Renal Flashcards

1
Q

What is the normal physiology of the blood flow through the kidney? How might abnormalities impact renal function?

A

metabolic waste products that are unneeded or in excess filter out of the blood and form into urine moving vis the ureter into the bladder and expelled through the urethra.

The kidneys reabsorb the substances that are needed in order to maintain the normal composition of the blood.

by adjusting blood composition, the kidneys are able to maintain blood volume

renin released into the bloodstream to inc blood pressure when there is a dec

abnormalities means that there will be a build up of metabolic waste in the blood
more calcium reabsorption because of pth, but less tubular absorption or phosphate which leads to dec bone density

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2
Q

What is acute kidney injury?

A
  • Rapid loss of kidney function with a progressive nitrogenous waste collection in the blood (azotenia)
  • rise in creatine ( or creatione in bun)
  • oliguria isn’t always guarantees
  • can be reversed by high mortality rate

most common cause of death: infection from invasive lines

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3
Q

What are potential causes of acute kidney injury?

A

pre-renaln (heart and circulation to kidneys) reduction of systemic circulation impacting renal blood flow
, intra-renal (kidneys) direct injury to the kidney resulting in impaired nephron function. , post renal (ureters and bladder) Mechanical obstruction of outflow that causes urine to reflux into the kidney, impairing function

Causes: Benign prostatic hyperplasia (overgrowth of cells), prostate cancer, trauma to lower GU tract, extra renal tumor , hydronephrosis

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4
Q

Differentiate pre-renal, intra-renal, and post-renal causes of acute kidney injury.

A

1.) Pre-renal - reduction of systemic circulation impacting renal blood flow (bleeding, hemorrhaging, heart failure, dysrhythmias, embolism, MI, hypovelimia, burns, dehydration, anything that decreases perfusion of kidneys)

if someone was hypovelimic, we could just give them fluids
no damage to actual kidney tissue , so readily reversible with treatment , but can lead to infrarenal disease if this ischemia is prolonged for a long amount of time, then kidney tissue cant compensate

2.) Intra-renal - direct injury to the kidney resulting in impaired nephron function.
Acute Tubular Necrosis account for most cases - from ischemia, nephrotoxins, and sepsis, antibiotics that cause interstitial nephritis (gentamycin and vancomycin can be nephrotoxic) . (destruction of basement membrane) BUT if the basement is not destroyed and the tubular epithelium can regenerate, its okay

Crush Injury- myoglobin comes from damaged tissues, that can clog the kidney and cause muscle damage
Lupus, Malignant HTN

3.) Post-renal - Mechanical obstruction of outflow that causes urine to reflux into the kidney, impairing function

Causes: Benign prostatic hyperplasia (overgrowth of cells), prostate cancer, trauma to lower GU tract, extra renal tumor , hydronephrosis

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5
Q

Explain the diagnostic studies for acute kidney injury.

A

Past medical/surgical history – helps identify etiology (prerenal, intra or post)
Current medication history
Allergies
Labs
Rate of increase of serum creatinine
Urinalysis
Kidney ultrasound
CT scan
Biopsy
TREAT THE UNDERLYING CAUSE

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6
Q

Differentiate the phases of acute kidney injury management. How might nursing assessments and interventions vary for each phase of management? How might priorities change?

A

Phases (from worse to better)
Oliguric – fluid and electrolyte abnormlalites (uremia is present) urie output may not always happen. Occurs 1-7 days post injuries. Metabolic acidosis, check K+, urinary chances, sodium balance
Some make not experience oliguria

Diuretic – excreting fluids , kidneys cant concentrate urine but excrete waste. If osmotic diuresis occurs, check electrolytes and fluids

Recovery – GFR inc. BUN and creatine is no longer building up so it is dec and plateu. Look at creatine and GFR. There can be a variety of reasons why the BUN is elevated.

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7
Q

What is chronic kidney disease?

A

progressive irreversible loss of kidney function

Clinical defintion:
- presence of kidney damage

or

GFR <60 mL/min for longer than 3 months

End Stage Renal Disease
GFR <15mL/min

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8
Q

How do you differentiate the stages of chronic kidney disease?

A

they’re deferientiated by the GFR

Starts from

stage 1 less than or equal to 90 GFR

by stage 4 (15-29) , you need dialysis or a kidney transplant

by stage 5, you need renal replacement therapy if uremia is present (presence of urea and nitrogenous waste in the blood)

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9
Q

What are the goals of treatment of chronic kidney disease? How might they vary for each stage? How might priorities change?

A

regulate…

Excess fluid volume

Electrolyte imbalance (serum albumin, creatinine, hemoglobin, hematocrit)

Imbalanced nutrition (maintain an acceptable weight and no more than 10% weight loss)

Grieving

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10
Q

Describe the management of chronic kidney disease? How might the management vary per stage?

A

stage 1 - diagnosis and treatment CVD risk reduction , slow progression

stage 2 - estimation of progression

stage 3a- evaluation and treatment of complications

stage 3b - more aggressive treatment of complications

by stage 4 (15-29) , you need dialysis or a kidney transplant

by stage 5, kidney failure, you need renal replacement therapy if uremia is present

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11
Q

Describe the nursing management of alteration in fluid balance.

A
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12
Q

What is metabolic acidosis?

A
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13
Q

What is hyperkalemia? Why is it important to know? How is it managed in kidney disease

A

The high concentration of potassium in the blood. It can be managed with insulin, sodium bicarbonate or calcium gluconate because it forces cells to uptake potassium instead of just letting it hang out in the blood

they’re also given kayexalate (causes osmotic diarrhea so it exchanges sodium for k+ and excretes it in the stool, )

renal replacement therapy (releases potassium and fluid MOST EFFECTIVE)

why is it important to know? : an inc in k+ can cause dyrhymthimas and cause a heart attack

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14
Q

What is hypertension? How is it managed in kidney disease?

A

High blood pressure: kidneys typically regulate blood pressure

Weight loss, lifestyle changes,
diet recommendations, antihypertensives, diuretics

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15
Q

What is anemia? How is it managed in kidney disease?

A

dec oxygen in blood, because kidneys have a decreased ability to make EPO so RBC’s are low

management: Epoetin alfa (Epogen, Procrit)
Iron supplementation
Blood transfusion
Goal to decrease use of this
May require diuretic

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16
Q

Describe disorders of calcium and phosphorus metabolism and how they are managed in kidney disease?

A

Recall: Kidneys activates Vitamin D
Calcium reabsorption

In kidney disease:
Body unable to excrete phosphate (is serum phosphate is high, than calcium is low)
Calcium drops
PTH stimulates calcium to be pulled from bone (bone demineralization)

Result: Irreversible bone disorder
Osteomalacia
Osteitis fibrosa

17
Q

What is dialysis?

A

substances moving from blood through semipermeable membrane into a dialysis solution (dialysate)

purpose:
- correct electrolyte imbalance
- removed fluid and waste

types:
hemodialysis (intermittent hemodialysis (HD) and Peritoneal dialysis (PD)

  • Alternative of Adjunctive Therapy (continuous renal replacement therapy) , if someone is hemodynamically unstable
18
Q

Explain the basic principles of dialysis.

A
19
Q

Describe the different types of dialysis. How does the nursing assessment vary for each?

What are some priorities of care for each type of dialysis?

Consider the medical, nursing, psychological, social, developmental, and financial factors related to dialysis.

A

peritoneal dialysis -

hemodialysis
intermittent hemodialysis (HD)

Peritoneal dialysis (PD)

  • Alternative of Adjunctive Therapy