The document outlines the agenda and content for a class on the endocrine system and diabetes mellitus. The class will review the hypothalamic-pituitary control of hormones, hypo- and hyper- functions of endocrine glands, the anatomy and physiology of the endocrine pancreas, classifications of diabetes, and the pathophysiology and clinical manifestations of type 1 and type 2 diabetes. Key differences between type 1 and type 2 diabetes will also be discussed.
SIGNIFICANCE
OVERVIEW
WHAT IS DIABETES?
DEFINITION
MECHANISM
PREVELANCE
EPIDEMIOLOGY
CLASSIFICATION
GESTATIONAL DIABETES
RISK FACTORS
DIAGNOSIS
COMPLICATIONS
MEDICAL TEST
MEDICAL NUTRITIONAL THERAPY
HERBS FOR DIABETES
MYTHS AND FACTS
REFERENCES
diagnosis & complication of Diabetes mellitus including Diabetic ketoacidosis & HHS
anaesthesia managment for patient with DM posted for surgery both emergency and elective surgery
gestational diabetes mellitus
SIGNIFICANCE
OVERVIEW
WHAT IS DIABETES?
DEFINITION
MECHANISM
PREVELANCE
EPIDEMIOLOGY
CLASSIFICATION
GESTATIONAL DIABETES
RISK FACTORS
DIAGNOSIS
COMPLICATIONS
MEDICAL TEST
MEDICAL NUTRITIONAL THERAPY
HERBS FOR DIABETES
MYTHS AND FACTS
REFERENCES
diagnosis & complication of Diabetes mellitus including Diabetic ketoacidosis & HHS
anaesthesia managment for patient with DM posted for surgery both emergency and elective surgery
gestational diabetes mellitus
DIABETES MELLITUS Definition :It is a clinical syndrome characterized by hyperglycemia due to absolute or relative deficiency of insulin.
Type 1 Diabetes :
Charactarized by an absolute deficiency of insulin secretion caused by pancreatic beta cell destruction usually resulting from auto immune attack
Type 2 Diabetes :
Caused by relative insulin deficiency due to combination of peripheral resistance to insulin action and an inadequate compensatory response to insulin secretion by pancreatic beta cells.
Introduction
pancreas
Pathology of insulin
Pathogenesis of DM
What is diabetes mellitus
Types of diabetes mellitus
Evaluation of plasma glucose levels
Clinical features of DM
Complications of DM
Treatment
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.
DIABETES MELLITUS Definition :It is a clinical syndrome characterized by hyperglycemia due to absolute or relative deficiency of insulin.
Type 1 Diabetes :
Charactarized by an absolute deficiency of insulin secretion caused by pancreatic beta cell destruction usually resulting from auto immune attack
Type 2 Diabetes :
Caused by relative insulin deficiency due to combination of peripheral resistance to insulin action and an inadequate compensatory response to insulin secretion by pancreatic beta cells.
Introduction
pancreas
Pathology of insulin
Pathogenesis of DM
What is diabetes mellitus
Types of diabetes mellitus
Evaluation of plasma glucose levels
Clinical features of DM
Complications of DM
Treatment
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.
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http://sandymillin.wordpress.com/iateflwebinar2024
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June 3, 2024 Anti-Semitism Letter Sent to MIT President Kornbluth and MIT Cor...Levi Shapiro
Letter from the Congress of the United States regarding Anti-Semitism sent June 3rd to MIT President Sally Kornbluth, MIT Corp Chair, Mark Gorenberg
Dear Dr. Kornbluth and Mr. Gorenberg,
The US House of Representatives is deeply concerned by ongoing and pervasive acts of antisemitic
harassment and intimidation at the Massachusetts Institute of Technology (MIT). Failing to act decisively to ensure a safe learning environment for all students would be a grave dereliction of your responsibilities as President of MIT and Chair of the MIT Corporation.
This Congress will not stand idly by and allow an environment hostile to Jewish students to persist. The House believes that your institution is in violation of Title VI of the Civil Rights Act, and the inability or
unwillingness to rectify this violation through action requires accountability.
