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NURS 2514 > Week 3 - Chronic Kidney Disease > Flashcards

Week 3 - Chronic Kidney Disease Flashcards

1
Q

what cuases chronic kidney disease

A
  • gradual irreversible destruction of nephrons & loss of renal function
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2
Q

what does the destruction of nephrons & loss of renal function result in (3)

A
  • increased workload on the remaining nephrons
  • increased glomerular filtration pressure
  • hyperfiltration ( of the remaining nephrons to attempt to maintain a normal GFR)
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3
Q

what does hyperfiltration predispose an individual to? (2)

A
  • glomerulosclerosis which causes increased rate of nephron destruction
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4
Q

what is glomerulosclerosis

A
  • fibrosis & scaring of the glomerulus
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5
Q

what are the top 3 causes of CKD

A
  1. diabetic nephropathy
  2. HTN
  3. glomerulosclerosis
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6
Q

end-stage renal failure presents as…

A
  • complex of symptoms called uremia
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7
Q

list 5 causes of uremia

A

retained:

  • fluid
  • electrolytes
  • waste products
  • hormones

and loss of renal endocrine function (renin & erythropoitein)

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8
Q

how does end-stage renal failure effect our BMR

A
  • causes reduced BMR = hypothermia
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9
Q

how does end-stage renal failure effect our blood lipoproteins? what causes this?

A
  • causes increased blood lipoproteins

- due to decreased Na/K ATPase activity & lipoprotein lipase activity

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10
Q

uremia (CKD) produces clinical abnormalities in… ?? (8)

A
  • fluid & electrolyte balance
  • bone metabolism
  • CNS
  • cardiovascular
  • pulmonary
  • skin
  • GI
  • hematologic
  • metabolic control (metabolic acidosis)
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11
Q

how many pathological stages of CKD are there?

A

3

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12
Q

describe pathological stage 1 of CKD (what is it, what % nephron lost, what happens if cause not detected)

A
  • reduced renal reserve
  • up to 50% of nephrons lost without causing S&S
  • if cause is not detected, damage will continue
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13
Q

describe pathological stage 2 of CKD (what is it, what % nephron lost)

A
  • renal insufficiency

- when more than 20% of nephrons remain

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14
Q

what does renal insufficiency result in? (4)

A
  • decrease in GFR, reabsorption & secretion capacity

- results in moderate azotemia (elevated BUN)

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15
Q

describe pathological stage 3 of CKD (what is it, what % nephron lost)

A
  • end-stage renal failure (uremia)

- occurs when less than 20% of nephrons remain

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16
Q

what does end-stage renal failure (pathological stage 3) result in (4)

A

GFR & tubular function greatly reduced =

  • oliguria/anuria
  • marked azotemia
  • failure to conc. urine
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17
Q

how many clinical stages of CKD are there

A

5

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18
Q

describe stage 1 of CKD

A
  • slightly diminished function

- kidney damage w normal or relatively high GFR (>90(

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19
Q

describe stage 2 of CKD

A
  • mild reduction in GFR (60-89) with kidney damage
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20
Q

describe stage 3 of CKD

A
  • moderate reduction in GFR (30-59)
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21
Q

describe stage 4 of CKD

A
  • severe reduction in GFR (15-29)

- preparation for renal replacement theraoy

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22
Q

describe stage 5 of CKD

A
  • established kidney failure (GFR < 15)

- permanent renal replacement therapy or end-stage kidney disease

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23
Q

what is normal GFR

A

125

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24
Q

describe CKD’s effect on sodium & fluid

A
  • get sodium & fluid overload bc we are consuming faster than the kidney’s can clear (exceed the GFR since it is so low)
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25
Q

excess water & sodium can cause.. (5)

A
  • circulatory congestion
  • HTN
  • ascites
  • edema
  • weight gain
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26
Q

what occurs with our water & sodium levels during times of loss (vomitting, diarrhea, etc.)

A
  • we have a diminished reserve to converse Na and water
    = hypovolemia & hyponatremia
    = can lead to circulatory shock
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27
Q

how do we treat/prevent sodium & volume overload during CKD (3)

A
  • restrict Na and water so we are not consuming it in excess
  • measure ins & outs
  • take multiple weight measuremenst throughout the day
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28
Q

describe CKD’s effect on potassium

A
  • for the most part it can be maintained thru diet if GFR is in stage 2/3
  • if GFR falls below 5, it can become a major problem
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29
Q

what 3 things increase the risk of hyperkalemia

A
  • hemolysis
  • acidosis
  • infection
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30
Q

how does hemolysis increase the risk of hyperkalemia

A
  • the rupture of RBC causes K to be leaked out
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31
Q

how does acidosis increase the risk of hyperkalemia

A
  • during acidosis, we have exchange of H+ into the cell, and K+ out of the cell
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32
Q

what clinical abnormality does uremia cause to our metabolic control

A
  • cause metabolic acidosis
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33
Q

at what point does metabolic acidosis occur during CKD? is it compensated

A
  • occur moderately when GFR is greater than 20 & is compensated by increased respiration
  • decompensated if GFR falls below 20 or if exposed to other acid loads
34
Q

list 3 examples of other acid loads

A
  • lactic acidosis
  • infection
  • pneumonia
35
Q

describe the role of the kidney’s regarding vitamin D; why is this important?

