NLE High-Risk Pregnancy & Obstetric Complications — Hypertensive & Metabolic Disorders of PregnancyRevision Notes

Exam tips

• NLE pattern: If the stem says 'after 20 weeks + high BP + protein in urine' → preeclampsia.
• If seizures occur on top of preeclampsia → eclampsia. First priority = AIRWAY (turn to side, do not restrain).
• Memorize the '20-week rule': before 20 weeks = chronic; after 20 weeks = gestational or preeclamptic.
• BP ≥160/110 is the magic number for SEVERE features — triggers emergency antihypertensive + MgSO4.
• The question 'Which group has the highest risk?' → Chronic hypertension with SUPERIMPOSED preeclampsia.

Key points

• Gestational hypertension: BP ≥140/90 mmHg after 20 weeks WITHOUT proteinuria; resolves postpartum.
• Preeclampsia: BP ≥140/90 after 20 weeks WITH proteinuria OR end-organ involvement (thrombocytopenia, impaired liver/renal function, pulmonary edema, cerebral/visual symptoms).
• Eclampsia: Preeclampsia PLUS tonic-clonic seizures not attributable to another cause.
• Chronic hypertension: Present BEFORE pregnancy or before 20 weeks.
• Chronic hypertension with superimposed preeclampsia: Pre-existing HTN + new proteinuria or worsening end-organ signs after 20 weeks — HIGHEST RISK GROUP.
• The 20-week threshold is the critical dividing line: before 20 weeks = chronic; after 20 weeks = gestational/preeclampsia.
• Proteinuria in preeclampsia: ≥300 mg in 24-hour urine OR protein:creatinine ratio ≥0.3 OR dipstick ≥2+ (least preferred).

Definitions

Common mistakes

• Confusing gestational hypertension with preeclampsia — remember: preeclampsia requires proteinuria OR end-organ involvement.
• Thinking hypertension must appear before 20 weeks to be chronic — chronic HTN is diagnosed at <20 weeks OR pre-pregnancy.
• Forgetting that superimposed preeclampsia (chronic HTN + new proteinuria/end-organ damage) carries the HIGHEST maternal-fetal risk.
• Assuming that normal BP before 20 weeks rules out preeclampsia — the disease manifests AFTER 20 weeks.
• Confusing 'severe hypertension' (≥160/110) with 'mild preeclampsia' (≥140/90) — the threshold for severe features is ≥160/110.

Exam tips

• NLE trap: 'The nurse should restrict sodium intake for preeclampsia' → FALSE. Sodium restriction and diuretics are both contraindicated.
• Think of preeclampsia as 'fluid in the wrong place' — overloaded tissues, depleted vessels. This explains why aggressive IV fluids cause pulmonary edema.
• Vasospasm → reduced kidney perfusion → proteinuria + oliguria → MgSO4 accumulates → toxicity risk. This chain explains why urine output monitoring is critical during MgSO4 therapy.

Key points

• Root cause: Generalized VASOSPASM from abnormal placentation and endothelial dysfunction.
• Abnormal placentation leads to decreased placental perfusion → release of antiangiogenic factors → endothelial damage → vasospasm.
• Vasospasm reduces perfusion to ALL organs: placenta (IUGR, abruption), kidneys (proteinuria, oliguria), liver (epigastric pain, elevated enzymes), brain (headache, seizures), eyes (visual changes).
• Increased vascular permeability: fluid shifts OUT of vessels → edema (tissue overload) + hemoconcentration (intravascular depletion).
• PARADOX: The woman is FLUID OVERLOADED in tissues but VOLUME DEPLETED in vessels — do NOT aggressively diurese or fluid load.
• Diuretics are CONTRAINDICATED in preeclampsia (worsens intravascular depletion and placental perfusion).
• IV fluids must be given cautiously, usually 125 mL/hr maximum, with strict intake/output monitoring to prevent pulmonary edema.
• Sodium restriction is also NOT recommended — it worsens volume depletion.

Definitions

Common mistakes

• Recommending sodium restriction for preeclampsia — this is WRONG; it worsens volume depletion.
• Ordering or endorsing aggressive diuresis in preeclampsia — diuretics are contraindicated.
• Thinking edema means the woman is well-hydrated intravascularly — she is paradoxically volume-contracted in the vessels.
• Confusing IUGR (fetal growth restriction) cause — it is due to decreased placental perfusion from vasospasm, not malnutrition.

