A 39-year-old male with a history of diabetes presented with abdominal pain, vomiting, lethargy, and dehydration. On examination, he had diffuse abdominal tenderness but no guarding or rigidity, and normal bowel sounds. He had been non-compliant with his insulin regimen. The most likely diagnosis is diabetic ketoacidosis.
A 62-year-old male diabetic presented with fever, right upper quadrant pain, and tachycardia. CT showed findings consistent with emphysematous cholecystitis.
A 42-year-old male diabetic with poor glucose control presented with facial asymmetry and was found to have right facial nerve palsy, suggesting an
CHRONIC DYSPEPSIA
Seminar Prepared by :-
Ali Abdulazeem
Shilan Adnan Abdulrahman
Alaa Shamil
Guldan Hameed
Internal Medicine
College of Medicine - University of Kirkuk
this was the first lecture which i delivered as a doctor. it was about dyslipidemia. i hope you will find information valuable to you here. please read. let me know about your ideas. comment.
CHRONIC DYSPEPSIA
Seminar Prepared by :-
Ali Abdulazeem
Shilan Adnan Abdulrahman
Alaa Shamil
Guldan Hameed
Internal Medicine
College of Medicine - University of Kirkuk
this was the first lecture which i delivered as a doctor. it was about dyslipidemia. i hope you will find information valuable to you here. please read. let me know about your ideas. comment.
This presentation is based on JBDS and BSPDE guidelines in adult and Paediatric DKA management. A comparison of adult vs paediatric management is included.
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
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
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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.
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
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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.
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.
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
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
- 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
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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
2. Questions
• A 39 year old Male patient presented to you in emergency
department for Acute Abdomen with H/O
vomiting,Restlessness,Lethargy,dehydration.On palpation of
abdomen diffuse tenderness+,no guarding/rigidity.On
Auscultation Bowel sounds heard. On eliciting History you
detect the patient is a known diabetic and is on insulin and
because of frequent travelling he is poorly complaint with
insulin.Your first probable diagnosis
a)Acute cholecystitis
b)Perforative peritonitis
c)Diabetic Ketoacidosis
d)Intestinal Obstruction
3. Questions
• A 62 yr old Diabetic Male presented to the Emergency with H/O fever,Right
Hypochondrial Pain,tachycardia for 2 days.CT abdomen done image is shown
below
The possible diagnosis
a)Emphysematous nephritis
b)Emphysematous cholecystitis
c)Perforative peritonitis
d)Alcoholic pancreatitis
4. Questions
• A 42 yr old Male known Diabetic for past 11 years with HbA1C 10.0
referred from an ENT surgeon to you the physician as a case of chronic
otorrhea,otalgia with hearing loss and now presenting with facial
asymmetry a provisional diagnosis of Rt. Facial N. palsy is made. You
suspect an infective pathology.The Probable organism could be
a)Streptococcus pneumonia
b)Hemophilus influenza
c)Pseudomonas aeruginosa
d)Clostridium perfringens
5. Questions
• A 54 yr old lady who is a diabetic for 12 years brought with h/o orbital cellulitis,6th
Nerve palsy and anosmia presenting with the following clinical picture
the Drug of choice for this patient?
a)Piperacillin Tazobactem
b)Amphotericin B
c)Mitomycin C
d)Actinomycin D
6. • Diabetic ketoacidosis
• Non ketotic hyperglycemic hyperosmolar
coma
• Hypoglycaemia & Hypoglycaemic coma
• Infections
7. Hyperglycemia
Ketosis
Acidosis
*
Definition of Diabetic Ketoacidosis
7
DKA is defined as the presence of all three of
the following:
(i) Hyperglycemia (glucose >250 mg/dL)
(ii) Ketosis,
(iii) Acidemia (pH <7.3).
Williams textbook of endocrinology 10th edition
8. Role of Insulin
• Required for transport of glucose into:
– Muscle
– Adipose
– Liver
• Inhibits lipolysis
• Absence of insulin
– Glucose accumulates
in the blood.
– Uses amino acids
for gluconeogenesis
– Converts fatty acids into ketone bodies :
Acetone, Acetoacetate, β-hydroxybutyrate.
12. Diabetic Ketoacidosis
PRECIPITATING EVENTS
Infection(Pneumonia / UTI / Gastroenteritis / Sepsis)
Inadequate insulin administration
Infarction(cerebral, coronary, mesenteric, peripheral)
Drugs (cocaine)
Pregnancy.
