Renal Disease Flashcards
1
Q
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MOA:
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Max dose:
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Monitoring:
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Drug-Drug/Food interactions:
A
Class:
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2
Q
ileus:
A
- inability of the intestine (bowel) to contract normally and move waste out of the body.
3
Q
(AKI): Acute Kidney Injury-
A
- a sudden loss of kidney function due to a non-renal condition (e.g. drugs). Often reversible (temporary) but can be permanent if the precipitating condition is not corrected.
- A common cause is dehydration (can present with BUN:SCr > 20:1 plus decreased urine output, dry mucus membranes, tachycardia.
4
Q
(CKD) Chronic Kidney Disease-
A
- a progressive loss of kidney function over months to years.
- The degree of kidney function is measured by the glomerular filtration rate (GFR) or creatinine clearance (CrCl), and by how much albumin is in the urine.
5
Q
Kidney Failure [End-Stage Renal Disease (ESRD)]-
A
- Total and permanent kidney failure.
- Fluid and waste accumulate.
- Requires Dialysis (or transplant) is needed to perform the functions of the kidneys.
6
Q
The most common causes of CKD are _______ and _________.
A
diabetes AND hypertension
7
Q
Proximal Tubule: the area in nephron where maximal reabsorption occurs*
large amounts of _____________ are reabsorbed here.
Blood pH is regulated by the exchange of ___________ and _________ ions.
Other ions and substances reabsorbed from the proximal tubule back into the blood include:
A
Ca, Cl, Na, and H2O are reabsorbed into the blood.
hydrogen ions and bicarbonate (HCO3) ions
K+, glucose, amino acids, vitamins, urea, choline
8
Q
Drugs that work here at the proximal tubule include:
A
SGLT2 inhibitors
9
Q
Descending Loop of Henle:
- as filtrate moves down the descending loop of Henle, ________ is reabsorbed into the blood.
-Nothing else is reabsorbed at this point, so the concentration of Na and Cl in the filtrate increases.
” So in the descending limb, __________ is mainly being reabsorbed, which leads to the filtrate becoming more concentrated.”
A
water
water
10
Q
Ascending Loop of Henle:
- as the filtrate moves up the ascending loop of Henle, ___1_______ is reabsorbed back into the blood but not _____2_____.
- If _______3_________ is present, water passes through the walls of the ascending limb and is reabsorbed into the blood; less water is then excreted into the urine
Electrolytes are reabsorbed at the ascending loop of Henle and are reabsorbed back into the blood, these include: _______4_______
A
1) Na, Cl ions are reabsorbed back into the blood
2) water usually.
3) (ADH) antidiuretic hormone
4) Na, Cl, Ca, K, Mg, NH4
11
Q
Drugs that work at ascending limp of Henle:
A
Loop diuretics:
- inhibit the Na/K pump. by blocking the pump, this causes less Ca reabsorption back into the blood, leading to Ca depletion.
- less Na is reabsorbed back into the blood. This increases the filtrate concentration of Na causing less water to be reabsorbed.
- Long-term use of loop diuretics can decrease done density because of this.
12
Q
Distal Convoluted Tubule:
- farthest point away from the entry point of nephron
- is involved in regulating K, Na, Ca and pH
A
13
Q
Drugs that work at Distal Convoluted Tubule:
A
Thiazide diuretics:
- inhibit the Na-Cl pump in the distal convoluted tubule.
- only about 5% of Na is reabsorbed here, making thiazide diuretics weaker than loops.
- thiazide diuretics increase Ca reabsorption at the Ca pump in the distal convoluted tubule. “ So long term use of thiazide diuretics has a protective effect on bones.”
Potassium (K) sparring diuretics:
Aldosterone Antagonists:
14
Q
Collecting Duct:
- is the final site of water and electrolyte balance
- is a network of tubules and ducts that connect the nephrons in each kidney to a ureters.
- is involved with water and electrolyte balance, which is affected by levels of ADH “antidiuretic hormone” also called vasopressin, and aldosterone.
