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167 Cards in this Set

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T/F:
Its not uncommon to see a patient on 15 to 20 drugs when suffering from AKF or CKF.
True, not uncommon usually 15-20 drugs
What is the focus of renal disease?
Management of complications and prevention of consequences
Name the organ systems effected by renal failure (5)
cardiac, vascular, dermatological,CNS, hematological, endocrine
What is the definition from the slides of chronic renal failure?
Progressive deterioration in renal function ultimately leading to irreversible nephron structural damage
CRF is based off the presence of ___/_____ for >3 months + a GFR of <_____ml/min/1.73m2
CRF is based off the presence of _proteinuria_/_albuminuria_ for >3 months + a GFR of <_90_ml/min/1.73m2
What are the GFR's for the 5 stages of CKD?
Stage 1: <90
Stage 2: 60-89
Stage 3: 30-59
Stage 4: 15-29
Stage 5 (ESRD): <15
What is the Cockcroft-Gault method of approximating GRF/CrCl?
Males:
(140-age)(TBW)/SCr72
Females multiple by .85
TBW up to 120% of IBW
otherwise use ABW:
IBW + [0.40(TBW-IBW)]
IBWM= 50+2.3(inches > 5ft)
IBWF=45+2.3(inches>5ft)
What is the equation for the 24 hour urine collection?
CrCl=UV/Pt
U=urine Cr
V=urine Volume
P=plasma Cr
t=time of collection
What are the most common causes of CKD in the US? (4)
DM, HTN, Glomerular nephoritis (GN), Polycystic kidney disease (PKD)
What are some susceptibility factors for CKD? (4)
Advanced age, low income or education (2), racial/ethnic minority
What are some initiation factors of CKD mentioned on the slide?
DM, HTN, GN, infections, ADRs and others
What are some progression factors that further kidney deterioration? (6 from slide)
Proteinuria, Hyperlipidemia, HTN, DM, obesity, Tobacco use
DM increasing the risk of developing CKD by what percent? What about Type 2?
40-50%
Type 2 have a 12 fold greater risk than nonDM
Agressive therapy in DM has been associated with a decrease in ____________
Agressive therapy in DM has been associated with a decrease in _risk for albuminuria_
What combo of factors leads to a 6 fold > risk of ESRD?
HTN+DM
T/F:
Early and agressive tx of HTN is associated with a decrease in progression of CKD
True that
What is considered nephrotic syndrome with proteinuria?
>5 gms/qd
When does treating proteinuria benefit the most?
With high levels of proteinuria
What are 2 characteristics of nephrotic syndrome as mentioned?
Proteinuria and hyperlipidemia
T/F:
The prevalence of hyperlipidemia decreases and renal function declines
False
The prevalence increases
What are some CV clinical presentations of CKD? (4)
HTN, hyperlipidemia, HF, angina pectoris
What are some CNS clinical presentations of CKD? (3)
Clouded sensorium, coma, seizures
What are some hematological presentations of CKD? (2)
Anemia, hemorrhage
What are some M.S. presentations of CKD? (2)
Renal osteodystrophy, osteoporosis
During ESRD what are some clincal presentations mentioned in the slides? (5)
decrease in thyroid, decrease in glucose (unable to clear insulin in ESRD), acidosis, DM, increase in PTH
T/F:
Some clincal presentations of CKD include: uremic syndrome, pruritus, altered fluids and electrolytes.
True, these are some "misc" clinical presentations
Generally, what are some emphasis on therapies known to slow renal deterioration? (3)
delay hemodialysis (improve pts QOL)
avoid tx that hasten renal det.
DC or minimize use of nephrotoxins
What is an important non drug tx approach in CKD?
decrease intake of PO4 and protein
For CKD treatment a no salt added diet is more restrictive in what risk factors?
HTN and edema
In Na restriction you can use what pharmalogical approach?
Use loop +/- a thiazide
Which thiazide is preferred in Na restriction?
Metolazone, it retains its diuretic properties even when CrCl is <30 ml/min
When is H2O restriction unnecessary when treating CKD?
If Na intake is "contolled" and stage < 5
T/F:
H2O restriction should be avoided in CKD when a pt is oliguric/anuric or ESRD.
