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Nutrition 8

front 1

Which A1C value alone diagnoses diabetes?
A. 6.4%
B. 5.7%
C. 6.2%
D. 6.5%

back 1

D. 6.5%

front 2

A patient has polyuria, polydipsia, weight loss. Random plasma glucose is over 200 mg/dL. Best interpretation?
A. Diabetes by symptoms + random
B. Prediabetes by random value
C. Diabetes only if fasting elevated
D. Needs OGTT to diagnose

back 2

A. Diabetes by symptoms + random

front 3

For diagnostic OGTT classification, the standard glucose load is:
A. 50 g oral glucose
B. 100 g oral glucose
C. 75 g anhydrous glucose
D. 1 g/kg oral glucose

back 3

C. 75 g anhydrous glucose

front 4

Which fasting plasma glucose meets diabetes criteria?
A. 125 mg/dL
B. 126 mg/dL
C. 110 mg/dL
D. 100 mg/dL

back 4

B. 126 mg/dL

front 5

Which fasting range defines impaired fasting glucose?
A. 90–99 mg/dL fasting
B. 126–139 mg/dL fasting
C. 80–89 mg/dL fasting
D. 100–125 mg/dL fasting

back 5

D. 100–125 mg/dL fasting

front 6

Which 2-hour OGTT range defines impaired glucose tolerance?
A. 120–139 mg/dL 2-hour
B. 200–239 mg/dL 2-hour
C. 140–199 mg/dL 2-hour
D. 100–119 mg/dL 2-hour

back 6

C. 140–199 mg/dL 2-hour

front 7

A 2-hour plasma glucose of which value diagnoses diabetes (75-g OGTT)?
A. 200 mg/dL
B. 199 mg/dL
C. 140 mg/dL
D. 125 mg/dL

back 7

A. 200 mg/dL

front 8

Which A1C range defines prediabetes?
A. 6.5–7.4%
B. 5.7–6.4%
C. 4.0–5.6%
D. 6.0–6.9%

back 8

B. 5.7–6.4%

front 9

Screening should be considered at any age when BMI ≥25 kg/m² plus:
A. Age >45 only
B. No symptoms present
C. At least one risk factor
D. Any normal fasting glucose

back 9

C. At least one risk factor

front 10

In adults without risk factors, testing should begin no later than:
A. Age 35
B. Age 40
C. Age 50
D. Age 45

back 10

D. Age 45

front 11

A teen presents with DKA and weight loss. The primary defect in type 1 diabetes is:
A. Autoimmune beta-cell destruction
B. Hepatic insulin overproduction
C. Muscle glucose transporter failure
D. Alpha-cell hyperplasia primary

back 11

A. Autoimmune beta-cell destruction

front 12

The hormonal state resulting from type 1 beta-cell loss is best described as:
A. Relative insulin excess
B. Absolute insulin deficiency
C. Isolated glucagon deficiency
D. Selective cortisol deficiency

back 12

B. Absolute insulin deficiency

front 13

Why can type 1 diabetes have months–years of silent progression?
A. Renal glucose threshold increases
B. Glucagon remains fully suppressed
C. Peripheral insulin sensitivity increases
D. Pancreas has large insulin reserve

back 13

D. Pancreas has large insulin reserve

front 14

Autoantibodies to GAD65 appear to provoke attack by:
A. Killer T lymphocytes
B. B lymphocytes
C. Neutrophils
D. Eosinophils

back 14

A. Killer T lymphocytes

front 15

Type 1 diabetes HLA association includes linkage to:
A. HLA-A and HLA-B
B. HLA-C and HLA-E
C. HLA-DGA and HLA-DQB
D. HLA-DP and HLA-DO

back 15

C. HLA-DGA and HLA-DQB

front 16

Which statement about HLA-DR/DQ alleles is correct?
A. DR/DQ alleles never protective
B. DR/DQ alleles can either be predisposing or protect
C. Only DRB is predisposing
D. Only DQB is protective

back 16

B. DR/DQ alleles can either be predisposing or protect

front 17

Insulin autoantibodies may be found in people who:
A. Always used insulin previously
B. Only have type 2 diabetes
C. Are only on metformin
D. Never received insulin therapy

back 17

D. Never received insulin therapy

front 18

In type 2 diabetes development, hyperglycemia requires:
A. Complete alpha-cell failure
B. Autoimmune islet destruction
C. Acute cortisol deficiency
D. Beta-cell secretory impairment

back 18

D. Beta-cell secretory impairment

front 19

By the time type 2 diabetes is diagnosed, beta-cell function loss can reach:
A. 50% loss
B. 10% loss
C. 90% loss
D. 25% loss

back 19

A. 50% loss

front 20

Early type 2 diabetes commonly features which insulin abnormality?
A. Excess first-phase insulin
B. Inadequate first-phase insulin
C. Absent basal insulin secretion
D. Increased insulin clearance

back 20

B. Inadequate first-phase insulin

front 21

Inadequate first-phase insulin fails to suppress which hormone?
A. Growth hormone
B. Cortisol
C. Epinephrine
D. Glucagon

back 21

D. Glucagon

front 22

The main consequence of glucagon hypersecretion is:
A. Increased hepatic glucose output
B. Increased muscle glucose uptake
C. Decreased gluconeogenesis
D. Increased peripheral insulin action

