Diabetes Screening Guidelines Quiz
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Questions and Answers

What is the preferred screening method for retinopathy in prepubertal children after 5 years of diabetes duration?

  • Spot urine sample for albumin:creatinine ratio
  • Lipid profile test
  • Fundal photography (correct)
  • Physical examination

    • How often should nephropathy screening occur in pubertal children after 2 years of diabetes duration?

  • 1-2 yearly
  • Every 5 years
  • Every month
  • Annually (correct)

    • What is the recommended frequency for screening macrovascular disease in children?

  • Every 2 years
  • Every 3 years
  • Every 5 years (correct)
  • Every 1 year

    • At what stage is thyroid disease screening recommended?

    <p>At diagnosis (A)</p> Signup and view all the answers

    When should screening for neuropathy begin in adults with type 2 diabetes?

    <p>Immediately at diagnosis (D)</p> Signup and view all the answers

    What is a primary factor contributing to β-cell failure in Type 2 Diabetes Mellitus (T2DM)?

    <p>Reduction of β-cell numbers (A)</p> Signup and view all the answers

    What role does glucolipotoxicity play in T2DM?

    <p>It leads to β-cell apoptosis. (C)</p> Signup and view all the answers

    In the feedback loop between β-cells and insulin-sensitive tissues, what change occurs in hyperinsulinemia?

    <p>Elevated insulin secretion from β-cells. (A)</p> Signup and view all the answers

    How does fasting glucagon behavior change in T2DM?

    <p>It is elevated compared to non-diabetic individuals. (A)</p> Signup and view all the answers

    What is a consequence of the pancreas being unable to renew β-cells after the age of 30?

    <p>Increased insulin resistance. (D)</p> Signup and view all the answers

    Which of the following best describes a typical change in insulin sensitivity in relation to T2DM progression?

    <p>Insulin sensitivity decreases over time. (C)</p> Signup and view all the answers

    What is a common effect of amyloid deposition in β-cells?

    <p>Reduction in β-cell function. (D)</p> Signup and view all the answers

    Which factors collectively play a significant role in the development of insulin resistance and β-cell dysfunction?

    <p>Genes, environment, and lifestyle together (B)</p> Signup and view all the answers

    What is the role of the gut microbiome in the development of T2DM?

    <p>It impacts the body's inflammation and glucose metabolism. (A)</p> Signup and view all the answers

    In the context of T2DM, what does increasing obesity typically lead to?

    <p>Decreased insulin sensitivity and increased β-cell stress. (B)</p> Signup and view all the answers

    Which of the following statements about the pathophysiology of T2DM is incorrect?

    <p>It is a straightforward process similar to a simple bicycle. (D)</p> Signup and view all the answers

    What are some environmental factors influencing the development of T2DM?

    <p>Exposure to arsenic and high saturated fat intake. (C)</p> Signup and view all the answers

    Which age group is increasingly prevalent for the diagnosis of T2DM?

    <p>Young children due to obesity. (D)</p> Signup and view all the answers

    What physiological changes occur due to insulin resistance in T2DM?

    <p>Decreased peripheral glucose uptake. (A)</p> Signup and view all the answers

    How does chronic inflammation relate to T2DM?

    <p>It exacerbates insulin resistance and β-cell failure. (C)</p> Signup and view all the answers

    What role do incretin hormones play in the regulation of blood sugar?

    <p>They enhance insulin secretion in response to meals. (B)</p> Signup and view all the answers

    Which factor is most commonly associated with triggering type 1 diabetes in genetically susceptible individuals?

    <p>Viral infection (D)</p> Signup and view all the answers

    What is the predominant abnormality observed in the early stages of type 2 diabetes mellitus?

    <p>Insulin resistance (B)</p> Signup and view all the answers

    Which dietary factor is suggested to potentially decrease the risk of developing type 2 diabetes?

    <p>Polyunsaturated fats (B)</p> Signup and view all the answers

    What is the primary method used to long-term monitor diabetes management?

    <p>Glycosylated Hemoglobin (HbA1c) (C)</p> Signup and view all the answers

    Which of the following lifestyle factors is least likely to contribute to the development of type 2 diabetes?

    <p>Consuming alcohol in moderation (D)</p> Signup and view all the answers

    What mediates the autoimmune attack in type 1 diabetes leading to beta cell loss?

