Chapter 47 - Foundation, Types, Diagnosis

Diabetes mellitus — core metabolic problem

Persistent hyperglycemia caused by impaired insulin secretion, impaired insulin action, or both; carbohydrate, fat, and protein metabolism become abnormal.

Pancreatic beta cells — hormone secreted when glucose rises

Insulin; it facilitates glucose uptake and storage and decreases liver glucose production.

Pancreatic alpha cells — response to falling blood glucose

Secrete glucagon, stimulating the liver to release glucose into the blood.

Pancreatic delta cells — hormone secreted

Somatostatin, which regulates insulin and glucagon secretion.

Insulin — meaning of anabolic or storage hormone

It promotes energy use and storage: glucose enters cells, glycogen and fat are stored, and protein and fat breakdown are inhibited.

Liver glycogenolysis — definition

Breakdown of stored glycogen to release glucose, especially early in fasting.

Liver gluconeogenesis — definition and timing

Making glucose from noncarbohydrate sources, such as amino acids; more important after about 8–12 hours without food.

Basal insulin — normal function between meals and overnight

A small continuous insulin release that controls liver glucose output even when no food is eaten.

Prandial insulin — normal function after a meal

An increase in insulin secretion that handles glucose absorbed from a meal.

Type 1 diabetes — primary cause of insulin deficiency

Autoimmune destruction of pancreatic beta cells leading to little or no endogenous insulin.

Type 1 diabetes — why lifelong insulin is required

The body cannot make enough insulin to sustain normal metabolism and prevent ketosis/DKA.

Type 1 diabetes — common onset and body habitus

Often begins in children or younger adults; recent weight loss or low weight may occur, but it can begin at any age.

Type 1 diabetes — autoantibodies associated with screening

Antibodies to insulin, glutamic acid decarboxylase (GAD), islet antigen-2, or zinc transporter 8.

Type 1 diabetes — stage when symptoms commonly become apparent

Clinical signs often do not appear until stage 3, after progressive beta-cell loss.

Type 1 diabetes — major acute hyperglycemic emergency

Diabetic ketoacidosis (DKA), especially when insulin is absent or interrupted.

Type 2 diabetes — two key pathophysiologic defects

Peripheral insulin resistance plus progressively insufficient insulin secretion from beta cells.

Insulin resistance in type 2 diabetes — what happens in tissues

Muscle and other tissues respond less well to insulin, so glucose uptake is reduced and liver glucose production remains high.

Type 2 diabetes — why pancreatic beta cells eventually fail

They must secrete more insulin to overcome resistance; over time they cannot meet demand, so glucose rises.

Type 2 diabetes — typical onset pattern

Gradual and often asymptomatic; chronic complications may be present before diagnosis.

Type 2 diabetes — relationship with body weight

Obesity is a major risk factor, but type 2 diabetes can occur without obesity.

Type 2 diabetes — whether insulin may eventually be necessary

Yes. Oral or noninsulin injectable agents may be insufficient over time, and stress or illness may require temporary insulin.

Type 2 diabetes — major acute hyperglycemic emergency

Hyperglycemic hyperosmolar syndrome (HHS), especially in older adults during illness.

Why ketoacidosis is less common in type 2 diabetes

Enough endogenous insulin is often present to suppress major fat breakdown and ketone formation.

Gestational diabetes — definition and pregnancy timing

New glucose intolerance during pregnancy, usually recognized in the second or third trimester, not preexisting diabetes.

Gestational diabetes — primary cause of hyperglycemia

Placental hormones produce insulin resistance during pregnancy.

Gestational diabetes — important fetal risk

Macrosomia, or a larger-than-expected newborn, with associated perinatal complications.

Gestational diabetes — recommended routine screening window

24–28 weeks of gestation, using the glucose challenge/OGTT approach described in the chapter.

Gestational diabetes — glucose target before breakfast

Fasting plasma glucose less than 95 mg/dL, per Chapter 47.

Gestational diabetes — target 1 hour after a meal

Less than 140 mg/dL, per Chapter 47.

Gestational diabetes — target 2 hours after a meal

Less than 120 mg/dL, per Chapter 47.

Gestational diabetes — first management steps

Individualized nutrition, activity, weight management, and blood glucose monitoring.

Gestational diabetes — preferred medication if lifestyle measures fail

Insulin, according to Chapter 47, because many other agents cross the placenta.

Gestational diabetes — postpartum long-term risk

Glucose often normalizes after delivery, but the person has a higher future risk for type 2 diabetes.

Gestational diabetes — recommended long-term follow-up

Screening for type 2 diabetes or prediabetes every 3 years after delivery, per Chapter 47.

Prediabetes — definition

Glucose values above normal but below the diagnostic threshold for diabetes; indicates increased future diabetes and cardiovascular risk.

Prediabetes — recommended weight-loss goal

Losing about 5–7% of body weight can improve glycemic control and reduce type 2 diabetes risk.

Diabetes Prevention Program — exercise target

At least 150 minutes of moderate-intensity physical activity per week, such as brisk walking.

Diabetes Prevention Program — weight-loss target in lecture

Aim to lose and maintain 7% of initial body weight in high-risk adults with excess weight.

