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PHAR123 > Chronic Kidney Disease > Flashcards

Chronic Kidney Disease Flashcards

1
Q

What is the definition of CKD?

A

abnormalities in kidney structure of function, present for 3 months or longer, and with implications for health

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2
Q

Which population is CKD more prevalent in?

A

the eldery

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3
Q

What is the classification system for CKD based mainly on?

A

GFR
albuminuria

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4
Q

What is the final stage of CKD?

A

end stage renal disease
-defined as GFR<15ml/min
-need dialysis or kidney transplant to live

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5
Q

What are the risk factors for CKD?

A

diabetes
high blood pressure
cardiovascular disease
obesity
family history of kidney disease
abnormal kidney structure
older age
smoking

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6
Q

What are the signs and symptoms of CKD?

A

signs and symptoms develop over time if kidney damage progresses slowly
nonspecific:
-nausea; vomiting; loss of appetite; fatigue and weakness;
sleep problems; changes in UO, decreased mental sharpness;
muscle twitches and cramps; swelling of ankles and feet;
persistent itching
-chest pain if fluid builds up around lining of heart
(pericarditis)
-shortness of breath if fluid builds up in lungs (pulmonary
edema)
-hypertension
ALL RELATED TO FLUID+WASTE BUILDUP

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7
Q

What are the classifications of CKD based on GFR?

A

G1 (normal-high): >90
G2 (mildly decreased): 60-89
G3A (mild-moderately decreased): 45-59
G3B (moderately-severely decreased): 30-44
G4 (severely decreased): 15-30
G5 (kidney failure): <15

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8
Q

What are the classifications of CKD based on albuminuria?

A

A1 (normal-mildly increased): <30
A2 (moderately increased): 30-300
A3 (severely increased): >300

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9
Q

What happens to prognosis of CKD as albuminuria and GFR get worse?

A

prognosis gets worse

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10
Q

True or false: CKD can be diagnosed without signs of kidney damage such as proteinuria

A

true
CKD can be diagnosed if:
GFR<60ml/min for at least 3 months (even without signs of kidney damage)
OR
if evidence of kidney damage such as proteinuria for at least 3 months (even if GFR>60ml/min)

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11
Q

Describe the kidney function for “normal”, the symptoms, and treatment options.

A

normal:
-kidney function: >60%
-symptoms: no symptoms observed
-tx options: identify cause and try to reverse it,
monitor albumin and GFR

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12
Q

Describe the kidney function for “mild”, the symptoms, and treatment options.

A

mild:
-kidney function: 45-59%
-symptoms: no symptoms observed
-tx options: monitor albumin and GFR, blood pressure, general
health and well-being, try to stop or slow down
the worsening of kidney function

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13
Q

Describe the kidney function for “moderate”, the symptoms, and treatment options.

A

moderate:
-kidney function: 30-44%
-symptoms: early symptoms may occur and could include
tiredness, poor appetite, and itching
-tx options: monitor albumin and GFR, and continue to try and
stop or slow down the worsening of kidney
function, learn more about CKD and tx options

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14
Q

Describe the kidney function for “severe”, the symptoms, and treatment options.

A

severe:
-kidney function: 15-29%
-symptoms: tiredness, poor appetite and itching may get
worse
-tx options: monitor albumin and GFR, and continue to try to
stop or slow down the worsening of kidney
function. Discuss and plan treatment choice:
dialysis access, assessment for transplant, or
information on non-dialysis supportive care

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15
Q

Describe the kidney function for “kidney failure”, the symptoms, and treatment options.

A

kidney failure:
-kidney function: <15%
-symptoms: severe fatigue, nausea, difficulty breathing, and
itchiness
-tx options: monitor albumin and GFR, and continue to try to
stop or slow down the worsening of kidney
function. Continue with non-dialysis supportive
care, plan for transplant or start dialysis

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16
Q

What are the potential underlying causes of CKD?

A

glomerular diseases
tubulointerstitial diseases
vascular diseases
cystic and congenital diseases

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17
Q

What are examples of systemic diseases that cause glomerular diseases?

A

diabetes
systemic autoimmune diseases
systemic infections
drugs
neoplasia

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18
Q

What are examples of systemic diseases that cause tubulointerstitial diseases?

A

systemic infections
autoimmune
sarcoidoisis
drugs
urate
environmental toxins (lead, aristolochic acid)
neoplasia (myeloma)

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19
Q

What are examples of systemic diseases that cause vascular diseases?

A

atherosclerosis
hypertension
ischemia
cholesterol emboli
systemic vasculitis
thrombotic microangiopathy
systemic sclerosis

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20
Q

What are examples of systemic diseases that cause cystic and congenital diseases?

A

polycystic kidney disease
Alports syndrome
Fabrys disease

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21
Q

How easy is it to identify CKD?

A

very difficult

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22
Q

Which stages of CKD are asymptomatic?

A

1 and 2

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23
Q

At what rate does GFR decline after the age of 20?

A

declines by 1ml/min/year in healthy people after the age of 20

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24
Q

What does the progression of CKD depend on?

