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Questions and Answers

What is the primary characteristic of type 1 diabetes?

Increased beta cell production

Excessive insulin secretion

Insulin resistance

T-cell-mediated autoimmune attack (correct)

At what stage is someone with type 1 diabetes typically diagnosed?

After a viral infection only

Often when otherwise healthy and of healthy weight (correct)

When insulin sensitivity is significantly impaired

During periods of obesity

What environmental factor is suggested to potentially trigger type 1 diabetes?

Low-fat diets

Viral infections (correct)

High sodium intake

Increased physical activity

Which lifestyle factor is NOT associated with type 2 diabetes?

Consuming whole grains Signup and view all the answers

What primarily causes the insulin resistance seen in type 2 diabetes?

Defective response of body tissues to insulin Signup and view all the answers

Which dietary factor is linked to an increased risk of developing type 2 diabetes?

Sugar-sweetened drinks Signup and view all the answers

Which test is considered the gold standard for long-term monitoring of diabetes?

Glycosylated Hemoglobin (HbA1c) Signup and view all the answers

What does a lack of exercise contribute to in relation to type 2 diabetes?

7% of diabetes cases Signup and view all the answers

What is a common side effect associated with long-term use of metformin?

Interference with vitamin B12 absorption Signup and view all the answers

Which of the following is NOT a contraindication for metformin use?

Diabetic ketoacidosis Signup and view all the answers

What is the primary mechanism of action for sulfonylureas?

Inhibit KATP channels of β-cells Signup and view all the answers

In which situation would insulin therapy be administered intravenously?

Acute conditions like diabetic ketoacidosis Signup and view all the answers

Which of the following complications can arise from insulin therapy?

Hypoglycemia Signup and view all the answers

What health aspect does diabetes care specifically help improve?

Blood glucose, blood pressure, and cholesterol levels Signup and view all the answers

Which insulin delivery method is typically used for long-term therapy?

Subcutaneous injection Signup and view all the answers

Which acute complication is NOT associated with diabetes mellitus?

Coronary artery disease Signup and view all the answers

What is the primary role of insulin in the body?

To transport glucose into fat and muscle cells Signup and view all the answers

What triggers the release of insulin from the beta cells in the pancreas?

Rising levels of blood glucose after eating Signup and view all the answers

What condition occurs when glucose levels remain excessively high over time?

Acidosis Signup and view all the answers

Which hormone acts in opposition to insulin in glucose metabolism?

Glucagon Signup and view all the answers

What happens to blood glucose levels if insulin is insufficient or ineffective?

Cells absorb glucose poorly Signup and view all the answers

What is the effect of glycosuria on the body?

Higher osmotic pressure in urine Signup and view all the answers

Which type of diabetes is characterized by the loss of insulin-producing beta cells?

Type 1 diabetes mellitus Signup and view all the answers

What leads to polydipsia in patients with high blood glucose?

Increased fluid loss from dehydration Signup and view all the answers

What does moderate or large ketones in the urine indicate when accompanied by hyperglycemia?

Insulin deficiency and risk of DKA Signup and view all the answers

In the case of negative or small ketones, how often should blood glucose be checked?

Every 2 hours Signup and view all the answers

What is the recommended carbohydrate distribution for a child on a split mix regime?

6 meals with 70% of total calories in major meals and 30% in midmeals Signup and view all the answers

What should be done if a child with hyperglycemia exhibits vomiting and large ketones?

Send the child to the emergency department Signup and view all the answers

What percentage of energy intake should come from complex carbohydrates for a healthy dietary plan?

50-60% Signup and view all the answers

Which type of foods is classified as high glycemic index (GI)?

Corn flakes and chocolates Signup and view all the answers

For children on a multiple dose injection (MDI) regime, what is the guideline on mid meals?

Mid meals should have less than 10-15 grams of carbohydrate Signup and view all the answers

What impact does exercise have on insulin requirements in diabetic individuals?

Decreases insulin requirement Signup and view all the answers

Which of the following complications is most commonly associated with diabetes due to damage in small blood vessels?

Diabetic nephropathy Signup and view all the answers

What is the approximate percentage of deaths in diabetics attributed to coronary artery disease?

75% Signup and view all the answers

Which treatment is recommended to decrease the progression of diabetic nephropathy?

ACE-inhibitors Signup and view all the answers

What is the most frequent acute complication in diabetes?

Hypoglycemia Signup and view all the answers

What condition is characterized by damage to the blood vessels in the retina of the eye?

Diabetic retinopathy Signup and view all the answers

Which of the following groups is primarily affected by sensory-motor polyneuropathy in diabetic patients?

