1) Beta blockers may help reduce mortality and improve outcomes in patients with traumatic brain injury by attenuating the hyperadrenergic response and decreasing cardiac complications.
2) Patients with TBI who have intracranial hemorrhage and a persistent hyperadrenergic state may benefit from beta blockers like propranolol or labetalol to control tachycardia, hypertension, and other symptoms.
3) Beta blockers may also improve outcomes for geriatric trauma patients and those with pre-existing cardiac conditions by reducing postoperative cardiac risks when started pre-operatively and continued peri-operatively.
Septic shock, updated presentation, including latest guidelines from Intensive care societies and how to approach to the diagnosis with few notes about Early Goal Directed Therapy and role of steroids
Latest definition of sepsis, application of qSOFA, latest evidence on treatment of septic shock,role of fluids, role of steroids, isobalance salt solution
Sepsis is leading cause of death in children. septic shock and multi organ dysfunction is final common pathway for death in various infections. We discuss here evidence based management of sepsis and septic shock in children.
Surviving Sepsis Campaign
International Guidelines for Management of Severe Sepsis and Septic Shock: 2012
Critical Care Medicine 2013 Feb;41(2):580-637
The recent definition, concept and terminologies of septic shock, surviving sepsis campaign, management techniques, SOFA score. Also includes antibiotics and supportive modalities.
Septic shock, updated presentation, including latest guidelines from Intensive care societies and how to approach to the diagnosis with few notes about Early Goal Directed Therapy and role of steroids
Latest definition of sepsis, application of qSOFA, latest evidence on treatment of septic shock,role of fluids, role of steroids, isobalance salt solution
Sepsis is leading cause of death in children. septic shock and multi organ dysfunction is final common pathway for death in various infections. We discuss here evidence based management of sepsis and septic shock in children.
Surviving Sepsis Campaign
International Guidelines for Management of Severe Sepsis and Septic Shock: 2012
Critical Care Medicine 2013 Feb;41(2):580-637
The recent definition, concept and terminologies of septic shock, surviving sepsis campaign, management techniques, SOFA score. Also includes antibiotics and supportive modalities.
Concept Map of Syndrome of Inappropriate (ly high) Anti-Diuretic Hormone (SIADH)riddler2008
Optimized for the BlackBerry, iPhone, Windows mobile phone, Symbian smartphone screen as a reviewer on-the-go.
Write to riddler2008@msn.com for similar slideshows.
Beta Blockers in current cardiovascular practice Praveen Nagula
betablockers are the drug of choice for prevention of progression of heart failure with mortality benefit, after the evolution of neurohormonal regulation as pathogenesis of heart failure
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.
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
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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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.
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.
2. Traumatic brain injury (TBI) is associated with
a systemic hyperadrenergic state.
Through activation of beta adrenoreceptors,
catecholamines may induce
hypermetabolism and increase both cardiac
and cerebral oxygen demands.
Common adverse effects of beta blockers were examined
including clinically significant hypotension, bradycardia,
bronchospasm and congestive heart failure.
3. The current body of
evidence is suggestive of a
benefit of beta blockers
following TBI.
4. Traumatic Brain Injury
A hyper-adrenergic state has long been
demonstrated in those patients with severe TBI,
as well as non-traumatic sub-arachnoid
hemorrhage.
This sympathetic hyperactivity may
present anywhere along the continuum; from a
mild and apparently benign SIRS state to
the disruptive and difficult to control
Paroxysmal sympathetic storms (PSS)
5. The most
severe form of the hyper-adrenergic states, PSS,
presents with paroxysmal sympathetic
system activation and adrenal release of
catecholamines.
These PSS events, with their
associated tachycardia, hypertension, tachypnea,
mydriasis, and diaphoresis, often
resemble those of pheochromocytoma and
Hyperthyroid storms
(Earning them the nickname
“Brain storms”).
6. Several investigators have evaluated the post-TBI
state (with
regards to the plasma and urinary correlates of a
hyper-adrenergic phenomenon) and
noted a greater than 7-fold increase in
norepinephrine, epinephrine, and their urine
excreted metabolites.
Elevations appear to correlate with significant
increases in
sympathetic hyperactivity and are most
pronounced during the first week following
injury.
7. Neil-Dwyer and
colleagues published several studies on the hyper-
adrenergic state following intra-cranial
hemorrhage.
Although the majority of these related to patients
with nontraumatic SAH,
the group later published findings in the TBI
population as well.
The authors noted that in
both groups, patients with a clinically and/or
biochemically significant hyper-adrenergic
state appeared to have an increased morbidity and
mortality.
