This document discusses the stages and types of shock. It begins by outlining the stages of shock as compensated, uncompensated, and irreversible. It then defines the main types of shock as hypovolemic, distributive, cardiogenic, and obstructive. For each type of shock, the document provides the etiology, clinical presentation, differentiation from other types, and general management approach. It particularly focuses on hypovolemic/hemorrhagic, cardiogenic, and septic shock, outlining their specific therapies which include fluid resuscitation, vasopressors, antibiotics, and other targeted interventions.
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.
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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.
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
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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
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Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
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Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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. Stages of Shock
Compensated
– Vital organ function maintained, BP
remains normal.
Uncompensated
– Microvascular perfusion becomes
marginal. Organ and cellular function
deteriorate. Hypotension develops.
Irreversible
4. Hypovolemic Shock
Most common form of shock world-
wide
Results in decreased circulating blood
volume, decrease in preload, decreased
stroke volume and resultant decrease in
cardiac output.
Etiology: Hemorrhage, renal and/or GI
fluid losses, capillary leak syndromes
5. Hypovolemic Shock
Clinically, history of vomiting/diarrhea
or trauma/blood loss
Signs of dehydration: dry mucous
membranes, absent tears, decreased
skin turgor
Hypotension, tachycardia without signs
of congestive heart failure
6. Hemorrhagic Shock
Most common cause of shock in the
United States (due to trauma)
Patients present with an obvious
history (but in child abuse history may
be misleading)
Site of blood loss obvious or concealed
(liver, spleen, intracranial, GI, long bone
fracture)
Hypotension, tachycardia and pallor
7. Hypovolemic/Hemorrhagic
Shock: Therapy
Always begin with ABCs
Replace circulating blood volume
rapidly: start with crystalloid
Blood products as soon as available for
hemorrhagic shock (Type and Cross
with first blood draw)
Replace ongoing fluid/blood losses &
treat the underlying cause
9. Cardiogenic Shock
Differentiation from other types of
shock:
– History
– Exam:
Enlarged liver
Gallop rhythm
Murmur
Rales
– CXR:
Enlarged heart, pulmonary venous congestion
10. Cardiogenic Shock
Management:
– Improve cardiac output::
Correct dysrhthymias
Optimize preload
Improve contractility
Reduce afterload
– Minimize cardiac work:
Maintain normal temperature
Sedation
Intubation and mechanical ventilation
Correct anemia
11. Inotropic support in cardiogenic shock:
If normotensive: dobutamine (5-20
mic/kg/min), milrinone (0.25-1 mic/kg/min)
or levosimendan(0.05-0.2 mic/kg/min)
If hypotensive: low dose adrenaline (0.05-0.3
mic/kg/min) then add one of the inodilators
mentioned above
DON‘T FORGET: any fluid bolus in cases of
cardiogenic shock should not exceed 5 cc/kg to
avoid overoad.
12. Obstructive Shock
Mechanical obstruction to ventricular
outflow
Etiology: Congenital heart disease,
massive pulmonary embolism, tension
pneumothorax, cardiac tamponade
Inadequate C.O. in the face of adequate
preload and contractility
Treat underlying cause.
13. Distributive Shock
Due to an abnormality in vascular tone
leading to peripheral pooling of blood with a
relative hypovolemia.
Etiology
– Anaphylaxis
– Drug toxicity
– Neurologic injury
– Early sepsis
Management
– Fluid
– Treat underlying cause
14. Dissociative Shock
Inability of Hemoglobin molecule to give up
the oxygen to tissues
Etiology:
• Carbon Monoxide poisoning,
methemoglobinemia, dyshemoglobinemias
Tissue perfusion is adequate, but oxygen
release to tissue is abnormal
Early recognition and treatment of the cause
is main therapy
18. Cold Shock rapidly progresses to mutiorgan
system failure or death if untreated
Multi-Organ System Failure: Coma, ARDS,
CHF, Renal Failure, Ileus or GI hemorrhage,
DIC
More organ systems involved, worse the
prognosis
Therapy: ABCs, fluid
Appropriate antibiotics, treatment of underlying
cause
20. Initial therapeutic end points of resuscitation
of septic shock:
1. Capillary refill time of ≤2 seconds.
2. Normal blood pressure for age.
3. Normal pulses with no differential between peripheral
and central pulses.
