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PAT202 WINTER > w6 kidneys AKI > Flashcards

w6 kidneys AKI Flashcards

1
Q

where is the kidney’s located?

A

in the back - retroperitoneal

retro(well protected)

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2
Q

do you ever palpate the kidneys?

A

no- but we can tap on them (CVA) we can make a fist and percuss the kidney area-but we don’t do it on the anterior surface on the abdomen exam

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3
Q

if a patient falls onto their back, what would we check?

A
  • kidney assessment

- assess for blood in the urine to see if there is injury

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4
Q

why can we survive with just one kidney?

A

because we have millions of nephrons-they are workhorses of the kidneys

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5
Q

how much CO goes into the kidneys?

A

20-25% goes to the kidney each minute

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6
Q

what is GFR?

A

pressure and volume related

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7
Q

what dose decrease preload cause =

A

decrease GFR

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8
Q

renin is a _ and _produced from _

A

enzyme and a hormone

produced from juxtaglomerular cells

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9
Q

what is the major electrolyte that our kidney’s is responsible for?

A

POTASSIUM

if our kidney’s fail, potassium skyrockets= dysthymia =can lead to death

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10
Q

the urinary system consists of

A
  • 2 kidneys
  • 2 ureters
  • 1 bladder
  • 1 urethra
  • each kidney contains more than 1 million nephrons (which are the structural and functional units of the kidney)
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11
Q

normal anatomy of the kidney’s

A

-once blood enters a nephron, it is filtered through a semipermeable membrane (called the Bowman’s capsule)
-water and small molecules pass through the Bowman’s capsule and enter the first section of the nephron –> the proximal tubule
-once the fluid is in the nephron it is called filtrate (fluid that was filtered by the Bowman’s capsule)
-after it leaves the proximal tubule, the filtration travels through the loop of Henle and the distal tubule
fluid that leaves the kidney’s is urine

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12
Q

what dose the kidney do?

A
  • excretion
  • primary organ that regulates fluid and electrolytes
  • they secrete renin (an enzyme that helps to regulate blood pressure)
  • erythropoietin ( a hormone that simulated red blood cell production
  • calcitrol (the active form of vitamin D)
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13
Q

what is reabsorption?

A

movement of filtered substances from the kidney tubule back into the blood

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14
Q

what is the most important molecule that is reabsorb in the tubule?

A

water

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15
Q

what are other molecules that are resorbed in the kidneys

A

-glucose, amino acids, and essential ions –> sodium, chloride, calcium, and bicarbonate

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16
Q

what is secretion?

A

movement of substances from the blood into the tubule after filtration has occurred
-potassium, phosphate, hydrogen, ammonium ions enter the filtrate through this mechanism

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17
Q

what is renal failure?

A

a decrease in kidney function that results in an inability to maintain electrolyte and fluid balance and excrete nitrogenous waste products
-can be acute or chronic

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18
Q

what is the primary treatment goal of renal failure?

A

-to maintain blood flow through the kidney and adequate urine output

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19
Q

what is the best marker for estimating kidney function?

A

the glomerular filtration rate (GFR)

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20
Q

what is GFR?

A

the volume of water filtered through the Bowman’s capsules per min

  • can be used to predict the onset and progression of kidney failure
  • indicates the ability for the kidney’s to excrete drugs from the body
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21
Q

what dose a progressive decline in GFR indicate?

A

-a reduction in the number of functioning nephrons

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22
Q

what happens when nephrons start to die?

A

the remaining healthy nephrons have the ability to compensate by increasing their filtration capacity
-this is why some pt’s w/ kidney damage are asymptotic until 50% or more of the nephrons have become non-functional and the GFR has fallen to less than half it’s normal value

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23
Q

what is azotemia?

A

accumulation of nitrogenous waste products in the kidneys that can result in death if left untreated

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24
Q

what is the most common cause of acute renal failure?

