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NUR 265 EXAM 1 STUDY GUIDE & EXAM QUESTIONS AND ANSWERS £11.09   Add to cart

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NUR 265 EXAM 1 STUDY GUIDE & EXAM QUESTIONS AND ANSWERS

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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 ra...

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  • February 8, 2022
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NUR 265 EXAM 1 STUDY GUIDE & EXAM QUESTIONS AND ANSWERS

• 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
chronickidney disease.
o 3 types of AKI
▪ prerenal - conditions that reduce blood flow / oxygen
tothe 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
thekidneys
• examples of perfusion reduction:
o blood/fluid loss- (surgery, sepsis,
hypovolemicshock)
o blood pressure drugs resulting in hypotension
o MI or HF → low ejection fraction → low
cardiacoutput
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
theglomeruli
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
hypoxemiafrom 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
kidneyperfusion!!!
▪ 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
waterdaily.
• 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
gravitydetermine hydration status.
o Contrast dyes
o MAP > 65 mmHg
• Diuretic therapy- happens after AKI is starting to
beresolved! (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
perfusionproblem
• 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
compromisesthe 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:

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