acute complication of diabetes mellitus. cardinal biochemical features for DKA. pathophysiology of DKA. clinical assesment of DKA. investigation and management for DKA. complications of DKA.
acute complication of diabetes mellitus. cardinal biochemical features for DKA. pathophysiology of DKA. clinical assesment of DKA. investigation and management for DKA. complications of DKA.
Diabetic ketoacidosis is a serious complication of diabetes that occurs when your body produces high levels of blood acids called ketones. The condition develops when your body can't produce enough insulin.
When your cells don't get the glucose they need for energy, your body begins to burn fat for energy, which produces ketones. Ketones are chemicals that the body creates when it breaks down fat to use for energy. The body does this when it doesn’t have enough insulin to use glucose, the body’s normal source of energy. When ketones build up in the blood, they make it more acidic.
Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria.
Acute kidney injury (AKI) is a potentially life-threatening
syndrome that occurs primarily in hospitalized patients
and frequently complicates the course of critically ill
patient.
Acute Kidney Injury is is (abrupt) reduction in kidney functions as evidence by changed in laboratory values; serum creatinine, blood urea nitrogen(BUN)and urine output
Diabetic ketoacidosis is a serious complication of diabetes that occurs when your body produces high levels of blood acids called ketones. The condition develops when your body can't produce enough insulin.
When your cells don't get the glucose they need for energy, your body begins to burn fat for energy, which produces ketones. Ketones are chemicals that the body creates when it breaks down fat to use for energy. The body does this when it doesn’t have enough insulin to use glucose, the body’s normal source of energy. When ketones build up in the blood, they make it more acidic.
Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria.
Acute kidney injury (AKI) is a potentially life-threatening
syndrome that occurs primarily in hospitalized patients
and frequently complicates the course of critically ill
patient.
Acute Kidney Injury is is (abrupt) reduction in kidney functions as evidence by changed in laboratory values; serum creatinine, blood urea nitrogen(BUN)and urine output
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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.
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
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.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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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
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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.
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.
2. Diabetic ketoacidosis (DKA) is an acute, major, life-
threatening complication of diabetes that mainly
occurs in patients with type 1 diabetes, but it can
occur in some patients with type 2 diabetes.
DKA is a complex disordered metabolic state
characterized by hyperglycemia, ketoacidosis, and
ketonuria.
DKA has high morbidity and mortality in paediatic
patients.
2/1/2019 DKA BY DR.BAKUNDA 2
3. Pathophysiology
Insulin normally elevates cellular uptake of
glucose from the blood
Insulin defciency with rised counter regulatory
hormones (glucagon,cortisol, catecholamines,
GH)
Can occur with lack of insulin (non-adherence,
inadequate dosage, 1st presentation) or
increased stress (surgery, infection, exercise)
2/1/2019 DKA BY DR.BAKUNDA 3
4. Unopposed hepatic glucose production
hyperglycemia cause osmotic diuresis
then dehydration and electrolyte
disturbance Na+ (water shift to ECF
causing pseudohyponatremia)
Fat mobilization increases FFA then
ketoacids then metabolic acidosis
2/1/2019 DKA BY DR.BAKUNDA 4
5. As a result of hyperglycemic
hyperosmolality, potassium shifts along
with water from inside cells to the
extracellular space and is lost in the
urine.
Insulin normally promotes cellular
potassium uptake but is absent in DKA,
compounding the problem.
2/1/2019 DKA BY DR.BAKUNDA 5
6. A total body potassium deficit therefore
develops in the body, although serum
potassium may be normal or even
paradoxically elevated.
