Diabetes is a condition where the body does not properly process glucose due to lack of insulin or insulin resistance. Diabetic ketoacidosis (DKA) occurs when a lack of insulin causes the body to break down fat and produce ketones, leading to hyperglycemia, ketosis and acidosis. DKA treatment involves rehydration, insulin therapy to lower blood glucose and ketone levels, electrolyte replacement, and identifying/treating the precipitating cause. Complications can include infection, shock, cerebral edema and death if not properly managed. Prevention relies on education about sick day management to avoid DKA during illness.
This presentation is based on JBDS and BSPDE guidelines in adult and Paediatric DKA management. A comparison of adult vs paediatric management is included.
This presentation is based on JBDS and BSPDE guidelines in adult and Paediatric DKA management. A comparison of adult vs paediatric management is included.
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
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
- 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
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.
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.
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
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.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Maxilla, Mandible & Hyoid Bone & Clinical Correlations by Dr. RIG.pptx
dkadrsyed2584-190602083813 (1).pdf
1.
2.
3. UNDERSTANDING DIABETES
Diabetes mellitus, often referred to simply as
DIABETES.
Diabetes is a condition in which the body:
• Does not produce enough insulin, and/or
• Does not properly respond to insulin
Insulin is a hormone produced in the pancreas. Insulin enables cells to
absorb glucose in order to turn it into energy.
3
4. Type 1 vs. Type 2
Type 1 diabetes Type 2 diabetes
Diagnosed in children
and young adults
Typically diagnosed in
adulthood
Previously known as
Juvenile Diabetes
Also found in overweight
children
Insulin-dependent Non-insulin-dependent
Body does not produce
insulin
Body fails to produce
and properly use insulin
9. DIABETIC KETOACIDOSIS (DKA)
• A state of absolute or relative insulin deficiency
aggravated by ensuing hyperglycemia, dehydration,
and acidosis-producing derangements in intermediary
metabolism, including production of serum acetone.
• Can occur in both Type I Diabetes and Type II
Diabetes
– In type II diabetics with insulin
deficiency/dependence
• The presenting symptom for ~ 25% of Type I
Diabetics.
10.
11. Diabetic KetoAcidosis (DKA)
1. 160,000 Admissions to private
hospitals/year
2. Cost = over 1 billion $ annually
3. 65% = <19 years old
4. Main cause of death in children with
diabetes (approximately 85%)
5. Cerebral edema in 69%
12. Hyperosmolar Hyperglycemic State (HHS)
• An acute metabolic complication of diabetes
mellitus characterized by impaired mental status
and elevated plasma osmolality in a patient with
hyperglycemia.
• Occurs predominately in Type II Diabetics
– A few reports of cases in type I diabetics.
• The presenting symptom for 30-40% of Type II
diabetics.
• Not commonly associated with ketonaemia and
acidosis
13.
14. The biochemical criteria for the diagnosis of DKA3,4
• Hyperglycemia - blood glucose greater than 11.1 mmol/L
• Ketosis - ketones present in blood and/or urine
• Acidosis - pH less than 7.3 and/or
bicarbonate less than 15 mmol/L
Classic Triad of DKA
15. DKA is generally categorized by the severity of the
acidosis.
• MILD – Venous pH less than 7.3 and/or
bicarbonate concentration less than 15 mmol/L
• MODERATE – Venous pH less than 7.2 and/or
bicarbonate concentration less than 10 mmol/L
• SEVERE – Venous pH less than 7.1 and/or
bicarbonate concentration less than 5 mmol/L
CLASSIFICATION OF DKA
16.
17. Risk factors for DKA at onset
• Age <12 yrs
• No first degree diabetic relative
• Lower socioeconomic status
• High dose glucocorticoids, atypical antipsychotics, diazoxide
and some immunosuppresive drugs
• Poor access to medical care
• Uninsured
• Usage of SGLT-2 inhibitor – euglycaemic DKA
SGLT2 inhibitors blunt insulin production in the face of stress
hormones leading to increased ketotic metabolism
18.
