Exam 2 Flashcards
what is the Cockroft and Gault equation for MEN
CrCl = (140-age)IBW/(SCr72)
what is the Cockroft and Gault equation for WOMEN
CrCl = ((140-age)IBW/(SCr72))*0.85
what is Cockroft and Gault used for
dosing drugs
what is MDRD
Modification of Diet in Renal Disorders
what is MDRD used for
staging kidney disease
IBW for females
45.5+2.3(inches over 5 ft)
IBW for males
50+2.3(inches over 5 ft)
what is the complication from a build up of excess waste products
Uremia
what is the definition or uremia
a cluster of sx which is associated with ESRD from any cause
cause of Sx in uremia
due to the accumulation of waste molecules in the blood that are normally removed by the kidney
how is uremia monitored
BUN
what effects happen to the body from uremia (hint: there are 8)
- CNS: Encephalopathy
- EENT: uremic fetor (pee breath)
- Pulmonary: non-cardiogenic pulmonary edema from volume overload
- Cardio: sodium retention, volume overload, LVH
- GI: anorexia, N, constipation, metallic taste
- musculoskeletal: mineral and bone disorder and restless leg syndrome
- anemia: EPO deficiency
- Skin frost: uremic frost
do you fluid restrict patients that have fluid retention from chronic kidney disease?
not generally if Na intake is controlled. AVOID large amts of water
will diruetics work without a funcitioning kidney
NO
what two stages of chronic kidney disease can you use diuretics in?
Stage 3 and 4
with what CrCl do thiazides become ineffective
<30 ml/min
what diuretic would work with CrCl work when CrCl < 30ml
loops!
why is furosemide oral dosing usually twice the IV dose
oral bioavailability is usually about 50%
as renal function declines, and you max loop dose, what drug class might be added on to overcome diuretic resistance
thiazide!
is there a need to severely Na restrict patients that have a Na imbalance
use IV saline with caution
Make pts aware of hidden Na content food (hot dogs, canned soups…)
what would you restrict a K imbalance patient’s diet to
3 grams per day
What electrolyte irregularity is a problem for nearly all ESRD patients
Hyperphophatemia
What must phosphate binders always be given with
given with meals
What are the three examples of calcium containing phosphate binders we discussed in class
Calcium carbonate (Tums) Calcium acetate (PhosLo)
why does calcium acetate produce fewer hypercalcemic events when compared to calcium carbonate
when given at the same elemental dose, calcium acetate will bind twice as much phosphate compared to calcium carbonate
what are the examples of non-calcium containing phosphate binders
Sevelamer carbonate (renvela)
Lanthanum carbonate (fosrenol)
sucroferric oxyhydroxide (velphoro)
ferric citrate (auryxia)
aluminum hydroxide (amphojel)
magnesium carbonate (Mag-Carb)
what should dietary phosphorus intake be restricted to if elevated phosphorus
800 to 1000 mg per day
how does hyperphosphatemia cause secondary hyperparathyroidism
since the kidneys are unable to activate vitamin D there is a subsequent decrease in serum Ca levels. This triggers the parathyroid gland to secrete more parathyroid hormone
when would you use ergocalciferol in CKD patients
stage 3 and 4
when would you use cholecalciferol in CKD patients
stage 3 adn 4
what class of drugs would you use in CKD stage 5 and some stage 3 and 4
Calcitriol (Rocaltrol and Calcijex), Paricalcitol (Zemplar), Doxercalciferol (Hectorol)
monitoring parameters for Calcitriol
S/Sx of hypercalcemia (fatigue, weakness, headache, nausea, vomiting, muscle pain, and constipation)
why might paricalcitol be used over other drugs
more favorable ADE profile, less calcemic activity compared to calcitriol
why might you not want to use Doxercalciferol in a liver disease patient
it is a prohormone that is activated in the liver
what electrolyte imbalance does doxercalciferol have a higher risk for
hyperphosphatemia
what drug class is cinacalcet (sensipar) in? what is it used for?
calcimimetic, mimics the action of calcium but does so by binding to the calcium sensing receptor and inducing a conformational change to the receptor, triggering the parathyroid gland to decrease PTH secretion
what are calcimemetic agents contraindicated?