Postsecondary education is a unique opportunity for students to learn and have their ideas and beliefs challenged. However, universities receiving hundreds of millions of federal funds annually have denied
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The House of Representatives will not countenance the use of federal funds to indoctrinate students into hateful, antisemitic, anti-American supporters of terrorism. Investigations into campus antisemitism by the Committee on Education and the Workforce and the Committee on Ways and Means have been expanded into a Congress-wide probe across all relevant jurisdictions to address this national crisis. The undersigned Committees will conduct oversight into the use of federal funds at MIT and its learning environment under authorities granted to each Committee.
• The Committee on Education and the Workforce has been investigating your institution since December 7, 2023. The Committee has broad jurisdiction over postsecondary education, including its compliance with Title VI of the Civil Rights Act, campus safety concerns over disruptions to the learning environment, and the awarding of federal student aid under the Higher Education Act.
• The Committee on Oversight and Accountability is investigating the sources of funding and other support flowing to groups espousing pro-Hamas propaganda and engaged in antisemitic harassment and intimidation of students. The Committee on Oversight and Accountability is the principal oversight committee of the US House of Representatives and has broad authority to investigate “any matter” at “any time” under House Rule X.
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Intro to Endocrine Disorder Unit-II.ppt
1. Hakim Shah
RN, BSN, MSN, PhD (Scholar)
September 06 & 07, 2022
1
Required Reading Book:
Carol, Porth M. (2014). Pathophysiology concept of altered health states (9th Ed). Philadelphia: J. B. Lippincott
Chaper-48 (Page# 1264), Chapet-50 (Page# 1303)
2. Class Agenda
Review the hypothalamic pituitary control
mechanism of hormone secretions in the body.
Differentiate between hypo & hyper function of
the endocrine glands.
Review of Anatomy & Physiology of endocrine
pancreas.
Briefly discuss the classification of diabetes
mellitus (DM)
Discuss etiology, pathophysiology, and clinical
manifestations of Type-1 DM & Type-2 DM.
Identify the main differences between Type-1 &
Type-2 DM.
2
3. Review of Endocrine System
Gland of Endocrine system
Hypothalamus
Posterior Pituitary
Anterior Pituitary
Thyroid Gland
Parathyroid Gland
Adrenals
Pancreatic islets
Ovaries and testes
3
7. Hypothalamus
Releasing and inhibiting hormones
Corticotropin-releasing hormone
Thyrotropin-releasing hormone
Growth hormone-releasing hormone
Gonadotropin-releasing hormone
Somatostatin-inhibiting hormone that
inhibits GH and TSH
7
8. Anterior Pituitary
Growth Hormone
Stimulates growth
Adrenocorticotropic hormone
Stimulates glucocorticoid and Mineralocorticoid
Thyroid stimulating hormone
Stimulate releasing of T3 & T4
Follicle stimulating hormone
Stimulates ovary in female, sperm in males
8
9. Cont…
Luteinizing hormone:
Stimulates corpus luteum in females, secretion of
testosterone in males
Prolactin:
prepares female breasts for lactation
9
10. Posterior Pituitary
Antidiuretic Hormone
Causes reabsorption of water and sodium from
the collecting tubule of kidney thus decrease urine
output.
Oxytocin
Causes contraction of uterus, and milk ejection
from breasts
10
11. Adrenal Cortex
Mineralocorticoid—aldosterone. Affects sodium
absorption, loss of potassium by kidney
Glucocorticoids (Cortisol). Affects metabolism,
regulates blood sugar levels, affects growth,
anti-inflammatory action, decreases effects of
stress
Adrenal androgens—dehydroepiandrosterone
and androstenedione. Converted to
testosterone in the periphery.