    <p>T-cells (B)</p> Signup and view all the answers

    Which of the following is a common diagnostic method for detecting diabetes?

    <p>Fasting Plasma Glucose (D)</p> Signup and view all the answers

    The sensitivity and responsiveness to insulin in type 1 diabetes at onset are usually described as:

    <p>Normal (C)</p> Signup and view all the answers

    Among the dietary factors, which is specifically mentioned as potentially leading to type 1 diabetes?

    <p>Gluten (A)</p> Signup and view all the answers

    Flashcards

    Retinopathy Screening

    Screening for eye problems caused by diabetes, done yearly in children based on age (5 years for prepubertal, 2 years for pubertal).

    Nephropathy Screening

    Screening for kidney problems, done annually in children based on age (5 years for prepubertal, 2 years for pubertal, by checking albumin:creatinine ratio in urine.

    Neuropathy Screening

    Screening for nerve damage in diabetes, unclear screening schedule for children, different protocols for type 1 & Type 2.

    Macrovascular Disease Screening

    Screening for large blood vessel problems, done every 5 years after age 2, using lipid profiles.

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    Thyroid Disease Screening

    Screening for thyroid issues, done at diagnosis and/or based on symptoms or antibodies every 2-3 years (or more frequently).

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    Classic T2DM

    Type 2 Diabetes Mellitus (T2DM) characterized by insulin resistance and beta-cell dysfunction. Reduced insulin sensitivity in peripheral tissues leads to diminished uptake of glucose. Beta-cell failure leads to decreased insulin secretion. Incretin defect reduces the response to rising glucose levels.

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    Incretin Defect

    A condition where incretins (hormones that enhance insulin secretion) are not working properly, leading to reduced insulin release in response to rising blood sugar. This contributes to the development of T2DM.

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    Hyperglycemia in T2DM

    High blood sugar levels in the body, a hallmark of T2DM. It results from insulin resistance, impaired insulin secretion, and other factors like increased hepatic glucose production and reduced renal glucose excretion.

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    Which came first: Hyperinsulinemia or Insulin Resistance?

    It is a debated question whether hyperinsulinemia (excessive insulin levels) in early stages of T2DM is the cause or merely the result of insulin resistance.

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    Feedback Loop in T2DM

    An intricate connection between beta-cells and insulin-sensitive tissues, where insulin secretion influences glucose uptake in tissues, which subsequently affects further insulin release. This loop contributes to the development and progression of T2DM.

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    Beta-Cell Loss in T2DM

    A characteristic feature of T2DM where the number of insulin-producing beta-cells in the pancreas declines, contributing to reduced insulin secretion. Glucolipotoxicity and amyloid deposition accelerate this process.

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    Alpha-Cell Dysfunction in T2DM

    A condition where alpha-cells in the pancreas malfunction, causing excessive glucagon release even after meals. This contributes to elevated blood sugar levels in T2DM.

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    Insulin Resistance

    A condition where the body's cells don't respond properly to insulin, preventing glucose from entering the cells for energy.

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    β-cell Dysfunction

    A condition where the pancreas, specifically the β-cells, fail to produce enough insulin to regulate blood sugar levels.

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    What causes Type 2 Diabetes (T2DM)?

    Both genetic factors and environmental factors like diet, exercise, and lifestyle contribute to the development of T2DM.

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    Environmental Factors for T2DM

    These factors can contribute to the development of T2DM: unhealthy diet, lack of exercise, obesity, arsenic exposure, and the gut microbiome.

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    Pancreatic Glucagon Secretion

    Glucagon is a hormone produced by the pancreas that increases blood sugar levels. It's often elevated in people with T2DM.

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    Hepatic Glucose Production

    The liver produces glucose, a process called gluconeogenesis, and this process is often increased in people with T2DM.

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    Renal Glucose Excretion

    The kidneys filter waste from the blood, including excess glucose. In T2DM, the kidneys may not filter all the excess glucose effectively.

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    T2DM: More than just 'simple mechanics'

    The pathogenesis of T2DM is complex, involving many factors beyond just insulin resistance and β-cell dysfunction. It's a system with interconnected parts.

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    Type 1 Diabetes

    An autoimmune disease where the immune system attacks and destroys beta cells in the pancreas, leading to a lack of insulin production.

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    What triggers type 1 diabetes?

