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70–110 mg/dL (lab-to-lab variation exists).
Liver (primary regulator)
Muscle
Adipose tissue
Pancreas (Islets of Langerhans)
Brain (uses glucose continuously)
Lowers blood glucose
How?
↑ Glucose uptake (muscle, adipose)
↑ Glycogenesis
↑ Lipogenesis
↑ Protein synthesis
↓ Gluconeogenesis
↓ Glycogenolysis
↓ Lipolysis
Raises blood glucose
↑ Glycogenolysis
↑ Gluconeogenesis
↑ Lipolysis
Rapid ↑ in glucose
↑ Glycogenolysis; ↓ insulin secretion
↑ Gluconeogenesis
↑ Protein breakdown
Causes hyperglycemia
Anti-insulin effect
↑ Lipolysis
↑ Insulin resistance
Mild ↑ glucose absorption & utilization
Dietary carbohydrates
Liver glycogen breakdown
Gluconeogenesis (lactate, glycerol, amino acids)
Collected in fluoride vial → inhibits glycolysis
Plasma preferred over serum
Glucose oxidase–peroxidase (GOD–POD)
Most common; specific
Hexokinase method
Reference method
Ortho-toluidine
Older method; less specific
Glucometer
Uses glucose oxidase or glucose dehydrogenase
Suspected diabetes
Gestational diabetes
Impaired glucose tolerance evaluation
3 days: normal carbohydrate diet
Overnight fast: 10–16 hours
No smoking/exercise during test
Fasting blood glucose measured
Administer 75 g anhydrous glucose orally
Measure plasma glucose at 2 hours
Normal: <100 mg/dL
IFG: 100–125 mg/dL
Diabetes: ≥126 mg/dL
Normal: <140 mg/dL
IGT: 140–199 mg/dL
Diabetes: ≥200 mg/dL
Fasting: <126 mg/dL
2 hours post-glucose: 140–199 mg/dL
Indicates pre-diabetes → high risk for progression.
Fasting glucose: 100–125 mg/dL
2-hour value: <140 mg/dL
Represents early glucose dysregulation.
From β-cells as proinsulin → insulin + C-peptide
C-peptide helps measure endogenous insulin levels.
Glucose (most potent)
Amino acids
Fatty acids
Incretins (GLP-1, GIP)
Via tyrosine kinase receptor
Activates:
GLUT-4 translocation in muscle + adipose
Glycogen synthesis
Lipogenesis
Protein synthesis
Any one:
Fasting glucose ≥126 mg/dL
Random glucose ≥200 mg/dL + symptoms
2-hour glucose ≥200 mg/dL
HbA1c ≥6.5%
Autoimmune β-cell destruction
Absolute insulin deficiency
Seen in children
Prone to ketoacidosis
C-peptide low
Insulin resistance + β-cell dysfunction
Associated with obesity
C-peptide normal/high early, low late
More common in adults
Detected at 24–28 weeks
75 g OGTT:
Fasting ≥92
1 hour ≥180
2 hour ≥153
DKA
HHS (Type 2)
Hypoglycemia
Microvascular: retinopathy, nephropathy, neuropathy
Macrovascular: CAD, stroke, PVD
Foot ulcers
Infections
HbA1c → reflects 3-month glucose
Fasting glucose
C-peptide → endogenous insulin
Urine ketones → DKA
Autoantibodies (GAD, IA-2) in Type 1 DM
Insulin ↓ glucose; glucagon ↑ glucose.
GOD–POD is the commonest glucose test.
OGTT uses 75 g glucose; 2-hour >200 = diabetes.
IFG = fasting 100–125; IGT = 2-hour 140–199.
Insulin acts via tyrosine kinase / GLUT-4.
Type 1 = autoimmune; Type 2 = insulin resistance.
HbA1c ≥6.5% = diabetes.
C-peptide = endogenous insulin marker.
Any degree of glucose intolerance first recognized during pregnancy (usually 2nd or 3rd trimester).