Exam tips

• HELLP memory trick: 'Hemolysis = H, Elevated Liver = EL, Low Platelets = LP' — memorize the lab triad.
• NLE key rule: 'Do NOT palpate the liver' in suspected HELLP — this is a safety priority question answer.
• If the stem shows RUQ pain + nausea + malaise in a pregnant woman after 20 weeks → think HELLP first.
• Management priority: Delivery + MgSO4 + blood products for DIC.

Key points

• HELLP = Hemolysis, Elevated Liver enzymes, Low Platelets — a severe variant of preeclampsia.
• Classic presentation: Right upper quadrant or epigastric pain, nausea, malaise, and general 'flu-like' symptoms in a pregnant woman after 20 weeks.
• Lab hallmarks: Low platelet count (<100,000/mm³), elevated AST/ALT, elevated bilirubin (hemolysis), elevated LDH.
• Complications: DIC (disseminated intravascular coagulopathy), hepatic rupture, placental abruption, acute kidney injury.
• CRITICAL nursing action: Do NOT palpate the liver — pressure can precipitate hepatic rupture, a life-threatening emergency.
• Management: Immediate delivery is the definitive treatment; magnesium sulfate for seizure prophylaxis; blood products (FFP, platelets) as needed for DIC.
• HELLP can occur WITHOUT hypertension or proteinuria in up to 20% of cases — do not rely on BP alone to suspect HELLP.
• Platelet transfusion is given if platelets fall below 50,000/mm³ before delivery or invasive procedures.

Definitions

Common mistakes

• Palpating the liver in a patient with suspected HELLP — this can cause hepatic rupture.
• Expecting HELLP to always present with high BP and proteinuria — up to 20% have neither.
• Confusing HELLP labs with normal pregnancy values — platelets fall, liver enzymes rise; this is ABNORMAL in pregnancy.
• Delaying delivery — delivery is the only definitive cure for HELLP; stabilize and deliver promptly.

Exam tips

• NLE classic question: 'What is the FIRST nursing action for a preeclamptic woman?' → Position left lateral recumbent.
• Room setup for preeclampsia: quiet + dim + padded rails + suction + O2 + calcium gluconate at bedside. All five elements are testable.
• DTR scale: 0 = absent (toxicity), 1+ = sluggish, 2+ = normal, 3+ = brisk, 4+ = hyperreflexia with clonus (seizure risk).
• Urine output <30 mL/hr during MgSO4 = HOLD infusion + notify physician immediately — this is a high-priority safety action.

Key points

• Monitor BP every 1–4 hours (more frequently with severe features), weight daily (sudden weight gain from fluid retention), and urine protein.
• Assess deep tendon reflexes (DTRs) and clonus: hyperreflexia indicates CNS irritability → seizure risk.
• Clonus test: Dorsiflex the foot sharply; beats of clonus (≥3 sustained beats) indicate CNS irritability.
• Strict intake/output: report urine output <30 mL/hr (oliguria = MgSO4 accumulation risk).
• Labs: CBC with platelet count, liver enzymes (AST, ALT), serum creatinine, uric acid, coagulation studies.
• Position: LEFT LATERAL recumbent — maximizes placental perfusion by relieving aorta/IVC compression.
• Environment: QUIET, DIM, LOW-STIMULATION room; limit visitors; avoid sudden loud noises — sensory stimulation can trigger seizures.
• Seizure precautions: padded side rails UP, suction at bedside, oxygen at bedside, emergency airway available.
• Fetal surveillance: non-stress test (NST), biophysical profile (BPP), kick counts, and electronic fetal monitoring.
• Only CURE for preeclampsia/eclampsia is DELIVERY — all management is supportive until fetal maturity allows safe delivery.

Definitions

Common mistakes

• Placing a preeclamptic woman flat on her back (supine) — this compresses the IVC and reduces placental perfusion.
• Keeping a preeclamptic woman in a bright, noisy ward — sensory stimulation increases seizure risk.
• Forgetting to raise and PAD the side rails — unpadded rails can cause injury during a seizure.
• Not reporting oliguria during MgSO4 infusion — oliguria means MgSO4 is not being excreted and toxicity will develop.
• Measuring protein by dipstick alone as the primary diagnostic method — 24-hour urine or protein:creatinine ratio is more accurate.

