Diabetes Mellitus Cheat Sheet
Core concepts, medications & acute complications. Everything high-yield for the NCLEX-RN in one organized, expert-reviewed sheet.
What's in this cheat sheet
This cheat sheet distills diabetes mellitus — one of the most heavily tested NCLEX-RN topics — into four focused sections. You'll review how diabetes develops and presents, the nursing interventions and patient teaching that matter most, the key insulin and oral medications with their safety rules, and the life-threatening acute complications (DKA and HHS) you must recognize fast. Use it for quick daily revision or last-minute cramming, then test yourself with the quiz at the end.
Pathophysiology & Assessment
The core mechanism of impaired glucose metabolism, Type 1 vs Type 2 differences, metabolic syndrome, the classic 3 P's (polyuria, polydipsia, polyphagia) and the chronic vascular damage signs of diabetes.
Interventions & Teaching
Glycemic control goals (A1C), first-line treatment, exercise guidelines, glucose self-monitoring, diet principles, diabetic foot care, and the hypoglycemia vs hyperglycemia comparison with the Rule of 15.
Medications
Insulin types and timing (rapid, short, intermediate, long-acting), critical nursing points around onset and potassium, plus oral T2DM medications — biguanides, incretins, SGLT-2 inhibitors and sulfonylureas.
Acute Complications
Diabetic Ketoacidosis (DKA) vs Hyperosmolar Hyperglycemic Syndrome (HHS) — triggers, pathophysiology, assessment findings, treatment priorities and prevention.
1. Pathophysiology & Assessment
Impaired glucose metabolism → cells starved of energy while glucose accumulates in the blood.
Type 1 vs Type 2
| Feature | Type 1 | Type 2 |
|---|---|---|
| Insulin | None produced | Produced but ineffective |
| Cause | Autoimmune β-cell destruction | Insulin resistance (chronic hyperglycemia) |
| Onset | Before early adulthood; often post-stressor | Gradual; often in adulthood |
| #1 Risk | Genetic / autoimmune | Obesity |
Metabolic syndrome (≥3 → ↑ T2DM & CVD risk): abdominal obesity · hyperglycemia · HTN · ↑ triglycerides · ↓ HDL.
The Classic 3 P's
Polyuria
Excess urination → osmotic diuresis
Polydipsia
Excess thirst → dehydration
Polyphagia
Excess hunger → cells starving
Chronic vascular damage signs
- · Frequent infections — impaired immune response
- · Poor wound healing — reduced perfusion
- · Blurred vision — retinopathy
- · Paresthesias / numbness — peripheral neuropathy
- · Elevated BP / proteinuria — nephropathy
2. Interventions & Teaching
Glycemic control, exercise, diet, foot care and recognizing glucose emergencies.
Glycemic control goals
≥6.5%
A1C = Diagnose DM
≤7.0%
A1C = Treatment goal
Hemoglobin A1C reflects average blood glucose over the past 3 months. First-line: diet + exercise + weight loss (all types). Insulin always required in T1DM.
Exercise guidelines
- Aim for 150 min/week of moderate activity (e.g. brisk walking)
- Eat 1 hour before exercise (glucose peaks during activity)
- Monitor glucose before, during, and after
- Wear a medical ID bracelet; carry fast-acting carbs
Do NOT exercise if ketonuria is present OR blood glucose >200 mg/dL.
Diet principles
- · Individualized plan focused on weight management
- · Choose complex carbs (whole grains, vegetables, fruit)
- · Limit simple/"empty" carbs — white bread, sugary drinks
- · Carbohydrate counting required for clients on high-dose insulin
Diabetic foot care
- · Inspect daily using a mirror — look for wounds, blisters
- · Well-fitted, closed-toed shoes only — no flip-flops or bare feet
- · Dry feet thoroughly; no soaking, no lotion between toes
- · Cut toenails straight across
- · No heating pads — peripheral neuropathy impairs sensation
Hypoglycemia vs Hyperglycemia
Hypoglycemia
"Cold & clammy? Need some candy."
- · Confusion, irritability
- · Tremor, diaphoresis
- · Palpitations, tachycardia
- · Severe → seizure, coma
Hyperglycemia
"Hot & dry? Sugar's high."
- · Lethargy, fatigue
- · Hot, flushed, dry skin
- · Polydipsia, polyuria
- · Severe (DKA) → fruity breath
Key rule: if no glucose meter available → assume hypoglycemia and treat. It is more dangerous (permanent neuron death, seizures).
Hypoglycemia management — Rule of 15
15g carbs → 15 min recheck
Repeat dose if still low · give carb + protein snack once stable
Patient is ALERT
- · ½ cup juice or regular soda
- · 5 hard candies
- · 1 tbsp (15 mL) honey
- · Glucose tabs / gel
Unconscious / confused
- · Glucagon IM or 50% dextrose IV
- · Turn patient to one side
- · Recheck in 15 min
- · Notify HCP
Avoid: fatty foods (slow absorption) & large sugar amounts (rebound hyperglycemia).
