This document provides guidelines for holding and restarting various anticoagulant and antiplatelet medications before, during, and after procedures involving neuraxial catheters. It lists medications such as heparin, warfarin, low molecular weight heparins, direct thrombin inhibitors, and others along with recommended hold times and when to restart each medication. It also includes each medication's mechanism of action and half-life.
Anticoagulants, antiplatelet drugs and anesthesiaRajesh Munigial
It is a presentation on anticoagulants and antiplatelets in anesthesia , starting from basis of coagulation , its tests and dugs and anesthetic implications
Based on latest ASRA (AMERICAN SOCIETY OF REGIONAL ANESTHESIA GUIDELINES)
Anticoagulants, antiplatelet drugs and anesthesiaRajesh Munigial
It is a presentation on anticoagulants and antiplatelets in anesthesia , starting from basis of coagulation , its tests and dugs and anesthetic implications
Based on latest ASRA (AMERICAN SOCIETY OF REGIONAL ANESTHESIA GUIDELINES)
Anticoagulation and Regional AnesthesiaRajnish Gupta
Discussing the ASRA Guidelines for Anticoagulation and Antithrombotics during Regional Anesthesia including the considerations for neuraxial anesthesia and deep blocks. We also discuss the use of the ASRA Coags app. Question and Answer included.
Direct oral anticoagulants (DOACs) have quickly become attractive alternatives to the long‐standing standard of care in anticoagulation, vitamin K antagonist. DOACs are indicated for prevention and treatment of several cardiovascular conditions. Since the first approval in 2010, DOACs have emerged as leading therapeutic alternatives that provide both clinicians and patients with more effective, safe, and convenient treatment options in thromboembolic settings. With the expanding role of DOACs, clinicians are faced with increasingly complex decisions relating to appropriate agent, duration of treatment, and use in special populations. This review will provide an overview of DOACs and act as a practical reference for clinicians to optimize DOAC use among common challenging scenarios. Topics addressed include (1) appropriate indications; (2) use in patients with specific comorbidities; (3) monitoring parameters; (4) transitioning between anticoagulant regimens; (5) major drug interactions; and (6) cost considerations.
Direct oral anticoagulants (DOACs)—dabigatran (Pradaxa), rivaroxaban (Xarelto), apixaban (Eliquis), edoxaban (Savaysa), and betrixaban (Bevyxxa) are anticoagulation pharmacotherapy used for the prevention of thrombosis in several cardiovascular contexts.1 DOACs are categorized into 2 main classes: oral direct factor Xa inhibitors (ie, rivaroxaban, apixaban, edoxaban, and betrixaban) and direct thrombin inhibitors (ie, dabigatran). In 2010, the US Food and Drug Administration (FDA) approved its first DOAC, dabigatran, followed by rivaroxaban, apixaban, edoxaban, and betrixaban in the following years. DOACs are relatively new agents demonstrating superiority or noninferiority to prior standards of care, anticoagulation with vitamin K antagonists (VKA; ie, warfarin), or low‐molecular‐weight heparins (LMWHs), in reducing risk of thromboembolic complications with similar or reduced bleeding risk.2, 3, 4, 5 Advantages of DOACs compared with VKAs include fewer monitoring requirements, less frequent follow‐up, more immediate drug onset and offset effects (important for periprocedural and acute bleeding management), and fewer drug and food interactions.6 As a result, DOAC prescriptions exceeded those for warfarin by 2013, with apixaban being the most frequently prescribed DOAC for patients with nonvalvular atrial fibrillation (NVAF).7
Over the past decade, DOACs have been the subject of extensive investigation in many clinical scenarios. Though guidelines and review articles have provided detailed and in‐depth analyses of the immense literature base, these can be too cumbersome and challenging to integrate into everyday clinical use
In general, FDA‐approved indications for each of the DOACs are comparable (see Table 1). Dabigatran, rivaroxaban, apixaban, and edoxaban are approved for the lowering the risk of stroke and embolism in NVAF as well as deep vein thrombosis and pulmonary embolism treatment/prophylaxis.8, 9, 10, 11 Unique indications
Learning Objectives:
After completing the topic, the student will be able to:
• Recognize the importance of hemostasis and thrombosis in health and disease.
• Describe the process that leads to platelet aggregation.
• Classify anti-platelets drugs and the mechanism by which they inhibit platelet
aggregation.
• Describe indications, contraindications, drug interactions & adverse effects of anti-
platelets drugs.
