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What is Glomerulonephritis (GN)?
Inflammation of the kidney glomeruli that damages the filtration membrane, leading to waste accumulation and leakage of blood and protein into urine.
What is the most common acute cause of Glomerulonephritis?
A recent streptococcal infection (Post-streptococcal glomerulonephritis).
What is the primary pathophysiology of Acute Glomerulonephritis?
Sudden inflammation reduces GFR, causing sodium and water retention, which leads to edema and hypertension.
What are the classic urinary manifestations of Acute Glomerulonephritis?
Hematuria ("tea" or "cola-colored" urine), mild proteinuria, oliguria, and increased specific gravity.
Where is edema most prominently seen in the morning for a patient with Acute Glomerulonephritis?
Periorbital edema (around the eyes).
What are the typical laboratory findings in Acute Glomerulonephritis?
Elevated BUN and Creatinine, decreased GFR, RBC casts in urinalysis, proteinuria, and an elevated ASO titer.
What is the priority nursing assessment for fluid status in renal disorders?
Daily weights and strict intake and output (I&O).
What does Chronic Glomerulonephritis eventually lead to?
Chronic Kidney Disease (CKD) and End-Stage Kidney Disease (ESKD).
What is the gold standard diagnostic test for Chronic Glomerulonephritis?
Kidney biopsy.
What skin manifestations are associated with uremia in late-stage Chronic Glomerulonephritis?
Yellow-gray skin color and severe pruritus (itching).
What causes Fluid Volume Excess in renal disorders and how is it managed?
Kidneys retain water; managed with daily weights, I&O, fluid restrictions, and diuretics.
What is the most life-threatening electrolyte abnormality in kidney failure?
Hyperkalemia.
What ECG changes are associated with life-threatening hyperkalemia?
Tall peaked T waves, wide QRS complexes, and ventricular dysrhythmias. (HYPERKALEMIA)
How is hyperkalemia managed pharmacologically to protect the heart?
Calcium gluconate (protects myocardium), followed by insulin and glucose to shift potassium into cells.
What causes hypocalcemia in renal failure?
Hyperphosphatemia (phosphorus binds calcium) and decreased activation of Vitamin D by the kidneys.
What are two positive physical assessment signs of hypocalcemia?
Chvostek's sign (facial twitching) and Trousseau's sign (carpal spasm with BP cuff).
Why does anemia occur in chronic kidney disease?
The kidneys fail to produce enough erythropoietin, which stimulates RBC production.
What are the diagnostic criteria for an Acute Kidney Injury (AKI)?
Creatinine increase of >=0.3 mg/dL within 48 hours, a 1.5x baseline increase within 7 days, or urine output less than 0.5 mL/kg/hr.
What is the underlying problem in Prerenal AKI?
A perfusion problem where decreased blood flow reaches the kidneys (e.g., dehydration, shock, hemorrhage).
What is the underlying problem in Intrarenal AKI?
Direct damage to the kidney tissue itself (e.g., Acute Tubular Necrosis, contrast dye, NSAIDs, aminoglycosides).
What is the underlying problem in Postrenal AKI?
An obstruction preventing urine from leaving the urinary tract (e.g., kidney stones, BPH, tumors).
What defines the Oliguric Phase of AKI?
Urine output less than 400 mL/day (or anuria less than 50-100 mL/day), accompanied by fluid overload and rising toxins.
What occurs during the Diuretic Phase of AKI?
Urine output surges to 1-5 liters/day because the kidneys can make urine but cannot concentrate it yet; puts patient at risk for dehydration and hypokalemia.
What is the mnemonic AEIOU used for in AKI management?
Indications for emergency dialysis: Acidosis, Electrolyte imbalances (Hyperkalemia), Intoxication, Overload of fluid, and Uremia. (AEIOU)
What nutritional restrictions are required for a patient with AKI?
Restriction of potassium, sodium, phosphorus, and fluids (if oliguric).