    Genetics play a role, but environmental factors like viral infections or diet may trigger the autoimmune attack in genetically susceptible individuals.

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    What are key lifestyle factors contributing to type 2 diabetes?

    Obesity, lack of physical activity, poor diet, and stress all increase the risk of developing type 2 diabetes.

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    How do dietary factors influence type 2 diabetes risk?

    Sugar-sweetened drinks, saturated and trans fats increase the risk, while polyunsaturated and monounsaturated fats decrease it.

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    Fasting Plasma Glucose Test

    A blood test that measures blood glucose levels after fasting overnight, used to diagnose diabetes.

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    Oral Glucose Tolerance Test (OGTT)

    A test that measures blood glucose levels at regular intervals after consuming a sugary drink, used to diagnose diabetes.

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    Glycated Hemoglobin (HbA1c)

    A blood test that measures the average blood sugar levels over the past 2-3 months, used to monitor diabetes control.

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    Urinalysis for Diabetes

    Checking urine for glucose (glycosuria) and ketone bodies, used to diagnose and manage diabetes.

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    Study Notes

    Definition of Diabetes Mellitus

    • A metabolic disorder caused by defects in insulin secretion, insulin action, or both.
    • Characterized by chronic hyperglycemia with disturbances of carbohydrate, fat, and protein metabolism.
    • Multiple etiologies exist for the disease condition.

    Old Classification (1985)

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

    New Classification (WHO)

    • Based on etiology, not treatment type or age.
    • Type 1 (Beta cell destruction-absolute insulin deficiency): Immune mediated, Idiopathic
    • Type 2: Predominant insulin resistance with relative insulin deficiency, or predominant secretory defect with insulin resistance.

    Other Specific Types

    • Genetic defect of beta cell function (MODY syndromes), mitochondrial mutations
    • Infections (congenital rubella, CMV)
    • Disease of pancreas (pancreatitis, trauma/pancreatectomy, neoplasia, cystic fibrosis)
    • Endocrinopathies (acromegaly, Cushing's Syndrome, Pheochromocytoma)
    • Drug or chemical induced (nicotinic acid, glucocorticoids, thiazides)
    • Genetic disorders associated with diabetes (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.
    • Most common endocrine disorder of childhood and adolescence.
    • Onset predominantly in childhood, with peaks at 5-7 years and puberty, but can occur at any age.
    • Prevalence in India: 10 per 100,000 population
    • Risk of development:
      • Mother with Type 1 DM: 2% risk in child
      • Father affected: 7% risk
      • Sibling of index case: 6% risk
      • Dizygotic twins: Risk 6-10%
      • Monozygotic twins: Risk 30-65%

    Stages of Type 1 Diabetes Natural History

    • Initiation of autoimmunity
    • Preclinical autoimmunity with progressive beta-cell loss
    • Onset of clinical disease
    • Transient remission ("honeymoon period")
    • Established disease
    • Development of complications

    Pancreas Anatomy

    • Beta cells: secrete insulin.
    • Alpha cells: secrete glucagon.
    • Autoimmunity occurs in islet of Langerhans against beta cells.

    Pathogenesis of Type 1 Diabetes

    • Genetic susceptibility + environmental triggers or chance.
    • Autoimmunity causes progressive β-cell loss.
    • Clinical diabetes.
    • Clinical remission (honeymoon period).
    • Complications

    Clinical Presentation

    • DKA (diabetic ketoacidosis): Most common presentation in pediatrics (children).
    • Classical symptom triad: Polyuria, polydipsia, weight loss.
    • Accidental diagnosis

    Diagnostic Criteria

    • Symptomatic (polydipsia, polyuria, weight loss): Random plasma glucose >11.1 mmol (200 mg) is diagnostic.
    • HbA1c ≥ 6.5%
    • Acute infections in young non-diabetic children may cause hyperglycemia without ketoacidosis.
    • Modified OGTT (oral glucose): 1.75 gm/kg (max 75 gm) may be used for asymptomatic children with hyperglycemia (RBS >140).
    • IGT: Fasting glucose level 6.0-6.9 mmol (100-126 mg/dl), and 2 hrs after oral glucose tolerance 7.8-11.0 mmol (140-200 mg/dl) – Impaired glucose tolerance
    • Diabetic: ≥7.0 mmol (126mg/dl) or ≥11.1 mmol (200 mg/dl)

    Treatment Elements

    • Education, insulin therapy, glycemic control monitoring, diet and meal planning, prevention and early detection of complications.

