Renal Flashcards
1
Q
basic unit of the kidney
A
nephron - very vascular
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
3
Q
what is the normal glomerular filtration rate
A
80-125 ml/min
4
Q
how does the kidney function to regulate acid/base bal?
A
reabsorbs bicarb
produce new bicarb
excretes small amts of hydrogen ions
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
6
Q
cardinal features of AKI
A
decreased GFR
azotemia (increased BUN and creat)
oliguria (output
7
Q
before determining AKI what do we need
A
a baseline creat, urine output
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
9
Q
what is rifle criteria (check into this)
A
a way of scaling AKI
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)
11
Q
what is prerenal AKI
A
reduction in renal blood flow (perfusion and filtration)
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
13
Q
what is post-renal AKI
A
mechanical obstruction of urine flow (urine back up)
14
Q
obstruction in post-renal AKI causes
A
increased intratubular pressure causing decreased GFR, and abnormal nephron fxn
15
Q
causes of post-renal AKI
A
kidney stone tumor foley with sediment injury/trauma abdominal surgeries benign prostatic hypertrophy
16
Q
can post-renal AKI be reversed
A
yes - potentially after removal of obstruction
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)
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
19
Q
most common type of intrarenal failure
A
ATN - acute tubular necrosis
20
Q
what is ATN
A
damage of basement membrane to tubular epithelium
necrotic tissue sloughs off
tubules become blocked
21
Q
what causes ATN
A
prolonged pre/post renal failure (shock scenario) ischemia (initiating cell death) increase in myoglobin hemolyzed RBC HTN
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)
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
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
25
3 phases of AKI
initiation, maintenance and recovery
26
the initiation phase of AKI
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
27
the maintenance phase of AKI
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
28
the recovery phase
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)
29
most common cause of AKI
ATN
| often associated with sepsis and shock
30
predisposing factors for AKI
```
htn
diabetes
liver disease (cirrhosis of the liver)
hypotensive incidence
exposure to nephrotoxic medications (metformin, contrast, antibiotics - *aminoglycosides, vancomycin, tetracycline)
```
31
if a pt with AKI is on a nephrotoxic med what do we want to check
peak and trough - make sure you are not overloading the patient
32
geriatric considerations r/t AKI renal fxn
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*
33
Manifestations of AKI
BP (high or low)
hyperventilation blowing off metabolic acidosis
electrolyte imbalances(hyperphosphatemia, hyperkalemia, hypocalcemia)
edema
dehydrated
uremia
metabolic acidosis
34
Uremia s/s of AKI
```
change in LOC (fatigue, malaise, disorientation)
build up of waste products
coma
tremors/convulsions
anorexia
n/v
pruritis
```
35
metabolic acidosis s/s of AKI
decreased bicarb re-absorption - kidneys aren't working anymore so we cant make ammonia and we can't excrete hydrogen
36
pt presents with signs of hypovolemia (oliguria, tachycardia, hypotension, dry mucous membranes, flattened neck veins) is this pre, intra or post renal
pre-renal
37
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
intra-renal - damaged actual kidney (CIN)
38
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
intra-renal - edema (increased daily weight), hypertension (retaining fluid), electrolyte imbalance (hyperkalemia)
39
lab values associated with AKI
urine - creatinine clearance, sediment
| serum - creatinine, BUN: creatinine ratio
40
how do we test for urine creatinine clearance
urine specimen - 24hr urine - estimate of GFR
| 88-137
41
how do we test for urine sediment
muddy brown casts - indicative of ATN (protein breakdown in tubules and glomerulus you have pcs that present like this
42
blood tinged urine is found in pre, intra or post renal
post renal
43
what is a normal creatinine (serum)
.6 to 1.2
44
BUN: Creatinine Ratio
Intra-Renal - BUN and Creatinine increase together
Pre-Renal - BUN increases; Creatinine increases slower
normal 10:1 to 20:1
45
the same serum creatinine can reflect a very different GFR, t or f
true - look beyond creatinine
46
common fluid and electrolyte imbalances with AKI
```
hyperkalemia (decreased excretion)
hyponatremia (fluid retention)
hypocalcemia (decreased excretion of phosphorous, decreased vit D)
hyperphosphatemia (decreased excretion)
hypermagnesium (decreased excretion)
```
47
2 types of dx studies r/t AKI
invasive and noninvasive
48
issues with invasive testing r/t AKI
must use dye
49
noninvasive testing r/t AKI
KUB-xray of kidneys, ureter, and bladder hydronephrosis?
renal u/s - stones?
