Diabetes Mellitus & Its Complications - Cheat Sheet
Your final 30-minute exam companion covering types, insulins, acute emergencies, and chronic complications. Every item here has appeared on the NLE.
Pathophysiology & Diagnostic Criteria
Common values
Value
70–100 mg/dL
Symbol
FPG
Quantity
Normal fasting plasma glucose
Value
≥126 mg/dL
Symbol
FPG
Quantity
Diabetes fasting glucose
Value
<5.7%
Symbol
HbA1c
Quantity
Normal HbA1c
Value
≥6.5%
Symbol
HbA1c
Quantity
Diabetes HbA1c
Value
<7%
Symbol
HbA1c target
Quantity
Treatment target HbA1c
Important facts
- Type 1 DM: autoimmune, absolute insulin deficiency, younger onset, lean, ALWAYS requires insulin, prone to DKA
- Type 2 DM: insulin resistance, relative deficiency, older/overweight (rising in youth), managed with diet/oral agents/insulin, prone to HHNS
- Classic 3 Ps: polyuria, polydipsia, polyphagia; plus fatigue, weight loss (Type 1), blurred vision, slow healing
- Diagnostic thresholds: fasting glucose ≥126 mg/dL; random ≥200 mg/dL with symptoms; 2-hr OGTT ≥200 mg/dL; HbA1c ≥6.5%
- Normal fasting glucose: 70–100 mg/dL; prediabetes: 100–125 mg/dL fasting or 100–199 mg/dL random
Key definitions
Diabetes Mellitus
Example
Type 1: autoimmune destruction of pancreatic beta cells; Type 2: insulin resistance + relative deficiency
Disorder of glucose metabolism from lack of insulin, resistance to insulin, or both, resulting in hyperglycemia and metabolic derangement.
Hyperglycemia
Example
A fasting glucose of 150 mg/dL confirms hyperglycemia and diabetes
Elevated blood glucose (>126 mg/dL fasting) due to insufficient insulin action or production.
HbA1c (Glycosylated Hemoglobin)
Example
HbA1c of 8% means average glucose ~185 mg/dL over the past 3 months
Average blood glucose over 2–3 months; diagnostic at ≥6.5%, treatment target <7%.
Diagrams to know
- Type 1 vs. Type 2 pathophysiology flow
- Diagnostic criteria decision tree
Insulin Types, Onset, Peak, Duration — THE MOST TESTED TABLE
Common values
Value
30 min–1.5 hr
Symbol
Peak (rapid)
Quantity
Rapid-acting peak time
Value
2–4 hr
Symbol
Peak (regular)
Quantity
Regular insulin peak time
Value
6–12 hr
Symbol
Peak (NPH)
Quantity
NPH peak time
Value
PEAKLESS
Symbol
Peak (glargine)
Quantity
Glargine peak time
Important facts
- RAPID-ACTING (lispro, aspart, glulisine): onset ~15 min, PEAK ~30 min–1.5 hr, duration 3–4 hr — give WITH meal (food must be ready first)
- SHORT-ACTING/REGULAR: onset ~30 min–1 hr, PEAK 2–4 hr, duration 5–8 hr — ONLY insulin given IV (DKA/HHNS drips)
- INTERMEDIATE/NPH: onset 1–2 hr, PEAK 6–12 hr (CLOUDY appearance — roll gently, don't shake), duration 12–18 hr
- LONG-ACTING (glargine, detemir): onset ~1 hr, PEAKLESS (no pronounced peak), duration ~24 hr — NEVER mixed with other insulins
- Mixing rule: draw CLEAR (regular) BEFORE CLOUDY (NPH); inject air into NPH vial first, then regular vial, then withdraw regular, then NPH
- Rotate injection sites within one anatomic area to prevent lipohypertrophy; abdomen absorbs fastest and most consistently
- In-use insulin stored at room temp (25°C) for 1 month; unopened vials refrigerated at 2–8°C
Key definitions
Onset
Example
Rapid-acting lispro has onset ~15 minutes; regular has onset ~30 min–1 hour
Time from injection until insulin begins to lower blood glucose.
Peak
Example
NPH peaks at 6–12 hours; this is when hypoglycemia is most likely if the patient skips a meal
Time of maximum insulin action (maximum hypoglycemia risk).
Duration
Example
Regular insulin lasts 5–8 hours; glargine lasts ~24 hours (peakless)
Total time insulin remains active in the body.
