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
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
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.
This presentation is based on JBDS and BSPDE guidelines in adult and Paediatric DKA management. A comparison of adult vs paediatric management is included.
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
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.
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.
This presentation is based on JBDS and BSPDE guidelines in adult and Paediatric DKA management. A comparison of adult vs paediatric management is included.
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
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.
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.
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
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.
- 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
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
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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2. Epidemiology
• Has increased 1.54 per 1000 under age 20
• 40% present in DKA
○ Vague symptoms
○ Delay diagnosis
• DKA -- Most frequent cause of death in children with Type 1
DM (0.15% - 0.3%)
○ ~1 in 350 children by age 18 in US have DM
3. Pathophysiology
• Insulin deficiency has three main effects:
1. Loss of insulin-dependent glucose transport into peripheral
tissues
2. Increased gluconeogenesis in the liver
3. Increased breakdown of fat, protein, and glycogen
Thus, insulin deficiency results in hyperglycemia (from
increased hepatic glucose production and decreased peripheral
uptake) and acidosis (primarily derived from hepatic fatty acid
oxidation into ketoacids).
Common Cause: New onset, intercurrent illness, insulin pump
malfunction, or purposeful insulin omission
2
4. Diagnosis/Biochemical
• Diabetes Hyperglycemia (BG>11mmol/L or 200 mg/dL)
• Keto Ketones in the urine or blood (Ketonuria or
Ketonemia) βhydroxybutyrate (BOHB); a level ≥3mmol/L is
indicative of DKA
• Acidosis Venous pH <7.3 or bicarbonate <15 mmol/L
○ Mild: venous pH<7.3 or bicarbonate <15mmol/L
○ Moderate: pH<7.2, bicarbonate <10mmol/L
○ Severe: pH<7.1, bicarbonate <5mmol/L.
3
5. Clinical Signs
• Dehydration (polyuria)
• Tachycardia
• Tachypnea
• Deep, sighing(Kussmaul)
respiration
• Acetone breath
• Nausea, vomiting
• Abdominal pain that may
mimic an acute abdominal
condition
• Confusion, drowsiness,
progressive loss of
consciousness.
4
6. Risk Factors
• Very young children
• Lower social economic
Background
• Prior poor compliance
• Concomitant psychiatric
disease
• Adolescent girls
5
7. Complications of DKA
• Cerebral Edema
• Cardiac Arrhythmias
• Severe Electrolyte abnormalities
• Severe Dehydration
• Thrombosis (CVL related, Stroke)
• Pulmonary edema
• Renal Failure
• Pancreatitis
• Rhabdomyolysis
• Severe Infections/Sepsis
• Death
6
8. Laboratory Investigation
• Glucose, urine dip
• Blood gas (venous or arterial)
• Electrolytes and other labs
Na is typically low. For every 100 mg/dL glucose above 200 mg/dL,
the measure Na should be reduced by 1.6 mEq/L
Nacorrected = Nameasured + 1.6 x [Glucose] - 200
100
K+ total body depletion
Ca and phosp typically low
BUN/Cr typically elevated in dehydration
WBC and left shift typically due to acute stress but also look
for infectious trigger process
7
9. Goals of Therapy
Correction of Dehydration, electrolyte deficits, hyperglycemia,
and acidosis.
A. Cardiovascular collapse
○ From dehydration
○ Treatment involves intravascular fluid expansion with
ISOTONIC fluids
B. Overwhelming acidosis
○ From ketoacid production and lactic acid accumulation
○ Volume expansion and tissue reperfusion to correct lactic acidosis
○ Prompt initiation of insulin to stop fatty acid oxidation and
ketone production
○ Consider use of sodium bicarbonate in patients with arterial pH <
6.9 and/or evidence of myocardial depression/collapse
• C. Hypokalemia
○ Insulin therapy is associated with rapid intracellular movement of
potassium
8
10. Treatment of DKA
9
Diagnose
• Hyperglycemia
• Ketoacidosis
Fluids
• Isotonic fluid bolus
• 1.5 to 2 X M (with NS)
Insulin
• 0.1 U/kg/hrstart after first fluid bolus
Dextrose
• Add when glucose drops below 300 mg/dL
K+
• Add if adequate renal function
11. What about Bicarb?
• No recommended for routine care
• Can lead to paradoxical worsening
• And associated with higher risk of cerebral edema
• Consider use of sodium bicarbonate in patients with arterial
pH < 6.9 and/or evidence of myocardial
depression/collapse
10
12. What about K?
• Potassium deplete
• Therapy (insulin and
correcting acidosis) cause
K to shift back into cells
• Check EKG/monitor
• Replete K if renal function
okay
11
14. Cerebral Edema
• Hypertonic dehydration in DKA is associated with the
production of osmotically active particles in the brain that act
to prevent neuronal cellular dehydration.
• Correction of hyperosmolar state leads to fluid influx into the
brain. Rapid rates of rehydration or correction of
hyperosmolarity may lead to cerebral cellular swelling
and brain herniation.
• It usually occurs 6-18 hours into therapy, just as the patient appears to
be clinically and biochemically improving.
• This is the most common cause of mortality in children with DKA !!!
⎯ Mortality rate of 20% and morbidity rate of 25%
13
15. Cerebral Edema
• Much of the etiology and pathophysiology of cerebral edema is
still unknown, but the risk should be minimized by attention to
the following:
• Slow fluid replacement (over 48 hrs) with isotonic fluids
• Frequent monitoring and slow rise of calculated CORRECTED Na values
• Close neurologic surveillance for early signs of increased ICP
(headache, lethargy, slurred speech, obtundation) and rapid
evaluation & action
• Don’t exceed 4L/m2/24 hours
14
17. Treatment of Cerebral Edema
• Initiate treatment as soon as the condition is suspected.
• Reduce the rate of fluid administration.
• Give mannitol, 0.5–1g/kg IV over 10–15min, and repeat if there
is no initial response in 30min to 2h
• Hypertonic saline(3%),suggested dose 2.5–5mL/kg over 10–
15min, may be used as an alternative to mannitol.
• Elevate the head of the bed to 30◦.
• Intubation may be necessary for the patient with impending
respiratory failure.
• After treatment for cerebral edema has been started, cranial
imaging may be considered.
○ The primary concern is whether the patient has a lesion requiring
emergency neurosurgery (e.g., intracranial hemorrhage) or a lesion
that may necessitate anticoagulation (e.g., cerebrovascular
thrombosis).
16
18. The High-Risk Patient
• Age < 3 years
• Significantly altered or deteriorating mental status
• pH < 7.2
• Glucose > 900 mg/dl
• Na (calculated)>160 or any patient with falling (calculated) Na
• K < 3.5 mEq/L on admission
• Severe hyperosmolality (Sosm > 350 mOsm)
• Other organ system dysfunction that complicates treatment
17
20. Hyperglycemia Hyperosmolar State (HHS)
formerly hyperosmolar nonketotic coma
• Plasma glucose concentration >33.3mmol/L (600mg/dL)
• Arterial pH>7.30; venous pH>7.25
• Serum bicarbonate >15mmol/L
• Small ketonuria, absent to small ketonemia
• Effective serum osmolality >320mOsm/kg
• Obtundation, combativeness, or seizures(in approximately
50%).
• Primarily Type 2 diabetics but can overlap with Type 1
especially in those with severe dehydration or those with high
carbohydrate load before hand
• Volume Resuscitation and insulin (often less)
19