back 22

A. Increased hepatic glucose output

front 23

Increased free fatty acids causing metabolic injury is termed:
A. Glucotoxicity
B. Ketosis
C. Lipotoxicity
D. Glycogenesis

back 23

C. Lipotoxicity

front 24

Increased free fatty acids directly cause which change?
A. Increased insulin sensitivity
B. Decreased insulin sensitivity
C. Increased GLUT4 translocation
D. Increased insulin receptor density

back 24

B. Decreased insulin sensitivity

front 25

Free fatty acids also tend to:
A. Impair insulin secretion
B. Improve beta-cell recovery
C. Reduce hepatic glucose output
D. Abolish glucagon secretion

back 25

A. Impair insulin secretion

front 26

A prediabetic patient asks about risk reduction. Supported weight loss target is:
A. 1–2% body weight
B. 3–4% body weight
C. 10–12% body weight
D. 5–7% body weight

back 26

D. 5–7% body weight

front 27

The physical activity target linked to benefit is:
A. 10 minutes brisk daily
B. 30 minutes brisk most days
C. 60 minutes jogging weekly
D. Resistance training only

back 27

B. 30 minutes brisk most days

front 28

Lifestyle changes can reduce diabetes risk by:
A. 5–10%
B. 10–20%
C. 29–67%
D. 70–90%

back 28

C. 29–67%

front 29

Lifestyle changes may delay type 2 diabetes onset for at least:
A. 10 years
B. 2 years
C. 6 months
D. 5 years

back 29

A. 10 years

front 30

For pharmacologic prevention, ADA recommends (with lifestyle):
A. Acarbose only
B. GLP-1 agonist only
C. Pioglitazone only
D. Metformin only

back 30

D. Metformin only

front 31

Metformin prevention is especially emphasized for:
A. BMI 24, age 66
B. BMI 28, age 62
C. BMI 36, age 58
D. BMI 23, age 41

back 31

C. BMI 36, age 58

front 32

Counterregulatory hormones have what net effect relative to insulin?
A. Same glucose-lowering effect
B. Opposite effect of insulin
C. No effect on metabolism
D. Only increase insulin secretion

back 32

B. Opposite effect of insulin

front 33

After eating, two “anticipatory” hormones amplify insulin release. Which pair fits?
A. Amylin and insulin
B. Cortisol and glucagon
C. Epinephrine and norepinephrine
D. GLP-1 and GIP

back 33

D. GLP-1 and GIP

front 34

A patient asks where incretins come from. Best answer?
A. Gastrointestinal tract after ingestion
B. Pancreatic alpha cells post-meal
C. Adipose tissue during fasting
D. Liver sinusoids during stress

back 34

A. Gastrointestinal tract after ingestion

front 35

A resident explains why incretins matter clinically. Key effect?
A. Delay insulin until absorption
B. Increase renal glucose reuptake
C. Anticipatory insulin rise pre-absorption
D. Trigger ketogenesis after meals

back 35

C. Anticipatory insulin rise pre-absorption

front 36

A1C measures:
A. Serum fructosamine
B. Glycosylated hemoglobin
C. Glycated albumin fraction
D. Total plasma glucose burden

back 36

B. Glycosylated hemoglobin

front 37

A patient’s A1C is reviewed. It best reflects glycemia over:
A. Prior 6–8 weeks
B. Prior 48–72 hours
C. Prior 10–14 days
D. Prior 6–12 months

back 37

A. Prior 6–8 weeks

front 38

Why does A1C rise with hyperglycemia over time?
A. Enzymatic hemoglobin phosphorylation
B. Rapid protein acetylation process
C. Insulin-driven hemoglobin oxidation
D. Nonenzymatic, concentration-dependent glycation

back 38

D. Nonenzymatic, concentration-dependent glycation

front 39

For many non-pregnant adults, ADA’s reasonable A1C goal is:
A. <6.5%
B. <7%
C. <7.5%
D. <8%

back 39

B. <7%

front 40

A highly motivated patient wants tighter control. Lower A1C may be reasonable if:
A. Advanced complications already present
B. Limited life expectancy expected
C. No significant hypoglycemia/adverse effects
D. Persistent postmeal excursions continue

back 40

C. No significant hypoglycemia/adverse effects

front 41

A frail patient has severe hypoglycemia history. A less stringent goal is most appropriate when:
A. Severe hypoglycemia, limited life expectancy, complications
B. Newly diagnosed, no comorbidities
C. Pregnancy planning this year
D. Early disease, low hypoglycemia risk

back 41

A. Severe hypoglycemia, limited life expectancy, complications

front 42

A pump user asks what drives rapid-acting bolus needs most. Best determinant?
A. Meal protein grams
B. Meal sodium content
C. Meal fiber density
D. Total meal carbohydrate grams

back 42

D. Total meal carbohydrate grams

front 43

A patient notices worse control after fried foods. High-fat meals primarily:
A. Improve insulin sensitivity acutely
B. Interfere with insulin signaling
C. Suppress hepatic glycogenolysis
D. Increase incretin release persistently

back 43

B. Interfere with insulin signaling

front 44

In nutrition counseling, lower-fat patterns are expected to:
A. Worsen insulin sensitivity
B. Increase hepatic glucose output
C. Reduce incretin secretion
D. Improve insulin sensitivity

back 44

D. Improve insulin sensitivity

front 45

Trials comparing eating patterns show similar A1C and weight improvements with:
A. High- or low-carbohydrate eating patterns
B. Zero-carbohydrate ketogenic diet only
C. Protein-only dietary pattern
D. Sodium-restricted pattern alone