Diagrams to know
- Insulin onset–peak–duration timeline (visual comparison of all types)
- Insulin mixing preparation sequence
Oral & Non-Insulin Agents (Type 2 Management)
Important facts
- Metformin: first-line, no hypoglycemia alone, HOLD around contrast and in renal disease, GI upset common, take with food
- Sulfonylureas: hypoglycemia + weight gain risk; use caution with alcohol
- Meglitinides (repaglinide, nateglinide): short-acting, skip dose if skipping meal
- Thiazolidinediones (pioglitazone): improve insulin sensitivity but fluid retention (contraindicated in heart failure), weight gain, hepatotoxicity
- DPP-4 inhibitors (sitagliptin): minimal hypoglycemia risk, well-tolerated
- SGLT2 inhibitors: EUGLYCEMIC DKA risk — patient may have normal/near-normal glucose during DKA, alert all providers
- GLP-1 agonists: weight loss benefit, GI side effects; injectable only
Key definitions
Biguanide (Metformin)
Example
HOLD metformin around contrast dye studies (contrast-induced nephropathy risk) and in renal impairment; risk of lactic acidosis
First-line oral agent that decreases hepatic glucose output and improves insulin sensitivity; does NOT cause hypoglycemia alone.
Sulfonylureas (Glipizide, Glyburide)
Example
Glyburide + alcohol → disulfiram-like reaction (flushing, nausea)
Insulin secretagogues that stimulate pancreatic beta cells; carry hypoglycemia risk and weight gain.
SGLT2 Inhibitors (Empagliflozin, Dapagliflozin)
Example
Dapagliflozin lowers glucose independent of insulin; patient may have normal glucose during DKA
Cause glucose excretion in urine; unique euglycemic DKA risk; watch for genital/urinary infections.
GLP-1 Receptor Agonists (Liraglutide, Semaglutide)
Example
Semaglutide is often given once weekly; excellent for weight reduction alongside glucose control
Injectable agents promoting weight loss, improve glycemic control; GI side effects (nausea, vomiting).
Diagrams to know
- Oral agent mechanism of action summary
Acute Complications: Hypoglycemia
Common values
Value
<70 mg/dL
Symbol
Glucose critical
Quantity
Hypoglycemia threshold
Value
15 g
Symbol
CHO
Quantity
Fast carbohydrate dose (Rule of 15)
Value
15 minutes
Symbol
Time interval
Quantity
Recheck time after treatment
Important facts
- Hypoglycemia signs ('cold and clammy — need some candy'): shakiness, sweating (diaphoresis), tachycardia, hunger, anxiety, pallor
- Severe hypoglycemia (brain deprived): confusion, slurred speech, blurred vision, seizures, loss of consciousness, coma
- CONSCIOUS patient: Rule of 15 — 15 g fast carbs (juice, soda, glucose tablets), recheck in 15 min, repeat if needed, then eat longer-acting snack/meal
- UNCONSCIOUS or unable to swallow: IV dextrose (D50) in hospital OR IM/subcutaneous glucagon out of hospital
- NEVER give oral fluids to unconscious patient (aspiration risk)
- Hypoglycemia unawareness: in chronic diabetes, loss of warning signs due to autonomic neuropathy — high risk for severe episodes
- Post-hypoglycemia: rebound hyperglycemia possible (Somogyi phenomenon)
Key definitions
Hypoglycemia
Example
A patient on NPH insulin who skips breakfast may become hypoglycemic at 10 a.m. (during the peak)
Blood glucose <70 mg/dL; most common acute diabetic emergency; rapid onset from too much insulin/oral agent, skipped meals, or extra activity.
Rule of 15
Example
½ cup fruit juice (15 g carbs) → wait 15 min → recheck glucose → if still <100, repeat; then give crackers with peanut butter
Treatment for conscious hypoglycemic patient: give 15 g fast-acting carbohydrate, recheck in 15 min, repeat if still low, then provide longer-acting snack.