Pregnancy hormones cause insulin resistance:
Human placental lactogen (hPL)
Progesterone
Cortisol
TNF-α
Growth hormone
Pancreas cannot compensate → hyperglycemia.
Obesity
Family history of diabetes
Previous GDM
PCOS
Macrosomic baby in past pregnancy
Multiple pregnancy
Age > 25 years
Unexplained stillbirth
75 g OGTT single-step test (DIPSI / WHO):
Venous plasma glucose:
Fasting ≥ 92 mg/dL
1 hour ≥ 180 mg/dL
2 hour ≥ 153 mg/dL
Any one abnormal value = GDM.
Type 2 DM later in life
Pre-eclampsia
Polyhydramnios
Preterm labor
Macrosomia
Shoulder dystocia
Neonatal hypoglycemia
RDS
Hyperbilirubinemia
Stillbirth (uncontrolled GDM)
Diet + exercise (first line)
Medical nutrition therapy
Insulin if needed
Metformin (allowed in many guidelines)
Continuous glucose monitoring in high-risk cases
Frequent fetal monitoring
Re-test mother at 6–12 weeks postpartum → 75 g OGTT
High risk of future Type 2 diabetes
Presence of glucose in urine after a high-carbohydrate meal, despite normal blood glucose.
Rapid intestinal absorption → sudden transient rise in blood glucose
Exceeds temporary renal threshold → glucose spills into urine
Often seen after heavy sweets/starch intake
Blood glucose is normal again by the time test is done.
No kidney disease.
No diabetes.
Common in:
Pregnancy
Large carbohydrate load
Individuals with low renal threshold
Benign condition
Does not progress to diabetes
Needs reassurance, not treatment
Glucosuria despite normal blood glucose because of defective glucose reabsorption in renal tubules.
Mutation in SGLT2 transporter (proximal tubule)
Glucose reabsorption impairment
Autosomal recessive
Completely benign
Fanconi syndrome
Pregnancy
Heavy metal poisoning
Certain drugs (e.g., SGLT2 inhibitors — intentionally cause glucosuria)
Blood glucose = normal
Persistent glucosuria
No ketones
No hyperglycemia
Normal GTT
No treatment usually required
| Feature | Alimentary | Renal Glucosuria |
|---|---|---|
| Cause | High CHO load | Tubular defect |
| Duration | Temporary | Persistent |
| Blood glucose | Normal | Normal |
| GTT | Normal | Normal |
| Pathology | None | Proximal tubule SGLT2 defect |
GDM → insulin resistance of pregnancy; diagnosed by 75 g OGTT; risk of macrosomia & neonatal hypoglycemia.
Alimentary glucosuria → glucose in urine after heavy carb intake; benign; transient.
Renal glucosuria → due to tubular SGLT2 defect; persistent glucosuria with normal sugars; benign.
Compounds that reduce cupric (Cu²⁺) to cuprous (Cu⁺) ions in Benedict’s / Fehling’s test.
Glucose (most common)
Fructose
Galactose
Lactose
Pentoses
Ascorbic acid
Certain drugs (salicylates, nalidixic acid)
Positive Benedict’s test ≠ Diabetes
Must confirm specific sugar (glucose oxidase dipstick is specific for glucose)
Galactosemia → galactose in urine
Hereditary fructose intolerance → fructose in urine
Alimentary glucosuria → transient glucose
Renal glucosuria → glucose with normal blood sugar
Presence of glucose in urine.
Occurs when:
Blood glucose exceeds renal threshold
(~ 180 mg/dL in normal adults)
Renal tubular reabsorption defect
(renal glucosuria)
Hyperglycemia exceeds renal threshold → glucose appears in urine.