11
13. Thyroid
Follicular cells—excretion of triiodothyronine
(T3) and thyroxine (T4) that Increase BMR,
increase bone and calcium turnover, increase
response to catecholamines, need for fetal
growth & development
Thyroid C cells—calcitonin. Lowers blood
calcium and phosphate levels
13
15. Pancreatic Islet cells (Islets of
Langerhans)
B- Cells
Secrete Insulin: Insulin stores glucose in liver and
muscle as glycogen. Metabolize glucose in the cells
A-Cells
Secrete Glucagon: Glucagon Stimulates
glycogenolysis and glyconeogenesis
D-Cells
Secrete Somatostatin: Somatosatin
decreases intestinal absorption of
glucose
15
16. Physiology of Glucose Metabolism
Blood Glucose
Normal serum level glucose 65 – 105 mg/dl
Inside CNS
Brain uses glucose as primary fuel
Brain cannot store/produce glucose
Outside CNS
Fatty acids converted to glucose and stored as
Glycogen (liver/muscles)
Triglycerides (fat cells)
16
17. Regulation of Glucose
Blood Glucose level is regulated by two Hormones:
Insulin and Glucagon
Endocrine portion of pancreas has group of cells
called ‘Islets of Langerhans’ which contains Beta
Cell & Alpha Cells
Beta cells make insulin
Allows body cells to store and use
carbohydrate, fats, and protein
Alpha cells make glucagon
“counterregulatory”, acts opposite of insulin
17
18. Function of Insulin
When blood glucose becomes high ,insulin
lowers glucose level in the following methods:
Liver
Helps in production and storage of glucose in the
form of glycogen
Inhibits glycogen breakdown
Increased protein & fat synthesis (VLDL
formation)
Muscles
Promotes protein and glycogen synthesis
Fat cells
Promotes storage of triglycerides
18
19. Function of Glucagon
Glucagon causes release of glucose from
liver
“Glycogenolysis (breakdown of glycogen
to glucose)
“Glyconeogenesis (formation of glucose) if
glucose not available
Lipolysis (breakdown of fat)
Proteolysis (breakdown of amino acids)
19
20. Diabetes Mellitus
A group of diseases characterized by high levels of blood
glucose resulting from defects in insulin production,
insulin action, or both which result in impaired
metabolism of carbohydrates, fats and protein
20
21. Prevalence of DM
Estimated 7% of US population is diabetic
Twice that many have prediabetes
21% of those over 60 have diabetes
45% of new diagnoses are being made in
children and adolescents
21
22. Types of Diabetes Mellitus
Type 1 Diabetes
Cells that produce insulin
are destroyed
Results in insulin
dependence
Commonly detected
before 30
10% diabetes is type I
Type 2 Diabetes
Blood glucose levels rise due to
Lack of insulin production
Insufficient insulin action (resistant
cells)
Commonly detected after 40
> 90% diabetes is type II
This type eventually leads to β-
cell failure (resulting in insulin
dependence)
Gestational Diabetes
3-5% of pregnant women in the world develop gestational diabetes
22
24. Pathophysiology of Diabetes II
Decresed level of circulatory insulin
Impaired metabolism of glucose
Decreased production of insulin by beta cells or increased
Insulin demand
Destruction or resistance of insulin receptors
24
25. Risk factor/Causes of Type I
Autoimmune: Destruction of beta cell by
antibodies
Destruction of beta cells by virus
Genetic factors
25
26. Risk Factors/Causes of Type II
Predisposing Factors:
Obesity (80%)
Heredity
Hypertension
Sedentary life style: lack of excersice
Consistent High caloric diet intake
Stress
High cholestrol level
26
27. Clinical Manifestation
3 P’s
Polyuria
Polydipsia
Polyphagia
Fatigue, tingling or numbness in hands, slow
healing wounds and recurrent infections
27
28. Diagnosi
s
Fasting Plasma Glucose Test
(FPG) –cheap & fast
Fasting B.G.L. 100-125 mg/dl
signals pre-diabetes
>126 mg/dl signals diabetes
Oral Glucose Tolerance Test
(OGTT)
Tested for 2 hrs after glucose-
rich drink
140-199 mg/dl signals pre-
diabetes
>200 mg/dl signals diabetes
Glycated Hemoglobin (A1C) tests
For people without diabetes, the normal range for the hemoglobin
A1c level is between 4% and 5.6%. Hemoglobin A1c levels
between 5.7% and 6.4% indicates prediabetes and a higher chance
of getting diabetes. Levels of 6.5% or higher signals diabetes.
