NUR 265 EXAM 1 STUDY GUIDE & EXAM QUESTIONS AND ANSWERS
• Nephrotic Syndrome:
o NS is a condition of increased glomerular permeability that allows
... [Show More] 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 [Show Less]