Week 9 Notes: Pathophysiology: emerging knowledge, complexity, diagnostics

(Week 8 included a simulation and a midterm exam, so no new theory was addressed)

Acute renal injury, chronic kidney disease, and endocrine disorders. Pathophysiology related to the same, nursing interventions or actions, lab and diagnostic tests.  

Acute Kidney Injury: Can onset within 48 hours; generally 2-48 hours and causes functional disturbances of all body systems. Multiple causes, which are categorized according to area of causation: prerenal, intrarenal, and postrenal.

  • Prerenal: factors prior to the kidney, such as hypovolemia, or other factors that would result in a reduced blood flow to the renals which further results in a decrease of glomerular perfusion and filtration.
  • Intrarenal: Direct damage to the renal tissue/parenchyma, resulting in altered nephron function such as ischemia, nephrotoxins, hemoglobin, myoglobin, acute tubular necrosis.
  • Postrenal: Often related to mechanical obstruction, such as BPH (benign prostatic hyperplasia), prostate cancer, calculi, trauma, and extrarenal tumours.

Hemoglobin causing intrarenal failure would be related to RBC hemolysis, while myoglobin causing intrarenal failure would be released from necrotic muscle cells. Acute Tubular Necrosis (ATN) is a result of ischemia, nephrotoxins, or sepsis. Hypovolemic shock likely results in prerenal failure; septic shock likely results with septic shock.

Acute Kidney Failure Chronic Kidney Failure
Sudden onset 3 Month onset, minimum of consistent reduction in renal function
Can be reversible Non-reversible
Can be caused by nephrotoxic medications (i.e. gentamicin), hypovolemia, benign prostatic hyperplasia, kidney stones, tumours, urine obstruction Can be caused by diabetes, hypertension, long-term medication, congenital defects..

Nursing management: Strict in and outs, monitor output, daily weights, blood pressure management, fluid and electrolyte balance. Actual urinary output, impaired gas exchange related to circulatory overload related to impaired output (hypervolumia).

Risk for hypercalcemia related to kidneys not being able to activate vitamin D. When renal failure gets to the point of multisystem effect, it becomes or causes uremia.

If hyperkalemia manifests, administer kayexalate. Hyperkalemia may result from decreased excretion by kidneys paired with breakdown of protein, bleeding, and metabolic acidosis: associated with diet, supplements, and IV infusions.

Common indication for renal replacement therapy includes fluid overload, elevated potassium levels, metabolic acidosis, BUN level greater than 43 mmol/L, significant change in mental status, or pericarditis, pericardial effusion, or cardiac tamponade.

Oliguria is defined as urinary output less than 400-500 mL/24 hours in an adult; 17-21 mL/hr. Azotemia is an accumulation of nitrogenous wastes.

May develop dilutional hyponatremia; sodium retention may lead to edema, CHF, HTN. Metabolic acidosis, can result from the impaired ability to excrete or control the level of acid (ammonia), paired with the inability to reabsorb or produce bicarbonate. Tachypnea.

As the kidneys are responsible for erythropoietin, normocytic, normochromic anemia may result. Platelet function may also be altered, causing an increased risk of bleeding.


Syndrome of raised blood urea and other nitrogenous wastes, may lead to the development of dyslipidemia. Pale/yellow glow, increased BUN -> uremic frost. In early CKD, polyuria occurs, GFR decreases, BUN and serum creatinine levels increase -> uremia. Hypertension and proteinuria are often the first signs, however, hyperglycemia, hyperinsulinemia,  and abnormal glucose tolerance tests might also be seen.

Labs potentially ordered: ABGs, ‘lytes, CBC with differential, BUNs, Creatinine, eGFR, etc.

Endocrine Issues

Antidiuretic hormone: Helps regulate water by encouraging kidney (at renal tubules) to retain water.
Produced by the hypothalamus; posterior pituitary gland secretes ADH and/or stores it. Treating SIADH can lead to diabetes insipidus, and treating diabetes insipidus can cause SIADH.

Syndrome of Inappropriate Antidiuretic Hormone (SIADH); increased ADH. Can be caused by lung cancer, damage to hypothalamus or pituitary gland, infections, gillian barre, chlorpropamide (often used to treat diabetes insipidus and works too well, causing SIADH).

Signs and Symptoms: high blood pressure, water retention, tachycardia, dilutional hyponatremia, confusion, seizures, anorexia, low urine output–concentrated, hypochloremia.

Nursing care is dependant on the cause: monitoring input and output, monitoring lab values, daily weights, fluid restriction, loop diuretics (lasix) and monitoring potassium levels with that; potentially hypertonic IV solution to remove fluid from cells and back into vascular system with care in monitoring fluid overload; declomycin (avoid giving with calcium foods) administration.