Formulas

Exam tips

• THE most important MgSO4 sequence to memorize for NLE: Loss of DTRs → Respiratory depression (RR <12/min) → Cardiac/respiratory arrest.
• Any ONE of these = HOLD infusion: absent DTRs, RR <12/min, urine output <30 mL/hr.
• Antidote dose: 1 g calcium gluconate = 10 mL of 10% solution, give IV slowly over ~3 minutes.
• Therapeutic level = 4–7 mEq/L. Above this → toxicity. Below this → seizure not prevented.
• MgSO4 also crosses the placenta → monitor newborn for respiratory depression, hypotonia, and hypocalcemia at birth.
• NLE tip: 'What is kept at the bedside during MgSO4 infusion?' → Calcium gluconate (not glucagon, not atropine).

Key points

• Drug of choice for PREVENTION and TREATMENT of eclamptic seizures in preeclampsia.
• Mechanism: CNS depressant; relaxes smooth muscle; raises seizure threshold by competing with calcium at neuromuscular junctions.
• LOADING DOSE: 4–6 g IV over 15–30 minutes.
• MAINTENANCE DOSE: 1–2 g/hour continuous IV infusion (ALWAYS on an infusion pump).
• THERAPEUTIC SERUM LEVEL: 4–7 mEq/L (approximately 4.8–8.4 mg/dL).
• MgSO4 is renally excreted — oliguria = drug accumulation = TOXICITY RISK.
• MgSO4 is a HIGH-ALERT medication under Joint Commission and Philippine hospital safety standards.

Definitions

Common mistakes

• Giving MgSO4 without an infusion pump — this is a medication error and safety violation.
• Forgetting to check the THREE pre-dose checks: DTRs, respiratory rate ≥12/min, urine output ≥30 mL/hr.
• Not having calcium gluconate at the bedside during MgSO4 infusion.
• Confusing calcium gluconate with calcium chloride — calcium gluconate is the preferred antidote (less irritating to veins); calcium chloride can be used by physicians centrally.
• Continuing MgSO4 infusion when DTRs are absent, RR <12/min, or urine output <30 mL/hr.
• Thinking MgSO4 is also the treatment for seizures in epilepsy — it is specifically for eclampsia, NOT general epilepsy.

Formulas

Exam tips

• NLE CRITICAL: 'First sign of MgSO4 toxicity' = LOSS OF DEEP TENDON REFLEXES (not respiratory depression — that comes second).
• Memory aid for toxicity order: 'DTR → RR → Output → LOC → Arrest' (Reflexes die first, then Respiration, then Renal output drops, then Consciousness, then Arrest).
• If NLE asks 'What is the priority nursing assessment before giving MgSO4?' → Check patellar reflex FIRST, then respiratory rate, then urine output.
• Calcium gluconate dose: '1 gram, 10 mL, 10%, 3 minutes' — four 'tens' to remember.
• Philippine nursing context: Under DOH and PhilHealth protocols in tertiary hospitals, MgSO4 administration by nurses requires physician's order and strict pump use per RA 9173 scope of practice.

Key points

• Signs appear in ORDER as serum levels rise — memorize this sequence for NLE:
• 1. LOSS OF DEEP TENDON REFLEXES (patellar reflex absent) — EARLIEST sign, occurs around 8–10 mEq/L.
• 2. RESPIRATORY DEPRESSION — RR <12 breaths/min, occurs around 10–12 mEq/L.
• 3. OLIGURIA — urine output <30 mL/hr (MgSO4 not being excreted, levels continue to rise).
• 4. Decreased level of consciousness, hypotension, flushing, feeling of warmth.
• 5. CARDIAC/RESPIRATORY ARREST — at very high levels (>15 mEq/L).
• PRE-DOSE SAFETY CHECKS (before every dose): DTRs present, RR ≥12/min, urine output ≥30 mL/hr.
• HOLD infusion immediately if: DTRs absent, RR <12/min, OR urine output <30 mL/hr.
• ANTIDOTE: Calcium gluconate 1 g (10 mL of 10% solution) IV over ~3 minutes.
• Calcium gluconate MUST be at the bedside whenever MgSO4 is infusing.
• Also monitor the FETUS: MgSO4 crosses the placenta → neonatal respiratory depression, hypotonia, and poor feeding are possible.

Definitions

Common mistakes

• Waiting for respiratory arrest before stopping MgSO4 — absent DTRs alone is enough to HOLD the infusion.
• Giving calcium chloride instead of calcium gluconate through a peripheral IV — calcium chloride is caustic and should only be given centrally.
• Forgetting that neonates can also show MgSO4 toxicity (floppy baby, respiratory depression) when the mother received MgSO4 close to delivery.
• Checking only respiratory rate and forgetting DTRs and urine output.
• Documenting 'DTRs intact' without specifying which reflex and the rating (e.g., patellar 2+).

