This document discusses hypertension, including its definition, prevalence, classification, etiology, consequences, pathophysiology, and perioperative and long-term management. Some key points include:
- Hypertension is defined as blood pressure ≥140/90 mmHg. About 970 million people worldwide have high blood pressure.
- Perioperatively, hypertension can occur during induction of anesthesia or post-operatively due to discontinuation of antihypertensive medications. It increases the risk of postoperative complications.
- Long-term treatment involves lifestyle modifications like reducing sodium intake and exercise, as well as pharmacological therapy using medications like thiazide diuretics, calcium channel blockers, ACE inhibitors, and ARBs to
A powerpoint explaining in detail about all the intravenous induction agents and their clinical uses, pharmacokinetics & pharmacodynamics, adverse effects and complications.
In critical care medicine the invasive life saving techniques are often employed and when all goes well such interventions will be withdrawn to all for normal physiology to resume. Identifying this point for safe withdrawal for the resumption of normal respiratory function is of utmost importance.
diagnosis & complication of Diabetes mellitus including Diabetic ketoacidosis & HHS
anaesthesia managment for patient with DM posted for surgery both emergency and elective surgery
gestational diabetes mellitus
DIABETES AND ITS ANAESTHETIC IMPLICATIONSSelva Kumar
This presentation deals with diabetes mellitus and its anaesthetic implications. All about preoperative investigations and intra-operative management are discussed.
The transversus abdominis plane, more commonly referred to as the TAP block,
Places local anesthetic in the lateral abdominal wall in a plane between the internal oblique and the transversus abdominis muscles.
Here, the local anesthetic block can block many of the abdominal nerves as they pass to the abdominal structures.
Hypertension Emergencies and their managementpptxUzomaBende
This Presentation talks about Hyprtension, the mode of presentation of hypertensive crisis and the effective management of hypertensive crisis to prevent case fatalities.
A powerpoint explaining in detail about all the intravenous induction agents and their clinical uses, pharmacokinetics & pharmacodynamics, adverse effects and complications.
In critical care medicine the invasive life saving techniques are often employed and when all goes well such interventions will be withdrawn to all for normal physiology to resume. Identifying this point for safe withdrawal for the resumption of normal respiratory function is of utmost importance.
diagnosis & complication of Diabetes mellitus including Diabetic ketoacidosis & HHS
anaesthesia managment for patient with DM posted for surgery both emergency and elective surgery
gestational diabetes mellitus
DIABETES AND ITS ANAESTHETIC IMPLICATIONSSelva Kumar
This presentation deals with diabetes mellitus and its anaesthetic implications. All about preoperative investigations and intra-operative management are discussed.
The transversus abdominis plane, more commonly referred to as the TAP block,
Places local anesthetic in the lateral abdominal wall in a plane between the internal oblique and the transversus abdominis muscles.
Here, the local anesthetic block can block many of the abdominal nerves as they pass to the abdominal structures.
Hypertension Emergencies and their managementpptxUzomaBende
This Presentation talks about Hyprtension, the mode of presentation of hypertensive crisis and the effective management of hypertensive crisis to prevent case fatalities.
Described the BP targets in Ischemic stroke with and without IV thrombolysis, with and without mechanic thrombectomy, Intra cerebral Heamorrhage, SAH and other Neurological emergencies with revised AHA/ ASA upated guidelines
ALSO showed different journal evidence of work on blood pressure management in acute ischemic and heamorrhagic stroke, BP tergets in SAH, PRES
The presentation covers definitions, identification, Treatment goals, Special situations, Practice points, and cardinal pharmacotherapy. Session presented in NBE learning session
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 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
- 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
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.
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
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...
Anesthesia in Hypertensive Patients.pptx
1. A DISCUSSION
Kristel R. Quintas-Quitaleg, MD
Pangasinan Provincial Hospital
August 22, 2017
1
2. INTRODUCTIO
N
2
Hypertension: elevated
BP, (≥140/90 mmHg)
Important:
• Must be based on the average of
≥2 stable readings of arterial
pressure, taken at ≥2 visits after
initial screening
• Not on a single isolated recording
About 970M people
worldwide have high BP.
• Estimated cases in 2025:
1.56B adults.
• Prevalence of undiagnosed
HTN: 1 in 15
BP values increase with age:
• <45 y/o: males > females
• ≥65 y/o: females > males
• 90% lifetime risk for those
≥55 y/o with normal BP
3. PERIOPERATIV
E
HYPERTENSIO
N
3
HTN is the 2nd most
common risk factor
associated with surgical
morbidity (1st is
smoking).
Perioperatively, may occur
during induction of anesthesia.
• Intra-op, it is associated with
PAIN-induced sympathetic
stimulation, HYPOTHERMIA,
and/or HYPOXIA.
