Reading...
Play button
Play button
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;
45 Cards in this Set
- Front
- Back
|
At what GFR would you expect a pt to have hyperK+?
|
< 20
|
|
|
CKD spans a continuum of __ values which divde it into __ ranging from __ to __. Stage __ is divided into __ and __. Stage __ is referred to as __.
|
CKD spans a continuum of GFR values which divide it into STAGES ranging from 1 to 4. Stage 3 is divided into 3a and 3b. Stage 5 is referred to as ESRD.
|
|
|
What is the GFR range for Stage 1 CKD?
|
> 90
|
|
|
What is the GFR range for Stage 2 CKD?
|
60-90
|
|
|
What is the GFR range for Stage 3a CKD?
|
45-60
|
|
|
What is the GFR range for Stage 3b CKD?
|
30-45
|
|
|
What is the GFR range for Stage 4 CKD?
|
15-30
|
|
|
What is the GFR range for Stage 5 ESRD (Kidney Failure)?
|
< 15, or dialysis/transplantation
|
|
|
The burden of chronic kidney failure assoc. w/ HTN in AA pts is __ times higher among 25-44 y/o than for whites.
|
20
|
|
|
How/why is APOL1 involved with increasing risk of CKD?
|
APOL1 variants are carried by 10-12% of the AA population. There is a recessive effect of having APOL1 variants on CKD. There is thought to be a heterozygous advantage b/c carriers of one mutated locus are immune to Trypanosoma (African sleeping sickness)
|
|
|
What is the most important factor in CKD progression?
|
HTN
|
|
|
Many factors are involved w/ CKD progression including __, __, __, __, __, and __. All of these lead to the final common pathway of __ --> __ --> __.
|
Many factors are involved w/ CKD progression including HTN, ACIDOSIS, PROTEINURIA, AGT2 RELEASE, INCREASED ALDO, and HYPERPHOSPHATEMIA. All of these lead to the final common pathway of INFLAMMATION --> TUBULOINTERSTITIAL FIBROSIS AND GLOMERULOSCLEROSIS --> CKD PROGRESSION.
|
|
|
What type of disease is APOL1 mutation associated with?
|
progressive non-diabetic kidney disease
|
|
|
What are some factors that lead to HTN in CKD?
|
1. ECFV expansion
2. Alteration in endotheilium-derived factors (NO/endothelin) 3. Decreased vascular compliance 4. Renal vascular dz and renal artery stenosis |
|
|
HTN is a __ and __ of CKD
|
cause and complication
|
|
|
What is the target BP for pts w/ CKD? How do you get them there?
|
130/80. ACE inhibitors or ARBs are 1st line.
|
|
|
What is the most common cause of secondary HTN?
|
Yo mamma! (actually, it's CKD)
|
|
|
How does proteinuria worsen CKD?
|
protein is taken up in the proximal tubule --> Cytokines released --> Injury and fibrosis
|
|
|
How do we treat proteinuria in pts w/ CKD?
|
1. CONTROL THE HTN!!
2. RAAS blockade 3. Dietary Na restriction 4. Diuretics |
|
|
What is common to see on the chem 7 in a pt w/ CKD?
|
Metabolic Acidosis (low HCO3), HyperK+, and (++) Serum Cr
|
|
|
Explain the pathogenesis of metabolic acidosis in CKD.
|
(--) GFR --> (--) NH3-genesis --> less buffer for H+ --> Normal AG metabolic acidosis
|
|
|
At what GFR do you start to see a fall in the serum bicarb?
|
45
|
|
|
At what GFR do you start to see a high AG met acidosis?
|
GFR < 25
|
|
|
How does metabolic acidosis contribute to progression of CKD?
|
Metabolic acidosis --> (++) NH3 generation --> activate cytokines --> interstitial fibrosis --> function and mass loss --> progression
|
|
|
What trends do you expect to see on the lab values of Ca++, Phosphorus, and PTH?
