The 11-step method provides a systematic approach to reading EKGs:
1. Gather data such as heart rate, intervals, and axis.
2. Diagnose rhythm, conduction blocks, enlargement, and infarction by applying specific criteria.
3. Potential diagnoses are identified through disturbances of rhythm, conduction, hypertrophy, and ischemia. The four questions framework is used to characterize rhythms.
Talk given on 29 Sep 2015 at the Royal College of Emergency Medicine annual meeting.
Key areas:
What are the issues with sepsis in children?
How will it apply to the UK Sepsis CQUIN?
The Paediatric Sepsis 6 and screening for sepsis in children.
Additional notes following main talk.
This slide contains neonatal jaundice by including real case senario and nursing management through by passing definition, pathophysiology and diagnosis modality
Talk given on 29 Sep 2015 at the Royal College of Emergency Medicine annual meeting.
Key areas:
What are the issues with sepsis in children?
How will it apply to the UK Sepsis CQUIN?
The Paediatric Sepsis 6 and screening for sepsis in children.
Additional notes following main talk.
This slide contains neonatal jaundice by including real case senario and nursing management through by passing definition, pathophysiology and diagnosis modality
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
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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.
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
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
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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
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.
1. The 11-Step Method for Reading EKGs
Data Gathering
1. Standardization. Make sure the standardization mark on the EKG paper is 10 mm high so that 10 mm = 1 mV. Also make sure that
the paper speed is correct.
2. Heart rate. Determine the heart rate by the quick three-step method = [ 3 : large squares]
3. Intervals. Measure the length of the PR and QT intervals and the width of the QRS complexes.
4. QRS axis. Is the axis normal, or is there axis deviation?
Diagnoses
5. Rhythm. Always ask The Four Questions:
o Are there normal P waves present?
o Are the QRS complexes wide or narrow?
o What is the relationship between the P waves and QRS complexes?
o Is the rhythm regular or irregular?
6. AV block. Apply the criteria
7. Bundle branch block or hemiblock. Apply the criteria
8. Preexcitation. Apply the criteria
(Note that steps 6 through 8 all involve looking for disturbances of conduction.
9. Enlargement and hypertrophy. Apply the criteria for both atrial enlargement and ventricular hypertrophy.
10. Coronary artery disease. Look for Q waves and ST segment and T wave changes. Remember that not all such changes
reflect coronary artery disease; know your differential diagnoses.
11. Utter confusion. Is there anything on the EKG you don't understand? Never hesitate to ask for assistance.
information only becomes knowledge with wisdom and experience
2. Calculating the Axis
Lead ILead AVF
Normal axis + +
Left axis deviation + –
Right axis deviation – +
Extreme right axis deviation – –
Atrial Enlargement
Look at the P wave in leads II and V1.
Right atrial enlargement is characterized by the following:
Increased amplitude of the first portion of the P wave
No change in the duration of the P wave
Possible right axis deviation of the P wave.
Left atrial enlargement is characterized by the following:
Occasionally, increased amplitude of the terminal component of theP wave
More consistently, increased P wave duration
No significant axis deviation.
3. Ventricular Hypertrophy
Look at the QRS complexes in all leads.
Right ventricular hypertrophy is characterized by the following:
Right axis deviation of greater than 100°
Ratio of R wave amplitude to S wave amplitude greater than 1 in V1 and less than 1 in V6.
Left ventricular hypertrophy is characterized by many criteria. The more that are present, the greater the likelihood that left
ventricular hypertrophy is present.
Precordial criteria include the following:
The R wave amplitude in V5 or V6 plus the S wave amplitude in V1 orV2 exceeds 35 mm.
The R wave amplitude in V5 exceeds 26 mm.
The R wave amplitude in V6 exceeds 18 mm.
The R wave amplitude in V6 exceeds the R wave amplitude in V5.
Limb lead criteria include the following:
The R wave amplitude in AVL exceeds 13 mm.
The R wave amplitude in AVF exceeds 21 mm.
The R wave amplitude in I exceeds 14 mm.
The R wave amplitude in I plus the S wave amplitude in III exceeds 25 mm.
