Atrial fibrillation (AF) is a common heart rhythm disorder that increases the risk of stroke, heart failure, and other cardiovascular issues. The document summarizes guidelines for managing AF, including establishing rate control with medications, assessing stroke risk using the CHA2DS2-VASc score to determine anticoagulation needs, and considering rhythm control options like ablation for symptomatic patients. An integrated care approach is recommended, involving specialists, primary care, and informed patients, to consistently manage AF and improve outcomes through treatment of underlying conditions, anticoagulation, and controlling heart rate and rhythm issues.
Atrial Fibrillation is the most common arrhythmia encountered by a physician. The global prevalence is increasing because of aging population and better detection methods. Prediction of new onset AF is possible. AF is also a lifestyle disease. Lifestyle therapy, rate or rhythm control and stroke risk stratification are are four main pillars of AF management.
During atrial fibrillation, the heart's upper chambers — called the atria — beat chaotically and irregularly. They beat out of sync with the lower heart chambers, called the ventricles. For many people, AFib may have no symptoms. But AFib may cause a fast, pounding heartbeat, shortness of breath or light-headedness.
Atrial Fibrillation is the most common arrhythmia encountered by a physician. The global prevalence is increasing because of aging population and better detection methods. Prediction of new onset AF is possible. AF is also a lifestyle disease. Lifestyle therapy, rate or rhythm control and stroke risk stratification are are four main pillars of AF management.
During atrial fibrillation, the heart's upper chambers — called the atria — beat chaotically and irregularly. They beat out of sync with the lower heart chambers, called the ventricles. For many people, AFib may have no symptoms. But AFib may cause a fast, pounding heartbeat, shortness of breath or light-headedness.
CONCLUSIONS:
- Cardiologist, obstetrician and anestesiologist should cooperate to each other
- The advantage of regional anesthesia is patients can communicate if symptoms occur
- If palpitations, chest pain and shortness of breath happened, immediate action should be performed
- RA should be given using lower dose of local anesthetics opioids and slow induction
- GA : standard technique “rapid sequence induction”
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.
CONCLUSIONS:
- Cardiologist, obstetrician and anestesiologist should cooperate to each other
- The advantage of regional anesthesia is patients can communicate if symptoms occur
- If palpitations, chest pain and shortness of breath happened, immediate action should be performed
- RA should be given using lower dose of local anesthetics opioids and slow induction
- GA : standard technique “rapid sequence induction”
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.
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Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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
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.
- 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
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
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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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.
2. • Treat underlying cardiovascular conditions adequately to prevent AF, such as
hypertension, ischaemia, valvular heart disease and heart failure.
• Evaluate AF-related symptoms using the modified European Heart Rhythm Association
(EHRA) score.
• Providing tailored information and education to AF patients can empower them to
support the management of their condition.
• Shared decision-making can ensure that care is based on the best available evidence
and fits the needs, values, and preferences of the patient.
• One in four strokes are estimated to be caused by AF.
• Use oral anticoagulation in all AF patients unless they are at low risk for stroke based
on the CHA2DS2-VASc score, or have absolute contraindications for anticoagulant
therapy.
• When initiating anticoagulation, a non-vitamin K oral antagonist (NOAC) is
preferred, except in patients with moderate-to-severe mitral stenosis, mechanical
heart valves or severe kidney disease.
• Anticoagulated patients with atrial flutter similar to atrial fibrillation.
• Do not use aspirin or other antiplatelets for stroke prevention in AF.
• Reduce modifiable bleeding risk factors in all AF patients on oral anticoagulation,
but do not restrict access to anticoagulation based on bleeding risks.
• A full cardiovascular evaluation, including an accurate history, careful clinical
examination, and assessment of concomitant conditions is recommended in all AF
patients, and transthoracic echocardiography can help to guide management.
• Weight loss for obese patients, reducing alcohol consumption and more regular
(moderate) exercise are useful lifestyle modifications.
Prevention & general management
Patient involvement
Stroke prevention
Diagnosis & screening
Atrial fibrillation (AF) is the most common heart rhythm disorder, with a steep
rise predicted in the number of patients in coming years. AF is one of the major causes
of stroke, heart failure, sudden death, and cardiovascular morbidity, and is associated
with poorer quality of life and adverse symptoms. The management of AF should include
treatment of acute AF, cardiovascular risk reduction and treatment of comorbidities,
stroke prevention using oral anticoagulation, heart rate control, and in selected
symptomatic patients, the use of rhythm control therapy.
• The diagnosis of AF requires an electrocardiogram (ECG) showing irregular RR
intervals and no distinct P waves for at least 30 seconds.
