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?

At diagnosis Signup and view all the answers

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

Immediately at diagnosis Signup and view all the answers

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

Reduction of β-cell numbers Signup and view all the answers

What role does glucolipotoxicity play in T2DM?

It leads to β-cell apoptosis. Signup and view all the answers

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

Elevated insulin secretion from β-cells. Signup and view all the answers

How does fasting glucagon behavior change in T2DM?

It is elevated compared to non-diabetic individuals. Signup and view all the answers

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

Increased insulin resistance. Signup and view all the answers

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

Insulin sensitivity decreases over time. Signup and view all the answers

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

Reduction in β-cell function. Signup and view all the answers

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

Genes, environment, and lifestyle together Signup and view all the answers

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

It impacts the body's inflammation and glucose metabolism. Signup and view all the answers

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

Decreased insulin sensitivity and increased β-cell stress. Signup and view all the answers

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

It is a straightforward process similar to a simple bicycle. Signup and view all the answers

What are some environmental factors influencing the development of T2DM?

Exposure to arsenic and high saturated fat intake. Signup and view all the answers

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

Young children due to obesity. Signup and view all the answers

What physiological changes occur due to insulin resistance in T2DM?

Decreased peripheral glucose uptake. Signup and view all the answers

How does chronic inflammation relate to T2DM?

It exacerbates insulin resistance and β-cell failure. Signup and view all the answers

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

They enhance insulin secretion in response to meals. Signup and view all the answers

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

Viral infection Signup and view all the answers

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

Insulin resistance Signup and view all the answers

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

Polyunsaturated fats Signup and view all the answers

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

Glycosylated Hemoglobin (HbA1c) Signup and view all the answers

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

Consuming alcohol in moderation Signup and view all the answers

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

T-cells Signup and view all the answers

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

Fasting Plasma Glucose Signup and view all the answers

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

Normal Signup and view all the answers

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

Gluten Signup and view all the answers

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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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.