3. Medications
Insulin timing and the major oral medication classes for T2DM.
Insulin types & timing
Rapid-acting
lispro, aspart
15–30 min onset · Peak 1–3 hr
Short-acting
regular
30–60 min onset · Peak 2.5 hr
Intermediate
NPH
1–2 hr onset · Peak 4–12 hr
Long-acting
glargine
1–2 hr onset · No peak · 24 hr
Critical nursing point: client must start eating before insulin onset (within ~15 min of rapid-acting). Insulin also drives K⁺ into cells → monitor electrolytes. Steroids ↑ glucose; beta-blockers can mask hypoglycemia symptoms.
Oral diabetes medications (T2DM only)
Biguanides
Metformin
First-line for T2DM
Mechanism
↓ glucose output from liver
Hold 48 hr before IV contrast → risk of lactic acidosis
Incretins (GLP-1 / DPP-4)
Semaglutide, Dulaglutide
Sitagliptin, Saxagliptin
Mechanism
↓ glucagon secretion · slows gastric emptying · aids weight loss
Monitor for pancreatitis: report jaundice or abdominal pain
SGLT-2 Inhibitors
Dapagliflozin
Empagliflozin
Mechanism
↑ glucose excretion in urine (osmotic effect)
↑ Risk of vaginal & urinary tract infections
Sulfonylureas
Glipizide
Glimepiride · Glyburide
Mechanism
↑ insulin secretion from pancreas
Hold if NPO · Risk of hypoglycemia · Avoid alcohol (disulfiram-like reaction)
4. Acute Complications
DKA vs HHS — recognize the difference and act fast.
Diabetic Ketoacidosis (DKA) T1DM
Trigger: severe insulin deficiency — often precipitated by infection or stressor.
Path chain: hyperglycemia → osmotic diuresis → dehydration + fat/protein metabolism → ketones → metabolic acidosis.
Assessment findings:
- · Nausea, vomiting, lethargy
- · Severe dehydration
- · Kussmaul respirations (deep, rapid)
- · Fruity breath (ketones)
- · Glucose >300 mg/dL · ketonuria · ↓ pH · hyperkalemia
Treatment priorities:
- 1. IV fluids → treat dehydration (#1 priority)
- 2. IV regular insulin → treats hyperglycemia & hyperkalemia
Monitor mental status · glucose (hourly) · K⁺ · ECG · perfusion. Switch to D5NS once glucose ≤250 mg/dL. IV sodium bicarbonate only if pH <7.
Hyperosmolar Hyperglycemic Syndrome (HHS) T2DM
Key difference from DKA: enough residual insulin prevents ketosis → no ketones, normal ABG.
DKA glucose
>300 mg/dL
HHS glucose
>800 mg/dL
Findings similar to DKA:
- · Extreme dehydration
- · Neurological changes (confusion, coma)
- · No ketones · normal ABG · no fruity breath
Treatment (same as DKA):
- · IV fluids — aggressive rehydration
- · IV insulin
- · Electrolyte replacement
Prevention (both): when sick, ↑ fluid intake and continue monitoring glucose & urine ketones — even if not eating.
NCLEX Star Points
High-yield facts most likely to appear on the exam.
Classic triad: Polyuria, Polydipsia, Polyphagia — caused by glucose build-up & cell starvation.
Tremor, diaphoresis & acute mental status change → signs of hypoglycemia. Always check glucose with any change in mental status.
Hypoglycemia Tx: Alert → 15g carbs, recheck in 15 min. Unconscious → glucagon IM or dextrose IV, turn to side, notify HCP.
Foot care: inspect daily with a mirror, closed-toed shoes, dry between toes — neuropathy means no sensation of injury.
DKA priorities: IV fluids first (dehydration is #1), then IV insulin. Monitor K⁺, glucose, mental status, ECG throughout.
Hold Metformin 48 hr before IV contrast (lactic acidosis risk). Hold sulfonylureas if NPO (hypoglycemia risk).
Diabetes Self-Test
6 quick questions — answers reveal after you submit.
Q1. A nurse is assessing a newly diagnosed client. Which classic triad of symptoms is most consistent with diabetes mellitus?
Q2. A client with diabetes is found diaphoretic, tremulous, and confused. No glucose meter is available. What should the nurse do?
Q3. An alert client has a blood glucose of 52 mg/dL. Using the Rule of 15, what is the correct intervention?
Q4. A client with Type 1 diabetes presents with Kussmaul respirations, fruity breath, and glucose of 420 mg/dL. What is the FIRST treatment priority for DKA?
Q5. A client taking metformin is scheduled for a CT scan with IV contrast. What is the nurse's priority action?
Q6. Which foot-care instruction is correct for a client with diabetic peripheral neuropathy?
Answered 0 / 6 — unanswered count as incorrect.