urologic problems: chronic kidney disease Flashcards
kidney function
-maintain fluid and electrolyte homeostasis
-rid the body of water soluble wastes via urine
-endocrine fxns:
*produces erythropoietin
*activates vit D
*produces renin (helps regulate BP)
RAAS system
- renin converts angiotensinogen to angiotensin I
- ACE converts angiotensin I to angiotensin II
- angiotensin II –> aldosterone
blood pressure regulation
- blood volume
- sodium reabsorption
- potassium secretion
- water reabsorption
BUN and Cr lab values
BUN = 10-20 mg/dL
Cr = 0.5-1.2 mg/dL
BUN:Cr = 10:1
GFR lab value
> 90 mL/min
when would you see a 20:1 BUN:Cr ratio?
glomerulonephritis and nephrotic syndrome
chronic kidney disease (CKD)
presence of kidney damage for > 3 months with/without GFR <60
-inability to maintain acid-base balance, remove end products of metabolism (build up of toxins), maintain fluid/electrolyte balance
CKD stage 1
kidney damage with normal or increased GFR
greater than or equal to 90
CKD stage 2
kidney damage with mild decrease in GFR
60-89
CKD stage 3
moderate decrease in GFR
30-59
CKD stage 4
severe decrease in GFR
15-29
CKD stage 5
ESRD
<15
causes of ESRD
diabetes (50%)
HTN (30%)
glomerulonephritis (10%)
other (10%)
risk factors for CKD
family history
>60
male
african american
HTN, DM
smoking
overweight/obesity
3 characteristics of CKD
- glomerulosclerosis: scar tissue in glomerulus – can’t filter blood properly (nonfunctional fibrotic tissue)
- interstitial fibrosis: obstruction of renal tubules and interstitial capillaries
- interstitial inflammation
what plays a major role in CKD
complement - part of inflammatory process that destroys kidney tissue
angiotensin II - an increase causes increased BP, thus increased damage
S/S stage 1 CKD
asymptomatic
S/S stage 2 CKD
asymptomatic, possible HTN
S/S stage 3 CKD
asymptomatic, possible HTN
S/S stage 4 CKD
manifestations becoming apparent
*diagnosis often occurs here
S/S stage 5 CKD
uremia
GFR < 15
uremia
high levels of waste in blood
-BUN
-Cr
-phenols
-hormones
-electrolytes
-water (retained)
seen when GFR < 10
psychologic/neurologic S/S of ESRD
anxiety and depression
fatigue
headache
sleep disturbances
encephalopathy
paresthesia
restless legs syndrome
cardiovascular S/S of ESRD
HTN
heart failure
CAD
pericarditis
peripheral artery disease
GI S/S of ESRD
anorexia
N/V
GI bleeding
gastritis
pulmonary S/S of ESRD
PE
uremic pleuritis
pneumonia
ocular S/S of ESRD
HTN retinopathy
endocrine S/S of ESRD
hyperparathyroidism
thyroid abnormalities
amenorrhea
erectile dysfunction
metabolic S/S of ESRD
carb intolerance
HLD
hematologic S/S of ESRD
anemia
bleeding
infection
integumentary S/S of ESRD
pruritus
ecchymosis
dry, scaly skin
MSK S/S of ESRD
vascular and soft tissue calcifications (hardness causing soreness)
osteomalacia (softening of bones bc decrease in Vit D)
osteitis fibrosa (loss of bone mass)
abnormal kidney functions
-no longer maintain F/E homeostatis
-no longer rids the body of wastes via urine
-decreased production of erythropoietin
-decreased activation of vitamin D
unable to maintain f/e homeostasis results in
edema
high potassium
high phos
high mag
metabolic acidosis
unable to rid body of wastes results in
anorexia
malnutrition
itching
CNS changes
*uremic frost (crystallized deposits on skin - white spots)
decreased production of erythropoietin results in
anemia
decreased activation of vit D results in
renal osteodystrophy (weakening of bones)
drugs can be used to
slow the rate of progression by decreasing BP < 140/90 and treating HLD <200 (cholesterol)
& treat complications of CKD
complications of CKD
volume overload
hyperkalemia
metabolic acidosis
hyperphosphatemia
renal osteodystrophy
anemia
how to control BP
ACE or ARB
maintain SBP 110-130
how to control lipids
statins
treatment for volume overload
loop diuretic
used with low salt diet
treatment for hyperkalemia
multiple – diuretics
addressed with hemodialysis in ESRD
treatment for metabolic acidosis
sodium bicarbonate
*alkaline agent
treatment for hyperphosphatemia
calcium carbonate
a phosphate binder
treatment for renal osteodystrophy
calcitrol
activated vitamin D
treatment for anemia
erythropoietin
*must have iron
BLACK BOX WARNING: increase CV problems
goal of sodium bicarbonate
metabolic acidosis
goal: slow CKD progression, prevent bone loss, improve nutritional status
administration of sodium bicarbonate
initiate when HCO3 <15 (tested with CO2 on BMP
titrate to a HCO3 of 18-20
consider switch to sodium citrate if bloating is a problem
calcium carbonate MOA + goal
MOA: binds to phosphate
GOAL: treat hyperphosphatemia
-keep phosphate levels normal (near)
-reduce mortality
considerations + SE’s with calcium carbonate
take with meals to increase absorption
SE: high Ca –> monitor levels (acts as sedative)
calcitriol MOA
activated form of vit D
stimulates intestinal absorption of calcium/phosphate and bone mineralization
calcitriol SE
high Ca - toxicity
high phosphate
signs of Ca toxicity
GI upset
bone pain
neuro effects
cardiac arrythmias
complications of drug therapy
many drugs are excreted through kidneys, so if the kidneys are functioning may need to have renal dosing (decreased dose + frequency)
drugs of concern when treating CKD
digoxin
diabetic agents (glyburide, metformin)
antibiotics (vancomycin)
opioids (morphine)