19. Why do ketones develop?
No carbohydrate intake
• fasting
• gastroenteritis
• Atkins diet, neonates fed high-fat milk
Prolonged exercise, pregnancy
Lack of insulin activity
• onset of diabetes (insufficient secretion)
• interruption of insulin delivery in established pt
Increase in insulin resistance
• infection, illness, surgery, stress
Alcohol, salicylate ingestion, inborn metabolic errors
20. Causes of DKA/HHS
• Stressful precipitating event that results in increased
catecholamines, cortisol, glucagon.
– Infection (pneumonia, UTI)
– Alcohol, drugs
– Stroke
– Myocardial Infarction
– Pancreatitis
– Trauma
– Medications (steroids, thiazide diuretics)
– Non-compliance with insulin
21.
22. PATHOPHYSIOLOGY OF DKA
Wolfsdorf J, Glaser N, Sperling MA; American Diabetes Association. Diabetic ketoacidosis in infants, children, and adolescents: A consensus statement from the
American Diabetes Association. Diabetes Care. 2006;29(5):1150-1159. Reprinted with permission from The American Diabetes Association.
26. DKA is a complex metabolic state of: hyperglycemia,
ketosis, and acidosis
Symptoms include:
– Deep, rapid breathing
– Fruity breath odor
– Very dry mouth
– Nausea and vomiting
– Lethargy/drowsiness
DKA is life-threatening and needs immediate treatment
30. Diagnostic Criteria for DKA and HHS
Mild DKA Moderate DKA Severe DKA HHS
Plasma glucose
mmol/L
> 14 > 14 > 14 > 33.3
Arterial pH 7.25-7.30 7.00-7.24 < 7.00 > 7.30
Sodium Bicarbonate
(mEq/L)
15 – 18 10 - <15 < 10 > 15
Urine Ketones Positive Positive Positive Small
Serum Ketones Positive Positive Positive Small
Serum Osmolality
(mOsm/kg)
Variable Variable Variable > 320
Anion Gap > 10 > 12 > 12 variable
Mental Status Alert Alert/Drowsy Stupor/Coma Stupor/Coma
Serum ketones positive if > 1mg/dl or < 0.1 mmol/L
Anion gap Na + K – Cl – Hco3 target < 10
31.
32.
33. Identify and Treat the Precipitating
Factor
• Insulin omission – MOST COMMON CAUSE of DKA
• New diagnosis of diabetes
• Infection / Sepsis
• Myocardial infarction
– Small rise in troponin may occur without overt
ischemia
– ECG changes may reflect hyperkalemia
• Thyrotoxicosis
• Drugs
34. Treatment of DKA
• Once resolved
– Convert to home insulin
regimen
– Prevent recurrence
• Initial hospital
management
– Replace fluid and
electrolytes
– IV Insulin therapy
– Glucose administration
– Watch for complications
– Disconnect insulin pump
35. Treatment of DKA
Fluids and Electrolytes
• Fluid replacement
–Restores perfusion of the tissues
•Lowers counterregulatory hormones
•Increase insulin sensitivity
–Average fluid deficit 3-5 liters
36. Initial fluid resuscitation
• 15 to 20 mL/kg lean body weight per hour
• (approximately 1000 mL/hour in an average-sized
person) for the first couple of hours
• Maximum of <50 mL/kg in the first four hours
• 1-2 liters of normal saline over the first 2 hours
• Slower rates of 500cc/hr x 4 hrs or 250 cc/hr x 4
hours-When fluid overload is a concern
• If hypernatremia develops ½ NS can be used
37. Treatment of DKA
Fluids and Electrolytes
• Hyperkalemia initially present
– Resolves quickly with insulin drip
– Once urine output is present and K<5.0, add 20-40
meq KCL per liter.