Feet Signup and view all the answers

Which of the following is NOT a sign of diabetic nephropathy?

Increased glomerular filtration rate Signup and view all the answers

Which lifestyle change is recommended for diabetic patients to help manage their condition?

Smoking cessation Signup and view all the answers

What condition is indicated by painless ulceration and decreased deep tendon reflexes?

Diabetic neuropathy Signup and view all the answers

What is a potential effect of autonomic neuropathy in diabetic patients?

Diabetic diarrhea Signup and view all the answers

What was the objective of the study on the effects of mechanical vibration in patients with type 2 diabetes mellitus?

To determine impact on transcutaneous oxygen levels Signup and view all the answers

In the study on whole body vibration, what increase was observed in transcutaneous oxygen levels?

7 mmHg Signup and view all the answers

Which of the following symptoms should be assessed in a patient's history during a nursing assessment?

Polyuria, polydipsia, and polyphagia Signup and view all the answers

Which nursing diagnosis relates to the intake of excess foods compared to activity expenditures?

Imbalanced nutrition: more than body requirements Signup and view all the answers

What is one reason to collect a patient's family history in diabetic nursing assessment?

To identify potential genetic predispositions Signup and view all the answers

Which aspect is NOT part of the physical examination during a nursing assessment?

Changes in skin temperature Signup and view all the answers

Study Notes

Definition of Diabetes Mellitus

A metabolic disorder with multiple causes.
Characterized by ongoing high blood sugar.
Caused by problems with insulin secretion, insulin action, or both.
Results in disturbances in carbohydrate, fat, and protein metabolism.

Old Classification (1985)

Type 1: Insulin-dependent (IDDM)
Type 2: Non Insulin-dependent (NIDDM)
- Obese
- Non-obese
MODY (Maturity-onset diabetes of the young) - onset between 18-25 years old.
IGT (Impaired glucose tolerance)
Gestational Diabetes Mellitus

New Classification (WHO)

Based on the cause (etiology), not the treatment or age of the patient.
Type 1: Beta cell destruction - Absolute insulin deficiency
- Immune mediated
- Idiopathic
Type 2: Predominant insulin resistance with some relative insulin deficiency.
- Predominant secretory defect with insulin resistance

Other Specific Types

Genetic defect of beta cell function (MODY syndromes)
Mitochondrial mutations
Infections (congenital rubella, CMV)
Pancreatic disease (pancreatitis, trauma/pancreatectomy, neoplasia)
Cystic fibrosis
Endocrinopathies (Acromegaly, Cushing's Syndrome, Pheochromocytoma)
Drug or chemical induced (nicotinic acid, glucocorticoids, thiazides)
Genetic disorders (Down syndrome, Turner syndrome, Klinefelter syndrome, Prader-Willi syndrome)
Gestational Diabetes Mellitus
Neonatal Diabetes Mellitus

Type 1 Diabetes Mellitus

Formerly called insulin-dependent diabetes mellitus (IDDM) or juvenile diabetes.
Characterized by low or absent levels of endogenously produced insulin.

Epidemiology

Most common endocrine disorder of childhood and adolescence.
Onset predominantly in childhood, with two peaks: one at 5-7 years and one at puberty, but can occur at any age.
In India, the average prevalence of type 1 diabetes is 10 per 100,000 population.
Risk of development:
- Mother with type 1 DM: 2% risk in child
- Father with type 1 DM: 7% risk in child
- Sibling with type 1 DM: 6% risk
- Dizygotic twins: 6-10% risk
- Monozygotic twins: 30-65% risk

Pathogenesis & Natural History

The natural history of type 1 diabetes includes distinct stages:
- Initiation of autoimmunity
- Preclinical autoimmunity with progressive ẞ-cell loss
- Onset of clinical disease
- Transient remission ("honeymoon period")
- Established disease
- Development of complications

The Pancreas

Key components:
- Islet of Langerhans
  - Beta cells: secrete insulin
  - Alpha cells: secrete glucagon
Autoimmunity is a major factor in damaging β-cells

Pathogenesis of Type 1 Diabetes

Immune dysregulation
Environmental triggers and regulators
Interactions between genes
Variable insulitis
B-cell sensitivity to injury
Loss of first-phase insulin response
Glucose intolerance
Absence of C-peptide
Prediabetes (IGT)
Overt Diabetes

Clinical Presentations

DKA (most common presentation in pediatrics)
Clinical symptom triad:
- Polyuria
- Polydipsia
- Weight loss
Accidental diagnosis