back 45

A. High- or low-carbohydrate eating patterns

front 46

When comparing carbohydrate type/amount versus energy intake, the more important driver is:
A. Glycemic index category
B. Total energy intake
C. Dietary cholesterol intake
D. Protein timing with meals

back 46

B. Total energy intake

front 47

A dietitian teaches “carb counting.” One average carbohydrate serving equals:
A. 10 g carbohydrate
B. 12 g carbohydrate
C. 15 g carbohydrate
D. 20 g carbohydrate

back 47

C. 15 g carbohydrate

front 48

A patient asks for a fiber target. Recommended intake is:
A. 14 g per 1000 kcal
B. 10 g per 1000 kcal
C. 25 g per day
D. 40 g per day

back 48

A. 14 g per 1000 kcal

front 49

A patient without renal disease asks about protein restriction. Best guidance?
A. Increase protein to 30% energy
B. Avoid protein entirely at dinner
C. Reduce protein below usual intake
D. Remain 15–20% of energy

back 49

D. Remain 15–20% of energy

front 50

Long-term high-fat and high saturated fat intake is associated with:
A. Reduced insulin resistance
B. Improved insulin sensitivity
C. Increased insulin resistance
D. No change in insulin action

back 50

C. Increased insulin resistance

front 51

A supplement-focused patient asks about antioxidants. Routine supplementation is:
A. Recommended for all diabetics
B. Required with metformin use
C. Preferred in hypertensive patients
D. Not advised routinely

back 51

D. Not advised routinely

front 52

A patient asks if sodium advice differs in diabetes. Appropriate target is:
A. Under 2300 mg per day
B. Under 1500 mg per day
C. Under 3500 mg per day
D. No sodium restriction needed

back 52

A. Under 2300 mg per day

front 53

Sodium reduction lowers blood pressure in:
A. Only hypertensive individuals
B. Only normotensive individuals
C. Normotensive and hypertensive individuals
D. Only patients with complications

back 53

C. Normotensive and hypertensive individuals

front 54

A patient plans exercise; pre-exercise glucose is 92 mg/dL. Best immediate step?
A. Skip carbohydrates before exercise
B. Eat carbohydrates before exercise
C. Take bolus insulin immediately
D. Delay exercise until bedtime

back 54

B. Eat carbohydrates before exercise

front 55

A patient on Amylin mimetics (pramlintide) asks what it does. Primary postmeal effects?
A. Stimulates hepatic glucose production
B. Inhibits DPP-4 enzyme activity
C. Decreased glucagon, delayed gastric emptying
D. Increases glucagon, accelerates emptying

back 55

C. Decreased glucagon, delayed gastric emptying

front 56

A patient has postprandial hyperglycemia despite lifestyle changes. Alpha-glucosidase inhibitors (acarbose, miglitol) work by:
A. Inhibiting intestinal α-glucosidase that digests carbs
B. Stimulating beta-cell insulin release
C. Blocking hepatic gluconeogenesis enzymes
D. Activating amylin receptors

back 56

A. Inhibiting intestinal α-glucosidase that digests carbs

front 57

A patient asks why Biguanides (metformin) helps without “pushing insulin.” They:
A. Enhance insulin secretion directly
B. Delay gastric emptying markedly
C. Inhibit intestinal α-glucosidase
D. Suppressing hepatic glucose production

back 57

D. Suppressing hepatic glucose production

front 58

DPP-4 inhibitors (sitagliptin, saxagliptin, linagliptin) normally degrades which peptides?
A. Amylin and insulin
B. GLP-1 and GIP
C. Cortisol and epinephrine
D. Glucagon and growth hormone

back 58

B. GLP-1 and GIP

front 59

Exenatide, Liragludite are:
A. GLP-1 receptor agonists
B. GLP-1 receptor antagonists
C. GLP-2 receptor agonists
D. GLP-2 receptor antagonists

back 59

A. GLP-1 receptor agonists

front 60

Sodium-glucose transporter 2 (SGLT-2) inhibitors (canagliflozin, dapagliflozin) cause glucosuria by preventing filtered glucose from returning to blood. What is the key mechanism?
A. Inhibit intestinal carbohydrate enzymes
B. Activate GLP-1 receptors
C. Increase beta-cell insulin synthesis
D. Block renal glucose reabsorption

back 60

D. Block renal glucose reabsorption

front 61

A patient worries a GLP-1 receptor agonist will cause hypoglycemia when fasting. Why is insulin release limited at normal glucose?
A. Only with hyperglycemia present
B. Works only during exercise
C. Requires hepatic glycogen depletion
D. Depends on insulin receptor upregulation

back 61

A. Only with hyperglycemia present

front 62

After starting exenatide, a patient reports early satiety and smaller post-meal spikes. Which effect set best explains this?
A. Increase glucagon, faster emptying
B. Reduce insulin, faster emptying
C. Reduce glucagon, delay emptying
D. Increase insulin, faster emptying

back 62

C. Reduce glucagon, delay emptying

front 63

A patient takes an insulin secretagogue (Meglinitres) at the start of meals for postprandial control. Which drugs fit?
A. Glipizide and Repaglinide
B. Repaglinide and Nateglinide
C. Canagliflozin and Nateglinide
D. Liraglutide and Repaglinide