Harrison’s Principle of internal medicine 18th edition p2977
13. DIAGNOSIS LAB INVESTIGATIONS
Complete blood count
Serum ketones/ Urine ketones and sugar
Calculate serum osmolality and anion gap
Urinalysis and urine culture
Consider blood culture
Consider chest radiograph
Acid-base assessment
Williams textbook of endocrinology 10th edition
14. TREATMENT OF DKA
Initial hospital management
– Replace fluid and electrolytes
– IV Insulin therapy
– Watch for complications
– Treat causes
Once resolved
– Convert to home insulin regimen
– Prevent recurrence
TYPICAL BODY DEFICIT OF WATER AND ELECTROLYTES
15. FLUIDS
FLUID RESUSCITATION IS A CRITICAL PART OF
TREATING PATIENTS WITH DKA.
Intravenous solutions replace extravascular and
intravascular fluids and electrolyte losses.
They also dilute both the glucose level and the levels of
circulating counterregulatory hormones.
Fluid it self leads to correction of acidosis to some
extent
Insulin is needed to help switch from a catabolic state
to an anabolic state, with uptake of glucose in tissues
and the reduction of gluconeogenesis as well as free
fatty acid and ketone production
16. FLUID REPLACEMENT
Administer NS as indicated to maintain hemodynamic status, then follow general guidelines:
NS for first 4 hr.
Consider half NS thereafter.
Change to D5 half NS when blood glucose ≤250 mg/dL.
Williams textbook of endocrinology 10th edition
Hours Volume
1st half-hour to 1 hour 1 L
2nd hr 1 L
3rd hr 500 mL– 1 L
4th hr 500 mL– 1 L
5th hr 500 mL– 1 L
Total 1st 5 hr 3.5 - 5 L
6th–12th hr 250– 500 mL/hr
May need to adjust type and rate of fluid administration in the elderly and in patients with
congestive heart failure or renal failure.
17. INSULIN MANAGEMENT
Regular insulin 10 U i.v. stat (for adults) or 0.15 U/kg i.v. stat.
Start regular insulin infusion 0.1 U/kg per hour or 5 U per hour.
Increase insulin by 1 U per hour every 1–2 hr if less than 10% decrease in
glucose or no improvement in acid-base status.
Decrease insulin by 1–2 U per hour (0.05–0.1 U/kg per hour) when glucose
≤250 mg/dL and/or progressive improvement in clinical status with decrease
in glucose of >75 mg/dL per hour.
Do not decrease insulin infusion to <1 U per hour.
Williams textbook of endocrinology 10th edition
18. INSULIN MANAGEMENT CONTD…
Maintain glucose between 140 and 180 mg/dL.
If blood sugar decreases to <80 mg/dL, stop insulin infusion for no more than
1 hr and restart infusion.
If glucose drops consistently to <100 mg/dL, change i.v. fluids to D10 to
maintain blood glucose between 140 and 180 mg/dL.
Once patient is able to eat, consider change to s.c. insulin:
Overlap short-acting insulin s.c. and continue i.v. infusion for 1–2 hr.
For patients with previous insulin dose: return to prior dose of insulin.
For patients with newly diagnosed diabetes: full-dose s.c. insulin based on 0.6
U/kg per day.
Williams textbook of endocrinology 10th edition
19. POTASSIUM REPLACEMENT
Do not administer potassium if serum potassium >5.5 mEq/L or patient is anuric.
Use KCl but alternate with KPO4 if there is severe phosphate depletion and patient is unable to
take phosphate by mouth.
Add i.v. potassium to each liter of fluid administered unless contraindicated.
Williams textbook of endocrinology 10th edition p 454
Serum K (mEq/L) Additional K required
3.5 - 4.0 - 40mEq/L
3.5–4.5 - 20mEq/L
4.5–5.5 - 10mEq/L
>5.5 - Stop K infusion
22. BICARBONATE
• Clinical trials do not support the routine use of bicarbonate replacement
• HCO3 replacement and rapid reversal of acidosis can impair cardiac function, reduce tissue
oxygenation and promote hypokalemia and hypocalcemia.
• However in presence of severe acidosis pH<6.9,in hemodynamic instability with pH<7.1 and
hyperkaemia with ecg finding bicarbonate therapy considered
• In the presence of severe acidosis (arterial pH <6.9), the ADA advises bicarbonate [50 mmol/L
(meq/L) of sodium bicarbonate in 200 mL of sterile water with 10 meq/L KCl per hour for 2 h
until the pH is >7.0].