True
What is the goal of K restriction in CKD?
50 to 80 mEq/day
When should avoid and not avoid NaHCO3 when restricting K in CKD?
Avoid: if pt is HTN or hyperkalemic
Not Avoid: when pt has acidosis
What is an approach to restricting K in CKD mentioned in the slide?
D/C or limit K retaining meds
T/F:
Loop diuretics are effective in restricting K in CKD
False, theyre actually ineffective
What is the agressive goal of bp for HTN in CKD w/o DM or proteinuria? What about with those disorders?
130/80 for just HTN
W/ DM or proteinuria its 125/75 mmHg
A goal of therapy in HTN in CKD is to minimize or eliminate ______
A goal of therapy in HTN in CKD is to minimize or eliminate _proteinuria_
These pharmacological treatments are 1st line in treating HTN in CKD while slowing the decline of renal function.
What is ACEI's and ARB's
ACEI's and ARB's are especially beneficial in these pt's, w/ or w/o HTN in CKD.
What is DM
Why should pt's be monitored in CKD in regards to HTN meds?
They can lead to ARF
What CCB is preferred in HTN for CKD? What are two examples of these class?
NDHP, diltiazem and verapamil
Why should an alpha agonist be avoided when taking a BB?
Can cause rebound HTN w/ poor compliance and sever bradycardia
What were then examples given of ACEI's?
Captopril, Enalapril, Lisonipril, Fosinopril, Trandolapril
What were then examples given of ARB's?
Losartan, Valsartan, Ibersartan, Candesartan
T/F:
BB mayb exacerbate renal dysfunction but are not really contraindicated in the tx of HTN in CKD.
True
What is the main MOA of BB in the tx of HTN in CKD?
decrease CO to decrease renal blood flow
Using water soluble agents such as ________ and _______ should be avoided when using BB to tx HTN in CKD because they can do what in the kidneys?
Using water soluble agents such as _atenolol_ and _nadolol_ should be avoided when using BB to tx HTN in CKD because they can _accumulate_ in the kidneys
ACEI's block the conversion of?
ANGI --> ANGII
ARB's block what receptor?
AT1
SCr is going to increase or decrease with a HTN medicine in CKD?
Increase up to 30-40% over 1st 3 months
When would you stop using an Rx for HTN in CKD in regards to CKD?
If increase in K developes
When do you start measuring Cr every 6 months when using a HTN Rx in CKD?
After check Cr and K every 1 to 4 weeks after starting until stable levels then every 6 months
What is metabolic acidosis?
Decrease in net acid excretion leading to acid accumulation
At what stage of CKD is metabolic acidosis clinically significant?
Stage 4
What are the clinical presentations of metabolic acidosis, mentioned in the slides? (5)
Exacerbates renal osteodystrophy
Decrease in Vit D synthesis
Fatigue (impairs O2 delivery)
Decrease in contractility (ionotrophic)
Increase in protein catabolism
What are the goals of tx in metabolic acidosis?
Normalize systemic pH (7.35-7.45) and HCO3 (22-26 mEq/L)
What is the normal pH range for a patient?
7.35-7.45
What is the normal HCO3 range in a patient?
22-26 mEq/L
What can be used to treat metabolic acidosis in a pt with CKD?
Citrate/citric acid solutions
Shohl's, Bicitra, Polycitra all cause an increase in what electrolyte to decrease metabolic acidosis?
Potassium
Citrate increases ______ when being used to treat M.A. in CKD.
Citrate increases _HCO3_ when being used to treat M.A. in CKD.
Citric Acid is converted to these two chemical compounds that allow the decrease in metabolic acidosis.
What is H2O and CO2
What should be avoided when using any citrate/citric acid solution?
Al
When using NaHCO3 in metabolic acidosis, what must be true of the pt in regards to HTN?
Their HTN must be controlled
What is renal osteodystrophy?
