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Vocabulary flashcards covering nutrition recommendations, DKA, HHS, SIADH, and DI—including causes, pathophysiology, clinical findings, lab patterns, treatments, and key nursing considerations.
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Carbohydrate-containing foods
Grains, fruits, dairy, legumes, sweets, sugary drinks, and starchy vegetables such as potatoes, corn, peas.
Starchy vegetables
Vegetables higher in starch (potatoes, corn, peas) that provide more carbohydrates per serving than non-starchy varieties.
Low- to no-carb foods
Meat, fish, poultry, most cheeses, nuts, oils, and other fats.
Daily fiber goal for people with diabetes
Approximately 25–30 g of fiber per day.
Fiber benefit in diabetes
Increases satiety, lowers A1C, and reduces cholesterol levels.
Common fiber supplements
Psyllium and β-glucan.
Consensus dietary advice for diabetes
Emphasize non-starchy vegetables, minimize added sugars/refined grains, choose whole foods, reduce total carbohydrate intake.
Diabetic ketoacidosis (DKA)
Acute complication (usually type 1 diabetes) characterized by insulin deficiency, hyperglycemia, ketosis, and metabolic acidosis.
Typical DKA triggers
Infection, illness, stress, inadequate or missed insulin, poor diabetes management.
Key DKA pathophysiology
Absolute insulin deficiency → ↑ lipolysis & proteolysis → ketone production → metabolic acidosis and osmotic diuresis.
Classic DKA triad
Hyperglycemia, ketosis, metabolic acidosis.
DKA clinical dehydration signs
Polyuria, polydipsia, poor skin turgor, tachycardia, hypotension.
DKA respiratory sign
Kussmaul respirations with fruity (acetone) breath.
Typical DKA blood glucose level
250 mg/dL (13.9 mmol/L).
DKA anion gap feature
Elevated anion gap metabolic acidosis (pH < 7.30, HCO₃⁻ < 18 mEq/L).
Electrolyte pattern in untreated DKA
Total body potassium depleted, but serum K⁺ may be normal or elevated until insulin given.
First treatment step in DKA
Initiate isotonic IV fluids (0.9 % NaCl) before insulin.
Insulin infusion rate for DKA
Regular insulin 0.1 U/kg IV bolus then 0.1 U/kg/h continuous infusion.
Potassium rule before insulin in DKA
Serum K⁺ must be > 3.3 mEq/L; replace K⁺ if lower.
DKA glucose threshold for adding dextrose
Add D5 + 0.45 % NaCl when serum glucose reaches 200 mg/dL to prevent hypoglycemia.
Bicarbonate use in DKA
Consider only if arterial pH < 6.9.
Resolution criteria for DKA
Blood glucose < 200 mg/dL plus pH > 7.3, HCO₃⁻ ≥ 18 mEq/L, and closed anion gap.
Hyperosmolar hyperglycemic syndrome (HHS)
Severe hyperglycemia with hyperosmolarity and dehydration, minimal or no ketosis, usually in type 2 diabetes.
Common HHS precipitants
Infection (pneumonia, sepsis), acute illness, undiagnosed type 2 diabetes.
Typical serum glucose in HHS
600 mg/dL (33.3 mmol/L).
Serum osmolality level in HHS
320 mOsm/kg.
Acid–base status in HHS
No significant acidosis; pH usually > 7.30.
Key HHS symptoms
Profound dehydration, hypotension, tachycardia, altered mental status, seizures or coma.
Primary fluid choice in HHS resuscitation
Isotonic saline (0.9 % NaCl) 1 L/h initially.
Insulin protocol for HHS
Regular insulin 0.1 U/kg IV bolus then 0.1 U/kg/h; begin only after fluids and if K⁺ > 3.3 mEq/L.
Target glucose reduction rate in HHS
Decrease by 50–70 mg/dL per hour; adjust insulin if not achieved.
Glucose threshold to add dextrose in HHS
Add D5 with 0.45 % NaCl when glucose reaches 250–300 mg/dL.
Syndrome of inappropriate antidiuretic hormone (SIADH)
Excess ADH release leading to water retention, dilutional hyponatremia, and low serum osmolality.
Most common cause of SIADH
Malignancy, especially small-cell lung cancer.
Diagnostic triad for SIADH
Serum Na⁺ < 135 mEq/L, serum osmolality < 280 mOsm/kg, urine specific gravity > 1.030 (uOsm > sOsm).
Key SIADH symptoms
Low urine output, fluid retention, thirst, dyspnea, muscle cramps, headache, seizures, possible coma.
