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PHAR 123 > Chronic Kidney Disease > Flashcards

Chronic Kidney Disease Flashcards

1
Q

What are the major functions of the kidneys?

A

Excretion of waste
Fluid balance
Electrolyte balance
pH balance
Calcium homeostasis
REgulation of RBC production

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2
Q

What is End stage renal disease defined as?

A

GFR < 15mL/min
need dialysis or kidney transplant o live

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3
Q

What is used to classify CKD?

A

GFR and Albuminuria

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4
Q

How long must an abnormaility in kidney structure or function be present that has health implications exist to be CKD

A

3 months or longer

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5
Q

What are risk factors of CKD?

A

diabetes
high BP
heart and blood vessel disease
obesity
family history
abnormal kidney structure
older age
smoking

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6
Q

How to symptoms and signs of CKD develop?

A

slowly; nonspecific hard to notice as it can be asymptomatic, can’t feel pain in kidneys.`

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7
Q

What does rhabdomyolysis cause in kidneys?

A

tubular necrosis

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8
Q

What is the GFR of G1?

A

> 90 mL/min
Normal/ high

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9
Q

What is the GFR of G2?

A

60-89 mL/min
Mildly decreased

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10
Q

What is the GFR of G3a?

A

45-59 mL/min
midly to moderately decreased

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11
Q

What is the GFR of G3b?

A

30-44 mL/min
moderately to severly decreased

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12
Q

What is the GFR of G4?

A

15-29 mL/min
severely decreased

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13
Q

What is the GFR of G5?

A

<15 mL/min
Kidney failure

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14
Q

What is the albumin:Creatinine ratio of A1?

A

< 30 mg/g
normal to midly increased

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15
Q

WHat is the albumin: creatinine ratio of A2?

A

30-300 mg/g
moderately increased

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16
Q

What is the albumin: creatinine ratio of A3?

A

> 300
severely increased

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17
Q

What paramaters are needed to diagnose CKD without signs of damage to the kidneys?

A

A GFR of < 60mL/min for atleast 3 months

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18
Q

Can CKD be diagnosed with a GFR > 60mL/min?

A

Yes, if evidence of kidney damage; proteinuria present for at least 3 months

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19
Q

What is needed if their is a loss of renal functions resulting in the build up of toxins?

A

Dialysis; Kidney transplant

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20
Q

What are symptoms of toxin build up?

A

Fatigue, weakness, shortness of breath, loss of apetite, cold intlerance

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21
Q

What are some signs of toxin build up?

A

Edema, weight gain, urine output change, abdominal distension, foaming of urine

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22
Q

At what GFR do thiazide diuretics lose their effectiveness?

A

less than 30 mL/min

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23
Q

What is ESRD?

A

End stage renal disease; kidneys permanently fail to worke

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24
Q

What are the treatment options for ESRD?

A

Dialysis treatment; peritoneal and hemodialysis
Kidney transplant is “curative” option

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25
Q

What kidney transplant makes up ~20% of kideny transplants and has a lower risk of rejection and improved survival rates as well as quality of life, lower treatment costs, and avoidance of dialysis?

A

Pre-emptive kidney transplant

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26
Q

How can hypertension contribute to CKD?

A

Increased glomerular pressure leading to damage
increased ANG2 promoting tissue remodeling
glomerular dysfunction leading to protein leakage

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27
Q

What are first line agents for Hypertension CKD?

A

ACEI or ARBs usually paired with a diuretic

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28
Q

How does proteinuria contribute to CKD progression?

A

Promotes additional loss of nephrons via direct cellular damage.

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29
Q

T or F. Proteins are toxic to tubular cells.

A

True

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30
Q

What can additional damage from proteinuria lead to?

A

Cause increased production of inflammatory cytokines and damage can lead to scarring, structural change, and progressive loss of renal function.

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31
Q

How can proteinuria be identified?

A

Albumin to creatinine ratio
Protein dipstick
Blood levels can decline in severe proteinuria

32
Q

How can daibetes impact CKD?

A

Glycated products can damage kidney structure directly

33
Q

How can CKD progression be slwoed in daibetes?

A

Glucose control

34
Q

What is the leading cause of death in all stages of CKD?

A

Cardiovascular disease

35
Q

What are non-traditionalrisk factors that appear to accelerate risk of atherosclerotic cardiovascular disease?

A

Anemia
High phosphate, high PTH
Generalized inflammaton

36
Q

What lower baseline correlates with overall reduced risk for ESRD?

A

SCr; lower albumin excretion

37
Q

What is a first line agent for CKD in patients with diabetes and nephropathy?

A

ACEI / ARBs

38
Q

At what GFR does hyperkalemia become a serious problem?

A

below 5mL/min

39
Q

What are some options for hyperkalemia treatment?

