This document discusses anti-thrombotic therapy in difficult clinical conditions. It summarizes various antiplatelet and anticoagulant drugs, difficult situations for their use including high ischemic or bleeding risk, and strategies for balancing thrombotic and hemorrhagic risks. Certain drugs like prasugrel and ticagrelor are preferred for high ischemic burden due to more potent platelet inhibition, while dose adjustments and shorter durations are recommended for high bleeding risk. Careful management is needed in situations like surgery, renal dysfunction, and pregnancy to minimize risks.
Oral Surgery in Patients on Anticoagulant TherapyVarun Mittal
Management of patients on Anticoagulant Therapy in Surgical Practice with special emphasis on Oral Surgical Procedures; along with Guidelines drawn from various Text Books and Journals
Oral Surgery in Patients on Anticoagulant TherapyVarun Mittal
Management of patients on Anticoagulant Therapy in Surgical Practice with special emphasis on Oral Surgical Procedures; along with Guidelines drawn from various Text Books and Journals
With the growing number of individuals prescribed anti-coagulants, a dilemma exists whether to discontinue the medication few days before the dental innervation or to keep continuing it to prevent the chances of stroke. This presentation covers in detail the pros an cons of discontinuing the anti-platelet medication.
Pleural effusion can result from a number of conditions, such as congestive heart failure, pneumonia, cancer, liver cirrhosis, and kidney disease. [1] The characteristics of the fluid depend on the underlying pathophysiologic mechanism. The fluid can be transudate, nonpurulent exudate, pus, blood, or chyle. Imaging studies are valuable in detecting and managing pleural effusions but not in accurately characterizing the biochemical nature of the fluid.
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
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.
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
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
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
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
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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.
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.
2. ▪ Anti – thrombotic therapy is a double edged sword
especially in certain critical situation .
▪ Attempts to reduce ischemic events is associated with
an increased risk of bleeding.
▪ Conversely, reducing bleeding complications may
increase coronary thrombotic ( ischemic ) events.
▪ Balancing both ends of the spectrum is essential.
3. ●Antiplatelet/Anti Coagulant drugs currently
available and their mechanism of action :
➢ASPIRIN : Irreversibly acetylates enzyme
cyclooxygenase . Selectively inhibits COX 1.
Thus prevents the synthesis of thromboxane
A2.This inhibits platelet aggregation.
4. ➢DIPYRIDAMOLE & CILOSTAZOL: Increases the
levels of c AMP in the platelets by blocking the
reuptake of adenosine and preventing c AMP
degradation( phosphodiesterase inhibition ). Thus
reducing the intracellular calcium levels which inturn
inhibits platelet activation and aggregation.
5. ➢CLOPIDOGREL, TICLOPIDINE & PRASUGREL:
Inhibit ADP activity by preventing its binding to
platelet receptor P2Y12. ADP stimulates expression of
GPIIb/IIIa receptor and mediate release of other
aggregation agonists .
Prasugrel is a pro drug( new thienopyridine ) and its
active form binds irreversibly to ADP P2Y12 receptor
on platelets.
6. ➢ABCIXIMAB , EPTIFIBATIDE & TIROFIBAN :
GPIIb/IIIa receptor antagonists block the final
common pathway in platelet activation. Due to high
affinity binding of abciximab to target receptor the
anti platelet effect of the drug persists for 24-48 hrs .
Residual platelet inhibition remains as high as 50-60%
for 24 hrs after the infusion ended.
7. ➢HEPARIN
Acts by activating plasma antithrombin.
Prevents conversion of fibrinogen to fibrin
Prevents conversion of prothrombin to thrombin.
➢WARFARIN
Indirectly interfere with the synthesis of vit k mediated
clotting factors in the liver.