MRI
50
what does a KUB test tell us about kidneys
size, shape, position of kidneys
51
invasive testing r/t AKI
IV pyelogram
renal angiography
renal scan
renal biopsy
52
mgmt of AKI
```
prevent infection
prevent injury (initial and progressing along)
```
53
biggest complication of AKI
infection
54
pre-renal mgmt of AKI
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
post-renal mgmt of AKI
alleviate obstruction - may require an indwelling urinary catheter (trans-urethral or supra-pubic)
stent placement
56
intra-renal mgmt (ATN-acute tubular necrosis) of AKI
conserve kidney fxn, prevent/manage complications
pharmacological
dietary
mgmt of fluid/electrolyte imbalances
renal replacement therapy (hemo-dialysis or continuous dialysis)
57
pharmacological therapy for AKI
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
meds no longer recommended for trt of AKI
```
renal dose dopamine
acetylcysteine IV (mucomyst)
diuretics (don't give with fluid overload)
```
59
mgmt of fluid and electrolyte imbalances r/t AKI
focus on fluid imbalance - don't want massive edema
focus on hyperkalemia
metabolic acidosis
60
s/s of metabolic acidosis
pH
61
hyperkalemia mgmt r/t AKI
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
dietary mgmt of AKI
need more calories than normal
| restrict sodium/potassium/fluid intake
63
mgmt of CIN (contrast induced nephropathy)
```
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
pt has AKI secondary to cardiac cath, which action should the nurse establish as priority
administer IV calcium gluconate
65
renal replacement therapy decisions making
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
types of renal replacement (3)
intermittent hemo-dialysis
CRRT (continuous renal replacement therapy)
peritoneal dialysis
67
reasons to initiate renal replacement therapy
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
what is dialysis
separation of solutes by differential diffusion through a porous or semi porous membrane
69
2 physical principles of dialysis that occur simultaneously
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
dialysis can be given
intermittent or continuous
71
2 main types of vascular access for dialysis
percutaneous venous catheter
| permanent fistula/vascular access
72
where is a percutaneous venous catheter placed/how long does it stay in
interventional radiology - bedside - OR
2 lumens
can stay in for a couple months
73
risk fxrs r/t percutaneous venous catheter - permacath
***infection, bleeding, clots
74
who gets a percutaneous venous catheter (permacath)
someone who needs dialysis now - not planned ahead
75
2 types of permanent access for dialysis
av fistula or av graft - used when planning ahead
76
vascular access of choice fistula or graft
fistula - because there is nothing foreign in the body
77
what is taking place with av fistula/graft
shunting arterial blood into the vein
78
what is used in an av graft
Teflon tubing anastomose's the artery and vein
79
how long does it take av fistula/graft to mature
2-4 weeks
80
can you give fluids/meds or draw labs from dialysis cath's?
no
81
what do we want to assess on the permanent vascular access?
when was it put in (has it matured)
| bruit/thrill and distal pulse
82
what should you do if you can't hear bruit/thrill
EMERGENCY, CALL PHYSICIAN
83
can you do BP or IV stick on side of fistula
no - should have limb alert bracelet
84
complications of hemodialysis
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
what is dialysis disequilibrium syndrome
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
s/s of dialysis disequilibrium syndrome
headaches, n/v, seizures
87
how do we prevent dialysis disequilibrium syndrome
start slow with treatments, more frequent and shorter
88
mgmt before dialysis
weigh the pt
check labs (baseline)
hold BP meds - unless BP is very high - assess pt.
hold water soluble meds
89
mgmt during and after dialysis
BP - vitals - I/O's, check access points
90
CRRT - continuous renal replacement when is it used
pt too unstable for hemodialysis
91
where is CRRT done
ICU bed - slowly and continuously
92
2 types of CRRT
CVVH - continuous venovenous hemofiltration - removal of fluid and SOME uremic wastes
CVVHD - continuous venovenous hemodialysis - removes fluid and MAX uremic waste
93
benefits of CRRT
remove solute more gradually
flexible with fluid administration
minimal heparin
done at bedside
94
complications of CRRT
```
volume depletion
disequilibrium syndrome
dysrhythmias
bleeding
hypoxemia
```
95
nursing responsibilities during CCRT
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)?