A
15
Q
Drugs that work in collecting duct:
A
Potassium (K) sparring diuretics:
Aldosterone Antagonists: spironolactone and eplerenone
- which do the opposite of aldosterone, decrease reabsorption of Na and H2O, and increase reabsorption of K.
16
Q
Aldosterone:
Works in the distal convoluted tubule & collecting duct to increase ____________ and __________ reabsorption and decrease _________ reabsorption.
A
Na and water
potassium
17
Q
Select Drugs that Cause Kidney Disease:
A
Aminoglycosides
Amphotericin B
Cisplatin
Cyclosporine
Loop Diuretics
NSAIDs
Polymyxins
Radiographic contrast dye
Tacrolimus
Vancomycin
18
Q
Risk Factors for Drug Induced Kidney Disease:
A
- multiple nephrotoxic drugs
- existing kidney disease
- decreased blood flow to the kidneys (heart failure, dehydration, hypotension)
- elderly
19
Q
Estimating Kidney Function:
Blood Urea Nitrogen (BUN): urea is a waste product of protein metabolism.
Creatinine: a waste product of muscle breakdown
normal serum creatinine (SCr) range is ________.
A
0.6-1.3mg/dL
20
Q
As Kidney function declines:
BUN will ______________
CrCl will ________________
SCr will _____________
A
BUN will increase.
CrCl will decrease.
SCr will increase.
21
Q
The accuracy of Creatinine-based estimation equations is decreased when a patient has __________.
A
very low muscle mass, which is often the case in frail elderly patients
(low muscle mass = low SCr)
This can lead to an overestimation of CrCl and inappropriate drug dosing for the patients true kidney function.
22
Q
A GFR < 60 mL/min/1.73m2 and/or albuminuria (ACR or AER > or = to 30) indicates that the patient has ________
A
Chronic Kidney Disease
albumin creatinine ratio (ACR)
albumin excretion rate (AER)
23
Q
An ACE inhibitor or ARB are 1st line for patient with CKD, hypertension and albuminuria (with or without diabetes).
Normal SCr increase up to 30%. This is expected, and treatment should not be stopped. If SCr increases by > 30% the treatment should be discontinued, and the patient will generally be referred to a nephrologist.
Do NOT Use ACE inhibitors and ARBs together.
They increase potassium (K), which can result in hyperkalemia.
Monitor SCr and K
The SCr and K should be monitored 1-2 weeks after initiating.
Patients should be counseled to avoid potassium supplements and salt substitutes (KCl).
A
ACE inhibitors and ARBs For albuminuria
Who?
All patients with albuminuria
Why?
To prevent kidney disease progression
How?
Inhibit RAAS causing efferent arteriolar dilation.
What?
Reduce pressure in the glomerulus.
24
Q
Patients with advanced kidney disease require monitoring of _______________
A
(PTH) parathyroid hormone,
phosphorus (phosphate, PO4),
Ca, and
Vitamin D levels
25
The Complications of (CKD) Chronic Kidney Disease:
The interactions of Ca, PO4 and Vitamin D in CKD are complex.
- (PO4) phosphate levels increase (because the kidneys ________1________)
- Vitamin D cannot be activated by the kidney, causing ____2____
- Both high (PO4) phosphate and low calcium cause ___3__
In a patient with healthy kidneys, PTH would cause the kidneys to increase calcium resorption, but in CKD this is not possible, and calcium is pulled from the bones, leading to bone demineralization and increased fractures. Normally, when calcium levels return to normal, PTH release is shut down, but the chronically high PO4 levels continue to stimulate ____4____.
In CKD, the kidneys produce less ____5___ resulting in decreased ____6___ production in the bone marrow which causes anemia.
1- cannot eliminate excess PO4 absorbed from the diet.
" Phosphate levels increase. These high levels of phosphate signal to the parathyroid gland to increase PTH."
2- dietary calcium absorption to decrease.