Williams textbook of endocrinology 10th edition p456
23. TREATMENT OF DKA
GLUCOSE ADMINISTRATION
Plasma glucose reaches 250 mg/dl in DKA or 300
mg/dl in HHS,
Decrease the insulin infusion rate to 0.05–0.1
unit/kg/h (3–6 units/h),
Add dextrose (5–10%) to the intravenous fluids.
Maintain the above glucose values until acidosis in
DKA or mental obtundation and hyperosmolarity in
HHS are resolved
Williams textbook of endocrinology 10th edition p 455
24. Criteria for resolution of DKA
glucose <200 mg/dl,
serum bicarbonate ≥18 mEq/l, and
venous pH of >7.3.
Once DKA is resolved, if the patient is NPO,
continue intravenous insulin and fluid
replacement and supplement with
subcutaneous regular insulin as needed every
4 h.
25. ONCE DKA RESOLVED…
• Most patients require 0.5-0.6 units/kg/day
• highly insulin resistant patients
– 0.8-1.0 units/kg/day
• Give subcutaneous insulin at least 2 hours prior to weaning insulin
infusion.
Williams textbook of endocrinology 10th edition p455
26.
27. CLINICAL ERRORS
Fluid shift and shock
Giving insulin without sufficient fluids
Using hypertonic glucose solutions
Hyperkalemia
Premature potassium administration before insulin has begun to
act
Hypokalemia
Failure to administer potassium once levels falling
Recurrent ketoacidosis
Premature discontinuation of insulin and fluid when ketones still
present
Hypoglycemia
Insufficient glucose administration.
28. Hyperglycemic-Hyperosmolar State (HHS)
HNC is a syndrome characterized by impaired
consciousness, sometimes accompanied by
seizures, extreme dehydration, , and extreme
hyperglycemia that is not accompanied by
ketoacidosis.
30. Physical examination
1. Severe dehydration is invariably present.
2. Various neurologic deficits (such as coma, transient
hemiparesis, hyperreflexia, and generalized areflexia) are
commonly present. Altered states of consciousness from
lethargy to coma are observed.
3. Findings associated with coexisting medical problems
(e.g., renal disease, cardiovascular disease) may be
evident.
31. Laboratory findings
1. Extreme hyperglycemia (blood glucose levels from 30 mmoll/l and
over are common.
2. A markedly elevated serum osmolality is present, usually in excess
of 350 mOsm/l. (Normal = 290 mOsm)
3. Serum ketones are usually not detectable, and patients are not
acidic.
4. Serum sodium may be high (if severe degree of dehydration is
present), normal, or high
5. Serum potassium levels may be high (secondary to the effects of
hyperosmolality) Low or normal
32. Treatment
This condition is a medical emergency and the patient
should be placed in an intensive care unit.
Many of the management techniques recommended for a
patient with DKA are applicable here as well.
The goals of therapy include:
• rehydration;
• reduction of hyperglycemia;
• electrolytes replacement;
• investigation of precipitating factors, treatment of
complications.
33. Hypoglycemia
It is a syndrome characterized by symptoms of
sympathetic nervous system stimulation or
central nervous system dysfunction that are
provoked by an abnormally low plasma
glucose level and it can occur at any time.
34. Precipitating factors
• irregular ingestion of food;
• extreme activity;
• alcohol ingestion;
• drug interaction;
• liver or renal disease;
• hypopituitarism and adrenal insufficiency.
37. Pathophysiology of hypoglycaemia
Inhibition of
endogenous
insulin secretion
Counter-
regulatory
hormone
release
• Glucagon
• Adrenaline
Onset of
symptoms
• Autonomic
• Neuroglycopa
enic
Neurophysiologic
al dysfunction
• Evoked
responses
Widespread
EEG
changes
Cognitive
dysfunction
• Inability to
perform
complex
tasksSevere
neuroglycop
aenia
• Reduced
level of
consciosn
ess
• Convulsio
ns
• Coma
83 mg/dL
58–50 mg/dL
68 mg/dL
54–43 mg/dL 54 mg/dL 50 mg/dL
<27 mg/dL
Arterialisedvenousbloodglucoseconcentration
(mmol/L)
2.
0
3.
0
4.
0
1.
0
0
5.
0
Cryer et al. Diabetes Care 2003;26:1902–12
EEG, electroencephalogram
38. Physical examination
1. The skin is cold, moist.
2. Hyperreflexia can be elicited.
3. Hypoglycemic coma is commonly associated
with abnormally low body temperature
4. Patient may be unconscious.
39. Treatment
• The most effective treatment of an insulin reaction is the immediate
ingestion of a concentrated carbohydrate source, such as sugar, honey,
candy, or orange juice.
