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Therapeutics 2 - Exam 1 > CKD pt 2 > Flashcards

CKD pt 2 Flashcards

Shepler 9-14

1
Q

Vit D and secondary hyperparathyroidism (SHPT)

A

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

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2
Q

treatment of SHPT drugs

A

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

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3
Q

ergocalciferol (calciferol)

A

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

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4
Q

cholecalciferol

A

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

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5
Q

calcitriol

A

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

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6
Q

signs and symptoms of hypercalcemia

A

fatigue
weakness
headache
NV
muscle pain
constipation

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7
Q

paricalcitol

A

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

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8
Q

doxercalciferol

A

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

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9
Q

calcimimetic drugs

A

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

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10
Q

cinacalcet (sensipar)

A

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

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11
Q

etelcalcetide

A

sensipar but via IV

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12
Q

erythropoietin (EPO)

A

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

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13
Q

mechanisms of anemia development

A

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)

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14
Q

signs and symptoms of anemia

A

fatigue
dizziness
headache
decrease cognition

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15
Q

low MCV

A

iron deficiency
aluminum toxicity

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16
Q

high MCV

A

folate deficiency
B12 deficiency

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17
Q

normal MCV

A

could be signs of chronic disease
GI bleed
EPO deficiency

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18
Q

treatment goals of anemia

A

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

19
Q

monitoring parameters of anemia

A

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

20
Q

iron supplementation in anemia

A

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

21
Q

oral iron

A

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)

22
Q

hepcidin

A

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

23
Q

IV iron

A

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

24
Q

iron dextran

A

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

25
Q

feraheme

A

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

26
Q

ESA

A

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)

27
Q

ESA in stage 3-5ND

A

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

28
Q

ESA in stage 5D

A

start when Hb is between 9 and 10 g/dL

29
Q

ESA drugs

A

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

30
Q

ESA SE

A

pure red cell aplasia (PRCA)
HTN

31
Q

PRCA with ESAs

A

antibodies develop to erythropoietin
discontinue drug permanently

32
Q

HTN with ESAs

A

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)

33
Q

causes of ESA therapy failure

A

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

34
Q

new therapy for anemia of CKD

A

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

35
Q

daprodustat

A

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

36
Q

acid base disorders

A

ESRD patients cannot excrete H+ ions and develop metabolic acidosis

37
Q

treatment of acid base disorders

A

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

38
Q

uremic bleeding

A

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

39
Q

diabetic kidney disease

A

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

40
Q

microalbuminuria

A

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

41
Q

treatment of DKD

A

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)

42
Q

HTN in CKD

A

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

43
Q

hyperlipidemia

A

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

Therapeutics 2 - Exam 1 (6 decks)

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