Why are older adults at a higher risk for AKI and medication toxicity?
They naturally experience a decreased number of nephrons, reduced GFR, and a diminished ability to concentrate urine.
What is the definition of Chronic Kidney Disease (CKD)?
Progressive, irreversible loss of kidney function lasting longer than 3 months.
What GFR level defines Stage 5 End-Stage Renal Disease (ESRD)?
A GFR less than 15 mL/min, requiring dialysis or a kidney transplant.
What is the purpose of Dialysis?
To remove waste products, excess fluid, potassium, and acids from the blood; it is a management strategy, not a cure.
What is the most common complication during Hemodialysis?
Hypotension due to rapid fluid removal.
What is Dialysis Disequilibrium Syndrome?
Cerebral edema caused by the rapid removal of systemic toxins during dialysis, resulting in headache, nausea, and seizures.
What items should a nurse hold before a patient goes to Hemodialysis?
Antihypertensive medications (to prevent severe hypotension) and water-soluble vitamins (which will be filtered out).
What is the primary, most dangerous complication of Peritoneal Dialysis?
Peritonitis.
What are the classic signs of Peritonitis in a Peritoneal Dialysis patient?
Cloudy drainage fluid, fever, abdominal pain, and rebound tenderness.
When is Continuous Renal Replacement Therapy (CRRT) indicated?
For critically ill ICU patients with AKI who are hemodynamically unstable and cannot tolerate standard hemodialysis.
What is an AV Fistula and how long does it take to mature?
A surgical connection between an artery and a vein that takes 2-4 months to mature before use.
How does a nurse assess the patency of an AV Fistula or Graft?
Palpate for a thrill (vibration) and auscultate for a bruit (whooshing sound) every shift.
What are the strict restrictions for an arm with an active AV Fistula or Graft?
No blood pressures, no blood draws, no IV insertions, no tight clothing, and no sleeping on that arm.
What is the most common causative organism of a Urinary Tract Infection (UTI)?
E. coli.
How do UTIs uniquely manifest in older adults?
Confusion, delirium, altered mental status, weakness, and falls, often without classic dysuria.
What urinary findings on a urinalysis indicate a UTI?
Positive nitrites, positive leukocyte esterase, and elevated WBCs.
What is Pyelonephritis?
An upper urinary tract infection that has spread into the kidneys.
What are the defining systemic symptoms of Pyelonephritis?
High fever, chills, flank pain, and costovertebral angle (CVA) tenderness.
What causes Stress Incontinence and how is it managed?
Weak pelvic floor muscles causing leakage during coughing, sneezing, or laughing; managed primarily with Kegel exercises.
What characterizes Overflow Incontinence?
An inability to empty the bladder completely, leading to constant dribbling, a weak stream, and a high post-void residual.
What is an abnormal Post-Void Residual (PVR) volume in an older adult?
A volume greater than 100 mL (with volumes over 200 mL strongly suggesting incomplete emptying).
Where is a Suprapubic Catheter placed and what is a key nursing priority?
Inserted through the abdominal wall directly into the bladder; the nurse must keep the site clean/dry and ensure the bag remains below bladder level.
What is the number one risk factor for Bladder Cancer?
Smoking.
What is the classic, early warning sign of Bladder Cancer?
Painless hematuria.
What is the most common risk factor for developing Kidney Stones (Renal Calculi)?
Dehydration.
What type of pain characterizes renal colic from kidney stones?
Sudden, severe flank pain that comes in waves and radiates to the groin or genitalia.
Why is a fever accompanying an obstructing kidney stone a medical emergency?
It indicates an infection trapped behind a blockage, which can rapidly progress to urosepsis.
What is a vital nursing action for a patient attempting to pass a kidney stone conservatively?
Strain all urine to collect the stone fragments for laboratory analysis.
What are the expected and unexpected outcomes after Extracorporeal Shock Wave Lithotripsy (ESWL)?