back 63

B. Repaglinide and Nateglinide

front 64

Which medication is a second-generation sulfonylurea?
A. Sitagliptin
B. Nateglinide
C. Glimepiride
D. Dapagliflozin

back 64

C. Glimepiride

front 65

A patient prefers long-term therapies that preserve beta-cell function. Which concern best matches sulfonylureas?
A. Primary hepatic glucose stimulation
B. Postmeal glucagon hypersecretion
C. Marked gastric emptying acceleration
D. Weight gain, beta-cell exhaustion

back 65

D. Weight gain, beta-cell exhaustion

front 66

A patient with insulin resistance is placed on pioglitazone and rosiglitazone (thiazolidinediones). Primary therapeutic effect?
A. Increase urinary glucose clearance
B. Increase insulin secretion acutely
C. Decrease peripheral insulin resistance
D. Inhibit intestinal carbohydrate digestion

back 66

C. Decrease peripheral insulin resistance

front 67

A patient needs background insulin to cover the post-absorptive state. Which insulins fit this role?
A. Lispro, Glargine, NPH
B. Glargine, Determir, NPH
C. Aspart, Determir, NPH
D. Regular, Determir, NPH

back 67

B. Glargine, Determir, NPH

front 68

A hospitalized patient is NPO overnight. Why is basal insulin still required?
A. Restrain hepatic glucose output
B. Prevent intestinal glucose absorption
C. Increase pancreatic insulin stores
D. Enhance renal glucose filtration

back 68

A. Restrain hepatic glucose output

front 69

Basal insulin also helps prevent excess substrate delivery to liver by:
A. Increasing glucagon secretion
B. Increasing hepatic ketone clearance
C. Accelerating adipose triglyceride breakdown
D. Limiting lipolysis and FFA flux

back 69

D. Limiting lipolysis and FFA flux

front 70

A patient asks when to inject detemir. Best guidance?
A. Only before breakfast
B. Only at bedtime
C. Any time, same daily
D. Only with largest meal

back 70

C. Any time, same daily

front 71

A patient wants to mix glargine with rapid-acting insulin in one syringe. Best advice?
A. Do not mix with others
B. Mix if dose is small
C. Mix only with NPH
D. Mix only at bedtime

back 71

A. Do not mix with others

front 72

A patient reports high glucose around waking despite stable daytime control. What phenomenon best fits?
A. Postprandial excursion
B. Dawn phenomenon
C. Reactive hypoglycemia
D. Exercise-induced hyperglycemia

back 72

B. Dawn phenomenon

front 73

A patient’s plasma glucose is 205 mg/dL and urinalysis shows glucose. The renal threshold is approximately:
A. 90–110 mg/dL
B. 120–140 mg/dL
C. 150–170 mg/dL
D. 180–220 mg/dL

back 73

D. 180–220 mg/dL

front 74

New-onset type 1 diabetes usually becomes clinically apparent after approximately what beta-cell loss?
A. 30–40% destruction
B. 50–60% destruction
C. 80–90% destruction
D. 95–99% destruction

back 74

C. 80–90% destruction

front 75

A conscious diabetic patient has tremor and diaphoresis with glucose 52 mg/dL. Preferred treatment?
A. Oral sucrose candy
B. Oral glucose
C. IV lipid emulsion
D. IM epinephrine

back 75

B. Oral glucose

front 76

Initial hypoglycemia treatment dose should be:
A. 15–20 g glucose
B. 5–10 g glucose
C. 25–30 g glucose
D. 40–50 g glucose

back 76

A. 15–20 g glucose

front 77

After giving oral glucose for hypoglycemia, expected initial response time is:
A. 1–3 minutes
B. 5–8 minutes
C. 10–20 minutes
D. 45–60 minutes

back 77

C. 10–20 minutes

front 78

An unconscious patient with hypoglycemia cannot take oral carbohydrates. Best immediate therapy?
A. Oral glucose tablets
B. Oral complex carbohydrates
C. IV fiber solution
D. Glucagon administration

back 78

D. Glucagon administration

front 79

In absolute insulin deficiency, adipose lipolysis increases partly due to:
A. Decreased adenylate cyclase activity
B. Increased adenylate cyclase activity
C. Increased insulin receptor signaling
D. Increased GLUT4 translocation

back 79

B. Increased adenylate cyclase activity

front 80

In insulin absence, fatty acid release also reflects reduced inhibition of:
A. Pyruvate dehydrogenase
B. HMG-CoA reductase
C. Glycogen phosphorylase
D. Hormone-sensitive lipase

back 80

D. Hormone-sensitive lipase

front 81

The liver generates ketone bodies in DKA primarily from increased:
A. Acetyl-CoA from FFA oxidation
B. Oxaloacetate from glycolysis
C. Lactate from anaerobic muscle
D. Citrate from TCA overflow

back 81

A. Acetyl-CoA from FFA oxidation

front 82

Which molecule is a major ketone body in DKA?
A. Oxaloacetate
B. Succinate
C. Beta-hydroxybutyrate
D. Malate

back 82

C. Beta-hydroxybutyrate

front 83

In DKA, the primary source of circulating glucose is:
A. Hepatic gluconeogenesis
B. Muscle glycogenolysis
C. Intestinal glucose absorption
D. Renal glucose reuptake

back 83

A. Hepatic gluconeogenesis

front 84

Insulin’s major hepatic effect on this pathway is to:
A. Activate hepatic gluconeogenesis
B. Inhibit hepatic gluconeogenesis
C. Replace hepatic glycogen stores
D. Increase hepatic ketone synthesis