Normal glucose but proximal tubule cannot reabsorb it
Seen in:
Familial renal glucosuria (SGLT2 defect)
Fanconi syndrome
Pregnancy (lowered renal threshold)
After heavy carbohydrate meal
Temporary and benign
Hormones increasing glucose:
Hyperthyroidism
Cushing syndrome
Acromegaly
Pheochromocytoma
Metabolic disorder characterized by:
Hyperglycemia
Disturbed metabolism of carbohydrates, fats, proteins
Due to insulin deficiency/resistance
Fasting plasma glucose ≥126 mg/dL
Random plasma glucose ≥200 mg/dL + symptoms
2-hour OGTT value ≥200 mg/dL
HbA1c ≥6.5%
Autoimmune destruction of β-cells
Absolute insulin deficiency
Younger age, thin body
Prone to DKA
Insulin resistance + β-cell dysfunction
Associated with obesity
Most common
May develop HHS
Onset during pregnancy
Diagnosed using 75 g OGTT
Pancreatitis, Cushing, acromegaly, steroid use, hemochromatosis
Polyuria
Polydipsia
Polyphagia
Often with weight loss
Blurred vision
Fatigue
Recurrent infections (UTI, candidiasis)
Slow wound healing
Ketonuria (Type 1)
DKA or HHS in severe cases
Retinopathy
Nephropathy
Neuropathy (peripheral, autonomic)
Coronary artery disease
Stroke
Peripheral vascular disease
Acanthosis nigricans (insulin resistance)
Skin infections (furuncles, candidiasis)
Erectile dysfunction
Neuropathic foot pain
Reducing substances ≠ glucose → Benedict’s detects all reducing sugars.
Dipstick detects only glucose (glucose oxidase).
Glycosuria occurs when blood glucose crosses renal threshold or tubular defect exists.
Diabetes diagnosed by FPG ≥126, 2 h OGTT ≥200, or HbA1c ≥6.5%.
Classical diabetes symptoms = polyuria, polydipsia, polyphagia, weight loss.
Type 1 → autoimmune → absolute insulin deficiency → DKA prone.
Type 2 → insulin resistance → obesity → HHS risk.
(Acute emergency of Type 1 DM)
Absolute insulin deficiency
↑ Glucagon → ↑ Lipolysis → ↑ Free fatty acids
FFAs enter liver → excess ketone bodies:
Acetoacetate
β-Hydroxybutyrate
Acetone
Results in metabolic acidosis (high anion gap)
Infection (most common)
Missed insulin doses
Myocardial infarction
Stroke
Trauma
Surgery
Polyuria, polydipsia, dehydration
Kussmaul breathing (deep, rapid)
Fruity (acetone) breath
Abdominal pain, vomiting
Altered consciousness
Blood glucose: 250–600 mg/dL
pH <7.3
HCO₃⁻ <18 mEq/L
Positive ketones
High anion gap metabolic acidosis
Potassium: initially high, body stores depleted
IV fluids (NS)
IV insulin infusion
Potassium replacement
Treat trigger (infection, etc.)
(Acute emergency of Type 2 DM)
Severe hyperglycemia → profound dehydration
Enough insulin present to prevent ketosis
Very high osmolality → CNS depression
Elderly, Type 2 DM
Profound dehydration
Confusion → coma
No Kussmaul breathing
No significant acidosis
Blood glucose: >600 mg/dL (often >1000 mg/dL)
pH: >7.3
HCO₃⁻ >18
Ketones: absent or mild
Serum osmolality: >320 mOsm/kg
Aggressive IV fluids
Insulin (lower dose than DKA)
Electrolyte replacement
| Feature | DKA | HHS |
|---|---|---|
| Type | Type 1 | Type 2 |
| Glucose | 250–600 | >600 |
| Ketones | Present | Absent/mild |
| pH | <7.3 | >7.3 |
| Osmolality | Mild ↑ | Very high ↑ |
| Onset | Rapid | Slow (days) |
| Mortality | Lower | Higher |
Accumulation of lactic acid → high anion gap metabolic acidosis.