8. Mechanism involved
included a severe hyper-metabolic state,
myocardial ischemia/infarction, and pulmonary
dysfunction.
Other severely injured patients without TBI lacked
the catecholamine surge and
were noted to have better survival rates.
Administration of beta-blockers (BB) in patients
with severe TBI could
attenuate the hyper-adrenergic response, thereby
decreasing cardiac complications and
improving neurological recovery.
9. Mortality following
severe TBI has remained unacceptably high. Poor
outcomes are generally attributed to
the severity of the primary brain injury and little (if
any) real progress has been made on
improving survival.
Poor outcomes from severe TBI were not a
consequence of the primary insult that could not
be prevented, but rather a failure to utilize less
“traditional” therapeutic approaches.
10. By
treating intra-cranial hypertension with a multi-
drug regimen, including scheduled
intravenous metoprolol and clonidine leading to
reduction in arterial inflow
pressure.
Through the use of this protocol, the Lund group
demonstrated a significant
reduction in mortality and improvement in
Glasgow Outcome Scale at six months
11. By investigating and treating the extra-cranial
manifestations (or non-neurological organ
dysfunction) of severe TBI, these previously
overlooked and harmful secondary insults
become potential avenues for improving survival in
this population.
We recently
demonstrated that exposure to beta-blockers in
patients with severe TBI was associated
with a significant reduction in mortality
12. This reduction in mortality is
even more impressive when considering
that the BB (+) group was older, more
severely
injured, had higher respiratory and
infectious complications, and had a
lower predicted
survival.
13. WHICH TBI PATIENTS GET BB?
All TBI patients with:
1) intra-cranial hemorrhage by CTH,
AND
2) persistent hyper-adrenergic state with
paroxysmal tachycardia, tachypnea and
hypertension; may also demonstrate diaphoresis,
mydriasis, agitation
14. WHICH BB TO USE AND HOW MUCH?
1. Propranolol and labetalol
are lipophilic, penetrate BBB, and exhibit
central &
peripheral actions.
2. Initiate propranolol @ 10 mg PT/PO
q8
3. If no gut access, use labetalol 10-20
mg I.V. q4
4. Utilize labetalol 10-40mg I.V. q2 prn
15. WHEN TO START AND HOW LONG TO
CONTINUE?
1. Initiate after 24-48 h, adequate
resuscitation.
2. Rule out sepsis, missed injuries, un-
addressed pain prior to initiating BB
3. Continue for at least 14 days.
May wean
as HR remains <100.
16. WHEN TO START AND HOW LONG TO
CONTINUE?
HOW TO TITRATE BB?
1. Consider titration to a mean HR< 90bpm
and/or improvement in symptom
severity/frequency
2. May also titrate for a return of CVRD to less
than 5%
17. Geriatric trauma
Numerous studies have documented the
beneficial effects of peri-operative beta
blockade
In patients undergoing non-cardiac surgery. In
addition to a significant reduction in
preoperative cardiac mortality, decreases in long-
term overall mortality, long-term
cardiac mortality, postoperative myocardial
infarction, and postoperative myocardial
ischemia have been demonstrated in patients
receiving beta-blockade in the peri-
operative period.
18. Geriatric trauma
The current ACC/AHA guidelines recommend
peri-operative beta
blockade as a Class I recommendation for
patients who required use of beta blockers in
the recent past for control of angina,
arrhythmia, or hypertension, and high-risk
patients with findings of ischemia on
preoperative testing undergoing vascular
surgery.
19. WHICH TRAUMA PATIENTS GET BB?
Use of beta-blockers in patients with (1)
prehospital use of BB, (2) known coronary artery
disease, or (3) age greater than 65 years
should be standard of care.
The College has placed this under the standards for
Patient Safety Practices along with DVT prophylaxis
and peri-operative antibiotics.
20. WHICH BB TO USE AND HOW
MUCH?
1. If patient is one home BB, this
medication should be restarted initially at ½
dose and
then titrated to full dose as tolerated.
2. If not on BB at home, but patient meets
indications, metoprolol should be utilized.
Start at 12.5-25 mg PO/PT q 12h. Titrate to
HR <80 bpm as BP tolerates.
21. WHICH BB TO USE AND HOW
MUCH?
3. If metoprolol proves ineffective,
propranolol can be utilized. Initiate @ 10
mg PT/PO q
8h.
4. If no gut access, use labetalol 10-20 mg
I.V. q 4h or metoprolol 5-10 mg I.V. q 4h
22. GOOD LUCK
SAMIR EL ANSARY
ICU PROFESSOR
AIN SHAMS
CAIRO
elansarysamir@yahoo.com