• Phosphate deficit
– May want to use Kphos
• Bicarbonate not given unless pH <7 or
bicarbonate <5 mmol/L
38. Treatment of DKA
Insulin Therapy
• IV bolus of 0.1-0.2 units/kg (~ 10 units) regular
insulin
• Follow with hourly regular insulin infusion
• Glucose levels
– Decrease 4 to 5.5 mmol/L per hour
– Minimize rapid fluid shifts
39. Treatment of DKA
Glucose Administration
• Supplemental glucose
– Hypoglycemia occurs
• Insulin has restored glucose uptake
• Suppressed glucagon
– Prevents rapid decline in plasma osmolality
• Rapid decrease in insulin could lead to cerebral edema
• Glucose decreases before ketone levels decrease
• Start glucose when plasma glucose < 16.6
mmol/L
41. Treatment of HHS
• Hydration!!!
– Even more important than in DKA
• Find underlying cause and treat!
• Insulin drip
– Should be started only once aggressive hydration has
taken place.
– Switch to subcutaneous regimen once glucose <
11mmol/L and patient eating.
• Serial Electrolytes
– Potassium replacement.
42. Pottasium Replacement
• If the initial K is below 3.3 mmol/L,
IV potassium chloride (KCl; 20 to 40
mmol/hour, before insulin therapy till raise
the serum potassium concentration into the
normal range of 4 to 5 mmol/L
• 3.3 to 5.3 given iv K with insulin infusion
• If above 5.3 not to given iv K till level less than
than
43. Resolution of ketoacidosis in DKA
• ●Normalization of the serum anion gap (less
than 12 mEq/L) and blood beta-
hydroxybutyrate levels
• ●Patients with HHS are mentally alert and the
effective plasma osmolality has fallen below
315 mOsmol/kg
• ●The patient is able to eat
44. Caveat
• Urinary ketones by the nitroprusside method can
be used for the initial diagnosis of ketoacidosis
• It should not be used for monitoring resolution of
DKA.
• Nitroprusside reacts mainly with acetoacetate, to
a much lesser degree with acetone (which is not
an acid), and not with beta-hydroxybutyrate.
• A positive nitroprusside test may persist for up to
36 hours after resolution of the ketoacidosis due
to a positive reaction with acetone, which is
slowly eliminated,
45. Once DKA Resolved
Treatment
• Most patients require 0.5-0.6 units/kg/day
• Pubertal or highly insulin resistant patients
– 0.8-1.0 units/kg/day
• Long acting insulin
– 1/2-2/3 daily requirement
– NPH, Lente, Ultralente or Lantus
• Short acting insulin
– 1/3-1/2 given at meals
– Regular, Humalog, Novolog
• Give insulin at least 2 hours prior to weaning insulin
infusion.
48. Complications of DKA
• Infection
– Precipitates DKA
– Fever
– Leukocytosis can be secondary
to acidosis
• Shock
– If not improving with fluids
r/o MI
• Vascular thrombosis
– Severe dehydration
– Cerebral vessels
– Occurs hours to days after DKA
• Pulmonary Edema
– Result of aggressive fluid
resuscitation
• Cerebral Edema
– First 24 hours
– Mental status changes
– Tx: Mannitol
– May require intubation with
hyperventilation
49.
50. Prevention of DKA / HHS
• Type 1 diabetes
– Education around sick day management
– Continuation of insulin even when not eating
– Frequent monitoring when ill
• Type 2 diabetes
– Education around sick day management
– Frequent monitoring when ill
51. Prevention of DKA
Sick Day Rules
• Never omit insulin
– Cut long acting in half
• Prevent dehydration
and hypoglycemia
• Monitor blood sugars
frequently
• Monitor for ketosis
• Provide supplemental
fast acting insulin
• Treat underlying
triggers
• Maintain contact with
medical team
52.
53.
54. Conclusion
• Successful management
requires
– Judicious use of fluids
• Establish good perfusion
– Insulin drip
• Steady decline
• Complete resolution of ketosis
– Electrolyte replacement
– Frequent neurological evaluations
– High suspicion for complications
• Determine etiology to avoid
recurrent episodes