NLE Endocrine & Metabolic Nursing — Diabetes Mellitus & Its ComplicationsExam Answer Templates

Examiner tip

Examiners distinguish between the DIAGNOSTIC value (HbA1c ≥6.5% = diabetes) and the TREATMENT TARGET (<7%). Confusing the two is the most common error on this item.

Model answer

The target HbA1c for a diabetic patient on treatment is less than 7% (less than 7 percent), reflecting average blood glucose control over the preceding 2 to 3 months.

Answer structure

• State the correct numeric target value with the correct unit (%) [1 mark]

Scoring breakdown

Common mark deductions

• Writing '6.5%' — that is the diagnostic threshold for diabetes, NOT the treatment target
• Omitting the percent sign or unit entirely
• Writing a range such as '6–7%' without specifying the target ceiling

Key phrases to include

• less than 7%
• HbA1c
• glycosylated hemoglobin
• 2 to 3 months

Examiner tip

Examiners reward specificity. 'Roll, do not shake' and the exact peak time '6–12 hours' are the two phrases that earn full marks. Generic answers about insulin administration earn zero.

Model answer

Before administering NPH insulin, the nurse must: (1) Gently roll the vial between the palms (never shake) to resuspend the cloudy, milky suspension evenly; and (2) Check the time of administration and plan to assess the patient during the peak action window of 6 to 12 hours after injection, when the risk of hypoglycemia is highest.

Answer structure

• Point 1: Identify the correct preparation technique for cloudy/NPH insulin [1 mark]
• Point 2: Identify the peak window and its clinical significance (hypoglycemia risk) [1 mark]

Scoring breakdown

Common mark deductions

• Saying 'shake the vial' instead of 'roll gently' — this is the opposite of correct technique
• Stating the wrong peak time (e.g., '2–4 hours' which belongs to regular insulin)
• Listing a generic consideration like 'check expiry' without the NPH-specific details

Key phrases to include

• cloudy
• gently roll
• do not shake
• peak 6–12 hours
• hypoglycemia risk
• NPH

Examiner tip

The words 'absolute' and 'relative' are examiner keywords. Including them shows you understand the mechanism, not just the label.

Model answer

Type 1 DM results from autoimmune destruction of pancreatic beta cells, leading to absolute insulin deficiency; the patient always requires exogenous insulin for survival. Type 2 DM involves insulin resistance combined with a relative insulin deficiency; it is initially managed with lifestyle modification and oral hypoglycemic agents, though insulin may be added over time.

Answer structure

• Line 1: Type 1 — autoimmune destruction, absolute deficiency, insulin-dependent [1 mark]
• Line 2: Type 2 — insulin resistance + relative deficiency, managed with OHAs initially [1 mark]

Scoring breakdown

Common mark deductions

• Reversing the descriptions (attributing insulin resistance to Type 1)
• Saying Type 2 'never' needs insulin — it can require insulin eventually
• Omitting the word 'absolute' for Type 1 or 'relative' for Type 2, which are the key differentiators

Key phrases to include

• autoimmune
• beta cells
• absolute insulin deficiency
• insulin resistance
• relative deficiency
• oral hypoglycemic agents

Examiner tip

Safety is the first mark. Any answer that recommends giving something by mouth to an unconscious patient not only loses marks but signals unsafe practice. State 'nothing by mouth' first, then the correct treatment.

Model answer

The patient is experiencing severe hypoglycemia (blood glucose 38 mg/dL, below 70 mg/dL). Because the patient is unconscious and cannot swallow, the nurse must NOT administer anything by mouth (aspiration risk). Immediate management: (1) Establish IV access and administer 50% Dextrose (D50W) as ordered — this rapidly raises blood glucose. (2) If IV access is unavailable, administer glucagon intramuscularly or subcutaneously. (3) Recheck blood glucose 15 minutes after treatment and continue monitoring neurological status and vital signs. Position the patient safely (lateral/recovery position) to protect the airway. Document findings and notify the physician immediately.

