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Therapeutics 1 Kappa Epsilon Version > CKD and ESRD Lecture > Flashcards

CKD and ESRD Lecture Flashcards

1
Q

Major causes of CKD

A

Diabetes; HTN; Glomerulonephritis

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2
Q

KDIGO definition of CKD

A

abnormalities of kidney structure present for more than 3 months with implications of health

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3
Q

KDIGO classifies CKD by what categories?

A

Cause, GFR, and albuminuria cateogry

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4
Q

What level does GFR have to be at to be considered CKD

A

GFR has to be below 60 mL/min/1.73 m^2

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5
Q

Kidney Failure has a GFR of _____ and has the category name of ____

A

< 15; G5

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6
Q

Albuminuria levels for CKD

A

normal - mild < 30

moderate: 30 - 300
severe: > 300

(units: mg/24 hours)

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7
Q

Normal GFR level

A

above 90 mL/min/1.73 m^2

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8
Q

Cockroft Gault Equation is an equation for what?

A

finding CrCl

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9
Q

What is the Cockroft Gault equation

A

If male: CrCl =
(140 - age) IBW/ (SCr x 72)

If female - same thing but x .85

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10
Q

Cockroft gault formula tends to _______ renal function in moderate to severe kidney impairment

A

overestimate

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11
Q

MDRD is used for what?

A

measure GFR and it is used to stage kidney disease

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12
Q

Components of MDRD equation

A

Age; Sex; Race

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13
Q

What does MDRD stand for

A

modification of Diet in renal disease

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14
Q

IBW equations

A

male: 50 kg + (2.3 x inches of 60 in)

Female: 45.5 + (2.3 x inches of 60 in)

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15
Q

Main functions of Kidney

A
  • excrete waste products
  • regulates body’s concentration of water and salt
  • maintain acid balance of plasma
  • secrete hormones
  • synthesize calcitriol
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16
Q

What waste products does the kidney get rid of from the blood

A

urea, ammonia, bilirubin, uric acid

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17
Q

If the kidney cannot get rid of waste products - the waste products build up and cause

A

UREMIA: increase in BUN; pruritis; confusion; nausea; vomiting; anorexia

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18
Q

If the body cant regulate the bodys water and salt concentrations - what happens

A

edema; fluid overload; CV complications

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19
Q

what happens if the kidney cant maintain acid balance of plasma

A

metabolic acidosis - because it CANT EXCRETE H+ ions

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20
Q

what hormones does the kidney secrete

A

erythropoeitin, rennin, PGAs

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21
Q

what happens if the kidneys cant secrete hormones

A

Anemia - erythropoeitin is needed to make RBCs

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22
Q

What happens if the kidney cant make synthesize calcitriol

A

mineral and bone disorder/ increased levels of PTH

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23
Q

another name for calcitriol

A

active form of Vit.D

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24
Q

Common effects of Uremia

A
  • Uremic fetor (urine breath)
  • encephalopathy (confusion)
  • Uremic frost (uric acid crystals on skin)
  • Nausea and Vomiting
  • Edema
  • Mineral and bone disorder
  • Anemia
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25
Q

How to regulate fluid retention in a CKD patient

A

regulate Na intake!!! not so much fluid restriction - but AVOID lots of free water

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26
Q

Do diuretics work when a patient does NOT make urine?

A

no they do not work

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27
Q

Explain Diuretic Resistance

A

When Loop diuretics are used - Distal tubule is exposed/”bathed” in lots of Na - which makes the distal tubule reabsorb more Na and therefore more water is absorbed too - thus making the loop less effective

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28
Q

How to treat diuretic resistane

A

give a thiazide diuretic to work at the Distal tubule to stop the NaCl transporter to stop absorbing Na (and water)

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29
Q

How to treat fluid overload when on dialysis

A

just adjust settings on dialysis machine

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30
Q

Electrolyte imbalance cautions for CKD

A

Na and K

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31
Q

K amount is restricted to _____

A

3 gm/day

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32
Q

Steps on how to treat hyperkalemia

A

1) calcium gluconate
2) insulin/D5W
2) albuterol
3) sodium polystyrene sulfonate
3) dialysis

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33
Q

What are high potassium foods

A

tomatoes; dried fruits; salt substitutes; fresh fruits

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34
Q

Sodium bicarbonate - not used for what kind of patients?