28
31. Cont…
Fasting plasma glucose—125 mg/dL
Random sugar >200mg/dL
According to text, OGTT and IV glucose tolerance
test no longer used routinely—see latest
guidelines
31
32. Complications
Acute Complications
Hyperglycemia
Diabetic Keto Acidosis (DKA) occurs in Type 1 DM
Hyperglycemic Hyperosmolar Non-ketotic Syndrome
(HHNK): Occurs in Type II DM
Hypoglycemia
Ussoally occurs in Type I due to insulin reaction, and rarely
in Type II due to increased intake of hypoglycemic drug
Chronic Complications
32
33. Hyperglycemia
A condition in which fasting blood glucose (FBS)
is greater than 125mg/dl, and Random Blood
Sugar (RBS) is greater than 200mg/dl
33
34. Clinical manifestation of
Hyperglycemia
Drowsiness, flushed face, increased thirst, blurred
vision
Polyuria
Sodium, chloride, potassium excreted
Electrolyte and fluid imbalance
Polydipsia from dehydration
Polyphagia: cells are starving, so person feels
hungry despite eating huge amounts of food.
Starvation state remains until insulin is available.
34
35. Diabetic Ketoacidosis (DKA)
Causes:
Three main causes are:
Illness,
Undiagnosed DM
Untreated DM, and decreased insulin
Other causes: patient error, intentional skipping of
insulin.
35
36. Manifestation of DKA
3 P’s
Orthostatic hypotension
Ketosis
GI s/s: N/V, diarrhea, abdomen pain
Acetone breath
Hyperventilation (Kuassmal breathing)
Dehydration and electrolyte loss
36
37. Diagnosis of DKA
BS between 300-800
Acidosis
Electrolyte abnormalities
Elevated BUN, creatinine and hematocrit related
to dehydration
37
38. Management
Rehydrate with normal saline, then follow with
.45% NaCl then D5.45NS (or other)
Restore electrolytes
ECGs
Hourly blood sugars
IV insulin
Avoid bicarbonate as can affect serum K+
38
39. Nursing management
Nursing Diagnosis
Body fluid and electrolytes imbalance R/L excessive
loss through GI (diarrhea, N/V)
Ineffective breathing pattern i.e hypoventilation R/L
increased acidity of blood
Altered thought process R/L increased blood sugar
level
39
41. Hyperosmolar Hyperglycemic Non
Ketosis Syndrome (HHNS)
Predominated by hyperosmolarity and
hyperglycemia
Minimal ketosis
Osmotic diuresis
Glycosuria and increased osmolarity
Occurs over time
Blood sugar is usually over 600
41
42. Cont…
Occurs more often in older people
Type 2 diabetes mellitus
No ketosis
Do not usually have the concomitant n/v
Hyperglycemia, dehydration and hyperosmolarity
may be more severe than in DKA
42
43. Medical Management
Similar treatment as seen in DKA
Watch fluid resuscitation if history of heart failure
ECG
Electrolytes monitoring
Fluids with potassium replacement
43
46. Chronic complications of DM are grouped in to the
following categories.
• Vascular disease
1. Macrovascularopathy
– Coronary artery diseases (CAD)
– Hypertension
– Stroke
2. Microvascularopathy
– Retinopathy
– Nephropathy
• Neuropathy
• Diabetic Foot problems (Due to both Vascular and
neuropathy)
46
47. Vascular Disease
• Macro vascular Disease: Thickening of the arteries-
Arthrosclerosis which leads to coronary artery disease
(CAD), Hypertension and heart failure.
