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CCM > Renal > Flashcards

Renal Flashcards

1
Q

basic unit of the kidney

A

nephron - very vascular

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2
Q

primary focus of the kidneys

A

maintaining homeostasis - regulation of fluid vol, electrolytes, acid/base bal, BP, erythropoieses
excretion of exogenous waste
metabolism of vit D

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3
Q

what is the normal glomerular filtration rate

A

80-125 ml/min

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4
Q

how does the kidney function to regulate acid/base bal?

A

reabsorbs bicarb
produce new bicarb
excretes small amts of hydrogen ions

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5
Q

what is acute kidney injury

A

sudden decline in kidney function leading to oliguria, azotemia and acid-base disturbances
loss in small solute clearance
decreased glomerular filtration rate
a disruption in homeostasis

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6
Q

cardinal features of AKI

A

decreased GFR
azotemia (increased BUN and creat)
oliguria (output

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7
Q

before determining AKI what do we need

A

a baseline creat, urine output

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8
Q

KDIGO dx guidelines define AKI as

A

increase in serum creat by 50% within 7 days OR
increase in serum creat by 0.3mg/dl within 2 days OR
oliguria

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9
Q

what is rifle criteria (check into this)

A

a way of scaling AKI

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10
Q

3 classifications of AKI

A 
prerenal injury (something above the kidneys causing injury)
intrarenal (in the kidneys)
postrenal (after the kidneys, ureter/bladder)
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11
Q

what is prerenal AKI

A

reduction in renal blood flow (perfusion and filtration)

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12
Q

what causes prerenal AKI

A 
decreased intravascular volume (shock/trauma)
decreased cardiac output
renal vasoconstriction
Diabetes Insipidus
Burns
overuse of diuretics
meds that impair auto regulation and GFR (ace inhibitors, nor-epinephrine)
systemic vasodilation
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13
Q

what is post-renal AKI

A

mechanical obstruction of urine flow (urine back up)

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14
Q

obstruction in post-renal AKI causes

A

increased intratubular pressure causing decreased GFR, and abnormal nephron fxn

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15
Q

causes of post-renal AKI

A 
kidney stone
tumor
foley with sediment
injury/trauma
abdominal surgeries
benign prostatic hypertrophy
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16
Q

can post-renal AKI be reversed

A

yes - potentially after removal of obstruction

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17
Q

what is intrarenal AKI

A

damage to kidney tissue intrinsic of the kidney (nothing else causing it)
quickly can become ATN (acute tubular necrosis)

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18
Q

causes of intrarenal AKI

A

can happen if we don’t address prerenal issues (shock, decreased Cardiac Output, decreased GFR and flow)
ATN - variable onset
contrast induced nephropathy (nephrotoxic exposure)
acute glomerulonephritis

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19
Q

most common type of intrarenal failure

A

ATN - acute tubular necrosis

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20
Q

what is ATN

A

damage of basement membrane to tubular epithelium
necrotic tissue sloughs off
tubules become blocked

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21
Q

what causes ATN

A 
prolonged pre/post renal failure (shock scenario)
ischemia (initiating cell death)
increase in myoglobin
hemolyzed RBC
HTN
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22
Q

***contrast induced nephropathy (CIN) risk factors

A

*screen patients baseline Creat and BUN, GFR
what meds are they taking-additional nephrotoxic meds?
dehydration, hypotension
advanced age
diabetes
admin of lg amt of contrast (contrast is better today)

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23
Q

CIN dx by

A

increase in serum creat of 25% or 0.5mg/dl (decreased urine output)
occurs 48-72 hours after contrast administration

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24
Q

CIN patho

A

contrast = toxic effect on renal tubule cells causing decreased blood flow
can be reversible - dependent on how bad injury is
adjustment of contrast type/amt can chg outcome

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25
Q

3 phases of AKI

A

initiation, maintenance and recovery

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26
Q

the initiation phase of AKI

A

precipitating event that causes AKI (before seeing a lot of injury) - urine output slightly decreases, electrolyte imbalances
potentially reversible at this point - good assessment
intrinsic damage has not occurred

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27
Q

the maintenance phase of AKI

A

intrinsic damage has set in - BUN and Creat are going up
GFR decreased
urine output less than 400ml/day
obvious signs of renal failure (fluid overload, electrolyte imbalance, acidosis)
renal replacement therapy is required
presents in 8-14 days and can last for months

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28
Q

the recovery phase

A

gradual return of tubular function - can happen with AKI
can take 6mos to a yr to reverse
may diurese 4-5L/day (avoid by implementing dialysis)
residual impairment of GFR (know history of pt)

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29
Q

most common cause of AKI

A

ATN

often associated with sepsis and shock

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30
Q

predisposing factors for AKI

A 
htn 
diabetes
liver disease (cirrhosis of the liver)
hypotensive incidence
exposure to nephrotoxic medications (metformin, contrast, antibiotics - *aminoglycosides, vancomycin, tetracycline)
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31
Q

if a pt with AKI is on a nephrotoxic med what do we want to check

A

peak and trough - make sure you are not overloading the patient

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32
Q

geriatric considerations r/t AKI renal fxn

A

decreased GFR, decreased renal blood flow, decreased muscle mass ldg to decreased ability to concentrate urine
at risk for hyperkalemia, hyponatremia, vol depletion and dehydration
drug and dye considerations - special considerations*