back 84

B. Inhibit hepatic gluconeogenesis

front 85

Which complication category is most tightly linked to chronic hyperglycemia?
A. Macrovascular aneurysm rupture
B. Primary valve calcification
C. Microvascular complications
D. Primary arrhythmia syndromes

back 85

C. Microvascular complications

front 86

Chronic microvascular complications prominently involve:
A. Lungs, skin, marrow
B. Eyes, kidneys, nerves
C. Liver, pancreas, spleen
D. Heart, aorta, carotids

back 86

B. Eyes, kidneys, nerves

front 87

Microalbuminuria signals increased risk for:
A. Hyperthyroidism and stroke
B. DKA and pancreatitis
C. Nephrolithiasis and anemia
D. Atherosclerosis and nephropathy

back 87

D. Atherosclerosis and nephropathy

front 88

A pump user snacks between meals. If the snack contains >15 g carbs, what is often needed?
A. Additional basal insulin only
B. No insulin adjustment needed
C. Rapid-acting insulin before snack
D. Glucagon before snack

back 88

C. Rapid-acting insulin before snack

front 89

A 19-year-old with type 1 diabetes starts HIIT training. To prevent exercise-related hypoglycemia, advise checking glucose:
A. Before and after exercise
B. Only during exercise
C. Only after exercise
D. Only if symptomatic

back 89

A. Before and after exercise

front 90

For general lifestyle counseling, patients should strive for how much moderate exercise weekly?
A. 60 minutes weekly
B. 150 minutes weekly
C. 300 minutes weekly
D. 30 minutes monthly

back 90

B. 150 minutes weekly

front 91

A 26-year-old with oligomenorrhea and hirsutism has labs “consistent with PCOS.” The key lab features are:
A. Insulin resistance, hyperandrogenism
B. Hyperthyroidism, hypogonadism
C. Hyperprolactinemia, low cortisol
D. Hypoandrogenism, low insulin

back 91

A. Insulin resistance, hyperandrogenism

front 92

In PCOS, hyperandrogenism is mainly driven by which source, with another contributing?
A. Adrenals primary, ovary minor
B. Pituitary primary, ovary minor
C. Ovary primary, adrenals contribute
D. Liver primary, adrenals contribute

back 92

C. Ovary primary, adrenals contribute

front 93

A patient’s fasting plasma glucose is 128 mg/dL on screening. This is:
A. Normal fasting glucose
B. Impaired fasting glucose
C. Diabetes by fasting criteria
D. Reactive hypoglycemia

back 93

C. Diabetes by fasting criteria

front 94

A 75-g OGTT shows 2-hour plasma glucose 206 mg/dL. Best interpretation?
A. Diabetes by 2-hour value
B. Impaired glucose tolerance
C. Normal glucose tolerance
D. Indeterminate, repeat in a week

back 94

A. Diabetes by 2-hour value

front 95

A patient has polyuria and polydipsia. Random plasma glucose is 201 mg/dL. This indicates:
A. Prediabetes by random glucose
B. Normal random glucose
C. Requires fasting confirmation
D. Diabetes with classic symptoms

back 95

D. Diabetes with classic symptoms

front 96

A fasting plasma glucose of 110 mg/dL is best classified as:
A. Diabetes mellitus
B. Prediabetes (IFG)
C. Normal fasting glucose
D. Postprandial hyperglycemia

back 96

B. Prediabetes (IFG)

front 97

A 2-hour OGTT glucose of 180 mg/dL is best classified as:
A. Normal glucose tolerance
B. Diabetes mellitus
C. Prediabetes (IGT)
D. Laboratory artifact

back 97

C. Prediabetes (IGT)

front 98

An A1C of 6.1% is best classified as:
A. Prediabetes by A1C
B. Diabetes by A1C
C. Normal A1C
D. Hypoglycemia risk state

back 98

A. Prediabetes by A1C

front 99

A patient’s diabetes screen is normal. When should routine re-testing occur?
A. Every 6 months
B. Every 3 years
C. Every 10 years
D. Only if symptomatic

back 99

B. Every 3 years

front 100

Overweight youth should be screened if they have how many additional diabetes risk factors?
A. Two or more
B. One only
C. Three or more
D. None required

back 100

A. Two or more

front 101

For at-risk overweight youth, start screening at:
A. Age 5 regardless puberty
B. Age 18 only
C. Age 13 regardless puberty
D. Age 10 or puberty onset

back 101

D. Age 10 or puberty onset

front 102

Which set meets “overweight” criteria used for youth screening?
A. BMI ≥95th percentile only
B. BMI <50th percentile only
C. BMI≥85th, wt/ht≥85th, wt≥120%
D. Height <5th percentile only

back 102

C. BMI≥85th, wt/ht≥85th, wt≥120%

front 103

Which type 1 diabetes autoantibody targets tyrosine phosphatases?
A. GAD65 antibody
B. IA-2 / IA-2B
C. Insulin autoantibody
D. Islet cell antibody

back 103

B. IA-2 / IA-2B

front 104

Which list best matches circulating autoantibodies linked to beta-cell destruction in type 1 diabetes?
A. ANA, dsDNA, Smith
B. TPO, TRAb, Tg
C. RF, CCP, ANCA
D. ICA, IAA, GAD65, IA-2