A

ESRD

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35
Q

Key Points of Mineral and Bone Disorder

A

1 - hyperphosphatemia
2 - decrease in (activated) Vit. D
3 - hypocalcemia

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36
Q

Why does hyperphosphatemia happen with kidney disease

A

Kidney cannot excrete it - therefore phosphorous accumulates

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37
Q

Why does decreased Vit. D happen with CKD

A

kidney is messed up - therefore cant make calcitriol

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38
Q

2 major classes of drugs to help treat Hyperphosphatemia

A

Phosphate binders -

Calcium containing OR Non-Calcium Containing

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39
Q

Overall Effect of Mineral - Bone Disorder (CKD)

A

increased iPTH - which leads to the bones being broken down to release more calcium form the bones

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40
Q

Renvela/ Sevelamer carbonate - facts about it

A
  • little bit of GI issues;
  • Not absorbed = low risk of toxicity
  • decrease uric acid serum concentrations
  • decreases LDL levels
    is a NON CALCIUM CONTAINING PHOSPHATE BINDER
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41
Q

Drugs that are NON-CALCIUM CONTAINING PHOSPHATE BINDER

A 
Sevelamer Carbonate (Renvela)
Lanthanum Carbonate (Fosrenol)
Sucroferric Oxyhydroxide (Velphoro)
Auryxia (ferric citrate)
Aluminum Hydroxide (Amphojel)
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42
Q

Drugs that are calcium containing phosphate binders

A

Tums (Calcium Carbonate) and Calcium acetate (PhosLo)

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43
Q

Important facts about Auryxia

A
  • contains iron that can be absorbed to affect TSAT and ferritin
  • is a non calcium containing phosphate binder
  • darken stool bc iron
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44
Q

important facts about lanthanum carbonate (fosrenol)

A
  • is eliminated in feces - no worry about accumulation of lanthanum long term
  • keeps it efficacy regardless of pH of stomach (3 - 5)
  • does not cross blood brain barrier
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45
Q

Two iron containing phosphate binders

A

Auryxia and Sucroferric oxyhydroxide

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46
Q

Dietary Restriction for Phosphate

A

800 - 1000 mg/ day

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47
Q

Foods that contain high amounts of phosphorus

A

meat, nuts, dry beans, dairy, cola, beets

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48
Q

Caution of Phosphate binders and TPN patients

A

phosphate binders work in GI tract - if TPN being used - GI tract is not being used - therefore no need to use phosphate binders in TPN

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49
Q

Stage 3/4 CKD pts vs Stage 5 (ESRD) pts -

Vitamin D supplementation

A

if 3 or 4 - give INACTIVE FORM - Ergocalciferol (Calciferol) - Vit D2 or Cholecalciferol - Vit D3

if 5 - give ACTIVE FORM (bc kidney cant make inactive form into active)

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50
Q

active forms of Vit. D to give ESRD pts

A

Calcitriol; Paricalcitol; Dexercalciferol

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51
Q

Inactive forms of Vit. D to give to CKD stage 3/4 pts

A

Ergocalciferol; Cholecalciferol

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52
Q

Out of the Active forms of Vit. D to give to a patient - which one has the biggest risk of hypercalcemia

A

Calcitriol

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53
Q

out of the active forms of Vit. D to give a patient - which one has least risk of causing hypercalcemia

A

Paricalcitol and Doxercalciferol

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54
Q

Which active form of Vit. D is a PRO-HORMONE

A

Doxercalciferol

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55
Q

Importnat note to Doxercalciferol

A

its a pro-hormone - must be metabolized by LIVER

also gives more even serum concentrations

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56
Q

Why is important for Vit. D supplements to have a LOW CALCEMIC activity

A

because patients already have high phos levels - if too much Ca = more risk for precipitation

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57
Q

Which active form of Vit. D has a higher risk of hyperphosphatemia

A

Doxercalciferol

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58
Q

What drug should be avoided in patients that are alcoholics or have multi organ failure?