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33
Q

Manifestations of AKI

A

BP (high or low)
hyperventilation blowing off metabolic acidosis
electrolyte imbalances(hyperphosphatemia, hyperkalemia, hypocalcemia)
edema
dehydrated
uremia
metabolic acidosis

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34
Q

Uremia s/s of AKI

A 
change in LOC (fatigue, malaise, disorientation)
build up of waste products
coma
tremors/convulsions
anorexia
n/v
pruritis
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35
Q

metabolic acidosis s/s of AKI

A

decreased bicarb re-absorption - kidneys aren’t working anymore so we cant make ammonia and we can’t excrete hydrogen

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36
Q

pt presents with signs of hypovolemia (oliguria, tachycardia, hypotension, dry mucous membranes, flattened neck veins) is this pre, intra or post renal

A

pre-renal

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37
Q

pt presents with oliguria, angiogram w/contrast 2 days ago, nausea, +2edema in lower/upper extremities b/l, crackles on auscultation is this pre, intra or post renal

A

intra-renal - damaged actual kidney (CIN)

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38
Q

pt has an AKI resulting from ATN (acute tubular necrosis) what will we expect to see on assessment. is this pre, intra or post renal

A

intra-renal - edema (increased daily weight), hypertension (retaining fluid), electrolyte imbalance (hyperkalemia)

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39
Q

lab values associated with AKI

A

urine - creatinine clearance, sediment

serum - creatinine, BUN: creatinine ratio

40
Q

how do we test for urine creatinine clearance

A

urine specimen - 24hr urine - estimate of GFR

88-137

41
Q

how do we test for urine sediment

A

muddy brown casts - indicative of ATN (protein breakdown in tubules and glomerulus you have pcs that present like this

42
Q

blood tinged urine is found in pre, intra or post renal

A

post renal

43
Q

what is a normal creatinine (serum)

A

.6 to 1.2

44
Q

BUN: Creatinine Ratio

A

Intra-Renal - BUN and Creatinine increase together
Pre-Renal - BUN increases; Creatinine increases slower
normal 10:1 to 20:1

45
Q

the same serum creatinine can reflect a very different GFR, t or f

A

true - look beyond creatinine

46
Q

common fluid and electrolyte imbalances with AKI

A 
hyperkalemia (decreased excretion)
hyponatremia (fluid retention)
hypocalcemia (decreased excretion of phosphorous, decreased vit D)
hyperphosphatemia (decreased excretion)
hypermagnesium (decreased excretion)
47
Q

2 types of dx studies r/t AKI

A

invasive and noninvasive

48
Q

issues with invasive testing r/t AKI

A

must use dye

49
Q

noninvasive testing r/t AKI

A

KUB-xray of kidneys, ureter, and bladder hydronephrosis?
renal u/s - stones?
MRI

50
Q

what does a KUB test tell us about kidneys

A

size, shape, position of kidneys

51
Q

invasive testing r/t AKI

A

IV pyelogram
renal angiography
renal scan
renal biopsy

52
Q

mgmt of AKI

A 
prevent infection
prevent injury (initial and progressing along)
53
Q

biggest complication of AKI

A

infection

54
Q

pre-renal mgmt of AKI

A

early recognition and mgmt - pt in shock with hypovolemia and low cardiac output
*improve renal perfusion - increase cardiac output
give fluids/blood - use isotonic solutions
antidysrhythmic agents if dysrhythmias
intra-aortic balloon pumps
hemodynamic monitoring to guide trt
prevent progression

55
Q

post-renal mgmt of AKI

A

alleviate obstruction - may require an indwelling urinary catheter (trans-urethral or supra-pubic)
stent placement

56
Q

intra-renal mgmt (ATN-acute tubular necrosis) of AKI

A

conserve kidney fxn, prevent/manage complications
pharmacological
dietary
mgmt of fluid/electrolyte imbalances
renal replacement therapy (hemo-dialysis or continuous dialysis)

57
Q

pharmacological therapy for AKI

A

hemodynamic support (fluids/vasopressors)
anemia (epoetin alfa)
hyperphosphatemia (calcium acetate)
dosage/schedule will be adjusted if pt has decreased renal fxn or is on dialysis
collaborate w/pharmacy for dosing

58
Q

meds no longer recommended for trt of AKI

A 
renal dose dopamine
acetylcysteine IV (mucomyst)
diuretics (don't give with fluid overload)
59
Q

mgmt of fluid and electrolyte imbalances r/t AKI

A

focus on fluid imbalance - don’t want massive edema
focus on hyperkalemia
metabolic acidosis

