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66 Cards in this Set

  • Front
  • Back
Renin is released mainly in response to??
Decreased BP/GFR
Where is renin secreted from?
Juxtaglomerlular cells
Goes to liver (converts to angio 1) then to lungs where ACE converts it to angio 2
Angio 2 fx's
1) Efferent arterole vasoconstr
2) Stims aldosterone-conserves Na/H2O
3) Stims ADH-conserves H2O (but not Na)
Aldosterone fx's
1) Increases Na/H2) reabsorption
2) Thus excretion of K
Aldosterone released in response to ??
1) Dec BP/GFR via RAAS
2) Hyponatremia thus increasing Na (and also H2O)
3) Hyperkalemia/acidosis
Where is aldosterone secreted
Adrenal gland (mineralocorticoid)
ADH released in response to??
1) Decreased BP/GFR via RAS thereby increasing circ volume and increaing GFR
2) Hyperosmolality via detected via osmoresceptors in hypothalamus-increases circ volume thereby diluting hyperosmolality
3) Dehydration/hypovolemia via pressure receptors in veins/atria/carotids-thereby increaing circ volume
ADH fx's
1) Conserves H2O (but not salt) by inserting H2O channels
2) moderate vasoconstr
Kidney/glomerular autoregulation is maintained when MAP is __-__
Hypernatremia regulated by what hormone??
Kidneys retain H2O via ADH
Hyponatremia regulated by what hormone?
Kidneys retain Na/H2O via aldosterone
Why does kidney failure result in Hyperkalemia
Can't excrete K
End up with metabolic acidosis
How long does it generally take kidneys to respond to acid/base d/o
48-72 hours
Renal threshold for glucose?
When glucose levels are higher then this the nephron doesn't have enough sie to allow for reabsorption and it spills into the urine
Proteinuria may indicate dmage to??
Glomerulus (usually will not allow particles of the size of protein to be filtered)
Occurs with glomerular nephritis or intra renal failure
Casts in the urine generally indicate??
Cellular breakdown, intrearenal failure
Dilute urine (low spec grav) generally indicates what in regards to H2O balance?
Water excess
Concentrated urin (high spec grav) generally indicates what in regards to H2O balance?
Water defecit
How/why is spec grav fx'd by renal Dx?
1) Can become fixed and low in d/o like ATN, acute nephritis and CRF

2) Can b/c falsely high d/t allowance of high molecular weight substance i.e. protein, glucose, radiocontrast

Thus osmolality is a better indicator
Urine osmol is ____ in relation to serum osmol

Urine osmol<150 with simultaneous increase in serum osmol indicates??
renal failure
Byproduct of muscle metab excreted solely in urine
Normal Creat clearance
Why does BUN tend to rise in dehydration state
Dehydration>low urine flow rate>more Na/H2O reabsorbed>consequently more urea reabsorbed

i.e. little urine being put out so BUN CAN'T get out essentially and so it starts building up

Increased BUN:Cr ratio as it's not a kidney problem

Also elev in increased protein intake, increased tissue brkdwn, reabsorption of blood in intestine second to GI bleed, decreased renal perfusion secondary to CHF
increased BUN/Creat ratio
renal Dx or not?
Not renal Dx

Renal Dx both should rise (at least the Creat will)
Fluid therapy in prerenal ARF
Appropriate aggressive fluid therapy
Blood loss=blood products
How do we support CO in prerenal ARF
Fluids may help too
Pressors generally not good as they will decrease renal perfusion further (except low dose dopamine)
Are diuretics utilized in prerenal ARF?
Yes, large doses of lasix
Mannitol not indicated
Why must fluid admin be cautioned in any oliguric state
Potential for fluid overlad

e.g. oliguric phase of ATN=fluid restriction
Type of nute therapy in RF
Term for intrarenal ARF in caused by prolonged hypoperfusion
Ischemic ATN
Term for intrarenanl ARF caused by offensive agent
Nephrotoxic ATN
How long after admin of Abx (e.g. eminoglycosides) does it take for nephtrotoxic ARF to set in
7-10 days
How long after admin of radiocontrast does it take for nephrotoxic ARF to set in
48 hours
Whats worse
-ischemic or nephrotoxic ATN
Ischemic is worse

