Type 1 diabetes is characterized by low or absent insulin production. It is an autoimmune disease where the body's immune system attacks the beta cells in the pancreas that produce insulin. The main treatment is lifelong insulin therapy via injections or insulin pump to control blood glucose levels. Strict glucose monitoring and management of diet and activity is needed to prevent complications like diabetic ketoacidosis and maintain overall health. Sick day management may require increased insulin dosing and monitoring of blood glucose and ketone levels.
Diabetes mellitus (DM) has routinely been described as a metabolic disorder characterized by hyperglycemia that develops as a consequence of defects in insulin secretion, insulin action, or both.
Such a deficiency results in increased concentrations of glucose in the blood, which in turn damage many of the body's systems, in particular the blood vessels and nerves.
1. Microvascular (due to damage to small blood vessels).
2. Macrovascular (due to damage to larger blood vessels).
Controlling blood sugar (glucose) levels is the major goal of diabetes treatment, in order to prevent complications of the disease.
Type 1 diabetes is managed with insulin as well as dietary changes and exercise.
Type 2 diabetes may be managed with non-insulin medications, insulin, weight reduction, or dietary changes.
Medications for type 2 diabetes are designed to
increase insulin output by the pancreas,
decrease the amount of glucose released from the liver,
increase the sensitivity (response) of cells to insulin,
decrease the absorption of carbohydrates from the intestine, and
slow emptying of the stomach, thereby delaying nutrient digestion and absorption in the small intestine.
Diabetes mellitus (DM) has routinely been described as a metabolic disorder characterized by hyperglycemia that develops as a consequence of defects in insulin secretion, insulin action, or both.
Such a deficiency results in increased concentrations of glucose in the blood, which in turn damage many of the body's systems, in particular the blood vessels and nerves.
1. Microvascular (due to damage to small blood vessels).
2. Macrovascular (due to damage to larger blood vessels).
Controlling blood sugar (glucose) levels is the major goal of diabetes treatment, in order to prevent complications of the disease.
Type 1 diabetes is managed with insulin as well as dietary changes and exercise.
Type 2 diabetes may be managed with non-insulin medications, insulin, weight reduction, or dietary changes.
Medications for type 2 diabetes are designed to
increase insulin output by the pancreas,
decrease the amount of glucose released from the liver,
increase the sensitivity (response) of cells to insulin,
decrease the absorption of carbohydrates from the intestine, and
slow emptying of the stomach, thereby delaying nutrient digestion and absorption in the small intestine.
Diabetes mellitus -INTRODUCTION,TYPES OF DIABETES MELLITUSvarinder kumar
INTRODUCTION
TYPES OF DIABETES MELLITUS
DIAGNOSE TEST FOR DIABETES MELLITUS
MECHANISM OF ACTION OF INSULIN (IDDM)
HERBAL DRUG TREATMENT FOR DIABETES
LIFESTYLE FOR TYPE 1 AND TYPE 2 DM
NEW ANTI DIABETIC DRUGS
The Diabetic coma is one the most dangerous and again emergent case experienced during dental care delivery. Actually it mistreated and aggravated-diabetic cases resulting coma, that is categorized into Hypoglycemic coma, Diabetic ketoacidosis and Hyperosmolar coma.
For More Medicine Free PPT - http://playnever.blogspot.com/
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Diabetes mellitus -INTRODUCTION,TYPES OF DIABETES MELLITUSvarinder kumar
INTRODUCTION
TYPES OF DIABETES MELLITUS
DIAGNOSE TEST FOR DIABETES MELLITUS
MECHANISM OF ACTION OF INSULIN (IDDM)
HERBAL DRUG TREATMENT FOR DIABETES
LIFESTYLE FOR TYPE 1 AND TYPE 2 DM
NEW ANTI DIABETIC DRUGS
The Diabetic coma is one the most dangerous and again emergent case experienced during dental care delivery. Actually it mistreated and aggravated-diabetic cases resulting coma, that is categorized into Hypoglycemic coma, Diabetic ketoacidosis and Hyperosmolar coma.
For More Medicine Free PPT - http://playnever.blogspot.com/
For Health benefits and medicine videos Subscribe youtube channel - https://www.youtube.com/playlist?list=PLKg-H-sMh9G01zEg4YpndngXODW2bq92w
A review of the investigation and management of diabetic ketoacidosis in newly diagnosed type I diabetes. Patient details have been changed and anonymised to protect the identity of the individual.
