This document provides an overview of diabetic ketoacidosis (DKA) presented by Dr. Jonathon Sargent at a noon conference. It discusses the clinical presentation of DKA, including symptoms like polyuria and abdominal pain. The pathophysiology of DKA is described as reduced insulin leading to increased gluconeogenesis, glycogenolysis, and ketone production. Precipitants, diagnostic testing, treatment including IV fluids, insulin and electrolyte repletion, and tips for management are reviewed. The goals of treatment are to rehydrate the patient and lower their blood glucose levels by 10% per hour with intravenous insulin.
This is a ppt presentation regarding Acute Hyperglycemic Emergencies we face in routine clinical practices and their management
from Harrison's Principles of Medicine and Paul Marino Emergency Management book
By
Dr.V.B.Kasyapa. J
(MD GM)
A review of the investigation and management of diabetic ketoacidosis in newly diagnosed type I diabetes. Patient details have been changed and anonymised to protect the identity of the individual.
This is a ppt presentation regarding Acute Hyperglycemic Emergencies we face in routine clinical practices and their management
from Harrison's Principles of Medicine and Paul Marino Emergency Management book
By
Dr.V.B.Kasyapa. J
(MD GM)
A review of the investigation and management of diabetic ketoacidosis in newly diagnosed type I diabetes. Patient details have been changed and anonymised to protect the identity of the individual.
this power point descripe diabetic ketoacidosis in pediatric age group .. we talk about the risk of it .. management specially (fluid management) as case study .. complications and the treatment of brain oedema .. i hope to be auseful one .. enjoy
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.
this power point descripe diabetic ketoacidosis in pediatric age group .. we talk about the risk of it .. management specially (fluid management) as case study .. complications and the treatment of brain oedema .. i hope to be auseful one .. enjoy
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.
This presentation is based on JBDS and BSPDE guidelines in adult and Paediatric DKA management. A comparison of adult vs paediatric management is included.
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.
Type 1 diabetes:
Diagnosed in children and young adults
Previously known as Juvenile Diabetes
Type 2 diabetes:
Typically diagnosed in adulthood
Also found in overweight children
Complications of blood glucose alterations
Hypoglycemia
Hyperglycemia
Ketosis
Acidosis
DKA (Hyperglycemia + Ketosis + Acidosis)
Normal fasting blood glucose level 4-6 mmol/L
definition:
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.
160,000 Admissions to private hospitals/year
Cost = over 1 billion $ annually
65% = <19 years old
Main cause of death in children with diabetes (approximately 85%)
Cerebral edema in 69%
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
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
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
Risk factors:
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
AETIOLOGY:
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
Causes:
Stressful precipitating event that results in increased cate
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.
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
Classic Triad of DKA:
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
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
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
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
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
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
Symptoms of DKA/HHS
Polyuria
Polydypsia
Blurred vision
Nausea/Vomiting
Abdominal Pain
Fatigue
Confusion
Obtundation
Physical Examination in DKA/HHS: Hypotension, tachycardia
Kussmaul breathing (deep, labored breaths)
Fruity odor to breath (due to acetone)
Dry mucus membranes
Confusion
Abdominal tenderness
Treatment of DKA:
Fluids and Electrolytes
Fluid replacement
–Restores perfu
14. a case study on diabetes mellitus type 1 with diabetic ketoacidosis cp in...Dr. Ajita Sadhukhan
A 26 year old male patient was admitted to the male medicine ward with complaints of nausea, vomiting, generalised weakness, anxiety, decreased appetite, headache since noon.
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
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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
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
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MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
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 lecture slides, by Dr Sidra Arshad, offer a quick overview of the 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 lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
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. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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.
10-30% of patients in DKA are DMII.
What are you worried about with the neurological symptoms? Cerebral edema
10-30% of patients in DKA are DMII.
10-30% of patients in DKA are DMII.
Stopping ketone production takes less insulin than lowering serum glucose, which explains the difference between HHS and DKA.
10-30% of patients in DKA are DMII.
Get these frequently, every 1-4 hours as needed. This is something to monitor closely until resolved.
Why was serum ketones negative but urine ketones positive?
wrong diagnosis
Test doesn’t’ measure betahydroxybutyrate
Serum ketones resolved, but urine ketones stay in bladder
DKA severity index
Pts are severely dehydrated due to osmotic diuresis. IVF helps correct acidosis and makes pts more responsive to insulin and other therapies.
Remember, K is osmotically active, and dka and hhs usually have a increased serum osmolality. Therfore adding K to ivf increases their tonicity. Adding K to ½ NS makes it more like ¾ NS.
Hypo K for 2 reasons: loss during osmotic diuresis and from hyperaldosteronism