Answer structure

• Line 1: Identify the problem — severe hypoglycemia; state why oral route is contraindicated [1 mark]
• Line 2: State the correct treatment — IV D50 (first choice) or IM/SC glucagon (if no IV) [1 mark]
• Line 3: State monitoring action — recheck glucose in 15 min, monitor neuro and vitals, notify physician [1 mark]

Scoring breakdown

Common mark deductions

• Recommending juice or oral glucose for an unconscious patient — this is a serious safety error worth zero marks
• Forgetting to state the rechecking/monitoring step
• Not identifying the reason why oral route is unsafe (aspiration)

Key phrases to include

• severe hypoglycemia
• less than 70 mg/dL
• nothing by mouth
• aspiration
• IV D50W
• 50% dextrose
• glucagon IM/SC
• recheck blood glucose
• 15 minutes

Examiner tip

The mnemonic 'air into cloudy first, then draw clear first' is the NLE standard. Write the steps in numbered order — examiners follow the sequence to award marks.

Model answer

The correct technique follows the principle 'clear before cloudy' to prevent contamination: (1) Inject air equal to the NPH (cloudy) dose into the NPH vial first — without withdrawing any insulin. (2) Inject air equal to the regular (clear) dose into the regular insulin vial. (3) Invert and withdraw the REGULAR (clear) insulin first, ensuring the exact prescribed dose. (4) Finally, withdraw the NPH (cloudy) insulin to the total required volume. This sequence prevents cloudy NPH from contaminating the clear regular insulin vial, which would alter future doses.

Answer structure

• Step 1: Inject air into NPH vial first (without withdrawing) [1 mark]
• Step 2: Inject air into regular vial, then withdraw regular insulin first [1 mark]
• Step 3: Withdraw NPH second; state rationale — prevents contamination of regular insulin [1 mark]

Scoring breakdown

Common mark deductions

• Reversing the sequence — drawing NPH before regular — is the most common error
• Omitting the air injection step entirely
• Failing to state the rationale for the sequence

Key phrases to include

• clear before cloudy
• air into NPH first
• withdraw regular first
• prevent contamination
• regular insulin
• NPH insulin

Examiner tip

The two '15s' (15 g and 15 minutes) are the marking points. Write both in one sentence to ensure you earn both marks.

Model answer

The Rule of 15 is the standard protocol for treating conscious hypoglycemia (blood glucose less than 70 mg/dL): give 15 grams of fast-acting carbohydrates (e.g., half cup of fruit juice, 3–4 glucose tablets, or half cup of regular soda), then recheck the blood glucose after 15 minutes. If the glucose remains below 70 mg/dL, repeat the 15 grams of carbohydrates and recheck again. Once the glucose normalizes, provide a longer-acting snack or meal to prevent recurrence.

Answer structure

• Line 1: State the two '15s' — 15 grams of fast-acting carbohydrates, wait 15 minutes [1 mark]
• Line 2: State the follow-up — recheck glucose, repeat if still low, then give a longer-acting snack [1 mark]

Scoring breakdown

Common mark deductions

• Stating '10 grams' or '20 grams' instead of the exact 15 grams
• Omitting the rechecking step — just treating without verifying effectiveness
• Forgetting to mention the follow-up longer-acting snack/meal

Key phrases to include

• 15 grams
• fast-acting carbohydrate
• recheck in 15 minutes
• blood glucose less than 70 mg/dL
• longer-acting snack
• repeat if still low

Examiner tip

Each 'P' should be a cause-and-effect explanation, not just a translation. Examiners want the mechanism, not just the definition.

Model answer

The three classic manifestations of DM are: (1) Polyuria — excess glucose in the blood spills into the urine (glucosuria), drawing water out via osmotic diuresis, causing increased urine output. (2) Polydipsia — the resulting fluid loss activates the thirst mechanism, leading to excessive thirst and water intake. (3) Polyphagia — because insulin is absent or ineffective, glucose cannot enter cells; starving cells send hunger signals to the brain, causing excessive appetite and eating despite elevated blood glucose.