    Education About

    • Diabetes type 1, life-long insulin therapy, self-monitoring, recognition of hypoglycemia and DKA, meal plan, sick-day management, possible long-term complications

    Insulin Therapy

    • Polypeptide made of 2 beta-chains.
    • Discovered by Bants & Best in 1921.
    • Animal-based insulin (porcine & bovine) used before human insulin (DNA-recombinant types).
    • Potent insulin analogs produced by altering amino acid sequence.

    Types of Insulin

    • Rapid-acting: Onset 5 minutes, Peak 1 hour, Duration 2-4 hours (insulin lispro or insulin aspart)
    • Regular or Short-acting: Onset 30 minutes, Peak 2-3 hours, Duration 3-6 hours (insulin regular)
    • Intermediate-acting: Onset 2-4 hours, Peak 4-12 hours, Duration 12-18 hours (NPH, Lente)
    • Long-acting: Onset 6-10 hours, Duration 20-24 hours (insulin glargine)

    Insulin Concentrations

    • Available in different concentrations: 40, 80, & 100 Unit/ml.
    • WHO recommends U100/ml to prevent confusion.
    • Special preparation for infusion pumps: soluble insulin 500 U/ml.

    Suggested Target Blood Glucose Ranges

    • Fasting or preprandial: 90-145 mg/dL
    • Postprandial: 90-180 mg/dL
    • Bedtime: 120-180 mg/dL
    • Nocturnal: 80-162 mg/dL; <5 years 90-200 during day, 150-200 at bedtime/night

    Key Aspects of Insulin Therapy

    • Mimic natural insulin secretion pattern.
    • Administered subcutaneously using syringes, pens, or pumps.
    • Dose (DKA/overt symptoms): 0.8-1 unit/kg/day
    • Incidentally diagnosed: lower doses (toddlers & pre-school 0.2-0.4 unit/kg/day, pre-pubertal 0.5-0.8 unit/kg/day, adolescents 0.8-1.5 unit/kg/day)
    • Injection sites (anterolateral thighs, abdominal wall, posterior aspect upper arms, superolateral aspects of buttocks)

    Insulin Therapy Regimes

    • Split-mix regime (Mixtard 30:70 or NPH 2/3 + Regular 1/3 twice daily, 2/3 dose 45 min before breakfast, 1/3 dose 45 min before bed)
    • Basal bolus regimen with multiple daily injections (MDI)(30-50% Long acting (glargine, detemir) 3-4 rapid acting remainder).

    Calculation of Bolus Dose

    • Carbohydrate to insulin ratio (CIR)
    • Amount of carbohydrate covered by one unit of insulin
    • Initial calculation = 500/Total daily dose
    • More accurate estimations based on meal carbohydrate intake, insulin amounts administered, pre and post-prandial glucose

    Insulin Pump Therapy

    • Continuous subcutaneous insulin infusion (CSII) via battery-powered pumps.
    • Provides closer approximation of normal plasma insulin profiles.
    • Delivers small baseline continuous insulin infusion, coupled with bolus therapy parameters.
    • Bolus insulin determined by carbohydrate intake and blood sugar levels.

    Monitoring of Glycemic Control

    • Self monitoring of blood glucose (SMBG), fasting, before & 2 hrs after meals & during night.
    • Real-time continuous glucose monitoring,
    • Urinary glucose reflects glycemic levels over preceding hours and is positive if renal threshold exceeded, crude indicator of hyperglycemia.
    • Measuring ketones in urine more sensitive and accurate (In-BG > 250mg/dl, Illness, fever, vomiting, abdominal pain, polyurea, drowsiness, rapid breathing)
    • Glycosated hemoglobin (HbA1c) every 3-4 months.

    Adverse Effects of Insulin Therapy

    • Hypoglycemia
    • Lipoatrophy
    • Lipohypertrophy
    • Obesity, Insulin allergy
    • Insulin antibodies.

    Practical Problems

    • Non-availability of insulin,
    • Injection sites and technique,
    • Insulin storage and transfer,
    • Mixing insulin preparations,
    • Insulin and school hours,
    • Adjusting insulin doses at home,
    • Sick-day management,
    • Recognition and treatment of hypoglycemia at home.