60
Q

s/s of metabolic acidosis

A

pH

61
Q

hyperkalemia mgmt r/t AKI

A

Reduce amt of potassium in the body - give kayexalate
Shift potassium into the cell - iv insulin (10 units iv push, followed by an amp of D50) *only regular insulin OR an amp of sodium bicarbonate or albuterol (monitor anxiety/palpitations)
Give calcium gluconate - decrease irritated effect of high K

62
Q

dietary mgmt of AKI

A

need more calories than normal

restrict sodium/potassium/fluid intake

63
Q

mgmt of CIN (contrast induced nephropathy)

A 
mucomyst PO
prevention strategies (pt. screens, best contrast for pt, limit exposure to contrast, give fluids)
pharmacological therapy (mucomyst PO bid, isotonic fluids w/norm saline or sodium bicarb solution)
64
Q

pt has AKI secondary to cardiac cath, which action should the nurse establish as priority

A

administer IV calcium gluconate

65
Q

renal replacement therapy decisions making

A

decision to begin therapy is based on fluid, metabolic and electrolyte status - what does pt look like?
are they getting intermittent hemo-dialysis, continuous renal replacement therapy (CRRT) or peritoneal dialysis

66
Q

types of renal replacement (3)

A

intermittent hemo-dialysis
CRRT (continuous renal replacement therapy)
peritoneal dialysis

67
Q

reasons to initiate renal replacement therapy

A

Fluid status - they’re overloaded, compromising cardiovascular and respiratory status
Elevated serum/potassium levels - regardless of trt (IV insulin)
Severe metabolic acidosis
Changes in mental status (get uremia under control)

68
Q

what is dialysis

A

separation of solutes by differential diffusion through a porous or semi porous membrane

69
Q

2 physical principles of dialysis that occur simultaneously

A

diffusion - movement of solutes from blood into dialysate across a hemofilter (semipermeable membrane)
ultra-filtration - removal of plasma water by pressure or osmotic gradient

70
Q

dialysis can be given

A

intermittent or continuous

71
Q

2 main types of vascular access for dialysis

A

percutaneous venous catheter

permanent fistula/vascular access

72
Q

where is a percutaneous venous catheter placed/how long does it stay in

A

interventional radiology - bedside - OR
2 lumens
can stay in for a couple months

73
Q

risk fxrs r/t percutaneous venous catheter - permacath

A

***infection, bleeding, clots

74
Q

who gets a percutaneous venous catheter (permacath)

A

someone who needs dialysis now - not planned ahead

75
Q

2 types of permanent access for dialysis

A

av fistula or av graft - used when planning ahead

76
Q

vascular access of choice fistula or graft

A

fistula - because there is nothing foreign in the body

77
Q

what is taking place with av fistula/graft

A

shunting arterial blood into the vein

78
Q

what is used in an av graft

A

Teflon tubing anastomose’s the artery and vein

79
Q

how long does it take av fistula/graft to mature

A

2-4 weeks

80
Q

can you give fluids/meds or draw labs from dialysis cath’s?

A

no

81
Q

what do we want to assess on the permanent vascular access?

A

when was it put in (has it matured)

bruit/thrill and distal pulse

82
Q

what should you do if you can’t hear bruit/thrill

A

EMERGENCY, CALL PHYSICIAN

83
Q

can you do BP or IV stick on side of fistula

A

no - should have limb alert bracelet

84
Q

complications of hemodialysis

A

hypotension (shift/removal of fluid) - try CRRT?
muscle cramping (legs do to shift of fluid)
reaction to dialyzer
infection if permacath*
dialysis disequilibrium syndrome

85
Q

what is dialysis disequilibrium syndrome

A

happens during the 1st few times being dialyzed

AKI pt has high K, BUN, Creat - blood brain barrier - osmotic shift causing temporary cerebral edema

86
Q

s/s of dialysis disequilibrium syndrome

A

headaches, n/v, seizures

87
Q

how do we prevent dialysis disequilibrium syndrome

A

start slow with treatments, more frequent and shorter

88
Q

mgmt before dialysis

A

weigh the pt
check labs (baseline)
hold BP meds - unless BP is very high - assess pt.
hold water soluble meds

89
Q

mgmt during and after dialysis

A

BP - vitals - I/O’s, check access points

90
Q

CRRT - continuous renal replacement when is it used

A

pt too unstable for hemodialysis

91
Q

where is CRRT done

A

ICU bed - slowly and continuously

92
Q

2 types of CRRT

A

CVVH - continuous venovenous hemofiltration - removal of fluid and SOME uremic wastes
CVVHD - continuous venovenous hemodialysis - removes fluid and MAX uremic waste

93
Q

benefits of CRRT

A

remove solute more gradually
flexible with fluid administration
minimal heparin
done at bedside

94
Q

complications of CRRT

A 
volume depletion
disequilibrium syndrome
dysrhythmias
bleeding
hypoxemia
95
Q

nursing responsibilities during CCRT

A

hourly assessments
assess for leaks, blood in lines
freq labs (BNP, electrolytes, clotting factors)
check hemodynamic stability
risk for metabolic alkalosis (citrate turns into bicarb)?

CCM (13 decks)

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