The presence of repolarization abnormalities (asymmetric ST segment depression and T wave
inversion) indicates clinically significant hypertrophy, is most often seen in those leads with tall R
waves, and may herald ventricular dilatation and failure.
4. The four basic types of arrhythmias are:
Arrhythmias of sinus origin
Ectopic rhythms
Conduction blocks
Preexcitation syndromes.
Whenever you are interpreting the heart's rhythm, ask The Four Questions:
Are normal P waves present?
Are the QRS complexes narrow (less than 0.12 seconds in duration) or wide (greater than 0.12 seconds)?
What is the relationship between the P waves and the QRS complexes?
Is the rhythm regular or irregular?
The answers for normal sinus rhythm are:
Yes, P waves are present.
The QRS complexes are narrow.
There is one P wave for every QRS complex.
The rhythm is regular.
6. Characteristics EKG
PSVT Regular
P waves are retrograde if visible
Rate: 150–250 bpm
Carotid massage: slows or terminates
Flutter Regular, saw-toothed
2:1, 3:1, 4:1, etc., block
Atrial rate: 250–350 bpm
Ventricular rate: one half, one third, one fourth,
etc., of the atrial rate
Carotid massage: increases block
FibrillationIrregular
Undulating baseline
Atrial rate: 350–500 bpm
Ventricular rate: variable
Carotid massage: may slow ventricular rate
MAT Irregular
At least three different P wave morphologies
Rate: 100–200 bpm; sometimes less than 100
bpm
Carotid massage: no effect
PAT Regular
Rate: 100–200 bpm
Characteristic warm-up period in the automatic
form
Carotid massage: no effect, or only mild slowing
7. Ventricular Arrhythmias
Rules of Aberrancy
VT PSVT
Clinical Clues
Carotid massage No response May terminate
Cannon A waves May be present Not seen
EKG Clues
AV dissociation May be seen Not seen
Regularity Slightly irregular Very regular
Fusion beats May be seen Not seen
Initial QRS deflectionMay differ from normal QRS complexSame as normal QRS complex
8. AV Blocks
AV block is diagnosed by examining the relationship of the P waves to the QRS complexes.
First degree: The PR interval is greater than 0.2 seconds; all beats are conducted through to the
ventricles.
Second degree: Only some beats are conducted through to the ventricles.
o Mobitz type I (Wenckebach): Progressive prolongation of the PR interval until a QRS is dropped
o Mobitz type II: All-or-nothing conduction, in which QRS complexes are dropped without PR interval
prolongation
Third degree: No beats are conducted through to the ventricles. There is complete heart block with AV
dissociation, in which the atria and ventricles are driven by independent pacemakers.
9. Bundle Branch Blocks
Bundle branch block is diagnosed by looking at the width and configuration of the QRS complexes.
Criteria for Right Bundle Branch Block
QRS complex widened to greater than 0.12 seconds
RSR' in leads V1 and V2 (rabbit ears) with ST segment depression and T wave inversion
Reciprocal changes in leads V5, V6, I, and AVL.
Criteria for Left Bundle Branch Block
QRS complex widened to greater than 0.12 seconds
Broad or notched R wave with prolonged upstroke in leads V5, V6, I, and AVL with ST segment depression and T wave
inversion
Reciprocal changes in V1 and V2
Left axis deviation may be present.
10. Hemiblocks
Hemiblock is diagnosed by looking for left or right axis deviation.
Left Anterior Hemiblock
Normal QRS duration and no ST segment or T wave changes
Left axis deviation greater than –30°
No other cause of left axis deviation is present.
Left Posterior Hemiblock
Normal QRS duration and no ST segment or T wave changes
Right axis deviation
No other cause of right axis deviation is present.
Bifascicular Block
The features of right bundle branch block combined with left anterior hemiblock are as follows:
Right Bundle Branch Block
QRS wider than 0.12 seconds
RSR' in V1 and V2.
Left Anterior Hemiblock
Left axis deviation.
The features of right bundle branch block combined with left posterior hemiblock are as follows:
Right Bundle Branch Block
RS wider than 0.12 seconds
RSR' in V1 and V2.