Mild hematuria and bruising are expected; a high fever, inability to void, or severe unmanaged pain require immediate notification.
How does the body's endocrine system utilize negative feedback?
When hormone levels are too low, production increases; when hormone levels are too high, production shuts down.
Where is Antidiuretic Hormone (ADH) stored and released?
The Posterior Pituitary Gland.
What is the primary pathophysiological difference between SIADH and Diabetes Insipidus (DI)?
SIADH involves an excess of ADH (water retention), while DI involves a deficit of ADH (massive fluid loss).
What happens to fluid and sodium levels in SIADH?
The body retains water, causing fluid overload, concentrated urine, and dilutional hyponatremia.
What is the primary, life-threatening danger associated with SIADH?
Cerebral edema and seizures due to severe hyponatremia.
What is the first-line treatment for a patient with SIADH?
Strict fluid restriction (typically 500-1000 mL/day).
What precautions must be taken when administering Hypertonic Saline (3%) for SIADH?
Administer very slowly to prevent Osmotic Demyelination Syndrome (permanent brain cell damage).
What are the cardinal clinical signs of Diabetes Insipidus (DI)?
Massive polyuria (4-20 L/day) of clear, dilute urine and extreme thirst (polydipsia).
What laboratory values confirm a diagnosis of Diabetes Insipidus (DI)?
Hypernatremia, elevated serum osmolality, and a very low urine specific gravity (<1.005).
What is the preferred synthetic hormone replacement medication for Diabetes Insipidus (DI)?
Desmopressin (DDAVP).
What are the classic manifestations of Hyperthyroidism (Graves Disease)?
Tachycardia, weight loss despite increased appetite, heat intolerance, tremors, anxiety, and exophthalmos (bulging eyes).
What laboratory values indicate primary Hyperthyroidism?
Decreased TSH with elevated T3 and T4 levels.
Why are Beta Blockers prescribed for a patient with Hyperthyroidism?
To rapidly control systemic symptoms like tachycardia, tremors, and anxiety.
What are the classic manifestations of Hypothyroidism?
Bradycardia, hypotension, weight gain, cold intolerance, dry skin, constipation, and extreme fatigue.
What laboratory values indicate primary Hypothyroidism?
Elevated TSH with decreased T3 and T4 levels.
What is the lifelong drug therapy requirement for Hypothyroidism?
Levothyroxine (Synthroid).
What are the key patient education points for taking Levothyroxine?
Take it every morning on an empty stomach at the same time daily, and never discontinue it suddenly. What dietary modifications help prevent constipation in hypothyroid patients? An increase in both dietary fiber and fluids.
Why must calcium and iron supplements be avoided within 4 hours of levothyroxine?
They significantly decrease the absorption of the thyroid hormone medication.
What are the defining clinical manifestations of Hyperthyroidism?
Weight loss, heat intolerance, tachycardia, diarrhea, sweaty skin, anxiety, tremors, and insomnia.(HYPERTHYROIDISM)
What are the defining clinical manifestations of Hypothyroidism?
Weight gain, cold intolerance, bradycardia, constipation, dry skin, depression, fatigue, and hypersomnia (excessive sleep).
What is Myxedema Coma?
A life-threatening medical emergency where severe, untreated hypothyroidism causes the body's metabolism to almost completely shut down. (MYEXDEMA COMA)
What are the most common triggers for Myxedema Coma?
Abruptly stopping thyroid medications, infection, trauma, surgery, sedatives, or acute cold exposure.
What is the classic clinical triad of Myxedema Coma?
Bradycardia, hypothermia, and a decreased level of consciousness (LOC).
What metabolic and respiratory imbalances occur in a Myxedema Coma?
Hypoventilation leading to carbon dioxide retention (CO2 retention), respiratory depression, severe hypotension, hypoglycemia, and hyponatremia.
