Javed Butler, MD, MPH, MBA, discusses heart failure in this CME activity titled, "New Frontiers in Managing Heart Failure: Are SGLT2 Inhibitors the Next Leap Forward in Optimizing Patient Care?" For the full presentation, downloadable infographics, monograph, complete CME information, and to apply for credit, please visit us at http://bit.ly/2JG2v9l. CME credit will be available until May 29, 2020.
Javed Butler, MD, MPH, MBA, discusses heart failure in this CME activity titled, "New Frontiers in Managing Heart Failure: Are SGLT2 Inhibitors the Next Leap Forward in Optimizing Patient Care?" For the full presentation, downloadable infographics, monograph, complete CME information, and to apply for credit, please visit us at http://bit.ly/2JG2v9l. CME credit will be available until May 29, 2020.
In a pregnant woman presenting with thrombocytopenia, the possibility of HELLP syndrome should always be considered by the treating clinician so as to initiate the therapy at the earliest to prevent the high perinatal mortality and postpartum morbidity. Here we report an unusual case of young Primigravida (postpartum) who presented at Indraprastha Apollo hospitals, New Delhi with altered sensorium, paraperesis, DIC and septic shock. On evaluation she was found to have HELLP syndrome for which Plasmapheresis was given and patient showed remarkable improvement.
An overview of the management of Rhabdomyolysis, put together for the weekly Emergency Medicine registrar teaching session at Wollongong Hospital ED. Information in the presentation is from both the journals and medicine 2.0 (and in particular "FOAMed" -the free open access medical education network that aims to improve sharing of medical education resources through the web). Enjoy. @trainthetrainer
Its leftover homework of our physician scientist & health care providers for the last 75 years indeed. Contemporary challenges are numerous , but there is a will there is a way ,today or tomorrow some body some where has to start .
Currently heart failure is being treated by every physician ,any where from community to academic institution ,and is based on old system of payment ( FFP ) fee for service ,we need to switch from FFS to Value based payment ( VBP ) .
Million Heart, ticking time bomb can we predict or preventasadsoomro1960
There are different stages of HF syndromes , stage B HF is grossly neglected by cardiology community ,which is a ticking bomb to prevent symptomatic HF
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.
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
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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
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.
- 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
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.
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.
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 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
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.
3. Executive Summary
52 year saudi male newly diagnosed diabetes, admitted through
ER to our CCU on 31/12/2012 at around 4.05am .
He was referred from one of the secondary care hospital as ACS
for further management ,where he presented with H/O sudden
severe retrosternal ,prolonged chest pain with sweating ,woke
up from deep slumber at mid night.
In KFHH ER he developed heart failure and became hypoxic
therefore intubated & ventilated.
Chest X-ray showed normal heart size with pulmonary edema
4. Conti,
He was immediately transferred to cath lab & coronary angiogram
showed ,normal left main, LAD totally occluded proximaly,LCX,OM1
osteal 70%,OM2 good, distal LCX diffusely diseased. RCA totally
occluded after RV branch, fills retrogradely from left system, looks
chronic .
Primary PCI done to LAD with 2DES.
At the end of procedure developed monomorphic ventricular
tachycardia, which was reverted with single 150 jouls of DC shock,
had short CPR indeed.
He was hypotensive therefore IABP was inserted ,and shifted to CCU on
Amiodarone, dopamine , aggrastat,& lasix infusion.
5. Cont,
He remained critical ,but conscious, his intial CPK was 5887,MB,
617 ,with ratio of 10.4% ,creatnine was 133. Post PCI EKG
showed new RBBB with persistent ST elevation in leads V 4-6
.Still on IABP & on ventilator.( he was on clopidogrel, ASA ,
&40mg statin.
On 3rd Jan 2013 ,left sided weakness was noticed by nurses, at
night.
Next day 4th Jan on morning round at around 11 am it was
discovered that patient has developed stroke with left sided
hemiplegia, he was conscious but febrile ( 39C) he was on
ceftriaxone and tazocin,
6. CT brain was done on the same day, which was reported as small
hypodense lesion at left cerebellum , ( ? Old infarction), no mid
line shift ,no bleeding. Initially heparine was stopped and later after CT
brain ,restarted because of IABP.
Transthoracic echocardiogram did not showed apparent thrombus .
EKG showed RBBB, with persistent ST elevation in same leads.
his creatnine progresively increased from 133 to 215mg, CPK & MB ,
showed a downward trend for the next four days ,from 5887 to
794,MB from 617 to 59 ( yet not normalized, until 5th post MI day) )
.He was persistently hypernatraemic , ( Na,>150) seen by
nephrologist ,at this stage his HB,WBC,PLT and LFT remain stable.
7. Cont,
On 6th January ( 7th day of MI & statin) profile of cardiac enzymes
showed rising of CPK from 794 to 1043, MB, 60 ( ratio 7.5%),
creatnine 249, Na 156.
On 7th January pm ,CPK further increased to 2522,MB,75 ( ratio
2.9%), creatnine 206,Na, 162,K, 3.6,Ca, 1.8 platelets 100.