• ECG screening is useful in populations at risk of AF or those at high risk of stroke,
including stroke survivors and older patients.
• The pattern of AF can be categorised as:
First diagnosed
Paroxysmal (self-terminating)
Persistent (lasting longer than 7 days)
Long-standing persistent (continuous for 1 year)
Permanent (AF accepted by patient and physician, hence rhythm control is not
pursued)
Acute rate
and rhythm
control
Manage
precipitating
factors
Assess stroke
risk
Assess heart
rate
Assess
symptoms
Haemodynamic
stability
Cardiovascular risk
reduction
Improved
life
expectancy
Improved
quality of life,
autonomy,
social
functioning
Lifestyle changes, treatment
of underlying cardiovascular
conditions
Oral anticoagulation in
patients at risk for stroke
Rate control therapy
Antiarrhythmic drugs,
cardioversion, catheter
ablation, AF surgery
Stroke prevention
Symptom improvement,
preservation of
LV function
Symptom
improvement
Treatment Chronic management Desired outcome Patient benefit
AF = atrial fibrillation; LV = left ventricular.
No
Yes
Mechanical heart valves or moderate or severe mitral stenosis
Estimate stroke risk
CHA2DS2-VASc 0
or women without
other risk factors
CHA2DS2-VASc 1 CHA2DS2-VASc ≥2
Other options* NOAC VKA
No antiplatelet
or anticoagulant
treatment
Oral anticoagulation
should be
considered
Oral anticoagulation
indicated
Assess for
contra-indications
Correct reversible
bleeding risk factors
NOAC = Non-vitamin K oral anticoagulant (apixaban, dabigatran, edoxaban, rivaroxaban).
VKA =Vitamin K oral anticoagulant (e.g. warfarin, with INR 2.0–3.0 and time in therapeutic range kept as high as
possible and closely monitored).
* No anticoagulation, or left atrial appendage exclusion if clear contra-indications for anticoagulation.
The five domains of integrated AF management
Stroke prevention in atrial fibrillation
Modified
EHRA score
Symptoms Description
1 None AF does not cause any symptoms
2a Mild
Normal daily activity not affected by symptoms
related toAFa
2b Moderate
Normal daily activity not affected by symptoms
related toAF,but patient troubled by symptomsa
3 Severe
Normal daily activity affected by symptoms
related toAF
4 Disabling Normal daily activity discontinued
AF = atrial fibrillation; EHRA = European Heart Rhythm Association.
a
EHRA Class 2a and 2b can be differentiated by evaluating whether patients are functionally affected by
their AF symptoms. AF-related symptoms are most commonly fatigue/tiredness and exertional shortness
of breath, or less frequently palpitations and chest pain.
CHA2DS2-VASc risk factor Points
Congestive heart failure
Signs/symptoms of heart failure or objective evidence
of reduced left-ventricular ejection fraction
+1
Hypertension
Resting blood pressure >140/90 mmHg on at least
two occasions or current antihypertensive treatment
+1
Age 75 years or older +2
Diabetes mellitus
Fasting glucose >125 mg/dL (7 mmol/L) or treatment
with oral hypoglycaemic agent and/or insulin
+1
Previous stroke, transient ischaemic attack, or
thromboembolism
+2
Vascular disease
Previous myocardial infarction,peripheral artery
disease,or aortic plaque
+1
Age 65–74 years +1
Sex category (female) +1
Modifiable bleeding risk
factors
Hypertension (especially
when systolic blood pressure
is >160 mmHg)
Labile INR or time in therapeutic
range <60% in patients on vitamin K
antagonists
Medication predisposing to bleeding,
such as antiplatelet drugs and non-
steroidal anti-inflammatory drugs
Excess alcohol (≥8 drinks/week)
Potentially modifiable
bleeding risk factors
Anaemia
Impaired renal function
Impaired liver function
Reduced platelet count or function
From the ESC Guidelines for the Management of Atrial Fibrillation published in the European Heart Journal (2016) 37:
2893–2962 - doi:10.1093/eurheartj/ehw210.
Corresponding authors:
Paulus Kirchhof,
Institute of Cardiovascular Sciences, University of Birmingham, SWBH and UHB NHS trusts, IBR, Room 136,
Wolfson Drive, Birmingham B15 2TT, United Kingdom,
Tel: +44 121 4147042, E-mail: p.kirchhof@bham.ac.uk and
Stefano Benussi,
Department of Cardiovascular Surgery, University Hospital Zurich, Rämistrasse 100, 8091 Zürich, Switzerland,
Tel: +41(0)788933835, E-mail: stefano.benussi@usz.ch.
Special thanks to Dipak Kotecha for his contribution.
