NUR 265 EXAM ONE STUDY GUIDE

NUR 265 EXAM ONE STUDY GUIDE  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