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nursing > 2450 renal failure (wk5) > Flashcards

2450 renal failure (wk5) Flashcards

1
Q

7 major funx of kidneys that are altered in renal fail

4 regulations, activation, excrete/secrete

A
  1. regulation of fluid balance
  2. regulation of electrolyte balance
  3. regulation of acid-base balance
  4. excretion of metabolic waste products & foreign chemicals
  5. activation of vita. D
  6. secretion of erythropoietin
  7. regulation of systemic BP
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2
Q

important factors in renal activation of vitamin D, secretion of erythropoietin,

A
  1. affects Ca+ absorp. in gut & reabsorb. in nephron

2. erythropoietin is a cytokine that regulates RBC produxn. and longevity

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3
Q

how do the kidneys regulate systemic BP

A

1 fluid balance (RAAS)
2. renal prostaglandins; cox 1 housekeeping are natriuretic & block Na+ & H2O cause vasodilation
cox -2 inflammatory, reabsorption

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4
Q

7 general assessments based on renal funx

A
  1. urine output pattern
  2. serum electrolytes
  3. acid-base status
  4. BUN creatinine levels
  5. S/S of hyperPO4-/hypoCa+
  6. CBC- Hgb, Hct, RBC
  7. blood pressure
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5
Q

how many nephrons needed to work to achieve kidney’s funx?
at what point will renal funx not be sustained?
what else occurs?

A
  1. 2 million
  2. renal funx sustained until 75% nephronal damage
  3. compensatory hypertrophy
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6
Q

3 facts about ARF or AKI

A

Acute Renal Fail, Acute Kidney Injury

  1. usually associated with acute injury or illness
  2. reversible if underlying etiologies corrected and renal hypoperfusion not prolonged
  3. usually affects all nephrons about equally
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7
Q

3 etiologies of ARF

A
  1. acute ischemic event or loss of renal perfusion (MI, bleeding, surgery, clot)
  2. acute nephrotoxic injury w/damage to renal tubules (drug bugs chemicals)
  3. obstruction to urine flow (rare)
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8
Q

3 facts about CRF or CKD

A

Chronic Renal Failure or Kidney Disease

  1. gradual onset & progression
  2. generally irreversible
  3. attack localized groups of nephrons, causing other nephrons to compensate
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9
Q

5 etiologies of CRF

A
  1. tubulointerstitial dz
  2. glomerulonephropathies
  3. renal vascular d/o
  4. nephrotic syndrome
  5. renal cancer
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10
Q

what is tubulointerstitial dz and how does it affect renal funx

A

spaces b/w kidney tubules become inflamed. This inflammation can affect kidney funx by affecting ability to filter waste

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11
Q

1 final pathway in end-stage renal fail
2 progression
3. 2 d/o’s that cause interstitial nephritis

A
  1. chronic hypoxia b/c of decreased nourishment,
    2 tubulointerstitial damage progresses & is associated with loss of peritubular capillaries which leads to apoptosis
  2. lupus or NSAID hypersensitivity
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12
Q

what does glomerulonephropathies or glomerulonephritis result from and what happens

A
  1. most result from immune dysregulation mediated by type 2 (cell lysis) or Type 3 (immune complex deposition) hypersensitivity rxns.
  2. damage to glomerulus results in changes in GFR & capillary wall structures which cause proteinuria & hematuria (ex: rusty pipes)
  3. diffuse (rather than local) lesions result in renal failure
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13
Q

3 renal vasc. d/o

A

HTN, stenosis (narrowing), atherosclerosis (plaque & thickens vessels)

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14
Q
  1. where does nephrosis start
  2. what it affects
  3. how
  4. who
  5. dz’s
A
  1. usually starts in glomerulus
  2. affects all of the kidney
  3. is the excretion of 3.5g or more of protein in the urine per day (characteristic of glomerular dz
  4. more common in children than adults
  5. DM, systemic lupus erythematosus, malignancies
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15
Q
  1. cancer associated with CRF
  2. who
  3. prognosis
A
  1. adrenocarcinomas that arise from tubular epithelium in the cortex (PCT DCT)
  2. seen more in males, 50-60yo, black ppl, smokers obese
  3. less than 50% w/o metastasis, 2% w/ metastasis
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16
Q