8. DIFFICULT SITUATIONS FOR GIVING ANTI-THROMBOTIC
THERAPY :
● High ischemic burden
● High bleeding risk
● Non- cardiac surgery , post angioplasty, stenting
● Poor drug compliance
● Presence of anti-platelet therapy
● Renal dysfunction
● Pregnancy with prosthetic heart valve
● High INR levels
● Embolic stroke on anti- coagulant therapy
9. ASSESSMENT OF ISCHEMIC AND BLEEDING RISK :
ISCHEMIC RISK SHARED RISK FACTOR BLEEDING RISK
Recent ACS , PCI Elderly h/o bleeding
ACS with dual antiplatelet
therapy
Female Recurrent h’agic peptic
ulcer
LVEF<30% Obesity Intracranial surgery
TVD , DM Heart failure Transurethral
prostatectomy
Stent length >25mm Renal failure Surgery with extensive
detachment
Vessel diameter < 2.5mm Co- morbidites
Stent thrombosis
10. :CRITICAL CLINICAL CONDITIONS :
1. HIGH ISCHEMIC BURDEN :
▪ Rapid and greater inhibition of platelets to reduce
ischemic burden
▪ Diabetics, post PCI , small vessel disease, recent ACS
come in this category
▪ CLOPIDOGREL : slow onset of action , inhibits 50%
platelets , 25 % incidence of resistance
▪ PRASUGREL : inhibits ADP induced platelet
aggregation more rapidly and to a greater extent than
CLOPDOGREL .
11. ● In the Trial to Assess Improvement in Therapeutic
Outcomes by Optimising Platelet Inhibiton with
Prasugrel –Thrombolysis in Myocardial Infarction
(TRITON –TIMI 38 ) -
● Patients who underwent PCI had 19% risk reduction in
cardiovascular death, non-fatal MI, non-fatal stroke when
treated with PRASUGREL compared to CLOPIDOGREL .
● 52% risk reduction in stent thrombosis .
● But, 39% incresed risk of major bleeding with PRASUGREL
compared to CLOPIDOGREL
12. ● TICAGRELOR : Reversible ADP receptor inhibitor , more
rapid onset and more platelet inhibition than clopidogrel .
● The Platelet Inhibition and Patient Outcomes (PLATO)
trial : At ONE year , cardiovascular death, MI, stroke
occurred in 9.8 % patients receiving TICAGRELOR as
compared to 11.7% of those receiving CLOPIDOGREL , with
a significant 16% relative risk reduction .
● Patients who underwent PCI, rate of stent thrombosis was
lower with TICAGRELOR than CLOPIDOGREL (1.3% Vs
1.9% )
13. ● TICAGRELOR was associated with higher rates of fatal ICH
& major bleeding unrelated to CABG.
● Thus, patients with high ischemic risk , PRASUGREL or
TICAGRELOR is preferred over CLOPIDOGREL .
● But, their use should be discouraged in patients with high
bleeding risk .
14. 2. HIGH BLEEDING RISK :
▪ Patients whose bleeding risks out – weighs the potential
rewards of an aggressive anti-thrombotic strategy .
▪ They require a conservative approach to anti-thrombotic
therapy .
▪ Prasugrel should be avoided .
▪ Aspirin should be given in low doses .
▪ Loading dose of Clopidogrel should be 300mg .
▪ Bivalirudin ( synthetic short acting direct anti-thrombin
agent that binds specifically to thrombin ) is becoming an
alternative to UFH in ACS undergoing PCI .
15. ● Fondaparinux ( synthetic pure factor Xa inhibitor that
selectively binds to anti-thrombin causing rapid inhibition
of Xa ) has lower bleeding complications like Bivalirudin .
It has become an alternative to Heparin in ACS .
● It should always be used with Heparin as it may lead to
catheter thrombosis during PCI.
16. THERAPEUTIC STRATEGIES IN PCI THAT MAY INCREASE ANTI-
THROMBOTIC EFFICACY IN PATIENTS AT HIGH RISK OF
ISCHEMIC EVENTS :
● Use high-dose aspirin (e.g., 325 mg daily) for the
longest recommended duration after PCI (1 month for
BMS, 3 months for DES)
● Use higher-dose maintenance aspirin (e.g., 150 mg
daily) after PCI
● Use higher loading doses of clopidogrel (e.g., 600 mg;
consider 900 mg) during PCI
● Extend duration of post-PCI maintenance clopidogrel
therapy to at least 15 months after stenting.
17. ● Do not use fondaparinux as the sole anticoagulant during PCI.
● If LMWH is used, given higher periprocedural bolus dose (e.g.
enoxaparin 0.75 mg/kg).
● Therapeutic Strategies That May Reduce Hemorrhagic
Complications Of PCI In Patients At Higher Risk Of Bleeding
Events.
● Consider low-dose aspirin (e.g., 75mg daily) during the immediate
post-PCI period .