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
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
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Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
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
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
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
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the 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 lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
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. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
2. DEFINITION
Metabolic disorder of multiple
etiologies characterized by chronic
hyperglycemia with disturbances of
carbohydrate, fat and protein
metabolism resulting from defects of
insulin secretion, insulin action or
both.
3. OLD CLASSIFICATION (1985)
Type 1, Insulin-dependent (IDDM)
Type 2, Non Insulin-dependent (NIDDM)
◦ obese
◦ non-obese
◦ MODY (between 18 to 25 years)
IGT
Gestational Diabetes Mellitus
4. New Classification (WHO)
Is based on etiology not on type of treatment
or age of the patient.
Type I(Beta cell destruction-absolute insulin
deficiency)
Immune mediated
Idiopathic
Type II
predominant insulin resistant with
relative insulin deficiency
predominant secretory defect with
insulin resistance
5. Other specific Types
Genetic defect of beta cell function
MODY (maturity onset diabetes of the young)
syndromes
mitochondrial mutions
Infections
Congenital rubella
CMV
Disease of pancreas
Pancreatitis
Trauma/pancreatectomy
Neoplasia
Cystic fibrosis
6. Endocrinopathies
Acromegaly
Cushing’s Syndrome
Pheochromocytoma
Drug or chemical induced
Nicotinic acid
Glucocorticoids
Thiazides
Genetic disorder with diabetes
Down syndrome
Turner syndrome
Klinefelter syndrome
Prader willi syndrome
Gestational Diabetes Mellitus
Neonatal Diabetes Mellitus
Other specific Types
7. Type 1 Diabetes Mellitus
Formerly called insulin-dependent
diabetes mellitus (IDDM) or juvenile
diabetes
T1DM is characterized by low or absent levels of
endogenously produced insulin
8. EPIDEMIOLOGY
• Most common endocrine disorder of
childhood and adolescence.
• The onset occurs predominantly in
childhood, with 2 peak one 5-7 yr, and
another at puberty but it may present at
any age.
• In india an average prevalence of Type I
diabetes is 10 per 100000 population.
9. Risk of development of Type 1 DM
If mother has Type1DM risk in child is
2%.
If father is affected risk is 7%.
In a sibling of the index case is
estimated as 6%.
Risk is 6-10% in diazygotic twins
& 30-65% in monozygotic twins
10. Pathogenesis & Natural
history
The natural history includes distinct
stages
1) Initiation of autoimmunity
2) Preclinical autoimmunity with
progressive loss of β-cell function
3) Onset of clinical disease
4) Transient remission( “Honeymoon
period”)
5) Established disease
6) Development of complications
11. Beta Cells: secrete
insulin.
The Pancreas
Alpha Cells: secrete
glucagon
Autoimmunity occurs in islet of Langerhans
against the beta cells...
12.
13.
14. CLINICAL PRESENTATIONS
DKA ( most common presentation
in pediatrics)
Classical symptom triad:
polyuria, polydipsia and weight loss
Accidental diagnosis
15. In symptomatic (polydipsia , polyurea,
weight loss) children a random plasma
glucose >11.1 mmol (200 mg) is
diagnostic.
Hemoglobin A1C >= 6.5 %
Remember: acute infections in young
non-diabetic children can cause
hyperglycemia without ketoacidosis.
DIAGNOSTIC CRITERIA
16. DIAGNOSTIC CRITERIA
Fasting blood glucose level
IGT (Impaired glucose
tolerance)
6.0-6.9 mmol (100-126
mg/dl)
Diabetic
>=7.0 mmol (126mg/dl)
2 hours after oral glucose
IGT (Impaired glucose
tolerance)
7.8-11.0 mmol (140-200
mg/dl)
Diabetic
>=11.1 mmol (200
mg/dl)
modified OGTT (oral glucose 1.75gm/kg max 75
gm) may be needed in
Asymptomatic children with
hyperglycemia (RBS >140)
Symptomatic with hyperglycemia
(RBS between 140 to 200)
17. TREATMENT ELEMENTS
Education
Insulin therapy
Glycemic control Monitoring
Diet and meal planning
Prevention and early dectection of
complication
18. EDUCATION
Educate child & care givers
about:
Diabetes type 1
life long Insulin therapy
self monitoring and maintaining records
Recognition of Hypoglycemia & DKA
Meal plan
Sick-day management
Possible long term complication
19. INSULIN Therapy
Insulin
A polypeptide made of 2 b-chains.