" since the kidneys cannot activate Vitamin D, there is decreased calcium levels in the blood serum. This signals again to the parathyroid gland, to increase PTH"
3- increased release of PTH
4- PTH release and hypercalcemia can persist, causing calcification and cardiovascular disease.
5- erythropoietin
6- RBC
26
In healthy kidneys, the kidneys activate vitamin D which helps us absorb calcium.
27
An increase in PTH, signals to the kidneys to reabsorb more ___1___.
In a patient with CKD, the kidneys cannot reabsorb more __2__. So instead, the PTH starts signaling to pull the ___3______ from the ____4_.
1- calcium into the blood, since the calcium in the blood is low.
2- calcium.
3-calcium
4- bones
" so patients with CKD can have bone fractures occur along with other complications if this is not corrected"
28
Hyperphosphatemia (PO4) Treatment:
- restrict diet (avoid dairy products, cola, chocolate and nuts)
Phosphate binders: (3 types)
- aluminum based
- calcium based: FIRST LINE
- aluminum and calcium free
29
Hyperphosphatemia contributes to chronically elevated PTH levels and must be treated to prevent ________ and _________
bone disease
fractures
30
Phosphate binders:
work by -
If a missed dose-
blocking the absorption of dietary PO4 by binding to it in the intestine.
They are taken prior to (or at the start of) each meal.
If a dose is missed (and the food is absorbed), the phosphate binder should be skipped, and the patient should resume normal dosing at the next meal or snack.
31
32
aluminum hydroxide
Class:
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aluminum based phosphate binder
Class: phosphate binder
Indications: hyperphosphatemia
MOA: drug blocks the absorption of dietary (PO4) phosphate by binding to it in the intestine.
Dosage forms: suspension
Dosing: 300-600mg PO TID with meals
**treatment limited to 4 weeks** or can get aluminum accumulation leading to aluminum toxicity, which is toxic to bone and CNS
Contraindications:
Warnings:
Side Effects:
aluminum intoxication, "dialysis dementia", osteomalacia, constipation, nausea
Monitoring:
Ca, PO4, PTH, signs and symptoms of aluminum toxicity
Pearls/Notes:
- potent, use short term. "Rarely used due to the risk of aluminum accumulation (which can cause nervous system and bone toxicity). Treatment duration is limited to 4 weeks"**
- toxic to bone and CNS
- Used LAST LINE essentially
- typically used in hospital setting when there is a need to lower phosphate level to a safer range urgently
Drug-Drug/Food interactions:
*- levothyroxine
*- quinolones and tetracyclines
*- oral bisphosphonates
*- Others
33
34
Phoslyra
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Calcium (Ca) Acetate
Calcium-based phosphate binder: First line
Class: phosphate binder
Indications: hyperphosphatemia CKD
MOA: drug blocks the absorption of dietary (PO4) by binding to it in the intestine.
Dosage forms: tablet, capsule, solution
Dosing: 1334mg PO TID with meals, titrate based on (PO4) levels
Contraindications:
Warnings:
Side Effects:
*Hypercalcemia, constipation, nausea*
Monitoring:
Ca, PO4, PTH
Pearls/Notes:
- hypercalcemia, is especially problematic with concomitant use of vitamin D (due to increased calcium absorption)
- constipation
- Calcium acetate binds more dietary phosphorus on an elemental calcium basis compared to calcium carbonate
Drug-Drug/Food interactions:
*- levothyroxine
*- quinolones and tetracyclines
*- oral bisphosphonates
*- others
35
PhosLo*
Class:
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Calcium (Ca) Acetate
Calcium-based phosphate binder: First line
Class: phosphate binder
Indications: hyperphosphatemia CKD
MOA: drug blocks the absorption of dietary (PO4) by binding to it in the intestine.