A

the Pro-hormone drug - Doxercalciferol

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59
Q

Name for calcimimetic agent for treating calcium homeostasis

A

Cinacalcet (Sensipar)

60
Q

Mechanism of Cinacalcet

A

it mimics action of calcium by binding to calcium sensing receptor on parathyroid - causes conformational change of receptor to send signal to parathyroid to decrease PTH production

61
Q

Cinacalcet is contraindicate in patients with what?

A

hypocalcemia

62
Q

Hypocalcemia is a contraindication for what drug

A

cinacalcet (if Calcium is less 7.5 mg/dL)

63
Q

Possible mechanisms for anemia in ESRD pts

A

1 - DECREASED PRODUCTION OF ERYTHROPOIETIN
2- uremia causes decreased half life span of RBCs
3- vitamin losses during dialysis (folate, B12, B6)
4- dialysis - loss of blood through dialyzer

64
Q

What is MCV

A

mean corpuscular volume - average size of RBCs

65
Q

what are the 3 main types of anemia (related to MCV)

A

microcytic, normocytic, macrocytic

66
Q

Iron deficiency causes what kind of anemia (micro, normo, macro - cytic)

A

micro!

67
Q

Vitamin deficiencies (folate, B12) cause what kind of anemia (micro, normo, macro - cytic)

A

macro!

68
Q

GI bleed or Erythropoetin deficiency can cause what kind of anemia (micro, normo, macro - cytic)

A

normocytic

69
Q

what is RDW?

A

red cell distribution width -

70
Q

when is RDW important?

A

if pt has both macrocytic and microcytic anemia - the blood cell volume range is much larger

71
Q

what is the average value for RDW

A

11.5 -14.5%

72
Q

What is the preferred way to assess anemia

A

Hemoglobin (not hematocrit)

73
Q

why is Hgb preferred over Hct for anemia monitoring parameters

A

Hgb is more stable

74
Q

Hemoglobin Levels to see if a patient is Anemic
Females: ?
Males: ?

A

Females: < 12 g/dL
Males: < 13 g/dL

75
Q

What is erythropoiesis and what does it require

A

makes RBCs - need IRON!!

76
Q

When to recommend iron supplementation

A

TSAT: < 30%
and
serum ferritin < 500 ng/mL

77
Q

when to give oral iron vs IV iron?

A

oral - stage 3 or 4 CKD patient

IV - stage 5 CKD patient

78
Q

Iron is best absorbed in what kind of environment?

A

acidic! (therefore avoid eating with it or taking antacids/PPIs/H2 antagonists)

79
Q

what drugs should be avoided/separated from iron supplements

A

antacids/H2 antagonists/PPIs - because they decrease acidity of stomach and therefore absorption

80
Q

Note about enteric coated iron tablets

A

enteric = absorbed in small intestine - but less acidic = less absorption

81
Q

iron and ___ should be separated from each other by about 2 hours due to _______

A

Calcium; tight binding

82
Q

Low molecular vs High Molecular weight IV iron

A

high = higher chance of anaphylactic reaction

83
Q

Which IV iron needs a test dose

A

iron dextran

84
Q

two kinds of Iron dextran and why they are different

A

Infed - low molecular weight

Dexferrum - high molec weight

85
Q

Heme iron qualities

A

absorbed in a different site - NOT relevant to the 200 mg elemental iron rule

86
Q

Oral iron: need ______ of elemental iron per day - at least!