What is the leading immediate cause of death in a patient experiencing Myxedema Coma?
Respiratory failure.
What are the immediate priority medical treatments for Myxedema Coma?
Airway support (ABCs), oxygenation, mechanical ventilation if needed, administration of IV levothyroxine, and careful fluid resuscitation.
Why is aggressive active rewarming (like heating blankets) contraindicated in Myxedema Coma?
It causes rapid, sudden vasodilation that can worsen hypotension and precipitate cardiovascular collapse; passive warming with standard blankets is preferred.
What is a Thyroid Storm?
A life-threatening medical emergency caused by a sudden, massive surge and release of thyroid hormone into the bloodstream. (THYROID STORM)
What typically triggers a Thyroid Storm?
Thyroid surgery, severe infection, physical trauma, extreme stress, or completely untreated hyperthyroidism.
What are the hallmark clinical manifestations of a Thyroid Storm?
An extremely high fever (often greater than 103 F), severe tachycardia (greater than 150 bpm), early hypertension, severe agitation, delirium, and diarrhea.
What are the immediate nursing and medical priorities for a patient in a Thyroid Storm?
Call the Rapid Response team, establish oxygen therapy, implement cooling blankets, deliver IV fluids, initiate continuous cardiac monitoring, and administer beta blockers and antithyroid drugs (e.g., PTU).
Why is an iodine solution administered after antithyroid medications in a Thyroid Storm?
To prevent the thyroid gland from using the new iodine to synthesize and release even more thyroid hormone.
What hormonal deficiencies characterize Addison's Disease?
A severe deficit in cortisol and often aldosterone due to adrenal insufficiency.
What are the primary structural causes of Addison's Disease?
Autoimmune destruction of the adrenal cortex (most common), tuberculosis, adrenal hemorrhage, or cancer.
How can long-term corticosteroid therapy inadvertently cause secondary Addison's Disease?
Long-term steroid therapy suppresses the body's natural adrenal function; if the steroids are withdrawn suddenly, the adrenal glands cannot produce cortisol.
What are the physiological consequences of decreased aldosterone in an Addisonian patient?
Massive sodium and water loss accompanied by potassium retention, resulting in profound hypotension, severe dehydration, and hyperkalemia. Addisonian)))
What is the classic, high-yield skin assessment finding in Addison's Disease?
Bronze hyperpigmentation, most notably on the elbows, knees, knuckles, skin folds, and oral mucosa.
What specific electrolyte and blood sugar imbalances occur in Addison's Disease?
Hyponatremia (low sodium), hypoglycemia (low glucose), and hyperkalemia (high potassium).
What is an Addisonian Crisis?
A life-threatening medical emergency where the body suddenly runs completely out of cortisol, triggered by stress, illness, trauma, or abrupt steroid withdrawal.
What are the hallmark signs of an Addisonian Crisis?
Severe, unmanageable hypotension, profound circulatory shock, dehydration, confusion, hypoglycemia, and hyperkalemia.
What is the immediate medical treatment for an Addisonian Crisis?
Aggressive administration of IV hydrocortisone, IV normal saline, and dextrose to treat hypoglycemia.
What crucial "stress dosing" education must be provided to an Addison's patient?
The daily steroid dose must be increased during periods of physical illness, extreme stress, or scheduled surgery.
What is Cushing Syndrome?
A condition characterized by a chronic, toxic excess of cortisol in the body.
What is the most common overall cause of Cushing Syndrome?
Long-term, high-dose exogenous corticosteroid therapy.
What is the physiological difference between Cushing Syndrome and Cushing Disease?
Cushing Syndrome is the broad condition of excess cortisol; Cushing Disease specifically refers to an excess of cortisol caused by a pituitary tumor.
What are the classic physical appearance changes seen in Cushing Syndrome?
Moon face (round, full face), buffalo hump (fat pad between shoulders), truncal obesity with large abdomen, and thin, wasted arms and legs.