renal Flashcards
functional unit of the kidney is the
nephron
glomerulus
bundle of capillaries where filtration occurs in nephron
Function of kidneys
remove toxins from blood, maintain electrolyte balance, regulate water balance
Renin Angiotensin Aldosterone System
regulates water balance and controls blood pressure; renin released by kidneys -> angiotensinogen -> angiotensin I -> angiotensin II -> aldosterone
renin is released when
decrease renal blood flow, sympathetic input, epi/norepi, early in day, when standing
Inhibits renin:
adenosine, angiotensin II, Adrenalin. lockers, aldosterone, later in day, lying down
Angiotensin II Receptor Blockers
Losartan; inhibits vasoconstrictor properties of angiotensin II
ACE inhibitor
blocks concessions of angiotensin I to angiotensin II, increases renin levels and decrease aldosterone leading to vasodilation
Loop diuretics
“ide”; act on loop of Henle to increase urine output by affecting sodium reabsorption within the nephron
Loop diuretics uses and monitoring
increase UO, edema, CHF, bp management; monitor potassium levels (considered potassium wasting), most effective of all diuretics
Thiazide diuretics
“thiazide”; decreases sodium reabsorption causing more
fluid loss in urine; htn, CHF; monitor electrolyte levels and bp
potassium sparing diuretics
spares potassium; htn, edema, swelling, hypokalemia; monitor potassium; not as strong as other diuretics so are often combine with a different diuretic
when kidneys have poor perfusion we will see
urine output go down
normal urine output
30ml/hr
UTI S&S
dark, cloudy urine, blood in urine, pain in pelvis, pain or burning while urinating (dysuria), strong or foul smelling, increase frequency or urgency
pyelonephritis
UTI that has reached the kidneys
UTI treatment
hydration (more fluids being filtered and put out bacteria will be flushed out), antibiotics
glomerulonephritis
acute inflammation of kidneys at level of nephron; happens d/t inflammatory reaction, antibodies get lodged into glomerulus, #1 cause is strep
glomerulonephritis S&S
sore throat, malaise, headache, flank pain, htn, edema, decreased UOP, increased BUN and Cr, increase specific gravity, dark, cloudy, sediment
glomerulonephritis tx
abx for strep, struck I&Os, bp, decrease protein and sodium, increased carbs
nephrotic syndrome
causes body to pass too much protein in urine; no protein in the blood = not being able to hold onto fluid which leads to third spacing - bp still low but RAAS activated due to low perfusion to kidneys water and sodium retained but not in cells = tons of edema
causes of nephrotic syndrome
anything that causes inflammation; infection, cancer, NSAID overuse, diabetes, lupus, diabetes, strep throat
Nephrotic Syndrome S&S
anasarca, blood clots, high cholesterol, proteinuria, hypoalbuminemia, edema, hyperlipidemia
nephrotic syndrome tx
fix the cause, prednisone, diuretics, ACE inhibitors, statins, anti coagulation, dialysis, high protein low sodium diet
pre renal failure
blood cannot get to the kidneys; hypotension, hypovolemia, shock
intra renal failure
damage inside the kidney; golemerulonephritis, nephrotic syndrome, nephrotoxic drugs
post renal failure
something is blocking urine from leaving the kidneys; kidney stone, tumor, urethral obstruction, enlarged prostate
Acute kidney injury
sudden, happens over few hours to few days, causes build up of waste products in blood
Phases of AKI
onset, oliguric, diuretic, recovery
onset phase of AKI
Injury occurs and output decreases, hours to days
oliguric phase
decreased output, becomes fluid volume overload, 10-14 days, oliguria, edema, SOB, increased BUN and Cr, metabolic acidosis, anemia, hyperkalemia, hyperphosphatemia, hypocalcemia, fatigue, confusion, nausea
Diuretic phase AKI
diuresis, 1-3 weeks, 3-5 L dilute urine per day, hypotension and hypovolemia, hypokalemka, hyponatremia, BUN and Cr begin to normalize
CKD
happens slowly over a long period of time, damage to kidneys accumulates over time, can no longer filter waste properly, and waste products build up
HTN and CKD
high bp put pressure on renal artery causes thickening of opening from blood vessels to kidneys = less blood flow to kidneys = kidneys ask for more blood and activate RAAS = causes more htn = eventually causes glomerulosclerosis and loss of nephrons
major causes or CKD
htn and uncontrolled diabetes
diabetic nephropathy
chronic high blood sugars = production of pro inflammatory cytokines causes changes to kidneys -> thickening of tubular basement membrane, thickening of renal arterial wall, sclerosis of nephrons; major intra renal cause of CKD
CKD is staged based off of the __________
GFR; as it decreases condition worsens
in CKD stages 2 and 3 we want to
protect kidneys, try to reverse damage
Stages 4 and 5 of CKD will require
dialysis
S&S early stages of CKD
GFR goes up, diuresis
S&S late stage CKD
htn, edema, hyperkalemia (muscle cramps, ECG changes, fibrillations), metabolic acidosis, osteodystrophy (not enough calcium = secondary hyperparathyroidism = causes osteoporosis), uremia, neuro changes, anorexia, vomiting, skin changes (uremic frost)
Labs in CKD will look like
Increased BUN and Cr, high potassium and phosphorus, low calcium, metabolic acidosis
renal diet
low sodium, low phosphorus, low protein, low potassium
CKD treatment
restrict fluid intake, no K+ sparing diuretics or ACE inhibitors, regular lab work, dialysis
hemodialysis
3-4 times/week, blood goes out IV in artery and gets filtered then goes back to body through IV in vein (has fistula), will cause rapid fluid shift, monitor bp and electrolytes
fistula nursing considerations
no BPs or IVs in arm of fistula, palpate for a thrill, and musculature a bruit
Peritoneal dialysis
not all can handle hemodialysis, peritoneal membrane is used to filter instead of machine; dialysate is infused into peritoneal cavity and dwells for 6hrs, fluid is drained taking
toxins with it; drainage should be clear (cloudy indicates infection), need to drain all dialysate (everything that goes in needs to come out) might need to turn pt side to side