Exam tips

• NLE top picks for antihypertensives in pregnancy: acute IV = hydralazine or labetalol; chronic oral = methyldopa.
• ABSOLUTELY AVOID: ACE inhibitors (captopril, enalapril) and ARBs (losartan) — teratogenic to fetal kidneys.
• Labetalol contraindications: ASTHMA + Heart failure + Bradycardia — these three are commonly tested.
• If a stem mentions a hypertensive pregnant woman with a history of asthma → do NOT choose labetalol.

Key points

• Antihypertensives are used for SEVERE hypertension (BP ≥160/110) to prevent maternal STROKE — the primary danger of uncontrolled severe HTN.
• HYDRALAZINE: 5–10 mg IV; first-line parenteral agent; watch for maternal hypotension and reflex tachycardia.
• LABETALOL: 20 mg IV initially, then escalating doses (20–40–80 mg); avoid in asthma, heart failure, and bradycardia (beta-blocker effect).
• NIFEDIPINE: oral immediate-release; vasodilator; watch for hypotension; DO NOT crush or chew; avoid with MgSO4 (additive hypotension).
• METHYLDOPA: oral; preferred for CHRONIC hypertension in pregnancy (long-term use, crosses placenta, safe record).
• ACE INHIBITORS (captopril, enalapril) and ARBs (losartan, valsartan): ABSOLUTELY CONTRAINDICATED in pregnancy — cause fetal renal agenesis, oligohydramnios, neonatal renal failure, and death.
• Goal of antihypertensive therapy: Reduce BP to 140–150/90–100 mmHg range — do NOT lower BP too aggressively (reduces placental perfusion).

Definitions

Common mistakes

• Giving ACE inhibitors or ARBs to a pregnant hypertensive — these are ABSOLUTELY contraindicated; causes fetal kidney damage.
• Using labetalol in a woman with asthma — labetalol is a beta-blocker and will cause bronchospasm.
• Dropping BP too low with antihypertensives — reduces uteroplacental blood flow and causes fetal distress.
• Confusing the route: hydralazine and labetalol are IV for acute; methyldopa and nifedipine are oral.

Exam tips

• NLE SEQUENCE for eclamptic seizure: DURING = turn left side + do not restrain + do not put anything in mouth. AFTER = suction + O2 + FHR assessment + MgSO4 + prepare for delivery.
• Priority framework (Maslow): PHYSIOLOGIC SAFETY = Airway (turn to side, clear airway) is ALWAYS first.
• Common NLE distractor: 'Insert padded tongue blade' — this is WRONG in modern practice. Choose 'turn to the side' instead.
• Remember: 'Delivery = only cure' → this is the rationale for all obstetric interventions in eclampsia.

Key points

• PRIORITY DURING SEIZURE: PATENT AIRWAY and PATIENT SAFETY.
• TURN woman to her LEFT SIDE — maintains airway patency, prevents aspiration, maintains placental perfusion.
• Do NOT restrain the patient — restraint can cause fractures and muscle injury.
• NEVER force anything into the mouth — risk of broken teeth, jaw fracture, and nurse injury.
• Protect from injury: clear surrounding area; do not insert tongue blade (outdated and dangerous).
• POST-SEIZURE ACTIONS (after convulsions stop):
• 1. Suction secretions from the airway.
• 2. Administer oxygen (8–10 L/min via face mask).
• 3. Assess fetal heart rate — fetal bradycardia is common post-seizure (hypoxia).
• 4. Prepare for delivery — delivery is the ONLY CURE; it follows maternal stabilization.
• 5. Administer MgSO4 as ordered (loading dose if not already on it).
• 6. Continuous monitoring of VS, LOC, DTRs, urine output.
• Delivery does NOT occur during the seizure — stabilize the mother FIRST, then deliver.

Definitions

Common mistakes

• Attempting to restrain the patient during a seizure — increases risk of injury to patient and nurse.
• Inserting a padded tongue blade or any object into the mouth — OUTDATED and DANGEROUS practice; airway management is via positioning and suction POST-seizure.
• Rushing to deliver the baby DURING the seizure — stabilize the mother first.
• Forgetting to assess fetal heart rate after a seizure — fetal hypoxia is expected and needs monitoring.
• Positioning the woman supine after a seizure — left lateral is maintained to preserve placental perfusion.