A

depends on:
-cause of kidney disease
-GFR at time of diagnosis
-degree of albuminuria
-presence of comorbid conditions such as:
–>hypertension
–>diabetes
–>congestive heart failure
–>ischemic heart disease
–>COPD

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25
Q

What is CKD a result of?

A

CKD is a result of irreversible injury-nephrons are lost

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26
Q

What do the healthy nephrons in someone with CKD have to do?

A

remaining nephrons take on more filtrate to accommodate for the loss in nephrons

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27
Q

What is the result of healthy nephrons taking on more filtrate in someone with CKD?

A

damaging the remaining nephrons
hyperfiltration effect

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28
Q

What % of nephrons can be lost without clinical signs?

A

50%
thats why you can donate one kidney

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29
Q

What happens when 80% of nephron loss occurs?

A

some degree of azotemia occurs but may still be asymptomatic

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30
Q

What are the clinical manifestations of CKD?

A

accumulation of toxins (e.g., protein metabolite)
consequences of non-excretory functions (fluid/electrolytes, hormones)
progressive inflammation

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31
Q

What is uremia?

A

caused by numerous toxins
hundreds of toxins have been implicated

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32
Q

As loss of renal function progresses, what might be needed?

A

routine dialysis or kidney transplant

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33
Q

What is the clinical presentation of toxin accumulation?

A

symptoms: fatigue, weakness, shortness of breath, mental confusion, nausea and vomiting, bleeding, loss of appetite, itching, cold intolerance, and peripheral neuropathies
signs: edema, weight gain (from accumulation of fluid), changes in urine output (volume consistency), “foaming” of urine (indicative of proteinuria), and abdominal distension

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34
Q

What is the excretion of Na and water based on in healthy kidneys?

A

adjustments of Na and water excretion are based on intake

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35
Q

What are the fluid and electrolyte problems in CKD?

A

in CKD, adjustments are lost so intake of Na and water exceeds excretion
results in Na retention and ECFV expansion (edema or HTN)

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36
Q

How do the fluid symptoms associated with CKD progress?

A

initially, asymptomatic
eventually, can become very difficult to manage, contributing to heart failure, hypertension, edema, and weight gain

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37
Q

What is the use of diuretics in CKD?

A

reduce blood pressure and treat swelling (edema)

38
Q

At what GFR do thiazide diuretics often lose their effectiveness?

A

GFR below 30ml/min

39
Q

Which diuretics are preferred in CKD?

A

loop diuretics preferred but higher doses are often needed

40
Q

What is the drug combination for diuretic resistance?

A

loop diuretic + thiazide diuretic (metolazone)

41
Q

What is required for untreatable edema and HTN?

A

dialysis

42
Q

What is ESRD?

A

end stage renal disease
kidneys permanently fail to work

43
Q

How is ESRD diagnosed?

A

blood tests-blood cell counts, electrolyte levels, kidney function
urine tests
sonography (renal ultrasound)
CT scan
kidney biopsy

44
Q

What are the treatment options for ESRD?

A

dialysis: not cure
-peritoneal dialysis
-hemodialysis
kidney transplantation
-deceased/living donor kidney transplant
-pre-emptive kidney transplant (~20% of kidney transplants)

45
Q

What are advantages of pre-emptive kidney transplants?

A

lower risk of rejection
improved survival rates
improved quality of life
lower treatment costs
avoidance of dialysis

46
Q

What is the link between hypertension and CKD?

A

increased glomerular pressure
chronic glomerular hypertension can lead to hypertrophy of tissues and loss of nephrons altogether
elevated ANG II may promote tissue remodelling over time

47
Q

What is first line for HTN and CKD?

A

ACEI and ARBs (along with diuretics depending on volume issues)

48
Q

As CKD progresses, proteinuria will exceed ___.

A

1g/24hrs

49
Q

What is the implication of proteinuria on the kidneys?

A

promote additional loss of nephrons through direct cellular damage
proteins are toxic to tubular cells
caused increased production of inflammatory cytokines (attracting inflammatory cells)
damage leads to scarring, structural changes, and progressives loss of renal function

50
Q

How is proteinuria identified?

A

ACR (albumin to creatinine ratio)
protein dipstick
blood levels can decline in severe proteinuria

51
Q

What is the correlation between diabetes and CKD?

A

diabetes is associated with glomerular mesangial matrix expansion and renal vascular damage
often associated with HTN
glycated products (sugar coated molecules) somehow damage kidney structures directly

52
Q

What is a benefit to the kidneys on controlling glucose in people with diabetes?

A

slows the progression of CKD

53
Q

True or false: CVD and CKD are closely interrelated

A

true

54
Q

What are the risk factors in a CKD patient for atherosclerosis and heart failure?

A

hypertension
lipid
sympathetic nervous system tone

55
Q

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

A

anemia
high phosphate, high parathyroid hormone
generalized inflammation

56
Q

What is the bottom line with ACEI/ARBs in CKD?

A

benefit to kidney increases in people with more severe disease
in lower risk people other drugs appear to provide similar protection
some BP-independent benefits on kidneys are likely in higher risk situations
ACEI/ARBs are first line in patients with diabetes+nephropathy

57
Q

Which hormone serves to excrete K+?