Shock
Sepsis
Severe anemia
Cardiac failure
Hypoxia
Carbon monoxide poisoning
Metformin
Alcohol
Liver disease
Malignancies
Drugs/toxins
Deep breathing
Hypotension
Severe acidosis
Altered sensorium
Lactate > 5 mmol/L
pH < 7.35
High anion gap metabolic acidosis
Non-proliferative → microaneurysms, hemorrhages
Proliferative → neovascularization
Risk increased by poor glycemic control
Microalbuminuria → macroalbuminuria → CKD
Kimmelstiel-Wilson nodules (nodular glomerulosclerosis)
Peripheral (glove-and-stocking)
Autonomic → gastroparesis, impotence, orthostatic hypotension
Coronary artery disease
Cerebrovascular disease (stroke)
Peripheral arterial disease
Foot ulcers
Infections (skin, UTI, candidiasis)
Gastroparesis
Diabetic dermopathy
Erectile dysfunction
Glycosylation of hemoglobin at N-terminal valine of β-chain
Reflects average glucose over 8–12 weeks
Normal: <5.7%
Pre-diabetes: 5.7–6.4%
Diabetes: ≥6.5%
Most patients: <7%
Stringent control (<6.5%) in young adults
Lenient control (<8%) in elderly/comorbid
No fasting required
Reflects long-term control
Useful for treatment monitoring
False values in:
Hemolytic anemia
Hemoglobinopathies
Recent blood transfusion
Chronic kidney disease (carbamylated Hb)
DKA = Type 1, ketones + acidosis + Kussmaul breathing.
HHS = Type 2, severe hyperglycemia + hyperosmolality, no ketones.
Lactic acidosis = high lactate, high anion gap acidosis.
Chronic complications = microvascular (retina, kidney, nerves), macrovascular (heart, brain, vessels).
HbA1c ≥6.5% = diabetes; reflects last 3 months.
Because of coordinated actions of insulin, glucagon, and other counter-regulatory hormones (cortisol, GH, adrenaline).
Insulin — only hormone that lowers glucose.
Serum takes time to clot → glucose falls due to glycolysis.
Plasma (with fluoride) prevents glycolysis.
Around 180 mg/dL.
Above this → glucose appears in urine.
Detects early abnormalities in glucose handling: IGT and GDM.
Pregnancy lowers renal threshold → benign glucosuria.
IFG = high fasting glucose
IGT = high 2-hour post-glucose value
Type 1 has absolute insulin deficiency, so lipolysis is uncontrolled → ketone production.
Type 2 has some insulin which suppresses ketosis.
Because metabolic acidosis stimulates respiratory compensation → deep rapid breathing.
Presence of enough insulin to inhibit ketogenesis.
Poor tissue perfusion → anaerobic glycolysis → excess lactate.
Microalbuminuria (30–300 mg/day).
RBC lifespan = 120 days, so glycation reflects ~3-month glucose.
No — hemolysis, transfusions, and CKD can give false results.
High glucose impairs neutrophil function, circulation, and immunity.
Combination of:
Peripheral neuropathy
Poor blood supply
Infection
Loss of sensation
Post-meal hyperglycemia produces oxidative stress → endothelial damage.
No insulin → lipolysis and proteolysis → muscle and fat loss.
Osmotic diuresis due to glucose in urine.
Acidosis shifts K⁺ out of cells, but total body K⁺ is low.
These are the most exam-relevant statements for rapid recall.
Insulin is the only hypoglycemic hormone; all others raise glucose.
GLUT-4 is insulin-dependent (muscle + adipose).
Liver controls fasting glucose via glycogenolysis and gluconeogenesis.
Fluoride inhibits glycolysis.
GOD–POD is the most common method; hexokinase is the reference method.
Glucometers use glucose oxidase or glucose dehydrogenase.
OGTT uses 75 g glucose.
IFG = fasting 100–125 mg/dL.
IGT = 2-hour 140–199 mg/dL.
Diabetes = 2-hour ≥200 mg/dL.
Type 1: autoimmune, ketosis-prone, low C-peptide.
Type 2: insulin resistance, associated with obesity, acanthosis nigricans.