Diagnostic Criteria

Symptomatic children (polydipsia, polyuria, weight loss): random plasma glucose >11.1 mmol (200 mg) is diagnostic.
Hemoglobin A1c (HbA1c) ≥ 6.5%
Modified OGTT (oral glucose tolerance test) may be needed in asymptomatic children with hyperglycemia (>140) or symptomatic patients with hyperglycemia (random blood sugar between 140 and 400)

Treatment Elements

Education
Insulin therapy
Glycemic control monitoring.
Diet and meal planning
Prevention and early detection of complications

Education

Educate children and caregivers about:
- Type 1 diabetes
- Life-long insulin therapy
- Self-monitoring and record-keeping
- Recognition of hypoglycemia and ketoacidosis
- Meal planning
- Sick-day management
- Potential long-term complications

Insulin Therapy

Insulin is a polypeptide made up of two β-chains.
It was discovered by Bants & Best in 1921.
Animal types (porcine and bovine) were initially used before human-like insulin (DNA-recombinant types).
More potent insulin analogs are now available via changing the aminoacid sequences.
Various types exist with different onsets, peak times, and durations of action (rapid-acting, short-acting, intermediate-acting, long-acting, premixed).

Insulin Pump Therapy

Continuous subcutaneous insulin infusion (CSII) using battery-powered pumps provides a closer approximation of normal plasma insulin profiles
Accurately delivers a small baseline continuous infusion of insulin, coupled with bolus therapy.
Bolus insulin is determined by the amount of carbohydrates ingested and the current blood sugar levels.

Monitoring of Glycemic Control

Self-monitoring of blood glucose (measuring fasting levels; before and 2 hours after meals; during nighttime)
Real-time continuous glucose monitoring
Urinary glucose (reflects glycemic levels over several hours)
Measuring ketones in urine (more sensitive and accurate for high blood sugar >250mg/dL, or illnesses such as fever or vomiting combined with abdominal pain, polyuria, or rapid breathing)
Glycosylated Hemoglobin (HbA1c) monitoring every 3–4 months

Adverse Effects of Insulin

Hypoglycemia
Lipoatrophy
Lipohypertrophy
Obesity
Insulin allergy
Insulin antibodies

Practical Problems

Non-availability of insulin in low-income countries
Injection site and technique issues
Insulin storage and transfer issues
Mixing insulin preparations
Insulin and school schedule adjustments
Sick-day management
Home recognition and treatment of hypoglycemia

Management on Sick Days

Insulin requirement may increase or decrease during illness.
Fever, dehydration, stress of illness may cause hyperglycemia; vomiting, loss of appetite, may result in hypoglycemia.
Risk of ketoacidosis is increased due to starvation and dehydration.
Ensure adequate fluid intake and frequent monitoring of blood glucose and urine ketones.

Diet Regulation

Regular meal plans and calorie exchange options are encouraged.
50-60% of required energy should be from complex carbohydrates.
Carbohydrate intake should be evenly distributed throughout the day, preferably with 3 meals & 2 snacks, avoiding simple sugars.
Encourage a low-salt, low-saturated fat diet with high fiber.
Avoid simple sugars.
For split mix regimens: 6 meals, 3 major(70%), 3 mid-meals (30%).
Medial meals not essential in children with MDI regimen, with ≤ 10-15g carbohydrates.
Glycemic Index is the ranking of carbohydrates on a scale of 0 - 100, based on the extent to which they raise blood sugar levels after ingestion.
Low GI foods are preferred (e.g., most fruits and vegetables (except potatoes & watermelon), pasta, pulses, milk, and curd. )

Exercise

Decreases insulin requirement in diabetic subjects by increasing muscle cell sensitivity to insulin and enhancing glucose utilization.
Can precipitate hypoglycemia in unprepared diabetic patients.
Exercise caution if blood sugar is high (>250mg/dl) or urine ketones are present.
Wear proper footwear and avoid extremes of heat or cold during activity.
Have snacks after exercise to prevent post-exercise hypoglycemia

Pitfalls of Management

Delayed diagnosis of IDDM
The honey-moon period
Problems with diagnosis & treatment of DKA & hypoglycemia
Somogyi effect & dawn phenomenon may go unrecognized.

Dawn Phenomenon

Blood glucose levels increase in early morning hours before breakfast due to declining insulin levels (resulting in elevated morning glucose).
This phenomenon is mainly caused by overnight growth hormone secretion and increased insulin clearance.
It's a normal physiological process among most adolescents who compensate with higher insulin output.
Children with Type 1 DM cannot compensate.

Somogyi Phenomenon

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 monitoring can detect and clarify ambiguously elevated morning glucose levels.