Diagrams to know
- Hypoglycemia recognition and management flowchart
Acute Complications: DKA (Diabetic Ketoacidosis)
Common values
Value
Usually 250–600 mg/dL (can exceed)
Symbol
Glucose
Quantity
DKA glucose range
Value
<7.35
Symbol
pH
Quantity
DKA pH threshold
Value
7.35–7.45
Symbol
pH normal
Quantity
Normal pH
Important facts
- DKA typical in Type 1 DM; triggered by infection, illness, omitted insulin, or other stress
- Classic triad: HYPERGLYCEMIA (usually 250–600 mg/dL, can exceed), KETONES (blood/urine), ACIDOSIS (pH <7.35, low HCO3–)
- Signs: Kussmaul respirations, fruity/acetone breath odor, dehydration, nausea/vomiting/abdominal pain, altered mental status
- Onset: hours (rapid, unlike HHNS which is days)
- Labs: glucose >250, positive serum/urine ketones, pH <7.35, low bicarbonate, elevated anion gap, elevated BUN/creatinine (dehydration)
- Mortality: lower than HHNS but still serious (~5%); cerebral edema is a complication, especially in children
Key definitions
Diabetic Ketoacidosis (DKA)
Example
Patient with Type 1 DM misses insulin injections → develops hyperglycemia, ketosis, and acidosis within hours
Life-threatening metabolic emergency in Type 1 DM: absolute insulin lack → uncontrolled lipolysis → ketone production and metabolic ACIDOSIS.
Kussmaul Respirations
Example
Patient breathing 35 times/min with deep breaths and fruity breath odor during DKA
Deep, rapid, labored breathing (compensatory response to metabolic acidosis to blow off CO₂).
Ketones
Example
Beta-hydroxybutyrate >3 mmol/L indicates significant ketosis
Acidic byproducts of uncontrolled fat metabolism; measured in blood and urine; present in DKA but NOT in HHNS.
Diagrams to know
- DKA pathophysiology cascade (insulin lack → lipolysis → ketones → acidosis)
Acute Complications: HHNS (Hyperglycemic Hyperosmolar Nonketotic Syndrome)
Common values
Value
Often >600, can exceed 1000 mg/dL
Symbol
Glucose
Quantity
HHNS glucose range
Value
>320 mOsm/kg
Symbol
Osmolality
Quantity
HHNS serum osmolality
Value
280–300 mOsm/kg
Symbol
Osmolality normal
Quantity
Normal serum osmolality
Important facts
- HHNS typical in Type 2 DM, often older patients; triggered by infection, illness, poor intake, or diuretic use
- Extreme hyperglycemia: glucose often >600, can exceed 1,000 mg/dL (often higher than DKA)
- Profound dehydration: water loss greater than electrolyte loss → high osmolality
- NO significant ketosis/acidosis: enough residual insulin to suppress lipolysis but not hyperglycemia control
- Labs: very high glucose, HIGH serum osmolality (>320), normal/near-normal pH, minimal/no ketones, elevated BUN/creatinine
- Signs: severe neurologic changes (lethargy, confusion, seizures, coma), absent Kussmaul respiration, no fruity breath
- Onset: days (slower than DKA)
- Mortality: HIGHER than DKA (~15%), especially in elderly; renal failure and thrombosis common
Key definitions
HHNS (HHS)
Example
Elderly Type 2 patient with infection develops glucose >1000 mg/dL, severe dehydration, but pH remains near-normal
Life-threatening metabolic emergency in Type 2 DM: enough insulin to prevent ketosis but not hyperglycemia → extreme hyperglycemia, profound dehydration, HIGH osmolality, WITHOUT significant ketosis/acidosis.
Serum Osmolality
Example
Osmolality >350 associated with seizures, coma, and high mortality
Concentration of dissolved particles in blood; elevated in HHNS (>320 mOsm/kg), causing cellular dehydration and CNS dysfunction.
Diagrams to know
- HHNS pathophysiology (insulin insufficiency for glucose control but enough to prevent ketosis)
DKA vs. HHNS — Critical Comparison
Important facts
- DKA: Type 1, glucose 250–600, KETONES + ACIDOSIS present, Kussmaul/fruity breath, hours onset
- HHNS: Type 2, glucose >600 (up to >1000), NO significant ketosis/acidosis, no Kussmaul, days onset
- DKA mortality ~5%; HHNS mortality ~15% (older, sicker patients)
- Both require IV fluids, insulin, and potassium monitoring but different precipitants and complications
Diagrams to know
- DKA vs. HHNS comparison matrix
DKA/HHNS Management — The CRITICAL Sequence
Common values
Value
200–250 mg/dL
Symbol
Glucose threshold
Quantity
Glucose target for dextrose addition
Value
50–100 mg/dL/hr
Symbol
Drop rate
Quantity
Expected glucose drop rate
Important facts
- STEP 1: IV NORMAL SALINE (0.9%) FIRST — correct profound dehydration and restore perfusion (alone lowers glucose by ~50 mg/dL/hr)
- STEP 2: Regular insulin IV continuous drip — lowers glucose gradually (~50–100 mg/dL/hr target to avoid cerebral edema, especially in children)
- STEP 3: POTASSIUM MONITORING — the classic NLE trap. At presentation, serum K may be normal/high (due to acidosis), but it is DEPLETED. Once you give insulin + fluids, K shifts into cells → HYPOKALEMIA → fatal arrhythmias.