Discovered by Bants & Best in 1921.
Animal types (porcine & bovine) were used
before the introduction of human-like insulin
(DNA-recombinant types).
Recently more potent insulin analogs are
produced by changing aminoacid sequence.
20. Rapid-acting Insulin
Examples: insulin lispro or insulin aspart
Onset: Begins to work at about 5
minutes
Peaktime: Peak is about 1 hour
Duration: Continues to work for about
2-4 hours
21. Regular or Short-acting
Insulin
Examples: insulin regular
Onset: Reaches the bloodstream within
30 minutes after injection.
Peaktime: Peaks anywhere from 2-3
hours after injection.
Duration: Effective for approximately 3-
6 hours.
25. INSULIN CONCENTRATIONS
Insulin is available in different
concentrations 40, 80 & 100 Unit/ml.
WHO now recommends U 100/ml to be the
only used insulin to prevent confusion.
Special preparation for infusion pumps is
soluble insulin 500 U/ml.
26. Suggested target blood glucose
range
Time of checking Target plasma
glucose(mg/dl)
1 Fasting or preprandial 90-145
2 Postprandial 90-180
3 Bedtime 120-180
4 Nocturnal 80-162
For children<5 yrs of age 90-200mg/dl during the day time and
between 150-200mg/dl at bed time and during the night are
optimal
27. Key aspect of Insulin Therapy
Aim-To mimic natural pattern of insulin secretion
Administration- insulin is administered subcutaneously
using insulin syringes, pens, or insulin pumps.
Dose-
DKA/with overt symptoms:
-Total daily dose(TDD)-0.8 to1 unit/kg/day
Incidentally diagnosed: at lower dose
Toddlers & pre-school (2-5 yrs)-0.2-0.4unit/kg/day
Pre-pubertal children(5-9 yrs)-0.5-0.8 unit/kg/day
Adolescents-(9-14 yrs) 0.8-1.5unit/kg/day
28. Injection sites
• Anterolateral thighs
• Anterior and lateral
abdominal wall
• Posterior aspect of upper
arms
• Superolateral aspects of
buttocks.
(site rotation : following a
regular pattern of using the
different sites and different
areas within the same site
is important)
Key aspect of Insulin Therapy
29. Regimes-
Split mix regime ( mixtard 30:70 or NPH 2/3 +
Regular insulin 1/3; twice a daily)
2/3 dose-45 min BBF
1/3 dose-45 min BD
1 IU of Mixtard takes care of BS 50mg/dl above
target
Basal bolus regime with multiple daily
injection(MDI)
30-50% of Total daily dose as one dose- long
action (Glargine,Detemir)
3-4 doses of rapid insulin as remainder
Key aspect of Insulin Therapy
30. Calculation of Bolus Dose –
CIR (carbohydrate to insulin ratio)
- Amount of carohydrate in gram covered by one unit of
insulin
- Initial calculation-500/Total daily dose
more accurate estimation is based on
- amount of carbohydrate consumed in a meal
- units of insulin administered
- pre and post prandial blood glucose
ISF-insulin sensitivity factor
- Reduction in blood glucose by one unit of insulin
- Initial calculation as 1800/Total daily dose
- For correcting Pre meal high sugar (actual BS- Target
BS/ISF)
Key aspect of Insulin Therapy
31. Example for 10 yrs old 33 kg wt child
Total insulin requirement 0.8 IU * 33=26 IU
Carbohydrate to Insulin Ratio = 500/26=20
Insulin sensitivity factor = 1800/26 = 70
Inj Glargine 40% = 11 IU
If child is taking 80 gm carbohydrates in
lunch , insulin needed is 80/ CIR =4 IU
If pre lunch BS is 200 than to correct pre
lunch BS insulin needed is 200-130/ISF
= 1
So Inj lispro is given 5 IU before lunch.
Key aspect of Insulin Therapy
32. Insulin Pump Therapy
Continuous subcutaneous insulin infusion
(CSII) via battery-powered pumps provides
a closer approximation of normal plasma
insulin profiles.
It accurately deliver a small baseline
continuous infusion of insulin, coupled with
parameters for bolus therapy.
The bolus insulin determined by amount of
carbohydrate intake and blood sugar level
33.