Dosage forms: tablet, capsule, solution
Dosing: 1334mg PO TID with meals, titrate based on (PO4) levels
Contraindications:
Warnings:
Side Effects:
*Hypercalcemia, constipation, nausea*
Monitoring:
Ca, PO4, PTH
Pearls/Notes:
- hypercalcemia, is especially problematic with concomitant use of vitamin D (due to increased calcium absorption)
- constipation
- Calcium acetate binds more dietary phosphorus on an elemental calcium basis compared to calcium carbonate
Drug-Drug/Food interactions:
*- levothyroxine
*- quinolones and tetracyclines
*- oral bisphosphonates
*- others
36
Tums
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calcium carbonate
Calcium-based phosphate binder: First line
Class: phosphate binder
Indications: hyperphosphatemia
MOA: drug blocks the absorption of dietary PO4 by binding to it in the intestine
Dosage forms: tablet, chewable tablet
Dosing: 500mg PO TID with meals (Can vary with formulation), titrate based on PO4 levels
Max dose:
Contraindications:
Warnings:
Side Effects:
*Hypercalcemia, constipation, nausea
Monitoring:
Ca, PO4, PTH
Pearls/Notes:
total daily dose of elemental calcium should be less than < 2000mg (from diet and supplements)
Drug-Drug/Food interactions:
*- levothyroxine
*- quinolones and tetracyclines
*- oral bisphosphonates
*- others
37
Velphoro
Class:
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sucroferric oxyhydroxide
Class: Al free & Ca free Phosphate Binder
Indications: Hyperphosphatemia CKD
MOA:
drug blocks the absorption of dietary PO4 by binding to it in the intestine
Dosage forms: chewable tablet
Dosing: 500mg PO TID with meals, titrate based on PO4 levels
Contraindications:
Warnings:
Side Effects:
diarrhea, constipation, discolored stool(black)
Monitoring:
iron, ferritin, PO4, PTH
Pearls/Notes:
- iron based products, absorption is minimal with sucroferric oxyhydroxide
- no aluminum accumulation, less hypercalcemia, but more expensive
Drug-Drug/Food interactions:
*- levothyroxine should NOT be used with sucroferric oxyhydroxide
*- quinolones and tetracyclines
*- oral bisphosphonates
*- others
- doxycycline should be 1 hour before
-
38
Auryxia
Class:
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ferric citrate
Class: Al free & Ca free Phosphate Binder
Indications: Hyperphosphatemia CKD
MOA:
drug blocks the absorption of dietary PO4 by binding to it in the intestine
Dosage forms: chewable tablet
Dosing: 2 tablets (420mg) PO TID with meals, titrate based on PO4 levels
Contraindications:
Warnings:
Side Effects:
diarrhea, constipation, discolored stool(black)
Monitoring:
iron, ferritin, TSAT* (only with ferric citrate), PO4, PTH
Pearls/Notes:
- iron based products
- no aluminum accumulation,
-less hypercalcemia,
-but more expensive
Drug-Drug/Food interactions:
*- levothyroxine
*- quinolones and tetracyclines
*- oral bisphosphonates
*- others
*- doxycycline should be 1 hour before
*- ciprofloxacin should be separated by 2 hours from ferric citrate**
39
Fosrenol
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lanthanum carbonate
Class: Al free & Ca free Phosphate (PO4) Binder
Indications: hyperphosphatemia CKD
MOA: drug blocks the absorption of dietary PO4 by binding to it in the intestine. They are taken just prior to (or at the start of) each meal.
Dosage forms: chewable tablet, powder
Dosing: 500mg PO TID with meals, titrate based on PO4 levels. Must chew tablet thoroughly to reduce risk of severe GI adverse effects.
- Use powder if unable to chew tablets
Contraindications:
** GI obstruction, fecal impaction, ileus**
ileus (inability of the intestine (bowel) to contract normally and move waste out of the body.