hypocalcemia
what are the basic monitoring parameters for CKD stage 3
Calcium: every 6 - 12 months
Phosphorus: every 6 - 12 months
25(OH)D: Baseline
Intact PTH
what are the basic monitoring parameters for CKD stage 4
Calcium: every 3-6 months
Phosphorus: every 3-6 months
25(OH)D: Individualized
Intact PTH: every 6-12 months
what are the basic monitoring parameters for CKD 5D
Calcium: every 1-3 months
Phosphorus: every 1-3 months
25(OH)D: individualized
intact PTH: every 3-6 months
what are the basic monitoring parameter goals for CKD
Calcium: 8.5-10.5 mg/dL Phosphorus: 2.5-4.5 mg/dL 25(OH)D: ~ 30 ng/dL Intact PTH: non-dialysis = 11-54pg/mL dialysis = 100-500 pg/mL
nearly all ESRD patients will develop what kind of blood disorder
anemia
what are the 4 ways a ESRD patient may contract anemia
- decreased production of erythropoetin
- uremia causes a decreased life span of red blood cells
- vitamin losses during dialysis - folate, B12, B6
- dialysis - loss of blood through dialyzer (hemolysis)
anemia S/Sx
- fatigue
- dizziness
- HA
- decreased cognition
why is Hb the be assessment parameter for anemia
due to its increased stability over the hematocrit
how many times a year should you monitor Hb in CKD3
once
how many times a year should you monitor Hb in CKD 4-5ND
twice per year
when should you monitor Hb in CKD 5D
every 3 months
why do you monitor Hb in CKD patients
as a means to screen for anemia
when would you diagnose anemia in females
Hb < 12 g/dL
when would you diagnose anemia in males
Hb < 13 g/dL
when would you suggest iron supplementation in patients with anemia
if TSAT < 30% and serum ferritin < 500 ng/mL
when can you use oral iron in anemic patients
in stages 3-4 (only used for CKD patients or peritoneal dialysis patients)
what dose of elemental iron must be given per day
200 mg
what route is preferred for CKD 5D patients
intravenous
which iron supplement requires a 25 mg test dose?
iron dextran (infed, dexferrum)
what diagnostic test do you have to be careful with when patients are taking feraheme iron supplementation
magnetic resonance imaging (3 months after second injection)
what does high molecular weight iron carry a higher incidence of?
anaphylaxis
when do you start ESAs (erythropoiesis stimulating agents)
after all other correctable cause of anemia have been addressed
when is it suggested to begin ESAs for CKD 3-5ND
Hb < 10 g/dL; Hb falling at a rapid rate; needed to avoid blood transfusion
when is it suggested to begin ESAs for CKD 5D
start when Hb is between 9 and 10 g/dL
as Hb increases the incidence of what adverse event also increases
cerebrovascular adverse events
do not use ESAs to push Hb above what
11.5 g/dL
what are the ESA drugs
epogen, aranesp, and mircera
what are the adverse effects of the ESA drugs
pure red cell aplasia (antibodies develop to erythropoietin) and HTN
what are the reasons that ESA therapy might fail
- lack of vitamins or iron
- aluminum toxicity
- active bleed
- drug induced bone marrow suppression
- acute inflammation or infection
when do acid/base disorders arrise
usually when bicarb < 20 mEq/L
ESRD patients cannot excrete H+ ions and develop what
metabolic acidosis
what are the protein nutritional requirements for CKD 3 and 4
1.2 g/kg/day
in what patient would you use water soluble vitamin replacement
for dialysis patients
what is DKD and mechanism of action
diabetic kidney disease, glucose in the blood enters the glomerular cells and through multiple biochemical mechanisms alters the ability of the glomerulus to filter waste products from the blood appropriately
what is microalumineria
it is one of the best predictors of DKD
how to treat DKD
SGLT2 inhibitors and metformin
what GFR limit does treating microalbuminuria have
you can treat if GFR > 30
what is an AV fistula
a surgically created anastamosis between an artery ad a vein, usually located in the forearm between the radial artery and cephalic vein used for HD access
what is an AV graft
an alternate to a fistula, the graft is created by surgically connecting an artery and vein with a polytetrafluoroethylene tube
what are the indications of RRT
(A, E, I, O, U) A: acid/base balance E: electrolyte balance I: intoxication O: overload (fluid) U: uremia
what are the two goals of dialysis
- general rule is to initiate when BUN > 100, SCr > 10
2. removal of “middle molecules” such as beta2microglobulin, uric acid, creatinine, etc…
what are the substances not removed in hemodialysis
- High Vd
- High lipophilicity
- Large molecular weight
- Highly protein bound
what are the two ways you could measure the effectiveness of dialysis sessions