-basement membrane remains inact
-necrotic areas more localized
-non-oliguric type more common
-healing more rapid
How can you prevent nephrotoxic ATN/ARF from radiocontrast
1) aggressive hydration before and after procedure
2) mucomyst 600mg bid before and after
How long does onset phase of ATN last and how is it's onset noticed?
hours to days
Onset=Sx of RF i.e. dec UP, inc Creat
Major goal for onset phase of ATN
Initiate Tx
Prevent irreversible damage
Oliguric phase of ATN
More commonly assoc with ischemic or nephrotoxic
S&S of oliguric phase of ATN
Fluid overlaod (d/t oliguria)
Azotemia (BUN, Creat) d/t oliguria
Lyte imbalances (Inc K, Phosp, dec Ca...)
Metab acidosis
main goals of oliguric phase of ATN/ARF
Support renal fxn
Keep pt alive-major causes of death:
-GI bleed
Non-oliguric phase of ATN/ARF more commonly assoc with ischemic or nephrotoxic?
Why is pt at risk of dehydration during diuretic phase of ATN/ARF
May diurese 4-5 L/day
Primary goals during diuretic phase of ATN/ARF
Keep hydrated
Replace Na/K (at risk for hypo Na/K)
major goals for recovery phase of ATN/ARF
-Precipitating factors
-Preventative measures
-Follow up care
In the intact nephron theory, what percentage of nephrons must be damaged for kidney failure to onset
Why is decreased renal reserve stage of CRF usually asymptomatic
Kidneys can maintain excretory and regulatory fxn thus BUN and Creat remains normal
At what stage of CRF do uremic symptoms become evident
2 most common causes of CRf
DM and HTN
Common Sx's during rnal insuff stage
Solute clearance, abil to concentrate urine and hormone secretion compromised
Sx's of renal failure begin to manifest including azotemia, lyte imbalances and anemia
Common Sx's include fatigue, polyuria and nocturia
What types of RF indicate fluid restriction and Na restriction
Oliguric phase of ATN
When are alkaline meds (IV NaHCO3) indicated
Metab acidosis
S&S of uremic pericarditis seen primarily in CRF pt's d/t urmeia
chest pain
Pericardial friction rub
Becks triad associated with tamponade/pericarditis
Mainstays of HTN therapy in RF
Fluid/Na restriction
ECG changes tend to manifest when K is ____
Tx of mild hyperkalemia i.e. K<6
Dietary K restriction
Tx of severe hyperkalemia i.e. K>6
Antagnize fx of K-IV Ca gluconate (first priority)
Promote cellular shifting-IV insulin w/ dextrose AND IV NaHCO3
Remove K-diuretic
Rx for restless leg syndrome
Tx of burning feet syndrome
Vit B
Cotton socks
Open shoes
General measures for increased bleeding tendecies thought to be d/t uremia
Monitor labs
Assess for bleeding
Admin blood prod PRN
Protect pt
Avoid Rx that alter Plt fxn i.e. NSAID's and ASA
General measures for immunosuppresion thought to be d/t uremia on WBC's
Assess infection
Monitor labs
Watch for ANY increase over baseline temp as it is signifigant
pathophys behind metastatic calcification
inc PO4/dec Ca
Adding to hypoCa-failure to convert Vit D to active form
In response to hypoCa, PTH secreted
Ca is reabsorbed into serum from bone BUT this is done at expense of bone density/mass
Eventually Ca and PO4 crytsal precipitate in brain
How are Ca/PO4 alteration managed
Ca-admin supp Ca
Vit D-Calcitrol supp
In a pre-renal cause of ARF, urinary excretion of Na is often??
How does lasix correct edema
Lasix blocks the reabsorption of Na from loop of Henle thereby pulling H2O with it. This creates hypotonic serum which then pulls more Na (and thus H2O) from interstitium.

Reduced edema with increased UO.