4 stages of CRF

A
  1. diminished renal reserve
  2. renal insufficiency
  3. end-stage renal dz (ESRD)
  4. uremic syndrome
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17
Q 
diminished renal reserve in CRF
1 Nephron loss
2. lab data
3. creatinine clearance
4. symptoms
A
  1. 50%
  2. serum creatinine doubles from baseline
  3. decreases to 1/2 norm. (norm~125mL/min down to 60-70)
  4. none
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18
Q 
renal insufficiency in CRF
1 Nephron loss
2. lab data
3. creatinine clearance
4. symptoms
A
  1. 75%
  2. serum CR x4
  3. 40-50
  4. HTN, anemia, bone dz (s/s begin)
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19
Q 
ESRD in CRF
1 Nephron loss
2. lab data
3. creatinine clearance
4. symptoms
A
  1. 90%
  2. serum electrolyte, & acid base alterations Serum CR > or = to 10X
  3. 10-15
  4. metab acidosis, increase of K+ Na+ h2o retention (require dialysis or transplant)
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20
Q 
uremic syndrome
1 Nephron loss
2. lab data
3. creatinine clearance
4. symptoms
A
  1. > or= 90%
  2. findings reflect multiorgan involve.
  3. = or < 10-15
  4. pigmentation pruritis uremic frost uremic pericarditis
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21
Q

describe normal urine output pattern

A

kidneys maintain body h2o homeostasis & norm. osmolality by adjusting concentration/dilution of urine. urine osmolality (200-1400 osmolality)

22
Q

3 alterations to Urine output, & associated risks

A
  1. anuria
  2. oliguria (risk for excess fluid volume)
  3. polyuria (deficient fluid volume)
23
Q

clinical manifestation of hypervolemia (EFV)

A
  1. generalized edema=anasarca
  2. pulmonary edema
  3. concentrated urine
  4. less than 30mL of urine output/hr
24
Q

clinical manifestations of hypovolemia (DFV)

A
  1. increased output
  2. decrease in BP
  3. dry mucus membranes, poor turgor
  4. dilute urine (low specific gravity)
25
Q

3 methods of normal electrolyte balance regulation

3 earliest detectable most harmful electrolyte imbalances

A
  1. diffusion, osmosis, & active transport of electrolytes at nephronal level
  2. hyperK+, hypoCa+, hyperPO4-
26
Q

What happens is Renal failure related hyperkalemia & manifestations & most important

A
  1. nephron’s inability to secrete K+ ion
  2. N/V/D fatigue
  3. EKG changes, tall T waves (indicated possible ischemia), wide QRS waves (indic. slow ventricular activation), disappearing P waves (loss of atrial contraction)–> can be life threatening arrhythmias Y brady<3
27
Q

etiology of renal failure related hypoCa+ & hyperPO4-

A

hypoCa+: kidney’s inability to activate vitamin D
hyperPO4-: kidney’s failure to excrete phosphate, excess PO4- binds to Ca+, eventually metastatic calicifications are risk & cause organ dysfunx–> <3, lungs, kidneys

28
Q

clinical manifestations (3) of hypocalcemia/hyperphophatemia

A
  1. neuromusc. excitability (tetany->chvostek/trousseau; adult form of rickets)
  2. bleeding d/o’s
29
Q

how do they kidneys maintain acid-base balance & etiology in renal failure

A
  1. secretion of H+ from tubular cells into urine & reabsorption of bicarbonate HCO3-
  2. inability to excrete acids & reabsorb bicarbonate which cause metabolic acidosis
30
Q

etiology of HTN in renal fail

A
  1. decreased renal perfussion sensed in juxtaglomerular apparatus ->stimulates RAAS (angiotensin 2 vasoconstrict -> increase BP, aldosterone Na+ & h2o retention -> increase blood volume)
  2. decrease GFR -> decrease h2o excretion=h2o retention ->BP increase
  3. decrease renal produxn of prostaglandins -> increase BP
31
Q

RBC Hgb Hct norm. & altered funx

A
  1. normal: renal secretion of erythropoietin in response to hypoxemia, stimulates RBC produxn in bone marrow & prolong life of existing RBC
  2. alteration: renal inability to secrete erythropoietin -> low RBC, Hgb, Hct -> symptomatic anemia (fatigue, SOB, palor, palpitations)
32
Q

normal funx of renal elimination of toxins and waste

A

renal excretion of nitrogenous waste, toxins, & waste products from blood & body

33
Q

in altered renal elimination of toxins & waste, what are 2 commonly measured nitrogenous waste products normal ranges