Warnings:
GI perforation
Side Effects:
*Nausea/vomiting, diarrhea, constipation, abdominal pain
Monitoring:
Ca, PO4, PTH
Pearls/Notes:
Drug-Drug/Food interactions:
*- levothyroxine, separate by 2 hours from lanthanum
*- quinolones and tetracyclines, should be given one hour before or 4 hours after
*- oral bisphosphonates
*- others
- can bind to Al, Ca or Mg containing antacids; administration of these products should be separated from lanthanum by 2 hours**
40
Renvela
Class:
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sevelamer carbonate
Class: Al free & Ca free Phosphate Binder that is NOT systemically absorbed
Indications: hyperphosphatemia CKD
MOA: drug blocks the absorption of dietary PO4 by binding to it in the intestine
Dosage forms: tablet, powder
Dosing: 800-1600mg PO TID with meals, titrate based on PO4 levels
Contraindications:
Bowel obstruction
Warnings: can reduce dietary absorption of vitamins D, E, K and folic acid; consider vitamin supplementation
Side Effects: nausea/vomiting/diarrhea (all>20%), dyspepsia, constipation, abdominal pain, flatulence
Monitoring:
Ca, PO4, HCO3, Cl, PTH
Pearls/Notes:
- can lower total cholesterol :) and LDL by 15-30% :)
- sevelamer carbonate can maintain bicarbonate concentrations
Drug-Drug/Food interactions:
*- levothyroxine, should be given several hours before dose of sevelamer
*- quinolones and tetracyclines, should be given 2 hours before or 6 hours after the sevelamer dose
*- oral bisphosphonates
*- others
41
Renagel
Class:
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sevelamer hydrochloride
Class: Al free & Ca free Phosphate Binder that is NOT systemically absorbed
Indications: hyperphosphatemia CKD
MOA: drug blocks the absorption of dietary PO4 by binding to it in the intestine
Dosage forms: tablet, powder
Dosing: 800-1600mg PO TID with meals, titrate based on PO4 levels
Contraindications:
Bowel obstruction
Warnings: can reduce dietary absorption of vitamins D, E, K and folic acid; consider vitamin supplementation
Side Effects: nausea/vomiting/diarrhea (all>20%), dyspepsia, constipation, abdominal pain, flatulence
Monitoring:
Ca, PO4, HCO3, Cl, PTH
Pearls/Notes:
- can lower total cholesterol :) and LDL by 15-30% :)
-
Drug-Drug/Food interactions:
*- levothyroxine, should be given several hours before dose of sevelamer
*- quinolones and tetracyclines, should be given 2 hours before or 6 hours after the sevelamer dose
*- oral bisphosphonates
*- others
42
problem #2 CKD
Vitamin D deficiency AND secondary hyperparathyroidism (High PTH)
*remember*- healthy kidneys hydroxylate vitamin D, activate it to its active form: 1,25-dihydroxy vitamin D
- impaired kidneys are unable to activate vitamin D, and therefore without active vitamin D we can't absorb dietary calcium.
- serum calcium levels are low in the blood, which signal to the parathyroid hormone to increase PTH
43
Vitamin D3-
Vitamin D2-
cholecalciferol, which is synthesized in the skin after exposure to ultraviolet light (the sun)
ergocalciferol, which is produced from plat sterols and is the primary dietary source of vitamin D.
44
Vitamin D deficiency worsens:
- bone disease
- impairs immunity
- increases the risk for cardiovascular disease
45
The vitamin D analogs are used in patients with pater stages of CKD or kidney failure, to increase calcium absorption from the gut, raise serum calcium concentrations and ____________________
inhibit PTH secretion.
By raising calcium levels in the blood, this signals to the parathyroid gland to STOP secreting PTH.
46
Another method of inhibiting PTH release is by increasing the sensitivity of the calcium receptor on the parathyroid gland.
calcimimetics- mimic the actions of calcium on the parathyroid gland and causes a further reduction in PTH.
"only used in dialysis patients"
47
48
Rocaltrol
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calcitriol
Class: Vitamin D analog CKD
Indications: vitamin D deficiency & secondary hyperparathyroidism
MOA: drug increases intestinal absorption of Ca from the gut, which increases serum Ca, so body stops pulling calcium from bones and it provides negative feedback to the parathyroid gland to inhibit PTH secretion
Dosage forms: capsule, solution, injection
Dosing:
Max dose:
Contraindications:
*Hypercalcemia, Vitamin D toxicity
Warnings:
digitalis toxicity potentiated by hypercalcemia.