Answer structure

• Point 1: Polyuria — define and explain osmotic diuresis from glucosuria [1 mark]
• Point 2: Polydipsia — link to fluid loss from polyuria activating thirst [1 mark]
• Point 3: Polyphagia — link to cellular starvation due to insulin lack/resistance [1 mark]

Scoring breakdown

Common mark deductions

• Only listing the three Ps without explaining the mechanism — worth 0 for the explanation marks
• Confusing polyphagia with weight gain — in Type 1, patients lose weight despite eating
• Not linking polydipsia to the fluid loss from polyuria (presenting them as unrelated)

Key phrases to include

• polyuria
• polydipsia
• polyphagia
• osmotic diuresis
• glucosuria
• cellular starvation
• insulin deficiency

Examiner tip

In a 5-mark case study, structure is everything. Use bold headers or numbered sections. Examiners scan for keywords: HHNS identification, NS first, Regular Insulin IV, potassium monitoring. Each of these is worth 1 mark.

Model answer

IDENTIFICATION: The patient is presenting with Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS/HHS). Key features supporting this diagnosis are: (1) extreme hyperglycemia greater than 600 mg/dL (here: 780 mg/dL), (2) markedly elevated serum osmolality greater than 320 mOsm/kg (here: 335 mOsm/kg), (3) profound neurological changes (confusion), (4) absence of significant ketones, and (5) Type 2 DM profile.

PRIORITY NURSING INTERVENTIONS (in order):

1. AIRWAY AND SAFETY: Position the patient in a lateral decubitus (recovery) position to protect the airway due to altered mental status. Apply supplemental oxygen as ordered. Maintain seizure precautions.
2. IV FLUID REPLACEMENT — FIRST PRIORITY: Administer 0.9% Normal Saline IV as the initial bolus to restore circulatory volume and correct severe dehydration. HHNS causes profound dehydration (fluid deficit may reach 8–10 liters). Fluid replacement alone significantly lowers blood glucose.
3. INSULIN THERAPY: After initiating IV fluids, administer Regular Insulin (the ONLY insulin given IV) via continuous infusion per physician order. Monitor blood glucose hourly.
4. POTASSIUM MONITORING: Monitor serum potassium closely. As insulin drives glucose into cells, potassium also shifts intracellularly, risking hypokalemia and fatal cardiac arrhythmias. Add potassium to IV fluids once urine output is confirmed and potassium is within normal or low-normal range. Monitor ECG continuously.
5. DEXTROSE TRANSITION: When blood glucose approaches 200–250 mg/dL, add dextrose to the IV fluids to prevent hypoglycemia and allow insulin infusion to continue.
6. MONITORING: Hourly blood glucose, vitals, neurological status (GCS), strict intake-and-output, and electrolytes. Identify and treat the precipitating cause (e.g., infection, dehydration).

PRIORITY NURSING DIAGNOSIS: Deficient Fluid Volume related to osmotic diuresis and severe hyperglycemia as evidenced by blood glucose 780 mg/dL, serum osmolality 335 mOsm/kg, and confusion.

Answer structure

• Part 1: Correctly identify HHNS with supporting clinical evidence [1 mark]
• Part 2: State IV Normal Saline as the first-priority intervention with rationale [1 mark]
• Part 3: State Regular Insulin IV as the pharmacologic intervention [1 mark]
• Part 4: Discuss potassium monitoring — the hypokalemia trap with rationale [1 mark]
• Part 5: State ongoing monitoring (glucose, vitals, I&O, ECG) and identify the priority nursing diagnosis [1 mark]

Scoring breakdown

Common mark deductions

• Misidentifying the condition as DKA — no ketones and Type 2 profile clearly indicate HHNS
• Starting insulin before IV fluids — fluids MUST come first in both DKA and HHNS
• Failing to discuss the potassium trap — this is the highest-yield safety point in the management section
• Not specifying Regular Insulin for IV use (no other insulin is given IV)
• Missing the monitoring components entirely

Key phrases to include

• HHNS
• glucose greater than 600 mg/dL
• serum osmolality greater than 320
• no significant ketones
• 0.9% Normal Saline first
• regular insulin IV
• hypokalemia
• potassium shift
• monitor ECG
• add dextrose at 200–250 mg/dL
• Deficient Fluid Volume

Examiner tip

A comparison table drawn in the answer booklet with DKA vs. HHNS as column headers and five features as rows is faster to write, easier to read, and earns full marks more reliably than paragraphs.