A

200 mg

87
Q

If iron doesn’t work - start using ______

A

erythropoesis stimulating agents

88
Q

When to start use ESAs?

If stage 3/4 vs stage 5

A

3/4: if Hb < 10 g/dL

5: when Hb is b/w 9 and 10

89
Q

Do not use ESA to push Hb above _____ g/dL

A

11.5

90
Q

2 kinds of ESAs

A

Recombinant human erythropoietin and Darbepoetin alfa

91
Q

Difference between the 2 ESAs

A

Darbepoetin alfa - has a longer half life!

92
Q

ESA adverse effects

A

Pure Red cell aplasia (PRCA) = antibodies develop to erythropoietin
AND
HTN

93
Q

Common reasons ESA fails

A

lack of IRON (and vitamins)

active bleed

94
Q

Protein Requirement for CKD and then ESRD

A

CKD: 0.8 g/kg/day (if GFR is < 30 mL/min)

ESRD: 1.2 g/kg/day

95
Q

What types of vitamins should be replaced when on dialysis

A

water soluble - B and C

96
Q

Two types of vascular access for Hemodialysis

A

AV fistula and AV graft

97
Q

Differences b/w AV fistula and graft

A

fistula - sew an artery into a vein to make it more strong

graft - “foreign body”/plastic put into body to make vein and artery connected

98
Q

AV graft or AV fistula?

Fewer complications

A

fistula

99
Q

AV graft or AV fistula?

Poses a problem for diabetics (due to PVD - weak veins)

A

Fistula

100
Q

AV graft or AV fistula?

Has the shortest time to “mature”

A

graft

101
Q

AV graft or AV fistula?

Hast the longest time to “mature”

A

fistula

102
Q

AV graft or AV fistula?

uses a synthetic material to

A

graft

103
Q

AV graft or AV fistula?

has higher infection rate

A

graft

104
Q

KEY NOTE about the ACESS ARM once a AV fistula or graft is made

A

NO needle pricks on that arm AND NO BP cuff on that arm

105
Q

What kind of substances are not removed by a dialysis machine

A
  • high molecular weight
  • high volume of distribution molecules (because a lot in tissue - not blood)
  • high lipophilicity (because blood deals with water like solutions)
  • highly protein bound (not free to be excreted)
106
Q

Ways to measure the effectiveness of dialysis sesssions

A

Kt/V and URR (urea reduction rate)

107
Q

what is Kt/V / what do the variables stand for

A

a way to measure the effectiveness of a dialysis session
K - clearance of urea
t - time on dialysis
V - volume of distribution of urea

108
Q

Goal Kt/V value

A

1.4 (and above)

109
Q

If Kt/V value is 0.9 - good or bad?

A

bad! - adjust the time on dialysis… to increase value

110
Q

what is URR measuring

A

measuring the reduction of BUN

111
Q

what is the goal URR

A

> 70%
(example of good session of dialysis:
BUN starts: 100
after dialysis BUN = 30)

112
Q

Types of Peritoneal Dialysis

A

CAPD; CCPD; NIPD; TPD

113
Q

Signs and Symptoms of Peritonitis

A 
cloudy effluent (fluid coming out is cloudy = infection);
fever, nausea; abdominal pain
114
Q

Different ways to treat peritonitis

A

1st and 3rd generation Cephs; Aminoglycosides

115
Q

Best way to give an antibiotic for peritonitis

A

intraperitoneal

116
Q

Why is intraperitoneal route the best route for peritonitis infectoins?