Side Effects:
Hypercalcemia, hyperphosphatemia, N/V/D (>10%)
Monitoring:
Ca, PO4, PTH, 25-hydroxy vitamin D (calcifediol)
Pearls/Notes:
-active form of Vitamin D3
- take with food or shortly after a meal to decrease GI upset
Drug-Drug/Food interactions:
49
Rayaldee
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calcifediol
Class: Vitamin D analog
Indications: vitamin D deficiency & secondary hyperparathyroidism
MOA: drug increases intestinal absorption of Ca from the gut, which provides negative feedback to the parathyroid gland to inhibit PTH secretion
Dosage forms: capsule, solution, injection
Dosing:
Max dose:
Contraindications:
Hypercalcemia, Vitamin D toxicity
Warnings:
digitalis toxicity potentiated by hypercalcemia.
Side Effects:
Hypercalcemia, hyperphosphatemia, N/V/D (>10%)
Monitoring:
Ca, PO4, PTH, 25-hydroxy vitamin D (calcifediol)
Pearls/Notes:
-active form of Vitamin D3
- take with food or shortly after a meal to decrease GI upset
Drug-Drug/Food interactions:
50
Hectorol
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doxercalciferol
Class: Vitamin D analog
Indications: vitamin D deficiency & secondary hyperparathyroidism
MOA: drug increases intestinal absorption of Ca from the gut, which provides negative feedback to the parathyroid gland to inhibit PTH secretion
Dosage forms: capsule, solution, injection
Dosing:
Max dose:
Contraindications:
Hypercalcemia, Vitamin D toxicity
Warnings:
digitalis toxicity potentiated by hypercalcemia.
Side Effects:
Hypercalcemia, hyperphosphatemia, N/V/D (>10%)
Monitoring:
Ca, PO4, PTH, 25-hydroxy vitamin D (calcifediol)
Pearls/Notes:
-active form of Vitamin D3
- take with food or shortly after a meal to decrease GI upset
Drug-Drug/Food interactions:
51
Zemplar
Class:
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paricalcitol
Class: Vitamin D analog
Indications: vitamin D deficiency & secondary hyperparathyroidism
MOA: drug increases intestinal absorption of Ca from the gut, which provides negative feedback to the parathyroid gland to inhibit PTH secretion
Dosage forms: capsule, solution, injection
Dosing:
Max dose:
Contraindications:
Hypercalcemia, Vitamin D toxicity
Warnings:
digitalis toxicity potentiated by hypercalcemia.
Side Effects:
Hypercalcemia, hyperphosphatemia, N/V/D (>10%)
Monitoring:
Ca, PO4, PTH, 25-hydroxy vitamin D (calcifediol)
Pearls/Notes:
-active form of Vitamin D3
- take with food or shortly after a meal to decrease GI upset
Drug-Drug/Food interactions:
52
Sensipar
Class:
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cinacalcet
Class: Calcimimetic
Indications: secondary hyperparathyroidism in dialysis patients
MOA: drug increases sensitivity of the calcium-sensing receptor on the parathyroid gland, which causes a decrease in PTH secretion, they shut down the pathway used to increase Ca in the blood, in doing so this causes
decreased Ca, decreased PO4 levels.
Dosage forms:
Dosing:
Dialysis: 30-180mg PO daily with food
Take tablet whole, do not crush or chew
Contraindications:
*Hypocalcemia
Warnings:
Caution in patients with a history of seizures
Side Effects:
Hypocalcemia, N/V/D, paresthesia, HA, fatigue, depression, anorexia, constipation, bone fracture, weakness, arthralgia, myalgia, limb pain, URTIs
Monitoring:
Ca, PO4, PTH
Pearls/Notes:
Drug-Drug/Food interactions:
53
Parsabiv
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etelcalcetide
Class: Calcimimetic
Indications: secondary hyperparathyroidism in dialysis patients
MOA: drug increases sensitivity of the calcium-sensing receptor on the parathyroid gland, which causes a decrease in PTH secretion, they shut down the pathway used to increase Ca in the blood, in doing so this causes
decreased Ca, decreased PO4 levels.