Model answer

DKA vs. HHNS — Comparison of Five Clinical Features:

1. TYPICAL PATIENT: DKA occurs predominantly in Type 1 DM patients (absolute insulin deficiency). HHNS occurs predominantly in Type 2 DM patients (often elderly), who retain enough insulin to prevent ketogenesis.
2. BLOOD GLUCOSE LEVEL: In DKA, glucose is usually above 250 mg/dL (typically 300–600 mg/dL). In HHNS, glucose is markedly higher — above 600 mg/dL and can exceed 1,000 mg/dL.
3. KETONES AND ACID-BASE STATUS: DKA is characterized by significant ketonemia/ketonuria and metabolic acidosis (pH less than 7.35, low bicarbonate) because without insulin, fat is broken down producing ketone bodies. In HHNS, there are no significant ketones and pH is near normal, because residual insulin prevents lipolysis.
4. RESPIRATORY PATTERN: In DKA, Kussmaul respirations (deep, rapid breathing) develop as a compensatory mechanism to blow off CO2 and correct acidosis; fruity/acetone breath is also present. In HHNS, respirations are not significantly affected (no acidosis to compensate).
5. ONSET AND NEUROLOGICAL CHANGES: DKA develops over hours (rapid onset). HHNS develops over days (insidious onset), and because of the extreme hyperosmolality, neurological changes (profound lethargy, seizures, coma) are more severe and mortality is higher in HHNS than in DKA.

Answer structure

• Feature 1: Typical patient type (Type 1 vs. Type 2) [1 mark]
• Feature 2: Blood glucose level (>250–600 vs. >600–1000 mg/dL) [1 mark]
• Feature 3: Ketones and acid-base — DKA acidosis vs. HHNS near-normal pH [1 mark]
• Feature 4: Respiratory pattern — Kussmaul and fruity breath in DKA only [1 mark]
• Feature 5: Onset and neurological changes — rapid vs. insidious, mortality [1 mark]

Scoring breakdown

Common mark deductions

• Saying both conditions have ketosis — HHNS specifically does NOT have significant ketones
• Stating glucose levels are the same for both conditions
• Omitting Kussmaul respirations entirely
• Not specifying that HHNS has higher mortality
• Presenting features without clear labeling of which applies to DKA and which to HHNS

Key phrases to include

• Type 1 DKA
• Type 2 HHNS
• Kussmaul respirations
• fruity/acetone breath
• metabolic acidosis pH less than 7.35
• no significant ketones
• glucose greater than 600
• osmolality greater than 320
• insidious onset
• higher mortality HHNS

Examiner tip

The causal chain is the key: Contrast → renal impairment → metformin accumulates → lactic acidosis. Write it in exactly that sequence to earn the mark.

Model answer

Metformin is a biguanide oral hypoglycemic agent that is the first-line treatment for Type 2 DM. It works by reducing hepatic glucose production and improving peripheral insulin sensitivity. It does NOT cause hypoglycemia on its own. Metformin is held 24–48 hours before and after contrast dye procedures because contrast media can cause transient renal impairment; if metformin is retained in the body under conditions of reduced kidney function, it can accumulate and cause potentially fatal lactic acidosis.