A

K-wasting diuretics
Potassium-binding resins
Sodium polystyrene sulfonate
Calcium polystyrene sulfonate
Minimal use of K-sparing diuretics/ medications
Altering diet; less K intake

40
Q

How does Sodium polystrene sulfonate work?

A

Binds K in GI tract in exchange for Na
Onset of effect is slow, not an emergency treatment

41
Q

What is the dosing of Sodium polystrene sulfonate? Dosage forms?

A

15-60 g per day, 100mg Na per 1 g drug
Powder, suspension, or recatal suspension

42
Q

How does Calcium polystrene sulfonate work?

A

Binds K in GI tract in exchange for Ca

43
Q

What is the dosing for calcium polystrene sulfonate?

A

15g, 3-4 times a day

44
Q

What is an issue with both Na/Ca polystrene sulfonates?

A

Borh have potential to bind to other orally administered medications

45
Q

What would be the emergency treatment for hyperkalemia?

A

Hemodialysis

46
Q

where is 80-90% of bicarbonate produced?

A

Kidneys

47
Q

What is the effect of CKD on bicarbonate?

A

Less production, causing metabolic acidosis from increased protons in the body

48
Q

What 2 factors are seen in CKD that cause acidosis?

A

diminshed capacity to excrete acid and diminished capacity to produce base

49
Q

What is the acid produced through metabolism?

A

Carbon dioxide

50
Q

What increases with carbon dioxide?

A

Hydrogen; protons

51
Q

What does Carbon dioxide retention in the lungs cause?

A

Respiratory acidosis

52
Q

How do the kidneys excrete “fixed acids”

A

Secretion of H ions that combine with NH3 to form NH4+ that is then secreted into tubular lumen

53
Q

what are 2 examples of fixed acids?

A

Lactic acid
Ketones

54
Q

What do NH3 and Co2 combine in the liver too?

A

Urea

55
Q

What characteritics does urea have that make it ideal for excretion?

A

odourless and highly soluble in water making it easily excreted

56
Q

What are the effects of pH, bicarbonate, and PaCO2 in metabolic acidosis?

A

pH decrased
bicarbonate decreased
PaCO2 normal

57
Q

What are the effects of pH, bicarbonate, and PaCO2 in respiratory acidosis?

A

pH decrased
bicarbonate normal
PaCO2 increased

58
Q

What are the effects of pH, bicarbonate, and PaCO2 in respiratory alkalosis?

A

pH increased
bicarbonate normal
PaCO2 decreased

59
Q

What are the effects of pH, bicarbonate, and PaCO2 in metabolic alkalosis?

A

pH increased
bicarbonate increased
PaCO2 normal

60
Q

at what GFR is metabolic acidosis no longer “mild”

A

<20mL/min

61
Q

What is the risk of using sodium bicarbonate to manage bicarbonate levels?

A

Sodium load becomes a risk

62
Q

How do the kidneys play a role in Ca homeostasis?

A

Through its role in activating Vitamin D

63
Q

With low Ca serum levels what else does the kidnet fail to excrete?

A

phosphate

64
Q

How can Ca/phosphate disorders be managed in CKD?

A

Decrease in phosphorous in diet
phosphate binding agents (sevelamer)
Calcitriol

65
Q

what does low Ca cause the parathyroid gland to excrete?

A

PTH

66
Q

How does PTH effect the kidneys?

A

Promote renal tublar Ca reabsorption
Promote phosphate excretion
stimulate production of 1,25 - dihydroxyvitamn D

67
Q

What does PTH stimulate in the bone?

A

Promotes catabolism of bone to release Ca and phosphorous into bloodstream

68
Q

What does the combination of low Ca and reduced Vitamin D level cause?

A

Increased PTH release.
As PTH increases only Ca source is bone causing accelerated bone loss

69
Q

What vitamin D product does not require activation; is already active?

A

Calcitriol

70
Q

What major structural changes happens to the glomerulus in diabetic patients?

A

change of podocytes
expansion of mesangial matrix
renal vascular damage

71
Q

What does EPO regulate?

A

stimulation of bone marrow to ONLY produce more RBC’s
NO lymphocytes or hormones

72
Q

What happens to the hematocrit in CKD patients?

A

Decreased; decreased RBC’s

73
Q

What is often given for anemia in CKD along with EPO replacement?

A

Iron supplements

74
Q

at what GFR can anemia often begin at?

A

when GFR falls below 30-45mL/min

75
Q

Why anemia treatment closely monitored (hemoglobin levels)

A

Increased RBC production can result in hypertension or thrombosis

76
Q

What can happen if there is poor disease recognition?

A

lapses in patient saftey

77
Q

what pharmacokinetics and pharmacodynamics need to be considered in CKD?

A

increased volume distribution in moderate to severe CKD
Metabolite accumulation
non-renal clearance
loading dose
maintenance dose
serum drug monitoring

PHAR 123 (18 decks)

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