NLE Endocrine & Metabolic Nursing — Diabetes Mellitus & Its ComplicationsCheat Sheet
Diabetes Mellitus & Its Complications cheat sheet — the reference card you wish you had on exam day. Condensed from the full study notes, this is the high-yield core of Diabetes Mellitus & Its Complications for NLE Endocrine & Metabolic Nursing. Download, print, revise.
Exam context
For the Philippine Nurse Licensure Examination (PNLE), Professional Regulation Commission (PRC) — Board of Nursing tests Endocrine & Metabolic Nursing under a "Core" label, with Diabetes Mellitus & Its Complications in the 3rd slot across 3 chapters. NLE candidates must clear the 75% weighted average with no sub-test below 60% cut on the 2026 paper, which draws about 50 Endocrine & Metabolic Nursing questions. Date to watch: Bi-annual.
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.
Sections
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
Section Title
Pathophysiology & Diagnostic Criteria
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
Term
Diabetes Mellitus
Example
Type 1: autoimmune destruction of pancreatic beta cells; Type 2: insulin resistance + relative deficiency
Definition
Disorder of glucose metabolism from lack of insulin, resistance to insulin, or both, resulting in hyperglycemia and metabolic derangement.
Term
Hyperglycemia
Example
A fasting glucose of 150 mg/dL confirms hyperglycemia and diabetes
Definition
Elevated blood glucose (>126 mg/dL fasting) due to insufficient insulin action or production.
Term
HbA1c (Glycosylated Hemoglobin)
Example
HbA1c of 8% means average glucose ~185 mg/dL over the past 3 months
Definition
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
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
Section Title
Insulin Types, Onset, Peak, Duration — THE MOST TESTED TABLE
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
Term
Onset
Example
Rapid-acting lispro has onset ~15 minutes; regular has onset ~30 min–1 hour
Definition
Time from injection until insulin begins to lower blood glucose.
Term
Peak
Example
NPH peaks at 6–12 hours; this is when hypoglycemia is most likely if the patient skips a meal
Definition
Time of maximum insulin action (maximum hypoglycemia risk).
Term
Duration
Example
Regular insulin lasts 5–8 hours; glargine lasts ~24 hours (peakless)
Definition
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
Section Title
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
Term
Biguanide (Metformin)
Example
HOLD metformin around contrast dye studies (contrast-induced nephropathy risk) and in renal impairment; risk of lactic acidosis
Definition
First-line oral agent that decreases hepatic glucose output and improves insulin sensitivity; does NOT cause hypoglycemia alone.
Term
Sulfonylureas (Glipizide, Glyburide)
Example
Glyburide + alcohol → disulfiram-like reaction (flushing, nausea)
Definition
Insulin secretagogues that stimulate pancreatic beta cells; carry hypoglycemia risk and weight gain.
Term
SGLT2 Inhibitors (Empagliflozin, Dapagliflozin)
Example
Dapagliflozin lowers glucose independent of insulin; patient may have normal glucose during DKA
Definition
Cause glucose excretion in urine; unique euglycemic DKA risk; watch for genital/urinary infections.
Term
GLP-1 Receptor Agonists (Liraglutide, Semaglutide)
Example
Semaglutide is often given once weekly; excellent for weight reduction alongside glucose control
Definition
Injectable agents promoting weight loss, improve glycemic control; GI side effects (nausea, vomiting).
Diagrams To Know
- Oral agent mechanism of action summary
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
Section Title
Acute Complications: Hypoglycemia
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
Term
Hypoglycemia
Example
A patient on NPH insulin who skips breakfast may become hypoglycemic at 10 a.m. (during the peak)
Definition
Blood glucose <70 mg/dL; most common acute diabetic emergency; rapid onset from too much insulin/oral agent, skipped meals, or extra activity.
Term
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
Definition
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
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
Section Title
Acute Complications: DKA (Diabetic Ketoacidosis)
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
Term
Diabetic Ketoacidosis (DKA)
Example
Patient with Type 1 DM misses insulin injections → develops hyperglycemia, ketosis, and acidosis within hours
Definition
Life-threatening metabolic emergency in Type 1 DM: absolute insulin lack → uncontrolled lipolysis → ketone production and metabolic ACIDOSIS.