First-line treatment for SIADH
Treat underlying cause and institute fluid restriction (800–1000 mL/day if Na⁺ > 125 mEq/L).
Safe sodium correction rate in SIADH
Increase serum Na⁺ by no more than 8–12 mEq/L in the first 24 h.
Pharmacologic options for SIADH
Hypertonic saline, salt tablets, loop diuretics (if Na⁺ > 125), demeclocycline, vasopressin receptor antagonists (vaptans).
Key nursing interventions in SIADH
Seizure precautions, strict I&O, monitor serum/urine Na⁺ and osmolality, provide ice chips or sugarless gum for thirst.
"No free water" order meaning
Patient may not receive plain water; all fluids must contain solute to avoid worsening hyponatremia.
Diabetes insipidus (DI)
Deficiency of ADH (central) or renal resistance to ADH (nephrogenic) leading to excessive dilute urine and hypernatremia.
Central vs. nephrogenic DI
Central: inadequate ADH secretion. Nephrogenic: kidneys unresponsive to ADH.
Core DI manifestations
Polyuria (2–20 L/day), polydipsia, low urine specific gravity < 1.005, high serum osmolality, hypernatremia.
Desmopressin (DDAVP)
Synthetic ADH analog used to treat central DI; given intranasally, orally, sublingually, or SQ/IV.
Monitoring effectiveness of DDAVP
Reduced urine output, increased urine specific gravity/osmolality, stabilized serum Na⁺ and osmolality.
Fluid management in DI
Encourage oral intake to thirst; provide hypotonic IV fluids (D5W) cautiously to avoid rapid sodium drop.
Key labs: SIADH vs. DI – serum sodium
SIADH ↓ Na⁺; DI ↑ Na⁺.
Key labs: SIADH vs. DI – urine specific gravity
SIADH ↑ specific gravity (> 1.030); DI ↓ specific gravity (< 1.005).
Key labs: SIADH vs. DI – serum osmolality
SIADH ↓ serum osmolality; DI ↑ serum osmolality.
Electrolyte caution with loop diuretics in SIADH
Give furosemide only if serum Na⁺ > 125 mEq/L to avoid worsening hyponatremia.
Vaptans mechanism
Vasopressin receptor antagonists that promote water diuresis without major sodium or potassium loss.
Polyphagia meaning in DKA
Excessive hunger caused by cellular glucose starvation despite hyperglycemia.
Osmotic diuresis definition
Increased urine output due to osmotic pull of excess glucose/ketones in renal tubules, leading to water and electrolyte loss.
Anion gap significance in DKA
Represents unmeasured anions (ketones); elevated gap indicates metabolic acidosis.
Kussmaul respirations
Deep, rapid breathing pattern that blows off CO₂ to compensate for metabolic acidosis.
Hyperviscosity complication in HHS
Increased blood thickness can cause thrombosis, seizures, and decreased tissue perfusion.
Priming insulin bolus in DKA
Initial 0.1 U/kg IV bolus to fill insulin receptors before continuous infusion.
Criteria to hold insulin in DKA/HHS
Serum potassium < 3.3 mEq/L—replace K⁺ first.
Reason ketosis rare in type 2 diabetes
Even small residual insulin secretion suppresses lipolysis and ketogenesis.
Thirst center location
Hypothalamus; activated by high serum osmolality (e.g., in DI).
Urine osmolality pattern in SIADH
Inappropriately high (> 100 mOsm/kg) despite low serum osmolality.
Urine osmolality pattern in DI
Low (< 100 mOsm/kg) due to inability to concentrate urine.
Fluid restriction goal in SIADH
Create negative water balance to raise serum sodium slowly.
Hemodynamic monitoring indication
Severe hypovolemia or cardiogenic shock in DKA/HHS management.
Magnesium trend in DKA/HHS
Serum Mg²⁺ often low due to osmotic diuresis; may require replacement.
Hypertonic saline concentration
3 % NaCl; used cautiously to treat severe symptomatic hyponatremia in SIADH.
Demeclocycline role in SIADH
Tetracycline derivative inducing nephrogenic DI to counteract water retention.
Central pontine myelinolysis risk
Neurologic damage from overly rapid correction of chronic hyponatremia.
Key nursing assessment in DI
Monitor I&O, daily weight, neurological status, serum/urine electrolytes.
Treatment end-point in HHS
Plasma osmolality ≤ 315 mOsm/kg and patient mentally alert with stable vitals.
Abrupt insulin cessation danger after IV infusion
Can lead to rebound hyperglycemia; overlap IV insulin with first subcutaneous dose for 1–2 h.
“No jokes about sodium?” answer
NA (the chemical symbol for sodium).