    Management on Sick Days

    • Insulin requirement may increase or decrease during illness.
    • Fever, dehydration, and stress of illness can cause hyperglycemia due to increase counterregulatory hormones.
    • Vomiting and loss of appetite can lead to hypoglycemia.
    • Risk of ketoacidosis increases due to starvation and dehydration.
    • Take plenty of fluids; monitor blood glucose and urine ketones frequently; "moderate" or "large" ketones in urine with hyperglycemia indicates insulin deficiency and risk of DKA.

    Diet Regulation

    • Regular meal plans with calorie exchange options are encouraged.
    • 50-60% of required energy from complex carbohydrates (low GI).
    • Distribute carbohydrate load evenly, avoiding simple sugars.
    • Encouraged low salt, low saturated fats, high-fiber diet.
    • Avoid simple sugars.
    • In split-mix regime, 6 meals (3 major, 3 midmeal).
    • In children with MDI, midmeal not essential.
    • Glycemic index: ranking of carbohydrates on scale from 0 to 100 according to their blood sugar raising effect after eating (High GI foods rapidly digested; Low GI foods result in gradual rise).

    Exercise

    • Decreases insulin requirement by increasing muscle cell and glucose utilization sensitivity.
    • Can precipitate hypoglycemia in unprepared diabetic patients.
    • Exercise should be at same time and duration each day; caution during poor metabolic control; consider possible hypoglycemia/have extra snack

    Pitfalls of Management

    • Delayed diagnosis of IDDM, the honey-moon period, problems with DKA & hypoglycemia management, Somogyi's effect & dawn phenomenon (may go unrecognized).

    Dawn Phenomenon

    • Blood glucose level increases in early morning hours before breakfast due to decline in insulin levels.
    • It is caused by overnight growth hormone secretion and increased insulin clearance.
    • Seen in adolescents without diabetes; children with T1DM cannot compensate.

    Somogyi Phenomenon

    • Theoretical rebound from late-night/early morning hypoglycemia (from exaggerated counter regulatory response).
    • Continuous glucose monitoring helpful in clarifying ambiguous morning glucose levels.

    Complications of Diabetes

    • Acute: Diabetic ketoacidosis (DKA), hypoglycemia, hyperosmolar coma.
    • Late-onset: Retinopathy, neuropathy, nephropathy, Ischemic heart disease & stroke.

    Prevention and Early Detection of Complication

    • Retinopathy: Screening after 5 years (prepubertal), 2 years (pubertal) using Fundal photography; Frequency: 1-2 yearly.
    • Nephropathy: Screening after 5 years (prepubertal), 2 years (pubertal) using Spot urine sample for albumin:creatinine ratio, annually.
    • Neuropathy: Screening in unclear in children; adults at diagnosis of Type 2 DM 5 years after diagnosis in Type 1 DM; Frequency unclear using physical examination.
    • Macrovascular Disease: Screening after 2 years by lipid profile test; frequency -every 5 years.
    • Thyroid Disease: Screening at diagnosis, every 2-3 years or more frequently based on symptoms or presence of antibodies; preferred method -TSH.
    • Celiac Disease: Screening at diagnosis, every 2-3 years using tissue transglutaminase and endomysial antibody

    Management of Acute Complications, Diabetic Ketoacidosis

    • True emergency.
    • Causes: Omitting insulin, increased insulin requirements (infection, trauma, myocardial infarction, stroke, surgery, emotional stress).
    • Mortality ~5%
    • Clinical presentation includes vomiting, stomach pain, rapid breathing, increased pulse, sleepiness, dry mouth, flushed face, fruity breath
    • Management includes fluid replacement (0.9% NaCl IV), insulin therapy, electrolyte correction, acidosis correction, and treating precipitating cause.

    Hyperglycemia, Hyperosmolar Coma

    • Insufficient insulin, enough insulin to prevent ketoacidosis.
    • Occurs in all types of diabetes, esp. Type 2.
    • Life-threatening medical emergency, characterized by Blood glucose severely elevated (>800 mg/dL), absence of or only slight ketosis, nonketotic acidosis, severe dehydration, abnormal neurological signs.
    • Plasma osmolarity is >350 mOsm/L.
    • Management includes rapid repletion of vascular volume deficit and very slow correction of hyperosmolar state (1/2 isotonic saline at an estimated rate).

