This document summarizes guidelines for treatment of diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) from the American Diabetes Association (ADA) and Joint British Diabetes Societies Inpatient (JBDS IP). Key points include:
1) Bedside beta-hydroxybutyrate testing is now the best way to monitor treatment response in DKA.
2) For DKA, guidelines recommend fixed rate insulin infusion of 0.1 unit/kg/hr without a priming dose and adjustments to meet metabolic targets.
3) For HHS, the goal of initial therapy is to expand intravascular volume and restore perfusion by replacing approximately 50
Diabetic ketoacidosis (DKA) is a state of absolute or relative insulin deficiency aggravated by ensuing hyperglycaemia, dehydration, and acidosis producing derangements in intermediary metabolism.
Diabetic ketoacidosis (DKA) is a state of absolute or relative insulin deficiency aggravated by ensuing hyperglycaemia, dehydration, and acidosis producing derangements in intermediary metabolism.
This presentation is based on JBDS and BSPDE guidelines in adult and Paediatric DKA management. A comparison of adult vs paediatric management is included.
How to manage status epilepticus, what drugs should be used and when to use what to avoid and need to know
everything you should have about status epilepticus is here.
This presentation is based on JBDS and BSPDE guidelines in adult and Paediatric DKA management. A comparison of adult vs paediatric management is included.
How to manage status epilepticus, what drugs should be used and when to use what to avoid and need to know
everything you should have about status epilepticus is here.
This presentation was present by my friend during emergency posting seminar with Dr.Mohd. Kamal Mohd. Arshad. I upload this ppt here for all of us and my own reference too. Good luck in your life.
Dr Abdullah Ansari
PG-2 (Medicine)
AMU ALIGARH
A general approach to periodic paralysis....
(including hypokalemic periodic paralysis and thyrotoxic periodic paralysis, and other “Channelopathies” or “Membranopathies)
Pathophysiology
Epidemiology
Primary or familial periodic paralysis
Secondary periodic paralysis
Conventional classification of periodic paralysis
Classification of primary periodic paralysis based on ion-channel abnormalities
Clinical approach to a case of periodic paralysis
History of muscle weakness
Age of onset
Family history
Timing
Intensity
History of administration of certain drugs
Clinical examination
Differential Diagnosis
Laboratory investigations
Serum K+
CPK and serum myoglobin
ECG
EMG
Nerve conduction studies
Provocative Testing
Muscle biopsy
Treatment
Prognosis
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 is the fifth lecture. it is based on guidelines by NHS UK. the guidelines based are freely available in internet. the source and the used literature are trusted and accurate. i hope this level of a knowledge about the management side of the DKA touches the all areas of patient survival. patho-physiology not discussed here but will be discussed in another lecture in details. to a intern and final year MBBS students or ERPM students must process a level of knowledge described by the lecture. definitely more you read more knowledge you get. get the idea in the lecture and principles of management. so you will be much accurate in a ward. always take superior advice while managing emergencies.
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
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
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
- 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
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
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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
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
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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
2. • Thyroid storm
• Myxedema coma
• Thyrotoxic periodic paralysis
• Hyperglycemic crisis
• Severe hypoglycemia
• Hypercalcemia
• Hypocalcemia
Somchodok Chakreeyarat, MD.
Endocrine Unit, Department of Medicine
Bhumibol Adulyadej Hospital
• Adrenal insufficiency
3.
4.
5.
6.
7. Hypokalemic periodic paralysis Thyrotoxic periodic paralysis
Age at onset First or second decade > 20 years
Attack frequency Infrequent Infrequent
Attack duration Hours to days Hours to days
Precipitants Exercise, CHO load, stress Exercise, CHO load, stress
K+ level during attack Low Low
Associated features Later onset myopathy Symptoms of thyrotoxicosis
Low TSH, high FT4 or FT3
Etiology AD inherited defect in calcium or
sodium ion channel on muscle
membrane
Thyrotoxicosis
Possible inherited predisposition
Penetrance Nonpenetrance common, esp in
woman
Epidemiology M > F M > F, high incidence in Asians
Preventive treatment Carbonic anhydrase inhibitors
K+ sparing diuretics
Euthyroid state
Propanolol
10. Occurs in early morning or late evening
Prodromal symptoms: muscle aches, cramps, muscle stiffness
Begins in proximal muscle of the lower extremities
progress to flaccid quadriplegia
Symmetrical, spared bulbar, respiratory and ocular muscle
Serum K+ ↓, but not always during attack
Spontaneous resolution within a few hours to 2 days
“Thyrotoxic myopathy” persistent muscle weakness, soreness
and normokalemia
TPP can occur with any causes of hyperthyroidism
11. ECG finding
- Sinus tachycardia or sinus arrhythmia
- First degree AV block
- LVH pattern
Electrolytes and biochemistry in blood and urine
- Hypo K+ with low urine excretion rate
- Relatively normal blood acid-base balance
- Hypo PO4 with low urine PO4 excretion
- Normal or increased serum calcium with hypercalciuria
- Hypocreatinemia ( increased GFR )
Therapeutic course
- Lower K+ dose to achieve recovery
- Rebound hyperkalemia if high K+ dose is given
13. Aim
- To raise serum K+ rather than to fill a large K+ deficit
- For the treatment of paralysis and prevention of fatal cardiac
arrhythmia
Close cardiac monitoring is absolutely warranted
Exogenous KCl administration rebound hyperkalemia
Total KCl dose given less than 50 mEq, ↓ risk of rebound
hyperkalemia
KCl should be given at the rate of no more than 10 mEq/hr
14. Nonselective beta blockers
Parenteral KCl might be given in saline instead of glucose
solution
Avoid oral route of KCl administration if bowel sounds are absent
or diminished
“ Hypokalemia-induced pseudointestinal obstruction”
“Paradoxical hypokalemia” , a further fall in plasma K+
concentration during KCl therapy, associated with more severe
hyperthyroidism and hyperadrenergic activity
The maximum dose of KCl should be kept at 20-40 mEq/hr in
case of ventricular arrhythmia or impending respiratory failure
15. Mechanism
- To block K+ uptake via Na-K-ATPase
Oral propanolol 3-4 mg/kg/day
Shorten the duration of attack and promote recovery in TPP
16. Life-threatening arrhythmia or
respiratory failure?