Complications of Diabetes

Acute:
- Diabetic ketoacidosis (DKA)
- Hypoglycemia
- Hyperosmolar coma
Late-onset:
- Retinopathy
- Neuropathy
- Nephropathy
- Ischemic heart disease & stroke

Guidelines Regarding Monitoring for Complications

HbA1c: 3-4 times per year
Height/Weight: 3-4 times per year
Nutritional counseling: At diagnosis, 4-6 weeks later, then annually.
Lipid profile: Pubertal children every 5 years; pre-pubertal children within 6-12 months of diagnosis, then annually after 10 years old.
Blood pressure: Annually after age 10 years.

Prevention and Early Detection of Complications

Retinopathy
- Screening (after 5 years in prepubertal children; after 2 years in pubertal children)
- Frequency: 1-2 yearly
- Method: Fundal photography
Nephropathy
- Screening (after 5 years in prepubertal children; after 2 years in pubertal children)
- Frequency: annually
- Method: Spot urine sample for albumin:creatinine ratio
Neuropathy
- Screening (unclear in children; adults at diagnosis of Type 2 DM and 5 years after diagnosis of type 1 DM)
- Frequency: unclear
- Method: Physical examination
Macrovascular disease
- Screening: after age 2 years
- Frequency: every 5 years
- Method: lipid profile test

Thyroid Disease

Screening: at diagnosis
Frequency: every 2-3 years or more frequently based on symptoms or antithyroid antibodies.
Method: TSH

Celiac Disease

Screening: at diagnosis
Frequency: every 2-3 years
Method: tissue transglutaminase and endomysial antibody

Management of Acute Complications

Diabetic Ketoacidosis

Diabetic Ketoacidosis

A life-threatening complication of diabetes mellitus, more common in children with Type 1 DM than Type 2 DM.
Defined by hyperglycemia (>200-300 mg/dL), metabolic acidosis (blood pH <7.3 with serum bicarbonate <15 mEq/L), and ketonemia (presence of ketones in blood).

Signs and Symptoms of Diabetic Ketoacidosis

Nausea, vomiting, abdominal pain
Fruity odor in breath
Tachycardia
Low-volume pulses
Hypotension
Impaired skin turgor
Delayed capillary refill time
Dehydration
Rapid, deep sighing (Kussmaul) respirations

Classification of Diabetic Ketoacidosis

Normal
Mild
Moderate
Severe

Diabetic Ketoacidosis Treatment Protocol

Replace fluids (10-20 mL/kg of 0.9% NaCl or LR intravenously)
Administer insulin drip (0.05-0.1U/kg/hr for children)
Potassium phosphates (20mEq/L) and (0.5 - 2.5% glucose)
Treat hypokalemia (if low: 0.5 - 1 mEq/kg)
Monitor for emesis, CO2, and electrolytes Note: Should be taken to emergency department if vomiting and large ketones are present, or frequent hypoglycemia occurs.

Transition to Subcutaneous Insulin Therapy

As oral feeds advance, IV fluids are reduced and the change to subcutaneous insulin is planned.
Administer immediate rapid-acting insulin prior to each meal (e.g., lispro or aspart 15-30 minutes before or regular 1-2 hours before the IV insulin infusion is discontinued), followed by a regular (or short acting) insulin.
The optimal dose of subcutaneous insulin therapy is 0.75 – 1 U/kg /day (pre-pubertal) and 1-1.2 U/ kg/day (pubertal)

Management of Cerebral Edema

Elevate the patient's head.
Administer Mannitol 0.5-1 g/kg intravenously; repeat as needed every 30-120 minutes if there is no response
Administer 3% hypertonic saline 5ml/kg intravenously over 30 minutes

Non-Ketotic Hyperosmolar Coma

Severe hyperglycemia (>800 mg/dL)
Absence or minor ketosis.
Severe dehydration
Depressed sensorium or coma
Miscellaneous neurological signs (seizures, hyperthermia, hemiparesis, and positive Babinski signs)

Treatment of Non-Ketotic Hyperosmolar Coma

Rapid fluid replacement with 0.45% NaCl (one-half of volume deficit in 1-12 hours, remainder in the next 24 hours)
Change to 5% dextrose in 0.2 normal saline when blood glucose levels approach 300 mg/dL.
Add potassium chloride (20 mEq/L) to fluids to correct hypokalemia.
Administer insulin (0.05 units/kg/hr, intravenously) after 2 hours of fluid therapy

Hypoglycemia

Blood glucose <70 mg/dL. Risks increase with the duration of diabetes.
Mild to moderate symptoms: Immediate oral consumption of 0.3 g/kg of glucose drink or candy (retesting every 10–15 minutes for adequate response and re-administering if inadequate).
Severe symptoms: Altered mental status (unconsciousness, or seizures): Administer glucagon 0.5 mg intravenously for children under age 12; administer 1mg for over 12 years