18. ● Use a lower leading dose of clopidogrel (300 mg
instead of 600 mg) during PCI
● Shorten the duration of post-PCI therapy to the
minimum recommended length (2 weeks for
angioplasty, 4 weeks for BMS, 12 months for DES);
discontinue at any time if bleeding events occur.
● Avoid prasugrel; if used, however, use lower
maintenance dose (5 mg daily)
19. ● If LMWH is used, give lower periprocedural bolus dose
(e.g. enoxaparin 0.5 mg/kg); if pre-PCI LMWH was
previously administered, give periprocedural
intravenous bolus dose (e.g., enoxaparin 0.3 mg/kg)
only if 8-12 hours have elapsed since the last
subcutaneous dose; avoid crossover from pre-PCI
heparin to procedural LMWH, and vice-versa.
20. ANTI-THROMBOTIC THERAPY IN PATIENTS UNDERGOING
NON-CARDIAC SURGERY POST ANGIOPLASTY AND STENTING :
● Cessation of antiplatelet therapy in the peri-operative
period can lead to rebound thrombotic phenomenon
which can result in stent thrombosis that can be fatal.
● At the same time continuing anti platelet therapy in
the peri-operative period may pose a threat of
increased risk of bleeding.
● American College of Cardiology recommends that you
delay any NCS for at least 12 months in case of DES
and 1 month in case of a bare metal stent .
21. ● Surgery with low bleeding risk e.g. cataract surgery,
oral dental surgery : Interruption of oral anti platelet
therapy is not necessary, irrespective of the ischemic
risk profile. Continue both aspirin and clopidogrel .
● Surgery with Intermediate bleeding risk e.g. GI
surgeries, cholecystectomy, appendicectomy etc :
Continue aspirin during peri-operative period. Stop
clopidogrel 5 days prior to surgery with
reintroduction as soon as possible.
22. ● Surgeries with high bleeding risk e.g. intracranial
surgeries, prostate surgery, aortic surgery, ENT
surgeries, and surgery in posterior segment of
eye: Stop Aspirin and Clopidogrel 5 days before
planned surgery,and substitute with alternative
antithrombotic therapies which may include low-
weight heparin (s.c. dose of 85– 100 iu per kg for 12
h). Regular treatment should be resumed as soon
as possible after surgery.
23. ANTI-THROMBOTIC THERAPY IN PATIENTS WITH POOR
DRUG COMPLIANCE :
WARFARIN :
● Cumbersome to use
● Multiple interactions to food and drugs.
● Regular INR monitoring required .
● Deviation from narrow therapeutic level can lead
to a fatal thrombotic episode or a bleeding
incident.
25. ● Lesser interactions with food and drugs .
● Various studies ( RELY , ROCKET-AF ,
ARISTOTLE ) have shown that these drugs have
an edge over Warfarin in terms of reduced
thrombotic events and bleeding events .
● When regular INR monitoring is a problem then
any of these 3 new oral anti-coagulants can be
used.
26. ANTI-COAGULANT THERAPY IN THE PRESENCE OF ANTI-
PLATELET THERAPY :
● Patients who undergo PTCA with a DES require a
long term dual antiplatelet drugs. If these patients
develop either an atrial fibrillation or left atrial
thrombus then they require an additional
Warfarin therapy .
27. ● When the triple therapy is needed : Dose of ASPRIN
should be kept as low as possible (i.e.75 mg). Clopidogrel
should be given at its standard dose of 75 mg/day.
Warfarin be administered under tight control to achieve a
slightly lower target INR of 1.5 to 2.0.
● PPIs should be administered prophylactically .
28. ● In patients who require long-term oral
anticoagulation: BMS prosthesis should be
considered for which dual antiplatelet treatment
is recommended for a shorter time .
● Newer anticoagulants ( Dabigatran, Rivaroxaban,
and Apixaban) have better predictable
pharmacodynamics and pharmacokinetics.
29. ANTI-COAGULANT THERAPY IN THE PRESENCE OF
RENAL DYSFUNCTION :
● Patients with renal failure have an increased risk of both
thrombotic and bleeding complications.
● A number of antithrombotic drugs undergo renal
clearance.
● In patients with severe renal insufficiency (creatinine
clearance [CrCl] < 30 mL/min) who require therapeutic
anticoagulation, the use of unfractionated heparin
(UFH) instead of LMWH is suggested.
● If LMWH is used, a 50% reduction of the total dose is
suggested.