A

1 - pt probably has N/V - cant do oral
2 - probably has vasular issues because they are periotneal (therefore no IV)
3 - infection usually isnt too deep - intraperitoneal is just fine

117
Q

when to use CRRT (continuous renal replacement therapy)

A
  • in ACUTE renal failure

- for patients that cannot handle normal dialysis sessions

118
Q

3 main kinds of CRRT

A

hemofiltration; hemodialysis; hemodiafiltration

119
Q

Hemofiltration (CAVH or CVVH) as a CRRT - key points about it

A

NO DIALYSATE bag; uses CONVECTION; ultrafiltrate added to keep BP up

120
Q

CVVHD - hemodialysis as a CRRT - key points about it

A

regular dialysis but all day long; uses DIFFUSION (works better than convection)

121
Q

CVVDHF - hemodiafiltration as a CRRT - key points about it

A

use diffusion AND convection; just like CRRT hemodialysis but the rate is increased (to create the convection)

122
Q

The decline of kidney function based on SCr values is a ________ curve

A

sigmoidal

123
Q

where is the biggest drop in kidney function when SCr increases

A

1 - 2

124
Q

How do you measure CrCl for AKI?

A

PSYCHE! YOU DONT! Its changing too much to calculate it

125
Q

Types of AKI (and how they are acquired)

A

Community (self inflicted) OR Hospital (hospital did it to ya)

126
Q

Since we can’t use SCr for AKI - what do we look at as monitoring parameters?

A
  • pts weight
  • BP
  • urine output
  • urinalysis (Specific gravity, hematuria/proteinuria; microscopic exam)
127
Q

Types of Urine Output Categories (related to AKI parameters)

A

anuria; oliguria; non-oliguria

128
Q

what is oliguria

A

less than 400 mL of urine production in a 24 hr period

129
Q

what is non-oliguria

A

more than 400 mL of urine production in a 24 hr period

130
Q

If specific gravity is high - what kind of AKI could it be?

A

pre-renal or functional AKI

131
Q

If Hematuria or proteinuria is present - what kind of AKI?

A

some kind of injury…. (?)

132
Q

what can be seen in a microscopic examination

A

RBCs and Casts (of RBCs)

133
Q

What is fractional excretion of Sodium?

A
  • way to differentiate b/w prerenal/functional renal failure and intrinsic renal failure
  • also means “can kidney still make concentrate urine”
134
Q

Preventing AKI/AKI management

  • Avoid ________ agents
  • __________ - if nephrotoxic agent has to be used - make sure to use this kind of therapy to increase urine output and flush out the toxin
  • _____ loading
  • identify at risk patients
A

nephrotoxic; hydration; Na;

135
Q

Patient groups that are at risk for AKI

A

Older pts; pts w/ abnormal renal function; diabetic pts; volume depleted pts

136
Q

Main Goals of treating AKI

A
  • remove primary cause
  • limit further nephrotoxic exposure
  • accelerate therapy
137
Q

Two ways to control volume with AKI patients

A

CRRT (the 3 diff. kinds) and diuretics (loops)

138
Q

List the common nephrotoxins

A
  • NSAIDs/Cox II inhibitor
  • Acetaminophen
  • Aminoglycosides
  • ACE inhibitors/Angiotensin II receptor blockers
  • PROTON PUMP INHIBITORS (caution bc OTC)
    (- Amphotericin B
  • Contrast Media
  • Cisplatin/Carboplatin
  • cyclosporine/tacrolimus
  • lithium)
139
Q

If filtration in the kidney decrease, _____ will increase

A

SCr

140
Q

General Rule to start hemodialysis:
If BUN is > ______
or
SCr is > ______

A

100; 10

141
Q

When starting a patient on an ACE inhibitor or ARB - what should be monitored closely

A

SCr - if it increase over 30% - dc the drug

142
Q

NSAIDs increase SCr because of what mechanism?

A

afferent arteriole (to the glomerulus) will VASOCONSTRICTION - causes decreases renal perfusion and filtration pressure

143
Q

ACEIs and ARBs increase SCr by what mechanism?

A

vasodilation of the efferent arterioles decrease the filtration pressure

144
Q

Definition of ultrafiltrate

A

waste products removed during continuous renal replacement therapy

145
Q

Most common reason that ESA treatment fails

A

lack of vitamins and iron

Therapeutics 1 Kappa Epsilon Version (17 decks)

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