Management of Hypoglycemia

Mild: Oral fast-acting carbohydrates (10–15 g).
Severe (semi-conscious or comatose): Intravenous hypertonic glucose (25% or 50% concentration) and glucagon 1mg intravenously

Diabetic Ketoacidosis

Life-threatening complication.
Causes: Omitting insulin, infections, trauma, myocardial infarction, stroke, surgery, emotional stress
Mortality rate: ~5%

Clinical Presentation of Diabetic Ketoacidosis

Vomiting
Sleepiness
Stomach pain
Rapid breathing
Increased pulse
Dry mouth
Flushed face
Fruity breath

Management of Diabetic Ketoacidosis

Fluid replacement (0.9% NaCl IV)
Insulin therapy (50 Units insulin in 50ml NS IV via infusion pump; 6U/hr initially; 3U/hr when < 270mg/dL; 2U/hr when < 180mg/dL).
Electrolyte correction
Correction of acidosis
Treatment of precipitating cause

Hyperglycemia, Hyperosmolar

Occurs when there is insufficient insulin to prevent hyperglycemia but enough insulin to prevent ketoacidosis.
Occurs in all types of diabetes, especially Type 2.
Life-threatening medical emergency.
Characterized by extremely high glucose levels(>800mg/dl,) & clinical presentation with osmolarity (>340 mOsm/L)

HHNKS (Hyperglycemia, Hyperosmolar Nonketotic Syndrome)

Major difference from Diabetic Ketoacidosis: lack of ketonuria (residual ability to secrete insulin in NIDDM).
Clinical presentation: Altered level of consciousness (lethargy to coma), neurological deficits (hyperthermia, motor and sensory impairment, seizures), dehydration (dry skin and mucous membranes, extreme thirst).

Macrovascular Complications

Ischemic heart diseases.
Cerebrovascular diseases.
Peripheral vascular diseases.
Diabetic patients have a 2–6 times higher risk.

Hypertension in DM

Commonly present at diagnosis.
Affects about 60% of patients.
Secondary to insulin resistance.
Increases the risk of retinopathy and nephropathy.
Abnormal lipid profile, predominantly low HDL and high triglycerides is common

Peripheral Vascular

Increased risk in type 1 & 2 diabetes.
Risk of arterial occlusion and thrombosis resulting in gangrene.
Gangrene is the most common cause of non-traumatic lower limb amputation

Screening for Macrovascular Complications

Examine pulses for cardiovascular diseases.

Lipid profile.
ECG
Blood pressure

Microvascular Complications

Microvascular complications are specific to chronic hyperglycemia.
Type 1 and 2 DM susceptible to microvascular complications.
Duration and quality of diabetic control are significant determining factors for microvascular abnormalities.

Diabetic Retinopathy

Affects 60% of Type 2 diabetics.
Progressive, irreversible vision loss.
Damage to the tiny blood vessels in the retina.
Presence of: Micro aneurysms, scattered exudates, cotton wool spots.

Diabetic Nephropathy (DN)

Defined by persistent albuminuria (>300 mg/day), decrease glomerular filtration rate, and rising blood pressure.
About 20-30% of diabetes patients develop diabetic nephropathy.
Manifested by microalbuminuria.
Progressive diabetic nephropathy leading to end-stage renal disease

Treatment to Prevent Diabetic Complications

Screen all diabetic patients annually for microalbuminuria.
Tight glycemic control and blood pressure management.
ACE inhibitors are recommended to mitigate nephropathy progression.
Smoking cessation.
Protein restriction.
Lipid reduction.

Diabetic Neuropathy

Damage to nerves throughout the body due to hyperglycemia.
Types: Sensory-motor polyneuropathy, Autonomic neuropathy.
- Sensory-motor polyneuropathy: numbness, paresthesias, mostly feet/less frequently hands; potential complications include painful ulceration (painless), Charcot arthropathy, and decreased deep tendon reflexes.
- Autonomic neuropathy: Affects many bodily systems with clinical presentation of orthostatic hypotension, diabetic diarrhea, erectile dysfunction, difficulty urinating

Research Input

Effect of mechanical vibration on transcutaneous oxygen levels in the feet of type 2 diabetes mellitus patients.
To determine whether whole-body vibration favorably impacts certain parameters related to diabetic foot syndrome, specifically transcutaneous oxygen levels above 40 mmHg.

Method

54 patients with DM participated in a 12-week exercise program based on whole-body vibration.
The study determined glycemic control through patients' HbA1c levels.
TcPO2 was recorded on each patient's foot.

