NUR 265 EXAM 1 STUDY GUIDE & EXAM QUESTIONS AND ANSWERS

NUR 265 EXAM 1 STUDY GUIDE & EXAM QUESTIONS AND ANSWERS • The 2 major functions of the kidneys are to secrete erythropoietin and renin, which stimulate red blood cell production and blood pressure respectively, and to make urine. • The number one objective sign of anemia is increased heart rate. • The number one subjective sign of anemia is fatigue. • The only difference between acute renal failure and chronic renal failure is that acute renal failure is reversible. • Kidney failure is defined by how many nephrons are dead. • Any condition that decreases the flow of blood to the kidneys is called Pre-renal Acute Kidney Failure. • Any condition that results in damage to the kidney tissue is called Intra-renal Acute Kidney Failure. • Any condition that obstructs the urine is called Post-renal Acute Kidney Failure. • NSAIDs and aminoglycosides are 2 common nephrotoxic drugs. o An example of an aminoglycoside is the antibiotic called Gentamicin. • A patient with heart failure may experience Acute Pre-Renal Failure, because the decreased cardiac output causes lower blood flow to the kidneys. • A patient with acute tubular necrosis may experience Acute Intra-Renal Failure, because necrosis is damaging the kidney tissue. • A patient with benign prostate hypertrophy may experience Acute Post-Renal Failure, because the prostate could obstruct the flow of urine. • In the oliguric phase of kidney failure, the BUN, serum creatinine, and specific gravity are all increased. • In the diuretic phase of kidney failure, urine specific gravity is decreased, because the urine is diluted. • In any acute care setting, preventing hypovolemia is a nursing priority, because it is the most common cause of Acute Kidney Injury. • Due to high blood concentration, the manifestations of hypovolemia are decreased pulse pressure, orthostatic hypotension, decreased urine output, thirst, and increased blood osmolality. • Nephrotic Syndrome: o NS is a condition of increased glomerular permeability that allows larger molecules to pass through the membrane into the urine and then be excreted. o Immunological Kidney disorder o This causes massive loss of protein in the urine, edema formation, and decreased plasma albumin levels. ▪ Proteinuria- severe protein loss more than 3.5 g in 24- hour urine sample. o Key features: ▪ Massive proteinuria >3.5g / 24hrs ▪ Hypoalbuminemia <3g/dL ▪ Edema (facial and periorbital) ▪ Lipiduria ▪ Hyperlipidemia ▪ Increased coagulation (renal vein thrombosis) ▪ Reduced kidney function (↑ BUN, ↑ Cr, ↓ GFR) o Treatment- immunosuppressant agents (if immunity based). ▪ ACE inhibitors (to decreased protein loss in urine & ↓BP) ▪ Statins (improve blood lipid levels). ▪ Heparin (↑ coagulation / risk of thrombosis → treat vascular effects and improve kidney function) o Diet: ▪ If GFR is normal- dietary intake of complete proteins is needed ▪ If GFR is decreased- dietary protein is decreased, diuretics and sodium restriction. • Acute Kidney Injury: o AKI is rapid reduction in kidney function resulting in a failure to maintain fluid and electrolyte balance, and acid-base balance. ▪ Can occur over a few hours or days o Severity of AKI is based on serum creatinine increase, and decreased urine output- an increase in specific gravity (meaning urine is more concentrated or the patient is dehydrated). o GFR isn’t used to measure acute injury or illness—only chronic kidney disease. o 3 types of AKI ▪ prerenal - conditions that reduce blood flow / oxygen to the kidney → decreased perfusion to kidneys • azotemia- nitrogenous waste/toxin build up o effects LOC, mood, change in personality o related directly to reduced perfusion to the kidneys • examples of perfusion reduction: o blood/fluid loss- (surgery, sepsis, hypovolemic shock) o blood pressure drugs resulting in hypotension o MI or HF → low ejection fraction → low cardiac output o NSAIDs, ASA o Anaphylaxis o Severe burns o Severe dehydration o Renal artery stenosis o Bleeding or clotting in kidney blood vessels o Atherosclerosis (cholesterol deposits obstructing blood flow to the kidneys) ▪ Intra-renal failure- tissue damage to the actual kidneys • Intra-renal- reflects injury to the glomeruli, nephrons, or tubules • Examples of intra-renal failure: o Bleeding in the kidney o Glomerulonephritis or inflammation of the glomeruli o Pyelonephritis o Thrombi or emboli in the kidney blood vessels o TTP → platelet disorder ↑ clotting o Sepsis or local infection o Lupus o Multiple myeloma o Scleroderma o Chemo/ ABTs / nephrotoxic drugs o Ischemia in kidney failure, including hypoxemia from respiratory and cardiac arrest ▪ Post-renal failure- Urine flow obstruction • Post-renal failure examples: o Bladder cancer o Colon cancer o Prostate cancer o Cervical cancer o Enlarged prostate o Kidney stones o Blood clots in urinary tract o Neurogenic bladder →Nerve damage o Mean atrial pressure is important in determining adequate kidney perfusion!!! ▪ MAP= (systolic+ 2[diastolic])/3 