Dosage forms:
Dosing:
Dialysis: 2.5-15mg IV 3 x weekly
Contraindications:
Warnings:
*Hypocalcemia, worsening HF, GI bleeding, decreased bone turnover
Side Effects:
*muscle spasms, paresthesia, N/V/D
Monitoring:
Ca, PO4, PTH
Pearls/Notes:
Drug-Drug/Food interactions:
54
Anemia of CKD:
anemia is defined as ___
a hemoglobin level less than < 13g/dL
55
Anemia of CKD:
It is common in CKD and is due to a combination of factors. The primary problem is a lack of ___________, which is normally produced by healthy kidneys and travels to the bone marrow to stimulate the production of red blood cells.
(EPO) erythropoietin
56
As kidney function declines, EPO production ___. This leads to reduced hemoglobin levels and symptoms of anemia (fatigue, pale skin). These processes are exacerbated by CKD, causing an inflammatory state, which contributes to decreased EPO production.
decreases
57
Treatment of Anemia in CKD:
ESAs - to produce RBCs
&
iron
58
(ESAs) erythropoiesis-Stimulating Agents:
these drugs work like EPO to produce more red blood cells and can prevent the need for blood transfusions.
59
(ESAs) erythropoiesis-Stimulating Agents include:
- epoetin alfa (Procrit, Epogen, Retacrit)
- longer acting formulation darbopoetin alfa (Aransep)
60
(ESAs) erythropoiesis-Stimulating Agents: Risks
-elevated blood pressure
- thrombosis
-
61
(ESAs) erythropoiesis-Stimulating Agents, should only be used when ____
The dose should be held or discontinued if the hemoglobin exceeds ________, as the risk for thromboembolic disease (DVT, PE, MI, stroke) is increased with higher hemoglobin levels.
the hemoglobin is less than < 10g/dL
11 g/dL
62
ESAs are only effective if adequate ____________ is available to make hemoglobin.
iron
"It is important to assess an iron panel (iron, ferritin, and TSAT) and provide supplementation to prevent iron deficiency.
63
Hyperkalemia- can be defined as a potassium level _____
a normal potassium level is ____________
> 5.3 or > 5.5 mEq/L, (ranges vary), though clinicians will be concerned with any level > 5 mEq/L
3.5-5 mEq/L
64
_________ is the most abundant intracellular cation and is esstenial for life.
potassium
65
Excess potassium intake is excreted primarily through the kidneys and partially via the gut. Renal potassium excretion is increased by the hormone __________, drugs ________, by a high urine flow (via osmotic diuresis) and by negatively charged ions in the distal tubule (bicarbonate).
aldosterone
diuretics (loop > thiazides)
66
High dietary potassium intake does not typically cause hyperkalemia unless there is significant renal damage. With normal kidney function, the acute rise in potassium from a meal would be offset by the release of ____________, which causes potassium (K) to shift ____________.
insulin
into the cells
67
Complications of CKD: recap
1) inability to excrete phosphate, so it accumulates, leading to hyperphosphatemia
2) inability to activate Vitamin D, leading to low serum Ca
3) decreased production of EPO
68
The most common cause of hyperkalemia is _________
decreased renal excretion due to kidney failure.
"Patients with diabetes are at a higher risk for hyperkalemia, as insulin deficiency reduces the ability to shift potassium into the cells or ARBs."
69
A patient with an elevated potassium level may be asymptomatic. When symptoms are present, they include ________.
muscle weakness, bradycardia and fatal arrhythmias
If the potassium is high or the heart rate/rhythm is abnormal, the patient is usually monitored with an ECG.
