This document discusses the challenges of managing diabetic emergencies like diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) in patients with heart failure. Aggressive fluid resuscitation is typically needed for DKA/HHS but can worsen heart failure, requiring cautious fluid administration and monitoring. Goals of treatment include managing hemodynamics, fluid balance, metabolic derangements like acidosis/electrolyte imbalances, and preventing complications like acute kidney injury or thromboembolism. Careful attention to fluid intake and output as well as electrolyte and acid-base status is important when treating hyperglycemic crises in patients with heart failure.
Educative power-point presentation for students in paediatrics, paediatric critical care, neonatology, And trainees or fellows in paediatric critical care
Acute kidney failure happens when your kidneys suddenly lose the ability to eliminate excess salts, fluids, and waste materials from the blood. Acute kidney failure is also called acute kidney injury or acute renal failure. It's common in people who are already in the hospital. It may develop rapidly over a few hours.
This power point is prepared from text books, guidelines and literature. so it will be up date based on the need and not used for management of patients.
Educative power-point presentation for students in paediatrics, paediatric critical care, neonatology, And trainees or fellows in paediatric critical care
Acute kidney failure happens when your kidneys suddenly lose the ability to eliminate excess salts, fluids, and waste materials from the blood. Acute kidney failure is also called acute kidney injury or acute renal failure. It's common in people who are already in the hospital. It may develop rapidly over a few hours.
This power point is prepared from text books, guidelines and literature. so it will be up date based on the need and not used for management of patients.
Intro to hyperglycemic emergencies - hhs vs dkaPritom Das
Some slides are taken from different textbooks of medicine like Davidson, Kumar and Clark and Oxford, and some from other presentations made by respected tutors. I'm barely responsible for compilation of various resources per my interest. These resources are free for use, and I do not claim any copyright. Hoping knowledge remains free for all, forever.
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
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.
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.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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
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.
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- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
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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
Double trouble: Diabetic emergency with heart failure
1. Double trouble: managing diabetic
emergencies in patients with heart
failure
Dr.Rahatul Quadir
MD Thesis student
NHFRI
rahatul.quadir@gmail.com
2. Introduction
• Heart failure and diabetes frequently coexist
• Although the management of heart failure in patients with stable
glycaemia is relatively straightforward, the management of the two
conditions becomes difficult during diabetic ketoacidosis (DKA) or
hyperosmolar hyperglycaemic state (HHS).
• Recently, it has become apparent that the relationship between
heart failure and diabetes is more bidirectional in nature rather
than just diabetes leading to heart failure
3. Introduction
• One postulated theory is that the decreased physical activity in
heart failure patients may lead to decreased insulin sensitivity.
• Furthermore, neuro-humoral activation, including increased
catecholamine levels and sympathetic activity stimulate
gluconeogenesis and glycogenolysis leading to hyperglycaemia.
• Poor cardiac output and increased venous congestion can cause
hypoperfusion of the pancreas and the liver thereby weakening
their potential to regulate metabolic homeostasis
4. Management of hyperglycaemic
emergencies in patients with heart failure
• Diuretics and fluid restriction are essential components of heart failure
management while aggressive intravenous fluid replacement is indicated
in DKA and HHS
• If they have concomitant heart failure, managing these patients may well
pose many challenges:
1. managing haemodynamic compromise
2. fluid management
3. managing associated metabolic derangement such as kidney function,
associated acidaemia and base excess.
5. Management
• The mainstay of treatment of these diabetic emergencies is insulin,
fluids and electrolyte correction
• ideally, these patients should also be managed in a high-care setting
• There are no specific guidelines to date on specific management of
hyperglycaemic emergencies in heart failure although UK guidelines
suggest that ‘fluid replacement may need to be modified’.
6. History
• It is important to take a focused history from the patient or
their family
• Last HbA1c
• Latest Echo
• Previous admission history
• Last weight
• Current cardiac medication
• Fluid status
7. Examination
• Assessing volume status in these patients can be difficult.
• Heart failure patients can have peripheral oedema
• Patients are often intravascularly depleted during the
hyperglycaemic state while appearing peripherally
overloaded.
• Therefore care should be taken while examining and
interpreting volume status.
8. Look for
• JVP
• Extent of edema
• Lung congestion
• IVC size & collapsibility
• CVP
• Thirst & mucous membrane
• Mean arterial pressure
• Urine output
• Conscious level
• Capillary refill time
10. Specefic Mx:Fluid balance
• The average fluid deficit is approximately 5–7 litres in DKA but may be as
much as 22 litres in HHS
• Normal saline with potassium is the fluid of choice
• A more cautious approach of giving 1–1.5 litres of normal saline over 1–2
hours with frequent haemodynamic and clinical monitoring could be
attempted as initial resuscitation in patients with heart failure
• Fluid resuscitation should be tailored to patients’ clinical status and
response. If there are signs of worsening haemodynamics, then this might
warrant use of vasoactive drugs and escalation of treatment to a critical
care setting
11. Fluid balance
• In DKA, once glucose has fallen to target levels but where
ketones/ acidosis have not yet resolved, a 10% dextrose
infusion is usually commenced to prevent hypoglycaemia.
• In patients with heart failure where fluid overload is
becoming a worry, this can be substituted with 20% dextrose
to maintain glycaemic targets with only half of the volume
infused
12. Renal impairment
• It may be necessary to withhold some of the prognostic heart
failure medications such as ACE-i ,ARNI and MRAs and adjust
diuretics to aid patients’ recovery from the acute phase.
• Measuring urine output and recording daily weights.
13. Metabolic derangement
• Acidosis can be seen in HHS and DKA patients
• Withhold metformin
• Care be taken in correcting acidosis gently, if
hyperglycaemia is the primary cause of the acidosis
• Bicarbonate should not be given to correct the metabolic
derangement as it can worsen central nervous system
acidosis and precipitate cerebral oedema
14. Electrolyte imbalance
• Abnormalities in sodium and potassium are common
• low sodium with hyperglycaemia is real in order to preserve osmolality
• normal or high measured serum sodium in this setting indicates a severe
state of dehydration
• Renal impairment and heart failure medications such ACE-i, ARBs and
MRAs can cause hyperkalaemia.
• A low potassium level therefore suggests severe total body potassium
depletion
15. Thromboembolic state
• During the acute phase of a hyperglycaemic emergency, patients
are at risk of clot formation due to the associated hyper-viscosity of
blood.
• Therefore thromboembolism prophylaxis should be administered in
all patients unless there is a significant contraindication