics in community trust services
A presentation describing pain, analgesia, formation of prostaglandins along with a detailed description of NSAIDS, the mechanism of action, classification and an in depth discussion of each class along with key points to be kept in mind for dentists
NSAIDs have an extremely safe profile when used for acute dental pain.
Within a group they tend to have similar characteristics & tolerability. There is little difference in clinical efficacy among the NSAIDs when used at equivalent doses.
Rather, differences among compounds usually relate to dosing regimens (related to compound’s elimination half –life), route of administration, & tolerability profile.
So, clinician should have a thorough knowledge of mechanism of action, pharmacokinetics, pharmacodynamics, dosage & adverse effects of each drug before prescribing the same.
Lecture slides for undergraduates medical (MBBS) Students. Source material for this presentation is Essentials of Pharmacology, KD Tripathi, Katzung and Goodman and Gillman. It deals with Local anaesthetics with their mechanism of action, pharmacokinetics , adverse effects and therapeutic uses.
A presentation describing pain, analgesia, formation of prostaglandins along with a detailed description of NSAIDS, the mechanism of action, classification and an in depth discussion of each class along with key points to be kept in mind for dentists
NSAIDs have an extremely safe profile when used for acute dental pain.
Within a group they tend to have similar characteristics & tolerability. There is little difference in clinical efficacy among the NSAIDs when used at equivalent doses.
Rather, differences among compounds usually relate to dosing regimens (related to compound’s elimination half –life), route of administration, & tolerability profile.
So, clinician should have a thorough knowledge of mechanism of action, pharmacokinetics, pharmacodynamics, dosage & adverse effects of each drug before prescribing the same.
Lecture slides for undergraduates medical (MBBS) Students. Source material for this presentation is Essentials of Pharmacology, KD Tripathi, Katzung and Goodman and Gillman. It deals with Local anaesthetics with their mechanism of action, pharmacokinetics , adverse effects and therapeutic uses.
Pharmacology of drugs for pain management important
Route of drugs administration change pharmacodynamic and pharmacokinetic of the drug must be explore to enrich our modality in pain management
Postoperative pain management not resolved completely still a problem for most of the physician involved in this area and the patients
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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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.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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
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.
- 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
5. Pharmacological actions of aspirin
and other NSAIDs
• Analgesic effect
– mainly used for relieving musculoskeletal pain.
– dysmenorrhoea and pain associated with
inflammation or tissue damage.
– Analgesic effect is mainly due to peripheral
inhibition of PG production.
– They also reduce pain by acting at subcortical
site. These drugs relieve pain without causing
sedation, tolerance or drug dependence
6. Pharmacological actions
• Antipyretic effect
– mainly due to inhibition of PGs in the hypothalamus.
– They promote heat loss by causing cutaneous
vasodilatation and sweating.
– They do not affect normal body temperature.
• Anti-inflammatory effect:
– These drugs produce only symptomatic relief. They
suppress signs and symptoms of inflammation such as
pain, tenderness, swelling, vasodilatation and
leukocyte infiltration but do not affect the
progression of underlying disease.
– mainly due to inhibition of PG, bradykinin, histamine,
serotonin, etc synthesis at the site of injury. thus
inhibit granulocyte adherence to the damaged
vasculature.
7. Pharmacological actions
• Antiplatelet (antithrombotic) effect
– Aspirin in low doses (50–325 mg/day) irreversibly
inhibits platelet TXA2 synthesis and produces
antiplatelet effect, which lasts for 8–10 days.
– Aspirin in high doses (2–3 g/day) inhibits both
PGI2 and TXA2 synthesis.
9. Pharmacological actions
• Cardiovascular system (CVS)
– Prolonged use of aspirin and other NSAIDs causes
sodium and water retention.
– They may precipitate congestive cardiac failure
(CCF) in patients with low cardiac output. They
may also decrease the effect of antihypertensive
drugs.
• For patients with cardiovascular disease or risk
factors for ischemic heart disease:
acetaminophen, aspirin, tramadol, opioidsare
recommended before moving to an NSAID
10. Adverse effects
• GIT
– Nausea, vomiting, dyspepsia, epigastric pain,
acute gastritis, ulceration and GI bleeding.