34. Monitoring of glycemic control
Self monitoring of blood glucose(SMBG)
-fasting
-before and 2 hours after meals
-during night
Real time continuous glucose monitoring
Urinary Glucose
-Reflects glycemic level over the preceding
several hours
-It is positive if renal theshold is exceeded.
-Crude indicator of hyperglycemia
35. Measuring ketones in urine-More
sensitive and accurate
In-BG>250 mg/dl
Illness with fever and or vomiting
abdominal pain , polyurea,
drowsiness, rapid breathing
Glycosylated Hemoglobin (HbA1C)
- every 3-4 monthly
Monitoring of glycemic control
37. PRACTICAL PROBLEMS
Non-availability of insulin in poor countries
injection sites & technique
Insulin storage & transfer
Mixing insulin preparations
Insulin & school hours
Adjusting insulin dose at home
Sick-day management
Recognition & Rx of hypoglycemia at home
38. Management on Sick days
Insulin requirement may increase or
decrease during illness.
Fever, dehydration, and the stress of
illness can cause hyperglycemia due
to increase production of
counterregulatory hormones , whereas
vomiting and loss of appetite can lead
to hypoglycemia.
The risk of Ketosis is increased due to
starvation and dehydration.
39. Take plenty of fluids.
Blood glucose and urine ketones monitered
frequently.
“moderate” or “large” ketones in the urine in
the presence of hyperglycemia indicate
insulin deficiency and risk of DKA.
Child should be given rapid acting analog or
regular insulin and oral fluids and ketones
should be rechecked in the next urine.
If there is vomiting with hyperglycemia and
large ketones , or persistent hypoglycemia,
child should be taken to emergency
department.
Management on Sick days
40. Management on Sick days
URINE KETONE
STATUS
INSULI
N
CORRECTION DOSE COMMENT
Negative or small q2hr q2hr for glucose
>250mg/dl
Check ketones
every other void
Moderate to large q1hr q1hr for glucose >250
mg/dl
Check ketones
each void go to
hospital if emesis
occurs.
RBS 2hrly
INSULIN short acting (0.1u/kg) or if
RBS >250
41. DIET REGULATION
Regular meal plans with calorie exchange
options are encouraged.
50-60% of required energy to be obtained
from complex carbohydrates.
Distribute carbohydrate load evenly during
the day preferably 3 meals & 2 snacks with
avoidance of simple sugars.
Encouraged low salt, low saturated fats and
high fiber diet.
42. Avoid simple sugar
In patient with split mix regime-
6 meals-3 major(70% of total calories)
-3midmeal(30% of total calories)
In children with MDI(multiple dose
regime)
mid meal is not essential
majority of the calories should be
consumed as a part of the meals,
mid meal should have less than 10-15
gm of carbohydrate.
DIET REGULATION
43. Glycemic Index :
ranking of carbohydrates on a scale from 0 to 100
according to the extent to which they raise blood
sugar levels after eating.
Foods with a high GI are those which are rapidly
digested and absorbed and result in marked
fluctuations in blood sugar levels. Like corn flakes,
potato, watermelon, biscuits, chocolates
Low-GI foods, by virtue of their slow digestion and
absorption, produce gradual rises in blood sugar
and insulin levels, and have proven benefits
diabetics. Like Most fruits and vegetables (except
potato & water melon), pasta, pulses, milk, curd,
DIET REGULATION
44. EXERCISE
Decreases insulin requirement in
diabetic subjects by increasing both
sensitivity of muscle cells to insulin &
glucose utilization.
It can precipitate hypoglycemia in the
unprepared diabetic patient.
45. PITFALLS OF MANAGEMENT
Delayed diagnosis of IDDM
The honey-moon period
Problems with diagnosis & treatment
of DKA & hypoglycemia
Somogyi’s effect & dawn phenomenon
may go unrecognized.
46. Dawn Phenomenon
Blood glucose levels increase in early
morning hours before breakfast due to
decline in insulin levels. Which results
in elevated morning glucose.
This phenomenon mainly caused by
overnight growth hormone secretion and
increased insulin clearance.
It’s a normal physiologic process seen in
most adolescents without diabetes, who
compensate with more insulin output.
Child with TIDM cannot compensate.
47. Somogyi Phenomenon
It’s a theoretical rebound from late-
night or early morning hypoglycemia,
thought to be from an exaggerated
counter-regulatory response.
