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PHRM 844 > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

what is the Cockroft and Gault equation for MEN

A

CrCl = (140-age)IBW/(SCr72)

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2
Q

what is the Cockroft and Gault equation for WOMEN

A

CrCl = ((140-age)IBW/(SCr72))*0.85

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3
Q

what is Cockroft and Gault used for

A

dosing drugs

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4
Q

what is MDRD

A

Modification of Diet in Renal Disorders

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5
Q

what is MDRD used for

A

staging kidney disease

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6
Q

IBW for females

A

45.5+2.3(inches over 5 ft)

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7
Q

IBW for males

A

50+2.3(inches over 5 ft)

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8
Q

what is the complication from a build up of excess waste products

A

Uremia

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9
Q

what is the definition or uremia

A

a cluster of sx which is associated with ESRD from any cause

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10
Q

cause of Sx in uremia

A

due to the accumulation of waste molecules in the blood that are normally removed by the kidney

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11
Q

how is uremia monitored

A

BUN

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12
Q

what effects happen to the body from uremia (hint: there are 8)

A
  1. CNS: Encephalopathy
  2. EENT: uremic fetor (pee breath)
  3. Pulmonary: non-cardiogenic pulmonary edema from volume overload
  4. Cardio: sodium retention, volume overload, LVH
  5. GI: anorexia, N, constipation, metallic taste
  6. musculoskeletal: mineral and bone disorder and restless leg syndrome
  7. anemia: EPO deficiency
  8. Skin frost: uremic frost
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13
Q

do you fluid restrict patients that have fluid retention from chronic kidney disease?

A

not generally if Na intake is controlled. AVOID large amts of water

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14
Q

will diruetics work without a funcitioning kidney

A

NO

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15
Q

what two stages of chronic kidney disease can you use diuretics in?

A

Stage 3 and 4

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16
Q

with what CrCl do thiazides become ineffective

A

<30 ml/min

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17
Q

what diuretic would work with CrCl work when CrCl < 30ml

A

loops!

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18
Q

why is furosemide oral dosing usually twice the IV dose

A

oral bioavailability is usually about 50%

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19
Q

as renal function declines, and you max loop dose, what drug class might be added on to overcome diuretic resistance

A

thiazide!

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20
Q

is there a need to severely Na restrict patients that have a Na imbalance

A

use IV saline with caution

Make pts aware of hidden Na content food (hot dogs, canned soups…)

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21
Q

what would you restrict a K imbalance patient’s diet to

A

3 grams per day

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22
Q

What electrolyte irregularity is a problem for nearly all ESRD patients

A

Hyperphophatemia

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23
Q

What must phosphate binders always be given with

A

given with meals

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24
Q

What are the three examples of calcium containing phosphate binders we discussed in class

A 
Calcium carbonate (Tums) 
Calcium acetate (PhosLo)
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25
Q

why does calcium acetate produce fewer hypercalcemic events when compared to calcium carbonate

A

when given at the same elemental dose, calcium acetate will bind twice as much phosphate compared to calcium carbonate

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26
Q

what are the examples of non-calcium containing phosphate binders

A

Sevelamer carbonate (renvela)

Lanthanum carbonate (fosrenol)

sucroferric oxyhydroxide (velphoro)

ferric citrate (auryxia)

aluminum hydroxide (amphojel)

magnesium carbonate (Mag-Carb)

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27
Q

what should dietary phosphorus intake be restricted to if elevated phosphorus

A

800 to 1000 mg per day

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28
Q

how does hyperphosphatemia cause secondary hyperparathyroidism

A

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

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29
Q

when would you use ergocalciferol in CKD patients

A

stage 3 and 4

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30
Q

when would you use cholecalciferol in CKD patients

A

stage 3 adn 4

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31
Q

what class of drugs would you use in CKD stage 5 and some stage 3 and 4

A

Calcitriol (Rocaltrol and Calcijex), Paricalcitol (Zemplar), Doxercalciferol (Hectorol)

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32
Q

monitoring parameters for Calcitriol

A

S/Sx of hypercalcemia (fatigue, weakness, headache, nausea, vomiting, muscle pain, and constipation)

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33
Q

why might paricalcitol be used over other drugs

A

more favorable ADE profile, less calcemic activity compared to calcitriol

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34
Q

why might you not want to use Doxercalciferol in a liver disease patient

A

it is a prohormone that is activated in the liver

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35
Q

what electrolyte imbalance does doxercalciferol have a higher risk for

A

hyperphosphatemia

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36
Q

what drug class is cinacalcet (sensipar) in? what is it used for?

A

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

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37
Q

what are calcimemetic agents contraindicated?