- Potassium replacement: Start K+ AFTER initial glucose drop and when K+ is normal/low AND urine output is adequate (to prevent hyperkalemia and renal accumulation). ADD POTASSIUM TO IV FLUIDS, not bolus IV (cardiac arrhythmia risk).
- STEP 4: Add DEXTROSE to IV fluids when glucose reaches 200–250 mg/dL — allows insulin drip to continue clearing ketones without causing hypoglycemia or too-rapid drop (cerebral edema risk, esp. children)
- Monitor: Glucose hourly, K+ and ECG closely, vitals, neuro status, I&O, pH, HCO3–, anion gap
- Identify and treat precipitating cause: usually infection (UTI, pneumonia, etc.); give antibiotics if indicated
Key definitions
Potassium Paradox
Example
Patient presents with K 5.2 mEq/L (appears high), but after IV fluids + insulin, K drops to 3.0 mEq/L (life-threatening hypokalemia)
Serum K may appear normal or HIGH initially (acidosis pushes K out of cells) but TOTAL BODY K is depleted; insulin + fluids drive K back INTO cells → HYPOKALEMIA.
Diagrams to know
- DKA/HHNS management flowchart (fluids → insulin → potassium → dextrose)
Chronic (Long-Term) Complications
Important facts
- MICROVASCULAR (tight glucose control prevents): retinopathy (leading cause adult blindness), nephropathy (leading cause ESRD), neuropathy (peripheral + autonomic)
- MACROVASCULAR: CAD, stroke, PAD (CV disease is #1 cause of death in diabetes)
- Retinopathy: prevent with tight glucose control, regular dilated eye exams (annually), treat hypertension, control lipids
- Nephropathy: monitor for microalbuminuria (earliest sign); ACE inhibitor/ARB protective; tight glucose control essential; manage hypertension
- Neuropathy — PERIPHERAL: loss of protective sensation → foot ulcers/amputation; autonomic: gastroparesis, silent MI, orthostatic hypotension
- Neuropathy screening: monofilament test (assess sensation), vibration sense, ankle reflexes
- FOOT CARE (huge NLE emphasis): inspect feet DAILY, wash/dry (especially between toes), wear proper closed shoes (never barefoot), cut nails straight across
- NEVER use heating pads/hot water bottles on diabetic feet (neuropathy masks burns → injury)
- Report any wound early (slow healing, infection risk); diabetic ulcer → infection → amputation cascade
Key definitions
Microvascular Complications
Example
Retinopathy, nephropathy, neuropathy (all three are tight-glucose-control preventable)
Damage to small blood vessels from chronic hyperglycemia and poor glycemic control; prevented by tight glucose control.
Macrovascular Complications
Example
Coronary artery disease, stroke, peripheral vascular disease (PAD) — cardiovascular disease is the #1 cause of death
Damage to large blood vessels from diabetes and atherosclerosis; leading cause of death in diabetes.
Diabetic Retinopathy
Example
Microaneurysms → background retinopathy → neovascularization → proliferative retinopathy → vision loss
Progressive damage to retinal blood vessels; leading cause of adult blindness; prevented by tight glucose control and regular eye exams (dilated fundus exam annually).
Diabetic Nephropathy
Example
Microalbuminuria (first sign) → overt proteinuria → declining GFR → need for dialysis
Progressive glomerular damage → proteinuria/microalbuminuria → chronic kidney disease → ESRD; leading cause of ESRD; prevented by tight glucose control and ACE inhibitor/ARB use.
Diabetic Neuropathy (Peripheral)
Example
Patient cannot feel pressure/pain in feet → skin breakdown → infection → amputation
Damage to peripheral nerves → numbness, tingling, loss of protective sensation; highest risk for foot ulcers and amputation.