Mean atrial pressure of 65 is needed to perfuse the kidney!! Manifestations (s/s) of AKI o Oliguria o Fluid Volume Overload ▪ Crackles ▪ Edema ▪ Anasarca (generalized edema) ▪ ↓ 02 sats ▪ ↑ RR o LOC changes o Labs (↑BUN, ↑Cr, urine specific gravity >1.030) o Nursing considerations / Interventions for AKI: ▪ Prevention is key! - urge patients to drink 2-3 L of water daily. • Monitor Fluid status (I&O, weight, ↑ hydration, characteristic of urine) • Report Output <0.5mL/kg/hr if persists >2hr <30mL/hr • Monitor for kidney functions o Labs (BUN, Cr, GFR, electrolytes, osmolarity) o I&Os ▪ You want output to be more than input ▪ Sodium, potassium, and specific gravity determine hydration status. o Contrast dyes o MAP > 65 mmHg • Diuretic therapy- happens after AKI is starting to be resolved! (Releasing extra fluid through the urine - This is a good sign!!! - Watch for dehydration! - Its normal to have fluids hanging during the diuretic phase! - Titrate fluids!) • Nutrition during AKI: o Low protein ▪ Because protein molecules are huge and put on the strain to process o Low sodium ▪ Since the body has high sodium concentration due to AKI • Fluid restriction o if AKI was due to anything except for perfusion problem • Hemodynamic Monitoring o Temporary Kidney Replacement Therapy ▪ → for Symptomatic Uremia (critical electrolytes, toxicity, metabolic acidosis, fluid overload that inhibits tissue perfusion) ▪ Removes toxins ▪ Requires immediate vascular access • If RRT occurs for 4 weeks or less, then there is no loss of kidney function • If RRT occurs for 3 months or more it is considered kidney failure • Chronic Kidney Disease o CKD- progressive, irreversible disorder and kidney function doesn’t recover. o Focus / Teach on reducing risk factors to slow Progression! o CKD is normally a result of another condition that compromises the kidneys and takes years to progress ▪ Hypertension ▪ Uncontrolled diabetes ▪ Renal stenosis ▪ Infection ▪ Glomerulonephritis ▪ Polycystic kidney disease ▪ African Americans are 4 times more likely to get it o Azotemia- nitrogenous waste build up o Uremia- azotemia with clinical manifestations ▪ Manifestations of uremia • Metallic taste in mouth • Anorexia • Nausea/vomiting • Muscle cramps • Uremic frost on skin • Itching • Fatigue and lethargy • Hiccups • Edema • Dyspnea • Paresthesia o Stages of chronic kidney disease: ▪ o effects of CKD on the kidneys: ▪ decreased urinary output • urine output decreases as the patient progresses through CKD until they reach oliguria ▪ increased potassium, BUN, Creatinine • put patient on tele monitor if they are in hyperkalemia!!! ▪ Decreased GFR ▪ Maintains homeostasis until late signs ▪ Salt wasting: • In early stages of CKD patients will lose the sodium and the water won’t follow!! So, excess fluid and hyponatremia • In late stages CKD- no urine output so salt and water stay and hypernatremia occurs! o Metabolic changes of CKD: • Urea and creatinine build up • Hyponatremia- early stages • Hypernatremia- late stages o Hyperkalemia- late stages → due to kidneys not excreting potassium though the urine. • Acid-base balance- o Metabolic acidosis occurs due to lack of urine excretion, and the body becomes more acidic! → kussmaul respirations! (deep rapid resp) → pt is compensating! o Patient is normally in a slight acidic state all the time. o Effects of CKD on the body: ▪ Cardiac- • Hypertension • Hyperlipidemia • Heart failure • Crackles • Pulmonary edema (pink frothy sputum) • Tachypnea • hyperpnea • Pericarditis, cardiac tamponade ▪ Integumentary • Uremic frost! - causes patient to be itchy! o Keep cold o Tepid water ▪ Hematological • Anemia (fatigued, SOB) →from lack of RBCs → from Ø erythropoietin o Put on fall precautions!!!- orthostatic hypotension ▪ Musculoskeletal • Bone pain • Muscle weakness • Pathological fx (↓Ca) ▪ Gastrointestinal • Stomatitis- huge ulcers in the mouth o Patient won’t want to eat o NG tube • PUD- GI bleeds • Uremic Fetor o Dietary restrictions of CKD ▪ Depends on the severity of the CKD and how well their kidneys are function • Protein: o Restriction early during the disease prevents complications of CKD, and preserves kidney function (↑ for dialysis) Monitor BUN and Albumin o Based on GFR and type of treatment being used • Fluid- May have restrictions! • Potassium- restriction! o Salt substitute is potassium! It is a big no no! o Kayexelate- excrete potassium in GI- diarrhea! • Give / ↑ Calcium, Vit D & Vit B • Magnesium o Avoid Mg and Mg containing antacids • Sodium o Restrict late, not early o ↑ for dialysis • Phosphorus o Restrict early in CKD! o Phosphate binders- GI excretion o Nursing Considerations / Interventions: ▪ Assess for FVO q4hr ▪ Daily weights (same time q day) 1 kg = 1 L of fluid ▪ Strict I&O ▪ Diuretics (do Not help in ESRD) ▪ Monitor Electrolytes ▪ Treat HTN → ACEs, CCBs, thiazides o Hemodialysis ▪ Most common Kidney replacement Therapy in ESKD ▪ Normally no urine output at all ▪ 3x a week- 4-5 hours. At clinic and go home ▪ pull blood