– Ulcerogenic effect is the major drawback of
NSAIDs, which is prevented/minimized by taking:
• NSAIDs after food.
• proton pump inhibitors/H2-blockers/misoprostol with
NSAIDs.
• Coated aspirin.
• selective COX-2 inhibitors.
11.
12. Adverse effects
• Hypersensitivity
– It is relatively more common with aspirin. The
manifestations are skin rashes, urticaria, rhinitis,
bronchospasm.
– Bronchospasm (aspirin-induced asthma) is due to
increased production of leukotrienes.
• Reye’s syndrome
– Use of salicylates in children with viral infection may
cause hepatic damage with fatty infiltration and
encephalopathy—Reye’s syndrome. Hence, salicylates
are contraindicated in children with viral infection.
13. Adverse effects
• Pregnancy
– These drugs inhibit PG synthesis, thereby delay onset
of labour and increase chances of postpartum
haemorrhage.
• Analgesic nephropathy
– Salt &water retention & edema of lower limbs
– Hyperkalemia
– Interstitial nephritis
– Slowly progressive renal failure may occur on chronic
use of high doses of NSAIDs. Renal failure is usually
reversible on stoppage of therapy but rarely, NSAIDs
may cause irreversible renal damage.
15. Clinical uses of NSAIDs
• As analgesic & Anti-inflammatory
– In painful conditions like toothache, headache,
backache, bodyache, muscle pain, other joint
pain, neuralgias, dysmenorrhoea, etc.
• As asntipyretic
– To reduce elevated body temperature in fever
paracetamol is preferred because:
• Gastrointestinal symptoms are rare.
• It does not cause Reye’s syndrome in children.
16. Clinical uses of NSAIDs
• Thromboembolic disorders
– The antiplatelet effect of low-dose aspirin is made
use of in the prophylactic treatment of various
thromboembolic disorders, such as:
• Transient ischaemic attacks (TIA)
• Myocardial infarction (MI)
– to reduce incidence of recurrent MI to decrease mortality in
post-MI patients
• Other uses:
– Colon and rectal cancer: Regular use of aspirin is
reported to reduce the risk of cancer.
– Reduce the risk and retard the onset of
Alzheimer’s disease.
17. Other NSAIDs
• They have similar mechanism of action,
pharmacological actions, therapeutic uses and
adverse effects.
• They vary mainly in their potency, duration of
action, analgesic and anti-inflammatory
effects.
24. Paracetamol
• Mechanism of Action
– The drug is only a weak COX-1 and COX-2 inhibitor in
peripheral tissues, which accounts for its lack of anti-
inflammatory effect.
– Evidence suggests that acetaminophen may inhibit a
third enzyme, COX-3, in the CNS.
• Uses
– As antipyretic
– As analgesic: To relieve headache, toothache,
dysmenorrhoea, etc.
– It is the preferred analgesic and antipyretic in patients
with peptic ulcer, bronchial asthma and children.
25. Paracetamol
• Adverse effects
– Side effects are rare, occasionally causes skin rashes and
nausea.
– Hepatotoxicity: with acute overdose or chronic use.
– Nephrotoxicity is commonly seen on chronic use
• Acute paracetamol poisoning
– Acute overdosage mainly causes hepatotoxicity—
symptoms are nausea, vomiting, diarrhoea, abdominal
pain, hypoglycaemia, hypotension, coma, etc.
– Death is usually due to hepatic necrosis.
• The usual adult dose is 2* 325-mg (regular-strength) tablets every 4-6 hours, 2
*650-mg (extra-strength) tablets every 6 hours, or 2* 500 mg caplets (extra-
strength) every 6 hours.
• No more than 10 regular-strength tablets or 6 extra-strength tablets should be
ingested by adults in 24 hours.
27. • The minimum toxic dose of acetaminophen for a
single ingestion is 7.5 to 10 g in adults and 150
mg/kg in children.
• The acute ingestion of more than 12 g of
acetaminophen in single ingestion is considered a
toxic dose and can poses a high risk for liver
damage.
• In children, the acute ingestion of 250 mg/kg
poses a high risk for liver damage, and the acute
ingestion of 350 mg/kg can cause severe
hepatotoxicity if not immediately treated.
28.