• Micro vascular disease: Thickening of the capillary
basement membrane that surrounds
the endothelial cells of the capillary, increased capillary
permeability and capillary occlusion
• Affects the areterioles, venules, & capillaries of eye,
kidney and other organs. Examples are Retinopathy &
Nephropathy
47
48. Diabetic Retinopathy
• Leading cause of blindness in the United
States
• Characterized by deterioration of the small
blood vessels in the retina
• After 10 years of having diabetes 50% of all
diabetics have it and 90% of those who have
poor control of blood glucose levels 48
49. Diabetic Nephropathy
• Occurs in patients with Type 1 diabetes after
15 -20 years (30% to 40% progress to end -
stage renal disease)
• Occurs after 5 to 10 years with Type 2
diabetics
• Deterioration of kidney function takes place
over many years - first sign is protein in the
urine
49
50. Manifestations of Nephropathy
• Frequent urinary tract infections and
incontinence
• Sexual - Impotence in men and inability to
have an orgasm
• Characterized by proteinuria,
hypertension,edema and renal insufficiency
50
51. Nephrotic Syndrome
• Nephrotic syndrome is diagnosed when
protein excreted exceeds 3.5 g/d.
• When protein is lost in the urine, the serum
protein also decreases.
• Low serum protein causes decreased oncotic
pressure and retention of fluid that leads to:
– Weight gain
– Edema
– Protein tissue wasting
51
52. Diabetic Neuropathy
• Occurs in 70% of diabetic patients
• Prevalence increases with age and severity of
hyperglycemia
• Results in loss of large and small myelin nerve
fibers, connective tissue proliferation and
thickening of the capillary basement
membrane
52
53. Cont..
• Can have mononeuropathy such as carpal
tunnel syndrome, extraocular motor paralysis
& foot-drop
• Most patients have numbness, tingling,
burning, dull ache & cramping that begins in
the digits & progresses to the foot and hand
(worse at night)
53
54. Cont…
• progresses to muscle weakness & sensory
loss, an unbalanced gait, foot ulcers and loss
of fine motor skills.
• Sensory neuropathy leads to loss of pain &
pressure sensation & increases the risk of
undetected injury, tissue ischemia or
infection
54
55. • Insulin ( Type 1 DM)
• Excersice
• Nutrition
• Medicine
• Insulin (in some cases in Type 2 DM)
55
56. 1.Sources: standard practice is use of human
insulin prepared by alteration of pork insulin
or recombinant DNA therapy
2. Clients who need insulin as therapy:
a. All type-1 diabetics since their bodies
essentially no longer produce insulin
56
57. Cont…
b. Some Type 2 diabetics, if oral medications are not
adequate for control (both oral medications and insulin
may be needed)
c. Diabetics enduring stressor situations such as
surgery, corticosteroid therapy, infections, treatment
for DKA, HHNS
d. Women with gestational diabetes who are not
adequately controlled with diet
e. Some clients receiving high caloric feedings including
tube feedings or parenteral nutrition
57
63. Cont…
• Alternative insulin administration
– Insulin pump
• Continuous subcutaneous infusion of a basal dose with
increases at meal times
– Implanted pumps
• Implanted into the peritoneal cavity
– Inhaled insulin
• Under developme
63
66. 1. Used to treat Diabetes Type 2
2. Client must also maintain prescribed diet and
exercise program; monitor blood glucose
levels
Not used with pregnant or lactating women
66
67. Cont…
4. Several different oral hypoglycemic agents
and insulin may be prescribed for the client
5. Specific drug interactions may affect the
blood glucose levels
6. Must have some functioning beta cells
67
68. Classifications and Action of
Hypoglycemic drugs
a.Sulfonylureas
Action: Stimulates pancreatic cells to secrete
more insulin and increases sensitivity of
peripheral tissues to insulin
Indication: to treat non-obese Type 2 diabetics
Example: Glipizide (Glucotrol),
Chlorpropamide (Diabinese), Tolazamide
(Tolinase)
68
69. b. Meglitinides
Action: stimulates pancreatic cells to secret
more insulin
Indication: Used in non-obese diabetics
Side effects: Taken just before meals, rapid
onset, limited duration of action. Major
adverse effects is hypoglycemia
Example: Repaglinide (Prandin), Nateglinide
(Starlix)
69
70. c. Biguanides
Action: decreases overproduction of glucose by
liver and makes insulin more effective in
peripheral tissues
Indication: Used in obese diabetics. Does not
stimulate insulin release
Contraindication: Metabolized by the kidney, do
not use with renal patients
Example: Metformin (Glucophage)
70
71. d. Alpha-glucoside Inhibitors
Action: Slow carbohydrate digestion and delay
rate of glucose absorption
• Take with first bite of the meal or 15 min.