A

hypocalcemia

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38
Q

what are the basic monitoring parameters for CKD stage 3

A

Calcium: every 6 - 12 months
Phosphorus: every 6 - 12 months
25(OH)D: Baseline
Intact PTH

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39
Q

what are the basic monitoring parameters for CKD stage 4

A

Calcium: every 3-6 months
Phosphorus: every 3-6 months
25(OH)D: Individualized
Intact PTH: every 6-12 months

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40
Q

what are the basic monitoring parameters for CKD 5D

A

Calcium: every 1-3 months
Phosphorus: every 1-3 months
25(OH)D: individualized
intact PTH: every 3-6 months

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41
Q

what are the basic monitoring parameter goals for CKD

A 
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
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42
Q

nearly all ESRD patients will develop what kind of blood disorder

A

anemia

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43
Q

what are the 4 ways a ESRD patient may contract anemia

A
  1. decreased production of erythropoetin
  2. uremia causes a decreased life span of red blood cells
  3. vitamin losses during dialysis - folate, B12, B6
  4. dialysis - loss of blood through dialyzer (hemolysis)
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44
Q

anemia S/Sx

A
  • fatigue
  • dizziness
  • HA
  • decreased cognition
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45
Q

why is Hb the be assessment parameter for anemia

A

due to its increased stability over the hematocrit

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46
Q

how many times a year should you monitor Hb in CKD3

A

once

47
Q

how many times a year should you monitor Hb in CKD 4-5ND

A

twice per year

48
Q

when should you monitor Hb in CKD 5D

A

every 3 months

49
Q

why do you monitor Hb in CKD patients

A

as a means to screen for anemia

50
Q

when would you diagnose anemia in females

A

Hb < 12 g/dL

51
Q

when would you diagnose anemia in males

A

Hb < 13 g/dL

52
Q

when would you suggest iron supplementation in patients with anemia

A

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

53
Q

when can you use oral iron in anemic patients

A

in stages 3-4 (only used for CKD patients or peritoneal dialysis patients)

54
Q

what dose of elemental iron must be given per day

A

200 mg

55
Q

what route is preferred for CKD 5D patients

A

intravenous

56
Q

which iron supplement requires a 25 mg test dose?

A

iron dextran (infed, dexferrum)

57
Q

what diagnostic test do you have to be careful with when patients are taking feraheme iron supplementation

A

magnetic resonance imaging (3 months after second injection)

58
Q

what does high molecular weight iron carry a higher incidence of?

A

anaphylaxis

59
Q

when do you start ESAs (erythropoiesis stimulating agents)

A

after all other correctable cause of anemia have been addressed

60
Q

when is it suggested to begin ESAs for CKD 3-5ND

A

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

61
Q

when is it suggested to begin ESAs for CKD 5D

A

start when Hb is between 9 and 10 g/dL

62
Q

as Hb increases the incidence of what adverse event also increases

A

cerebrovascular adverse events

63
Q

do not use ESAs to push Hb above what

A

11.5 g/dL

64
Q

what are the ESA drugs

A

epogen, aranesp, and mircera

65
Q

what are the adverse effects of the ESA drugs

A

pure red cell aplasia (antibodies develop to erythropoietin) and HTN

66
Q

what are the reasons that ESA therapy might fail

A
  1. lack of vitamins or iron
  2. aluminum toxicity
  3. active bleed
  4. drug induced bone marrow suppression
  5. acute inflammation or infection
67
Q

when do acid/base disorders arrise

A

usually when bicarb < 20 mEq/L

68
Q

ESRD patients cannot excrete H+ ions and develop what

A

metabolic acidosis

69
Q

what are the protein nutritional requirements for CKD 3 and 4

A

1.2 g/kg/day

70
Q

in what patient would you use water soluble vitamin replacement

A

for dialysis patients

71
Q

what is DKD and mechanism of action

A

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

72
Q

what is microalumineria

A

it is one of the best predictors of DKD

73
Q

how to treat DKD

A

SGLT2 inhibitors and metformin

74
Q

what GFR limit does treating microalbuminuria have

A

you can treat if GFR > 30

75
Q

what is an AV fistula

A

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

76
Q

what is an AV graft

A

an alternate to a fistula, the graft is created by surgically connecting an artery and vein with a polytetrafluoroethylene tube

77
Q

what are the indications of RRT

A 
(A, E, I, O, U) A: acid/base balance
E: electrolyte balance
I: intoxication
O: overload (fluid)
U: uremia
78
Q

what are the two goals of dialysis

A
  1. general rule is to initiate when BUN > 100, SCr > 10

2. removal of “middle molecules” such as beta2microglobulin, uric acid, creatinine, etc…