back 104

D. ICA, IAA, GAD65, IA-2

front 105

Type 1 diabetes can be diagnosed at any age, but it occurs mostly:
A. Over age 65
B. Under age 30
C. Only in toddlers
D. Only after menopause

back 105

B. Under age 30

front 106

Peak type 1 incidence occurs between which ages in girls?
A. 5–7 years
B. 15–17 years
C. 10–12 years
D. 20–22 years

back 106

C. 10–12 years

front 107

Peak type 1 incidence occurs between which ages in boys?
A. 12–14 years
B. 6–8 years
C. 16–18 years
D. 22–24 years

back 107

A. 12–14 years

front 108

At type 1 diabetes diagnosis, approximately what fraction have ≥1 circulating autoantibody?
A. 10–20%
B. 30–40%
C. 50–60%
D. 85–90%

back 108

D. 85–90%

front 109

The HLA association in type 1 diabetes is most classically tied to:
A. HLA-A/B alleles
B. HLA-DR/DQ alleles
C. HLA-C alleles
D. HLA-E alleles

back 109

B. HLA-DR/DQ alleles

front 110

Within this HLA association, linkage is described to which genes?
A. HLA-A and HLA-B
B. HLA-C and HLA-E
C. DGA and DQB genes
D. DPB and DPC genes

back 110

C. DGA and DQB genes

front 111

This HLA association is also influenced by which gene?
A. DRB gene
B. HBB gene
C. INS gene
D. VHL gene

back 111

A. DRB gene

front 112

The type 1 “honeymoon phase” can last up to:
A. 6 months max
B. 2 years max
C. 4 years max
D. 8–10 years max

back 112

D. 8–10 years max

front 113

In type 2 diabetes, hyperglycemia does not manifest until what has occurred?
A. Alpha-cell hyperplasia predominates
B. Impaired beta-cell function present
C. Autoimmune beta-cell destruction occurs
D. Complete insulin absence develops

back 113

B. Impaired beta-cell function present

front 114

Insulin resistance in adipocytes increases circulating free fatty acids. Which change is expected?
A. Increased insulin secretion
B. Decreased hepatic glucose output
C. Increased insulin sensitivity
D. Decreased insulin secretion

back 114

D. Decreased insulin secretion

front 115

Elevated circulating free fatty acids contribute to fasting hyperglycemia primarily by:
A. Increasing hepatic glucose production
B. Increasing renal glucose reabsorption
C. Decreasing gastric emptying
D. Suppressing glucagon secretion

back 115

A. Increasing hepatic glucose production

front 116

Which combined triad best matches effects of elevated free fatty acids on insulin?
A. ↑ secretion, ↑ sensitivity, ↓ production
B. ↓ secretion, ↓ sensitivity, ↑ production
C. ↓ secretion, ↑ sensitivity, ↓ production
D. ↑ secretion, ↓ sensitivity, ↑ production

back 116

B. ↓ secretion, ↓ sensitivity, ↑ production

front 117

Multiple drugs reduced diabetes incidence in prevention trials. Which set matches those tested?
A. Metformin, acarbose, orlistat, rosiglitazone
B. Metformin, liraglutide, glipizide, insulin
C. Acarbose, sitagliptin, dapagliflozin, NPH
D. Orlistat, pramlintide, glargine, metoprolol

back 117

A. Metformin, acarbose, orlistat, rosiglitazone

front 118

ADA prevention pharmacotherapy is recommended for IGT/IFG or A1C:
A. 6.5–7.4%
B. 5.7–6.4%
C. 4.8–5.6%
D. 6.0–6.9%

back 118

B. 5.7–6.4%

front 119

Metformin prevention is also especially emphasized for:
A. Prior gestational diabetes
B. Prior nephrolithiasis
C. Prior asthma exacerbations
D. Prior hyperthyroidism

back 119

A. Prior gestational diabetes

front 120

Grain recommendation within prevention lifestyle guidance:
A. Avoid grains entirely
B. Whole grains ≥ half intake
C. Whole grains only at dinner
D. Whole grains < quarter intake

back 120

B. Whole grains ≥ half intake

front 121

Replacing saturated fats with which improves insulin resistance?
A. Trans fatty acids
B. Monounsaturated fats
C. Short-chain saturated fats
D. Dietary cholesterol

back 121

B. Monounsaturated fats

front 122

Another acceptable replacement for saturated fats is:
A. Polyunsaturated fats
B. Medium-chain triglycerides
C. Animal-based saturated fats
D. Hydrogenated oils

back 122

A. Polyunsaturated fats

front 123

Alcohol guidance in diabetes prevention is to limit to:
A. 3–4 drinks per day
B. 0 drinks always
C. 1–2 drinks per day
D. 1 drink per week

back 123

C. 1–2 drinks per day

front 124

A dietary pattern encouraged for prevention is:
A. Ketogenic pattern
B. Mediterranean-style pattern
C. Carnivore pattern
D. Very-low fiber pattern

back 124

B. Mediterranean-style pattern

front 125

Dietary cholesterol should be limited to:
A. <100 mg per day
B. <150 mg per day
C. <200 mg per day
D. <300 mg per day

back 125

C. <200 mg per day

front 126

Continuous glucose monitors primarily measure glucose in:
A. Interstitial fluid
B. Capillary blood
C. Venous plasma
D. Intracellular cytosol