Formulas

Exam tips

• NLE key fact: GDM screening = 50-g GCT at 24–28 weeks; if ≥140 mg/dL at 1 hour → do 3-hour OGTT to CONFIRM.
• Insulin is the safest because it does NOT cross the placenta — this statement appears directly in NLE options.
• Macrosomia → shoulder dystocia at delivery → Erb's palsy; neonatal hypoglycemia → feed early. Know this chain.
• Filipino context: Filipino women are at higher risk for GDM and type 2 DM; GDM prevalence is rising with urbanization and dietary changes — relevant to community health questions.
• Postpartum care: GDM woman needs OGTT at 6–12 weeks postpartum and annual fasting glucose thereafter.

Key points

• GDM = glucose intolerance first RECOGNIZED during pregnancy (may have been pre-existing but undiagnosed).
• Mechanism: Placental hormones (human placental lactogen/HPL, progesterone, cortisol, growth hormone) cause INSULIN RESISTANCE — pancreas cannot compensate → hyperglycemia.
• Risk factors: Obesity, family history of type 2 DM, previous macrosomic baby (>4,000 g), previous GDM, age >25, polycystic ovarian syndrome (PCOS), ethnicity (Filipino women have higher risk).
• SCREENING: 50-g Glucose Challenge Test (GCT) at 24–28 weeks (non-fasting).
• SCREEN POSITIVE if 1-hour glucose ≥140 mg/dL → proceed to DIAGNOSTIC test.
• DIAGNOSTIC: 3-hour 100-g Oral Glucose Tolerance Test (OGTT) — requires fasting; positive if ≥2 values are met/exceeded.
• OGTT thresholds (Carpenter-Coustan criteria): Fasting ≥95 mg/dL, 1-hour ≥180 mg/dL, 2-hour ≥155 mg/dL, 3-hour ≥140 mg/dL.
• GLYCEMIC TARGETS in pregnancy: Fasting <95 mg/dL, 1-hour postprandial <140 mg/dL, 2-hour postprandial <120 mg/dL.
• Management FIRST LINE: Medical Nutrition Therapy (MNT) + regular exercise.
• INSULIN is added when MNT fails — safest because it does NOT cross the placenta; remains the GOLD STANDARD.
• Oral agents (metformin, glyburide) cross the placenta to varying degrees; some centers use them but insulin remains the standard in the Philippines.
• After delivery: GDM usually resolves but 50% risk of developing type 2 DM within 10 years; postpartum OGTT at 6–12 weeks is recommended.

Definitions

Common mistakes

• Saying insulin crosses the placenta — INSULIN DOES NOT cross the placenta; only glucose does. This is the reason insulin is safe in pregnancy.
• Starting insulin before attempting diet therapy — MNT (diet and exercise) is ALWAYS tried first for 2 weeks before adding insulin.
• Forgetting to early-feed the GDM newborn — neonatal hypoglycemia occurs within 1–3 hours of birth.
• Thinking GDM always resolves permanently — 50% lifetime risk of type 2 DM; postpartum OGTT is mandatory.
• Confusing the GCT (50-g screening, non-fasting, 1-hour) with the OGTT (100-g diagnostic, fasting, 3-hour).

Exam tips

• NLE classic: 'First-line antiemetic for HG' = PYRIDOXINE (Vitamin B6) ± doxylamine. NOT metoclopramide, NOT ondansetron.
• Electrolyte pattern: HG → hypokalemia + metabolic alkalosis (from HCl loss). Know this combination.
• Thiamine BEFORE glucose: critical safety rule. If you see 'prolonged vomiting + IV fluid initiation' → give thiamine first.
• Ketonuria = HG diagnosis confirmed. Normal NVP does not cause ketones in urine.
• Dietary teaching for HG: 'Dry crackers before rising from bed in the morning' + small frequent meals + separate fluids from solids + avoid cooking smells.

