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This Presentation covers Pharmacology of different antiplatelet agents their Mechanisms, Kinetics, Therapeutic uses, Adverse drug reactions and also Recent advances ..benefiting the Medical ,Dental graduates..
PH1.28 Describe the mechanisms of action, types, doses, side effects, indicat...Dr Pankaj Kumar Gupta
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This Presentation covers Pharmacology of different antiplatelet agents their Mechanisms, Kinetics, Therapeutic uses, Adverse drug reactions and also Recent advances ..benefiting the Medical ,Dental graduates..
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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
3. Antiplatelet Agents/
Antithrombotic Agents
These are drugs which interfere with platelet function.
They are useful in the prophylaxis of thromboembolic
disorders.
(Why them ?????)
DO we not have the Thrombolytic Medications?
Antithrombotic Agents Vs Thrombolytic Agents
5. The Platelets
• Platelets provide the initial hemostatic plug at sites of
vascular injury.
• They also participate in pathological thromboses that lead
to
• myocardial infarction,
• stroke, and
• peripheral vascular thromboses.
• Antiplatelet drugs when used in combination with
anticoagulants their effects are additive or even synergistic.
6. Platelet phase
• Blood vessel wall (endothelial cells) prevents platelet adhesion
and aggregation via- NO & PGI2.
• Platelets contain glycoprotein receptors (fibrinogen) and von
Willebrand factor (collagen)
• Following vessel injury platelets adhere & aggregate.
• Loose their membrane and form a viscous plug known as the
platelet plug.
7. Platelet Plug
• Sharp object pierces skin.
• Platelets are attracted to the
exposed collagen and will start
to form a plug by connections
of their glycoprotein
receptors.
• A substance called von
Willebrand's Factor (vWF)
bridges the gap between the
platelets and the collagen, but
receptors also link the platelets
straight to it.
8.
9. Platelet Plug
• Platelets are stuck together with fibrinogen linking
their glycoprotein receptors.
• Along with neutrophils and monocytes, platelets
release ADP to try and help the situation, which helps
the platelets come together to form a plug.
• PAF or Platelet activating factor which
activates platelets to release more chemicals;
and 5-HT ( 'Serotonin') and TXA2 (Thromboxane
A2), which cause vasoconstriction.
10. NO and PGI2
• The endothelial cells lining blood vessels, release Nitric oxide (NO)
and Prostacyclin (PGI2), which inhibit the pro-aggregatory and
vasoconstrictor effects of ADP, PAF, 5-HT and TXA2.
• Prostacyclin (PGI2) synthesized in the intima of BVs increases
platelet cAMP and thereby acts as a strong inhibitor of platelet
aggregation.
• Nitric oxide (NO) – also increases cAMP, thus inhibiting
thrombogenesis.
• TXA2 lowers cAMP
• NOTE: Drugs that modulate the intraplatelet concentration of cAMP
do not prolong bleeding time.
11. A balance between TXA2 released from platelets and PGI2
released from vessel wall appears to control intravascular
thrombus formation.
12. When do you think will the antiplatelet drugs be
more useful?
1. Venous thrombus
2. Arterial thrombus
• WHY??
1. Anticoagulants---RBCs (main constituents)
2. Antiplatelet Drugs---Platelets
13. Drug Class Prototype Action Effect
1.
Anticoagulant
Parenteral
Heparin Inactivation of clotting
factors
Prevent DVT
Oral Warfarin Decrease synthesis of
clotting factors
Prevent DVT
2. Antiplatelet Aspirin Decrease platelet
aggregation
Prevent arterial
thrombosis
3. Thrombolytic Streptokinase Fibrinolysis Breakdown of
thrombi
Drugs used to reduce clotting
17. NSAIDS-Aspirin
Mechanism:
• Acetylates and irreversibly
inhibits COX and TX-synthase
• Inhibits platelet aggregation
• Aspirin also inhibits the release
of ADP from platelets and their
sticking to each other.
• Long acting--because new
proteins must be synthesized
owing to irreversible inactivation
of enzymes.
• Thus, it also induces prolongation
of bleeding time lasting for 7 days.
18. Aspirin--COX-Inhibition
Platelets (lacking nucleus) Can’t produce TXA2
Endothelial cells(nucleated) Produce COX, and then produce
some PGI2,
hence the antiplatelet effect is seen.
• New platelets need to be formed for Aspirin effects to wear off.
• Endothelial cells being nucleated, can form fresh enzyme and
therefore enzyme activity returns rapidly.
• Therefore PGI2 is still produced at low doses that depress the
TXA2 production. Dose being 75-150 mg/day or 300 mg twice
weekly.
• High dose >900mg daily decrease both TXA2 and PGI2
production.
19. NSAIDS-Aspirin
Use: Low dose aspirin (Baby aspirin 75-150 mg)
• MI
Prophylaxis of MI
Prevention of recurrent infarcts in patients with myocardial infarction
• Prevention of stroke
• Antiplatelet prophylaxis for
– DVT –Deep Vein Thrombosis
– PE – Pulmonary Embolism
• Venous Thromboembolism reduction
Low-dose aspirin, compared with placebo, reduces by 36% the risk of
VTE (Venous Thromboembolism) after orthopedic surgery
20. • Phosphodiesterase Inhibitor
• Phosphodiesterase break down the
cyclic nucleotides cAMP, cGMP.
