This document discusses diabetic ketoacidosis (DKA), providing information on its pathophysiology, classification, precipitating factors, signs and symptoms, laboratory investigations, management, and goals of treatment. It classifies DKA as mild, moderate or severe based on plasma glucose, arterial pH, serum bicarbonate, urine ketones, and anion gap. The key aspects of management include fluid resuscitation to restore intravascular volume, insulin therapy to reduce glucose and ketone levels, and potassium supplementation to correct deficiencies. Bicarbonate supplementation is only recommended if the pH is less than 6.9.
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)
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)
to download this presentation from this link
https://mohmmed-ink.blogspot.com/2020/11/diabetic-ketoacidosis.html
Diabetic Ketoacidosis, diabetus type 1 complection. diagnosisi and managment
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 (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.
to download this presentation from this link
https://mohmmed-ink.blogspot.com/2020/11/diabetic-ketoacidosis.html
Diabetic Ketoacidosis, diabetus type 1 complection. diagnosisi and managment
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 (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.
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of 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 leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
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. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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.
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
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.
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
- 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 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
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.
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.
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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.
3. A&E(VINAYAKA)
IntroductionIntroduction
• Acute life threatening complication of DM
• DKA predominantly seen in type 1 DM
• DKA represents body’s response to cellular
starvation due to insulin deficiency & counter
regulatory hormone excess
7. A&E(VINAYAKA)
• Facilitate uptake
of glucose &
conversion into
glycogen
• Inhibits
glycogenolysis &
gluconeogenesis
• Increase
lipogenesis
• Inhibit
lipolysis
• Uptake of
amino acids into
muscle cell
• Prevents release
of amino acids
from muscle
8. A&E(VINAYAKA)
Pathophysiology
Insulin Deficiency is the primary defect in
patients with DKA
Muscle Hepatocyte Adipose
Glucose
Amino
Acids
Glucose-P
Glycogen
Pyruvate, CO2
Glucose
Free
fatty
acidsKetoacids
Normal Insulin Activity
20. A&E(VINAYAKA)
Clinical featuresClinical features
• Increased PGI2 and PGE2peripheral
vasodilation ,nausea, vomiting and abdominal
pain.
• Vomiting maladaptive response to counter
acidosis exacerbates the potassium losses
21. A&E(VINAYAKA)
Signs of DKASigns of DKA
• Dehydration
• Hyperventilation
• Ketotic breath
• Tachycardia and hypotension
• Disturbed conscious state and shock
• Alteration of consciousness correlate better with
elevated serum osmolality (>320 mOsm/L) than with
severity of metabolic acidosis
33. A&E(VINAYAKA)
Approach to therapyApproach to therapy
• Correcting the hyperosmolar state and
dehydration is the initial aim of therapy.
• Insulin therapy should be undertaken only
after the patient is stable hemodynamically.
Glucose and H2O
H2O lost in urine Loss of ECF, vascular collapse and death
34. A&E(VINAYAKA)
Fluid ResuscitationFluid Resuscitation
• Single most important step
• Fluid deficit around 100ml/kg (5-10L)
• Helps in Restore I/V volume
• Perfuse vital organs
• Increase GFR
• Decrease serum Glucose & Ketone levels
• To restore normal tonicity
35. A&E(VINAYAKA)
Fluid balance in diabeticFluid balance in diabetic
hyperosmolarityhyperosmolarity
ECF = 14 L ICF = 28 L
H2O
ECF ICF
H2O
Osmotic Diuresis
Osmotic Diuresis ECF hyperosmolar from ICF autotransfusion
ECF and ICF both hyperosmolar
38. A&E(VINAYAKA)
Fluid ResuscitationFluid Resuscitation
• 2–3 L of 0.9% saline over first 1–3 h (10–15
mL/kg per hour)
• 0.45% saline at 150–300 mL/h; change to 5%
glucose and 0.45% saline at 100–200 mL/h
when plasma glucose reaches 250 mg/dl.
41. A&E(VINAYAKA)
Insulin therapyInsulin therapy
• Ideal way to administer insulin by continuous
infusion of small doses of regular insulin
0.1unit/kg/hr once hypokalemia is excluded.
• I/M or S/C administration of regular insulin
should be avoided as insulin absorption may be
erratic in volume depleted & vasocostricted
patient
42. A&E(VINAYAKA)
Insulin therapyInsulin therapy
• Goal is to decrease Glucose by 50-75mg/dl/hr.50-75mg/dl/hr.