A

aldosterone

58
Q

What causes hyperkalemia in CKD?

A

as tubules are lost, the ability to excrete K+ becomes more problematic
-distal tubules are the target for aldosterone

59
Q

At what GFR is hyperkalemia a serious problem?

A

<5ml/min

60
Q

What are the drug options for hyperkalemia?

A

K-wasting diuretics
minimization of K-sparing medications
potassium-binding resins
-sodium polystyrene sulfonate
-calcium polystyrene sulfonate

61
Q

Describe sodium polystyrene sulfonate.

A

used for hyperkalemia
bind potassium in GIT (in exchange for Na+)
supplied as powder, suspension, or rectal suspension
not absorbed
onset of effect is slow (days)
-should not be used as an emergency treatment for life-
threatening hyperkalemia

62
Q

Describe calcium polystyrene sulfonate.

A

used for hyperkalemia
binds potassium in exchange for Ca
not absorbed
dispensed as powder

63
Q

True or false: both calcium/sodium polystyrene sulfonate have the potential to bind to other orally administered medications

A

true

64
Q

What is normal arterial blood pH?

A

7.35-7.45

65
Q

What is the reaction that serves as a very important regulator of pH?

A

H + HCO3 <–> H2CO3 <–> CO2 + H2O

66
Q

Which organ maintains bicarbonate concentration?

A

the kidney at the proximal tubule

67
Q

How much bicarbonate is re-absorbed at the proximal tubule?

A

85-90%

68
Q

True or false: metabolic acidosis is common in advanced CKD

A

true

69
Q

Why is metabolic acidosis common in advanced CKD?

A

diminished capacity to excrete acid and generate base
day to day cellular metabolism produces large quantities of acid (much of which is CO2, as CO2 increases so does H)

70
Q

What are some acids that cannot be eliminated by respiration?

A

lactic acid (produced by anaerobic glycolysis)
ketones (fatty acid oxidation)
kidneys must eliminate these acids

71
Q

What are the two ways that H+ is eliminated?

A

secretion of H+ ions
-secreted into lumen directly
-combines with NH3 already circulating
secretion of NH4+ ions
-within tubular cells and secretion into tubular lumen

72
Q

What does circulating NH3 combine with?

A

circulating NH3 combines with CO2 in the liver to form urea

73
Q

Describe urea.

A

odorless and colourless
highly soluble in water
easily excreted by kidney

74
Q

Which foods contain nitrogen?

A

meats
fish
potatoes
milk
eggs
cereals
legumes

75
Q

What is metabolic acidosis characterized by?

A

decreased pH
decrease in HCO3
PaCO2 is normal

76
Q

Metabolic acidosis is normally mild in CKD until GFR ___.

A

<20ml/min

77
Q

How does the kidney play a role in calcium homeostasis?

A

activation of vitamin D
in addition to low serum calcium, the kidneys fail to excrete phosphate

78
Q

What are the management strategies for Ca/phosphate disorders in CKD?

A

decrease phosphorus in diet
phosphate binding agents such as Sevelamer
calcitriol

79
Q

How is PTH secreted?

A

parathyroid gland senses level of calcium in blood
if Ca 2+ falls, the gland secretes PTH

80
Q

What are the effects of PTH?

A

kidney
-promotes renal tubular calcium reabsorption
-promotes phosphate excretion
-production of 1, 25-dihydroxyvitamin D
bones
-promotes catabolism of bone to release calcium and
phosphorus

81
Q

What are some common vitamin D products?

A

alfacalcidol
-requires conversion to calcitriol in liver
calcitriol
-active
cholecalciferol
-synthesized in skin, requires 2 step activation
-fatty fish, fish oils
ergocalciferol
-occurs in nature (wild mushrooms)
-similar to D3 as it requires 2 step activation

82
Q

How are the kidneys involved in regulation of RBC production?

A

contain specialized cells that detect low oxygen levels
-hypoxia-induced erythropoietin production
-act as a critimer to maintain hematocrit

83
Q

What is the hematocrit?

A

ratio of volume of red blood cells to the total volume of blood
-men 47 +/-5%
-women: 42 +/- 5%

84
Q

What is erythropoietin?

A

naturally occurring hormone that stimulates the bone marrow to produce more RBC

85
Q

At what GFR does anemia often begin?

A

<30-45ml/min
present in virtually all patient with ESRD

86
Q

What are some erythropoiesis-stimulating agents?

A

epoetin alfa (recombinant EPO with same amino acid sequence)
darbepoetin alfa (modified amino acids for longer duration of action)

87
Q

What are some adverse effects of increasing RBC production?

A

hypertension or thrombosis

88
Q

Approximately half of patients with GFR ___ are at risk for ___.

A

<60ml/min
ADRs

89
Q

What are some PK and PD considerations in CKD?

A

increased Vd in moderate to severe CKD
metabolite accumulation
non-renal clearance
loading dose
maintenance dose
serum drug monitoring

90
Q

What are the risk factors for CKD patients and ADRs?

A

Age
ACEI/ARB usage
Diabetes
Advanced CKD

PHAR123 (15 decks)

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