A
  1. urea: waste of protein metab., filtered in the glomerulus & reabsorbed @ several different sites along nephron (BUN=8-20)
  2. creatinine: waste of muscle metabolism, amt produced per day is proportional to body’s muscle mass & occurs @ constant rates (.6-1.2)
34
Q

define azotemia & 2 examples of non-renal etiology

A

high levels of blood urea nitrogen

high protein diet & starvation (muscle waste product)

35
Q

describe Cr & GFR correlation

A
  1. increase Cr= Decrease GFR

2. decrease in GFR = decrease in Cr clearance

36
Q

pathophysiology of prerenal failure (acute)

A
  1. decreased renal blood flow (RBF)
  2. renal adaptation to decreased RBF
  3. result: concentrated urine, high BUN, no change in creatinine (creatinine is never reabsorbed)
37
Q

etiology of decreased RBF in acute prerenal fail

A
  1. decreased renal cellular metab & tubular transport systems (starves renal cell = no funx)
  2. decrease driving force for glomerular filtration = decrease in hydrostatic pressure
38
Q

how does renal adaptation to decrease in RBF occur

A
  1. autoregulation (can occur when sys BP b/w 80-180 to maintain norm GFR, if < 80 AKI risk)
  2. stimulation of RAAS
39
Q

causes of high BUN

A
  1. increased Na+ reabsorption
  2. increased h2o reabsorption
  3. decreased urine flow rate through nephron
40
Q

2 pathophysiology for postrenal failure

A
  1. complete bilateral obstruction -> anuria

2. unilateral obstruction -> oliguria

41
Q

etiology for anuria caused by bilateral obstruction

A
  1. urine accumulates-> increase pressure in collecting system & back into nephron
  2. Na+, h2o, urea reabsorbed
  3. increased hydrostatic pressure in Bowman’s capsule -> increased force oppose filtration -> decreased GFR
42
Q

what happens if bilateral obstruction is prolonged

A
  1. tubular dilation & damage
  2. interstitial compression
  3. decreased renal tubular funx ->intrarenal failure
43
Q

what happens in unilateral obstruction

A

same a bilat obstruct just progresses @ slower rate & hypertrophy of unobstructed kidney

44
Q

2 dz of Acute intrarenal failure

A
  1. ischemic acute tubular necrosis

2. nephrotoxic acture tubular necrosis

45
Q

2 causes of ischemic acute tubular necrosis

A

may be a reperfusion injury (release of free radicals)

  1. renal vascontriction d/t: persistent stimulation of RAAS related to decreased renal perfusion & decreased renal prostaglandin produxn b/c of overwhelmed autoregulation mechanisms to counteract RAAS
  2. tubular injury & dysfunction
46
Q

etiology of tubular injury & dysfunx

A
  1. damage to renal tubule cell=basement membrane
  2. renal tubule cell membrane disrupted -> loss of renal tubule cell funx
  3. increased tubule permeability
47
Q

what happens when renal tubule is too permable

A
  1. tubular fluid & protein leak back in to interstitium ->cause inflammation
    2, casts form and found in urine
  2. some nephrons may collapse
48
Q

3 steps in nephrotoxic acute tubular necrosis

A
  1. injury to renal tubule cell (inside nephron) drugs bugs or chemicals
  2. epithelial cells of nephron affected 1st -> microvilli slough off, casts formed -> decrease nephron funx
  3. oliguria- nonoliguria and even polyuria occur
49
Q

4 phases of ARF

  1. beginning
  2. duration
  3. s/s
A
  1. onset/ initiating phase (begins with acute renal injury lasts 24-48hrs until oliguric phase low urine output rising BUN)
  2. oliguric phase (begins 1-2 days after trauma/illness lasts for 1-3 wks) marked loss of nephron funx need to replace renal funx during this phase
  3. diuresis phase (begins 2-4 weeks after trauma/ischemia, last 1-2 wks if underlying caused removed) nephrons healing but may be unable to concentrate urine
  4. recovery phase (3-12 months for full recovery), 30% never recover
50
Q

2 facts about diuresis phase (skip, & careful)

A
  1. PTs w/ nephrotoxic injury d/t drugs or toxins may skip oliguric phase & go straight to diuresis phase
  2. careful fluid & electrolyte monitoring & replacement is essential
51
Q

Treatment for Acute intrarenal failure

A
  1. rest kidney (dialysis)
  2. treat underlying cause
  3. replace lost renal funx until renal funx returned (blood transfusion electrolytes)

nursing (15 decks)

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