Answer structure

• Line 1: Classify metformin and state its mechanism and that it does not cause hypoglycemia [1 mark]
• Line 2: Explain why it is held — contrast impairs kidneys → metformin accumulates → lactic acidosis [1 mark]

Scoring breakdown

Common mark deductions

• Saying metformin causes hypoglycemia — it does not when used alone
• Vaguely saying 'it is dangerous with contrast' without explaining the lactic acidosis mechanism
• Not specifying the kidney as the link between contrast and metformin accumulation

Key phrases to include

• biguanide
• first-line Type 2 DM
• no hypoglycemia
• hepatic glucose production
• contrast dye
• renal impairment
• lactic acidosis
• hold 24–48 hours

Examiner tip

This is a one-word answer with clinical extension. The mark is earned by naming Regular insulin. The IV route distinction is frequently tested in the NLE because it is a safety-critical fact.

Model answer

Regular insulin is the ONLY insulin that can be administered intravenously. It is the insulin of choice for IV infusion in managing DKA and HHNS, and blood glucose must be monitored hourly during IV infusion.

Answer structure

• State: Regular insulin — the only insulin given IV (accept: short-acting insulin) [1 mark]

Scoring breakdown

Common mark deductions

• Naming NPH, lispro, or glargine — none of these are given IV
• Saying 'any insulin can be given IV with dilution' — this is incorrect and dangerous

Key phrases to include

• regular insulin
• IV
• intravenous
• DKA
• HHNS
• hourly glucose monitoring

Examiner tip

The 2–3 AM glucose check is the diagnostic key and the NLE loves to test this. Low at 2–3 AM = Somogyi (reduce insulin); normal/high at 2–3 AM = Dawn (increase insulin).

Model answer

Both present as morning hyperglycemia but have different causes. The Somogyi phenomenon is caused by nocturnal hypoglycemia (low blood glucose during the night, usually 2–3 AM) followed by a rebound hyperglycemia in the morning due to counter-regulatory hormone release. Treatment: reduce the evening or bedtime insulin dose or add a bedtime snack. The Dawn phenomenon is morning hyperglycemia caused by a normal physiological surge in counter-regulatory hormones (cortisol, growth hormone) in the early morning, WITHOUT any preceding nighttime hypoglycemia. Treatment: adjust or increase insulin timing. The 2–3 AM blood glucose check differentiates them: low in Somogyi, normal or elevated in Dawn.

Answer structure

• Somogyi: nocturnal hypoglycemia → rebound hyperglycemia → reduce evening insulin [1 mark]
• Dawn: morning hormone surge → morning hyperglycemia, no nocturnal low → increase/adjust insulin [1 mark]

Scoring breakdown

Common mark deductions

• Reversing the descriptions — saying Somogyi has no nocturnal low
• Giving the same treatment for both conditions
• Omitting the management (treatment) for each phenomenon

Key phrases to include

• Somogyi
• nocturnal hypoglycemia
• rebound hyperglycemia
• reduce evening insulin
• Dawn phenomenon
• morning hormone surge
• no nocturnal low
• 2–3 AM blood glucose
• increase insulin

Examiner tip

The NLE frequently tests the contraindications — heating pads and hot water are the 'trap' answers. Always include at least one safety-based instruction (no heating pads, no barefoot) for maximum marks.

Model answer

Foot care instructions for a diabetic patient with peripheral neuropathy: (1) Inspect both feet daily for cuts, blisters, redness, or swelling — neuropathy may prevent the patient from feeling injuries. (2) Wash feet daily with mild soap and lukewarm water; dry thoroughly, especially between the toes, to prevent fungal infection. (3) Wear properly fitted, closed-toe shoes and cotton socks at all times — never walk barefoot indoors or outdoors. (4) NEVER use heating pads, hot water bottles, or soak feet in hot water — neuropathy impairs heat sensation and thermal burns may occur unnoticed. Additional: cut toenails straight across (not curved) to prevent ingrown nails.