Key points

• Definition: SEVERE, PERSISTENT nausea and vomiting beyond normal morning sickness, causing dehydration, weight loss >5% of pre-pregnancy weight, electrolyte disturbances, and KETONURIA.
• Distinguishing from normal morning sickness: HG causes weight loss, ketonuria, electrolyte imbalance, and dehydration; normal NVP does not.
• Pathophysiology: Elevated hCG levels (HG is more common with molar pregnancy and multiple gestation) and possibly thyroid, estrogen, and helicobacter pylori involvement.
• Assessment findings: Dry mucous membranes, poor skin turgor, tachycardia, orthostatic hypotension, concentrated amber urine, weight loss, ketonuria on urinalysis.
• Electrolyte disturbances: HYPOKALEMIA (loss of gastric potassium) and METABOLIC ALKALOSIS (loss of gastric hydrochloric acid) — most common. Starvation ketosis can also cause metabolic acidosis.
• Complication: WERNICKE ENCEPHALOPATHY from thiamine (Vitamin B1) deficiency due to prolonged vomiting and poor intake — presents with confusion, ataxia, and ophthalmoplegia.
• THIAMINE (Vitamin B1) must be given BEFORE glucose/dextrose infusion in severely malnourished patients to prevent precipitating Wernicke encephalopathy.
• Management: NPO initially → small frequent dry bland carbohydrate meals → IV fluid and electrolyte replacement → antiemetics.
• FIRST-LINE antiemetic: PYRIDOXINE (Vitamin B6) ± DOXYLAMINE.
• Second-line: Metoclopramide, promethazine, or ondansetron.
• Separate fluids from solids; elevate head of bed after meals; avoid triggers and strong odors.
• Monitor daily weight, intake/output, urine ketones, electrolytes, and signs of dehydration.

Definitions

Common mistakes

• Confusing HG with normal morning sickness — normal NVP resolves by 12–16 weeks and does NOT cause ketonuria or significant weight loss.
• Giving IV dextrose before thiamine in a severely vomiting patient — this precipitates Wernicke encephalopathy by depleting the last thiamine reserves for glucose metabolism.
• Starting oral feeding too quickly after NPO — advance diet GRADUALLY: clear liquids → small dry crackers → bland foods.
• Giving large volumes of fluid too quickly — can cause electrolyte dilution and pulmonary edema.
• Choosing ondansetron as first-line — pyridoxine ± doxylamine is FIRST-LINE; ondansetron is added later.

Exam tips

• NLE community health context: In Philippine rural areas (barangay health centers), nurses often do initial BP screening and prenatal monitoring independently under RA 9173 — know danger signs to refer promptly to a physician/hospital.
• PhilHealth Z-Benefit package covers hypertensive disorders of pregnancy in accredited hospitals — relevant to Philippine healthcare delivery context.
• For GDM: 'Insulin does not cross the placenta' is the NLE-tested rationale for its safety in pregnancy.
• Kick count teaching: 10 movements in 2 hours is the standard; report if less — simple but frequently tested.

Key points

• DANGER SIGNS to report IMMEDIATELY for preeclampsia (ACOG warning signs):
• 1. Severe headache (unresponsive to paracetamol)
• 2. Visual changes (blurring, spots, flashing lights, double vision)
• 3. Epigastric or right upper quadrant pain
• 4. Sudden swelling of face, hands, or feet
• 5. Decreased urine output
• 6. Decreased fetal movement (kick counts <10 movements in 2 hours)
• Home BP monitoring: Check BP twice daily, same arm, same time, after 5-minute rest — record readings.
• Rest in left lateral position; avoid prolonged standing or strenuous activity.
• DO NOT take diuretics, sodium restriction, or non-prescribed medications (avoid NSAIDs — raise BP and reduce renal clearance).
• Adequate protein intake: 60–80 g/day; adequate fluid intake: 8–10 glasses/day.
• Attend ALL prenatal visits for BP, weight, and urine protein checks — compliance is critical.
• GDM teaching: SBGM technique (timing, targets), insulin storage (refrigerate, do not freeze), injection technique, carbohydrate-controlled diet, exercise, recognize hypo/hyperglycemia.
• GDM postpartum: Breastfeeding is encouraged (lowers mother's glucose); OGTT at 6–12 weeks postpartum; annual FBS screening for life.
• HG teaching: Dry crackers before rising, small frequent bland meals, separate fluids from solids, avoid strong food odors, rest after meals with head elevated.

Common mistakes

• Telling a preeclamptic woman to restrict salt — NOT recommended; may worsen intravascular volume depletion.
• Advising diuretic use for edema in preeclampsia — CONTRAINDICATED.
• Forgetting to teach fetal kick counts — decreased fetal movement is a warning sign of fetal compromise.
• Not including postpartum follow-up in GDM teaching — the OGTT at 6–12 weeks is essential for detecting persistent DM.
• Teaching GDM patients to store insulin at room temperature long-term — unopened insulin should be REFRIGERATED (2–8°C); in-use insulin can be at room temperature for up to 28–30 days.