    HHNKS (Hyperosmolar Hyperglycemic Nonketotic Syndrome)

    • Differentiated from DKA by lack of ketonuria.
    • Residual ability of insulin secretion in NIDDM.
    • Clinical manifestations include altered level of consciousness (e.g., lethargy to coma), neurological deficits (e.g., hyperthermia, motor and sensory impairment, seizures), and dehydration (dry skin, mucous membranes, extreme thirst).
    • Management includes rapid replacement of lost fluids (0.45% NaCl at estimated rate to replace 50% of volume deficit in 1st 12 hours, remainder administered in ensuing 24 hours), changing hydrating fluids to 5% dextrose in normal saline as blood glucose approaches 300 mg/dL, and supplementing fluids with 20 mEq/L of KCl.
    • Insulin infusion started at 0.05 units/kg/hr beginning 2nd hour of fluid therapy.

    Macrovascular Complications

    • Ischemic heart disease, cerebrovascular disease, peripheral vascular disease.
    • Higher risk for diabetic patients than general population.
    • Screening includes examining pulses, Lipid profile, ECG, and blood pressures.

    Hypertension in DM

    • Often present at diagnosis.
    • Affects around 60% of patients.
    • Secondary to insulin resistance.
    • Increased risk for retinopathy and nephropathy.
    • Abnormality is low HDL and high triglycerides.

    Peripheral Vascular Disease

    • Increased risk in Type 1 and Type 2 diabetics.
    • Develop arterial occlusion and thrombosis resulting in gangrene.
    • Gangrene is frequent cause of non-traumatic lower limb amputation.

    Microvascular Complications

    • Specific to longstanding hyperglycemia.
    • Susceptible in Type 1 and Type 2 DMs.
    • Duration and quality of diabetic control determinants of abnormalitites.

    Diabetic Retinopathy

    • Affects 60% of Type 2 diabetics.
    • Progressive and irreversible vision loss.
    • Damage to tiny blood vessels supplying the eyes (Micro aneurysms, scattered exudates).

    Diabetic Nephropathy

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

    Treatment to Prevent Complications

    • All diabetic patients should be screened annually for microalbuminuria.
    • Tight glycemic control and management of blood pressure.
    • ACE inhibitors recommended to decrease progression of nephropathy.
    • Smoking cessation, protein restriction, and lipid reduction.

    Diabetic Neuropathy

    • Damage to the nerves due to hyperglycemia.
    • Types: Sensory-motor polyneuropathy (numbness, paresthesias; affects feet more than hands).
    • Complicated by ulceration (painless), Charcot arthropathy.
    • Decreased deep tendon reflexes.
    • Autonomic neuropathy: affects almost any system, manifested by orthostatic hypotension, diabetic diarrhea, erectile dysfunction, difficulty in urination.

    Research Input

    • Effect of mechanical vibration on transcutaneous oxygen levels in feet of Type 2 DM patients.
    • Favors some parameters related to diabetic foot syndrome (TcPO2 > 40 mmHg cases prognosis).

    Method

    • 54 patients with DM included in a 12-week exercise program based on whole body vibration.
    • Glycemic control determined by HbA1c and sensitivity; TcPO2 levels of each foot recorded

    Conclusion

    • Whole body vibration may increase TcPO2 levels, prevention or management of complications associated with restricted blood perfusion.

    Hypoglycemia

    • Most frequent acute complication.
    • Common when blood glucose levels fall < 60 mg/dL
    • Causes: Missing meals, excessive exercise, alterations/errors in insulin dosage, alcohol ingestion.
    • Clinical manifestations include hunger, tremors, palpitations, anxiety, pallor, sweating

    Management of Hypoglycemia

    • Mild (self-treated): Oral fast-acting carbohydrates (10-15g) like glucose drink or candy.
    • Severe (semi-conscious/comatose): IV hypertonic glucose (25% or 50%) concentration or glucagon injection (1mg IM).

    Diabetic Ketoacidosis

    • True emergency.
    • Causes: Omitting insulin, increased insulin requirements - infection, trauma, myocardial infarction, stroke, surgery, stress.
    • Mortality approximately 5%.
    • Classic presentation includes vomiting, stomach pain, rapid breathing, increased pulse, sleepiness, dry mouth, flushed face, fruity breath.