NO YES
Standart IV KCl infusion
≤ 10 mEq/hr
Rapid IV KCl infusion
20-40 mEq/hr, then ≤ 10 mEq/hr
Paradoxical hypokalemia
after KCl infusion
NO YES
Worsening hypokalemia and
life-threatening arrhythmia
YES
Keep the rate and stop KCl
Infusion when muscle strength
Increased
Consider IV or oral non-selective
beta blocker
Recover from paralysis
Chronic treatment for the
underlying hyperthyroidism
TPP
NO
18. Most patients with TPP do not manifest typical
symptoms and signs related to hyperthyroidism
• Lab tests and ECG may help establish the diagnosis of TPP
• In acute therapy, the dose of KCl should be minimal to
rebound hyperkalemia, except in case of ventricular
arrhythmia or impending respiratory insufficiency
• High-dose non-selective beta blockers may be used to
terminate muscle paralysis , esp for those who developed
paradoxical hypokalemia
27. Joint British Diabetes Society Inpatient (JBDS IP);2013
recommend :
- Rapid near-patient technology 3-beta-hydroxybutyrate
(BHB, ßHBA))
28. DKA
• To improve circulatory
volume and tissue
perfusion
• Decrease blood glucose
• Correct the acidosis
and electrolyte
imbalances
HHS
• To gradually and safely
normalize the
osmolarity
• Replace fluid and
electrolyte loss
• Normalize blood
glucose
Other goals include prevention of :
• Arterial or venous thrombosis
• Other potential complications e.g.
cerebral oedema/ central pontine
myelinolysis
• Foot ulceration
29. ADA 2009
• Blood glucose > 250 mg/dL
• Ketonemia
• Metabolic acidosis (pH ≤ 7.3)
or serum HCO3 < 18 mEq/L
JBDS IP 2013
• BHB > 3 mmol/L or Urine
ketone ≥ 2+ on standard
urine sticks
• Blood glucose > 200 mg/dL or
known DM
• Venous or arterial HCO3 < 15
mEq/L and/or pH < 7.3
31. 1. Bedsides ketone (BHB) testing now represents the best
practice in monitoring the response to treatment
2. Fixed Rate Insulin Infusion (FRII) with short acting or
rapid acting insulin 0.1 unit/kg/hr should be used with
an infusion pump
3. Do not use a priming (bolus) dose of insulin
32. 4. Adjusted insulin dose if the metabolic target are not met
- Reduction of blood ketone(BHB) at least 0.5
mmol/L/hour
- Increase in venous HCO3 at least 3 mEq/L/hour
- Reduction in CBG at least 50 mg/dL/hour
5. Increase insulin infusion rate by 1.0 unit/hr increments
hourly until the ketones are falling at target rates
6. Measure venous blood gas for pH,HCO3, and K+ at 60
min, and then q 2 hr
33. The difference between venous and arterial pH is
0.02- 0.15 pH units
The difference between arterial and venous bicarbonate
is 1.88 mmol/L
It is not necessary to use arterial blood to measure acid
base status
34. Fluid Volume
1 L 0.9% NaCl 1,000 mL over first hour
1 L 0.9% NaCl with KCl 1,000 mL over next 2 hr
1 L 0.9% NaCl with KCl 1,000 mL over next 2 hr
1 L 0.9% NaCl with KCl 1,000 mL over next 4 hr
1 L 0.9% NaCl with KCl 1,000 mL over next 4 hr
1 L 0.9% NaCl with KCl 1,000 mL over next 6 hr
* A slower infusion rate should be considered in young adults
35. K+ Level in first 24 hr
(mEq/L)
K+ Replacement in mEq/L
of infusion solution
> 5.5 Nil
3.5-5.5 40 mEq/L
< 3.5 Senior review
36. DKA : Criteria for diagnosis and Resolution
ADA 2009 JBDS IP 2013
Diagnosis • Blood glucose > 250 mg/dL
• Ketonemia
• Metabolic acidosis(pH ≤ 7.3)
or serum HCO3 < 18 mEq/L
• BHB > 3 mmol/L or
Urine ketone ≥ 2+ on
standard urine sticks
• Blood glucose > 200 mg/dL
or known DM
• Venous or arterial HCO3
< 15 mEq/L and/or
pH < 7.3