Soft tissue mestatic calcification (in the joints, blood vessels, kidneys, intestine, and eyes, etc)
Ca ppt into tissue causing hypocalcemia
PO4 is elevated in the blood causing hyperphosphotemia
This then leads to an increase in PTH which then causes Ca to be removed from the bones leading to osteodystrophy
What are some pulmonary consequences of renal osteodystrophy? (3)
decrease in pulmonary function test
pulmonary fibrosis
pulmonary HTN
What is a vascular consequence of RO?
organ ischemia
What are some M.S symptoms of RO?
pain, bone pain, myopathy, fatigue, tendon rupturre
What are some pulmonary sx of RO?
SOB, CP (chest pain)
What are some cardiac sx of RO?
CP, AMI, death
T/F:
The evidence of RO is amenable due to the quick onset of symptoms.
False:
The evidence of RO is not amenable, the onset is too slow and when symptoms come about its too late
What are the risk factors for RO? (4)
Hyperphosphatemia
Ca-P product > 55mm2/dL2
2ndary hyperparathyroidism
Excessive Ca intake
How is the Ca-P product calculated?
Ca level * PO4 level
What is the Ca-P product level at which mortality risk is increase?
<70 mm2/dL2
What 4 things mentioned in the slide can lead to excessive Ca intake, a risk factor of RO?
Diet
Dialysis
Ca containing P binding agents
Ca supplement
What are 3 general pharmacological tx for RO?
PO4 binders, Vit D, and calcimimetic
At what level of CrCl should a pt be at to initiate dietary PO4 restriction in regards to RO and CKD?
CrCl <60 ml/min
In PO4 restriction, other than protein, what can a pt limit in their diet?
meats, dairy, beans, dark cola, peanut butter, beer, and chocolate
What is the name of the surgery involved in RO for those pts resistant to therapy?
Parathyroidectomy
What needs to be done with PO4 binding agents in order to have maximal effect?
Take just before or with a meal
What is the MOA of a PO4 binding agent?
Bind to and sequester PO4 in the GI lumen so its not absorbed and thus excreted
What are some examples of PO4 binding agents (PBA)?
Ca salts
Aluminum salts
Non Ca/Al/Mg
When does Ca carbonate, a Ca salt (PBA), have a max effect? What do you do if there are ADR?
At acidic gastric pH
Give with a meal
What drugs should be avoided when using Ca carbonate (PBA)?
H2 receptor blocked and PPIs
What are the 3 Ca salts that are PO4 binding agents?
Ca carbonate, Ca acetate, Ca citrate
T/F:
Ca carbonate binds twice as much PO4 as Ca acetate.
False
Ca ACETATE binds twice as much PO4 as Ca CARBONATE
What is the advantage of Ca acetate over Ca carbonate in regards to gastric pH?
Ca acetate is more effective over a wider range of gastric pH than Ca carbonate
Why is there a greater likelihood of hypercalcemia with Ca acetate compared to Ca carbonate?
Ca acetate has greater systemic absorption
Ca citrate has _____ PO4 binding capacity and _____ Al absorption
Ca citrate has _Low_ PO4 binding capacity and _increased_ Al absorption
What therapeutic agent is used in combo with Ca salts that is also a PBA?
Non Ca/Al/Mg such as sevelamer and lanthanum carbonate (fairly expensive!)
When would a non Ca/Al/Mg PBA be used?
When pt arent responding to Ca salts or if the pt becomes hypercalcemic
The Al salt PBA are considered 3rd line. When should a pt be prescribed them?
If there is severe hyperphosptemia or in combo with Ca compounds or Sevelamer when response to the other single agents are inadequate
What is the limit of duration for Al salt PBAs?
</= 4 weeks
What are some consequences of Al salts?
Osteomalacia, encephalopathy, and anemia
During CKD and onward to RO, _______ can be used to increase GI absorption of Ca, decrease PTH, and increase renal PO4 absorption
During CKD and onward to RO, _Vitamin D therapy_ can be used to increase GI absorption of Ca, decrease PTH, and increase renal PO4 absorption
Vitamin D therapy minimizes the likelihood of?
hypercalcemia and hyperphosphotemia
What stage of CKD should Vitamin D be started?
Stage 3 or after
Can Vitamin D (such as calcitriol, paricalcitriol, or doxercalcefitriol) be administered with a calcimimetic (such as cinacalet)?