Term
Kussmaul Respirations
Example
Patient breathing 35 times/min with deep breaths and fruity breath odor during DKA
Definition
Deep, rapid, labored breathing (compensatory response to metabolic acidosis to blow off CO₂).
Term
Ketones
Example
Beta-hydroxybutyrate >3 mmol/L indicates significant ketosis
Definition
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)
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
Section Title
Acute Complications: HHNS (Hyperglycemic Hyperosmolar Nonketotic Syndrome)
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
Term
HHNS (HHS)
Example
Elderly Type 2 patient with infection develops glucose >1000 mg/dL, severe dehydration, but pH remains near-normal
Definition
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.
Term
Serum Osmolality
Example
Osmolality >350 associated with seizures, coma, and high mortality
Definition
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)
Section Title
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
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
Section Title
DKA/HHNS Management — The CRITICAL Sequence
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
Term
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)
Definition
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)
Section Title
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
Term
Microvascular Complications
Example
Retinopathy, nephropathy, neuropathy (all three are tight-glucose-control preventable)
Definition
Damage to small blood vessels from chronic hyperglycemia and poor glycemic control; prevented by tight glucose control.
Term
Macrovascular Complications
Example
Coronary artery disease, stroke, peripheral vascular disease (PAD) — cardiovascular disease is the #1 cause of death
Definition
Damage to large blood vessels from diabetes and atherosclerosis; leading cause of death in diabetes.
Term
Diabetic Retinopathy
Example
Microaneurysms → background retinopathy → neovascularization → proliferative retinopathy → vision loss
Definition
Progressive damage to retinal blood vessels; leading cause of adult blindness; prevented by tight glucose control and regular eye exams (dilated fundus exam annually).
Term
Diabetic Nephropathy
Example
Microalbuminuria (first sign) → overt proteinuria → declining GFR → need for dialysis
Definition
Progressive glomerular damage → proteinuria/microalbuminuria → chronic kidney disease → ESRD; leading cause of ESRD; prevented by tight glucose control and ACE inhibitor/ARB use.
Term
Diabetic Neuropathy (Peripheral)
Example
Patient cannot feel pressure/pain in feet → skin breakdown → infection → amputation
Definition
Damage to peripheral nerves → numbness, tingling, loss of protective sensation; highest risk for foot ulcers and amputation.
Term
Autonomic Neuropathy
Example
Gastroparesis causes delayed gastric emptying, nausea, unpredictable glucose control
Definition
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
Section Title
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
Term
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
Definition
Nocturnal HYPOGLYCEMIA (low 2–3 a.m.) → rebound HYPERGLYCEMIA at morning (morning glucose is high). Treatment: REDUCE evening insulin dose or add bedtime snack.
Term
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)
Definition
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
Section Title
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
Term
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
Definition
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
Rows
Values
- Autoimmune destruction of beta cells → absolute insulin deficiency
- Insulin resistance + relative deficiency
Property
Pathophysiology
Values
- Younger (children, adolescents, young adults)
- Older (usually >40, but rising in youth)
Property
Typical onset
Values
- Lean
- Obese/overweight
Property
Body habitus