after
• Adjunct to diet to decrease blood glucose
levels
Example: Acarbose (Precose), Miglitol (Glyset)
71
72. e. Thizaolidinediones (Glitazones)
Action: Sensitizes peripheral tissues to insulin
Indication: Used in obese diabetics
• Inhibits glucose production
• Improves sensitivity to insulin in muscle, and
fat tissue
Example: Rosiglitazone (Avandia), Pioglitazone
(Actos)
72
73. • Patients with Type 2 DM who are obese have
insulin resistance, they produce enough
insulin
– Should use Glucophage, Actos or Avandia
– Enhances insulin secretion in tissue, but does not
increase amount of insulin secreted
73
74. A.Goals for diabetic therapy include
1.Maintain as near-normal blood glucose levels
as possible with balance of food with
medications
2.Obtain optimal serum lipid levels
3.Provide adequate calories to attain or
maintain reasonable weight
74
75. Diet Composition
1. Carbohydrates: 60 – 70% of daily diet
– Carbohydrates convert quickly to sugars
• Advice patient to consume a similar amount of carbs at
each meal
• Medications can work on a consistent glucose response
from foods
2. Protein: 15 – 20% of daily diet
3. Fats: 10% of daily diet
– No more than 10% of total calories from saturated fats
75
76. • Fiber: 20 to 35 grams/day; promotes
intestinal motility and gives feeling of fullness
• 5. Sodium: recommended intake 1000 mg
per 1000 kcal
• 6. Sweeteners approved by FDA instead of
refined sugars
• 7. Limited use of alcohol: potential
hypoglycemic effect of insulin and oral
hypoglycemics
76
77. A. Assessment, planning, implementation
with client according to type and stage of
diabetes
B. Prevention, assessment and
treatment of complications through
client self-management and keeping
appointments for medical care
77
78. Cont…
C.Client and family teaching for diabetes
management
D.Health promotion includes education of
healthy life style, lowering risks for developing
diabetes for all clients
E.Blood glucose screening at 3 year intervals
starting at age 45 for persons in high risk
groups
78
79. Common Nursing Diagnoses and
Specific Teaching Interventions
A. Risk for impaired skin integrity: Proper
foot care
1.Daily inspection of feet
2.Checking temperature of any water before
washing feet
3.Need for lubricating cream after drying but not
between toes
4. Patients should be followed by a podiatrist
5. Early reporting of any wounds or blisters
79
80. Cont…
B.Risk for infection
1.Frequent hand washing
2.Early recognition of signs of infection and seeking
treatment
3.Meticulous skin care
4.Regular dental examinations and consistent oral
hygiene care
80
81. Cont…
C. Risk for injury: Prevention of accidents, falls
and burns
D. Sexual dysfunction
1.Effects of high blood sugar on sexual functioning,
2.Resources for treatment of impotence, sexual
dysfunction
E.Ineffective coping
1.Assisting clients with problem-solving strategies
for specific concerns
81
82. Cont…
2.Providing information about diabetic
resources, community education programs,
and support groups
3.Utilizing any client contact as opportunity to
review coping status and reinforce proper
diabetes management and complication
prevention
82
83. References
Brunner & Suddarth (2008). Text book of Medical-Surgical
Nursing (10th Ed). Lippincott
Renuka C. P. et.al (2002) J. Biol. Chem. 277, 22590–4
Zoltan V. AND William C. D. (2001) Pharm. Rev. 52, 1-9
Lauge S. et. Al (2003) PNAS 100, 4435-9
Mark R. B. (1997) J. of Clin. Endoc.& Met. 82, 3-7
Gianni C. (1992) FEBS 307, 66-70
Irl B. H., (2001) Clin. Diabetes 19, 146-7
BRUCE W. B. and POUL S. (2001) Diabetes care 24,69-72
http://www.indstate.edu/thcme/mwking/diabetes.html
83