|
Low Calcium
High Phosphorus High PTH |
|
|
Phosphorus __ is dependent on __
|
Phosphorus EXCRETION is dependent on GFR
|
|
|
Bone Dz: Decreased renal __ leads to increased __which binds with __, reducing circulating levels. It also downregulates __, the enzyme responsible for converting __ to usable __.
|
Bone Dz: Decreased renal MASS leads to increased PHOSPHORUS which binds with CALCIUM, reducing circulating levels. It also downregulates 1-ALPHA-HYDROXYLASE, the enzyme responsible for converting 25(OH)D3 to usable 1,25(OH)2D3.
|
|
|
Bone Dz: Decreased levels of __ trigger release of __ which causes __ of __ from bone. This can lead to __ __ __, which causes pain and fractures. These increased levels of __ can lead to __ __.
|
Bone Dz: Decreased levels of CALCIUM trigger release of PTH which causes RELEASE of CALCIUM from bone. This can lead to OSTEITIS FIBROSA CYSTICA, which causes pain and fractures. These increased levels of CALCIUM can lead to VASCULAR CALCIFICATION.
|
|
|
If you are deficient in __ __ you will have __ absorption of it which __ the ongoing __.
|
If you are deficient in ACTIVE VITAMIN D you will have DECREASED absorption of it which ENHANCES the ongoing HYPOCALCEMIA.
|
|
|
__ __ __ is a consequence of calcemia of the microvasulature leading to __ of the __. 6 month mortality is X%.
|
CALCIFIC UREMIC ARTERIOLOPATHY is a consequence of calcemia of the microvasulature leading to ISCHEMIA of the SKIN. 6 month mortality is 100%.
|
|
|
What is Cinacalcet?
|
Drug that sensitizes the CaR to serum Ca++. Basically fools the parathyroid into thinking that there is more serum Ca than there really is, inhibiting PTH release.
|
|
|
In order of importance, how do you control CKD related bone disease?
|
1. Manage the levels of phosphorus (preferably w/ non-Ca binders, sevelamer and lanthanum)
2. Use vitamin D analogs to suppress PTH (dangerous --> can get bone dz or Ca deposition in vasculature) 3. Cinacalcet (high PTH) |
|
|
What levels of PTH do you try to maintain in pts w/ CKD?
|
150-600
|
|
|
What are the options for ESKD?
|
1. Nothing
2. Kidney Transplant 3. Peritoneal dialysis 4. Hemodialysis |
|
|
At what GFR do you see symptoms of uremic syndrome?
|
< 60 mL/min
|
|
|
What GFR is the threshold to list somebody for kidney transplant?
|
GFR < 20
|
|
|
At what GFR do you begin dialysis?
|
GFR < 10-15
|
|
|
Why is Stage 3 CKD subcategorized into 3a and 3b?
|
Because GFR < 45 seems to be the tipping point for increasing the risk of CVD
|
|
|
T or F: Most pts w/ CKD die of CVD before reaching ESRD?
|
TRUE
|
|
|
What is the leading cause of death in pts w/ ESRD?
|
CVD
|
|
|
Why do you need to have a high index of suspuscion for ACS w/ CKD pts?
|
they often present atypically. pts on dialysis are more likely to present w/ cardiogenic shock
|
|
|
Why are pts w/ CKD at increased risk of developing cardiomyopathy?
|
Volume overload, ischemic heart disease, HTN, uremic toxins, etc. all contribute
|
|
|
Why are pts w/ CKD at increased risk of developing anemia?
|
decreased production of EPO and decreased RBC lifespan
|
|
|
What is the best way to treat anemia in CKD pts?
|
treat the iron deficiency first
|
|
|
What therapeutic agents should be avoided in pts w/ CKD?
|
Mg and Phosphorus containing cathartics
NSAIDs, COX-2 inhibitors Bisphosphonates Iodinated contrast Gadolinium |