Continuous glucose monitoring
systems or night time blood glucose
may help clarify ambiguously elevated
morning glucose levels.
48. COMPLICATIONS OF DIABETES
Acute:
DKA
Hypoglycemia
Hyperosmolar Coma
Late-onset:
Retinopathy
Neuropathy
Nephropathy
Ischemic heart disease & stroke
49. Guidelines regarding monitoring
for complications
Parameter Recommendation
HbA1c 3-4 times per year
Height and Weight 3-4 times per year
Nutritional
counseling
At diagnosis, 4-6 weeks later
,then annually.
Lipid profile Prepubertal child :every 5 yr
Pubertal child: within 6-12
months after diagnosis, then
every 2 yrs.
Blood pressure Annually after age 10 yrs.
50. RETINOPATHY :
Screening - after 5 yr duration in prepubertal children
- after 2 yr in pubertal children
Frequency- 1-2 yearly
Method preferred- fundal photography
NEPHROPATHY:
Screening - after 5 yr duration in prepubertal children
- after 2 yr in pubertal children
Frequency- annually
Preferred method- spot urine sample for
albumin:creatinine ratio
Prevention and Early
detection of complication
51. NEUROPATHY:
Screening-unclear in children ; adults at
diagnosis in type 2 DM and 5yr after
diagnosis in type 1DM
Frequency- unclear
Method preferred-physical examination
MACROVASCULAR DISEASE:
Screening- after age 2 yrs
Frequency- every 5 yrs
Method preferred- lipid profile test
Prevention and Early
detection of complication
52. THYROID DISEASE
Screening- at diagnosis
Frequency- every 2-3 yr or more frequently
based on symptoms or the presence of
antithyroid antibodies.
Method preferred- TSH
CELIAC DISEASE:
Screening- at diagnosis
Frequency- every 2-3 yr
Method preferred- tissue transglutaminase
endomysial antibody.
Prevention and Early
detection of complication
54. Diabetic Ketoacidosis
DKA,a life threatning complication of
diabetes mellitus,occurs more
commonly in children with type 1 DM
than type 2 DM.
DKA in children is defined as
hypgerglycemia(serum glucose conc.
>200-300mg/dl) in the presence of
metabolic acidosis (blood pH<7.3 with
serum bicarbonate level<15 mEq/L)
and ketonemia(presence of ketones in
blood).
56. Classification of diabetic
ketoacidosis
NORMAL MILD MODERATE SEVERE
Co2 mEq/L
venous)
20-28 16-20 10-15 <10
pH 7.35-7.45 7.25-7.35 7.15-7.25 <7.15
clinical No change Oriented,
alert but
fatigued
Kussmaul
respirations;
oriented but
sleepy;
arousable
Kussmaul or
depressed
respirations;
sleepy to
depressed
sensorium to
coma
57. DIABETIC KETOACIDOSIS TREATMENT
PROTOCOL.
1ST hr 10-20 ml/kg IV bolus 0.9% NaCl
or LR
Insulin drip at 0.05 to 0.10
u/kg/hr
Quick volume expansion;may be
repeated.NPO.Monitor I/O,neurological
status.Usefloe sheet. Have Mannitol at
bedside;1 g/kg IV push for cerebral edema
2nd hr until
DKA resolution
0.45%NaCl:plus continue
Insulin drip
20 mEq/l Kphos and .5%
glucose if blood sugar <250
mg/dl
IV rate= 85 ml/kg+maintainence-
bolus/23hr
If K<3mEq/L,give 0.5 to 1 mEq/kg as oral K
solution OR increase IV K to 80 mEq/L
After
correction of
dehydration
and acidosis
Oral intake with subcutaneous
insulin
No emesis;CO2> 16 mEq/L;normal
electrolytes
TIME THERAPY COMMENTS
58. Transition to subcutaneous insulin
therapy
• As oral feeds advanced iv fluids reduced and change to
subcutaneous insulin planned.
• Timing-ideal time to begin is just before a meal.
• Rapid acting insulin(lispro,aspart) are administered sc
15-30 mins prior and regular insulin 1-2 hr prior to
stopping infusion to avoid rebound hyperglycemia.
• Dose-For pt with DKA at ds onset,recommended TDD
is 0.75-1 u/kg(pre pubertal) and 1-1.2 u/kg(pubertal).