Diagnostic criteria:
Fasting ≥126
Random ≥200
2 hr OGTT ≥200
HbA1c ≥6.5%
DKA: Type 1, ketones + metabolic acidosis + Kussmaul breathing.
HHS: Type 2, very high sugars, hyperosmolarity, no ketones.
Lactic acidosis: lactate >5 mmol/L, high anion gap.
Retinopathy
Nephropathy (first sign = microalbuminuria)
Neuropathy (stocking–glove)
CAD, Stroke, PAD
Foot ulcers
Infections
Gastroparesis
Erectile dysfunction
Reflects 3-month glucose.
Target in most diabetics: <7%.
False low: hemolysis, blood loss, CKD.
False high: iron deficiency anemia.
Renal glucosuria: tubular defect (SGLT2).
Alimentary glucosuria: transient after heavy carbs.
Diabetic glucosuria: blood glucose > renal threshold.
Occurs due to pregnancy-induced insulin resistance.
Diagnosed by 75 g OGTT at 24–28 weeks.
HbA1c ≥6.5% = diabetes.
IGT = 2-hour 140–199 mg/dL; IFG = 100–125 mg/dL.
DKA → ketones + acidosis + dehydration.
HHS → glucose >600 mg/dL, osmolality >320, no ketosis.
Microalbuminuria = earliest sign of nephropathy.
Post-prandial glucose predicts CV risk better than fasting.
Type 1 = autoimmunity (GAD antibodies).
A. Glucagon
B. Cortisol
C. Growth hormone
D. Insulin
Answer: D. Insulin
A. Glucagon
B. Insulin
C. Cortisol
D. Thyroxine
Answer: B. Insulin
A. GOD–POD
B. Hexokinase
C. Benedict’s test
D. Glucose oxidase strip
Answer: B. Hexokinase
A. 50 g
B. 60 g
C. 75 g
D. 100 g
Answer: C. 75 g
A. Diabetes mellitus
B. Impaired fasting glycemia
C. Impaired glucose tolerance
D. Normal
Answer: B. Impaired fasting glycemia
A. Normal
B. Diabetes
C. IGT
D. Renal glucosuria
Answer: C. IGT
A. >5.7%
B. >6.0%
C. ≥6.5%
D. ≥7.0%
Answer: C. ≥6.5%
A. Calcitonin
B. Cortisol
C. Oxytocin
D. ADH
Answer: B. Cortisol
A. 90 mg/dL
B. 140 mg/dL
C. 180 mg/dL
D. 220 mg/dL
Answer: C. 180 mg/dL
A. Type 2 DM
B. Type 1 DM
C. Renal glucosuria
D. Uncontrolled DKA
Answer: C. Renal glucosuria
A. Exercise
B. High-fat meal
C. Infection
D. Dehydration
Answer: C. Infection
A. pH > 7.4
B. HCO₃⁻ > 20
C. High anion gap metabolic acidosis
D. Low ketones
Answer: C. High anion gap metabolic acidosis
A. DKA
B. HHS (Hyperosmolar state)
C. Lactic acidosis
D. Hypoglycemia
Answer: B. HHS
A. Hypoglycemia
B. HHS
C. DKA
D. Renal glycosuria
Answer: C. DKA
A. 1 mmol/L
B. 2 mmol/L
C. 3 mmol/L
D. 5 mmol/L
Answer: D. 5 mmol/L
A. Fasting glucose
B. HbA1c
C. 75 g OGTT
D. Random glucose
Answer: C. 75 g OGTT
A. Diabetes mellitus
B. Kidney disease
C. High carbohydrate meal
D. Fanconi syndrome
Answer: C. High carbohydrate meal
A. Proteinuria
B. Edema
C. Microalbuminuria
D. Reduced GFR
Answer: C. Microalbuminuria
A. Retinopathy
B. Neuropathy
C. Nephropathy
D. Coronary artery disease
Answer: D. Coronary artery disease
(Macrovascular.)
