3.2 Gastrointestinal, Renal & Endocrine Disorders Management

Key Takeaways

  • Peptic Ulcer Disease (PUD) differentiates gastric ulcers (pain worsened by food) from duodenal ulcers (pain relieved by food).
  • Acute Kidney Injury (AKI) features oliguria and elevated creatinine; monitor for life-threatening hyperkalemia.
  • Diabetic Ketoacidosis (DKA) presents with Kussmaul respirations and fruity breath; prioritize IV fluid resuscitation and regular insulin infusion.
  • Hyperosmolar Hyperglycemic Syndrome (HHS) occurs in Type 2 Diabetes with extreme hyperglycemia (>600 mg/dL) without significant ketosis.
  • Thyroid Storm is a life-threatening complication of hyperthyroidism requiring immediate beta-blockers, antithyroid medications, and cooling measures.
Last updated: July 2026

Gastrointestinal Nursing Management

Peptic Ulcer Disease (PUD)

PUD involves the deep erosion of the mucosal lining of the stomach or duodenum, primarily caused by Helicobacter pylori (H. pylori) infection or chronic nonsteroidal anti-inflammatory drug (NSAID) use. The disruption of the mucosal barrier exposes the underlying tissue to gastric acid and pepsin, leading to profound inflammation, ulceration, and potential bleeding.

Disease Comparison Table: Gastric vs. Duodenal Ulcers

CharacteristicGastric UlcerDuodenal Ulcer
LocationStomach (often lesser curvature)Duodenum (proximal portion)
IncidenceLess common, typically older adultsMore common, often younger adults
Pain Timing1-2 hours after meals2-4 hours after meals, often awakens patient at night
Effect of FoodPain is WORSENED by eatingPain is RELIEVED by eating
WeightWeight loss is commonWeight gain may occur
MalignancyHigher risk, requires biopsyVery low risk

Nursing Priority Interventions for PUD

  • Medications: Administer Proton Pump Inhibitors (PPIs, e.g., pantoprazole) to decrease acid secretion, H2-receptor antagonists, and a combination of antibiotics if H. pylori positive. Mucosal protectants (Sucralfate) should be given on an empty stomach. Antacids should be given 1-2 hours apart from other medications to prevent impaired absorption.
  • Complication Monitoring: Monitor vigilantly for perforation (characterized by a sudden, severe, rigid, board-like abdomen and shoulder pain), hemorrhage (hematemesis, "coffee-ground" emesis, or melena), and gastric outlet obstruction.
  • Education: Advise strict smoking cessation, avoidance of NSAIDs, reduction of stress, and eating small, frequent, non-irritating meals.

Cirrhosis and Liver Failure

Cirrhosis is the end-stage of chronic liver disease, characterized by extensive degeneration, necrosis, and destruction of liver parenchymal cells, which are replaced by fibrotic scar tissue. This structurally alters the liver, obstructing blood flow and impairing hepatic function.

Clinical Manifestations and Interventions

  • Portal Hypertension: Increased pressure in the portal venous system leads to esophageal varices (fragile, distended veins prone to rupture) and ascites. Interventions include administering non-selective beta-blockers (propranolol) to reduce portal pressure. In acute bleeding, prepare for endoscopic variceal ligation or balloon tamponade.
  • Hepatic Encephalopathy: Caused by elevated ammonia levels crossing the blood-brain barrier due to the liver's inability to convert ammonia to urea. Symptoms range from confusion to coma. Administer Lactulose to trap ammonia in the gut for excretion via stool. Monitor neurological status and assess for asterixis (flapping tremor of the hands).
  • Ascites and Edema: Perform daily weights, measure abdominal girth, strictly restrict sodium intake, administer diuretics (Spironolactone and Furosemide), and prepare for therapeutic paracentesis if respiratory compromise occurs due to fluid pressure on the diaphragm. Monitor for spontaneous bacterial peritonitis.
  • Coagulopathy: The liver synthesizes clotting factors and requires Vitamin K. Cirrhosis patients have an increased PT/INR and are at high risk for bleeding. Institute bleeding precautions.

Renal Nursing Management

Acute Kidney Injury (AKI) vs. Chronic Kidney Disease (CKD)

Kidney disorders profoundly impact fluid balance, electrolyte homeostasis, acid-base balance, and the excretion of metabolic waste products.

Diagnostic Lab Thresholds

  • BUN: Normal 10-20 mg/dL. Elevated in renal failure, dehydration, and high-protein diets.
  • Serum Creatinine: Normal 0.6-1.2 mg/dL. The most specific and reliable indicator of renal function.
  • GFR (Glomerular Filtration Rate): Normal > 90 mL/min. A GFR < 15 mL/min indicates Stage 5 CKD (End-Stage Renal Disease, ESRD).
  • Potassium: Normal 3.5-5.0 mEq/L. Hyperkalemia is a critical, life-threatening risk in renal failure leading to fatal dysrhythmias.