29. CLINICAL CASE STUDY
James Smith is 45 years old and is new to your practice. This is your first
meeting with him, and you would like to ask him some questions
regarding his medication/health history. During the course of your
conversation you learn that he has a history of coronary heart disease
and is currently taking a baby aspirin each day. He takes acetaminophen
for general aches and pains. During the course of his examination you
and the dentist find two cavities, which are filled that day. Mr. Smith is
experiencing some mild pain after the procedure.
1. What is the rationale for using acetaminophen instead of an NSAID instead
to treat Mr. Smith’s pain?
2. What dose and duration of therapy should be recommended for Mr. Smith?
3. At what doses does hepatotoxicity occur with acetaminophen?
4. How can acetaminophen toxicity be avoided in Mr. Smith?
5. Compare and contrast acetaminophen to aspirin in terms of pharmacology,
adverse effects, and therapeutic effects.
6. What is the role of aspirin in the prevention of heart attack or stroke?
7. Are any dental concerns associated with low-dose aspirin therapy?
8. Can Mr. Smith take a drug like ibuprofen?
9. What should be said to Mr. Smith during a counseling session regarding
acetaminophen?
30. Case
1. A 64-year-old male presents with mild to moderate
musculoskeletal back pain after playing golf. He states
he has tried acetaminophen and that it did not help.
His past medical history includes diabetes,
hypertension, hyperlipidemia, gastric ulcer (resolved),
and coronary artery disease. Which of the following is
the most appropriate NSAID regimen to treat this
patient’s pain?
A. Celecoxib.
B. Indomethacin and omeprazole.
C. Naproxen and omeprazole.
D. Naproxen.
Prostaglandins
Prostaglandins (PGs) are products of long-chain fatty acids. Arachidonic acid is the precursor for
the biosynthesis of all PGs. The enzyme involved in the formation of PGs from arachidonic acid is
cyclooxygenase (COX). The main PGs in humans are prostaglandin E2 (PGE2), prostaglandin F2 (PGF2)
and prostacyclin (PGI2). Another class of substances obtained from arachidonic acid by the action of
lipoxygenase is leukotrienes.
There are two forms of COX, COX-1 and COX-2 (Fig. 7.2). COX-1 is constitutive (it is always
present) and is widely distributed. It participates in various physiological functions such as protection
of gastric mucosa, homeostasis, regulation of cell division, etc. COX-2 is induced during infl ammation
by cytokines and endotoxins.
Gastrointestinal tract (GIT): Aspirin irritates the gastric mucosa and produces nausea, vomiting and dyspepsia. The salicylic acid formed from aspirin also contributes to these effects. Aspirin also stimulates chemoreceptor trigger zone (CTZ) and produces vomiting
The increased risk of arterial thrombosis
is believed to be due to the COX-2 inhibitors having a greater
inhibitory effect on endothelial prostacyclin (PGI2) formation
than on platelet TXA2 formation. Prostacyclin promotes vasodilation
and inhibits platelet aggregation, whereas TXA2 has the
opposite effects
Autacoids and Respiratory System
Mechanism of toxicity and treatment (Fig. 7.5) The toxic metabolite of paracetamol is detoxified by conjugation with glutathione and gets elimi- nated.
High doses of paracetamol cause depletion of glutathione levels. In the absence of glutathione, toxic metabolite binds covalently with proteins in the liver and kidney and causes necrosis.
Alcoholics and premature infants are more prone to hepatotoxicity.
N-acetylcysteine or oral methionine replenishes the glutathione stores of liver and protects the liver cells.
Activated charcoal is administered to decrease the absorption of paracetamol from the gut.
Charcoal haemoperfusion is effective in severe liver failure.
Haemodialysis may be required in cases with acute renal failure.
1. Correct answer = C. This patient is at high risk of future
ulcers, due to the history of gastric ulcer. Therefore, using a
regimen that includes an agent that is more COX-2 selective
or a proton pump inhibitor is warranted. Therefore,
D is incorrect. Choices A and B are incorrect because this
patient has significant cardiovascular risk and a history
of coronary artery disease. Naproxen is thought of as the
safest NSAID regarding cardiovascular disease, though it
still can present risks. Therefore, C is correct as it uses the
first-choice NSAID with the GI protection of a proton pump
inhibitor.