Diabetes Insipidus; decreased ADH. Causes extreme diuresis.  Can be related to a decrease in production or a reduced efficacy on the kidneys.

Signs and Symptoms: Urinating up to 24 L fluid per day, polydipsia, dehydration, hypotension, potentially hypovolemia and shock, low urinary-specific gravity, hypernatremia, increased plasma osmolality. Central (damage or alterations of the brain), nephrogenic (ADH levels are find; kidneys just aren’t responding to it), or psychogenic (due to increased water intake, potentially due to damage to thirst center).

Nursing care: early detection, maintenance of hydration, patient teaching, daily weights, monitoring input and output, providing foods and nutrition that do not encourage diuresis, diabinese (increases diuretic hormone)–can cause hypoglycemia and photosensitivity of skin; desopressin (form of ADH replacement)–signs of hyponatremia if given;

Hyperthyroidism can be caused by toxic nodular goitre, thyroiditis, excess iodine levels, pituitary gland tumours, or thyroid cancer. Manifests as tachycardia, weight loss, insomnia, exophthalmoses (bug eyes).

Thyrotoxicosis effects or clinical syndrome of hypermetabolism related to excessive T4, T3, or both.

Grave’s Disease, the most common cause of hyperthyroidism. Autoimmune in nature, diffuse enlargement of thyroid gland and excessive thyroid hormone release. Might be related to genetics and begins after interactions with infection, poor iodine supply, or stress. Signs and symptoms enlarged thyroid gland/goitres, bruits auscultated to goitre, exophthalmos. Treatment antithyroid medications, radioactive iodine therapy, subtotal thyroidectomy.

Thyrotoxic crisis aka thyroid storm: severe tachycardia, heart failure, shock, hyperthermia, restlessness, agitation, seizures, abdominal pain, nausea, vomiting, diarrhea, delirium, and coma.

Hypothyroidism can be primary or secondary. Can be related to thyroiditis or discontinuation of thyroid hormone therapy; poor iodine levels, but the most common cause is thyroid gland atrophy which is often the end result of grave’s or hashimoto’s. S&S: fatigue, lethargy, personality changes, mental changes,  decreased cardiac output, anemia, constipation. May demonstrate myxedema: an accumulation of hydrophilic mucopolysaccharides in the dermis and other tissues -> periorbital edema, puffiness, and masklike face.

Potentially leads to Myxedema Coma, which is often precipitated by infection, drugs (barbiturates, narcotics, tranquilizers), exposure to cold or trauma. S&S: subnormal temps, hypotension, bradypnea, treat with IV thyroid hormone replacement.

Hyperparathyroidism causes increased secretion of parathyroid hormone leading to hypercalcemia and hypophosphatemia. S&S: muscle weakness, loss of appetite, constipation, emotional disorders, and shortened attention span.

hypoparathyroidism causes hypocalcemia, sudden decrease in calcium levels may lead to tetany, tingling of lips and fingertips or feet, increased muscle tension, paresthesia, stiffness, tonic spasms.

Relating to adrenal cortex

Cushing’s Syndrome: too much corticosteroid in the bloodstream. Often caused by an adrenocorticotrophic hormone (ACTH) secreting pituitary tumour if Cushing’s disease; cushing’s syndrome is often linked with the use of corticosteroids, such as prednisone. 
Signs and Symptoms:
Skin fragile
Truncal obesity
Ecchymosis and Elevated BP
Sugar levels: hyperglycemia and hypokalemia
Excessive body hair
Dorsocervical fat deposits (buffalo hump)

Adrenocortical insufficiency (Addison’s Disease): A decrease in cortisol (glucocorticoids, mineralocorticoids, and androgens) as well as aldosterone levels.
Signs and Symptoms:
Sodium and sugar levels low
Tired and weak
Electrolyte imbalances (K+ and Ca)
Reproductive changes
lOw blood pressure
Increased pigmentation
Diarrhea and nausea

Treated with mineralcorticoids, fludrocortisone acetate, increased dietary salt,

Addisonian Crisis occurs when there is an acute adrenal insufficiency, triggered by stress, infection, hemorrhage, trauma, sudden withdrawal of corticosteroids, adrenal surgery, pituitary gland destruction, or surgery. S&S postural hypotension, tachycardia, dehydration, hyponatremia, hyperkalemia, hypoglycemia, fever weakness, and confusion.

Treatment: shock management, high-dose hydrocortisone therapy, NS solution with 5% dextrose to stabilize blood pressure.

Corticosteroid Therapy Used for immunosuppression, anti inflammation, blood pressure, carbohydrate, and protein metabolism.  Suppresses adrenal gland and can lead to cushing’s disease.