Left Posterior Hemiblock
Right axis deviation.
11. Preexcitation
Criteria for WPW Syndrome
PR interval less than 0.12 seconds
Wide QRS complexes
Delta wave seen in some leads.
Criteria for LGL Syndrome
PR interval less than 0.12 seconds
Normal QRS width
No delta wave.
Arrhythmias commonly seen include the following:
Paroxysmal supraventricular tachycardia—narrow QRS complexes are more common than wide ones.
Atrial fibrillation—can be very rapid and can lead to ventricular fibrillation.
12. Myocardial Infarction
The diagnosis of a myocardial infarction is made by history, physical examination, serial cardiac enzyme determinations, and serial
EKGs. During an acute infarction, the EKG evolves through three stages:
The T wave peaks (A), then inverts (B).
The ST segment elevates (C).
Q waves appear (D).
Criteria for Significant Q Waves
The Q wave must be greater than 0.04 seconds in duration.
The depth of the Q wave must be at least one third the height of the R wave in the same QRS complex.
Criteria for Non–Q Wave Infarctions
T wave inversion.
ST segment depression persisting for more than 48 hours in the appropriate setting.
13. Localizing the Infarct
Inferior infarction: leads II, III, and AVF
Often caused by occlusion of the right coronary artery or its descending branch
Reciprocal changes in anterior and left lateral leads.
Lateral infarction: leads I, AVL, V5, and V6
Often caused by occlusion of the left circumflex artery
Reciprocal changes in inferior leads.
Anterior infarction: any of the precordial leads (V1 through V6)
Often caused by occlusion of the left anterior descending artery
Reciprocal changes in inferior leads.
Posterior infarction: reciprocal changes in lead V1 (ST-segment depression, tall R wave)
Often caused by occlusion of the right coronary artery.
14. The ST Segment
ST segment elevation may be seen:
With an evolving infarction
In Prinzmetal's angina.
ST segment depression may be seen:
With typical exertional angina
In a non–Q wave infarction.
ST depression is also one indicator of a positive stress test.
Miscellaneous EKG Changes
Electrolyte Disturbances
Hyperkalemia: Evolution of peaked T waves, PR prolongation and P wave flattening, and QRS widening. Ultimately,
the QRS complexes and T waves merge to form a sine wave, and ventricular fibrillation may develop.
Hypokalemia: ST depression, T wave flattening, U waves
Hypocalcemia: Prolonged QT interval
Hypercalcemia: Shortened QT interval.
Hypothermia
Osborne waves, prolonged intervals, sinus bradycardia, slow atrial fibrillation; beware of muscle tremor artifact.
15. Drugs
Digitalis: Therapeutic levels associated with ST segment and T wave changes in leads with tall R waves; toxic
levels associated with tachyarrhythmias and conduction blocks; PAT with block is most characteristic .
Sotalol, quinidine, procainamide, amiodarone, tricyclic antidepressants, erythromycin, the quinolones, the phenothiazines,
various antifungal medications, some antihistamines: Prolonged QT interval, U waves.
Other Cardiac Disorders
Pericarditis: Diffuse ST segment and T wave changes. A large effusion can cause low voltage and
electrical alternans.
HOCM: Ventricular hypertrophy, left axis deviation, septal Q waves
Myocarditis: Conduction blocks.
Pulmonary Disorders
COPD: Low voltage, right axis deviation, poor R wave progression. Chronic cor pulmonale can produce P
pulmonale and right ventricular hypertrophy with repolarization abnormalities.
Acute pulmonary embolism: Right ventricular hypertrophy with strain, right bundle branch block, S1Q3 .
Sinus tachycardia and atrial fibrillation are the most common arrhythmias.
CNS Disease
Diffuse T wave inversion, with T waves typically wide and deep; U waves.
The Athlete's Heart
Sinus bradycardia, nonspecific ST segment and T wave changes, left and right ventricular hypertrophy, incomplete right
bundle branch block, first-degree or Wenckebach AV block, occasional supraventricular arrhythmia.