Answer structure

• Two correct and specific foot care instructions [1 mark — any 2 of the 4]
• Two more correct and specific foot care instructions [1 mark — any 2 more of the 4]

Scoring breakdown

Common mark deductions

• Listing general health teaching (e.g., 'eat healthy') instead of foot-specific instructions
• Saying to cut nails in a curved shape — correct is straight across
• Recommending hot water soaks — contraindicated due to neuropathy

Key phrases to include

• inspect daily
• never barefoot
• no heating pads
• cut nails straight across
• dry between toes
• properly fitted shoes
• lukewarm water
• peripheral neuropathy
• loss of protective sensation

Examiner tip

The word 'peakless' is the examiner's target answer. Write 'peakless' explicitly — do not just say 'it works for a long time.' The 'never mix' rule is the second mark.

Model answer

Glargine (Lantus) is a long-acting insulin analog prescribed as basal insulin therapy. It has an onset of approximately 1 hour and a duration of approximately 24 hours with NO pronounced peak (peakless action), providing a steady, continuous background level of insulin that mimics the body's normal basal insulin secretion. Because it has no peak, it does NOT cause the high-risk hypoglycemic episodes associated with peak-acting insulins like NPH. It is given once daily (usually at bedtime), is clear in appearance, and must NEVER be mixed with any other insulin.

Answer structure

• Pharmacologic rationale: long-acting, peakless, basal coverage, 24-hour duration [1 mark]
• Clinical advantage: no peak = reduced hypoglycemia risk; administration note: never mix, clear, once daily [1 mark]

Scoring breakdown

Common mark deductions

• Stating glargine has a peak — it is PEAKLESS and this is its defining characteristic
• Saying it can be mixed with regular insulin — this is explicitly contraindicated
• Confusing glargine with NPH (which is intermediate-acting and cloudy)

Key phrases to include

• long-acting
• peakless
• basal insulin
• 24-hour duration
• no pronounced peak
• never mix
• reduced hypoglycemia risk
• clear appearance

Examiner tip

This is the most nuanced 5-mark question in diabetes nursing. Examiners specifically look for the paradox: 'initially normal/high serum K despite total body depletion.' If you explain this contradiction and then explain why treatment drops the K+, you earn the first two marks automatically. Then the protocol and monitoring earn the rest.

Model answer

PATHOPHYSIOLOGY OF POTASSIUM IMBALANCE IN DKA:

In DKA, the body experiences TOTAL BODY POTASSIUM DEPLETION — potassium has been lost through osmotic diuresis and vomiting. However, the SERUM potassium at presentation may appear NORMAL or even ELEVATED (hyperkalemia). This occurs because: (1) Metabolic acidosis causes hydrogen ions (H+) to move into cells; to maintain electrical neutrality, potassium (K+) shifts OUT of cells into the extracellular fluid (transcellular shift). (2) Absolute insulin deficiency also impairs potassium uptake by cells. Therefore, the MEASURED serum potassium may be falsely reassuring, masking total body depletion.

WHEN TREATMENT BEGINS — THE DANGER POINT:
Once insulin administration and IV fluid resuscitation are started: (1) Insulin drives glucose AND potassium back INTO the cells. (2) Acidosis is corrected, reversing the transcellular shift of K+ back into cells. (3) IV fluids dilute the serum potassium. These three mechanisms rapidly LOWER the serum potassium → HYPOKALEMIA. Hypokalemia can cause life-threatening cardiac arrhythmias (ventricular tachycardia, ventricular fibrillation).

NURSING MANAGEMENT:

1. ASSESS: Obtain baseline serum potassium level BEFORE initiating insulin therapy. Monitor potassium levels every 1–2 hours during treatment.
2. CARDIAC MONITORING: Place the patient on continuous ECG monitoring. Hypokalemia signs on ECG: flattened T waves, U waves, ST depression, prolonged QT.
3. POTASSIUM REPLACEMENT RULE: If serum K+ is LESS THAN 3.5 mEq/L — hold insulin and replace potassium first (giving insulin without correcting severe hypokalemia risks fatal arrhythmia). If K+ is 3.5–5.5 mEq/L — add potassium to IV fluids and continue insulin. If K+ is GREATER THAN 5.5 mEq/L (hyperkalemic) — do NOT add potassium yet; begin insulin and fluids.
4. POTASSIUM IV ADMINISTRATION SAFETY: Potassium must NEVER be given as an IV bolus (risk of cardiac arrest). Always administer potassium replacement via slow IV infusion with a controlled infusion pump, with continuous cardiac monitoring.
5. ONGOING MONITORING: Hourly blood glucose, urine output (confirm renal function before giving potassium), neurological status, and electrolytes.