back 126

A. Interstitial fluid

front 127

A stable patient meeting goals asks about A1C testing frequency. Minimum is:
A. Once yearly
B. Twice yearly
C. Quarterly
D. Monthly

back 127

B. Twice yearly

front 128

A patient with therapy changes is not meeting goals. A1C testing should be:
A. Every 6 months
B. Every 12 months
C. Four times per year
D. Every 2 years

back 128

C. Four times per year

front 129

Medical nutrition therapy (MNT) improves which metabolic outcomes?
A. Glucose, A1C, lipids, BP, weight
B. Only A1C and weight
C. Only triglycerides and HDL
D. Only blood pressure

back 129

A. Glucose, A1C, lipids, BP, weight

front 130

In diabetes, MNT is associated with A1C reductions of:
A. 0.1–0.3%
B. 0.3–0.7%
C. 1–2% average
D. 3–5% average

back 130

C. 1–2% average

front 131

Cardioprotective MNT implemented by RDs reduced which lipid marker 7–21%?
A. HDL-cholesterol
B. Total cholesterol
C. Lipoprotein(a)
D. Apolipoprotein B

back 131

B. Total cholesterol

front 132

At what timepoint should medication changes be assessed to meet targets?
A. At 1 week
B. At 1 month
C. At 3 months
D. At 12 months

back 132

C. At 3 months

front 133

Effective nutrition interventions include which set?
A. Reduced energy/fat, MNT, portion control
B. High sodium, low fiber, skipping meals
C. High saturated fat, low activity, fasting
D. Low fluid, high alcohol, low protein

back 133

A. Reduced energy/fat, MNT, portion control

front 134

A complementary effective set includes:
A. High glycemic meals, random snacks
B. Healthy choices and carb counting
C. Low sodium only, no carbs
D. Cholesterol loading, high fat

back 134

B. Healthy choices and carb counting

front 135

Metabolic improvements often require what weight loss range with activity and RD meetings?
A. 1–3% weight loss
B. 3–5% weight loss
C. 5–7% weight loss
D. 7–8.5% weight loss

back 135

D. 7–8.5% weight loss

front 136

Which group often consumes ~65–75% energy from carbohydrate with reported benefits?
A. Competitive powerlifters
B. Vegans or vegetarians
C. Carnivore dieters
D. Ketogenic dieters

back 136

B. Vegans or vegetarians

front 137

Observational studies in diabetes report A1C benefits from which pattern?
A. Lower carb, higher fat
B. Higher carb, lower fat
C. Higher protein, lower carb
D. Higher fat, higher carb

back 137

B. Higher carb, lower fat

front 138

As weight loss progresses in type 2 diabetes, patients may become more:
A. Insulin resistant than deficient
B. Insulin deficient than resistant
C. Glucagon deficient than resistant
D. Amylin resistant than deficient

back 138

B. Insulin deficient than resistant

front 139

This shift helps explain why some type 2 patients eventually need:
A. ACE inhibitors
B. Insulin injections
C. Antioxidant supplements
D. Glucagon injections

back 139

B. Insulin injections

front 140

A patient notices better control when meal carbs are consistent. This implies:
A. Carb-consistent diet improves sugars
B. Protein variability improves sugars
C. Fat cycling improves sugars
D. Sodium loading improves sugars

back 140

A. Carb-consistent diet improves sugars

front 141

After a protein-only meal, plasma glucose barely changes. Which immediate hormonal pattern is expected?
A. Insulin rises, glucagon falls
B. Glucagon rises, insulin falls
C. Neither insulin nor glucagon rises
D. Insulin and glucagon both rise

back 141

D. Insulin and glucagon both rise

front 142

Which amino acid category is a substrate for gluconeogenesis?
A. Nonessential amino acids
B. Essential amino acids
C. Branched-chain amino acids
D. Aromatic amino acids

back 142

A. Nonessential amino acids

front 143

In type 2 diabetes, which dietary component lowers total and LDL cholesterol?
A. Omega-3 fish oil capsules
B. Plant sterol/stanol esters
C. Dietary cholesterol supplements
D. Medium-chain triglyceride oil

back 143

B. Plant sterol/stanol esters

front 144

ADA-recommended bariatric surgery for type 2 diabetes is best captured by:
A. BMI 32, good medical control
B. BMI 35, no comorbidities
C. BMI 38, comorbidities hard to control
D. BMI 40, comorbidities easily controlled

back 144

C. BMI 38, comorbidities hard to control

front 145

A patient on glyburide plans to drink alcohol tonight. Best advice?
A. Avoid all alcohol permanently
B. Drink fasting to prevent spikes
C. Omit dinner to offset calories
D. Consume with food to reduce hypoglycemia

back 145

D. Consume with food to reduce hypoglycemia

front 146

Which statement about moderate alcohol intake is supported in these notes?
A. Increases CVD mortality substantially
B. Associated with lower CVD mortality
C. Eliminates hypoglycemia risk on insulin
D. Requires skipping meals to compensate

back 146

B. Associated with lower CVD mortality

front 147

A patient asks how to “count” alcohol in their meal plan. Best guidance?
A. Replace dinner carbs with alcohol
B. Skip meals to balance calories
C. Add to meal plan; omit none
D. Use alcohol as bedtime snack

back 147

C. Add to meal plan; omit none

front 148

Which basal insulin is typically dosed twice daily?
A. Glargine
B. Detemir
C. Degludec
D. NPH

