Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
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 __-__
|
90-250
|
|
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?
|
200
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
|
inverse
Serum=285-293 Urine=300-900 |
|
Urine osmol<150 with simultaneous increase in serum osmol indicates??
|
renal failure
|
|
Byproduct of muscle metab excreted solely in urine
|
Creatinine
|
|
Normal Creat clearance
|
80-120
|
|
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 etc |
|
How do we support CO in prerenal ARF
|
Inotropes-dopa/dobutamine
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
|
Nepro
|
|
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
nephrotoxic: -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 |
Ischemic
|
|
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 Uremia |
|
main goals of oliguric phase of ATN/ARF
|
Support renal fxn
Keep pt alive-major causes of death: -hyperK -GI bleed -Infection |
|
Non-oliguric phase of ATN/ARF more commonly assoc with ischemic or nephrotoxic?
|
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
|
Education
-Precipitating factors -Preventative measures -Follow up care |
|
In the intact nephron theory, what percentage of nephrons must be damaged for kidney failure to onset
|
80%
|
|
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
|
ESRD
|
|
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
CRF |
|
When are alkaline meds (IV NaHCO3) indicated
|
Metab acidosis
pH<7.2 HCO3<14 |
|
S&S of uremic pericarditis seen primarily in CRF pt's d/t urmeia
|
chest pain
Fever Pericardial friction rub |
|
Becks triad associated with tamponade/pericarditis
|
JVD
Inc CVP Hypotension |
|
Mainstays of HTN therapy in RF
|
Fluid/Na restriction
Diuretics ACEI/ARB, BB, CCB Dialysis |
|
ECG changes tend to manifest when K is ____
|
6-7
|
|
Tx of mild hyperkalemia i.e. K<6
|
Dietary K restriction
Diuretics |
|
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
|
Mirapex
|
|
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
|
PO4-Phoslo
Ca-admin supp Ca Vit D-Calcitrol supp |
|
In a pre-renal cause of ARF, urinary excretion of Na is often??
|
Decreased<10
|
|
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. |