A. 1 week
B. 2 weeks
C. 1 month
D. 2–3 months
Answer: D. 2–3 months
A. Type 2
B. LADA
C. Type 1
D. MODY
Answer: C. Type 1
A. Type 2 DM
B. Renal failure
C. Type 1 DM
D. Alimentary glucosuria
Answer: C. Type 1 DM
A. Severe ketosis
B. Glucose < 200 mg/dL
C. Severe dehydration
D. Low serum osmolality
Answer: C. Severe dehydration
A. Insulin
B. Aldosterone
C. Glucagon
D. Thyroxine
Answer: C. Glucagon
A. Fasting glucose
B. Postprandial glucose
C. HbA1c
D. Random glucose
Answer: C. HbA1c
A 17-year-old boy presents with 3 weeks of polyuria, excessive thirst, fatigue, and weight loss. Random glucose is 320 mg/dL. Urine ketones are positive.
Diagnosis:
➡️ Type 1 Diabetes Mellitus
Reason:
Hyperglycemia + weight loss + ketosis strongly suggest Type 1 DM.
A 45-year-old sedentary man has:
Fasting glucose: 112 mg/dL
2-hour OGTT: 125 mg/dL
HbA1c: 5.8%
Diagnosis:
➡️ Impaired Fasting Glycemia (IFG)
A 50-year-old woman undergoes OGTT:
Fasting: 95 mg/dL
2-hour: 172 mg/dL
Diagnosis:
➡️ Impaired Glucose Tolerance (IGT)
A 70-year-old diabetic woman presents with lethargy, dehydration, and confusion.
Investigations:
Glucose: 880 mg/dL
Serum osmolality: 340 mOsm/kg
pH: 7.38
No ketones
Diagnosis:
➡️ Hyperosmolar Hyperglycemic State (HHS)
A 21-year-old Type 1 diabetic skipped insulin. Now breathing deeply and rapidly (Kussmaul).
Lab:
Glucose: 420 mg/dL
pH: 7.12
HCO₃⁻: 10
Ketones: Positive
Diagnosis:
➡️ Diabetic Ketoacidosis (DKA)
A 60-year-old man in septic shock shows:
Lactate: 8 mmol/L
pH: 7.21
High anion gap acidosis
Diagnosis:
➡️ Lactic Acidosis (Type A) due to hypoperfusion.
A 52-year-old obese man has recurrent fungal infections.
HbA1c = 9.8%
Interpretation:
➡️ Poor glycemic control over the last 3 months.
28-year-old pregnant woman at 26 weeks:
Fasting = 95 mg/dL
1 hr = 182 mg/dL
2 hr = 168 mg/dL
Diagnosis:
➡️ Gestational Diabetes Mellitus (GDM)
A 20-year-old woman:
Fasting glucose: 88 mg/dL
Urine glucose: positive
OGTT: normal
Diagnosis:
➡️ Renal Glucosuria (tubular SGLT2 defect)
A boy eats a lot of sweets at a party. Urine next morning shows glucose.
Fasting sugar = 90 mg/dL.
Diagnosis:
➡️ Alimentary Glucosuria (benign)
A 34-year-old diabetic on SGLT2 inhibitors presents with abdominal pain, nausea, and ketonuria but glucose of only 180 mg/dL.
Diagnosis:
➡️ Euglycemic DKA (SGLT2 inhibitor–related)
A 60-year-old diabetic complains of burning sensation and loss of vibration sense in feet.
Diagnosis:
➡️ Diabetic Peripheral Neuropathy
A 48-year-old diabetic has blurred vision. Fundus: microaneurysms & cotton-wool spots.
Diagnosis:
➡️ Non-proliferative Diabetic Retinopathy
A 55-year-old diabetic has urine albumin: 75 mg/day.
Diagnosis:
➡️ Early Diabetic Nephropathy (Microalbuminuria)
A smoker has:
HbA1c: 7.0%
Fasting glucose: 95 mg/dL
Fructosamine: normal
Reason:
➡️ Falsely high HbA1c (carbonylation / hemoglobin abnormalities)
A 45-year-old man has recurrent hypoglycemia.