Autonomic Neuropathy
Example
Gastroparesis causes delayed gastric emptying, nausea, unpredictable glucose control
Damage to autonomic nerves → gastroparesis, orthostatic hypotension, silent MI, hypoglycemia unawareness.
Diagrams to know
- Microvascular vs. macrovascular complication pathways
- Foot ulcer cascade: neuropathy + poor circulation + infection → amputation
Two Look-Alike Morning Hyperglycemia Scenarios
Important facts
- Somogyi: nocturnal hypoglycemia is the PROBLEM → reduce evening insulin or add snack; 2–3 a.m. check will show LOW glucose
- Dawn: normal/high 2–3 a.m. glucose → morning high is from hormone surge → increase insulin or adjust timing
- Distinguish by checking 2–3 a.m. glucose: if LOW = Somogyi (reduce insulin); if NORMAL/HIGH = Dawn (increase/adjust insulin)
Key definitions
Somogyi Phenomenon
Example
Patient's 2 a.m. glucose is 45 mg/dL, but 7 a.m. glucose is 280 mg/dL — reduce NPH evening dose or add snack before bed
Nocturnal HYPOGLYCEMIA (low 2–3 a.m.) → rebound HYPERGLYCEMIA at morning (morning glucose is high). Treatment: REDUCE evening insulin dose or add bedtime snack.
Dawn Phenomenon
Example
Patient's 2 a.m. glucose is 120 mg/dL, and 7 a.m. glucose is 220 mg/dL — adjust insulin timing (not reduce evening dose)
Morning hyperglycemia from normal early-morning hormone surge (cortisol, growth hormone); 2–3 a.m. glucose is NORMAL/HIGH (no nocturnal hypoglycemia). Treatment: adjust/increase insulin timing or dose.
Diagrams to know
- Somogyi vs. Dawn phenomenon glucose pattern comparison
Sick-Day Management & Self-Care Teaching
Important facts
- Illness raises glucose (stress hormones counteract insulin) even if patient is not eating → NEVER omit insulin during sick days
- Monitor glucose and ketones more frequently (every 2–3 hours or as directed)
- Maintain hydration: sugar-free fluids if glucose is high; small frequent meals/carbs even if nausea (crackers, juice, broth)
- Call provider if: glucose consistently >250 mg/dL, presence of ketones, persistent vomiting, severe illness, or uncertainty about insulin dose
- Regular self-care: SMBG (self-monitoring blood glucose) before meals and bedtime; carb-consistent diet; regular exercise (adjust insulin/carbs to avoid hypoglycemia); A1c checks every 3 months
Key definitions
Sick-Day Rules
Example
Patient with flu has fever and nausea — DO NOT skip insulin shots; instead, check glucose every 2–3 hours, drink sugar-free fluids, and call the provider if glucose >250 or ketones present
During illness (infection, fever, stress), glucose rises even if eating less; NEVER omit insulin, monitor frequently, maintain hydration and carbohydrate intake.
Must remember
- INSULIN PEAKS ARE HYPOGLYCEMIA RISK: Rapid ~30 min–1.5 hr, Regular 2–4 hr, NPH 6–12 hr, Glargine PEAKLESS. Know these cold — they determine patient safety.
- POTASSIUM TRAP in DKA/HHNS: Serum K may appear normal/HIGH initially (acidosis), but TOTAL BODY K is depleted. Insulin + fluids drive K INTO cells → HYPOKALEMIA → fatal arrhythmias. Monitor K+ and ECG closely; replace AFTER initial glucose drop and when K+ is normal/low.
- DKA = Type 1, KETONES + ACIDOSIS, Kussmaul breathing, fruity breath, rapid hours onset. HHNS = Type 2, NO ketosis, profound dehydration, glucose often >600–1000, days onset, HIGHER mortality.
- Type 1 = ALWAYS requires insulin; Type 2 = diet/oral agents first, then insulin later. Type 1 prone to DKA; Type 2 prone to HHNS.
- Regular insulin is the ONLY insulin given IV (used in DKA/HHNS drips). All others are subcutaneous/IM only.
- Mixing insulins: Draw CLEAR (regular) BEFORE CLOUDY (NPH); inject air into NPH first, then regular, then withdraw regular, then NPH. Glargine is NEVER mixed.