A

renal hypoperfusion- lack of sufficient blood flowing through the kidney
-hypoperfusion can lead to permanent damage

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25
Q

what are potential causes of hypoperfusion ?

A

-heart failure, dysrhythmias, hemorrhage, and dehydration and pharmacotherapy w/ nephrotoxic drugs

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26
Q

what is the most common causes of chronic renal failure?

A

diabetes and long-standing hypertension

-it may go undiagnosed for many years

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27
Q

what are the treatments for end-stage renal disease?

A

dialysis and kidney transplantation

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28
Q

pathogenesis of anemia

A
  • hypoperfusion of kidneys result in less erythropoietin synthesis
  • treatment–> erythropoietin injection
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29
Q

hyperkalemia pathogenesis

A
  • kidneys are unable to excrete potassium

- treatment–> diet restricted potassium

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30
Q

hyperphosphatemia- pathogenesis

A
  • kidneys are unable to adequately excrete phosphate

- treatment–> dietary restriction of phosphate; phosphate binders such as calcium carbonate

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31
Q

hypervolemia- pathogenesis

A

hypoperfusion of kidney leads to water retention

-treatment –> dietary restriction of sodium; loop diuretics in acute conditions, thiazide diuretics in mild conditions

32
Q

hypocalcemia- pathogenesis

A

hyperphosphatemia leads to loss of calcium

-treatment–> usually corrected by reversing the hyperphospatemia but additional calcium supplements may be necessary

33
Q

metabolic acidosis- Pathogenesis

A

kidneys are unable to adequately excrete metabolic acids

treatment–> sodium bicarbonate or sodium citrate

34
Q

what are nephrotoxic drugs

A

NSADIS (nonsteroidal anti-inflammatory drugs)

  • aminoglycoside antibiotici
  • amphotericin B (Fungizone)
  • ACE inhibitors
  • many antieoplastic agents
35
Q

MOA of diuretics

A

most act by blocking sodium (NA+) reabsorption in the nephron, sending more NA+ to the urine.

  • Chloride ion (CI-) follows sodium
  • water also follows sodium, blocking the reabsorption of NA+ will increase the volume of urination known as diuresis
  • the amount of diuresis produced by a diuretic is directly r/t the amount of sodium reabsorption that is blocked
  • diuretics also affect the renal from excretion ions (magnesium, potassium, phosphate, calcium, and bicarbonate)
36
Q

loop diuretics

A
  • prevents the reabsorption of NA+ in the loop of Henle
  • there is an abundance of NA+ in the filtrate w/in the loop of Henle
  • most effective diuretic
37
Q

thiazides

A
  • act by blocking NA+ in the distal tubule
  • b/c most NA+ has already been reabsorbed from the filtrate by the time it reaches this part of the nephron, the thiazide produce less diuresis than the loop diuretics
38
Q

what can loop diuretics lead to?

A

hypokalemia

39
Q

considerations when giving furosemide?

A

-blood pressure decrease, blood volume decreases, and urine output increases

40
Q

prior to initiation of a loop diuretic the nurse should do what?

A
  • obtain baseline values for weight
  • baseline values for blood pressure (sitting and supine)
  • baseline pulse, respiration, and electrolytes
  • any prescene or hx of edema and its extent should be recorded
  • measure the abdomen girth of clients w/ fluid in the abdomen (ascites)
41
Q

what should u do daily if a patient is on a diuretic?

A

monitor weight daily to help evaluate the effectiveness` of therapy

42
Q

what should be monitored regularly w/ a diuretic?

A
  • blood pressure -if a substantial drop in B/P occurs hold themed
  • pulse rate
  • intake and output should be monitored
  • evaluate fore decrease of edema
  • potassium levels should be monitored closely
  • monitor lab values- elevated BUN, hypreglucemyia, and anemia
  • tell pts to report hearing loss or ringing in the ears
  • rapid and excessive diuresis can result in dehydration, hypovolemia, and circulatory collapse
43
Q

CBC should be monitored in clients receiving furosemide. why?