• Describe treatment recommendations for antiplatelet agents
Acetylsalicylic Acid (Aspirin)
• Irreversibly inhibits COX1 and, in higher doses, COX2.
• COX1 inhibition (main antithrombotic mechanism); the formation of prostaglandin H2 is blocked, thus
thromboxane A2 cannot be synthesized (TxA2 stimulates platelets aggregation).
Drug interactions
• Co-administration of non-selective COX1 inhibitors may impair its efficacy.
• About one-third of patients receiving aspirin manifest treatment failure (Thrombotic Complication or
Death).
Adverse Events
• Resulting from rebound thrombocyte activation after aspirin withdrawal.
• Single binding site and does not influence other thrombocyte receptors results in aspirin having less
antithrombotic effect than many other agents
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
- 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
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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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.
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.
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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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.
2. MEDICATIO
N
HOLD
MEDICATIO
N
(before
procedure)
RESTART
MEDICATIO
N
(after
procedure)
HOLD
MEDICATION
(before
catheter
removal)
RESTART
MEDICATIO
N
(after
catheter
removal)
MECHANISM HALF LIFE
HEPARIN
IV Heparin Wait until PTT
<40 Usual
hold time: 4-6
hours
1 hour 4-6 hours after
last heparin
dose and
confirm PTT <
40
1 hours
Indirect thrombin inhibitor
by inhibiting factors II a and
Xa
Heparin also increases the
release of tissue factor
pathway inhibitor(TFPI)
Monitored by testing aPTT
1-2 hours
SC Heparin
5000 units
or TID
4-6 hours or
check PTT
No delay 4-6 hours prior
to catheter
removal
No delay
SC Heparin
7500-10,000
units BID (or
20,000 units
per day)
12 hours and
PTT < 40
Avoid while
catheter is in
place
Avoid while
catheter is in
place
Perform
checks 12
hours after
catheter
removal
SC Heparin
>20,000 per
day
24 hours and
check PTT<
Assess
individual
case; monitor
Assess
individual case;
monitor neuro
Assess
individual
case; monitor
4. (before
procedure)
(after
procedure)
catheter
removal)
(after
catheter
removal)
LMWH
Therapeutic
Dosing:
EXONAPARIN
(LOVENOX):
1mg/kg SC
BID or
1.5mg/kg QD
Dalteparin:
120units/kg
BID or 200
units/kg QD
Tinzaparin:
175 units/kg
Q
24 hours;
consider
checking anti-
factor XA
activity level
elderly/renal
insufficiency
24-72 hours
(24 hours
after nonhigh
risk bleeding
surgery; 48-
hours after
high risk
surgery)
Catheter
should be
removed
before
initiation
LMWH
4 hours prior
to the first
postoperative
dose and at
least 24 hours
after neuraxial
procedure
Indirect factor X-a inhibitor
by causing conformational
change in AT-III
4-7 hours
Prophylactic
Dosing:
ENOXAPARIN
(LOVENOX):
30mg SQ BID,
40 mg SQ Q
At least 12
hours
12 hours Avoid 4 hours, no
earlier than 12
after neuraxial
procedure
5. MEDICATIO
N
HOLD
MEDICATIO
N
(before
procedure)
RESTART
MEDICATIO
N
(after
procedure)
HOLD
MEDICATION
(before
catheter
removal)
RESTART
MEDICATIO
N
(after
catheter
removal)
MECHANIS
M
HALF LIFE
Factor X-a Inhibitors
FONDAPARINU
X (ARIXTRA®)
ASRA Regional-
no
recommendatio
Pain- 4 day (5
half lives)
Avoid while
Catheter is in
place
Avoid while
Catheter is in
place
6 hours Indirect factor
X-a inhibitor by
causing
conformational
change in AT-III
17-21 hours
RIVAROXABAN
(XARELTO®)
72 hours At least 6 hours;
Avoid while
Catheter is in
plac
22-26 hours 6 hours If
bloody tap,
discuss risks and
benefits with
proceduralist
Direct Factor X-a
Inhibitors
5-9 hours
APIXABAN
(ELIQUIS®)
72 hours At least 6 hours;
Avoid while
Catheter is in
place
26-30 hours 6 hours If
bloody tap,