On 8th CPK further increased to 8926, MB,184 ( ratio, 2.0%)
creatnine 185, Na,164.K, 3.9, Ca 1.7
He remain on ionotropic support, he was extubated on 8th jan
2013.
Blood culture grew coagulase negative staphlococcus, and was
only susceptable to vancomycin, and was started
8. Cont,
IABP was tried to wean off but became hypotensive
60/30 on dopamine & levophed, he remain febrile
38C,ABG showed metabolic alkalosis, urinary out
put was 100-150ml/hour lasix infusion was reduced
from 5mg to 3mg/hour.
On 9th Jan became confused, developed hypotension
on dopamine & levophed, he was still febrile and
hypernatraemic.
9. Cont
On 12th jan because of persistent hypernatraemia ,he
was suspected for, diabetes insipidious,& pitutary
adenoma, seen by endocrinologist. After evaluation
,considered as sick thyroid, no DM insipidous,
discharged from his side and to be followed by
nephrologist for hypernatraemia. Results of hormonal
assays ( serum cotisol, ACTH, testosteron, FSH, LH &
prolactin) were with in normal range.
. Hepatitis Hbs, HCV& HIV remain negative
10. Cont,
He remain under care of nephrologist for renal failure and
hypernatraemia.
His CPK progressively incread to 18213, ( 9th jan) to, 21530,
38040 ,
On 15th jan highest peak of CPK 68405, renal function also
deteriorated ( from 168 to 322 & 404),Na 150,K
,4.9,Ca,1.7,Phos, 3.2, became oligouric , 30-40ml / hour and
later anuric at night .
Liver enzymes also increased significantly ( LDH,2640,GPT,824)
.
11. Cont,
On 16th jan , in acute renal failure, ( High creat,
Na, K Uric acid ,& posphorus, low Ca), he was
tachypnoeic ( ABG showed ,PH,7.3, PCO2,35,
PO2,95,Osat,97%, HCO3,18.6), Electively intubated
again.
He was reviewed by a nephrologist and first time CRRT
was started at 12.30pm.
Remain anuric on CRRT, however after dialysis, all
biochemical parameters started to regress , but CPK and
liver enzymes were still on higher side, despite on
CRRT,which was continued.
12. Until 19th jan ( 20th admission of day ,) he remain on 40mg
statin. ( undiagnosed rhabdomyolysis for two weeks)
At evening ,specialist on call evaluated the patient and first
time discover & diagnosed to have “statin induced
massive rhabdomyolyis”,& hepatic injury,
preceded by hypernatraemia, and progressed to acute
renal failure.
He was on ( HMG -co reductase inhibitor) statin( atorvastatin
40mg Qd, monotherapy) which was stopped ,& CRRT was
continued.
First time Urinary myoglobinurea done & came positive,
troponin T was negative .
13. Cont,
He remain anuric from 15th to 22nd jan,( 8 days) and ,on CRRT, which
was stopped on 23rd jan 5.20am ( on 8th day) because of
hypotension.
Subsequently on 24 th jan ,his 24 hour urinary out put became 2800,yet creatnine
was 171& 199,95 &55 electrolytes were stablized CPK became 278,136&97
LDH,476, 324& 264,GPT 131&98.
Urinary out put without dialysis remain between 2500 to 3000,with negative
balance of 700 to 1000ml.
On 2nd feb sputum culture grew Klebsiella pneumoni.
Still in CCU, conscious ,cardiologically compensated, renal function ,CPK
& liver enzymes have normalized, yet left sided dense hemiplegia, with
spiky fever.
23. Statin induced Myotoxicity
Rhabdomyolytic Syndrome
Statins are generally well tolerated, most cost effective& widely prescribed drugs
currently available for treatment of dyslipidaemia& coronary artery syndromes.
They are rapidly absorbed in 1-2 hours , & Mean plasma half life is
approximately 14hours. They under go metabolism via cytochrome P3A4 -A5.
98% Statins are bound to plasma proteins , because of this, haemodialysis is
not expected to significantly enhance statin clearance due to extensive drug
binding.
Statin induced myopathy occuring in 0.1% to 0.5% of population ,may
progress toward rhabdomyolysis while patients continue to take the drug.
The true incidence of statin associated rhabdomyolysis is not exactly clear because
of rarity of this condition.
The fatal rhabdomyolysis is rare, 0.12per one million
24. Cont,
Elevation in CK are conventionally used in the diagnosis of both
rhabdomyolysis & acute coronary syndromes, along with other
markers and may cause diagnostic confusion when both
conditions co-exist.
Skeletal muscle release of CK & MB generally remain elevated
for longer time, than myocardial release with temporal rise &
fall, rise after 4-8 hours and peak at 24 hours and decline after
48 to 72 hours.
Troponin may accurately distinguishes skeletal from cardiac
muscle damage.
25. Cont,
A frequent cause of drug induced Rhabdomyolysis today is
administration of HMG-CO, reductase inhibitors ,which are
most important & frequently prescribed cardiac drugs in ACS
due to their pleomorphic effect.