Results

A statistically significant increase was observed in the TcPO2 level (7mmHg).

Conclusion

Whole-body vibration potentially elevates TcPO2 levels and may be useful in preventing or managing complications from diabetic foot syndrome with restricted blood perfusion

Diabetes Prevention 101

Monitor and/or lower your blood pressure and cholesterol.
Manage your weight and body mass index (BMI).
Quit smoking.
Maintain a healthy diet (decrease fat intake; increase fiber intake; add more whole grains, fruits, vegetables, lean meats).
30 minutes of daily activity five days per week, potentially reducing the risk of developing type 2 diabetes by 58%.

Nursing Management

Obtaining a thorough patient history, including current and general health, family history, symptoms experienced (polyuria, polydipsia, polyphagia), length of time since diagnosis, and symptoms of complications.
Performing a thorough physical examination, encompassing general condition (weight loss/gain, fatigue, and anxiety), skin (lesions, infections, and dehydration assessment); eyes (vision changes, “floaters,” halos; and cataracts); cardiovascular (orthostatic hypotension, and claudication); gastrointestinal (diarrhea, increased hunger and thirst); genitourinary (polyuria, nocturia); and neurological (numbness and tingling) assessment

1. Imbalanced Nutrition

Assess current meal timings and content.
Advise patient on individualized meal plan and weight loss goals.
Explain the importance of exercise in maintaining/reducing weight.
Assist patient in creating goals for weekly weight loss and provide incentives.

2. Risk for Injury (Hypoglycemia)

Closely monitor blood glucose levels to detect hypoglycemia.
Instruct the patient on the accuracy of insulin preparation and meal timings to avoid hypoglycemia.
Quickly treat hypoglycemia with 15-20 g of fast-acting carbohydrates.
Teach the patient for carrying sugar candy or cubes and wearing an identification bracelet.

3. Deficient Knowledge

Assess patient's knowledge of the disease and ability to care for themselves.
Assess their adherence to the prescribed diet, monitoring procedures, medication, treatment, exercise regimen.
Assess for signs of hyperglycemia or hypoglycemia.
Perform skin and extremity assessments for peripheral neuropathy or injuries of feet.

4. Risk for Impaired Skin Integrity

Assess feet and legs for skin temperature variations/soft tissue injuries, presence of corns, dryness, hammer toes.
Ensure patient safety by ensuring foot protection from break down; use heel protectors, special mattresses, and foot cradles for bed-ridden patients.
Avoid using drying agents such as alcohol on skin; use moisturizers tomaintain skin elasticity and prevent the formation of fissures.
Instruct patients in foot care guidelines

5. Ineffective Coping

Discuss diabetes' perceived effect on lifestyle, finances, family life, and occupation.
Explore prior coping strategies and skills.
Encourage patient and family involvement in diabetes self-management.
Provide emotional support to the patient and family.

Special Patient Population

Adolescent Type 2 Diabetes Mellitus
Type 2 DM is on the rise among adolescents.
Lifestyle modification is essential for these patients, and metformin may be initiated as an oral medication.

Definitions

Endocrinology : the study of hormones, glands, diabetes, and thyroid.
Hormones: biologically active substances secreted by glands
Endocrine: hormones have effects far away
Paracrine: hormones have effects nearby
Autocrine: hormones have local effects

Hormone Classification

Proteins: thyroid stimulating hormone, insulin, parathyroid hormone
Amino Acids: thyroid hormone, epinephrine
Steroids: cortisol, aldosterone, testosterone

Mechanism of Action of Hormones

Hormones circulate in blood streams, bound to carrier proteins or free.
Free hormones are the active hormones.
Enter cells to alter biological activity

Coordination of Body Functions

Nervous systems: neurotransmitters into synaptic junctions.
Endocrine systems: hormones into blood by secretions.
Neuroendocrine: neurohormones into blood
Paracrine hormones: secreted into the extracellular fluid; affects neighbors
Autocrine hormones: affect the same cells
Cytokines: peptides (interleukins, lymphokines), adipokines (leptin)

Blood Sugar Control

Hyperglycemic: >120mg %; insulin causes body cells to take up glucose, livers store glucose as glycogen
Hypoglycemic: <80 mg %; glucagon stimulates liver to break down glycogen into glucose

Type 1 Diabetes

Also known as Juvenile diabetes (IDDM) or Insulin Dependent
Characterized by low endogenous insulin production.
Pronounced hyperglycemia (frequently presenting with polydipsia, polyphagia, and polyuria; weakness; and weight loss).
Patients left untreated may result in ketoacidosis.