• Or excessive IVF therapy –
persists 24-48hrs post-op
Post-operatively:
• Due to discontinuation
of antihypertensives
• Incidence: 4-30%
following surgery
5. ETIOLOGY
5
• Cannot be cured but can be controlled
• Genetic factors play an important role
• Develop gradually over many years
>90% UNKNOWN: classified as
PRIMARY or ESSENTIAL HTN
• MCC: HTN associated with kidney
impairment like CKD and renovascular HTN
• Appear suddenly, and causes higher BP
values
<10% have SPECIFIC CAUSES:
classified as SECONDARY HTN
6. Causes
of
Secondary
Hypertension
(JNC
VIII:
2015)
6
DISEASE STATES DRUGS AND OTHER PRODUCTS
• Kidney disease
• Adrenal gland
tumors
• Thyroid disease
• Congenital blood
vessel disorders
• Alcohol abuse or
chronic alcohol
abuse
• Obstructive sleep
apnea
• NSAIDs: e.g., ibuprofen, naproxen
• Birth control pills
• Decongestants: pseudoephedrine,
phenylephrine
• Cocaine
• Amphetamines: e.g.,
amphetamine, methylphenidate,
lisdexamfetamine
• Corticosteroids: e.g., prednisolone,
methylprednisolone,
dexamethasone, hydrocortisone
• Food: foods high in sodium such as
canned or processed foods, salad
dressings, cheese, chips, sweets
• Alcohol
7. CONSEQUENCE
S
Important cause of
premature death: 7.5M
deaths annually
HTN damages blood
vessels and organ
function: ending up with
heart attack, stroke,
CHF and kidney disease
If it causes
atherosclerosis in the
HEART: angina, CHF or
MI
In the brain: may
weaken blood vessels
forming aneurysms, or
atherosclerosis causing
stroke
7
10. PREOPERATIV
E
HYPERTENSIO
N
At least 25% of
patients undergoing
noncardiac surgery
Usually doesn’t
involve end-organ
damage, with enough
time to reduce BP
DBP ≥110 mmHg:
marker of
perioperative cardiac
complications in px
with chronic HTN
Associated with:
• Perioperative bradycardia,
tachycardia, hypertension
• 3.8x increase in post-op
death (compared with
normotensive patients)
10
11. PREOPERATIV
E
HYPERTENSIO
N
Work-up for secondary
causes:
• Pheochromocytoma – rare, but
may produce vasoconstriction and
hypovolemia, complicating
management
Clonidine withdrawal
syndrome – present 18-24
hrs after sudden
discontinuations of
clonidine
• Treated with IM clonidine or
labetalol and methyldopa
11
12. INTRAOPERATIV
E
HYPERTENSION
Considered HYPERTENSIVE
EMERGENCY if there is >20%
acute increase in BP during
surgery
Occur more commonly in
patients undergoing surgery of:
• Carotids
• Abdominal aorta
• Peripheral vascular procedures
• Intraperitoneal surgery
• Intrathoracic surgery
May precipitate MI or CHF in a
patient with preexisting LV
dysfunction
12
14. Interactions
Between
Anesthetics and
Antihypertensiv
e Drugs
Main concern: effect of anesthetics on the
sympathetic NS
• Especially during fast or extended sympathetic
blockade
• Propofol: reduces vascular response to
norepinephrine, angiotensin II & vasopressin (effect
amplified in hypertensive patients)
• Hence, catecholamine-resistant hypotension (or
refractory hypotension).
But, no evidence justifies withdrawal of
antihypertensives prior to surgery
• Chronic tx should be given till the day of surgery if
rebound HTN can occur (e.g., on beta-blockers or
clonidine)
• Or stopped the day before for most treatments
14
15. ACUTE
POSTOPERATIVE
HYPERTENSION
Definition:
• SBP >190 mmHg and/or
• DBP >100 mmHg
• On 2 consecutive readings
after surgery
Usually occur in the
first 20 minutes of the
post-op period
• Resolution can require up
to 3 hours
If untreated,
increases risk of:
• MI
• CVA
• Bleeding
Characterized by:
• Peripheral
vasoconstriction
• Catecholamine release
• Reduced baroreceptor
sensitivity
15
17. Management
of
Hypertensive
Patients
Other causes of HTN should be
addressed:
• Pain
• Hypoxia
• Hypercarbia
• Agitation
• Bladder distention
• Hypervolemia
Distinguish between
Hypertensive Urgency and
Emergency:
• Emergency: with coexistent end organ
damage, requires IV antihypertensive
Goal BP:
• 25% decrease in systolic BP
• Reduce DBP by 10-15% or to 110 mmHg
in 30-60 minutes
17
18. Management
of
Hypertensive
Patients
Pre-op
Know the HTN classification
Determine the kind/number
of anti-HTN drugs being used
Identify end-organ damage
Ideally, 2D-echo must be
done to assess LV
hypertrophy
Intra-op
Anesthesia induction should
be titrated
BP monitoring: thru an
automated cuff
(intermittent), or an arterial
line (continuous)
18
19. Management
of
Hypertensive
Patients
For Hypotension
IV fluids
Sympathetic agonists:
ephedrine, phenylephrine
Terlipressin: vasopressin
agonist, as effective as
norepinephrine, but
increases serum lactate
For Hypertension
Adequate pain control
Prevent shivering
Titratable IV treatment:
• Nicardipine
• Urapidil
• Esmolol
19
23. LONG-
TERM
TREATMEN
T
Lifestyle
Modification
Limit sodium intake to
<1.5g per day.
DASH diet – high in fruits,
veggies, whole grains,
poultry & fish
Restrict alcohol intake:
•0-2 drinks/day for males
•0-1 drinks/day for females
40 minutes of moderate to
vigorous intensity aerobic
exercises 3-4x a week
Pharmacological
Therapy
Thiazide diuretics
Long-acting calcium-
channel blockers
ACE-inhibitors
Angiotensin II Receptor
Blockers (ARBs)
23