PRIORITY NURSING DIAGNOSIS: Risk for Decreased Cardiac Output related to electrolyte imbalance (hypokalemia) secondary to insulin therapy and fluid resuscitation in DKA.

Answer structure

• Part 1: Explain WHY serum K+ appears normal/high initially despite total body depletion (acidosis-driven shift + insulin deficiency) [1 mark]
• Part 2: Explain why serum K+ drops dangerously when treatment starts (insulin + fluid + acidosis correction) [1 mark]
• Part 3: State the assessment priority — check serum K+ BEFORE giving insulin; ECG monitoring [1 mark]
• Part 4: State the potassium replacement protocol based on K+ levels; never give K+ as bolus [1 mark]
• Part 5: State comprehensive ongoing monitoring plan and priority nursing diagnosis [1 mark]

Scoring breakdown

Common mark deductions

• Stating that DKA causes hyperkalemia without explaining the total-body depletion paradox
• Not explaining why potassium drops when treatment starts — just saying 'potassium goes down'
• Omitting the potassium replacement protocol entirely
• Saying potassium can be given as an IV bolus — this is dangerous and incorrect
• Missing the ECG monitoring component

Key phrases to include

• total body potassium depletion
• serum potassium normal or elevated initially
• transcellular shift
• acidosis
• insulin drives potassium into cells
• hypokalemia
• cardiac arrhythmia
• check K+ before insulin
• continuous ECG
• never IV bolus potassium
• hold insulin if K+ less than 3.5

Do

• Write the exact numeric value with the correct unit (e.g., 'less than 7%' not 'low')
• Use the precise clinical term (e.g., 'Regular insulin' not 'fast insulin')
• Answer directly — first word of your answer should address the question
• Include one clinical implication if space allows (shows understanding, may protect partial marks)

Don't

• Do NOT write a paragraph for a 1-mark question — wastes time
• Do NOT use vague language like 'high,' 'low,' or 'some' — be specific
• Do NOT confuse diagnostic thresholds with treatment targets (e.g., HbA1c 6.5% vs. target <7%)

Do

• Number your two points (1. and 2.) to make the structure unmistakable
• Include the mechanism or rationale for each point, not just the name
• Use clinical vocabulary — 'osmotic diuresis' not 'a lot of urination'
• Connect each point directly to the question asked

Don't

• Do NOT write one long paragraph that blends both points — examiners may only award 1 mark
• Do NOT list more than 2 points hoping extras earn marks — stay focused on quality
• Do NOT repeat the question back as part of the answer

Do

• Use numbered or bolded headings for each of the 3 points
• State the correct clinical values/doses where applicable
• Link pathophysiology to clinical signs and nursing actions
• Prioritize your most important point first (Maslow/ABC priority)

Don't

• Do NOT write only 2 points for a 3-mark question
• Do NOT use the same word or concept twice dressed differently to look like separate points
• Do NOT omit the rationale — '3 points of what' earns less than '2 points with why'

Do

• Write bold/underlined section headers so examiners can locate each mark
• Apply Maslow's hierarchy and ABC (Airway, Breathing, Circulation) for priority ordering
• Use NANDA-format nursing diagnoses: Problem + R/T + AEB
• Include specific values, timelines, and drug names — not general statements
• End with an evaluation or monitoring statement to show full nursing-process thinking

Don't

• Do NOT write a narrative paragraph without structure — examiners cannot award 5 separate marks from one block of text
• Do NOT omit the nursing diagnosis — it is almost always worth 1 mark in a 5-mark question
• Do NOT prioritize pharmacological interventions before safety/fluid management (IV fluids come before insulin in DKA/HHNS)
• Do NOT repeat introductory phrases — use the marks to add new clinical content