4. Warm extremities.
5. Urine output >1 mL/kg/hr.
6. Normal mental status.
7. Scvo2 saturation ≥70%.
8. Cardiac index between 3.3 and 6.0 L/min/m2 should
be targeted thereafter (grade 2C)
21. B. Antibiotics and Source Control:
All children with septic shock should receive coverage
for methicillin-resistant Staphylococcus aureus
(MRSA).
Coverage for enteric organisms should be added
whenever clinical features suggest genitourinary (GU)
and/or gastrointestinal (GI) sources.
Treatment for Pseudomonas species should be
included for children who are immunosuppressed or at
risk for infection with these organisms (ie, those with
cystic fibrosis).
22. Listeria monocytogenes and herpes simplex virus are
important pathogens in neonates≤ 28 days of age.
When treating empirically, antibiotics which can be
given by rapid intravenous bolus (eg, beta-lactam
agents or cephalosporins) should be administered first
followed by infusions of antibiotics, such as
vancomycin, that must be delivered more slowly.
Ongoing antimicrobial therapy should be modified
based upon culture results, including antimicrobial
susceptibility and the patient's clinical course.
23. C. Fluid Resuscitation:
isotonic crystalloids or albumin with boluses of
up to 20 mL/kg crystalloids (or albumin
equivalent) over 5–10 minutes, titrated to
reversing hypotension, increasing urine output,
and attaining normal capillary refill, peripheral
pulses, and level of consciousness without
inducing hepatomegaly or rales.
24. If hepatomegaly or rales exist then inotropic
support should be implemented, not fluid
resuscitation. In non-hypotensive children with
severe hemolytic anemia (severe malaria or
sickle cell crises) blood transfusion is
considered superior to crystalloid or albumin
bolusing.
25. D. Inotropes/Vasopressors/Vasodilators:
Children with severe sepsis can present with
low cardiac output and high systemic vascular
resistance (cold septic shock), high cardiac
output and low systemic vascular resistance
(warm septic shock), or low cardiac output
and low systemic vascular resistance shock.
26. A child may move from one hemodynamic
state to another, Vasopressor or inotrope
therapy should be used according to the
hemodynamic state.
Dopamine refractory shock may reverse with
epinephrine if cold or norepinephrine infusion
if warm.
27. In the case of extremely low systemic vascular
resistance despite the use of norepinephrine,
the use of vasopressin and terlipressin has been
described in a number of case reports, yet
evidence to support this in pediatric sepsis, as
well as safety data, are still lacking.
When vasopressors are used for refractory
hypotension, the addition of inotropes is
commonly needed to maintain adequate
cardiac output.
28. E. Corticosteroids:
Timely hydrocortisone therapy in children with
fluid refractory, catecholamine resistant shock
and suspected or proven absolute (classic)
adrenal insufficiency.
29. F. Blood Products and Plasma Therapies:
In cases of low superior vena cava oxygen
saturation (< 70%), maintain hemoglobin
levels of 10 g/dL.
After stabilization and recovery from shock
and hypoxemia then a lower target > 7.0
g/dL can be considered reasonable.
30. Administer platelet prophylactically when counts
are <10,000/mm3 in the absence of apparent
bleeding.
We suggest prophylactic platelet transfusion when
counts are < 20,000/mm3 if the patient has a
significant risk of bleeding. Higher platelet counts
(≥50,000/mm3) are advised for active bleeding,
surgery, or invasive procedures.
31. Use plasma therapies in children to correct
sepsis-induced thrombotic purpura disorders,
including progressive disseminated
intravascular coagulation, secondary
thrombotic microangiopathy, and thrombotic
thrombocytopenic purpura.
33. H. Glycemic Control:
Control hyperglycemia using a similar target as
in adults ≤ 180 mg/dL. Glucose infusion
should accompany insulin therapy in
newborns and children.
34. I.Diuretics and Renal Replacement Therapy:
Use diuretics to reverse fluid overload when
shock has resolved, and if unsuccessful then
continuous venovenous hemofiltration (CVVH)
or intermittent dialysis is suggested to prevent
> 10% total body weight fluid overload.