discuss risks and
benefits with
proceduralist
Direct Factor X-a
Inhibitors
6-12 hours
EDOXABAN
(SAVAYSA®)
72 hours At least 6 hours;
Avoid while
Catheter is in
20-28 hours 6 hours If
bloody tap,
discuss risks and
Direct Factor X-a
Inhibitors
10-14 hours
7. MEDICATION HOLD
MEDICATION
(before
procedure)
RESTART
MEDICATION
(after
procedure)
HOLD
MEDICATION
(before
catheter
removal)
RESTART
MEDICATION
(after catheter
removal)
MECHANISM HALF LIFE
Anti-Platelet Agents*
ASPIRIN No restrictions No restrictions No restrictions No restrictions inhibits COX enzyme irreversibly
TXA2 synthesis inhibiton leading to
anti-aggregatory effects
CLOPIDOGREL
(PLAVIX®)
5-7 days Immediately if
NO loading
does; 6 hours
1-2 days
24 hours postop
0 post neuraxial
procedure
0 hours
6 hours if
loading dose
Irreversible antagonists of P2Y12
receptor of ADP thus preventing
activation of platelets
~6 hours
(metabo lites
longer)
CILOSTAZOLE
(PLETAL®)
48 hours 6 hours
Avoid while
Catheter is in
place
Avoid 6 hours Phosphodiesterse 3 inhibitor
leading to inc. cAMP levels and
dec platelet aggregation +
peripheral vasodilation
11-13 hours
DIPYRIDAMOLE
/A SA
(AGGRENOX®)
24 hours 6 hours; Avoid
while Catheter
in place
Avoid while
catheter is in
place
6 hours Inhibits phosphodiesterase (PDE)
which potentiates prostacyclins and
thus anti- aggregation
10-12 hours
(dipyrid amole
compon ent
8. MEDICATION HOLD
MEDICATION
(before
procedure)
RESTART
MEDICATION
(after
procedure)
HOLD
MEDICATION
(before
catheter
removal)
RESTART
MEDICATION
(after catheter
removal)
MECHANISM HALF LIFE
Anti-Platelet Agents*
PRASUGREL
(EFFIENT®)
7-10 days Immediately if
no loading
dose; Avoid
while Catheter
in place. See
app TPO- 6
hours
Avoid 24 hours
postop;
Immediately
post neuraxial
procedure;
6 hours if
loading dose
TPO- 6 hours
Irreversible antagonists of P2Y12
receptor of ADP thus preventing
activation of platelets
2-15 hours
TICAGRELOR
(BRILINTA®)
5-7 days Immediately if
no loading
dose; Avoid
while Catheter
in place. See
app TPO- 6
hours
Avoid 24 hours
postop;
Immediately
post neuraxial
procedure;
6 hours if
loading dose
See app TPO- 6
hours
Oral Reversible antagonists of
P2Y12 receptor of ADP thus
preventing activation of platelets
~7 hours
hours for
metabolit e)
TICLODIPINE
(TICLID®)
10 days Avoid while
Catheter is in
place
6 hours 24 hours
postop;
Immediately
Irreversible antagonists of P2Y12
receptor of ADP thus preventing
activation of platelets
~13 hours
9. MEDICATION HOLD
MEDICATION
(before
procedure)
RESTART
MEDICATION
(after
procedure)
HOLD
MEDICATION
(before
catheter
removal)
RESTART
MEDICATION
(after catheter
removal)
MECHANISM HALF LIFE
Fibrinolytics
STREPTOKINAS
E
10 days
48 hours +
normal clotting
studies including
fibrinogen
Avoid while
Catheter is in
place
Avoid while
Catheter is in
Place;
If unanticipated
event neurologic
checks Q2 hrs,
Check
Fibrinogen Level
Indirectly forms a complex with
plasminogen which acts as tPA
and activates other
plasminogen molecules to
plasmin
18-83
minutes
ALTEPLASE 10 days
48 hours +
normal clotting
studies including
fibrinogen
Avoid while Catheter is in place If
unanticipated event- neurologic
checks Q2 hrs, change infusion to
able to monitor
Check
Fibrinogen Level
They are recombinant tPA.
Directly Activates plasminogen
to form plasmin and thus help
lysis of thrombus
26-46 hours
TENECTEPLA
SE
10 days
48 hours +
normal clotting
studies including
fibrinogen
Avoid while Catheter is in place If
unanticipated event- neurologic
checks Q2 hrs, change infusion to
able to monitor
Check
Fibrinogen Level
115 minutes
RETEPLASE 10 days
48 hours +
normal clotting
studies including
fibrinogen
Avoid while Catheter is in place If
unanticipated event- neurologic
checks Q2 hrs, change infusion to
able to monitor
Check
Fibrinogen Level
13-16
minutes