- Hypoglycemia (<70 mg/dL) = RAPID onset, cold/clammy/sweaty, trembling, hungry, confused → Rule of 15 (15 g fast carbs, recheck in 15 min, repeat if needed, then snack). Unconscious = IV D50 or IM glucagon (NEVER oral to unconscious patient).
- Metformin: first-line, no hypoglycemia alone, HOLD around contrast dye and in renal disease (lactic acidosis risk). Sulfonylureas: hypoglycemia risk + weight gain. SGLT2 inhibitors: euglycemic DKA risk (patient may have normal glucose during DKA).
- DKA/HHNS management sequence: IV NORMAL SALINE first (corrects dehydration), then Regular insulin IV drip, then POTASSIUM replacement, then add dextrose when glucose reaches 200–250 mg/dL (prevents hypoglycemia and cerebral edema).
- Chronic complications: MICROVASCULAR (retinopathy = leading cause adult blindness, nephropathy = leading cause ESRD, neuropathy) prevented by TIGHT GLUCOSE CONTROL. MACROVASCULAR (CAD, stroke, PAD) is the #1 CAUSE OF DEATH in diabetes. Diabetic foot: inspect daily, no heating pads, cut nails straight, report wounds early (neuropathy + poor circulation + infection = amputation).
Last minute tips
- When you see 'cloudy insulin,' think NPH (intermediate); when you see 'peakless,' think glargine (long-acting). Never mix glargine with anything.
- If an exam question mentions a patient skipping a meal after taking rapid-acting insulin, the answer is hypoglycemia within 30 min–1.5 hours. If NPH is taken in the evening and the patient skips breakfast, hypoglycemia risk is 6–12 hours later (during the peak).
- In DKA/HHNS, if potassium is HIGH (>5.5) at presentation, DO NOT yet add K to fluids; start IV fluids + insulin first. If potassium is NORMAL/LOW (<3.5), add K+ to fluids immediately (with caution to avoid hyperkalemia). The TRAP is that initial high K from acidosis will drop dangerously once insulin/fluids are given.
- Somogyi = nocturnal low → morning high (check 2–3 a.m. to confirm); reduce EVENING insulin. Dawn = morning high from normal hormones (2–3 a.m. is normal/high); INCREASE insulin. One requires reducing insulin; the other requires increasing it — opposite strategies.
- On the NLE, if you see euglycemic DKA (normal/near-normal glucose but ketones present), suspect SGLT2 inhibitor use. This is a trick because patients think 'DKA = high glucose' — but SGLT2 inhibitors cause glucose in urine while insulin prevents severe hyperglycemia, creating a dangerous 'hidden' DKA.
Comparison tables
Type 1 DM vs. Type 2 DM — Key Distinguishing Features
| Feature | Type 1 | Type 2 |
|---|---|---|
| Pathophysiology | Autoimmune destruction of beta cells → absolute insulin deficiency | Insulin resistance + relative deficiency |
| Typical onset | Younger (children, adolescents, young adults) | Older (usually >40, but rising in youth) |
| Body habitus | Lean | Obese/overweight |
| Insulin requirement | ALWAYS required | Diet/oral agents initially; later insulin |
| Acute emergency | DKA (prone) | HHNS (prone) |
| Ketosis tendency | High (easily develops DKA) | Low (protected by residual insulin) |
DKA vs. HHNS — Complete Feature Comparison (NLE Favorite)
| Feature | DKA | HHNS |
|---|---|---|
| Typical patient type | Type 1 DM | Type 2 DM (often older) |
| Blood glucose | Usually 250–600 mg/dL | Often >600, can exceed 1000 mg/dL |
| Ketones | YES (serum/urine) | NO or minimal |
| Acidosis (pH) | YES (pH <7.35) | NO (pH near normal) |
| Serum osmolality | Mildly elevated | VERY HIGH (>320) |
| Kussmaul respiration | YES (deep rapid breathing, fruity breath) | NO |
| Dehydration | Significant | PROFOUND |
| Onset speed | Hours (rapid) | Days (gradual) |
| Mortality | ~5% | ~15% (higher; older patients) |
| Neurologic status | Mild to moderate changes | SEVERE (lethargy, seizures, coma) |
Insulin Types — Complete Onset-Peak-Duration Reference
| Insulin Type | Examples | Appearance | Onset | Peak (Hypoglycemia Risk) | Duration | Key Nursing Note |