70
Treatment of Hyperkalemia:
1)
2)
3)
1) stabilize the heart - to prevent arrhythmias
2) Shift (K) intracellularly, move it out
3) Remove (K) eliminate it from the body
71
Stabilize the heart - use _________
calcium gluconate IV
onset 1-2 minutes
does not decrease potassium. Stabilizes myocardial cells to prevent arrhythmias
72
Move it - Shift K intracellularly
1- regular insulin IV
*- dextrose IV
- sodium bicarbonate IV
- albuterol nebulized
onset 30 minutes
1- Co-administered with glucose or dextrose to prevent hypoglycemia
*- stimulates insulin secretion, but does not shift K intracellularly on its own
- Used when metabolic acidosis is present
- monitor for tachycardia and chest pain
73
Remove it: Eliminate K from the body
- furosemide IV
-
-
-
-
- furosemide IV
- eliminates K in urine, Onset 5 minutes
- monitor volume status
- Sodium polystyrene sulfonate
- Binds K in the GI tract
- Due to adverse effects (GI necrosis), used for emergency situations only
- oral may take hours to days to work ~ 2-24 hours
- rectal route has a faster onset and can be used in acute (emergency)
treatment
- patiromer
- Binds K in the GI tract
- Delayed onset limits use in life-threatening emergencies
- onset ~ 7 hours
- sodium zirconium cyclosilicate
- Binds K in the GI tract
- Potassium binder with fastest onset of action; may be preferred for
emergency situations
- onset 1 hour
- hemodialysis
- onset immediate, once started
- removes K from the blood
- takes several hours to set up/complete dialysis
- other methods are generally used in conjunction
74
Kayexalate
Class:
Indications:
MOA:
Dosage forms:
Dosing:
Max dose:
Contraindications:
Warnings:
Side Effects:
Monitoring:
Pearls/Notes:
Drug-Drug/Food interactions:
sodium polystyrene sulfonate
Class:
Indications:
MOA:
Dosage forms:
Dosing:
Max dose:
Contraindications:
Warnings:
Side Effects:
Monitoring:
Pearls/Notes:
Drug-Drug/Food interactions:
75
SPS
Class:
Indications:
MOA:
Dosage forms:
Dosing:
Max dose:
Contraindications:
Warnings:
Side Effects:
Monitoring:
Pearls/Notes:
Drug-Drug/Food interactions:
sodium polystyrene sulfonate
76
Kionex
Class:
Indications:
MOA:
Dosage forms:
Dosing:
Max dose:
Contraindications:
Warnings:
Side Effects:
Monitoring:
Pearls/Notes:
Drug-Drug/Food interactions:
sodium polystyrene sulfonate
77
Veltassa
Class:
Indications:
MOA:
Dosage forms:
Dosing:
Max dose:
Contraindications:
Warnings:
Side Effects:
Monitoring:
Pearls/Notes:
Drug-Drug/Food interactions:
patiromer
78
Lokelma
Class:
Indications:
MOA:
Dosage forms:
Dosing:
Max dose:
Contraindications:
Warnings:
Side Effects:
Monitoring:
Pearls/Notes:
Drug-Drug/Food interactions:
sodium zirconium cyclosilicate
79
Metabolic Acidosis:
-the ability of the kidney to reabsorb (HCO3) bicarbonate decreases as CKD progresses
- this can result in metabolic acidosis
- treatment of metabolic acidosis in initiated when the serum bicarbonate concentration is less than < __________
Treatment:
22 mEq/L
80
Drugs to replace bicarbonate include:
sodium bicarbonate (Neut)
Sodium citrate/citric acid solution (Cyta-2, Oracit, Shohl's solution)
81
*remember* bicarbonate is a ______
So as kidney disease progresses, bicarbonate reabsorption back into the blood ______ .
So since patients don't have enough base, less base is in the blood, patients become ____
base
decreases
acidodic
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