Values
- ALWAYS required
- Diet/oral agents initially; later insulin
Property
Insulin requirement
Values
- DKA (prone)
- HHNS (prone)
Property
Acute emergency
Values
- High (easily develops DKA)
- Low (protected by residual insulin)
Property
Ketosis tendency
Columns
- Feature
- Type 1
- Type 2
Table Title
Type 1 DM vs. Type 2 DM — Key Distinguishing Features
Rows
Values
- Type 1 DM
- Type 2 DM (often older)
Property
Typical patient type
Values
- Usually 250–600 mg/dL
- Often >600, can exceed 1000 mg/dL
Property
Blood glucose
Values
- YES (serum/urine)
- NO or minimal
Property
Ketones
Values
- YES (pH <7.35)
- NO (pH near normal)
Property
Acidosis (pH)
Values
- Mildly elevated
- VERY HIGH (>320)
Property
Serum osmolality
Values
- YES (deep rapid breathing, fruity breath)
- NO
Property
Kussmaul respiration
Values
- Significant
- PROFOUND
Property
Dehydration
Values
- Hours (rapid)
- Days (gradual)
Property
Onset speed
Values
- ~5%
- ~15% (higher; older patients)
Property
Mortality
Values
- Mild to moderate changes
- SEVERE (lethargy, seizures, coma)
Property
Neurologic status
Columns
- Feature
- DKA
- HHNS
Table Title
DKA vs. HHNS — Complete Feature Comparison (NLE Favorite)
Rows
Values
- lispro, aspart, glulisine
- Clear
- ~15 min
- 30 min–1.5 hr (earliest peak)
- 3–4 hr
- Give WITH meal (food ready first)
Property
Rapid-acting
Values
- Regular insulin
- Clear
- 30 min–1 hr
- 2–4 hr
- 5–8 hr
- ONLY insulin given IV; used in DKA/HHNS drips
Property
Short-acting (Regular)
Values
- NPH
- Cloudy
- 1–2 hr
- 6–12 hr
- 12–18 hr
- Roll gently; never shake; NEVER mix with glargine
Property
Intermediate (NPH)
Values
- glargine, detemir
- Clear
- ~1 hr
- PEAKLESS (no pronounced peak)
- ~24 hr
- NEVER mixed with other insulins; basal (background) coverage
Property
Long-acting
Columns
- Insulin Type
- Examples
- Appearance
- Onset
- Peak (Hypoglycemia Risk)
- Duration
- Key Nursing Note
Table Title
Insulin Types — Complete Onset-Peak-Duration Reference
Rows
Values
- Metformin
- Decreases hepatic glucose output; improves sensitivity
- NO (alone)
- HOLD around contrast dye; risk of lactic acidosis in renal impairment
Property
Biguanide
Values
- Glipizide, glyburide, glimepiride
- Stimulates beta cells → insulin secretion
- YES (high)
- Avoid alcohol (disulfiram-like reaction); weight gain
Property
Sulfonylurea
Values
- Repaglinide, nateglinide
- Short-acting insulin secretagogue
- YES
- Skip dose if skipping meal
Property
Meglitinide
Values
- Pioglitazone
- Improves insulin sensitivity
- NO
- Fluid retention (avoid in HF); weight gain; hepatotoxicity
Property
Thiazolidinedione
Values
- Sitagliptin
- Enhances GLP-1 effect
- Minimal
- Well-tolerated
Property
DPP-4 inhibitor
Values
- Empagliflozin, dapagliflozin
- Glucose excretion in urine
- NO
- EUGLYCEMIC DKA risk; genital/UTI infections
Property
SGLT2 inhibitor
Values
- Liraglutide, semaglutide, exenatide
- Promotes GLP-1 effect; weight loss
- NO
- Injectable only; GI side effects (nausea)
Property
GLP-1 agonist
Columns
- Class
- Examples
- Mechanism
- Hypoglycemia Risk
- Key Caution
Table Title
Oral Agents — Mechanism & Hypoglycemia Risk
Rows
Values
- RAPID (minutes)
- Gradual (hours to days)
Property
Onset
Values
- Cold, clammy, sweaty (diaphoresis)
- Dry, flushed
Property
Skin
Values
- Normal
- Kussmaul (deep rapid) if DKA
Property
Breathing
Values
- Normal
- Fruity/acetone if DKA
Property
Breath odor
Values
- Confusion (early), agitation, loss of consciousness
- Gradual confusion, lethargy, coma
Property
Mental status
Values
- YES (prominent)
- NO
Property
Tremor/shakiness
Values
- Rule of 15 (fast carbs); unconscious = IV D50 or IM glucagon
- IV fluids, insulin IV drip, K+ monitoring
Property
Treatment
Columns
- Feature
- Hypoglycemia (<70 mg/dL)
- Hyperglycemia (>250 mg/dL)
Table Title
Hypoglycemia vs. Hyperglycemia — Quick Recognition
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