• Infusion should continue until anion gap normalized
• S/C insulin should bridge for atleast one hour before
discontinuation of I/V insulin
• Insulin administration should be W/H if K <3.3 mEq
till K is supplemented
43. A&E(VINAYAKA)
DKA: Switch to S.C. insulinDKA: Switch to S.C. insulin
Can consider switch to SC insulin when:
• AG normalized
• BS < 250 mg/dl
• Insulin IV requirements < 2U/h
• Patient able to eat
• Hemodynamically stable
44. A&E(VINAYAKA)
DKA: Switch to S.C. insulinDKA: Switch to S.C. insulin
• Overlap insulin IV with 1st
SC insulin by 2-4h
to avoid recurrent ketosis
• T2 DM patients with DKA:
• Don’t necessarily have to be continued on
insulin
• Once acute stress resolved, many do well on
OHA
47. A&E(VINAYAKA)
Goal of K ReplacementGoal of K Replacement
• To maintain a normal extracellular K+
conc during
the acute phase of therapy and to replace intra-
cellular deficits over a period of days
48. A&E(VINAYAKA)
K SupplementationK Supplementation
Serum Potassium < 3 mEq/L Give 60mEq/l to IVF
3-3.9 mEq/L 40mEq/l to IVF
4-5.4 mEq/L 20 mEq/L to IVF
> 5.5 mEq/L No Replacement necessary
Verify Normal kidney function &
Urine output before treatment
50. A&E(VINAYAKA)
ADA RecommendationADA Recommendation
If PH 6.9-7.0 50mEq of NaHCo3+200ml sterile
water+10mEq KCl over 1 hour
If Ph <6.9 100mEq of NaHCo3+400ml sterile
water+10mEq KCl over 2 hours
Repeat dose of bicarb every 2 hours till PH>7
51. A&E(VINAYAKA)
Theoretical AdvantagesTheoretical Advantages
• In case of severe acidosis
• Improve myocardial contractility
• Improve catecholamine tissue response
• Decrease work of breathing
• In case of Hyperkalemia
• Elevate ventricular fibrillation threshold
65. A&E(VINAYAKA)
Correction of acidosisCorrection of acidosis
Don’t use bicarbonate as
• It will increase chances of cerebral edema
by 4 times.
• can lead to volume overload,
hypernatremia, paradoxical cerebral
acidosis, accelerated K+
loss
Is there any role for bicarbonate in DKA?
66. A&E(VINAYAKA)
Indication for bicarbonateIndication for bicarbonate
• pH < 7.0
• Hemodynamically unstable
• Not responding to fluids
• Depressed cardiac contractilty
• Poor perfusion
Dose: 0.5 – 2 mEq/kg over 1-2 hrs
Stop correction once pH >7.0
67. A&E(VINAYAKA)
Major complication of DKAMajor complication of DKA
• Cerebral Edema: most dreaded complication
• 57-87% of all pediatric DKA-associated
deaths
• More in < 5yrs Rare in > 20 yrs.
68. A&E(VINAYAKA)
Reasons for Cerebral EdemaReasons for Cerebral Edema
• Over aggressive fluid correction
• Failure of Na+
to rise with fall of glucose
during treatment
• Cerebral ischemia due to severe dehydration
and hypocarbia
Onset : 6-12 hrs. after onset of therapy
72. A&E(VINAYAKA)
IntroductionIntroduction
• A metabolic emergency that occurs in
diabetic patient usually Type 2 Diabetes
Mellitus
• Characterised by uncontrolled hyperglycemia
that induces hyperosmolar state and
dehydration without significant ketoacidosis.
73. A&E(VINAYAKA)
Diagnostic featuresDiagnostic features
• Plasma glucose level of 600 mg/dL or greater
• Effective serum osmolality of 320 mOsm/kg
or greater
• Profound dehydration (8-12 L) with elevated
serum urea nitrogen (BUN)-to-creatinine ratio
79. A&E(VINAYAKA)
Clinical features
• Severe dehydration invariable
• May have associated lactic acidosis due to
hypoxia
• Precipitating factors similar to DKA
• Mortality rate is high
81. A&E(VINAYAKA)
SymptomsSymptoms
A wide variety of focal and global neurologic
changes may be present :
• Drowsiness and lethargy
• Delirium
• Coma
• Focal or generalized seizures
• Visual changes or disturbances
• Hemiparesis
• Sensory deficits