CKD pt 2

Question 1

Vit D and secondary hyperparathyroidism (SHPT)

Answer 1

hyperphosphatemia + lack of kidney function –> no activation of Vit D –> decrease in calcium serum concentration –> triggers parathyroid gland –> more PTH secreted –> increase calcium mobilization

Question 2

treatment of SHPT drugs

Answer 2

ergocalciferol (stage 3/4)
calcitriol, paricalcitol, doxercalciferol (stage 5)
increase vit D concentrations and decrease PTH concentrations through negative feedback mechanism

Question 3

ergocalciferol (calciferol)

Answer 3

UNACTIVATED vit D2
for vit d insufficiency in CKD stage 3/4

Question 4

cholecalciferol

Answer 4

UNACTIVATED vit d3
for vit d insufficeincy in ckd stage 3/4

Question 5

calcitriol

Answer 5

activated vit d3 for CKD stage 5 and some stage 3/4
approved for pediatric usage
greatest risk of hypercalcemia (monitor for signs)
cheap

Question 6

signs and symptoms of hypercalcemia

Answer 6

fatigue
weakness
headache
NV
muscle pain
constipation

Question 7

paricalcitol

Answer 7

activated d2
same monitoring parameters as calcitriol
over 30% reduction in PTH
approved for peds
most favorable ADE profile
less calcemic activity

Question 8

doxercalciferol

Answer 8

activated vit D2
prodrug activated in the liver (so don’t use in pts with hepatic issues)
produced a more even serum concentration
over 30% reduction in PTH
higher incidence of hyperphosphatemia
lower incidence of hypercalcemia in comparison to calcitriol

Question 9

calcimimetic drugs

Answer 9

cinacalcet (sensipar)** type 2
etelcalcetide
contraindicated in hypocalcemia (do not use if Ca is below 7.5, wait until it reaches 8mg/dL

Question 10

cinacalcet (sensipar)

Answer 10

TYPE 2 calcimimetic agent
mimics the action of Ca by binding to Calcium sensing receptor (CaR) and inducing a conformational change to the receptor to trigger decrease PTH secretion via PT gland

Question 11

etelcalcetide

Answer 11

sensipar but via IV

Question 12

erythropoietin (EPO)

Answer 12

promotes production of mature red blood cells in the bone marrow
when there is too many red blood cells, it is suppressed via the hypoxia-inducible factor
anemia occurs when too few RBCs are circulating leading to increased transcription of EPO to account for it

Question 13

mechanisms of anemia development

Answer 13

decreased production EPO
uremia causes a decreased life span of RBCs
vitamin losses during dialysis (like folate, B12, and B6)
dialysis with loss of blood through dialyzer (hemolysis)

Question 14

signs and symptoms of anemia

Answer 14

fatigue
dizziness
headache
decrease cognition

Question 15

low MCV

Answer 15

iron deficiency
aluminum toxicity

Question 16

high MCV

Answer 16

folate deficiency
B12 deficiency

Question 17

normal MCV

Answer 17

could be signs of chronic disease
GI bleed
EPO deficiency

Question 18

treatment goals of anemia

Answer 18

reverse signs and symptoms of tissue oxygen deprivation and left ventricular hypertrophy
increase exercise tolerance and capacity
optimize survival
increase or quality of life

Question 19

monitoring parameters of anemia

Answer 19

Hb is best due to stability
should be monitoring annually in 3, biannually in 4, and q3m in 5 unless previously diagnosed
males - under 13
females - under 12

Question 20

iron supplementation in anemia

Answer 20

recommended if TSAT is under 30% and serum ferritin is under 500 ng/mL
monitor q3m
best absorbed in an acidic environment
food decreases absorption
should be separate from other meds by 2 hours
SE – stomach upset

Question 21

oral iron

Answer 21

will likely not be sufficient in correcting and maintaining iron stores for HD patients
may be used for CKD or PTD patients
NOT FOR STAGE 5
drugs –> ferrous salts (sulfate, gluconate, and fumerate)

Question 22

hepcidin

Answer 22

destroys FPN make it so that iron cannot be moved out of the duodenum

Question 23

IV iron

Answer 23

preferred route for CKD
drugs –> iron dextran, sodium ferric gluconate, iron sucrose, ferric carboxymaltose, ferumoxytol (feraheme)

Question 24

iron dextran

Answer 24

IV iron
test dose of 25mg needs to be done as dextran is a common allergy

Question 25

feraheme

Answer 25

interferes with MRI so should not be used for up to 3 months after second injection

Question 26

ESA

Answer 26

erythropoiesis stimulating agents used after all other correctable causes of anemia have been addressed although QOL benefits increase as the Hb increases, the incidence of CV AE also increases so do not use ESA to push Hb above 11.5 g/dL decrease dose by 1/2 if the pt has hepatic impairment do not give with strong CYP2C8 inhibitors (genefobrizil)

Question 27

ESA in stage 3-5ND

Answer 27

Hb under 10 g/dL Hb falling at a rapid rate needed to avoid blood transfusion

Question 28

ESA in stage 5D

Answer 28

start when Hb is between 9 and 10 g/dL

Question 29

ESA drugs

Answer 29

recombinant human erythropoietin (epogen) darbepoetin alfa (aranesp) methoxy polyethylene glycol - epoetin beta (mircera)

Question 30

ESA SE

Answer 30

pure red cell aplasia (PRCA) HTN

Question 31

PRCA with ESAs

Answer 31

antibodies develop to erythropoietin discontinue drug permanently

Question 32

HTN with ESAs

Answer 32

23% of patients will seen an increase not a reason to not give the drug even if they have pre-existing HTN (more important to keep them alive with this)

Question 33

causes of ESA therapy failure

Answer 33

lack of vitamins or iron aluminum toxicity active bleed drug induced bone marrow suppression acute inflammation or infection

Question 34

new therapy for anemia of CKD

Answer 34

HIF inhibitors, PHI inhibitors, or HIF-PHIs Daprodustat for patients who have been on dialysis for at least 4 months

Question 35

daprodustat

Answer 35

approved in feb 2023 injection leads to more adherence increased CV effect thugh

Question 36

acid base disorders

Answer 36

ESRD patients cannot excrete H+ ions and develop metabolic acidosis

Question 37

treatment of acid base disorders

Answer 37

1) dialysis - increase bicarbonate in dialysate (usually corrects problem) 2) Shohl's solution 3) sodium bicarbonate tablets 4) administer over several days

Question 38

uremic bleeding

Answer 38

common complication of CKD patients not fully understood but could be partially due to impaired binding of Von Willebrand factor to platelet membrane glycoprotein receptors

Question 39

diabetic kidney disease

Answer 39

excess glucose in the blood enters the glomerular cells and alters ability of glomerulus to filter waste products from blood appropriately

Question 40

microalbuminuria

Answer 40

best predictor of DKD (also risk factor for heart attack and stroke)

Question 41

treatment of DKD

Answer 41

SGLT2 inhibitors (flozins) and metformin to control BG if eGFR is above 30 life style mods HgbA1 below 6.5 to 8% in non-dialysis dependent CKD antihypertensives (ACE-i and ARBs to decrease proteinuria in addition to lowering BP)

Question 42

HTN in CKD

Answer 42

target SBP below 120 mmHg (weak evidence) salt intake below 2 g/d of sodium or 5 g/d of sodium chloride drug of choice: 1) ACE inhibitors 2) ARBs 3) diuretics

Question 43

hyperlipidemia

Answer 43

common in CKD patients due to altered metabolism of serum lipoproteins elevated serum LDL concentrations