Type 2 Diabetes

Also known as Adult-onset diabetes (NIDDM) ,
Results from inadequate insulin binding to cells. Results in less pronounced hyperglycemia,
Accounts for 90% of all diagnosed cases.

Risk Factors for Type-2 Diabetes

Age (45 or more),
Race (e.g., African American, Asian American, Hispanic or Latino)
Family history (parents, siblings with diabetes)
Pre diabetes,
Cardiovascular disease,
Hypertension,
Low HDL cholesterol,
high triglycerides.
Obesity,
Polycystic ovary syndrome,
Physical inactivity,
Saturated and trans fat in diet,
Frequent sugar-sweetened drinks.

Central nervous system involvement includes polydipsia, polyphagia, lethargy, and stupor.
Weight loss
Systemic symptoms with polyuria.
Respiratory symptoms include Kussmaul breathing.
Gastrointestinal symptoms include nausea, vomiting, abdominal pain.
Eyes may be affected with blurred vision.
Urinary signs/symptoms include polyuria and glycosuria.
Breath may have an acetone-like odor.

Type 1 Summary

Autoimmune pancreatic destruction
Need for insulin replacement therapy.
Often/frequently present with diabetic ketoacidosis(DKA)
At risk of other autoimmune diseases.
Evaluation of coping strategies is an important part of care.

Type 2 Summary

Usually not obese,
Frequently diagnosed with diabetic ketoacidosis (DKA)
Require exogenous insulin in cases of metabolic decompensation.

Diabetes Epidemiology

Globally, the incidence of diabetes is significantly increasing by 2-5% each year.
In Europe, the Middle East, and Australia, the incidence rates for Type 1 diabetes are increasing by 2–5% annually.
The prevalence of type 1 diabetes is highest in Scandinavian countries (~~20% of the total diabetes population), whereas, the lowest rates are found among people in China and Japan (~~<1%).

Type 1 DM is more common in males than in females.
In populations of European origin, the male-to-female ratio is generally greater than 1.5:1.
Type 1 DM is most frequently diagnosed in non-Hispanic whites, and less frequently in African Americans and Hispanic Americans.
It is comparatively uncommon in Asians.

Prognosis for Type 1 Diabetes

High risk of morbidity and premature mortality.
More than 60% of patients with Type1 DM will not develop serious complications in the long term; but those with ongoing chronic complications might experience early death, blindness, end-stage renal disease (ESRD), or other complications.

Patient Education for Type 1 Diabetes

Education is a critical aspect of diabetes management, coordinating by the patient’s long-term diabetes care team.
Make patients aware of the signs and symptoms, particularly related to hypoglycemia, and educate them on how to recognize and manage the condition appropriately.
Provide dietitians to educate patients and their families about dietary control.
Nurses/Health care providers should educate patients on self-insulin injection techniques & monitoring blood glucose through fingerstick tests.

Self-monitoring of Glucose levels

Symptoms of a cold, flu, or other intercurrent illness (nausea, vomiting, abdominal pain, polyuria)
An unexpectedly high glucose level on monitoring
Persistent, rapid, and marked fluctuation in the degree of hyperglycemia

Self-Monitoring of Blood Glucose (SMBG) Levels

A blood sample is placed onto a test strip,
The test strip is inserted into a blood glucose meter
Fasting/Pre-meal blood glucose levels are typically 70-100 mg/dL.
Post-meal blood glucose levels are typically 70-140 mg/dL.

Diabetes Care Schedule

Every 3 months: Doctor's office visit, HbA1c blood test, blood pressure, weight, and foot check
Every 6 months: HbA1c blood test (if glucose levels are stable); teeth and gums evaluation by dentist
Yearly: Complete physical exam, foot exam, lipid profile test, eye exam, flu shot, and kidney test

Continuous Glucose Monitoring (CGM)

Provides real-time interstitial glucose levels every 1-5 minutes.
Provides alarms for high or low glucose readings & rapid fluctuations.
Used in conjunction with transcutaneous or subcutaneous sensors, based on device use

Management of Hypoglycemia(Symptoms of low blood sugar)

Mild: Administer oral fast-acting carbohydrates (10–15 g).
Severe: Administer intravenous hypertonic glucose (25% or 50% concentration) and glucagon 1mg intravenously,

Diabetic Ketoacidosis (DKA) Causes/Triggers

Missed or omitted insulin doses in Type 1 DM patients.
Infections
Trauma
Myocardial infarction
Stroke
Surgery
Emotional stress

Diabetic Ketoacidosis (DKA) Clinical Presentation

Vomiting
Lethargy/sleepiness
Stomach pain
Rapid deep breathing
Increased pulse
Dry mouth
Flushed face
Fruity breath

Diabetic Ketoacidosis Management

Fluid replacement with 0.9% NaCl IV.
Insulin therapy with 50U insulin in 50 mL NS IV via infusion pump (6U/hr; reducing to 3U/hr when <270mg/dL; reducing to 2U/hr when <180mg/dL).
Electrolyte correction
Correction of acidosis
Treatment of the precipitating factor.

