Nur 265 Exam One Study Guide, Complete Solution
NUR 265 EXAM ONE STUDY GUIDE, COMPLETE SOLUTION •Nephrotic Syndrome: oNS is a condition of increased glomerular permeability that allows larger molecules to pass through the membrane into the urine and then be excreted. oImmunological Kidney disorder oThis 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. oKey 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) oTreatment- 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) oDiet: ▪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: oAKI 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 oSeverity 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). oGFR isn’t used to measure acute injury or illness—only chronic kidney disease. o3 types of AKI ▪prerenal - conditions that reduce blood flow / oxygen to the kidney → decreased perfusion to kidneys •azotemia- nitrogenous waste/toxin build up oeffects LOC, mood, change in personality orelated directly to reduced perfusion to the kidneys •examples of perfusion reduction: oblood/fluid loss- (surgery, sepsis, hypovolemic shock) oblood pressure drugs resulting in hypotension oMI or HF → low ejection fraction → low cardiac output oNSAIDs, ASA oAnaphylaxis oSevere burns oSevere dehydration oRenal artery stenosis oBleeding or clotting in kidney blood vessels oAtherosclerosis (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: oBleeding in the kidney oGlomerulonephritis or inflammation of the glomeruli oPyelonephritis oThrombi or emboli in the kidney blood vessels oTTP → platelet disorder ↑ clotting oSepsis or local infection oLupus oMultiple myeloma oScleroderma oChemo/ ABTs / nephrotoxic drugs oIschemia in kidney failure, including hypoxemia from respiratory and cardiac arrest ▪Post-renal failure- Urine flow obstruction •Post-renal failure examples: oBladder cancer oColon cancer oProstate cancer oCervical cancer oEnlarged prostate oKidney stones oBlood clots in urinary tract oNeurogenic bladder →Nerve damage oMean 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 oOliguria oFluid Volume Overload ▪Crackles ▪Edema ▪Anasarca (generalized edema) ▪↓ 02 sats ▪↑ RR oLOC changes oLabs (↑BUN, ↑Cr, urine specific gravity 1.030) oNursing 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 oLabs (BUN, Cr, GFR, electrolytes, osmolarity) oI&Os ▪You want output to be more than input ▪Sodium, potassium, and specific gravity determine hydration status. oContrast dyes oMAP 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: oLow protein ▪Because protein molecules are huge and put on the strain to process oLow sodium ▪Since the body has high sodium concentration due to AKI •Fluid restriction oif AKI was due to anything except for perfusion problem •Hemodynamic Monitoring oTemporary 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 oCKD- progressive, irreversible disorder and kidney function doesn’t recover. oFocus / Teach on reducing risk factors to slow Progression! oCKD 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 oAzotemia- nitrogenous waste build up oUremia- 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 oStages of chronic kidney disease: ▪ oeffects 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! oMetabolic changes of CKD: •Urea and creatinine build up •Hyponatremia- early stages •Hypernatremia- late stages oHyperkalemia- late stages → due to kidneys not excreting potassium though the urine. •Acid-base balance-
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