79
Q

what are the substances not removed in hemodialysis

A
  1. High Vd
  2. High lipophilicity
  3. Large molecular weight
  4. Highly protein bound
80
Q

what are the two ways you could measure the effectiveness of dialysis sessions

A 
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%
81
Q

what are some common complications of hemodialysis

A
  1. hypotension
  2. pruritus
  3. muscle cramps
82
Q

what is peritoneal dialysis

A

a form of dialysis that uses the peritoneal membrane as a dialysis membrane

83
Q

what is peritoneal dialysis mostly reserved for

A

pediatrics or ESRD patients already receiving PD

84
Q

what are the 4 different types of peritoneal dialysis

A

CAPD, CCPD, NIPD, TPD

85
Q

S/Sx of peritonitis

A
  1. cloudy effluent
  2. abdominal pain
  3. fever
  4. N/V
  5. Chills
  6. abdominal tenderness
86
Q

what is the predominant organism in peritonitis

A

staph epidermidis (40-50%)

87
Q

how to treat peritonitis

A

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*)
88
Q

what are the three routes that Tx can be administered

A

intraperitoneal, IV, oral

89
Q

what can you use IP route if peritonitis present

A
  1. infection is usually limited to the 1st few layer of the mesothelium, confined to the peritoneal cavity
  2. perionitis - N/V which can eliminate the oral route
  3. pts may have poor vascular access (that’s why they are on PD) so it would be prohibited
90
Q

what is CRRT primarily used for

A

acute renal failure

91
Q

why were contiuous renal replacement therapy developed

A

for patients who could not tolerate regular hemodialysis sessions

92
Q

can you use cockroft and gault in AKI patients

A

NOOOOOOOOOOOO

93
Q

why is CrCl not accurate in AKI patients

A
  1. it may be changing rapidly

2. other waste products build up out of proportion to SCr rise

94
Q

what are the two reasons someone can acquire AKI

A

Community acquired and hospital acquired

95
Q

what is azotemia

A

an elevation in nitrogenous waste products which leads to the clinical syndrome uremia

96
Q

what is prerenal azotemia

A

hypoperfusion of the kidney

97
Q

what is functional ARF

A

a decrease in the glomerular hydrostatic pressure which leads to a decrease in glomerular filtration rate

98
Q

what is functional ARF caused by

A

NSAIDs and ACE inhibitors

99
Q

what is acute intrinsic renal failure

A

damage to the kidney itself

100
Q

what is an example of a post renal obstruction

A

kidney stone

101
Q

what monitoring parameters do you look at in AKI (since you can’t look at SCr)

A
  1. patient’s weight
  2. blood pressure
  3. urine output
    a) acute anuria (<50 ml/24 hrs)
    b) oliguria (<400 ml/24 hrs)
    c) non-oliguria (>400 ml/24 hrs)
  4. urinalysis
    a) specific gravity (if high = prerenal)
    b) hematuria, proteinuria (intrinsic)
    c) microscopic examination ((+) for RBCs and casts = injury)
  5. FE(na) - fractional excretion of sodium
102
Q

what is the numerical difference between PR or functional AKI and intrinsic damage

A

if < 1% : PR or functional AKI

if >= 1% : intrinsic damage

103
Q

how do you prevent an AKI

A
  1. use less nephrotoxic agent
  2. hydration
  3. sodium loading
  4. identify patients at risk
    a) older adults
    b) patients with abnormal renal function or diabetes
104
Q

what are the goals of treating an AKI

A
  1. remove the primary cause of AKI
  2. limit further nephrotoxin exposure
  3. accelerate the recovery
105
Q

what is the supportive therapy for AKI

A
  1. if critically ill, may need insulin therapy
  2. 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
  3. Volume control
    a) CRRT
    b) diuretics (ONLY if urine output)
106
Q

what are the two common nephrotoxins emphasized in class

A

NSAID/Cox 2 inhibitors and ACEs/ARBs

107
Q

what is the MOA of AKI with NSAID/Cox 2 inhibitors

A

there is a decreased synthesis of renal vasodialator prostaglandins and afferent vasoconstriction resulting in reduced renal perfusion and filtration pressure

108
Q

is Tylenol AKI reversible

A

typically yes

109
Q

what is different about aminoglycoside AKI that other AKI

A

the rise in SCr usually occurs 5 - 10 days after the start of therapy

110
Q

how do ACEs/ARBs cause AKI

A

vasodilation of the efferent arterioles resulting in decreased filtration pressure, lowering GFR and urine ouput

111
Q

can PPIs (proton pump inhibitors) cause AKI

A

yes - by actue interstitial nephritis - its often reversible but can progress to CKD

112
Q

what is criteria for diagnosis of diabetes

A

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

113
Q

what is the basic understanding of Type 1 Diabetes Mellitus

A

lose the ability to secrete insulin in response to glucose

PHRM 844 (2 decks)

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