A

b/c it can cause agranulocytosis, anemia, leukopenia, and thrombocytopenia

44
Q

what medication should be avoided with furosemide?

A

digoixin -b/c of the risk of hypokalemia

45
Q

renal insufficiency refers to_

A

a decline in renal function of about 25% of normal or a GFR of 25 to 30mL/minute

46
Q

end stage kidney disease

A

-less than 10% of renal function remains

47
Q

what is uremia

A
  • a syndrome of renal failure that includes elevated blood urea and creatinine levels accompanied by fatigue, anorexia, nausea, vomiting, pruritus, and neurologic changes
  • includes retention of toxic wastes, deficiency states, electrolytes disorders and immune activation promoting and proinflammatory state
  • accumulation of nitrogenous waste products in the blood
48
Q

what is azotemia?

A

characterized by increased serum urea levels and frequently increased creatinine levels

  • renal insufficiency or renal failure causes azotemia
  • accumulation of nitrogenous waste products in the blood
49
Q

what is the normal creatinine levels?

A

normal is 0.7 to 1.4 mg/dL

50
Q

what is a AKI? acute kidney injury?

A

-a sudden decline in kidney function w/ a decrease in glomerular filtration and urine output w/ accumulation of nitrogenous waste products in the blood as demonstrated by elevation in plasma creatinine and blood urea nitrogen levels.

51
Q

what is the Pathophysiology of AKI?

A
  • results from extracellular volume depletion
  • decreased renal blood flow
  • or toxic/inflammatory injury to kidney cells that results in alternation in renal function
52
Q

what are the 3 etiologies of AKI?

A

1) prerenal AKI - renal hypoperfusion
2) intrarenal or intrinsic AKI- disorders involving the renal parenchymal or interstitial tissue
3) post renal AKI- disorders associated w/ acute urinary tract obstruction

53
Q

what is prerenal AKI?

A

-most common cause of AKI -results from inadequate kidney perfusion
-poor perfusion can be caused by: long-standing hypotension, hypovolemia associated w/ hemorrhage, fluid loss (burns), sepsis, inadequate CO (MI), kidney edema, or renal vasoconstriction (caused by NSAIDS) etc.
GFR decline b/c of a decrease in filtration pressure

54
Q

what is the most common cause of AKI?

A

Sepsis/Septic shock and cardiogenic shock following cardiac surgery

55
Q

what happens if we don’t treat prerenal acute kidney injury?

A

failure to restore blood volume or blood pressure and oxygen delivery can cause cell injury and acute tubular necrosis and apoptosis or acute interstitial necrosis
a more severe form of AKI

56
Q

what is postrenal acute kidney injury?

A
  • rare
  • occurs when there is a urinary tract obstruction that affects the kidneys bilaterally (i.e., a stone)
  • the obstruction causes an increase in intraluminal pressure upstream from the site of obstruction w/ a gradual decrease in GFR
  • findings–> pt will have several hours of anuria w/ flank pain followed by polyuria
57
Q

what is oliguria?

A

it is less than 400ml of urine output per day

or less than 30ml/hr

58
Q

oliguria- and alternations in renal blood flow

A
  1. alterations in renal blood flow- in response to ischemia blood flow is directed to the highly metabolic renal medulla
    - w/ continued ischemia, tubular sodium chloride reabsorption fails and tubuloglomerular feedback at the macular dense activates the RAAS
    - there is an increase in afferent arteriolar vasoconstriction and decrease in GFR
    - damaged endothelium and leukocyte activation activates coagulation and further impede microcirculatory blood flow =contributing to ischemic reperfusion injury and decreased GFR
59
Q

oliguria -and tubular obstruction

A
  1. necrosis of the tubules causes sloughing of cells, cast formation, and ischemic edema that result in tubular obstruction, which in turn causes a retrograde increase in pressure and reduces the GFR
    - renal failure can occur w/in 24 hours
60
Q

oliguria- and tubular backleak

A
  • glomerular filtration remains normal, but tubular reabsorption or “leak” of filtrate is accelerated as a result of permeability caused by ischemia and increased tubular pressure from obstruction
  • obstruction and backless probably occur concurrently
61
Q

what is intrarenal (intrinsic) acute kidney injury?