|---|---|---|---|---|---|---|
| Rapid-acting | lispro, aspart, glulisine | Clear | ~15 min | 30 min–1.5 hr (earliest peak) | 3–4 hr | Give WITH meal (food ready first) |
| Short-acting (Regular) | Regular insulin | Clear | 30 min–1 hr | 2–4 hr | 5–8 hr | ONLY insulin given IV; used in DKA/HHNS drips |
| Intermediate (NPH) | NPH | Cloudy | 1–2 hr | 6–12 hr | 12–18 hr | Roll gently; never shake; NEVER mix with glargine |
| Long-acting | glargine, detemir | Clear | ~1 hr | PEAKLESS (no pronounced peak) | ~24 hr | NEVER mixed with other insulins; basal (background) coverage |
Oral Agents — Mechanism & Hypoglycemia Risk
| Class | Examples | Mechanism | Hypoglycemia Risk | Key Caution |
|---|---|---|---|---|
| Biguanide | Metformin | Decreases hepatic glucose output; improves sensitivity | NO (alone) | HOLD around contrast dye; risk of lactic acidosis in renal impairment |
| Sulfonylurea | Glipizide, glyburide, glimepiride | Stimulates beta cells → insulin secretion | YES (high) | Avoid alcohol (disulfiram-like reaction); weight gain |
| Meglitinide | Repaglinide, nateglinide | Short-acting insulin secretagogue | YES | Skip dose if skipping meal |
| Thiazolidinedione | Pioglitazone | Improves insulin sensitivity | NO | Fluid retention (avoid in HF); weight gain; hepatotoxicity |
| DPP-4 inhibitor | Sitagliptin | Enhances GLP-1 effect | Minimal | Well-tolerated |
| SGLT2 inhibitor | Empagliflozin, dapagliflozin | Glucose excretion in urine | NO | EUGLYCEMIC DKA risk; genital/UTI infections |
| GLP-1 agonist | Liraglutide, semaglutide, exenatide | Promotes GLP-1 effect; weight loss | NO | Injectable only; GI side effects (nausea) |
Hypoglycemia vs. Hyperglycemia — Quick Recognition
| Feature | Hypoglycemia (<70 mg/dL) | Hyperglycemia (>250 mg/dL) |
|---|---|---|
| Onset | RAPID (minutes) | Gradual (hours to days) |
| Skin | Cold, clammy, sweaty (diaphoresis) | Dry, flushed |
| Breathing | Normal | Kussmaul (deep rapid) if DKA |
| Breath odor | Normal | Fruity/acetone if DKA |
| Mental status | Confusion (early), agitation, loss of consciousness | Gradual confusion, lethargy, coma |
| Tremor/shakiness | YES (prominent) | NO |
| Treatment | Rule of 15 (fast carbs); unconscious = IV D50 or IM glucagon | IV fluids, insulin IV drip, K+ monitoring |
Diagrams
Insulin Types: Onset-Peak-Duration Timeline & Hypoglycemia Risk
Visual timeline comparing all insulin types: when they start working, when they peak (maximum hypoglycemia risk), and how long they last. Rapid-acting is fastest; glargine is peakless (basal).
DKA vs. HHNS: Rapid Differential Diagnosis
Decision tree for rapidly distinguishing DKA from HHNS in an exam. Key differentiators: ketones + acidosis = DKA; no ketones + profound dehydration + very high glucose = HHNS.
Hypoglycemia Recognition & Emergency Management (Rule of 15)
Step-by-step flowchart for recognizing and managing hypoglycemia using the Rule of 15. Shows the branching decision: conscious vs. unconscious, and when to use oral carbs vs. IV dextrose vs. IM glucagon.
DKA/HHNS Emergency Management Sequence: IV Fluids → Insulin → Potassium
Critical management flowchart showing the exact sequence: fluids first, then insulin drip, then careful potassium replacement (the trap is that K appears high initially but is depleted), then dextrose when glucose reaches 200–250 mg/dL.
Diabetes Mellitus: Complete Pathophysiology & Complications Overview
Comprehensive mind map showing the entire diabetes chapter structure: types, diagnosis, acute crises, treatments, and chronic complications. Each branch shows key details to memorize.
Somogyi vs. Dawn Phenomenon: Distinguishing Morning Hyperglycemia
State diagram showing how to distinguish Somogyi phenomenon (nocturnal low → morning high) from Dawn phenomenon (morning high from hormones, no nocturnal low). The 2–3 a.m. glucose check is the key differentiator.