Pancreas & Islet Cell Transplantation

Pancreas transplantation for end-stage renal disease.
Islet cell transplantation- is a potential treatment option; however, graft rejection and recurrence of autoimmunity are limitations.

Immune Modulation

Immunosuppressive therapy (for newly diagnosed patients, patients in the prolonged honey-moon period, and high-risk children)
Immunomodulating drugs (e.g., nicotinamide and mycophenolate).

Gene Therapy

Immunological attack against islet cells by introducing DNA-plasmids coding for self antigens
- Using cytokine inhibitors.
- Modifying antigens like GAD65

Prediction of Diabetes

Sensitive and specific immunologic markers: GAD, GLIMA, IA-2 antibodies.
Consider the risk associated with single or multiple antibody positivity during diagnosis.

Prevention of Diabetes

Primary prevention: Identification of diabetes genes, prevention of autoimmune factors/environmental triggers
Secondary prevention: Immunosuppressive therapy
Tertiary prevention: Tight glycemic control and monitoring

Conclusions

Hormones are essential for normal growth, development, metabolism, energy requirements, and reproduction.
Hormonal activity/secretion is tightly regulated by multiple systems within the body.
Over or under production of hormones is linked to clinical diseases.

Type 2 Diabetes Mellitus (T2DM) Pathogenesis

Multifactorial etiological factors & complex pathophysiology
Combinations of genetic predisposition, environmental factors, and lifestyle choices.

Type 2 Diabetes Mellitus (T2DM) Natural History

The development of prediabetes, characterized by elevated fasting blood glucose or impaired glucose tolerance (IGT).
The diagnosis of type 2 diabetes, characterized by elevated fasting blood glucose and/or impaired glucose tolerance.
The progression of disease- with the gradual decline in β-cell function, as well as insulin resistance progressing.
Macrovascular changes (e.g., coronary artery disease).
Microvascular changes (e.g., diabetic neuropathy, nephropathy).

Type 2 Diabetes Mellitus (T2DM) Classifications

Classic view: Insulin resistance, and a deficiency of incretin.
There is a deficiency in β-cell function, which leads to inadequate secretion of insulin.

Role of Intestines

Secretes digestive enzymes into the small intestine.
Endocrine tissues secrete hormones such as GLP-1

Role of Intestine in Diabetes

Gut microbiota plays a significant role in diabetes by influencing several factors including metabolism, immunity, and the activity of several hormones.

Role of the Brain

Sympathetic Nervous System and Insulin Secretion
Parasympathetic Nervous System and Insulin Secretion

Alzheimer's Disease (AD)

Proposed as type 3 diabetes (T3DM).
Features insulin resistance within the brain.
Presence of insulin and insulin-like growth factor (IGF) receptors within neurons.
Insulin resistance is observable in patients with AD

Role of Sleep Deprivation in Diabetes

Sleep deprivation and prolonged wakefulness may disrupt the body's diurnal patterns of hormone secretion, such as leptin, glucagon, insulin, and melatonin.
Sleep disruption can result in significant impacts on glucose metabolism.

Role of Inflammation in Diabetes

Obesity leads to systemic inflammation.
Preclinical evidence reveals links between systemic inflammation and β-cell dysfunction.
Inflammatory markers (e.g., CRP, IL-6) and its upstream regulators demonstrate association with insulin sensitivity and β-cell function.

Role of Environmental Factors in Diabetes

Energy expenditure and caloric intake
Environmental chemicals,
Gut microbiome,
Body adiposity genes are also considered environmental factors that influence the risk for type 2 diabetes

Association Between Maternal Smoking, Obesity, and Offspring Diabetes

Several studies show a relationship between maternal smoking during pregnancy, potential for overweight/obesity, and an increased risk for developing diabetes in the offspring.

Association Between Arsenic and Diabetes

Several studies demonstrate a correlation between arsenic exposure and the risk of developing diabetes among populations experiencing high levels of arsenic exposure.

Classic View of Type 2 Diabetes.

Classic view suggests a combination of factors including insulin resistance and β-cell deficiency to result in hyperglycemia.

Summary

Describes the various mechanisms and factors that work together to cause both Type 1 and Type 2 DM and subsequent disease complications.

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