1. Kt/V: measure of fraction of TBW that is cleared of urea GOAL: 1.4 (the higher the better) 2. urea reduction ratio: measure of reduction of BUN GOAL >= 70%
what are some common complications of hemodialysis
- hypotension
- pruritus
- muscle cramps
what is peritoneal dialysis
a form of dialysis that uses the peritoneal membrane as a dialysis membrane
what is peritoneal dialysis mostly reserved for
pediatrics or ESRD patients already receiving PD
what are the 4 different types of peritoneal dialysis
CAPD, CCPD, NIPD, TPD
S/Sx of peritonitis
- cloudy effluent
- abdominal pain
- fever
- N/V
- Chills
- abdominal tenderness
what is the predominant organism in peritonitis
staph epidermidis (40-50%)
how to treat peritonitis
1st gen cephs (cefazolin, cephalothis Gm(+) coverage)
3rd gen cephs (ceftazidime Gm(-) coverage + pseudomonas) OR Aminoglycosides (gentamycin, tobramycin Gm(-) + pseudomonas (*NOT USED FOR THOSE WITH RESIDUAL RENAL FUNCTION*)
what are the three routes that Tx can be administered
intraperitoneal, IV, oral
what can you use IP route if peritonitis present
- infection is usually limited to the 1st few layer of the mesothelium, confined to the peritoneal cavity
- perionitis - N/V which can eliminate the oral route
- pts may have poor vascular access (that’s why they are on PD) so it would be prohibited
what is CRRT primarily used for
acute renal failure
why were contiuous renal replacement therapy developed
for patients who could not tolerate regular hemodialysis sessions
can you use cockroft and gault in AKI patients
NOOOOOOOOOOOO
why is CrCl not accurate in AKI patients
- it may be changing rapidly
2. other waste products build up out of proportion to SCr rise
what are the two reasons someone can acquire AKI
Community acquired and hospital acquired
what is azotemia
an elevation in nitrogenous waste products which leads to the clinical syndrome uremia
what is prerenal azotemia
hypoperfusion of the kidney
what is functional ARF
a decrease in the glomerular hydrostatic pressure which leads to a decrease in glomerular filtration rate
what is functional ARF caused by
NSAIDs and ACE inhibitors
what is acute intrinsic renal failure
damage to the kidney itself
what is an example of a post renal obstruction
kidney stone
what monitoring parameters do you look at in AKI (since you can’t look at SCr)
- patient’s weight
- blood pressure
- urine output
a) acute anuria (<50 ml/24 hrs)
b) oliguria (<400 ml/24 hrs)
c) non-oliguria (>400 ml/24 hrs) - urinalysis
a) specific gravity (if high = prerenal)
b) hematuria, proteinuria (intrinsic)
c) microscopic examination ((+) for RBCs and casts = injury) - FE(na) - fractional excretion of sodium
what is the numerical difference between PR or functional AKI and intrinsic damage
if < 1% : PR or functional AKI
if >= 1% : intrinsic damage
how do you prevent an AKI
- use less nephrotoxic agent
- hydration
- sodium loading
- identify patients at risk
a) older adults
b) patients with abnormal renal function or diabetes
what are the goals of treating an AKI
- remove the primary cause of AKI
- limit further nephrotoxin exposure
- accelerate the recovery
what is the supportive therapy for AKI
- if critically ill, may need insulin therapy
- nutritional needs
a) total energy intake 20-30 kcal/kg/day
b) protein requirements vary, may need up to 1.7 g/kg/day for CRRT patients in hypercatabolic states
c) KDIGO does not support the use of low-dose dopamine, fonoldopam or atrial natriuretic peptide for prevention or treatment of AKI
d) avoid amino glycosides - Volume control
a) CRRT
b) diuretics (ONLY if urine output)
what are the two common nephrotoxins emphasized in class
NSAID/Cox 2 inhibitors and ACEs/ARBs
what is the MOA of AKI with NSAID/Cox 2 inhibitors
there is a decreased synthesis of renal vasodialator prostaglandins and afferent vasoconstriction resulting in reduced renal perfusion and filtration pressure
is Tylenol AKI reversible
typically yes
what is different about aminoglycoside AKI that other AKI
the rise in SCr usually occurs 5 - 10 days after the start of therapy
how do ACEs/ARBs cause AKI
vasodilation of the efferent arterioles resulting in decreased filtration pressure, lowering GFR and urine ouput
can PPIs (proton pump inhibitors) cause AKI
yes - by actue interstitial nephritis - its often reversible but can progress to CKD
what is criteria for diagnosis of diabetes
A1C >= 6.5%
OR
Fasting plasma glucose (FPG) >= 126 mg/dL
OR
2-h plasma glucose >= 200 mg/dL during an OGTT
OR
Random plasma glucose >= 200 mg/dL
what is the basic understanding of Type 1 Diabetes Mellitus
lose the ability to secrete insulin in response to glucose