back 148

D. NPH

front 149

For a simplified insulin regimen, which premixed insulin is usually prescribed for type 2 diabetes?
A. Humulin/Novolin 70/30
B. Lispro only regimen
C. Aspart correction
D. Glargine plus pramlintide

back 149

A. Humulin/Novolin 70/30

front 150

In insulin-treated patients, glucose 30–60 minutes after a meal is typically:
A. Near fasting nadir
B. Near postprandial peak
C. Unchanged from baseline
D. Below baseline typically

back 150

B. Near postprandial peak

front 151

In many patients, glucose about 2 hours after a meal is ideally:
A. Still rising sharply
B. At absolute minimum
C. Doubles above baseline
D. Returning toward baseline

back 151

D. Returning toward baseline

front 152

First-line pharmacotherapy for most type 2 diabetes is:
A. Exenatide monotherapy
B. Glyburide monotherapy
C. Metformin monotherapy
D. Canagliflozin monotherapy

back 152

C. Metformin monotherapy

front 153

Why do many type 2 diabetics benefit from combination therapy?
A. Avoid all lifestyle changes
B. Address different pathophysiologic defects
C. Eliminate need for monitoring
D. Guarantee insulin independence lifelong

back 153

B. Address different pathophysiologic defects

front 154

Over time, many type 2 diabetics require:
A. Insulin therapy, alone or combined
B. Lifelong diet alone
C. Only alpha-glucosidase inhibitors
D. Only GLP-1 agonists

back 154

A. Insulin therapy, alone or combined

front 155

A patient starts pramlintide for postmeal spikes. What is the key effect pair?
A. Increase glucagon; speed emptying
B. Increase insulin; speed emptying
C. Decrease glucagon; delay emptying
D. Block renal glucose reabsorption

back 155

C. Decrease glucagon; delay emptying

front 156

Acarbose lowers postprandial glycemia primarily by:
A. Enhance GLP-1 receptor signaling
B. Inhibit intestinal α-glucosidase enzyme
C. Increase renal glucose excretion
D. Activate PPAR-gamma in adipose

back 156

B. Inhibit intestinal α-glucosidase enzyme

front 157

Metformin lowers glucose mainly by:
A. Suppress hepatic glucose production
B. Stimulate pancreatic insulin secretion
C. Increase gastric emptying speed
D. Block intestinal fat absorption

back 157

A. Suppress hepatic glucose production

front 158

Which statement about metformin is true?
A. Promotes insulin secretion acutely
B. Acts as GLP-1 agonist
C. Blocks DPP-4 degradation
D. Does not stimulate insulin secretion

back 158

D. Does not stimulate insulin secretion

front 159

Sitagliptin works primarily by:
A. Block SGLT2 in proximal tubule
B. Inhibit DPP-4 degrading incretins
C. Directly open beta-cell KATP
D. Bind PPAR-gamma receptors

back 159

B. Inhibit DPP-4 degrading incretins

front 160

DPP-4 inhibition most directly causes:
A. Increase glucagon and insulin
B. Decrease insulin; increase glucagon
C. Glucose-dependent insulin rise; glucagon falls
D. Insulin rise independent of glucose

back 160

C. Glucose-dependent insulin rise; glucagon falls

front 161

GLP-1 receptor agonists typically:
A. Increase glucagon; speed emptying
B. Decrease insulin; increase appetite
C. Increase insulin always; hypoglycemia
D. Delay emptying; lower glucagon; raise insulin

back 161

D. Delay emptying; lower glucagon; raise insulin

front 162

Which hormone set directly stimulates gluconeogenesis?
A. Insulin, leptin, GLP-1
B. Thyroxine, calcitonin, PTH
C. Amylin, GIP, somatostatin
D. Cortisol, adrenaline, glucagon

back 162

D. Cortisol, adrenaline, glucagon

front 163

Which set correctly lists ketone bodies?
A. Lactate, pyruvate, alanine
B. Acetoacetate, acetone, beta-hydroxybutyrate
C. Citrate, succinate, fumarate
D. Glucose, glycogen, galactose

back 163

B. Acetoacetate, acetone, beta-hydroxybutyrate

front 164

Ketone bodies in insulin absence derive primarily from:
A. Oxaloacetate from glycolysis
B. Glucose-6-phosphate from glycogen
C. Malonyl-CoA from lipogenesis
D. Acetyl-CoA from FFA oxidation

back 164

D. Acetyl-CoA from FFA oxidation

front 165

At type 1 diabetes diagnosis, an initial total daily insulin dose is about:
A. 0.1–0.2 units/kg/day
B. 1.0–1.2 units/kg/day
C. 0.5–0.6 units/kg/day
D. 2.0–3.0 units/kg/day

back 165

C. 0.5–0.6 units/kg/day

front 166

Initial total daily insulin is typically divided as:
A. All basal, no bolus
B. Mostly bolus, minimal basal
C. One-third basal, two-thirds bolus
D. Half basal, half bolus

back 166

C. One-third basal, two-thirds bolus

front 167

Alcohol should be consumed with food to reduce hypoglycemia risk in:
A. Patients on metformin only
B. Patients on ACE inhibitors
C. Insulin or secretagogue users
D. Patients on SGLT2 inhibitors

back 167

C. Insulin or secretagogue users

front 168

During physiologic stress, which hormone directly stimulates gluconeogenesis?
A. Insulin
B. Leptin
C. Amylin
D. Glucagon

back 168

D. Glucagon