Rhabdomyolysis may range from asymptomatic subclinical rise in
CK to life threatening acute renal failure. In one of the study of
812 patients of statin induced rhabdomyolysis ,mean age was
64.4 yrs,35.5% were females.
The worst outcome reported were renal dysfunction in
17%,acute renal failure in 19.8%,dialysis in 5.2%,and death in
7.6% ( rhabdomyolysis is dose related 10mg statin 3.8% &
with 40mg 11.3%) .
26. Statin induced Myotoxicity
Rhabdomyolytic Syndrome
Skeletal muscle is a complex heterogenous mixture of cell types that
composes 40% adult body mass. CK,MM is abundantly present in skeletal
muscle,and is most specific test for diagnosis of rhabdomyolysis, typically
peaks 2-5 days after initial insult, CK remain in circulation longer than
myoglobin.
Rhabdomyolysis is literally dissolution of skeletal muscle, potentially life
threatening condition, may lead to fatal irreversible renal damage
through series of biochemical reactions. It is characterized by ,
1) Markedly elevated CPK > ten times ( >16000 likely to cause renal failure)
2) Myalgia, myositis & myopathy.
3) Dark( Port wine/ tea color) urine, due to myoglobinurea
27. Hypernatraemia & Rhabdomyolysis
Hypernatraemia in rhabdomyolysis is reported to be associated
as both cause and effect.
The pattern of persistent hypernatraemia with elevated CK raised
the suspicion of rhabdomyolysis in spite of the absence of other
clinical feature.
The persistent hypernatraemia caused by rhabdomyolysis guide us to
correct diagnosis.
The hypernatraemia in this setting should not be treated with free water
as in usual case of hypernatraemia and dialysis would be more
appropriate method of treatment.
28. Statins & liver
Mild increase in liver enzymes approximately occur
in 1-3%.Clinically important & idiosyncratic, liver
injury is probably very rare, and can be associated
with severe outcome, mostly occur 3-4 month after
statin treatment.
It can be cholestatic or hepatocellular injury
,and similar pattern of liver injury can be
reproduced on re-exposure.
29. Complications of Rhabdomyolysis
Early complications of rhabdomyolysis includes, electrolyte
abnormalties, like hypokalemia (causing cardiac arrhythmias and
possibly cardiac arrest), hypocalcemia, hypernatremia ,hyperkalemia
&hepatic dysfunction.
Late complications occuring after 12-24hours include acute renal
failure ( 4 to 33% due to direct toxic effect of myoglobin on epithelial
cells of proximal convoluted tubules, full recovery of renal function is common
irrespective of rhabdomyolysis cause, however mortality may still be as high as
8%.
Compartmental syndrome is rare but if not addressed with in 6-8 hours,
irreversible ischemic muscle & nerve damage may occur,
Finally disseminated intravascular coagulation ( DIC) and multi-organ failure are
dreaded complications in adults.
30. Precipitating Factors &Cautions.
1) Hepato-renal impairment
2) DM, Hypothyroidism
3) Personal or familial H/O hereditary muscular disorders
.
4) Previous H/O myotoxicity with statins or fibrates.
5) If CPK level are significantly elevated > 5times,or
concomitant drugs, fibrates, gemfibrozil, treatment
should not be started
6) Treatment should be stopped if > 10 times or evidence
of rhabdomyolysis.
31. Excess intracytoplasmic calcium causes muscle
destruction and fiber necrosis, leading to excessive
potassium, phosphate myoglobin, creatne kinase
and urate release in to systemic circulation
The most sensitive biochemical indicator ,a creatine
kinase reading at least 5 times higher than normal,
is the accepted diagnostic standard.
A ratio of blood urea nitrogen to serum creatinine of
6:1 or less indicates increased creatinine release
from skeletal muscle and renal dysfunction. An
increase or decrease in K, Po4 or Ca may occur,
depending on severity,duration & management of
rhabdomyolysis.
32. Management & prevention
The treatment goal is to stop muscle destruction. The following steps
should be taken,
1) Eliminate exposure to the toxic agent
2) Begin symtomatic treatment immediately in pts with acute
rhabdomyolysis.
3) Correct and controll hyponatraemia, hypernatraemia,
hyperglycaemia, hypocalcemia and decrease phosphorus.
4) Restore intravascular volume.
5) Alkalinizing the urine and mannitol may be effective in some patients
with acute renal failure. Patient with severe metabolic abnormalties
and renal dysfunction may require dialysis.
33. Conclusion
1) In hospital acquired acute renal failure if etiology is sorted out
,one can prevent iatrogenically induced renal injury ,and may
reverse the course of acute renal failure.
2) If rhabdomyolysis is recognized early & promptly treated , the
complications are preventable and syndrome has excellent
prognosis.
3) Finally patient, nurses,& doctors education should focus on
preventing and minimizing adverse effects of statins. It may cause
silent progressive renal failure ( days to year) therefore regular
monitoring in high risk patients is mandatory to avoid irreversible
renal failure.