A

Acute tubular necrosis (ATN) caused by ischemia most common cause of intrarenal AKI
Other factors: nephrotoxic ATN (i.e., exposure to radiocontrast media or antibiotics), acute glomerulonephritis, vascular disease, allograft rejection, or interstitial disease
ATN → Post-ischemic or nephrotoxic or combination of both

62
Q

what is the initiation phase- ATN

A
  • phase of reduced perfusion or toxicity in which renal injury is evolving, usually lasting 24 to 36 Horus.
  • prevention of injury is possible during this phase
63
Q

what is the extension phase-ATN

A

-with progressive ischemia, there is infiltration of inflammatory cells, mostly neutrophils; release of cytokines, inflammation; and cell injury contributing to tubular obstruction and backleak

64
Q

what is the maintenance of oliguric phase-ATN

A

the period of established renal injury and dysfunction after the initiating event has been resolved and may last from weeks to months
-urine output is the lowest during this phase, and serum creatinine, blood urea nitrogen, and serum potassium levels increase; metabolic acidosis develops, and there is salt and water overload

65
Q

what is the recovery phase-ATN

A

-the interval when renal injury is repaired and normal a
-renal function is reestablished
GFR return to normal but the regenerating tubules cannot concentrate the filtrate
-diruesis is common with a decline in serum creatinine and urea levels
-ployuria can result in excessive loss of sodium, potassium, and water
- assess for F&E imbalance carefully

66
Q

what is anuria

A

-urine output that is less than 50ml/day
it is uncommon in ATN
-anuria involves both kidneys and suggests bilateral renal artery occlusion, obstructive uropahty, or acute cortical necrosis

67
Q

what is nonoliguric renal failure?

A

usually represent less severe injury and is associated w/ toxin exposure or drug toxicity

  • the renal tubules have impaired reabsorption and concentration and dilution function
  • the urine output may be greater than 2L/day but the blood urea nitrogen (BUN) and plasma creatinine concentrations increase
68
Q

individuals who have experienced trauma or surgery or people in a catholic state may have a more _?

A

rapid elevations in BUN levels
+they are more prone to hyperkalemia and metabolic acidosis
-renal phosphate excretion is decreased, causing hyperphosphatemia

69
Q

diagnosis- prerenal causes

A

are associated w/ a hx of blood volume depletion or other causes of poor kidney perfusion (e.g., shock, heart failure, renal artery thrombi)

70
Q

diagnosis- intrinsic causes

A

-include exposure to nephrotoxins and infection

71
Q

diagnosis- postrenal causes

A

-associated w/ obstructive uropatheis (e.g., an enlarged prostate or stone)

72
Q

management of hyperkalemia

A
  • restrict dietary sources of potassium
  • use nonpotassium-spraking diuretic agents or use cation-ion exchange resins
  • administer glucose and insulin or sodium bicarbonate to drive potassium into the cells
  • administer calcium
  • may need dialysis or Continuous renal replacement therapy (CRRT)
73
Q

management- azotemia

A

low-protein, high carbohydrate diet (slows protein catabolism and prevent release of K+ from cellular breakdown)

74
Q

management and prevention of AKI

A

1) correcting fluid and electrolyte imbalances
2) management of blood pressure
3) preventing and treating infections
4) maintaining nutrition
5) remembering that certain drugs or their metabolites are not excreted and can be toxic

75
Q

continuous renal replacement theory (CCRT hemodialysis)

A

mechanical removal of water, electrolytes, and toxins from the blood

  • is indicated for uncontrollable hyperkalemia or acidosis or severe fluid overload
  • usually promising in critically ill people w/ multiple organ dysfunction or sepsis

PAT202 WINTER (16 decks)

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