Insulin: High
C-peptide: High
Diagnosis:
➡️ Insulinoma
A chronic alcoholic presents with:
Ketones high
Glucose normal
pH: 7.19
Diagnosis:
➡️ Alcoholic Ketoacidosis
A 64-year-old diabetic has a chronic foot ulcer with reduced pulses in the limb.
Diagnosis:
➡️ Peripheral Arterial Disease (macrovascular complication)
Diagnosis:
➡️ Metabolic Syndrome (Syndrome X)
A 25-year-old has:
HbA1c = 4.8%
Recurrent osmotic symptoms
Fasting glucose = 142 mg/dL
Diagnosis:
➡️ Diabetes (HbA1c misleading due to hemolysis/high RBC turnover)
A woman with anemia has:
HbA1c = 12.4%
Fasting glucose = 115 mg/dL
Interpretation:
➡️ False high HbA1c due to prolonged RBC survival in iron deficiency.
A child with newly diagnosed DM has severe dehydration, deep breathing, and fruity breath.
Diagnosis:
➡️ DKA (classic presentation)
A 70-year-old bedridden diabetic:
Glucose: 780 mg/dL
Osmolality: 345 mOsm/kg
pH: 7.39
Ketones: none
Diagnosis:
➡️ HHS (Hyperosmolar state)
A 62-year-old diabetic on metformin has:
Lactate: 7.2 mmol/L
pH: 7.19
Diagnosis:
➡️ Metformin-induced lactic acidosis
Fundus: vitreous hemorrhage, neovascularization.
Diagnosis:
➡️ Proliferative Diabetic Retinopathy
70–110 mg/dL.
Insulin (the only hypoglycemic hormone).
The liver.
GLUT-4 (muscle and adipose tissue).
Around 180 mg/dL.
Hexokinase method.
It inhibits glycolysis (preserves glucose).
Diagnosing diabetes, IGT, and GDM.
75 g anhydrous glucose.
Fasting glucose 100–125 mg/dL.
2-hour OGTT value 140–199 mg/dL.
2-hour plasma glucose ≥200 mg/dL.
Glycation of hemoglobin that reflects 2–3 months’ average blood glucose.
≥6.5%.
Hemolysis, recent transfusion, anemia, CKD.
Polyuria, polydipsia, polyphagia.
Osmotic diuresis due to glucose in urine.
Type 1 diabetes.
Assess endogenous insulin production.
Fat and muscle breakdown due to absence of insulin.
Microalbuminuria.
Retinopathy, nephropathy, neuropathy.
CAD, stroke, peripheral arterial disease.
Chronic hyperglycemia damaging retinal vessels.
Sorbitol accumulation + microvascular ischemia.
Impaired immunity and high glucose environment.
Insulin deficiency → lipolysis → ketone production → metabolic acidosis.
Kussmaul breathing (deep, rapid).
<7.3.
High anion gap metabolic acidosis.
Insulin drives K⁺ into cells.
Enough insulin present to block ketogenesis.
600 mg/dL (often >1000 mg/dL).
Severe dehydration and hyperosmolarity leading to coma.
320 mOsm/kg.
Accumulation of lactate causing metabolic acidosis.
Metformin (especially in renal failure).
Tissue hypoxia → anaerobic glycolysis → lactate accumulation.
Glucose intolerance first diagnosed in pregnancy.
75 g OGTT at 24–28 weeks.
Lowered renal threshold for glucose.
Glucose in urine despite normal blood glucose due to tubular SGLT2 defect.
Glucosuria after heavy carbohydrate intake (benign; transient).
Protein kinase C activation and microvascular damage.
Endothelial dysfunction + accelerated atherosclerosis.
Strong predictor of atherosclerosis and cardiovascular events.
Obesity + high BP + high TG + low HDL + high fasting glucose.
DKA with near-normal glucose (seen with SGLT2 inhibitors).
Elevated LDH + low haptoglobin.
Short-term glycemic control marker (2–3 weeks).
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