• Before Breakfast-2/3 tdd(1/3 regular and 2/3 NPH
insulin)
• Before dinner-1/3 tdd(1/3 regular and 2/3 NPH insulin)
59. Cerebral Edema.
Management
•Head end elevation
•Give Mannitol 0.5-1 gm/kg and repeat if there is
no response in 30 mins-2hrs
•3% Hypertonic saline (5 ml/kg over 30 mins) can
be given
•Restrict iv fluids to 2/3
•Replace fluid deficit in 72 hr rather than 24 hr
•Intubation and ventilation if required
60. Non-Ketotic Hyperosmolar
Coma
Severe hyperglycemia(blood
glucose>800mg/dl), absence of or only slight
ketosis, nonketotic acidosis, severe
dehydration, depressed sensorium or frank
coma, and various neurological signs that
may include grand mal seizures,
hyperthermia,hemiparesis, and positive
babinski signs.
Respirations are usually shallow , but
coexistent metabolic acidosis may be
manifested by kussmaul breathing .
Serum osmolarity is commonly 350mOsm/kg
or greater. This condition is uncommon in
children.
61. Treatment of Nonketotic
Hyperosmolar coma
Rapid repletion of the vascular volume deficit and very
slow correction of the hyperosmolar state.
One half isotonic saline(0.45% NaCl) administered at a
rate estimated to replace 50% of the volume deficit in
the 1st 12hr,and remainder is administered in ensuing
24hr.
When blood glucose concentration approaches to
300mg/dl, the hydrating fluid should be changed to
5%dextrose in 0.2 normal saline.
Approximately 20mEq/L of potassium chloride should be
added to each of these fluids to prevent hypokalemia.
Insulin can be given by continuous intravenous infusion
beginning with the 2nd hr of fluid therapy. The IV insulin
dosage should be 0.05 units/kg/hr.
62. Hypoglycemia
Blood glucose <70mg/dl. Risk increases as
the duration of diabetes increases.
Mild to moderate symptoms- immediate oral
intake of 0.3 g/kg of glucose dissolved in
small amount of water, raises the blood
glucose value by 45-65 mg/dl. Blood glucose
is retested after 10-15 min. and glucose
readministered if the response is inadequate.
Chocolate, milk, sweets containing fat are not
a good choices as fat delays the absorption
of glucose. Treating it with child’s favourite
sweets or beverages should be avoided.
63. Severe hypoglycemia (altered mental
status, unconsciousness or seizures)-
glucagon is administered
subcutaneously or intramuscularly.
DOSE:
0.5 mg for <12yrs.
0.1 mg for>12 yrs.
(if glucagon injections are not available
glucose gel, honey can be administered
into buccal pouch.)
64. Nelson textbook of paediatrics 20 Edition
Harrison’s Textbook of Internal Medicine
Case based reviews of paediatric endocrinology
National Diabetes Fact Sheet 2003, DEPARTMENT OF HEALTH
AND HUMAN SERVICES Centres for Disease Control and
Prevention
World Health Organization. Definition, Diagnosis and Classification
of Diabetes Mellitus and its Complications. Report of WHO.
Department of Non-communicable Disease Surveillance. Geneva
1999
References
67. Pancreas & Islet Cell Transplantation
Pancreas transplants are usually given
to diabetics with end stage renal
disease.
Islet cell transplants, the ultimate
treatment of type 1 diabetes is under
trial in many centers in the US &
Europe with encouraging results but
graft rejection & recurrence of
autoimmunity are serious limitations.
68. IMMUNE MODULATION
Immunosuppressive therapy for
Newly diagnosed
Prolonged the honey moon
For high risk children
Immune modulating drugs
Nicotinamide
mycophenolate
69. GENE THERAPY
Blocks the immunologic attack against
islet-cells by DNA-plasmids encoding
self antigen.
Gene encode cytokine inhibitors.
Modifying gene expressed islet-cell
antigens like GAD.
70. PREDICTION OF DIABETES
Sensitive & specific immunologic
markers
GAD Antibodies
GLIMA antibodies
IA-2 antibodies
For single antibody risk is 2-6 %
Two antibodies ; risk is 21-40 %
more than 2 antibodies risk is 59-80 %
71. PREVENTION OF DIABETES
Primary prevention
• Identification of diabetes gene
• Tampering with the immune system
• Elimination of environmental factor
Secondary prevention
• Immunosuppressive therapy(cyclosporin,
GLP-1 agonist)
Tertiary prevention
• Tight metabolic control & good monitoring