30. ● Both tirofiban (PRISM-PLUS trial) and eptifibatide
(ESPRIT trial) have shown increased bleeding rates
in moderate to severe renal dysfunction.
● Although the manufacturer recommends reducing
both the bolus and infusion doses of tirofiban by
50% in CrCl < 30mL/min, the proper dose of
tirofiban and eptifibatide in such patients is
uncertain.
32. ANTI-COAGULANT THERAPY IN PREGNANCY WITH
PROSTHETIC HEART VALVE :
● The anticoagulant approach for a pregnant woman
with mechanical valve needs to be individualized.
● Women with mechanical valves who become pregnant
- it is suggested to use either adjusted dose LMWH or
UFH throughout pregnancy, or adjusted-dose LMWH
or UFH (doses adjusted to keep APTT at least twice
control) until the thirteenth week with substitution by
VKAs until LMWH or UFH are resumed close to
delivery.
33. ● The use of warfarin throughout pregnancy until the 36
weeks has also been recommended when warfarin
dose is below 5 mg per day during the first trimester.
34. ● For a woman with older generation or tilting disc
mitral prosthesis ( which has a higher chance of
thrombosis) the safer approach : Warfarin for the first
34 weeks of pregnancy particularly if her dose is less than
5 mg/day.
● For a woman at lesser risk (aortic prosthesis or
bileaflet valves) : Heparin therapy may be selected as
soon as pregnancy is diagnosed, Warfarin substituted at
13 to 14 weeks and Heparin restarted at approximately 34
weeks in anticipation of delivery
35. ● For women with antiphospholipid antibodies and
recurrent (three or more) pregnancy loss or late
pregnancy loss and no history of venous or arterial
thrombosis - recommended actions include,
antepartum administration of prophylactic or
intermediate-dose UFH or prophylactic LMWH
combined with aspirin.
36. ● Lactating woman on antithrombotics - For lactating
women using warfarin or UFH, it is recommended to
continue these medications.
37. (CVA) in a patient on antithrombotics :
Initial response - It is recommended that both Warfarin
and heparin be stopped immediately when CVA occurs
(heparin shown to have a 15-25% chance of converting a
non hemorrhagic into a hemorrhagic stroke).
CT scan reveals no hemorrhage - Heparin should be
administered to maintain an aPTT at the lower end of
therapeutic level until Warfarin started.
38. CT scan reveals hemorrhage – antithrombotic
therapy should be withheld until the bleed is
stabilized (7 to 14 days)
39. ANTI-COAGULANT THERAPY IN PATIENTS WITH HIGH
INR LEVELS :
● For patients with INRs of > 9.0 and no significant
bleeding recommended actions include, holding
warfarin therapy and administering a higher dose
of vitamin K (2.5 to 5 mg) orally.
● Serious bleeding and elevated INR - regardless of
the magnitude of the elevation,hold warfarin
therapy and giving vitamin K (10 mg) by slow IV
infusion supplemented with fresh frozen plasma
40. ● For patients with INRs > 5.0 but < 9.0 and no
significant bleeding - omitting the next one or two
doses, and monitoring.
41. ● If bleeding occurs when INR is normal then occult
malignant disease should be ruled out.
● If INR varying then ensure : Lab value is real ,
drug compliance is adequate, drug and food
interactions .
● If still INR varying : Newer anti-coagulants should
be started .
42. ANTI-COAGULANT THERAPY IN PATIENTS WITH
EMBOLIC STROKE WHILE ON ANTI-COAGULANT :
● The anti-coagulant intensity should be increased
to a maximum target INR of 3-3.5 instead of
adding anti-platelet agents .
● Newer anti-coagulants ( Dabigatran, Rivaroxaban ,
Apixaban ) should be considered .
43. RISK OF DVT IN HOSPITALISED PATIENTS
PATIENT GROUPS DVT PREVALENCE %
MEDICAL 10-20
SURGICAL 15-40
GYNAECOLOGIC SURG 15-40
HIP OR KNEE
ARTHROPLASTY/HIP
FRACTURE SURG
40-60
MAJOR TRAUMA 40-60
SPINAL CORD INJURY 60-80
CRITICAL CARE 10-80
44.
45. ● Balancing both ends of the spectrum with the proper
antithrombotic strategy is essential.
● An individualized approach to therapy is essential.