2/1/2019 DKA BY DR.BAKUNDA 6
7. Signs and symptoms
Polyuria ,Polydipsia
Recent weight loss
Nausea and vomiting
Signs of volume depletion (i.e., dry
mucous membranes, decreased skin
turgor), hypotension, circulatory collapse
2/1/2019 DKA BY DR.BAKUNDA 7
8. Neurological abnormalities
Altered mental status
Lethargy
coma
Other neurological
exam abnormalities such
as blurred vision and weakness
2/1/2019 DKA BY DR.BAKUNDA 8
9. Rapid onset (< 24 h)
Abdominal pain
Fruity odor on the breath (from
exhaled acetone)
Hyperventilation: Kussmaul respirations: deep
breaths at a normal respiratory rate
2/1/2019 DKA BY DR.BAKUNDA 9
10. Diagnostic
Initial approach
ABCs: airway, breathing, and circulation
Mental status check
Fingerstick glucose
History (taken from family members or
friends if need be), including possible
precipitating factors
2/1/2019 DKA BY DR.BAKUNDA 10
11. Diagnostic tests
◦ ↑ Serum glucose(< 600 mg/dL > 250 mg/dL ,Urine ketones
Serum electrolytes, including bicarbonate (with anion gap
calculation)
◦ Hypertonic hyponatremia
◦ But if fluid loss due to osmotic diuresis is not
replaced, hypernatremia
◦ serum bicarbonate is reduced
◦ Urine dipstick with increased glucose and ketones
◦ Osmolarity (increased to >290 mOsm/L)
2/1/2019 DKA BY DR.BAKUNDA 11
12. Additional tests
Indications: may be ordered to rule out
serious precipitating factors, such
as myocardial infarction, pneumonia,
or pancreatitis
↑ Blood urea nitrogen (BUN) and creatinine
Full blood count,ABG
Blood or urine cultures
ECG
Chest x-ray
2/1/2019 DKA BY DR.BAKUNDA 12
13. Management
Principles
Admission in high dependency area of Medical
Ward or ICU.
Correction of fluid loss with intravenous fluids
Correction of hyperglycemia with insulin
Correction of electrolyte disturbances, particularly
hypokalemia
Correction of acid-base balance but most of time
corrected with above mentioned measures
Treatment of concurrent infection, if present
2/1/2019 DKA BY DR.BAKUNDA 13
14. Correction of fluid loss
Normal Saline or Ringer’s Lactate
Administer 1-3 L during the first hour
Administer 1 L during the second hour
Administer 1 L during the following 2 hours
Administer 1 L every 4 hours, depending
on the degree of dehydration
2/1/2019 DKA BY DR.BAKUNDA 14
15. Correction of hyperglycemia
critical to resolve acidosis, not only
hyperglycemia
Do not use with hypokalemia , until serum K+ is
corrected to >3.3 mmol/L
– short-acting insulin(R)
– maintain on 0.1 U/kg/h insulin R infusion
– check serum glucose hourly
If blood glucose stable and urine ketones
negative, then stop insulin infusion and start
standard insulin regimen
2/1/2019 DKA BY DR.BAKUNDA 15
16. K+ replacement
with insulin administration, hypokalemia may develop
if serum K+<3.3 mmol/L, hold insulin and give 40
mEq/L K+ replacement
if serum K+3.3-4.5 mmol/L, give 20 mEq/L K+
replacement
when K+ 4.5-6.0 mmol/L add KCL 10 mEq/L IV fluid to
keep K+ in the range of 3.5-5 mEq/L
2/1/2019 DKA BY DR.BAKUNDA 16
Increase in BG by 10 mmol/L there is a decreases in Na+ by 3 mmol/L
Osmolarity (increased to >290 mOsm/L) Calculation = 2 (Na + K) + urea/3 + glucose(mg/dl)/18
Anion gap (elevated) Calculation = ([Na + K] - [Cl + HCO3] >13 mEq/L)
Te maximum decrease rate of glucose is100 mg/dL/h Blood glucose should not fall below 200mg/dl during the frst 6 hours
Serum anion gap reduced to normal (12 ± 2 mEq/L), or serum BOHB ≤1 mmol/L (10.4 mg/dL)
Venous pH >7.30, or serum bicarbonate (HCO3) >15 mEq/L● Blood glucose <200 mg/dL (11.1 mmol/L)● Patient is tolerating oral intake