A
  • skin makes inactive vitamin D
  • the kidneys are response for activating it
  • imp so we can absorb Ca
36
Q

describe the activation of vitamin D during CKD

A
  • the kidneys get a reduced ability to activate vit D
37
Q

describe the relation between vit D and calcium & how this is effected during CKD

A
  • vitamin D allows Ca to be absorbed
  • without activated vit D, consumed calcium cannot be absorbed in the gut and is lost in the feces = decreased Ca serum levels
38
Q

what does a fall in serum Ca levels cause

A
  • stimulates PTH secretion
39
Q

what is the function of parathyroid hormone

A
  • parathyroid hormone is released from the parathyroid gland when we have low Ca
  • PTH activated osteoclasts which cause bone breakdown in an attempt to raise serum calcium
40
Q

what 2 things does the bone contain that gets released when it is broken down?

A
  • collagen

- hydroxyapatite (Ca++ and phosphate)

41
Q

what else contributes to bone breakdown

A
  • chronic acidosis
42
Q

what does increased Ca and phosphate cause?

A
  • calcifications in arteries, tendons, soft tissues, skin
43
Q

kidney failure causes decreased GFR. How does this contribute to the formation of calcification in vascularture & soft tissues

A

decreased GFR = decreased PO4 excretion (can’t clear it out) = increased serum PO4 = calcifications

44
Q

kidney failure causes decreased activation of vit D. Explain how this contributes to the formation of calcifications

A

decreased vit D activation = impaired Ca absorption from gut = decreased serum Ca = release of PTH = bone dimineralization (activation of osteoclasts) = increased Ca and PO4 = calcification

45
Q

what is a consequence of increased parathyroid hormone

A
  • osteitis fibrosa
46
Q

what is osteitis fibrosa? what does this cause?

A
  • patches of dimineralization in bones

- causes weak & easily fractured bones

47
Q

what is a consequence of bone dimineralization due to the release of PTH

A
  • ostesomalacia
48
Q

what is osteomalacia

A
  • softening/dimineralization of the bones due to vit D deficiency and increased PTH
49
Q

what is the difference between osteomalacia and osteoporosis

A
  • osteomalacia = decreased BD due vit D deficiency & increased PTH
  • osteoporosis = decreased BD in absence ofvit D deficiency or PTH response (both PTH and vit D in range)
50
Q

what cardiovascular & pulmonary symptoms does CKD cause r/t sodium & volume overload (3)

A
  • circulatory congestion
  • HTN
  • edema & pulmonary edema
51
Q

hypereninemia????

A

come back to this

52
Q

what can irritation of uremic toxins cause in the CVS system?

A
  • pericarditis
53
Q

what is pericarditis

A

-inflammation of the pericardium (sac around the heart)

54
Q

describe the effect of uremia on atherosclerosis?

A
  • causes accelerated atherosclerosis
55
Q

what causes accelerated atherosclerosis r/t CKD (2)

A
  • elevation in bp (due to Na & water overload & hyperreninemia)
  • hyperlipidemia caused by inhibition of lipoprotein lipase
56
Q

what effect does CKD have on the hematological system (3)

A
  • causes decreased production of erythropoietin
  • abnormal hemostasis
  • abnormal white cell function
57
Q

what does decreased production of erythropoietin cause? how is this corrected?

A
  • anemia with hematocrits of 20-25%

- NOT corrected by dialysis, and requires erythropoietin treatment

58
Q

what does abnormal hemostasis & white cell function cause (2)

A
  • bleeding

- immunosuppression

59
Q

what effect does CKD have on the neurological system? (8)

A
  • sleep disorders
  • poor concentration
  • memory loss
  • seizures
  • hiccups
  • twitching
  • coma
  • sensory peripheral neuropathy
60
Q

what causes the neurological effects of CKD (3)

A
  • due to urea

- elevated organic acids or phenols

61
Q

what causes elevated organic acids & phenols

A
  • protein catabolism
62
Q

what is a way we can prevent neurological symptoms of CKD

A
  • protein restricted diet
63
Q

what corresponds well with the degree of CNS disturbance?

A
  • BUN
64
Q

what are the effects of CKD on the GI (4)

A
  • anorexia
  • nausea
  • vommiting
  • uremic fetor (bad breath)
65
Q

what causes uremic fetor

A
  • when salivia enzymes breakdown urea into ammonium
66
Q

what are the effects of CKD on the skin

A
  • uremic frost & colour
67
Q

what are 2 ways we can manage CKD

A
  1. drug therapy

2. nutritional therapy

68
Q

what drugs can we give to treat hyperkalemia (4)

A
  • Kayexalate
  • insulin/glucose
  • albuterol
  • furosemide (lasix)
69
Q

what is kayexalate

A

potassium binding agent

70
Q

describe the use of insulin/glucose for hyperkalemia

A
  • very quick response

- but does not last super long

71
Q

why do we give glucose with insulin for hyperkalemia

A
  • to prevent hypoglycemia
72
Q

what is albuterol? how does it help with hyperkalemia

A
  • short-acting beta adrenergic receptor agonist

- increases insulin

73
Q

what is lasix

A
  • a K+ losing diuretic (loop diruetic)
74
Q

what med can we give to treat HTN and fluid overload associated with CKD

A
  • furosemide (lasix)
75
Q

what drug can we give to treat hyperphosphatemia r/t CKD

A
  • sevelamer (renagel)
76
Q

what is sevelamer

A
  • phosphate binding agent
77
Q

what can be given o treat anemia r/t CKD

A
  • erythropoietin
78
Q

what type of meds can be given to treat dyslipidemia r/t CKD

A
  • statins
79
Q

what is a potential complication of drug therapy

A
  • many meds are 1st metabolized by the liver to produce water-soluble metabolites = then they need to be cleared by the kidneys
  • if GFR is rlly low, the med metabolites will accumulate and can become toxic
80
Q

list 4 types of nutritional therapy for management of CKD

A
  • protein restriction (for neuro symptoms)
  • na and fluid restriction
  • potassium restriction
  • phosphate restriction

NURS 2514 (75 decks)

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