Disease Comparison: AKI vs. CKD

FeatureAcute Kidney Injury (AKI)Chronic Kidney Disease (CKD)
OnsetSudden (hours to days)Gradual (months to years)
ReversibilityOften reversible if treated earlyProgressive and irreversible
CausesPrerenal (hypovolemia, shock), Intrarenal (nephrotoxins like contrast dye), Postrenal (stones, BPH)Diabetes Mellitus (leading cause), Uncontrolled Hypertension
Urine OutputOliguric phase (<400 mL/day), followed by diuretic phasePolyuria early, progressing to oliguria and anuria in ESRD

Nursing Interventions for Renal Failure

  • Hyperkalemia Management: Assess for peaked T-waves on ECG. Administer IV Calcium Gluconate (protects the myocardium from dysrhythmias), IV Regular Insulin with 50% Dextrose (drives potassium intracellularly), and Sodium Polystyrene Sulfonate (Kayexalate) for gastrointestinal excretion.
  • Fluid Management: Maintain strict I&O, record daily weights (the most accurate indicator of fluid status), and enforce fluid restriction as ordered.
  • Dietary Modifications: Low protein (unless the patient is on dialysis, which removes amino acids), low potassium, low sodium, and low phosphorus. Administer phosphate binders (e.g., Sevelamer) with meals.
  • Anemia Management: Administer Erythropoietin (Epogen/Procrit) subcutaneously, as the failing kidneys cease to produce this hormone, leading to severe anemia.

Endocrine Nursing Management

Diabetes Mellitus Emergencies: DKA vs. HHS

Diabetes emergencies require rapid identification, aggressive fluid resuscitation, and careful insulin administration to prevent mortality.

Disease Comparison Table: DKA vs. HHS

CharacteristicDiabetic Ketoacidosis (DKA)Hyperosmolar Hyperglycemic Syndrome (HHS)
Patient PopulationPrimarily Type 1 DiabetesPrimarily Type 2 Diabetes, typically older adults
Blood GlucoseUsually 250-600 mg/dLUsually extremely high, > 600 mg/dL (often >1000 mg/dL)
Ketones/AcidosisPositive serum/urine ketones, severe metabolic acidosis (pH < 7.3)Minimal or absent ketones, normal pH > 7.3
Clinical SignsKussmaul respirations, fruity (acetone) breath odor, abdominal painProfound dehydration, severe neurological changes (seizures, profound lethargy, coma)

Priority Interventions for DKA/HHS

  1. Fluids: Initiate rapid IV fluid replacement (0.9% Normal Saline) to treat severe intracellular and intravascular dehydration. This is always the first priority. When blood glucose drops to approximately 250 mg/dL, add 5% Dextrose to the IV fluids to prevent sudden hypoglycemia and cerebral edema.
  2. Insulin: Start a continuous IV infusion of Regular Insulin (the only insulin given IV). Monitor blood glucose hourly, aiming for a steady decrease.
  3. Potassium: Monitor levels constantly. IV Insulin drives potassium back into the cells, rapidly causing severe hypokalemia. Potassium replacement is often required even if initial serum levels appear normal or high, provided renal function is adequate.

Thyroid and Adrenal Disorders

Hyperthyroidism vs. Hypothyroidism

FeatureHyperthyroidism (Graves' Disease)Hypothyroidism (Hashimoto's)
MetabolismHypermetabolic stateHypometabolic state
TSH LevelDecreased (in primary hyperthyroidism)Elevated (in primary hypothyroidism)
SymptomsWeight loss despite appetite, heat intolerance, tachycardia, exophthalmos, diarrheaWeight gain, cold intolerance, bradycardia, severe fatigue, constipation
TreatmentPropylthiouracil (PTU), Methimazole, Radioactive Iodine, ThyroidectomyLifelong Levothyroxine (Synthroid) replacement (take on empty stomach)
ComplicationThyroid Storm (fever >104F, extreme tachycardia, delirium)Myxedema Coma (hypothermia, hypoventilation, severe bradycardia)

Nursing Care for Thyroidectomies

  • Airway Maintenance: Monitor closely for respiratory distress, stridor, or bleeding at the incision site. Keep a tracheostomy kit, oxygen, and suction equipment at the bedside at all times.
  • Hypocalcemia: Monitor for accidental parathyroid gland removal or damage. Assess for Chvostek's sign (facial muscle twitching when the facial nerve is tapped) and Trousseau's sign (carpal spasm when a blood pressure cuff is inflated). Keep IV Calcium Gluconate readily available.

Adrenal Insufficiency (Addison's Disease) vs. Cushing's Syndrome

  • Addison's Disease: Lack of cortisol and aldosterone. Presents with bronze hyperpigmentation, hypoglycemia, postural hypotension, weight loss, and hyperkalemia. Requires lifelong corticosteroid replacement. Stress requires "stress dosing" (increased steroids) to prevent Addisonian Crisis (profound shock).
  • Cushing's Syndrome: Excess cortisol. Presents with truncal obesity, moon face, buffalo hump, purple striae, hyperglycemia, hypernatremia, hypokalemia, and increased risk for infection and osteoporosis. Treatment involves surgical removal of pituitary or adrenal tumors or tapering of exogenous steroids.
Test Your Knowledge

A patient with Type 1 Diabetes is admitted with Diabetic Ketoacidosis (DKA). Which of the following is the INITIAL priority nursing intervention?

A
B
C
D
Test Your Knowledge

When assessing a patient with a duodenal ulcer, what classic symptom should the nurse expect?

A
B
C
D
Test Your Knowledge

Which assessment finding is the most reliable indicator of effective fluid resuscitation in a patient with Acute Kidney Injury (AKI)?

A
B
C
D