Resolution • Venous pH > 7.3
• Serum bicarbonate ≥ 15
mEq/l
• Blood glucose < 200 mg/dl
• Calculated anion gap ≤12
mEq/l
• Venous pH > 7.3
• Bicarbonate > 15 mEq/L
• BHB level < 0.6 mmol/L
(rather than < 0.3 mmol/L)
37. DKA : Insulin (RI or RAA) and IV fluid
ADA 2009 JBDS IP 2013
Start
insulin
• 0.1 unit/kg IV bolus
• 0.1 unit/kg/hr CII
• No bolus
• 0.1 unit/kg/hr CII
Adjust
insulin
Bolus 0.14 unit/kg if
• serum glucose < 10%/hr
Increase insulin infusion
rate by 1.0 unit/hr If
• BHB < 0.5 mmol/L/hr
• Venous HCO3 < 3
mEq/L/hour
• CBG < 50 mg/dL/hour
IV fluid • Change IV to 5% glucose
if glucose < 200 mg/dL
• Add 10% glucose if
glucose < 250 mg/dL
38.
39. Characteristic features of a person with HHS:
• High osmolality, often 320 mosmol/kg or more
• High blood glucose, usually 30 mmol/L
• •
(540 mg/dL) or more
• Severely dehydrated and unwell
41. General rules
1. The goal of initial therapy is to expand the intra- and
extravascular volume and to restore peripheral
perfusion
2. An optimal rate of decline in serum sodium of 0.5
mEq/L/hr has been recommended for hypernatremic
dehydration and not fall exceed 10-12 mEq/L/day
3. If BHB > 1 mmol/L = hypoinsuilinemia start insulin
If BHB is not present insulin should not be started
42. Is
4. Insulin treatment prior to adequate fluid
replacement may result in cardiovascular collapse
5. The recommended insulin dose is an FRII given at
0.05 units/kg/hr . A fall of glucose at a rate of up to
90 mg/dL/hr is ideal
6. Avoid hypoglycemia. Target blood glucose is 180-270
mg/dL in the first 24 hr
7. If blood glucose < 180 mg/dL commence 5% or 10%
dextrose at 125 mL/hr with NSS
43. The target:
The aim of treatment should be to replace
approximately 50% of estimated fluid loss within the
first 12 Hours
The remainder in the following 12 hours
A target blood glucose of between 180 and 270 mg/dL
Complete normalisation of electrolytes and osmolality
may take up to 72 hours.
44. HHS : Criteria for diagnosis and Resolution
ADA 2009 JBDS IP 2013
Diagnosis • Blood glucose >600
mg/dL
• Effective serum
osmolarity ≥320
mosm/kg
• High osmolality, often
320 mosm/kg or more
• High blood glucose,
usually 30 mmol/L
(540 mg/dL) or more
• Severely dehydrated
and unwell
Resolution • Normal osmolality
• Regain of normal
mental status
• Normal osmolality
• Regain of normal
mental status
45. HHS : Insulin (RI or RAA) and IV fluid
ADA 2009 JBDS IP 2012
Start
insulin
• 0.1 unit/kg IV bolus
• 0.1 unit/kg/hr CII
• No bolus
• 0.05 unit/kg/hr CII if
BHB > 1 mmo/L or
serum glucose < 90
mg/dL after adequate
fluid resuscitation
Adjust
insulin
Bolus 0.14 unit/kg if
• serum glucose < 10%/hr
• Increase insulin
infusion rate by 1.0
unit/hr if not achieve
target
IV fluid • Change IV to 5% glucose
if glucose < 300 mg/dL
• Add 5% or 10% glucose
if glucose < 180 mg/dL
47. Tetany, seizures, laryngospasm, or cardiac dysfunction
with proven or strong suspicion of low calcium
10-20 mL of 10% calcium gluconate in 50-100 mL 5% dextrose
(or 0.9% saline) given over 10 min with EKG monitoring
Repeat above treatment until symptom-free
• Treat hypomagnesemia (if present) with IV magnesium
sulfate
Start IV infusion of 100 mL of 10% calcium gluconate in 1 L of
normal (0.9%) saline (or 5% dextrose) at a rate of 50-100 mL/hr
Adjust rate to normalize calcium
Start oral calcium and potent vitamin D
(eg, calcitriol or alfacalcidol)
• Investigate the underlying cause (if not known) and treat