• Alternative methods for increasing blood glucose may be required when
the person having the reaction is unconscious or unable to swallow:
– Glucagon may be given intramuscularly or subcutaneously.
– In situations of severe or life-threatening hypoglycemia, it may be
necessary to administer glucose intravenously.
40. • BG = 40 mg%: Give
(100-40) x 0.8 = 60 x
0.8= 48 ml of IV 25%
Dextrose.
• Repeat BG q 15 mins
until BG > 70mg%.
Example • If BG < 70mg% : 25% dextrose as per
calculation. Check BG q15 mins
• If BG > 70mg% : Check BG q30 mins till
BG > 90mg%
• If BG > 90mg% : Check BG q1hrly, Hold
Infusion
• If BG > 140mg%: Restart infusion at 50%
of previous rate
BG ≤70 – Suspend Insulin, Give 25% Dextrose (100-BG) X 0.8**
41. Infections
Complement:
some studies have detected a deficiency of the C4 component in DM,this reduction of C4 is
probably associated with polymorphonuclear dysfunction and reduced cytokine response
Polymorphonuclear and mononuclear leukocytes:
Decreased mobilization of polymorphonuclear leukocytes, chemotaxis, and phagocytic activity
may occur during hyperglycemia.
hyperglycemic environment inhibits glucose-6-phosphate dehydrogenase (G6PD), increasing
apoptosis of polymorphonuclear leukocytes, and reducing polymorphonuclear leukocyte
transmigration
In tissues that do not need insulin for glucose transport, the increased intracellular glucose levels
are then metabolized, using NADPH as a cofactor and the low NADPH prevents the regeneration
of molecules that play a key role in antioxidant mechanisms of the cell, thereby increasing the
susceptibility to oxidative stress.
the glycated hemoglobin (HbA1c) is <8.0%, to maintain the proliferative function of CD4 T
lymphocytes and their response to antigens.
42. Infections• Respiratory infections
Streptococcus pneumoniae and influenza virus
• Tuberculosis
• Urinary infections
• Bacterial pyelonephritis
E.Coli & Proteus
• Emphysematous pyelonephritis
E.Coli & Proteus followed by enterobacter.
• Emphysematous cystitis
The most frequent pathogen is E. coli, followed by Enterobacter, Proteus, Klebsiella,
and Candida
• Perinephric abscess
gram-negative bacilli (predominantly E. coli) or polymicrobial infection
• Emphysematous cholecystitis
The emphysematous cholecystitis is more frequent in males with DM.The main
pathogens are Salmonella enteritidis and Campylobacter
• Invasive external otitis
Invasive external otitis is an infection of the external auditory canal that can extend to
the skull base and adjacent regions.It often affects elderly diabetic individuals and the
etiologic agent is usually Pseudomonas aeruginosa
43. Questions
• A 39 year old Male patient presented to you in emergency
department for Acute Abdomen with H/O
vomiting,Restlessness,Lethargy,dehydration.On palpation of
abdomen diffuse tenderness+,no guarding/rigidity.On
Auscultation Bowel sounds heard. On eliciting History you
detect the patient is a known diabetic and is on insulin and
because of frequent travelling he is poorly complaint with
insulin.Your first probable diagnosis
a)Acute cholecystitis
b)Perforative peritonitis
c)Diabetic Ketoacidosis
d)Intestinal Obstruction
44. Questions
• A 62 yr old Diabetic Male presented to the Emergency with H/O fever,Right
Hypochondrial Pain,tachycardia for 2 days.CT abdomen done image is shown
below
The possible diagnosis
a)Emphysematous nephritis
b)Emphysematous cholecystitis
c)Perforative peritonitis
d)Alcoholic pancreatitis
45. Questions
• A 42 yr old Male known Diabetic for past 11 years with HbA1C 10.0
referred from an ENT surgeon to you the physician as a case of chronic
otorrhea,otalgia with hearing loss and now presenting with facial
asymmetry a provisional diagnosis of Rt. Facial N. palsy is made. You
suspect an infective pathology.The Probable organism could be
a)Streptococcus pneumonia
b)Hemophilus influenza
c)Pseudomonas aeruginosa
d)Clostridium perfringens
46. Questions
• A 54 yr old lady who is a diabetic for 12 years brought with h/o orbital cellulitis,6th
Nerve palsy and anosmia presenting with the following clinical picture
the Drug of choice for this patient?
a)Piperacillin Tazobactem
b)Amphotericin B
c)Mitomycin C
d)Actinomycin D