Latent autoimmune diabetes in adults (LADA) — defining feature

Adult-onset autoimmune diabetes with type 1–associated autoantibodies and slower beta-cell destruction; can resemble type 2 initially.

Maturity-onset diabetes of the young (MODY) — defining feature

Rare inherited monogenic diabetes, often with diabetes across multiple generations; treatment depends on mutation.

Secondary diabetes — examples of causes

Pancreatic disease such as pancreatitis or cystic fibrosis, hormonal disorders, or medications such as corticosteroids.

Corticosteroid therapy — diabetes-related concern

Steroids can increase blood glucose and may cause medication-induced diabetes or worsen existing diabetes.

Type 2 diabetes risk — family-history clue

Having a parent or sibling with diabetes increases risk.

Type 2 diabetes risk — lifestyle-related clues

Physical inactivity, excess body weight, and a history of impaired fasting glucose or glucose tolerance.

Type 2 diabetes risk — comorbid conditions

Hypertension, cardiovascular disease, dyslipidemia, or polycystic ovary syndrome.

Type 2 diabetes risk — lipid thresholds in Chapter 47

HDL at or below 35 mg/dL or triglycerides at or above 250 mg/dL increase risk.

Metabolic syndrome — characteristic abnormalities

Central obesity, elevated blood pressure, abnormal lipids, and elevated fasting glucose/insulin resistance.

Metabolic syndrome — waist circumference cutoffs in lecture

Greater than 40 inches in men or greater than 35 inches in women.

Metabolic syndrome — HDL cutoffs in lecture

Below 40 mg/dL in men or below 50 mg/dL in women.

Metabolic syndrome — triglyceride threshold in lecture

Greater than 150 mg/dL.

Metabolic syndrome — blood pressure criterion in lecture

Blood pressure greater than 130/85 mmHg.

Metabolic syndrome — fasting glucose criterion in lecture

Fasting blood glucose greater than 100 mg/dL.

Diabetes screening — routine starting age in lecture

Start screening all people at age 35; assess some adults earlier if overweight plus additional risk factors.

Diabetes screening — lower Asian American BMI threshold in lecture

A BMI of 23 kg/m² plus other risk factors can warrant diabetes screening.

Fasting plasma glucose — diagnostic threshold for diabetes

At least 126 mg/dL after no caloric intake for at least 8 hours.

A1C — diagnostic threshold for diabetes

A1C at least 6.5%.

75-g oral glucose tolerance test — diabetes threshold at 2 hours

Plasma glucose at least 200 mg/dL, measured 2 hours after the glucose load.

Random plasma glucose — diabetes diagnosis with symptoms

At least 200 mg/dL PLUS classic hyperglycemia symptoms such as polyuria, polydipsia, or weight loss.

Abnormal diagnostic tests — when confirmation is needed

Without unequivocal hyperglycemia, confirm with two abnormal results obtained together or on separate days.

Hemoglobin A1C — what time period it reflects

Approximate average glucose exposure over the preceding 3 months, due to glucose binding to hemoglobin.

A1C — commonly used treatment goal in source

Less than 7% for many adults with diabetes, provided significant hypoglycemia is avoided; individualize when needed.

A1C — less strict target cited for selected vulnerable patients

Less than 8% may be more suitable for certain older or frail patients or those with limited life expectancy, per Chapter 47.

A1C — monitoring frequency when treatment goals are met

At least twice yearly, per Chapter 47.

A1C — monitoring frequency after a therapy change or poor control

Every 3 months (quarterly), per Chapter 47.

Polyuria in diabetes — mechanism

Hyperglycemia causes glucosuria and osmotic diuresis, pulling water and electrolytes into urine.

Polydipsia in diabetes — mechanism

Increased thirst caused by fluid loss and dehydration from osmotic diuresis.

Polyphagia in diabetes — mechanism

Increased hunger related to poor cellular glucose utilization and breakdown of stored fat and protein.

Unintentional weight loss in uncontrolled type 1 diabetes — mechanism

Glucose calories are lost in urine and the body breaks down fat and protein for fuel.

Blurred vision during marked hyperglycemia — clinical significance

A possible manifestation of elevated glucose; new or sudden vision changes should be evaluated.

Slow-healing wounds and recurrent infections — diabetes connection

Long-standing hyperglycemia impairs tissue healing and host defense.

New-onset type 1 diabetes — symptoms suggesting possible DKA

Polyuria, thirst, weight loss with nausea, vomiting, abdominal pain, or fruity breath.

Diabetes baseline physical assessment — key items

Blood pressure, BMI, eye and visual assessment, oral and skin assessment, foot pulses and sensation, and injection sites.

Diabetes baseline lab assessment — key items

A1C, lipids, urine albumin, serum creatinine/eGFR, and urinalysis; ECG when indicated by assessment.

Diabetes assessment — why check urine albumin and eGFR

To screen for diabetic kidney disease and monitor renal function.

Diabetes assessment — why test foot sensation with a monofilament

To identify loss of protective sensation and ulcer or amputation risk.

Diabetes social determinants — why the nurse assesses food access and cost

Housing, food availability, insurance, treatment costs, and education can affect diabetes risk and self-management.