Yes
T/F:
Cinacalet, a calcimemtic, is approved for any stage of CKD.
False,
Only approved for Stage 3 and greater in CKD
What is the MOA of a calcimemetic?
Increases the sensitivity of calcium- sensing receptors of the PT gland to Ca thus supressing PTH secretions
Can cinacelet (calcimemetic) be administered with Ca salts (PBA) and sevelamer (PBA)?
Yes
What are the cutoffs of Hb for male and female for anemia?
Male <13mg/dl
Female <12mg/dl
Anemia in CKD is defined as?
The inability to produce erythropoeitin (EPO) due to renal insuffieciency
How much circulating EPO is produced by a normal functioning kidney?
90%
Hypoxia or a decrease in Hct leads to and increase in __________ production
Hypoxia or a decrease in Hct leads to and increase in _EPO production_
If Fe, FA, and B12 are WNL the inability to produce EPO results in a ____chromic, _____cytic anemia
If Fe, FA, and B12 are WNL the inability to produce EPO results in a _normo_chromic, _normo_cytic anemia
What GFR does anemia usually develope at?
</ 50-60 ml/min
The lifespan of a RBC in anemia is _______
The lifespan of a RBC in anemia is _shortened_
(from 120 days to 60 days)
What are some s&s of anemia?
dypsnea, fatigue, dizziness, HA, pallor, angina, CHF, mental state changes
What is the adaption phenomenon in anemia?
Where there are no symptoms present
If the RBC present as hypochromic (pale) and microcytic (smaller) then what kind of anemic deficiency does the pt have?
Fe deficiency
When RBC present as macrocytic (very large and immature) what type of anemic deficiency does the pt have?
B12 and/or FA (folic acid)deficiency
What are the goals of therapy for anemic pts with CKD?
Increase the O2 carrying capacity of RBC and minimize symptoms
In iron deficiency anemia (IDA) Serum Fe is insenstive
Transferrin sat'n is ___ normal
Ferretin is ____
TIBC is ____
In iron deficiency anemia (IDA) Serum Fe is insenstive
Transferrin sat'n is _below_ normal
Ferretin is _low_
TIBC is _high_
What are 4 oral iron tx for treating anemia in CKD?
Ferrous sulfate
Ferrous gluconate
Polysaccharides
Heme iron polypeptides
When is absorption best for oral iron agents?
On an empty stomach
What are some ADRs of oral iron agents? (4)
Constipation
Nausea
Abdominal cramping
Black stools
When are iron oral agents not useful?
When there is functional iron deficiency, w transferrin sat'n less than 20% but normal or elevated ferritin
What iron tx can be given IV?
Ferric gluconate, iron sucrose, iron dextran
What is the preferred route of administration in functional iron deficiency?
IV
IV iron tx can lead to what ADRs? (5)
allergic rxn (iron dextran)
hypotension
dizziness
dypsnea
HA
What should be given with Fe to prevent an Fe overload?
Deferoxamine
For megablastic (macrocytic) anemia, what should be prescribed?
FA and B12 supplement
What is the DOC for long term management of anemia?
ESA (epoetin alfa, darbepoetin)
What comorbidities are resistant to ESA tx? (8)
Fe deficiency, Al toxicity, bleeding, malnutrition, CA, chemo, HIV, infections
What are 2 ADRs of ESA?
HTN, seizures
What is the normal dosing for epoetin alfa?
50-100 units/kg IV/SC 3 times a week
What is the normal dosing for darbepoetin?
0.45 mcg/kg/week
Transfusion for anemic pts are reserved for what occassions? (3)
Acute symptoms
Major blood loss
Before surgery
T/F:
Hyperlipidemia slows the rate of decline of CrCl
True
T/F:
There is no known reversal therapy for established ARF
True
What is the focus of tx for ARF?
Supportive therapy, managing other diseases, D/c nephrotoxins
What is the definition of ARF?
Decrease in GRF over hours to days and accumulated waste products including Cr in urea
Abrupt increase of SCr >50%
or
Abrupt decrease of GFR >25%
Reduction in urinary output >6 hrs
Why is the cockcroft-gault equation not useful in ARF?