    Management of Diabetic Ketoacidosis

    • Fluid replacement (0.9% NaCl IV), insulin therapy, electrolyte correction, acidosis correction and treatment of precipitating cause.
    • Start with 50U insulin in 50mlNS through continuous intravenous infusion pumps 6U/hr initially, 3U/hr at blood glucose <270mg/dl, 2U/hr when <180/mg/dL

    Hyperosmolar Hyperglycemic State

    • Insufficient_insulin to prevent hyperglycemia, but enough insulin to prevent ketoacidosis.
    • Occurs in all types of diabetes, especially Type 2 diabetes. A life-threatening medical emergency.
    • Characterized by blood glucose severely elevated (>800 mg/dL), absence or minimal ketosis, nonketotic acidosis, severe dehydration, abnormal neurological signs.
    • Plasma osmolarity is usually > 350mOsm/kg
    • Management includes rapid volume repletion (1/2 isotonic saline), changing hydrating fluids to 5% dextrose in normal saline as blood glucose approaches 300mg/dL , and supplementing fluids with 20mEq/L of KCl..
    • Begin insulin infusion (0.05U/kg/hr) at 2nd hr of fluid treatment

    Other Complications

    • Microvascular: retinopathy (affects 60% of Type 2 diabetics causing progressive irreversible vision loss), nephropathy (defined as persistent albuminuria resulting from sustained hyperglycemia), neuropathy (damage to nerves due to sustained hyperglycemia, types include sensory-motor polyneuropathy, and autonomic neuropathy manifesting as orthostatic hypotension, diabetic diarrhea, erectile dysfunction, difficulty in urination.
    • Macrovascular diseases: Includes ischemic heart disease, cerebrovascular disease and peripheral vascular disease.
    • Hypertension: Often present and secondary to insulin resistance. Most common abnormality is decreased HDL and increased triglycerides.

    Nursing Management

    • Obtain comprehensive patient history (current problems, general health, family history, symptoms (polyuria, polydipsia, polyphagia, weight loss)), years since diagnosis, and complications.
    • Physical examination: evaluate general condition (weight, fatigue, anxiety), skin (lesions, infections, dehydration), eyes (changes in vision), cardiovascular (orthostatic hypotension, claudication), GI (diarrhea, increased hunger and thirst), GU (polyuria, nocturia), and neurological system (numbness and tingling).
    • Assess nutrition related to body requirements and activity expenditure. Provide education on individualized meal planning and exercise importance for weight loss.
    • Assess knowledge about disease, self-care, and oral hypoglycemic agents, adherence to diet and exercise, and symptoms of hyperglycemia and hypoglycemia

    Risk for Injury (Hypoglycemia)

    • Implement interventions to prevent potential injury or harm related to hypoglycemia; Closely monitor glucose levels, educate patients on accurate insulin preparation and meal timing; treat promptly with 15-20g fast acting carbohydrates and have sugar candy, and wear identification information

    Deficient Knowledge

    • Assess patient's knowledge about their disease and self-care ability.
    • Check the level of adherence related to diet therapy, monitoring, medication, and exercise.
    • Assess signs of hyperglycemia and hypoglycemia.
    • Conduct skin & extremities assessments for peripheral neuropathy or injuries in feet & lower extremities

    Foot Care

    • Regular foot checks; wash daily, keep toenails short, & protect feet.
    • Always wear socks & shoes, check shoes for injuries.
    • Gradually break in new shoes, avoid applying drying agents (alcohol).
    • Use heel protectors, special mats & foot cradles for bed rest.
    • Apply moisturizers

    Ineffective Coping

    • Discuss impact on lifestyle, finances, family, and occupation.
    • Explore previous coping strategies and positive skills
    • Encourage patient's and family participation in diabetes self-care regimens
    • Provide emotional support

    Special Patient Population

    • Adolescent Type 2 DM: Increasing in adolescents, lifestyle modifications essential, and metformin, the only labeled oral medication appropriate for children (10-16 years old),

    Conclusions

    • Type 2 diabetes is a "lifestyle disease," characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both; caring for diabetes helps prevent other health issues.

    References

    • Various research articles/studies, reports from the US Centers for Disease Control and Prevention, and the World Health Organization are cited.

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    Diabetes 3 PDF

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    Test your knowledge on diabetes screening protocols for children and adults. This quiz covers important screening methods for retinopathy, nephropathy, macrovascular disease, thyroid disease, and neuropathy. Perfect for healthcare professionals or students in the medical field.

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