• Dipyridamole inhibits the uptake of
adenosine into platelets, endothelial
cells and erythrocytes.
• This increases local concentrations of
adenosine that acts on the platelet A2-
receptor thereby stimulating platelet
adenylate cyclase and increasing
platelet cAMP levels.
Thus Dipyridamole increases the
cellular concentration of cAMP.
Increased cAMP causes potentiation
of action of PGI2 & opposes actions
of TXA2.
Dipyridamole
21. Dipyridamole
USES
Only for prevention of thromboembolism after heart valve
replacement surgery. Dipyridamole alone has little clinically
significant effect, but improves the response to warfarin.
• Used with Aspirin to prevent ischemic stroke.
S/Es
• Dizziness, headache
• Stomach upset, diarrhea, vomiting
• Flushing
• Serious S/Es: chest pain, confusion, slurred speech
22. Ticlopidine and Clopidogrel
• ADP Receptor Antagonists
• Oral antiplatelet drugs whose effects similar to aspirin; to
patients who cannot tolerate aspirin.
[Expensive ]
Mechanism
• Irreversible blockade of ADP
receptors on platelet surface
• No effect on PG metabolism
• It prevents fibrinogen binding
to platelets without modifying
GP IIB/IIIA receptor.
23. Ticlopidine and Clopidogrel
• Used for prevention of ischemic stroke and MI
• Also useful in
– intermittent claudication,
– unstable angina,
– coronary artery bypass grafts
Adverse Effects-
• Diarrhoea, vomiting, abdominal pain
• Serious: bleeding, neutropenia, thrombocytopenia and
jaundice; deaths recorded
Clopidogrel is known to have low toxicity.
More in use in Nepal.
24. Abciximab
• A monoclonal antibody against GP IIB/IIIA.
• Given along with Aspirin + Heparin during angioplasty
it has markedly reduced the incidence of restenosis
subsequent MI and death.
• After a bolus dose platelet aggregation remains
inhibited for 12-24 hr, while the remaining antibody is
cleared from blood with a T ½ of 10-30 min.
• Non-antigenic
S/Es
• Main risk is hemorrhage
• Thrombocytopenia
• Constipation, ileus and arrhythmias
25. Glycoprotein IIb/IIIa Receptor
• GP IIB/IIIA is a platelet-surface integrin receptor.
• This glycoprotein is a receptor for
– fibrinogen
– von Willebrand factor,
which anchor platelets to foreign surfaces and to each other, thereby
mediating aggregation.
26. Clinical Uses
Coronary Artery Disease
• Aspirin is useful for prevention of MI
• Low dose aspirin immediately after MI reduce
mortality and prevent re-infarction. Ticlopidine
and Clopidogrel are alternatives.
• Aspirin is now routinely used to prevent
reocclusion after thrombolytic therapy.
• Clopidogrel or Abciximab with Aspirin useful in
angioplasty and stenting.
• Aspirin reduces risk of MI and sudden deaths in
patients with unstable angina.
27. Clinical Uses
Cerebrovascular Disease
• Aspirin reduces incidence of TIAs (Transient Ischemic
Attacks), and strokes.
• Ticlopidine and Clopidogrel can also be used for it.
Coronary angioplasty, stents, bypass implants
• Aspirin with Clopidogrel is used to maintain
recanalization of coronary artery or implanted bypass
vessel; decreasing re-occlusion.
• Abciximab with Aspirin and Heparin markedly reduces
restenosis and subsequent MI after coronary
angioplasty.
28.
29. Clinical Uses
Prosthetic heart valves and arteriovenous shunts
Antiplatelet drugs with Warfarin reduce microthrombi formation on
artificial heart valves and thereby decreasing incidence of embolism.
Since Aspirin increases risk of bleeding with Warfarin, Dipyridamole is
used with Warfarin.
Venous thromboembolism
Anticoagulants are better preferred (RBCs)
Peripheral Vascular Disease
Aspirin/Clopidogrel –for Intermitted claudication
30. Peripheral vascular disease/
Intermittent claudication
• Usually affects men over age 50
• A condition of the blood vessels that leads to narrowing
and hardening of the arteries that supply the legs and
feet, thereby injuring the nerves and other tissues.
• Symptoms are pain, achiness, fatigue, burning, or
discomfort in the muscles of your feet, calves, or thighs.
These symptoms usually appear during walking or
exercise and go away after several minutes of rest.
Precipitating factors:
Abnormal cholesterol, Hypertension, Heart disease,
Diabetes, Smoking, Stroke, Kidney disease involving
hemodialysis
31. Angina pectoris
• Sudden, severe, pressing chest pain starting
sub-sternal that radiates to left arm.
1. Exertional/Atherosclerotic angina (90%)
Stable, Atherosclerotic, Classic,
Due to obstruction of coronaries by atheroma.
2. Variant, Vasospastic angina
Occurs at rest, sleep. Due to Spasm of coronaries.
3- Unstable angina
Due to spasm and partial obstruction of coronaries.
Immediate precursor of myocardial infarction (MI)