Because weight and CrCl is rapidly changing
What are the risk factors for ARF? (7)
age>60,preexisting renal, liver, CV/vascular, or lung disease, infection, hemorrhage, volume depletion, DM, male, nephrotoxins
What medications are considered nephrotoxic in ARF? (11)
Contrast media dyes, NSAIDs, chemo, ACEI or ARB, antiviral medicine, diuretics,cyclosporine/tacrolimus,AntiBs,amphoterecin B, metformin
What complication of ARF is the most common cause of death?
Infection
What type of CV complications are associated w ARF? (3)
CHF, increase/decrease of BP, Arrythmias
What are the electrolyte complications associated w ARF?
Increase K, PO4, Mg
Decreased/increased Na
Metabolic acidosis
What hematological complications are associated with ARF?
Hemorrhage (GI), anemia
What complication of ARF results in anorexia, N/V, MS changes and seizures or comas?
Uremic syndrome (the clinical syndrome associated with uremia)
Azotemia is a complication of ARF, what exactly is azotemia?
Elevation in circulating concentrations of nitrogenous waste products (i.e Cr and BUN)
Can have no clinical sx
What is functional ARF characterized by?
Decrease in GFR due to decrease in glomerular hydrostatic pressure
No structural damage
What is a common cause of functional ARF?
ACEI or ARB usage
T/F
Pre-renal ARF is considered azotemia
True
What are the characteristics of pre renal ARF?
renal parachymal hypoperfusion w/ or w/o hypotension
T/F:
In post renal ARF Na and Fe are elevated suggesting there is structural damage to the tubules
False,
Na and Fe are normal suggesting there is NO structural damage to the tubules
What are the compensatory responses in pre renal ARF? (4)
SNS, RAAS, afferent arteriolar vasodilation, efferent arteriolar vasoconstriction
If presented with Pre renal ARF, a pt should be administered fluid and/or D/C of offending meds except?
HF, cirrhosis, RAS
What type of ARF has direct structural damage to the kidney?
Intrinsic ARF
What in the lab values tells you that there is structural damage to the kidney?
Na and FE are increased showing no reabsorption taking place
What is the most common intrinsic ARF?
ATN (Acute tubule necrosis)
What is the flow of damage when tubular injury occurs?
cell necrosis-->loss of cells--> decrease in filtration--> fluid/electrolyte imbalance--> dilute urine--> decrease in Na reabsorption--> decrease in GFR
In ATN there is a ____ in Scr and a ____ in urine output
In ATN there is a _increase_ in Scr and a _decrease_ in urine output
What are the clinical phases of ATN? (4)
Polyuria
Oliguria
Maintenence/diuresis
Recovery
How does post renal ARF develop?
When theres an obstruction from the renal tubule to the urethra
What are some causes of Post renal ARF? (4)
Malignancy, BPH, neprolithiasis, tumor lysis syndrome
What drugs are related to the cause of post renal ARF?
Indinavir (HIV), sulfonamides, acyclovir, probenecid
For ARF, what could you do to decrease the nephrotoxicity of amphoterecin B if the pt needed to be on it?
Limit the use/slow infusion
use liposomal formulation
use fluconazole or itraconazole
T/F:
Aminoglycosides should be used 2-3 times a day for pts w ARF?
False, should be d/c or down to once a day
What is really important for pts to do before getting a cardiofxn scan with radiocontrast dyes?
Rehydration!
Na load w/ 5% dextrose better
D/C Metformin!
What does NAC (N-acetylcysteine) help prevent? What are the doses and circumstances?
Helps prevent ARF IF there is previous renal impairment
600mg po bid 2-4 days
1200 po bid 2 day
What are some non pharmalogical therapies for ARF? (4)
Fluid restriction
Remove obstruction (postrenal)
electrolyte management
Renal replacement tx (dialysis)
What are 2 renal replacement tx?
hemodialysis and peritoneal dialysis
What role does dopaminergic agonist play in ARF? What are the dosings?
Improve renal blood/plasma flow, not necessarily outcome
Dosing 0.5-3 ug/kg/min